NCM 112: NGIMPEC LECTURE NOTES

Lesson 1: ALTERED LEVEL OF  Delirious: patient is restless and

CONSCIOUSNESS disoriented to time, place, and person.
Confusion with periods of agitation
Symptoms of metabolic and psychogenic
alternating with depressed arousal.
problems
 Obtunded: patient is having mark
psychomotor retardation but can still
Consciousness
be awakened. Marked decrease
- State of awareness of self and
arousal with some response to touch or
environment.
voice.
Level 3: Stuporous, responds only to
LEVEL OF CONSCIOUSNESS
noxious stimuli.
- subjective
- Sensitive indicator of neurologic status  Stuporous: can only be aroused using
- We can subjectively describe and strong (pain) stimuli. Using a strong or
perform it. loud sound but if not responsive to this,
- Consciousness is a state of awareness we will be using pain stimulation.
and arousal is controlled by reticulo- Patient will be asleep all the time but
activating system of the reticular maybe be awakened if pain stimuli is
formation of brain stem given.
- Cognitive ability or awareness of self
and environment including the affective  Types of Stimuli:
stage is controlled by cerebral cortex.
- Brain stem and cerebral cortex are parts 1. Trapezius pinch
of the brain which maintain level of - Central stimulation
consciousness - Pinch about 2 inches of the
muscle.
Level 1: Conscious, Coherent, and - Involves the gripping or twisting a
Cognitive portion of trapezius muscle in the
patient’s shoulder.
 Awake, coherent, and able to think
- If the patient opens his eyes to
clearly.
this stimulation it will be a score
 Whatever factor that will affect the LOC,
of 2.
it will descend down. LOC is a
descending continuum.
Level 2: Confused, Lethargic or
Somnolent, Delirious, and Obtunded.

 Confused: awake but disoriented to

time, place and person. You have to
ask about the time, place, and person.
Impaired attention but adequate
arousal to perform simple mental tasks.
 Lethargic or somnolent: the patient is
drowsy, sleeps all the time, but if 2. Supraorbital pressure
stimulated he/she can still be - Central stimulation
awakened. Mildly depressed LOC or - Apply pressure on the
alertness. Someone in this state can be supraorbital area of the patient.
aroused with little difficulty. Somnolent - This is a manual stimulation of
means sleepiness, the state of feeling the supraorbital nerve by
drowsy, ready to fall asleep. s pressing a thumb into the

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indentation above the eye, near organized response to stimuli. GCS of
the nose. 8 down to 4 is light coma.
- If patient responds by opening his  Deep Coma: no response to internal
eyes, this will be a score of 2 and external stimuli

GLASGOW COMA SCALE

 Most objective assessment of level of
consciousness.
 Used in 1974 to assess LOC after head injury.

3. Sternal rub
- Central stimulation
- Involves creating and turning
pressure (akin to grinding motion
with a pestle and mortar) on the
patient’s sternum.
- Performed by rubbing the
knuckles of a closed fist firmly
and vigorously on the patient’s
sternum. Because the stimulus is
applied to the core of the body-
central painful stimulus. Eye Opening
- Check in other institutions
because some do not use this  Used a s a reflection of the intensity of
especially on elders because this impairment of activating functions.
might cause fracture. Eye Opening
Spontaneous (even
4 if simple approach)

To sound (responds
after calling the
3
patient)

To Pain (after
2 painful stimulus is
applied
1 No response

Verbal Response
4. Peripheral (nailbed) stimulation
- Apply pressure to the edge of the  Index of higher cortical function
finger, just below the Verbal Response
interphalangeal joint. DO not Oriented to time,
apply pressure directly over the person, and place
nail bed. 5
(orientation to 3
spheres)
Level 4: Coma
Confused (he
 Light Coma: response by grimace, answers with
4
withdrawing limb from pain, primitive confusion)

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 NCM 112: NGIMPEC LECTURE NOTES
Inappropriate
words (patient
3 answered with
inappropriate words)

Incomprehensible
sounds (patient
2 produces sounds
that cannot be
understood)
No response
(normal for patients
1 with endotracheal
and tracheostomy
tube)

Motor Response
- Best motor response is knowing
the integrity of the nervous
system in patients who are not
speaking.
Motor Response
6 Obeys command (if
patient is paralyzed with
1 ext. if only 1 is raised
score him 6)
5 Localizes pain (patient
attempts to push the
examiner when pain is
stimulated, he knows
where the pain is)
4 Normal Flexion (flexion
of elbows)

3 Abnormal flexion
(decorticate posturing:
flexes arms at the elbow
with inward rotation of the
wrists, extension of lower
extremities, and plantar
flexion)
Rubrospinal tract is a descending tract
2 Abnormal extension Tegmentum is located at the mid brain
(decerebrate posturing:
all four extremities are Two Parts of decorticate posturing
extended with 1. Flexion of the elbow because of the
hyperpronation of the
disinhibition of red nucleus and facilitation
hand, and plantar flexion)
of rubrospinal tract or the flexion found at
1 No response
(compression is at the cervical spinal cord supplying the flexor
medulla oblongata) muscles of the upper ext.

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2. Extension of lower extremities due to
disruption of lateral corticospinal tract
which facilitates motor neurons in the lower
spinal cord supplying flexor muscles of the
lower ext.

In the case of ICP, the compression is at

the mid brain the patient will decorticate, if
the compression is going down at the brain
stem the patient will decerebrate (more
severe) and when it reaches the medulla
oblongata there are no more responses.
- The blue one, (located in the brain
Decerebrate posturing indicates brain stem stem) this is called the “reticular
damage, specifically below the level of the red formation (RF).” this is a circuit that
nucleus (mid-collicular lesions). It is exhibited helps to coordinate the activity of
by people with lesions or compression in the neurons in these cranial nerve nuclei,
mid brain and lesions in the cerebellum. and thus is involved in the regulation of
simple motor behaviors.
- For example: the reticular formation
neurons in the medulla facilitate motor
activity associated with the vagus nerve
(CN#10, that is responsible for the
cardiovascular functioning)

> Brain stem - The life center, because the

SCORING reflexes for survival are located here.
>Pons-respiratory center located here and
Score Indication upper medulla oblongata
>Medulla oblongata- CN# 10 that is
3-8 Deep coma
responsible for cardiovascular system.
>Thalamus - (part of diencephalon) that relay
6-8 Light Coma
the motor and sensory information. This
serves as the triage area
*Consciousness involves (part of the brain
that is responsible for arousal and content Note:
of thought) - it is possible that if the cerebral cortex is
1. Arousal (RAS) damaged but the brain stem is still intact, your
- State of awakeness patient can still survived (but without ability to
- It is in the brain stem, the reticular think)
activating syste, scattered all throughput
the brain stem in the reticular formation.
2. Content of thought
- Cerebral cortex
- Responsible for cognition/ability to think
clearly.
- Encompasses all cognitive functions
including awareness of self,
environment and affective states

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- the reticular activating system which is

the network that is scattered all through
out the brain stem that is responsible for
the interpretation of the information.
They are scattered diffusely from the
midbrain down to the medulla oblongata.
- This is the one that convey the impulses
connecting the brain stem, cerebellum
and the cerebral with the ascending and
descending tracts.
- This is the network that will convey the
information to the thalamus.
- When the sensory reaches the reticular
formation, it activates or arouses the
cerebral cortex for interpretation of these
impulses/information

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 NCM 112: NGIMPEC LECTURE NOTES
- this is the work of the network
*STATE TO THE LEVEL OF ALTERED
CONSCIOUSNESS
1. Coma:
- Deep coma: Total absence of
awareness
- The patient is in coma for a period of 2
to 4 weeks and after that it is replaced
by another state of the altered level of
consciousness
- was forming a pyramid.
2. Persistent Vegetative State (sleep-wake
cycle)
- Crude waking state maintained by the
RAS (only) when a person loses
cerebral function
- Sleep-wake cycles devoid of cognitive or
effective mental function but can still
survived
- The patient can still eat, breathe,
eliminate. The basic function of life will
maintained with the intact brain stem. It
is just that, the patient will be devoid of
thinking, cognition or defective mental
function.
3. Locked-in Syndrome (pseudo-coma)
- The patient is in Complete paralysis
(upper and lower extremities) of
voluntary muscles in all parts of the body
except for those that control eye
movement.
- The patient can here you but cannot
speak.
- The patient still has eye movement due
to CN-III and CN-IV which are still intact
in the Mid brain
- CN# 6 - located in the pons
NCM 112 NGIMPEC LECTURE NOTES
- Conscious, can think, can reason, but
unable to speak and move
- Caused by any damage in the pons
- The cause of the lock-in syndrome is the
infarct after a stroke in the pons. But the
Cranial nerves in the midbrain is still
intact (CN # 3 and 4). But there might be
a problem in the lateral movement
because CN#6 is located in the pons
- Cortocospinal tract, which is your
descended tract coming from the left
and right cerebral cortex.it is a pyramidal
tract. It is going to converge at the
middle in the internal capsule, located in
the deincephalon and it will go down to
your brain stem. From the mid-brain,
down to the medulla oblongata. And
there at the medulla oblongata, this
corticospinal tract will cross
(decussation). This means that the left
corticospial, will descent to the right
spinal cord and vice versa.
o In the medulla oblongata, in here, it
o This corticospinal tract, carries the
voluntary motor functioning that will
descend down to the different
segment of the spinal cord (anterior
and lateral of the cervical spine )
o To the thoracic lumbar spine,
lateral and anterior
o To the lumbar spine, lateral and
anterior
o Example: when there is a tumor
that is located in the pons, this tract
may be affected. This cannot
function anymore, as is it going to
descend down to the spinal cord.
This is the reason why there is a
paralysis for the lower and upper
extremities.
- Causes: can be use of the drugs, heroin,
abscess, infection and tumours.
4. Akinetic mutism
- A - means is absence
- Kinetic - means is movement
- Mutism - means is unable to speak
- Damage to frontal lobe of the brain
- Unable to speak and move
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 NCM 112: NGIMPEC LECTURE NOTES
- With intact LOC and sensorimotor
capacity but with a simultaneous
decrease in goal-directed behavior and
emotions
- The patient is unable to move, speak but
is awake with profound apathy.
- In a wakeful state of profound apathy,
seemingly indifferent to pain, thirst, or
hunger.
- This can cause expressive aphasia.
*Causes of the different level of Alterations
in Arousal/ consciousness
> 3 major categories: (35:43)
- Structural | Metabolic | Psychogenic
I. Structural Causes
1. Infections: ex. Encephalitis - abscess or
infection inside the brain may cause
compression in the other structures
within the brain. This may result to
increase intracranial pressure.
2. Vascular causes: ex. CVA /stroke
because blood vessel can be occluded or
rupture
o stroke is a vascular problem
because the blood vessels
can be occluded by a clot or it
may rupture. If occlusion may
occur, it may cause ischemic
stroke .
o if there is rupture, it may
cause bleeding or
hemorrhagic stroke
o these problems may increase
the intracranial pressure and
will alter the level of
consciousness
3. Neoplasms: tumors, these are space
occupying lesions that will cause
compression of structures in the brain
causing increased ICP and altered LOC
4. Trauma: like car accidents
o due to the accidents, the patient
may bleed and can cause
hematoma formation inside the
brain causing the increased ICP
and alter the level of
consciousness.
NCM 112 NGIMPEC LECTURE NOTES
5. Congenital:ex. congenital hydrocephalus
- there is an obstruction of pathway of the
flow of the cerebrospinal fluid, increasing
CSF volume which causes increased ICP
and altered LOC
6. Degenerative disorders : ex.
Huntington’s chorea and the Parkinson’s
disease
II. Metabolic
1. Hypoxia: decreased oxygen
- conditions that can result to hypoxia
will going to have an altered level of
consciousness
2. Electrolyte imbalance: ex. Diabetes
insipidus (decreased antidiuretic
hormone) and SIAHD (increased
antidiuretic hormone) both results to
increased urine output.
> diabetes insipidus - thirst is one of the
manifestation because there is a poly
urea.
- There a deficiency in the secretion of
the antidiuretic hormone which is
secreted in the posterior portion of the
pituitary gland.
- antidiuretic hormone - is a hormone
for the retention of the fluid
- in here, water is lost by excessive
urination
- the patient need to drink plenty of
water
- along the water which is lost through
urination, sodium may loss as well.
- where the water is, the sodium follows
- remember, sodium and water are
necessary for the blood volume
expansion. In this case, the blood
volume is depleted and this can cause
hemoconcentration. This can result
to many problems like seizure and
altered level of consciousness
> SIAHD (Syndrome of inappropriate
antidiuretic hormone secretion) – there is
increased level of antidiuretic hormone
- due to this, there is a retention of water
in the tissues
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 NCM 112: NGIMPEC LECTURE NOTES
- the water will go into the tissues and the Blink Equal Asymmetric
sodium also. This is will cause dilutional
hyponatremia Optic Discs Flat, good papilledema
- the tissues that has a plenty of fluids will pulsation
swell and may result to cerebral edema EOM (CN III, Roving eye Gaze
IV, and VI) movements, paresis;
that may alter the level of
normal doll’s nerve palsy
consciousness. This can cause the
eye, calorics
increase of ICP Pupils CN II Equal, Asymmetric;
>These two condition are usually result to the and III reactive, non-
intracranial surgery and complication of the dilated reactive;
increase intracranial pressure. (atropine); mid-position
>whenever you have a problem to the pinpoint (midbrain);
hypothalamus, to the vascular supply to the (opiates); mid- pinpoint
hypothalamus and pituitary gland, this will position/fixed (pons)
complications occurs (glutethemide)
Corneal reflex Symmetric Asymmetric
3. Hypoglycemia: in DM, reversible
Grimace to Symmetric Asymmetric
complication
pain CN VII
- Hypoglycemia - decreased blood
Motor Symmetric Asymmetric
glucose
- Normal level of blood glucose: 60- Tone Symmetric Spastic
100 mg/dl flaccid
- Hypoglycemia – blood glucose Posture Symmetric Decorticate
level of 40 and below Decerebrate
- This is usually occurs in the
patient’s with DM, this is one DTR Symmetric Asymmetric
reversible complications in which
the patient can go to coma Babinski Symmetric/ Present
- Severe hypoglycemia is absent
Sensation Symmetric Asymmetric
manifested by the neurologic
manifestation such as loss of
consciousness. Blink
- DKA (Diabetic ketoacidosis) and
- Sensory: CN V Trigeminal (pons)
HHNK (Hyperglycemic
specifically the ophthalmic branch
hyperosmolar nonketotic diabetic
- Motor: CN VII Facial (pons), also has
coma) – these 2 are the
sensory function which innervates at the
reversible/short-term
anterior 2/3 of the tongue for sense of
complications of DM that will
taste.
cause coma
- Open the eyes with the wisp of a cotton,
- Coma caused by DM, DKA, HHNK then the sensation is felt by the client it
are reversible if immediate
is the innervation of CN V and the blink
intervention is given of the client is innervated by the CN VII.
4. DRUGS - Metabolic: equal in both eyes
5. Toxins: like in Parkinsonism - Structural: unilateral or in one eyes

III. Psychogenic
1. Psychiatric problems Optic discs
- The head of CN II or Optic for sense of
Manifestations Metabolic Structural vision, located at the retina of the eye at
the cerebral hemisphere.

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 NCM 112: NGIMPEC LECTURE NOTES
- Using an ophthalmoscope, the optic disc
is seen as a physiologic cap at the
center about 1.5cm pinkish to orange.
- Metabolic: flat with good pulsation
- Structural: papilledema or swelling of
the optic disc. Example, increases ICP
you can have unilateral papilledema,
early sign of increased ICP
EOM (CN III, IV and VI
- CN III and IV are located at the midbrain
and VI is at the pons
- CN III movements of the eye up and
inward
- CN IV depression of the eye
- CN VI is lateral outward
- Metabolic: Roving eye movements,
normal doll’s eye (Special examinations
especially for unconscious patients),
calorics. Eye movements are present in
both eyes.
a. Doll’s eye phenomenon or
oculocephalic reflex test
o Check for cervical spine fracture
because we cannot perform this if
there is due to involvement of head
movement.
o Open the eyes of the unconscious
client using your two fingers then
observe the movement of the eyes
as you move the head up.
o Normal: when you move the head
up the eyes will move the eyes
downward in conjugate or parallel
manner (move at the same time),
when you move the head down the
eyes will move upward, if you move
the head to the left, the eyes will
move towards the right, if you move
the head to the right the eyes will
move to the right. So that, with
movement of head, you have
opposite direction movement of the
eyes, but it must be parallel.
o Abnormal: take note for paralysis in
the movement of the eyes. If there
is, it is structural
b. Eyes or cold caloric testing
o Prepare cold water in a syringe
o Position client at 60-degree angle,
almost sitting (to drain out the
NCM 112 NGIMPEC LECTURE NOTES
water), open up the eyes of the
unconscious client instill cold water
in ear to the auditory canal
o Normal: observe movement of eyes
which will normally go to where the
stimulus is, where you instill the cold
water in conjugate manner and
rapidly it will move away from the
stimulus in rapid, jerky motion or
nystagmus.
o Abnormal: paralysis, weakness,
and fixation of the pupil.
- Structural: Gaze paresis (weakness of
the gaze); nerve palsy (paralysis)
CN II and III
- Using penlight, assess for equality of the
pupil by striking the light at the temporal
side, not directly to the eyes
- Assess the pupil’s reaction and equality
to light
- CN III will constrict the pupil and located
at the mid brain. Vulnerable to
compression due to its location which is
anterior to the midbrain
- Check for direct and consensual
constriction
- Metabolic: briskly reactive to light.
Equal, reactive, dilated (atropine);
pinpoint (opiates); mid-position/fixed
(glutethemide). You need to find cause
through thorough history of medications
because if there will be an overdose of
atropine sulfate, pupils will be dilated.
Without structural lesions, pupils are
dilated. If there is overdose of narcotics
or opiates, pupils can be pinpoint. If
there is glutethemide overdose, pupils
will be fixed or in mid-point.
- Structural: inequality of the pupil
(anisocoric) only one pupil responds to
the light, asymmetric; non-reactive
(paralysis of CN III); mid-position or fixed
at the middle which can be unilateral or
bilateral (midbrain paralysis of CN III
paralysis); pinpoint (paralysis in pons)
Corneal Reflex
- Strike the light at the nasal bridge and
the light be reflected in both eyes.
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 NCM 112: NGIMPEC LECTURE NOTES
- Metabolic: light is symmetrically
reflected in both eyes
- Structural: light is asymmetrically
reflected in the eye (unilateral).
Grimace to pain CN VII
- CN VII facial, motor to facial expression
- Metabolic: symmetrical facial
expression and motor movement
- Structural: asymmetrical facial
expression, e.g. bels palsy, defect in CN
VII where you only have paralysis of one
side of the face, and asymmetrical motor
movement
Muscle Tone
- Firmness of the muscle, in a relaxed
face muscle are normally contracted
- Metabolic: symmetrical firmness of the
muscles
- Structural: hypertonicity (spastic), hypo
tonicity (flaccid)
Posture
- Metabolic: symmetrical and no problem
- Structural: Increased ICP- if you
perform GCS you will see decorticate
scored 3 (abnormal flexion, flexion at
the elbows, internal rotation of the
wrists, extension of the lower extremities
and plantarflexion where there is
interruption of the red nucleus and
facilitation of rubrospinal tract which
facilitates the flexion of the upper
extremities and disruption of the
corticospinal tract where you have the
extension of lower extremities) or
decerebrate scored 2 (abnormal
extension, four extremities are extended
with hyperpronation of the hand
plantarflexion which is also a problem in
the corticospinal tract passing along the
brainstem)
DTR
- Metabolic: reflexes are symmetrically
functioning
- Structural: Asymmetrical dysfunction of
these muscle stretch reflexes
Babinski
- Using the handle of the reflex hammer
stroke an inverted J on the patient’s foot.
NCM 112 NGIMPEC LECTURE NOTES
- Metabolic: Normal flexion of the toes
- Structural: Presence of fanning of the
toes and dorsiflexion of the big toe
(related to upper motor neuron lesion
which is the corticospinal tract)
Sensation
- Metabolic: Function of parietal lobe is
symmetrically present
- Structural: asymmetrically abnormal, it
may not be present in one side or
unilateral only.
CARE OF THE UNCONSCIOUS CLIENT
- Generalized whether it is metabolic or
structural cause
A. AIRWAY: maintain patency
1. Side lying position
o Patient’s reflex for swallowing may
be loss.
o Prevent aspiration of secretions and
saliva.
o Allow the tongue to fall because it
may obstruct the airway.
2. Oral airway if tongue is obstructing
o Made of plastic which is curved, fit
inside the mouth to keep the mouth
open and keep the tongue that
obstructs the airway
o If you do the suctioning, just do it at
the sides, lower and upper portion
o This one is a hollow at the center,
you may insert suction tip in there at
the opening.
3. Prepare ET insertion
o Check for airway patency always if
the patient needs the ET tube or
tracheostomy tube insertion to keep
the airway patent
o May be attached to mech. Vent. Or
respirator.
4. Suction PRN
o To remove secretions to keep the
airway patent
o The patency of the tube is ensured
by suctioning it at a specific times
PRN if not contraindicated
o But if with ICP suctioning is
scheduled because this may trigger
the gag reflex which can cause
coughing that will increase ICP.
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5. Check RR, depth q1-2h
o Check and assess as often as 1-2
hours to check if the patient is still
breathing to make sure that the O2
delivery is adequate to the cerebral
tissues.
6. Auscultates BS for crackles, rhonchi
o In an unconscious client one of the
problems that arise is pneumonia
that is why we need to assess the
respiratory status always.
o We need to check for adventitious
breath sounds like crackles and
rhonchi which is a sign of
pneumonia
o PNA develops because the client is
lying on the bed all the time so lungs
are not expanded efficiently and
secretions accumulate which may
be good for growth of
microorganisms.
o If patent is immobile may develop
thrombus formation on the small
blood vessels like the vein which
can cause DVT, or clot formation
which can cause obstruction to the
flow of the blow through the veins
which can cause decrease venous
return to the heart. It may be
dislodged and becomes an
embolus, it may travel to the heart
and pulmonary artery to the lungs
causing pulmonary embolism.
B. VS and Neuro Checks
- In clinical area there is a form in neuro
and vital signs monitoring where you are
going to document the neuro VS.
- Very often as every 5-15 minutes
especially to unconscious clients.
- Check the VS and GCS and document,
check the pupillary size, document the
reaction to light.
C. Fluid and Electrolyte Balance/ Nutrition:
1. IVF, NGT feedings as ordered
o Monitor the IV rate and the NGT
feedings as ordered
o Precaution in NGT feeding for
unconscious client, we have to
prevent aspiration. Check the
patency of the tube, aspirate the
gastric contents, position client in
NCM 112 NGIMPEC LECTURE NOTES
upright position, give the feeding
and flush with water after.
2. MIO
o Measure for the intake and output
3. Check hydration status: skin turgor,
mucous membranes
o Check skin turgor by pinching the
skin. If it goes back immediately, the
skin turgor is good.
o Check for mucous membranes, this
is a must for unconscious client
because their mouth is dry
especially if with ET tube, difficulty
in swallowing, some collect at the
side and we suction it. If the mouth
is dry there is a tendency of skin
break down.
4. Mouth care to keep mouth moist, clean
and intact.
o Done by nurses every shift.
o Uses mouthwash for antiseptic
(betadine)
D. Safety
- Clients who are unaware are always at
risk for injury.
- Checklist for falls to ensure safety
1. Keep side rails up
o Judicious use of the side rails must
be done. Be cautious.
2. SZ precaution
o Most patients with metabolic causes
of altered LOC or structural causes
even psychogenic undergoes
seizure.
o Manifestation which is to be watch
out
o Doctors give anticonvulsants for the
prevention of seizures that will
aggravate the condition
o A nurse prepares a suction
apparatus, ET tube, and O2, at the
bed side but there are rooms that
has built-in apparatus, just check if
they are functioning and efficiency.
o In wards, you as a nurse must
prepare them.
o Prepare the anticonvulsant that is
usually ordered by the doctor.
Compute how much you are going
to use. Anticonvulsants ordered
usually are under the
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benzodiazepine groups like
trazipam, diazepam, and valium (for
short term use)
3. Avoid restraints
o In other countries, it must be
ordered by the doctor some are
good for 24h because some
restraints can cause hematoma to
the tied hand or feet.
4. Touch gently
o Prevent jarring of the bed, no noise
in stimulating the patient. Darken
the room, no stimulation, no visitors.
o Touch and speak to the client gently
and maintain compassion.
o Handle the with dignity
5. Speak softly
o Speak to the client softly because
the patient’s dignity must be
maintained.
o We talk to them softly when we do
procedures because their sense of
hearing remains intact and that is
proven.
6. Protect eyes from corneal irritation’
instill artificial tears as ordered, eye
patch.
o There are some patients with
altered LOC in which their eyes
have an inability to close so the
cornea exposed to the environment
which is at risk for irritation and
eventually infection
o Get an order from the doctor for the
artificial tears instillation and apply
eye patch or shield.
E. Prevent Complications of Immobility
1. Keep skin clean, dry, and pressure free
o If the patient is immobile, pressures
especially on the body prominences
may occur and it may cause
decubitus ulcer where in there is
impaired skin integrity.
o Keep skin from moisture because
this can soften the skin which cause
skin breakdown and do the
cleansing of the skin. Perform CBB
o Keep the linens wrinkle free
because this may cause pressure
on the skin.
NCM 112 NGIMPEC LECTURE NOTES
2. Turn q2h
o To prevent destruction of skin
integrity.
o This will expansion of the lungs and
allow circulation.
o This will also prevent some
deformities.
3. ROM q4h
o Perform passive range of motion
every 4 hours to promote circulation
and prevent deformities.
o One deformity that may occur would
be foot drop and stiffness.
4. Prevent deformities: footboard, splint to
prevent wrist drop, high toped tennis
shoes
o To prevent foot drop and stiffness
o Wear high toped tennis shoes
keeps the position of the function of
the foot
o Apply splint in the wrist to prevent it
from dropping
F. Bowel/Bladder elimination
1. Indwelling catheter
o Incontinent especially in stroke
patients because they may be hypo-
reflexive during the first phase of the
disease process
o But if the bladder function is
restored to normal, indwelling
catheter is removed.
o This can introduce UTI, if it is to stay
for long period, this must be
changed every 2 weeks.
2. Stool softeners as ordered.
o The usual complication in immobile
patients is constipation.
o It is not due to the disease but the
immobility. The peristaltic will also
slow down.
o Doctors will usually order stool
softeners like senocot (Senna).
o Refer if the patient did not have any
BM.
o High fiber diet is one of the
management, it is already
formulated in NGT feeding. If not
contraindicated increase fluid intake
through NGT
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 NCM 112: NGIMPEC LECTURE NOTES
o With very high or low blood
pressure, this may cause decrease
O2 to the brain and may alter the
pressure inside.
2. Venous pressure
o If obstructed, flow of venous
circulation to the heart like for
example, the jugular vein is
obstructed, it drains venous blood
Lesson 2: INCREASED INTRACRANIAL
flow to the vein. If it is obstructed,
PRESSURE
this may affect the pressure inside.
3. Intra-abdominal intra-thoracic
Definition
pressure
- Not a disease process itself but a
o Example, there is abdominal
symptom of several neurologic
distention, this can cause pressure
problems.
on the inferior vena cava that carries
- Maybe related only to neurological
venous circulation to the heart. The
problems.
blood flow will stop, which can
- Defined as CSF > 15mmHg
cause an altered pressure inside the
cranial vault.
The pressure inside the cranial vault is made
o When there is a tumor in the
up of 3 components inside the brain. Three
thoracic area, this will cause
components making the volume inside the
increase venous pressure affecting
cranial vault:
the pressure inside the cranial vault.
1. CSF of 10%
4. Temperature
2. Blood of 12%
o When the patient is febrile, there is
3. Brain Tissue 78%
headache, this proves that the
TOTAL of= 1,500-1,900 ml
pressure inside the brain is affected.
- This volume will cause pressure inside
The blood vessels inside the brain
the vault.
are dilated, this increases the
Normal ICP= 5 to 15mmHg (as long as it
volume of blood in the dilated blood
does not exceed 15mmHg it is normal)
vessels. The circulation is slow
decreasing the oxygenation.
o When making an NCP for febrile
patients our goal is decreasing the
temperature 30 mins after the
nursing interventions. We will not
allow the temperature to increase to
go on for a longer period of time
because this affects the pressure
inside the cranial vault.
5. Blood gases
o Normally the PaO2 is 80-100mmHg.
PaCO2 is 35-45 mmHg. Whenever
the oxygen tension is decreased,
this will affect oxygenation inside
Factors Affecting Homeostasis of cranial the brain. This will affect the flow of
vault the delivery of O2 to the cerebral
tissues. The cerebral hemisphere is
1. Arterial Blood Pressure sensitive to deficiency of oxygen.

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 NCM 112: NGIMPEC LECTURE NOTES
o Whenever there is decrease from the skull, there are meningeal
oxygen, ischemia will occur. layers that cover the brain namely the
Whenever this happens, CO2 will dura mater, arachnoid layer, and the pia
compensate, the compensatory mater.
mechanism of CO2 in its attempt to - If anyone of the 3 components will
increase the O2 tension in the blood increase in its volume the brain will still
is to dilate the blood vessels. compensate. Example, the brain tissue
However, when there is has increased, the blood and CSF will
vasodilation, the blood volume compensate. However, this
increases, slowing down the compensatory mechanism is limited due
circulation and slowing delivery of to its rigidity.
O2.
o The CO2 will also make an acidic
environment so that excitatory cells
will get in to fuel the action potential
of the brain cells. Neurons are
always in action potential, and
needs energy. If there is less
energy, there is less O2, there is
less delivery so there will also less COMPENSATORY MECHANISM
energy from the glucose. However,
these excitatory cells are acids that 1. Autoregulation
will add up to the acidic environment o Automatic
caused by the CO2. The effect of alteration in the
this is to dilate the blood vessels diameter of
even more. If there is vasodilation, cerebral blood
there is increase volume of blood vessels to
which leads to a slower circulation maintain a
making it more difficult for the O2 to constant blood
be delivered in the brain. flow to the brain
6. Posture during changes
o Normally the posture is standing in arterial
o The circulation to the brain is unique pressure. The small blood vessels
because it has to go against the will constrict to accommodate
pressure of the gravity. limited amount of blood flowing
o The person is upside down, the through the constricted blood
venous circulation will stop and the vessels. Whenever some changes
venous pressure will increase of pressure will occur inside, let us
affecting the pressure inside the say with increasing volume inside
cranial vault. the brain.

Monro Kellie Doctrine Normal compensatory Adaptations

- The brain is enclosed within a rigid skull. Expanding Lesions

- It is composed in a close box that there __________________|__________________
is no room for expansion because of _
the rigidity of its protective structure | |
such as the skull. Increase CSF absorption vasoconstriction
- Skull is made up of 8 cranial bones Decrease CSF formation |
| |
covering the brain inside and 14 facial
Decrease CSF volume decrease
bones. Aside from the covering inside

NCM 112 NGIMPEC LECTURE NOTES 14 | P a g e

 NCM 112: NGIMPEC LECTURE NOTES
| Intracranial
| blood volume
| |
Allowing the brain to expand without serious
effects
Compensation Stage-Stage 1
- The brain still allows the growth of the
lesions without deleterious effect there is
no symptoms yet.
CEREBRAL BLOOD FLOW
- There are two metabolic requirements of
the brain, oxygen (20%) and glucose
(25%). These must be delivered without
interruption because the brain does not
store oxygen and also it does not store
glucose.
- Normally the brain should receive:
a. 50 ml/min/100g of brain
tissue- global circulation
b. 25 ml/min/ 100g- white matter
c. 75 ml/min/100g- gray matter.
- Uses….
a. 20 %- body’s O2
b. 25%- body’s glucose
MEAN ARTERIAL PRESSURE
- Average pressure in arteries during one
cardiac cycle, indicator or perfusion to
vital organs.
- Normal: 50 to 150 mmHg
MAP= DBP + (SBP – DBP)
3 o Expandability of the brain
Example: BP of 120/80
MAP= 80 (120-80)
3
MAP= 80 + 13.3333333
|MAP= 93.34|- Normal (average pressure that
is necessary to ensure that there is adequate
perfusion for every tissues)
Explanation…
With blood pressure changes the MAP will
also be altered, we are not sure if there is
adequate pressure to the brain. And, that
would mean it dilates, as it goes down, the
blood vessels are slowly dilation.
MAP= > 50 mmHg (ISCHEMIA)
NCM 112 NGIMPEC LECTURE NOTES
If the oxygen decreases, the CO2 increases to
dilate the blood vessel, too much dilation due
to CO2, plus excitatory cells (acids) will cause
more vasodilation and more pulling of the
blood so pressure increases. The circulation is
slowed down causing ischemia.
With BP changes, it will cause BP to rise
constantly causing blood vessels to constrict
until it reaches the maximum of 150 and
autoregulation is exhausted. The
autoregulation is impaired. The very narrow
blood vessels are too constricted, there is
decrease delivery of oxygen that will result to
ischemia which causes an increase in CO2
plus the excitatory cells that will cause
vasodilation that would still increase the
volume of blood in the dilated blood vessels,
decrease circulation and O2 delivery.
CEREBRAL PERFUSION PRESSURE (CPP)
- Normal 70 to 100mmHg
- 50 to 60 mmHg adequate CBF
- <50 mmHg is ischemia
- <30 mmHg death of the neurons
Formula:
CPP= MAP- ICP (If with ICP monitor)
Pressure changes
1. Elastance
o Stiffness of the brain
2. Compliance
Stages of Increased ICP
Stage 1 (Compensatory stage): Increase
compliance (allow expansion) | decrease
elasticity (not yet stiff to resist the pressure
inside) No manifestation yet
Stage 2: increase compliance (slowly
decrease the ability to expand) | decrease
elasticity (early signs if increased
ICP=papilledema)
Stage 3: Decrease compliance (very stiff) |
increase elasticity (less able to comply with the
expanding lesion) can see the Cushing’s triad
Stage 4: Increased ICP to terminal levels,
herniation (movement of structures inside the
brain)
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 NCM 112: NGIMPEC LECTURE NOTES
3. Space-occupying lesions, tumor, or
Causes of increased ICP mass, hematoma.
- Tumor may cause cerebral edema due
1. Cerebral edema to inflammation surrounding the tumor.
- Normal with gyri Distorts the structure inside the brain.
- If there is swelling gyri is flattened Movement of the cingulate gyrus.
- Can be related to infections, tumors,
intracranial surgery, hydrocephalus, or
radiation therapy.
- Complication of increased ICP

4. Infarct
2. Abscess
- Space occupying lesions
- It can move and compress the structures
inside the brain.
- A: cingulate gyrus below the fax cerebri
(divides two cerebral hemispheres). Due
to the abscess the structures will move
down and go to the other side of the
cerebral hemisphere.
- Corona radiate: bonds of nerve fibers,
located deep inside the brain at the
diencephalon. Due to the space
occupying lesion, it is moved towards
the other sides of the brain. And, that is
an example of brain herniation.
- Infections and abscess can cause
increased ICP and herniation.
- Cause by ischemic type of stroke
- Middle cerebral artery, terminal of
internal carotid artery coming from the
heart to the internal carotid artery and
will divide into two mid cerebral arteries,
supplying the upper temporal lobe and
latterly outward of the frontal and
outward of the frontal and parietal lobes.
- A clot or thrombus obstructs the
oxygenated blood flow to the areas. It
will die because it does not receive
oxygen requirements.
- Infarcts may be space occupying lesions
that can cause increased ICP.

5. Bleeding or hematoma
- Bleeding, hematoma in hemorrhagic
stroke can cause increased ICP
- Subdural hematoma: bleeding below the
dura mater and involves bridging veins
that can be damages and tear causing

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 NCM 112: NGIMPEC LECTURE NOTES
hematoma formation, compressing the
structures inside the brain. Venous in
nature, the pressure is lower than
arterial.
6. Intracranial surgery
- During the operation, the tissues are
being manipulated.
- After the operation, we are going to
prevent ICP increased due to a danger
that there will be rebound cerebral
edema after the operation for the first 24
hours because it can swell after the
operations. Watch out and monitor S/S
of increased ICP 8. Radiation therapy
- After surgery management would be for - During the exposure to the radiation
prevention of increased ICP therapy the tumor cells are being
destroyed by radiation, manipulated.
- This is like an intracranial surgery where
cells are brain tissues are manipulated.
- We expect a rebound cerebral edema
after the therapy.

7. Hydrocephalus
- Normal: from the lateral ventricles to the
saggital sinuses absorbed inti the
arachnoid villi, into the venous
circulation. It has to be continuous and
no interruption.
- Extra CSF in the ventricles Pathophysiology
- Hydrocephalus: there is obstruction to
the flow of CSF and it will be dumped
back to the ventricles causing increased
volume of CSF and swelling.
- This is a buildup of CSF in the hollow
places inside the brain. This can cause
interstitial edema.

Brain injury -> Local tissue pressure

(compression on small blood vessels below
the tumor) -> obstruction of venous drainage
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 NCM 112: NGIMPEC LECTURE NOTES
(swelling due to blockage) -> edema -> brain
swelling
Brain injury -> Local tissue pressure
(compression on small blood vessels below
the tumor) -> interruption of blood supply
(artery that carry oxygenated blood to tissues
can be compressed by the tumor below it) ->
local ischemia -> local acidosis (if there is local
ischemia there is decreased oxygen so there
is increased CO2 which makes the
environment acidic, causing vasodilation plus
with the decrease O2, there is decrease action
potential of the neurons so excitatory cells like
pyruvic acid, lactic acid, glutamic acid will
influx in the acidic environment) ->
vasodilation (dilated vessels still be filed with
blood due to pulling of blood in dilated vessels
-> cerebral edema -> brain swelling
Brain injury -> impaired autoregulation ->
vasodilation or vasoconstriction with BP
changes -> increased CBF -> increased CBV
-> edema -> brain swelling
Explanation
Continue to monitor BP, if it is going down
below 50, mean ischemia, BV are dilated,
increased volume and decrease oxygen will
result to ischemia
With increasing blood pressure, impaired
constriction, due to limited compensatory
mechanisms which is the constriction of small
blood vessels until such time, the MAP is
increased, very narrowed blood vessels
limited flow of blood decreasing perfusion of
oxygen leading to ischemia. Increased CO2
and influx of excitatory cells which are acids
will result to acidosis, dilating the BV,
increased blood volume cause vertebral
edema or swelling.
Increase mass effect (Brain swelling cause
mass effect, considered as space occupying
lesion, and is already complication of primary
injury) -> increased ICP -> decreased CPP ->
ischemia (becomes viscous cycle) -> local
acidosis (more acidic environment due to
increase CO2 and more excitatory cells will
NCM 112 NGIMPEC LECTURE NOTES
influx increasing the vasodilation, blood
volume, brain swelling and mass effect.
Increase mass effect -> brain shift and
herniation (due to very high ICP, moving
structures inside the brain) -> obstruction of
CSF pathways -> increased CSF volume
No CPP (below 30 mmHg, no blood that will
push blood to the tissues) -> brain death
(deprived oxygen requirements)
In 2 minutes without perfusion or oxygen
inside the brain everything inside will stop
In 5-6 minutes without oxygenation, it will
cause brain death.
Complications of increased ICP
A. Cerebral edema
1. Vasogenic
o Neurolglial cells double in number
with neurons
o Astrocytes form networks to support
the neurons, together with the
epithelial cells and the small blood
vessels, this will form the network
BBB.
o BBB is selective in substances that
gets into it that even antibiotics
cannot easily get through it. Only
when BBB is disrupted they can
pass.
o With the increasing pressure the
BBB is disrupted and will allow the
outflow of the large molecules
especially the proteins to go out of
the extravascular compartment.
Since proteins are highly
concentrated because they are
large molecules, it will draw fluids
from other compartments of lesser
pressure by osmotic pressure. From
lower to higher concentration.,
causing cerebral edema.
o BBB disruption=extravascular
o cerebral edema= vasogenic
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 NCM 112: NGIMPEC LECTURE NOTES
the white matter in the interstitial
tissues)
o Also known as periventricular
cerebral edema.

B. Brain Herniation

Falx Cerebri
2. Cytotoxic
o The membrane of the cerebral
tissues is disrupted, allowing influx
of water influx of water to the tissues
causing swelling.
o In the case of water intoxication,
your fluids will go in the cells
causing swelling of cerebral tissues.
o Refers to the brain swelling caused
by ions Na+ and Cl-, and water
entering the cells of neurons or
astrocytes
- From the outside, the cerebral
hemisphere is divided into two by a
fissure.
- From the inside it is divided into two by
the thick layer of dura matter (yellow
color) falling down the cerebral
hemisphere so that structures from the
left will not go to the right.
- Thick layer of dura mater

Tentorium cerebelli
- A dura mater which is thinner than the
falx cerebri
- Forms a tent at the top of the cerebellum
dividing the brain into two fossa, the
supratentorial (above the tentorium) and
the infratentorial (consist of cerebellum
and brain stem)
3. Interstitial - The tentorium cerebelli forms like a tent
that protects the cerebellum form the
o Results from the outflow of CSF
from the intravascular space to the weight of the cerebrum
- Tentorium is a Greek word which means
interstitial areas of the brain.
o Whenever one of the pathways of TENT
the cerebrospinal fluid will be
obstructed, there will be backflow of
CSF into the ventricles causing
swelling of ventricles. Ones swollen
walls of ventricles are stretching
causing increased permeability so
CSF will sip out to the ventricles to
the periventricular areas (tissues
around the ventricles of the brain at

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 NCM 112: NGIMPEC LECTURE NOTES
o Also known as central transtentorial
herniation or downward because it
will traverse the tentorium cerebilli.
3. Uncal
o Number 3: Lateral type of
herniation.
o Structures at the side that can be
moved by the hematoma is lateral
lobe where the floor of the cerebrum
or the 5th lobe the INSULA.
4. Tonsilar
o Number 4: Tonsils can be moved
downward.
Types of Brain Herniation
A. Assessment
1. Change in LOC
o Indicator if neurologic status and
perform GCS
o R/T impaired CBF affecting cerebral
cortex and RAS
o Falling score of GCS <7 coma
o Early behavioral changes:
a. Restlessness (initial sign LEVEL
2)
b. Irritability
c. Drowsiness
d. Confusion
1. Cingulate
e. Apathy
o Number 1: cingulate gyrus just
o Difficulty or inability to follow
below the falx cerebri.
commands
o Also known as subfalcial in clinical
o Changes in response to painful
charting it is subfalcine herniation.
o The cingulate gyrus is being moved stimuli
o Difficulty or inability in verbalization
due to the tumor.
or responding to auditory stimuli
2. Changes in V/S
2. Transtentorial
o r/t to pressure on the thalamus,
o Number 2: Corona radiate and
hypothalamus, pons, medulla
capsule, basal ganglia at the center
oblongata
of the brain can be moved due to the
o damage to vascular supply r/t
pressure.
increasing of pressure
o As these structures at the center
o Cushing’s triad:
moved towards the other side, the
 Reflex response with severe
gyri may be flattened when it strikes
decrease oxygenation to the
the skull. Impact there causing
brain
movement of brain towards the
 Can only be seen in Stage 3
center. So movement will be from
increased ICP
the center to the side, back again to
the center then downward because
there is opening at the foramen
a. BP wide pulse pressure
magnum.

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 NCM 112: NGIMPEC LECTURE NOTES
 High systolic pressure (250-
300mmHg) with very low
diastolic pressure.
b. Decreased cardiac rate-
bradycardia
 Reflex response will increase,
this is sympathetic regulated by
hypothalamus, parasympha is
regulated by hypothalamus will
compensate by regulation of
CN X located at the medulla
oblongata decreasing heart rate
c. Decreased respiratory rate-
bradypnea
 Pons and medulla are
respiratory centers are located,
RR will be affected
Note:
With the impairment or damage to the
hypothalamus this may cause moderately
increased temperature. So, immediately lower
the temp because this can cause dilation of the
blood vessels.
Lesson 3: HEAD INJURY
HEAD INJURY
- otherwise known as traumatic brain
injury (TBI)
- injury affecting the scalp, skull, and the
brain
Classification
Mild/Minor TBI: GCS 13-15
o Loss of consciousness to 15 min
o Mortality 0.1%
Moderate TBI: GCS 9-12
o Loss of consciousness for up to 6 hours
NCM 112 NGIMPEC LECTURE NOTES
o Mortality 10%
Severe TBI: GCS <9
o Loss of consciousness > 6 hours
o Mortality 40%
- usually for patients in vehicular
accidents, who died on increased
intracranial pressure on the spot related
to bleeding or fracture
Etiology
1. Vehicular accidents (motorcycles)
- number one cause of traumatic brain
injury
2. Falls
- especially for the young who have no
sense of safety
- for the very old who have problems with
eyesight and mobility
3. Assault
- penetrating injury
Gunshot wound related to assault.
Ecchymosis - the collection of blood in the
subcutaneous tissue
Mechanisms of Brain Injury
Closed head injury
o there is no opening or communication
from the inside to the outside
o coup (primary injury)
o countercoup (secondary injury)
Open head injury
o there is a break
o there is communication from the
outside to the inside
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 NCM 112: NGIMPEC LECTURE NOTES
Example:
There is a fixed object (wall), and the head is
mobile. The person is walking without seeing
the wall, and the head hits the wall.
This will cause acceleration or movement of
brain forward.
The injury caused by the acceleration of the
brain inside is called the coup or primary
injury.
The impact with the acceleration of the brain
will likewise cause an impact which is going to
move the brain backward—deceleration.
The rapid acceleration and rapid deceleration
of the brain inside can cause another injury—
countercoup injury (secondary injury)
Impact injury on the head can cause primary
or coup injury that will also cause movement
of the brain inside causing secondary or
countercoup injury.
Head injuries may cause lacerations (which
greatly bleeds). The blood vessels on the
NCM 112 NGIMPEC LECTURE NOTES
scalp are less constrictive compared to other
blood vessels in the body.
Even with minor lacerations, the bleeding is
profuse if it is in the head.
Types of Brain Injury
1. Scalp lacerations
- there is profuse bleeding
2. Skull fractures:
- break in the continuity of the bone
a. Linear
o hair-line fracture
o there is no fragmentation of the bones
(not separated into particles which is
why it is still aligned)
o impact injury may cause bleeding
below the dura mater of the subdural
hematoma
d. Comminuted
o there
is
fragmentation of the bones which are
separated into particles and we call this
fracture as comminuted fracture
o depression fracture – cause
indentation of the brain inside
o this one with opening is called as
compound fracture
o considered as an open head injury
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 NCM 112: NGIMPEC LECTURE NOTES
The brain has different layers which come in
3. Concussion different depth.
- jarring of the brain tissue When there is an impact injury, a layer will
- minor TBI move in different directions, and there are
- caused by a bump, blow, or jolt to the axons running through the different layers
head or by a hit to the body that causes which will be damaged
the head and brain to move rapidly back
If these layers will move in different directions,
and forth
these may be stretched.
- with rapid acceleration and
deceleration of the brain These are the new mechanisms of the injury in
- patient may manifest symptoms of DAI. The axons may be stretched, twisted,
headache, dizziness, amnesia and loss compressed or sheared, and also edema
of consciousness after TBI and will causing diffuse axonal injury.
persist up to 3 months
- this is the reason why with TBI, patient
is admitted and to be observed for 24
hours where you can also perform
several examinations to see if there is a
serious brain damage

4. Contusion
- bruising or tearing to the brain tissue
itself
- example in the photo: contusion of
temporal lobe

5. Diffuse axonal injury (DAI)

- is the shearing (tearing) of the brain’s
long connecting nerve fibers (axons)
that happens when the brain is injured
as it shifts and rotates inside the bony - the injured structure are the axons
skull
- this is considered as major as it 6. Hematoma
damages many axons in the brain - involves the blood vessels
which may be diffuse or global (all parts Epidural hematoma
of the brain are affected)
- bleeding outside the dura mater
- usually causes coma and injury to
- profuse bleeding with artery damaged
many different parts of the brain
- since it is arterial, accumulation of
hematoma is rapid
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 NCM 112: NGIMPEC LECTURE NOTES
Most common artery involved: middle  Battle’s sign
meningeal artery - ecchymosis behind the ear (bluish
discoloration at the mastoid process)
- indicates traumatic brain injury

Subdural Hematoma
- below the dura mater and usually
involves the bridging veins (venous in
nature)
- with veins, bleeding here is slower as
compared to arterial bleeding (slow
formation of hematoma)
- may be acute, subacute, or chronic
Intracerebral hematoma
ICP
one
Severe
 Scalp wounds
 Lacerations
 Fracture
 Swelling, bruising Brad
 Stiffness of the neck – nuchal rigidity;
indication of meningeal irritation
 Discharges from nose – may contain
cerebrospinal fluid; rhinorrhea which
indicates frontal bone fracture
 Discharges from ear – otorrhea which
indicates temporal basilar fractures
If there is cerebrospinal fluid contained in
these discharges, that is an indication of an
open head injury (there is already
communication from the inside to the outside)

0 0
raccoon's

eye

- rupture of the blood vessel causing How do we know that the drainage contains
hematoma formation inside the cerebrospinal fluid?

Pathophysiology of Head Injury 1. Halo sign – drop a small amount of these

discharges into a small piece of white cloth
- due to ICP increase and observe for the formation of these
o Neurologic deficits result from shearing concentric rings (concentric form of the blood
of white matter in the middle and a lining in the blood which is
o Ischemia and mass effect from clear compared to the blood)
hemorrhage and cerebral edema of o The lining is the cerebrospinal fluid.
surrounding brain tissue o Blood collects in the middle because it
is heavier than the cerebrospinal fluid.
Clinical Manifestations

NCM 112 NGIMPEC LECTURE NOTES 24 | P a g e

Concussions

manifestations

Acute 24 484
Subacute 484 2wks
Chronic Weeksmonths 720Days

Brainatrophy canstretch

Awh
depressant

L blood supply Brain

acute
DXStudies riskforsubdural hematoma

CTscan is pressured afterextractionfornomin

skull X ray Bleeding affgfsfff.ggsite
Cerebral Angiography
checkforserum
creatinine
tocheckkidney functionafteradministrationof contrastmedia
BloodStudies
lumbartap Cl forPx w t ICP brain
ofthelumbarfluid riskfor
movement
L when postdraining
complications
riskforherniation

Cerebral Edema
Hydrocephalus
Meningitis Encephalitis

81ADH DI
Brain Herniation
Death
Intervention

t CSFleak

Instruct Px not to blow nose

Head elevation 30
administer antibiotics to prevent
Observe for s s of meningitis d

meningitis
Place a cotton ball ear to absorb otorrhea replace frequently

Prepare for surgery

opening into the cranium w a drill

Bar hole
Craniotomy

Craniectomy
cranioplasty
 NCM 112: NGIMPEC LECTURE NOTES
2. The other test is to put a small amount of supply in all tissues. This
discharge in the gluco test tape. Insert into the condition is called
glucometer. If you can see the result that there arteriosclerosis
is presence of sugar, there is cerebrospinal o At 15 years old, a person starts
fluid in the discharge. to deposit fat which can cause
atherosclerosis
o Normally, the CSF contains sugar. o Blood pressure: normal adult –
120/80 however in people who
are aging, especially for those
Lesson 4: CEREBROVASCULAR people who are past age of 40,
ACCIDENT systolic BP of 130-140 is normal
3. Gender
STROKE o During the productive years of
women with the same age group
in men, stroke is more likely to
Cerebrovascular Accident
occur on men because during
- Layman’s terms: stroke or brain attack
the productivity years of female
- Considered an emergency
has still estrogen which will help
- Decreased blood supply to a part of a
to transport of lipoproteins away
brain or related to rupture or bursting of
from blood vessels
blood vessel that will result to death of
o Men are more vascular
brain cells
4. Race
o African Americans
 Develop truncal obesity at
middle age
 Carnivorous
o Hispanics
 Develops truncal obesity
at middle age
o American Indians
 They love to eat meat
 Develops truncal obesity
o Alaska natives
 Live in very cold climates
 If they don’t warm
Risk Factors for Stroke themselves the blood
- Divided into non-modifiable and vessels constricts
modifiable o Asian Americans
 Develops truncal obesity
Non-Modifiable o Japanese
1. Heredity  Low cases of stroke
o Cannot be changed because they love
o Genetic tendency with familial vegetables and fish
history of hypertension or stroke
in the family Modifiable
2. Age 5. Hypertension
o Inevitable o If the person has a tendency to
o In young ones, the blood vessels develop this, they must live a
are very elastic and these can healthy lifestyle to delay the
accommodate large volume of onset of hypertension and
blood but as the person is aging prevent development of stroke
the elasticity of blood vessels o Cause both hemorrhagic and
also decreases and this causes ischemic stroke
the narrowing of the lumen of the 6. Hyperlipidemia
blood vessels decreasing the

NCM 112 NGIMPEC LECTURE NOTES 25 | P a g e

 NCM 112: NGIMPEC LECTURE NOTES
o After the age of 15, the person
deposits fats especially based
on lifestyle that will later on
cause atherosclerosis
o Main triglycerides mustHDLintake
o Normally we need 50-60 percent
CHO as main source of energy
7. Heart Disease duetoabnormalrythm back now hafnut
o Cause embolic type of stroke
o Atrial Fibrillation will dispose clot
formation and this clot will
dislodge from its focus it will go
up in the circulation and cause
embolic stroke
o Rheumatic Heart Diseases,
example rheumatic heart fever,
the valves are damaged and
does not keep the circulation
o Cardiomyopathies and
Myocardial Infarction
8. Increase Alcohol Intake and Smoking
o Malt is CHO so it deposits fats
whoCNSdepressant
o Develops atherosclerosis
riskforatherosclerosis
o Drink moderately
o When the person is smoking,
blood vessels constricts and at
the same time they inhale CO
100 percent
cadmium o Passive smoker must not stay in
environment that is full of smoke
predisposes
because they may inhale CO 60
value damage percent
sruptsvitamin o The CO will bind with
absorption oxygenated hemoglobin that
carries oxygen to tissue
9. Drug Abuse
o Cause vasoconstriction that
results to hypertension because
it has excitatory
neurotransmitters such as
serotonin
10. Physical Inactivity
o Sedentary lifestyle
o Decreases circulation in all parts
of the body
11. Poor Diet
o Excessive fat intake
o Trans fat
o Fats will deposit on wall of blood
vessels and cause
atherosclerosis
12. Obesity
o With excessive intake of food,
there are a lot of deposits of fat
NCM 112 NGIMPEC LECTURE NOTES
and makes them inactive
sometimes
13. Carotid Artery Stenosis
o Major artery that delivers
oxygenated blood to the anterior
part of the brain
o With narrowing it will decrease
the delivery of oxygen into the
brain
14. Diabetes Mellitus
o DM will develop 50 percent
acceleration of atherosclerosis
19 4
blood
because there are many
complications that will result to
predisposed to stroke from DM
thrombosisformation In
o DM, there is relative
deficiency of insulin which
means there is production of
insulin but it is not sufficient, this
is called insulin resistance or
another one is absolute
deficiency of insulin where the
pancreas no longer produce
insulin. As a result, there is a
high concentration of sugar in
the blood or hyperglycemia
15. Oral Contraceptive use and Smoking
o Oral contraceptives are
combination of progesterone
and estrogen.
o With progesterone, the person
retains sodium and water that
will increase the blood volume
o May not be indicated to ages 35
years old and above I
Priskfor HPN o Smoke constricts the blood
vessel and with the increase of
blood volume due contraceptive
as a result there will be increase
pressure through constricted
blood vessel that will predispose
to hypertension and eventually
stroke
16. Hypercoagulability
o This is a condition where the
blood clot easily
o Polycythemia vera – in which
there is increase platelet count
and hemoglobin count which can
cause clot formation easily
17. Sickle Cell Disease
o Sickle cell anemia
o Can cause stroke
o Normally, the RBC is round
however in sickle cell anemia it
26 | P a g e
 NCM 112: NGIMPEC LECTURE NOTES
is crescent shaped which
causes the clumping or sickling
of cells which may obstruct the
flow or circulation
18. Inflammatory States
o Releasing of proinflammatory
cytokines which causes
vasodilation which causes
pooling of the blood and
decreasing the blood supply and
oxygenation to all the cells
o It can activate the coagulation
pathway where there will be
increase amount platelets which
can cause clotting which
microembolization may occur - There are 2 sets of blood vessels which
19. Hyperhomocysteinemia gives oxygen to the brain which are the
o Increase homocysteine in the right and left carotid artery from the
blood heart
o Homocysteine is a sulfur type of - The two carotid arteries will go up to the
amino acid which came from base of the brain, it will pass by
dietary protein especially meat anteriorly at the neck
o Homocysteine will cause - At the base of the brain, it will divide into
destruction of endothelial cells in two
the blood vessel that will going to o External carotid artery that will
cause the release of toxins or serving the face and the other
substances that will cause parts of the head
vasospasms o Internal carotid artery will get
o Endothelin thromboxane will inside the base of the brain
cause the constriction of blood - From the heart, the right and left
vessel and promote formation of subclavian arteries will go up
atherosclerosis posteriorly through the cervical spine
20. Sleep Apnea CPAP and will enter the foramen magnum at
o When the person is asleep, he is the base of the brain that will be serving
not breathing the posterior position of the brain.
o Predispose to stroke and MI - Since left and right subclavian pass the
21. Migraine spine, they will be known as vertebral
o Brain is insensitive to pain, it is arteries
the spasm of blood vessels that
will cause the headache
o Manifested by severe throbbing
headache on one side of the
head
o There is constriction of blood
vessels
o Can be primary or manifestation
of underlying problem
22. Depression
o Cause is not yet known
o Depressed person may be
inactive which cause decreased
circulation or excessive intake of
food or alcohol or some people
do not eat at all - From the carotid artery, the internal will
Circulation of Blood to Brain get inside the base of the brain and will
NCM 112 NGIMPEC LECTURE NOTES 27 | P a g e
 NCM 112: NGIMPEC LECTURE NOTES
terminate into two major blood vessels
which are the two Middle Cerebral
Artery (MCA)
- The two MCA will go laterally into the
brain and will go outside that will be
serving the outer frontal and parietal
lobes
- As they passing laterally, this will serve
the upper temporal lobe
- MCAs are vulnerable to stroke because
when the blood passes from the
internal carotid artery, the pressure is
increased to be able to distribute the
blood
o Increased pressure may
predispose stroke
- Branching out the anterior cerebral
arteries that will be joined together at
the base of brain by anterior
communicating artery
- The two anterior cerebral arteries will
be serving the middle portions of the
frontal and parietal lobes
- From the subclavian arteries, arises the
two vertebral arteries will be fuses into
one by basilar artery and will divided
into two posterior cerebral arteries
- Two posterior cerebral arteries will be
serving posterior parts of the brain
- From the basilar artery, the anterior as
superior cerebellar arteries serving the
cerebellum and the pontine arteries that
will be serving the brainstem
- Going up the basilar artery will divide
into two posterior cerebral arteries
- From the MCA, the posterior
communicating arteries that will
completely form the circle of Willis
Areas that will be served by posterior cerebral
arteries
- Middle and lower portions of temporal
- Occipital lobe
- Brainstem
- Parts of ventricles of the brain
- The choroid plexus
- Third and lateral ventricles of the brain
Purpose of Circle of Willis
- Provide collateral circulation to the
brain that whenever one of the arteries
is obstructed, the other will still serve
blood to the brain
NCM 112 NGIMPEC LECTURE NOTES
- From MCA, there are still branches
coming out from the middle cerebral
arteries that will be serving the deeper
portions of the brain, these are called
the penetrating arteries or arterioles
o Left lenticulostriate arteries will
be serving the deeper portions of
the brain like basal ganglia,
thalamus, internal capsule, and
pons
- From the MCA, passing laterally will be
serving the upper temporal and will go
outside of the brain will be serving the
frontal and parietal lobes
Anterior Communicating Artery (ACA)
- Supplies medial and superior parts of
frontal love and anterior parietal lobe
Posterior Communicating Artery (PCA)
- Supplies occipital lobe, medial surface
of the temporal lobe, midbrain,
thalamus, choroid plexus 3rd and lateral
ventricles
MCAs Supply
1. Parietal Lobe – processes sensory
information related to touch, taste, and
temperature
2. Temporal lobe – processes audio and
encodes memory
3. Internal capsule – aids communication
between areas o the brain
4. A portion of the frontal lobe – important
for movement, expressive language,
and the ability to work toward a goal
Types of Stroke
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 NCM 112: NGIMPEC LECTURE NOTES
1. Hemorrhagic Stroke
o Rupture of blood vessel which
will result to formation of
hematoma and will cause
increase ICP
2. Ischemic Stroke
o Related to obstruction of the flow
of blood or thrombus that is
going to cause injury to the part
which is involved
o Cannot receive oxygen which
may cause an infarct or death of
the brain
o If there is marginal perfusion of
blood, the part which is not
perfused with blood is penumbra
Precipitating events of Acute Ischemic
Stroke
- All the risk factors will result to
formation of clot cutting the flow of
cerebral circulation or it can be an
embolus that is travelling into cerebral
circulation resulting to obstruction of
flow of oxygenated blood
AFib
Embolism
Atherosclerosis
Pathophysiology of Ischemic Type of
Stroke
NCM 112 NGIMPEC LECTURE NOTES
ischemiacascade
- When the flow of the blood is obstructed
it will result to decrease delivery of
oxygen to the cerebral tissues by a
thrombus
- Normal cerebral blood flow should be
50mL per 100 grams of brain tissue in
a minute, it has to be continuous
- If the cerebral blood flow will be less
than 25mL per 100 grams per minute
this will result to beginning of ischemic
cascade, which you will have decrease
delivery of tissues in the brain and
decrease delivery of glucose to the
cells
o Glucose is needed for action
potential
- With decreased delivery, there is also
decreased delivery of glucose which
will result to energy failure
- Energy failure will result from decrease
ATP which is derived from glucose and
will affect the action potential of
neurons
- Decreased oxygenation to the tissues,
this will result to acidosis, which is the
increase amount of CO2 resulting to
vasodilation and increasing the volume
of blood but decreasing delivery of
oxygen
- Acidosis will result to ion imbalance,
because neurons have energy failure, it
is also deprived with oxygen
- The influx of other excitatory
neurotransmitters mainly glutamate or
glutamic acid and the influx of calcium
to intensify the action potential this will
result to depolarization of the ischemic
cell
- Depolarized cell will cause breakdown
of the cell membranes that will going to
cause the movement of the protein cells
exert osmoticpressure cellinjury
29 | P a g e
 NCM 112: NGIMPEC LECTURE NOTES
site and the breakdown of proteins
which is necessary for building and
repair resulting to the formation of free
radicals and protein production would
be decreased and cause cell death and
injury
- Death of neurons and injury that will
predispose the formation of infarct
- The infarct will become the space
occupying lesion that may increase the
pressure inside the cranial vault and
may cause increase ICP

lake may
exhibitmanifestations purelymotorsense
Transient Ischemic Attack causemicro emboli Lacunar Stroke
- Mini stroke - The small blood vessel stroke
- The manifestation is same to major - Cause formation of small infarcts about
stroke attack 1.5 to 2 cm
- Temporary loss of function of one of the - After a few days, infract will lysis and
vascular territories of the brain lasting this ischemic infarct will be placed by a
less than 24 hours, lasting less than 15 cavity and will be filled with fluids
minutes - Common sites: basal ganglia,
- Related to obstruction of blood supply thalamus, internal capsule, pons
due to formation of micro emboli that - With development of cavity in place of
will dissolve by itself infarct tissue AKA LakeLacunar
pyridamole
- However, TIA must be treated because
rep there will be a major stroke attack
- Treated with antiplatelets aggregators
jiggle or blood thinners such as aspirin,
ticlopidine, dipyridamole lowdose80100mg
5mg - Anticoagulants can be given such as
warfarin, oral anticoagulants
- Hypertension must be treated

3 types of Ischemic Stroke

1. Embolic Stroke
2. Thrombotic Stroke
3. Lacunar Stroke

Thrombotic Stroke Embolic Stroke

- Large blood vessel stroke such as - Related to heart disease such as Atrial
vertebral arteries, basilar artery, Fibrillation where there is abnormal
carotid, MCA, ACA, PCA rhythm of the heart that will predispose
- Accounts for 61% of all cases and may to clot formation which the clot will go
occur regardless of activity up to cerebral circulation causing
- Common is in the MCA embolic type of stroke
- Related to hypertension and - RHD, Cardiomyopathies, MI
accelerating atherosclerosis related to
diabetes

NCM 112 NGIMPEC LECTURE NOTES 30 | P a g e

 NCM 112: NGIMPEC LECTURE NOTES

- Example of rupture blood vessel of the

Hemorrhagic Stroke Patient isactiveduring
- Resulting from the rupture of blood
this penetrating artery
headache - There is bifurcation which has increase
vessel
blood pressure
weakness- This may result vasoconstriction or
- Common causes
BU deposits of fats on the walls of blood
o Hypertension
vessels that is going to narrow the
causedby lumen which the flow of blood will
o Ruptures aneurysm
o Congenital causes like
alcageof increase
Arteriovenous Malformation or
loud - Later in the walls of blood vessel will AVM
dilate as a result the walls of bloods
 Ruptures at the age of 18
vessel will weaken until it will become
or 19
thinner which will cause outpouching of
wall of blood vessels called aneurysm

- Fusiform type of aneurysm

- Every time there is increasing pressure
the pouch will rupture which will result
to formation of hematoma that will
increase the ICP
- Accounts for 15% of all stroke cases
- Occurs in subarachnoid space and
ventricles of brain, and inside the brain
tissue
- Associated most often during activity
- More fatal than ischemic
- Prognosis is very poor especially in
subarachnoid space
significant morbidity
Intracerebral hemorrhage
- Bleeding inside and rupture of the blood
vessel inside the brain tissue.
Subarachnoid hemorrhage
- Bleeding into CSF filled space between
arachnoid and pia matter.
- Rupture of the blood vessel inside the
subarachnoid space where the
cerebrospinal fluid is flowing. Poor
prognosis because you have already
there the CSF volume and if the blood
vessels rupture this will cause much

NCM 112 NGIMPEC LECTURE NOTES 31 | P a g e

 NCM 112: NGIMPEC LECTURE NOTES
increased volume inside because blood
volume and CSF volume increase.
- Manifested by SEVERE HEADACHE
which is considered as the worst
headache in one’s life.
- Some patients are still able to verbalize
that they have severe headache.
- Prognosis: poor; death or with significant
morbidity. With devastating neurologic
problems.
Types of Aneurysm and the surgeries
Surgical microvascular procedures are
done to prevent rupture of the blood
vessels.
1. Saccular or belly aneurysm usuallycongenital
- One side of the blood vessel is
weakened and whenever pressure is
increased it will balloon. Surgery
performed is clipping. Clipping the
aneurysm, popping the aneurysm and
ensuring the blood flow in the blood
vessel. Then they repair it after.
2. Fusiform Aneurysm
- The whole diameter of blood vessel is
dilated. Surgical clipping is not
applicable because it will stop the
circulation through the BV. Instead it will
be wrapped, biological wrapping.
Perform craniotomy and microvascular
clipping. In biologic wrapping, they wrap
the aneurysm to prevent its rupture but
the blood will still pass.
3. Occlusion of aneurysm with embolic
coil
NCM 112 NGIMPEC LECTURE NOTES
- Insert catheter, BV is widened by stent
to facilitate widening and insert micro
catheter to fill the aneurysm with
embolic coil. If filled with coil blood will
no longer pass through the aneurysm
and not be considered as part of BV.
Carotid endarectomy
- Surgical procedure opening the carotid
artery to remove the atherosclerotic
plaque to widened the lumen of the
carotid artery to serve the anterior parts
of the brain.
- Bleeding may occur postoperatively
since major artery is opened.
Medical Management of Stroke
Interventions – increased ICP same as stroke
HHH may be ordered (especially when BP is
decreased). To optimize the cerebral blood
flow during symptomatic vasospasm.
Symptomatic vasospasm occurs especially in
hemorrhagic type of stroke. Blood clot will
dissolve after the 4th day and peak till the 7th
day. Continues lysis after 14th day. The lysis of
the blood will release the toxin endothelin
causing vasospasm that will result to ischemia
decreasing the blood in spastic BV.
Note:
Monitor BP, MAP, and CPP. MAP is going to
depend in BP, precipitate monitoring of BP to
check adequate perfusion to the brain. MAP
will differ if BP will change. If it dilates, MAP
will decrease resulting to ischemia. If BP is
increased, MAP is increased meaning there is
vasoconstriction resulting to ischemia.
1. Hypervolemia
o Volume expanders
o If BP is decreased blood volume is
decreased so we need to ensure
adequate blood flow to the brain.
o The doctor will prescribe volume
expanders like albumin to increased
CO to deliver adequate oxygen to
the brain.
2. Hemodilution
32 | P a g e
 NCM 112: NGIMPEC LECTURE NOTES
o Crystalloids (IV fluids like PNSS,
LR), has sodium to maintain
adequate amount of fluids.
o So that there will be available fluids
for the blood volume
3. Induced Hypertension
o Administrations of inotropic
medications to induce hypertension
such as the phenylephrine,
dopamine, and dobutamine. To
increase BP.
Medications
1. Calcium channel blockers
o Symptomatic vasospasm is
prevented by administration of
calcium channel blockers.
o Used as antihypertensive, but if
given in strokes patients, this is
primarily to prevent cerebral
vasospasm.
o Calcium is an ECF ion. K will move
out Ca will move in to intensify the
action potential. To prevent this to
occur, we need to block the influx of
the calcium.
o Verapamil, Nephinipin, Delgiosem.
Nimotop is an example.
2. Thrombolytic therapy 2414monitoring
o For ischemic type of stroke.
o Not given for patients with
hemorrhagic stroke because it will
dissolve the blood clot
o Given with criteria, qualify the
patient.
o Perform CT scan immediately at the
ER to check whether it is ischemic
or hemorrhagic CVA
o If identified is ischemic, hypodensity
(area of ischemia)
o If hemorrhagic, hyperdensity (area
with bleeding)
o Criteria:
 BP- over 200 with narrow pulse
pressure (hemorrhagic stroke
with severe headache)
 CT scan
 There is no recent surgery
 No recent medications that may
result to bleeding like
anticoagulants and antiplatelet
therapy.
NCM 112 NGIMPEC LECTURE NOTES
 Get the bleeding profile. aPTT.
PT, CBC
o After qualifying for ischemic type of
CVA, thromoblytic Tx is given.
Recombinant tissue plasminogen
activator or R- tpa should be given 3
hours after symptoms onset of CVA
because after 3 hours it will no
longer be effective and results if
given within 3hrs will result to
revascularization of blood vessel
which is obstructed. Perfuse with
oxygenated blood and penopra, the
area that is marginally perfused by
obstruction of the clot.
 Dose: 0.9mg/kg
 Maximum: 90 mg
 10% of calculated dose given IV
bolus x 1 min
 90% by IV via infusion pump x
1h (given within 3h)
o Monitor for side effects such as
bleeding.
o Example of R-tpa is streptokinase
still used in ICU. New brands
altiplase and activase.
3. Anticoagulant
o Oral: Warfarin (Coumadin)
o Parenteral: Low molecular weight
heparin (LMWH), like clexane given
SQ, arixtra (with spring and syringe
that can be withdrawn after) given
SQ, these refilled syringes with
prepared dose.
4. Antiplatelet agrregators
o Blood thinners like Aspirin,
dipyridamole, clopidogrel,
ticlopidine.
o Aspirin can be used in large doses
as antinflammatory, antipyretics,
and analgesic. Like asagrangeten
(300mg) grangeten in the apathcary
system, metric is mg. With
headache and inflammation. Low
does is blood thinner about 80-100
mg/tab, like the aspilet chewable
OD especially with TIA and DM to
prevent blood clotting.
5. Statins
o Atorvastatin, simvastatins
33 | P a g e
 hematoma
Medical Mng

Ctexane
3 40 14day
Arixtra
endothelin Lovenox
Streptokinase
v
Cerebralraso
spasm

ISCHEMIA
 NCM 112: NGIMPEC LECTURE NOTES
o Hydroxymethylglutarate or HMG - Problem in pain sensations, in the tracts
COA reductase Inhibitors, which that carry sensation from the body to the
facilitates synthesis of fast brain like PCP and STT.
especially during starvation that 6. Confusion
occur from 12mn-5am. So that the - Disorientation to 3 spheres
inhibitors as usually given HS to 7. Dizziness
facilitate synthesis of fast at night. 8. Severe Headache
Can be given anytime of the day but - Manifestation of hemorrhagic stroke.
effective at night time at 8pm after - Helps us differentiate the two types of
supper. CVA.
6. Anti HTN - Sign of hemorrhagic type of stroke
CPrill B blockers, Calcium
o Ace inhibitors, severe subarachnoid
channel blockers Clinical Manifestations
o Ace inhibitors will prevent - Affect various functions inside the body
conversion of Angiotensin 1 to because the brain regulates a lot of
angiotensin 2 in the lungs. ANG 2 is functions in the body.
potent vasoconstrictor to prevent 1. Motor Activity
high blood pressure. 2. Elimination
3. Intellectual Functioning
7. Diuretics 4. Perceptual alterations
o In patients with hypertension to 5. Personality
enhance the flow of Na and H20 to 6. Sensation
decrease blood volume that 7. Communication
decreases the blood pressure but if
the BP is decrease they can According to scientists, the functions in both
regulate the flow of diuretics. cerebral hemispheres are the same but there
is dominance about 70% over the other.
A. Assessment Findings
Right handed- dominant brain is left
WARNING SIGNS OF STROKE Left handed- dominant brain is right.
Bring the patient immediately to the
hospital Left Handed (Right Right handed (Left
brain) brain)
1. Face drooping 1. Good in arts and 1. Good in
- With damage to the tracts from the music mathematics and
cerebral cortex like corticobulbar tracts 2. Good in calculations
that innervates the cranial nerves in engineering and 2. Good in
brain stem architecture- languages and
Spatial interpretation
2. Arm Weakness
perception is (Speech
- R/t damage to the tracts coming from the
good, position in centers).
cerebral cortex that carries the motor space and good 3. Good in
function to the spinal cord crossing at at judging systematic
medulla oblongata to the spinal cord distances. analysis.
causing weakness or paralysis to the 3. Prolonged focus, 4. Good in
one side of the body orientation to 3 judgements.
3. Difficult Speech expressive nonfluent aphasia spheres is good.
- R/t MCA left obstruction serving the
Broca’s or Wernicke’s area.
4. Trouble Seeing Right brain Left brain damage
5. Numbness rit totracts damage

NCM 112 NGIMPEC LECTURE NOTES 34 | P a g e

 NCM 112: NGIMPEC LECTURE NOTES
6. Impaired Preference of
judgment. Very looking at the right
short attention side of the body.
span and 4. Slow
become irritable performance,
because cautious with
orientation to 3 safety
spheres are lost, precautions
there is because they are
disorientation. aware that there
is problem on the
(stroke on right side (stroke on left side of right side of the
of the brain) the brain) body.
5. Aware of defects’
1. Paralyzed left 1. Paralyzed right depression,
side: hemiplegia. side: hemiplegia. anxiety. Seen with
Corticospinal Corticospinal and one sided
tract will cross to corticobulbar damage as well.
the opposite side tracts are 6. Impaired
to the left side of affected. Damage comprehension
the spinal cord to the related to
that will synapse corticospinal tract language, math.
with lateral and that carries motor Can cause
anterior lower voluntary receptive aphasia
motor neurons movements to the or fluent aphasia,
located in spinal spine at the right mathematician
cord. Which may side of the body will be lost.
result to left causing
hemiplegia or hemiparesis or
left hemiparesis weakness and
or weakness. hemiplegia or
There is left paralysis of one
sided neglect. side of the body. Long Term Disabilities
Not aware that 2. Impaired speech-
there is problem language If the brain is in fault, it will cause disabling
on the left side. (aphasia). neurologic deficits for long term. This will be
2. Spatial- Expressive affecting activities of daily living.
perceptual aphasia or non-
defects. fluent aphasia Motor function
Dominant is the damage to the a. Loss of skilled voluntary movements-
right side so Broca’s area. Akinesia
patient neglects Damage to
b. Impairment in the integration of movement
the left side. Wernicke’s area
3. Tends to deny or located at the left especially for those tasks that they had
minimize superior, posterior learned before the stroke. They cannot
problems. temporal lobe perform it anymore. They know the task
4. Rapid supplied by the but they cannot perform it. - Apraxia
performance, middle cerebral c. Alteration in muscle tone
short attention artery. Or, can be o Flaccidity- during the hypo reflexive
span. Due to global or both. stage or acute phase r/t nerve
negligence of 3. Impaired right-left damage (6-8 weeks) if prolonged
the left side of discrimination. prognosis is not good
the body. agraphestesia o Spasticity- hypertonicity r/t
5. Impulsive; safety and interruption of UMN or upper motor
problems. asteriognosis.

NCM 112 NGIMPEC LECTURE NOTES 35 | P a g e

 Quadrantanopsia
NCM 112: NGIMPEC LECTURE NOTES
neuron which is the corticospinal a. Bitemporal heteronymous
tract hemianopsia
d. Alteration of reflexes (documented in the b. Homogenous hemianopsia
stick man) o That can complicate these abilities.
o Hyporeflexia
o Hyperreflexia
e. Hemiparesis/hemiplegia contralateral
o r/t damage on corticospinal tract
f. Dysphagia a 10
o r/t damage in CN IX and CN X

Languages and speech problem in voice

pitch or quality
a. Dysarthria- r/t to coordination of muscles
of the tongue. No problem in interpretation
of the language but there is problem in
articulation of words. There is long pauses
between the words. Problem in
coordination r/t problems in cerebellum
and CN.
b. Aphasia- MCA left vascular lesions
c. Dysphasia
o Non fluent Diagnostic tests
o Fluent
o Global 1. CT san
o Expressive - As soon as the patient arrives
o Receptive - Without contrast medium
- Indicate size, location of lesion,
Affect differentiate ischemic and hemorrhagic.
a. Depression- r/t damage on the axons on - Ischemic: hypodensity
the white matter of the brain and also - Hemorrhagic: hyperdensity
secondary to body disturbance in patients
with neurologic disability. Slurring of
speech and disturbed gait could disturb
body image.

Elimination
- Least affected in stroke patients.
a. Urinary and bowel problems-
disturbances here may be initial or
temporary and later will be restored to
normal. Bowel problem is not directly
related to stroke but to immobility caused 2. MRI
by the stroke. - Magnetic Resonance Imaging is a
Visual medical imaging technique that uses a
- Can be complicated more if there is magnetic field and computer-generated
problem with the CN that are radio waves to create detailed images of
responsible for extraocular movements the organs and tissues in the body. Can
resulting to the different types of identify the extent of the injury.
blindness on the visual fields. 3. Diagnostic Cerebral Angiography

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 NCM 112: NGIMPEC LECTURE NOTES
- Invasive, cause puncturing of the blood
vessel, access is the femoral introducing
a dye.
- Before performing assess allergy to
iodine, because it is from shells. After
the dye is introduced there is a feeling of
heat
- Guided by an X ray.
- After, monitor for signs of bleeding
because this involves the blood vessel.
4. Transcranial Doppler V72
- Measures the speed or velocity of blood
flow in cerebral arteries.
- TCD ultrasound is a painless test that
uses sound waves to detect medical
problems that affect blood flow in your
brain.
- There are sound waves that measure
the flow of blood inside the cerebral
circulation.
5. Lumbar tap or puncture
- Get the CSF for examination
- Not indicated with increased ICP
because this can cause brain herniation.
Implementations/ Interventions
onlyremoved prevent stasis of blood and prevent clot
duffowers
NCM 112 NGIMPEC LECTURE NOTES
1. Respiratory:
a) Airways—ET, tracheostomy,
b) Assist in mechanical ventilation: Mech
vent for assistance of O2 requirement
c) Perform pulse oximetry to monitor O2
saturation Normal 95-100 mmHg.
d) Prevent Aspiration
e) Maintain adequate oxygenation
2. Neurologic system:
a) Monitor LOC
b) Monitor mental status
c) Perform GCS
d) Monitor pupillary response
e) Monitor extremity movement and
strength (corticospinal tract carries the
voluntary motor movement, assess
using appropriate scoring and
document in stickman)
f) Monitor V/S, S/S or increased ICO,
CPP
3. Cardiovascular system
- Maintain adequate cardiac output to
)deliver vertebral circulation adequately.
a) Monitor VS
b) Monitor Cardiac Rhythms
c) Monitor I&O to ensure that there is
enough fluids that maintain CO to
increased blood volume. Ensuring
balance in I&O
d) Regulate IVF to ensure that the rate is
correct according to its prescription to
make sure that there will be enough
fluid for the expansion of the blood
volume.
e) Adjust fluid intake to individual needs.
f) Monitor heart sounds.
g) Monitor lungs sounds for crackles and
rhonchi indicating pulmonary
congestion especially if there is lad of
fluid administration. This may
complicate cardiac output.
Prevent DVT
a) Perform active of passive ROM
b) Positioning to prevent dependent
edema.
c) Compression stocking to prevent
dilatation of blood vessels and promote
2411 venous return of blood to heart. To
formation.
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 NCM 112: NGIMPEC LECTURE NOTES
d) Use of LMW heparin example is
Lovenox prefilled don'taspirate
e) Measure the thigh and calf OD. This is
done to observe for swelling. Document
with separate sheet.
f) Observe swelling of lower ext.
g) Note unusual warmth at the LE.

4. Musculoskeletal System (prevent

contractures and deformities)
a) Posterior, legs splints, footboard, high
topped-tennis shoes.
b) Use of tronchanter to prevent external
rotation of the hip
c) Hand cones to maintain the position of
function of the hands, not rolled towels.
d) Hand splints to prevent contracture of
the hand
e) Avoid pulling by the arm when moving
up support the back to avoid frozen
Hand splint to support the hand to prevent
shoulder.
contracture
f) Arm support with slings especially with
hypotonic muscles. We can support the
hypotonic muscles with slings.

Performing ROM
Support the patient when moving fully to
expand lungs
Considerations when moving the patient q2h
into one side example when 1 side is
paralyzed and with compromised circulation,
let the patient stay on that side for 20 minutes
then turn again inconsideration with the
compromise flow on the weak side of the body.

Footboard to prevent foot drop

To maintain the position function of the
foot

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Self-care activities
Undressing: Start from unaffected side, this
can help the affected part to move.
Dressing: Start at the affected part then the
unaffected part. Unaffected will help the
affected side insert the clothes.
bladder
training
during
waking
hours
5. Integumentary
a) Pressure relief by position changes
o If early mobility is not possible, turn
the patient in prone position many
times a day, this can relieve back
pressure and promote lungs
expansion. (Done in covid patients
even with tubes)
NCM 112 NGIMPEC LECTURE NOTES
b) Good skin hygiene
c) Emollients
d) Early mobility
6. GIT System
a) Feed the patient after the acute phase
is controlled.
b) IVF
c) TPN
d) NGT
e) Oral feeding- assess for gag,
swallowing and chewing reflexes to
facilitate eating, as well as pocketing
(gakabilin ang food sa sulod and indi
ma swallow). If these reflexes are
present, start with mouth care, high
fowler’s position, foods that are easy to
swallow are given (consistency of
oatmeal like lugaw) Place the food on
unaffected side. No milk products
because this can mix with saliva and
difficult to swallow. No pureed foods
and thin liquids because this is highly
liquid and can cause aspiration.
f) Manage constipation. Increase fluid
intake if not contraindicated. Administer
high fiber diet. Formulate din NGT if
present. Administer stool softeners and
mobility to help peristaltic movement
inside the GIT
7. Urinary System
a) Indwelling catheterization acute phase
to manage diuresis. Temporary,
because it can be restored after the
acute phase.
b) Clump the catheter and instruct the
patient or family that whenever the
patient will feel like voiding, open the
clump and after draining the urine
clump again. Observe if patient can
feel the urge to void, open the clump
again, until there is 2-3 sensation.
After removal if there is no urge to void,
do the intermittent catheterization.
Straight catheter, not indwelling.
c) Bladder retraining program:
o Adequate fluid intake 8am-7pm
o Toileting q2hrs- bedpan,
commode, bathroom.
o Note signs for restlessness
o Indicate need for urination
8. Communication
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a) Gestures: Sign languages
b) Speak slowly and calmly
c) Use simple words and sentences that
can easily be understood
d) Give time to respond
e) Present ideas one at a time
f) Let the person speak do not supply the
words
g) Do not interrupt
9. Sensory-perceptual alterations
a) Homonymous hemianopsia-
arrange environment within perceptual
field.
b) Arranging food tray on unaffected side
c) Teach to scan neglected side.
d) Check paralyzed side for adequacy for
dressing, hygiene, for trauma.
e) Eye patch for diplopia
f) Absent corneal reflex: use artificial
tears or gel; eye shield at night to
prevent injury of cornea.
10. Coping
a) Give simple clear explanation
b) Educate the patient and family about
simple pathophysiology and
manifestations of stroke and how to
cope. Involve the family.
11. Rehabilitation
a) 12-24 hours after the stroke
b) Refer to a specialist, departmentalized;
referred to physiotherapist
c) To preserve life
d) To lessen disability
e) To attain optimal function
f) Refer to physiatrist
Lesson 5: PARKINSON’S DISEASE
- A problem of nervous system
- Degenerative, there is a progressive
decline in function in a part that is
affected which is the basal ganglia
- Manifested by poverty of movements or
slowness of movement
- Related to repeated blows in the head
Incidence
- Higher among the aged population form
50-60 years old and commonly among
male
- Secondary type of parkinsonism occurs
at younger age, 30s to 40s,
NCM 112 NGIMPEC LECTURE NOTES
o Secondary type of parkinsonism
such as use of antipsychotic
agents, having abused drugs,
antihypertensive medications
Etiology
- Unknown
Risk Factors
1. Degeneration of the substantia nigra
o Primary form of parkinsonism in
which there is an unknown
cause of degeneration
o Related to aging, increase
incidences of this case among
50 years old or above
o Substantia nigra is one of nuclei
reiof basal ganglia located at
midbrain where dopamine is
secreted posterior of substantia
nigra
o Paralysis agitans, first describe
by James Parkinsons in 1817
which entitled Shaking Palsy
2. Genetics
o A gene that can predispose this
disease is called parkin gene
o Cause familial tendency of
parkinsonism
3. Post Encephalitic Syndrome
o Infections in the brain can cause
movements just like in
parkinsons
o Found out in 1930s to 1940s
when there is an epidemic of
encephalitis
o Levodopa is a drug of choice for
parkinsonism but not a cure only
palliative
4. Repeated Head Trauma
o due to continuous blows on head
such as in boxing can cause
parkinsonism
5. Antipsychotic: phenothiazines,
haloperidol, lithium, Prozac
o Secondary
o Antidepressants which are used
in psychotic patients and causes
extrapyramidal symptoms
affecting the basal ganglia
descending down to the spinal
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 NCM 112: NGIMPEC LECTURE NOTES
cord and delays the reuptake of - 5 nuclei present in both cerebral
dopamine hemisphere: head of caudate,
o Neurotransmitters that release putamen, Globus pallidus, subtantia
to the vesicles have agents and nigra, subthalamic nucleus
substances called enzymes - Putamen and caudate nucleus
which degrades the collectively called the striatum are the
neurotransmitter and reuptakes chief input areas of motor impulses
in the vesicles for next use, this coming from cerebral cortex
is rapidly occurring for dopamine - Forwarded into nigrus striatal pathway,
to be used putamen and caudate has the
abundance of acetylcholine which is
6. Antihypertensives: methyldopa, excitatory and natural inhibitory
reserpine neurotransmitter which is GABA and
o Side effect will be on basal the excitatory movement will be passed
ganglia which is extrapyramidal into substantia nigra
symptoms - Substantia nigra function in basal
ganglia is to modulate the initiation,
7. Toxins that cause damage to the brain execution, and completion of voluntary
o Such as organic solvents and automatic movements associated
o Exposure to chemicals such as with skeletal muscle activity so if this is
paint thinner damaged it will cause movement
o Manganese disorders as seen in Parkinson’s
o MPTP or methylphenyl Disease and Huntington’s Chorea
tetrahydropyridine produce from
narcotic agents
o Exposure to lead cause poising
o Well water contains different
minerals
o Carbon monoxide poisoning
o Carbon disulfide
o Pesticide
o Methanol
o Cyanide

- Globus pallidus is the chief output area

Part of Nervous System involved in
Parkinson’s Disease
- Basal ganglia which is comprised of 5
nuclei
of basal ganglia
- Subthalamic nuclei serves as input
area from the cerebellum
- Substantia nigra located at the midbrain
is responsible for secretion of
dopamine
- Striatum (putamen and caudate
nucleus) have the abundance of
excitatory acetylcholine responsible for
excitement of movement

Substantia Nigra

- Anterior cut of the brain

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 NCM 112: NGIMPEC LECTURE NOTES
Pathophysiology of Parkinson’s

Normally, the cerebral cortex is going pass the

- Black in color because reach in crude motor movement to basal ganglia while
substance melanin processing and the chief input areas are
- This is where dopamine is secreted caudate nucleus and putamen which have the
posteriorly abundance of excitatory neurotransmitter
- Dopamine will regulate all over acetylcholine to excite the movements, these
excitability caused by acetylcholine in movements will be processed or forwarded
circuit from the nigrostriatal pathway to into substantia nigra where dopamine is being
putamen and caudate nucleus then to secreted which will going to pass through
globus pallidus to thalamus to motor nigrostriatal pathway from here dopamine will
circuit refine the movements or regulate the crude
movements from striatum. From the
What happens in primary time of substantia nigra already with dopamine, these
Parkinsonism? movement will go back to the striatum which
- Paralysis agitans have the has dopamine will regulate the excitability
degeneration of substantia nigra which caused by acetylcholine so that with dopamine
is paler than normal already in the circuit it will regulate the over all
excitability of movement along the circuit going
Action Potential to the globus pallidus which is the chief output
area but there are circuits attached to globus
pallidus that no longer part of circuit which will
be affected in parkinsonism. This movement
regulated by dopamine, balance between
acetylcholine and dopamine to make this
movements refined this will now be forwarded
from globus pallidus to thalamus. Thalamus
will serve as triage area for this inputs and the
chief output of thalamus will be the refined
motor movement which will be forwarded to
the motor cortex which is responsible
releasing the refined and smooth muscle
movement. So, you have here the interplay of
2 excitatory acetylcholine and 1 inhibitory
Dopamine dopamine.
- Function of dopamine is to cause the
muscle to work smoothly, under precise In paralysis agitans or parkinsonism,
control, and without unwanted substantia nigra will decrease production of
movement dopamine as a result when the motor functions
- Whenever we have a decrease in will be forwarded to substantia nigra, less
dopamine this will result to crude dopamine will be going along with it going back
movement which is not refined to the striatum so you will have a relative
increase in acetylcholine or same amount

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 NCM 112: NGIMPEC LECTURE NOTES
being secreted in striatum, so there is
imbalanced of acetylcholine which is
increased and dopamine which is decreased
so the movements produce are more crude
and more excited which produces tremors
which is the outstanding signs of parkinsonism
Clinical Manifestations
1. Tremor
o Cardinal sign of Parkinson’s
o Describe as pill-rolling of the
thumb and index finger
o At first unilateral but later
bilateral and even involved the
face
o Resting tremor, while the person
is at rest shaking will continue
but whenever holding something
it will disappear
o Pill-rolling tremor is a significant
characteristic in parkinsonism,
rhythmic oscillating contractions
or movements of muscle
2. Rigidity
o Cardinal sign of Parkinson’s
o Resistance to movement
o Seen when performing
assessment of muscle tone by
passive movement
o Describe as cogwheel or
ratchet-like movements
3. Bradykinesia
o Cardinal sign of Parkinson’s
o Slowness in movement
o Masked-like face with decrease
expression of emotion
o Loss of blinking reflex
o Failure to express emotion
o Dysphagia
i. related to rigidity muscles
in swallowing
ii. difficult to swallow saliva
as a result there is
drooling of saliva
iii. In parkinson’s there is
hypersalivation which
also accounts for drooling
of saliva
iv. Rigidity of throat muscles,
palate, and tongue
v. Slow monotonous voice
called hypophonia
o Hypokinesia
NCM 112 NGIMPEC LECTURE NOTES
i. Also called freezing,
where there is slowness
in movement or making a
pivot
o Micrographia
i. Small crumpled hand
writing
o Bradyphrenia
i. Slow answers to
questions
4. Loss of Postural Reflexes
o Posture is stooped: the head is
bent forward which is potential
for injury
o Gait is shuffling with festination:
short steps as if the foot is glued
to the floor
5. Other Manifestations
o Affecting ANS functioning
o Hyperhidrosis or excessive
swearing
o Hypohidrosis or decreased
sweating
o Hypersalivation which results to
drooling of saliva
o Seborrhea or excessive
accumulation of fats on the skin
o Orthostatic hypotension when
happens commonly when there
is sudden getting up from bed
o Gastric and Urinary Retention
o Sexual Dysfunction
6. Cognitive: Dementia
o Related to problems in cerebral
cortex
o Late in the disease progression
there is loss of memory which is
dementia
o Progressive dementia have
about 80% damaged in the brain
o Affect: depression because
basal ganglia is center for
emotions
Assessment and Diagnostic Findings
- Diagnosis for Parkinson’s disease
would be only observations and
collection of data from thorough health
history because there is no specific test
for parkinsonism
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- If 2 out of 4 cardinal signs present in the
patient, parkinsonism can be
diagnosed
- PET scan can help but not definitive of
parkinsonism
o Functional imaging technique
using radioactive substances
such as radiotracers to visualize
changes in metabolic processes
and in other physiological
activities such as blood flow,
regional chemical composition,
and absorption
Nursing Interventions
1. Improve Mobility
- Physical therapy
- Passive and active ROM to prevent
contractures and promote circulation
- Stretch exercises can be taught to
patient
- If client freezes suggest of something to
walk over
2. Use of Assistive Devices
- Such as canes, walkers, crutches, and
wheel chair
3. Warm baths and massage to relax the
muscles
- Whirlpool water can improve circulation
and relax muscles
4. Encourage independence in self-care
- Teach the patient because
parkinsonism is chronic
5. Improve communication abilities
- read aloud because of hypophonia
- listen to own voice
- enunciate each syllable
- refer to speech therapy if necessary
NCM 112 NGIMPEC LECTURE NOTES
6. Maintain adequate nutrition
- Weigh weakly
- Provide small frequent feedings
- Cut food into bite-size pieces to prevent
aspiration
- Give supplemental feedings
7. Teach patient on how to swallow
effectively
- upright position during mealtime
- semisolid foods with thick liquids
- teach to place food in the tongue, close
lips and teeth, lift tongue up then back
and swallow
- chew first on one side of mouth then on
the other
- to control build up of saliva, remind to
hold head upright and make a
conscious effort to swallow
8. Manage constipation
- Maintain adequate bowel elimination
- Increase fiber, fluids if not
contraindicated, mobility
- Stool softener
9. Provide psychological support
- Refer to support groups such as prayer
groups
10. Administer Antiparkinsonian Medications
- Levodopa is drug of choice
o MOA is converted to dopamine
in the basal ganglia
o no foods rich in pyridoxine
because can interfere with
absorption
o sweat and urine may be
darkened
- Carbidopa-Levodopa (Sinemet)
o MOA is preventing breakdown of
dopamine in the periphery
o Levodopa is combined with
carbidopa to reduce nausea side
effects and to ensure that
levodopa is converted to
dopamine in the brain and not in
the intestine or blood
- Anticholinergic Therapy
o Inhibits acetylcholine production
to relieve tremor and rigidity
 Trihexyphenidyl (artane)
 Benztropine (Cogentin)
 Procyclidine (Kemadrine)
- Antiviral Therapy
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 NCM 112: NGIMPEC LECTURE NOTES
o MOA is augmenting the release
of dopamine from intact
dopaminergic terminals in
nigrostriatal pathway
 Amantadine HCL
(Symmetrel)
o Block the action of the
neurotransmitter glutamate
which allows for an increase in
dopamine release
- Dopamine Agonists
o MOA is acting directly to
stimulate dopamine receptors
 Bromocriptine mesylate
(parlodel)
 Pergolide (permax)
 Ropinirole (ropinirole)
 Pramipexole (sifrol)
o Agents that mimic dopamine and
bind to the receptors in the
neuron’s synapse
- Monoamine Oxidase Inhibitors
o MOA is inhibiting dopamine
breakdown and slows
progression of the disease
 Selegeline (eldepryl)
- Antihistamines
o MOA is reducing tremors with
mild anticholinergic and sedative
effects
 Diphenhydramine HCL
(Benadryl)
 Orphenadrine citrate
(baniflex)
- Catecho-O-Methyltransferase
inhibitors
o MOA is blocking an enzyme that
metabolizes levodopa making
more levodopa available for
conversion to dopamine in the
brain
 Entacapone (comtan)
 Tolcapone (tasmar)
Surgical Management
- Guarantee of most surgeries will only
be five years
- Most common is stem cell
1. Deep Brain Stimulator
NCM 112 NGIMPEC LECTURE NOTES
o Electrodes are inserted into 5
nuclei of basal ganglia with
connective wires that can be
regulated attached to a
pacemaker and will be regulated
by patient
o Thalamic Stimulation
o Electrodes are inserted into the
brain and fed with thalamic
pacemaker implanted in the
thorax
o Performed with O-ARM imaging
system
o Electrodes are placed deep
within the brain through small
holes in the skull. The electrodes
are connected by an extension
wire to a battery-powered
stimulator placed under the skin
of the chest. Because the left
side of the brain controls the
right side of the body and vice
versa, BDS is commonly
performed on both sides of the
brain. The patient is able to turn
the stimulator off and on with a
handheld controller
2. Thalamotomy or opening of the
thalamus and Pallidotomy or opening of
the globus pallidus
o Interfere nerve pathway and
thereby alleviate tremor or
rigidity
o High frequency energy current is
used to permanently destroy the
cells
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Lesson 6: HUNTINGTON’S CHOREA
- Inherited medical condition where there
is progressive degeneration or
breakdown of nerve cells in the brain
- The choric movements will just
continue as long as the patient is awake
- Involves the basal ganglia, there is an
imbalanced in acetylcholine and
dopamine
- Decreased acetylcholine related to
damaged of striatum and dopamine will
relatively increased
- Progressive involuntary choreiform
movement and dementia
- Treatment is only symptomatic
Pathophysiology

- In Huntington’s chorea, there is

enlargement of frontal horns of the
lateral ventricles
- Huntington’s chorea is the name
because it taken from Greek word
chorea which is dance-like
- Movements are jerky, expressive, and
coordinated more graceful than
parkinsonism
Cause
- Unknown
Onset
- 35 to 45 years old, middle aged
- Occur in younger people
Genealogy
- An autosomal dominant genetic
disorder each child has 50% risk
- In Huntington’s disease this results
from a mutation of huntingtin (HTT)
gene on chromosome 4
- Abnormal repetition of DNA sequence
CAG, which codes for the amino acid
glutamine
o Amino acid glutamine is the
precursor or building block of
protein
- Resulting gene product, a large protein
called huntingtin has an expanded
stretch of polyglutamine residues
- Accumulation of glutamine within
neurons and lead to disease via
unknown mechanisms
o Repeats of this abnormal gene
may be 10x up to 35x until
matured that accounts why the
manifestation of Huntington’s
can be seen mid life

Glutamine

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o Raising of eyebrows
o Rolling of eyes
o Protrusion and withdrawal of
tongue
o Shoulders are elevated,
depressed or rotated
o Piano-playing type movements
with alternating extensions and
flexion of fingers
2. Speech: slurred, hesitant, explosive,
eventually unintelligible
3. Bladder bowel control is lost
4. Chewing swallowing are difficult
- Building block of protein 5. Gait: disorganized until ambulation is
- Abnormally collects in the cell nucleus impaired
- Premature striatum of the basal ganglia 6. Personality Changes
o In which there is abundance of o Irritable
acetylcholine excitatory o Nervous
neurotransmitter however if o Impatient
damaged will be decreased and o Anxious
dopamine will increase relatively o Apathetic
over acetylcholine o Euphoria
o Decreased acetylcholine, o Psychoses
decrease excitement and have o Uncontrollable fits of anger
an overregulation of dopamine o Profound suicidal depression
on the same circuit as of 7. Cognitive
Parkinson’s o Hallucinations, seeing things
- Death of cells in the cortex involve in which is not present
thinking, memory, perception and o Delusions, believing things
judgement which are untrue
o Damaged from cerebral cortex o Paranoia, suspicious of many
with abnormal accumulation of things
glutamate o Judgement and memory are
- Death of cells in the cerebellum that impaired
coordinates muscle activity o Dementia
o Manifestations can be seen
which is problem in balance and Assessment/Diagnostic Findings
coordination of muscles 1. Depending on the clinical presentation
- Choreiform Movement Dementia of the patient
o Choreiform movement related to 2. Thorough health history must be taken
relative increase in dopamine 3. DNA testing
over acetylcholine
o Dementia related to loss of Management
function in cerebral cortex - No cure because cause is unknown
- Management is focused on
Clinical Manifestations symptomatic relief of symptoms
1. Choreiform Movements 1. To improve chorea:
o Sudden, jerky, irregular but o MOA is blocking dopamine
coordinated and graceful receptors
o Distal limb, face, tongue, o Protects the nerves in the brain
swallowing muscles are affected and spinal cord from too much of
o Accentuated by environmental a natural substance called
stimulation and movement glutamate that may be part of the
o Grimacing of face cause of nerve damage

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 Thiohexene HCL  Should continue unless
(Navane) and until disease
 Haloperidoldeconoate progression prohibits it
(Haldol)  People with HD should
 Riluzole (Rilutek) participate in outside
2. Antidepressants activities, socialize, and
o Palliative management pursue hobbies, and
3. Antipsychotics interests
o Palliative management
4. Promoting Home and Community-
based Care
o As support for patient and family
o Teach family and patient Lesson 7: SPINAL CORD INJURY
strategies to manage symptoms
− Which causes temporary or
such as chorea, swallowing
problems, limitation in permanent loss of functioning
ambulation, loss of bowel and − Translated to loss of motor muscle
bladder function functioning, sensation, and autonomic
5. Consultation with Speech Therapist functioning of the parts of the body that
o To improve communication
are served by the spinal cord below
6. Genetic Counselling
o Because of familial tendency, the level of injury
couples are advised to consider
counselling Brief Review of the Spinal Cord
7. Nutrition and Eating − The spinal cord is a two-way
o Give more time for meals
conduction pathway, and it exits to the
o Food cut into small pieces,
softened, or pureed foramen magnum down to just below
o Avoid diary products the ribs (the last of the ribs, towards
o Consume enough calories the back)/ the lumbar spine.
o Thicken water with additives to  Brings impulses from the parts of
the consistency of syrup before
the body to the brain and vice
drinking is possible
o Large quantities of fluids are versa.
given − About 18 inches long, whitish and
o If oral feeding is impossible, gelatinous, about the size of a thumb
NGT feeding is used − It is also a reflex center
8. Physical Rehabilitation
o Physical activity
 Daily exercise promotes
physical and mental well-
being ‘protect from falls
 Wearing special padding
during walks
 Small weights worn
around the ankles and
sturdy that when ever he
walks small weights can
balance the weight
 Well-fitting shoes that slip
on and off easily can help
improve stability − Spinal cord is protected by the vertebral
o Social Activity bodies and the meninges
− Spinal cord is still part of the CNS

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 NCM 112: NGIMPEC LECTURE NOTES
− Inside is the gray matter, which looks like
a butterfly or letter H, made up of nerve
cells bodies
− Outside is the white matter, contains the
cells coated with myelin; the reason why it
is whitish in appearance
− Posterior roots are located at the back and
branches off the back of the vertebral
column which carry the sensory impulses
− The anterior root branches off in front of
the spinal column, which carries motor
impulses
 These two roots will come together to
create the spinal nerves outside of the
spinal cord
 Spinal nerves are bout 1 inch long and
thhe function will be carried out by the
rami/ramus to the dermatum/skin or
the myotum/glands that will carry the
motor and sensory impulses
 Spinal nerves are both motor and
sensory; 31 pairs
SPINAL NERVES
− Named after their location
− 7 cervical spines; 8 cervical nerves, start
above C1
 C1 and C2 responsible for head and
neck functioning
 C3-C5 responsible for the diaphragm
 C5-C6 responsible for deltoids,
biceps, brachioradialis; wrist
i extenders by the C6 also
 Triceps have overlapping functions of
C6-C8 extensionreflex
− Thoracic spinal nerves will start at T1
down to T12
 T1 down to T7 are responsible for the
chest muscle
 T7 down to T12 responsible for the
abdominal muscles
− Lumbar nerves L1 to L5 responsible for
the leg muscles
− Sacral nerves S1-S5 responsible for the
functions of the bowel, bladder, and sexual
functioning
NCM 112 NGIMPEC LECTURE NOTES
COMMON CAUSES
 Vehicular accidents- 46%
 Falls- 22%
 Violence- 16%
 Sports- 12%
PREDOMINANT RISK FACTORS OF SCI
 Age- 15 to 35 years old: Age group which
is very active because they are still very
young
 Gender- male: because males are more
adventurous than females so they are
more at risk for accidents
 Alcohol and drug use
PATHOPHYSIOLOGY
Mechanisms of Injury ranges:
− Concussions: jarring or jolting of the
spinal cord which may be minor
− Contusions: more major; already have
the tearing of the tissues of the spinal
cord
− Lacerations
− Compression injuries which may
cause complete or incomplete cord
transections leading to paralysis
below the level of the injury; most
devastating effect of most neurologic
problems
2 CATEGORIES OF SCI
1. Primary: result of initial trauma, permanent
2. Secondary: result of contusion or tear injury
in which the nerve fibers begin to well and
disintegrate and produces: ischemia, hypoxia,
edema, hemorrhagic lesions resulting to
destruction of the myelin and axons
− Example: Hemorrhage will cause
breakdown of RBCS, breaking it into
hemoglobin and iron, increasing the
free radical formation. With injury it
can cause the release of arachidonic
acid: the release of this will result to
the production of pro-inflammatory
cytokines and prostaglandins, which
49 | P a g e
 if positive

negative

slightly

Pathophysiology

concussions
contusions
lacerations
compression

complete transection

paralysisbelow level
ofinjury
 NCM 112: NGIMPEC LECTURE NOTES
are initiated to cause the inflammatory CLASSIFICATION: MECHANISM OF
response INJURY
− Secondary injury causing hypoxia:  Flexion
With injury, there will be an increase of  Hyperextension
neutrophils and the production of  Flexion-rotation
Leukotrienes (as we had the release  Extensive rotation
of the arachidonic acid), activation of  Compression
kallikrein-kinin system, initiating the
inflammatory processes causing
vasospasm and edema. These
vasospasms and edema will result to
the decrease of spinal cord blood flow
causing tissue hypoxia
− Another thing with injury, it will cause
the activation of the coagulation
pathway, where you have the platelet
aggregation causing the formation of
microemboli, and likewise activating
the sympathetic nervous system. In
times of stress, to compensate which
will cause the release of
norepinephrine which will cause − Whiplash Injury: with impact injury, this will
vasoconstriction predisposing the cause the movement of the head with rapid
formation of thrombos or blood clots. acceleration and deceleration,
These formation of blood clots may hyperextension and hyperflexion of the neck,
cause occlusion on the circulation which causes a sprain or strain of cervical
decreasing the spinal cord blood flow tissues
resulting the the secondary injury:  Resulting from forceful, rapid back-and
tissue hypoxia. forth movement of the neck
− If treated immediately, this is to
prevent the secondary cascade that
will result to devastating neurologic
deficits.

− With hyperflexion, which is bending forward,

the facets joint in motion compressing the disc
inside and likewise, the inside of the spinal
cord.
− Hyper/extension or bending backward, there
is movement which causes the compression
of the contents inside

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 NCM 112: NGIMPEC LECTURE NOTES
The fragmentation of the vertebral
bone, these will be broken into several
pieces which will cause the
compression on the inside.

CLASSIFICATION: Level of Injury and extent

of paralysis

− Flexion-rotation Injury
Examples:
1. Heavy blow onto one shoulder
causing the trunk to be in flexion and
rotation to the opposite side
2. A blow or fall on postero-lateral
aspect of the head
Results:  Cervical spinal cord injury down to C6 will
1. Dislocation of the facet joints in one cause paralysis of both upper and lower
or both sides extremities.
2. Fracture dislocation of the cervical  Will cause tetraplagia or quadriplegia
vertebra  T6 injury will cause paraplegia: paralysis
While dislocating, the upper vertebra of the lower extremities
takes a slice of the body of lower  L1 injury: paraplegia
vertebra with it.  Sacral and coccygeal injury may cause
It is highly unstable injury. bowel, bladder and sexual dysfunction

− Axial Loading
 Compression of the spine
- Shallow water diving
- Jumping from height CLASSIFICATION: Degree of Injury
head first; will cause a compression of
the spine that may cause injuries such 1. Complete Spinal Injury: All functions
as: below the injured area are lost, whether or
 Ruptured disks not the spinal cord is severed. The shaded
 Vertebral fractures area shows the level of injury. This will
cause complete loss of movement and
sensation below the level of injury.
Complete cord transection

Both white matter brain

NCM 112 NGIMPEC LECTURE NOTES 51 | P a g e

 2
Tangiotensin

PlateletAggrivating factors
leukotrienes mediators

cause vasopermeability
vasodilation
broncho
spasm
 NCM 112: NGIMPEC LECTURE NOTES
2. Incomplete Spinal Cord Injury: Involves
the preservation of motor or sensory
function below the level of injury in the
spinal cord.
c. Brown Sequard Syndrome: shaded
a. Central cord injury: Shaded part of
the spinal cord is located at the center,
this is where control of the functions of
the upper extremities found. Below this,
there is loss of movement on the upper
extremities, if it central cord injury, with
incomplete loss below the level of
injury. The only movement and
sensation that is lost is the upper
extremity.
b. Anterior cord injury: Anterior part of
the spinal cord is responsible for the
motor functioning and the posterior is
for the sensation. The anterior portion
NCM 112 NGIMPEC LECTURE NOTES
of the spinal cord is injured and the
shaded part is the level of injury. Loss
of movement, pain, and temperature
because the location of spinothalamic
tract is located at the anterior portion
carries sensation of pain and
temperature and crosses at the spinal
cord to the brain. Still able to feel
position, vibration, and touch because
this is the function of posterior column
pathway.
part is half of the spinal cord. Posterior
and anterior damage. ½ posterior and
½ anterior on 1 side of the spinal cord
that is damaged.
o A. lateral corticospinal tract,
pyramidal tract that originates from
the cerebral cortex and descend
down crossing the medulla
oblongata to the spinal cord and
innervate at the lower motor
neurons at the different segments
of the spinal cord, cervical,
thoracic, and lumbar.
o B. Lateral spinothalamic tract
which crosses at the level of the
spinal cord and ascends to the
brain stem, decussating carrying
sensations to the brainstem to the
thalamus.
o Dark blue (left side): Loss of
vibration, motor function, deep
touch, and position on ipsilateral
side. Damage on the lateral
corticospinal tract.
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 NCM 112: NGIMPEC LECTURE NOTES
o Light Blue (Right side): Loss of
pain, temperature and light touch
on contralateral side, related to the
decussation of spinothalamic tract.
Damage on the lateral
spinothalamic tract.

Actions of the spinal nerves

Functions after complete cervical spinal
Level Motor function
cord injury
C1-C6 Neck flexors
Level Motor Respiratory
C1-T1 Neck extensors
Function Function
C3, C4, C5 Supply Diaphragm Both
C1-C4 Full paralysis of Cannot
motor and sensory
the limbs breathe
(Mostly C4). Phrenic
without
nerve innervated for
endotracheal
diaphragm functioning
tube attached
for respiratory purposes.
to mechanical
C5-C6 Move shoulders, raise
ventilator
arms (deltoid); flex
C5 Paralysis of the Difficulty
elbow (biceps and
wrists, hands, coughing, may
brachioradialis)
and triceps. need help
C6 Externally rotate
clearing
(supinate) the arm
secretions.
C6, C7 included Extend elbow and wrist
Needs
C8 with (triceps and wrist
endotracheal
overlapping extensors); pronate
tube attached
functioning wrist
to mechanical
C7-T1 Flex wrist; supply small
ventilator
muscles of the hand
C6 Paralysis of the Difficulty
T1-T6 Intercostals and trunk
wrist flexors, coughing, may
triceps, and need help above the waist.
hands clearing T7-L1 Abdominal muscles
secretions. L2, L3, L4 Adduct thigh; extend leg
C7-C8 Some hand Need at the knee (quadriceps
muscle mechanical femoris)
weakness, ventelator L4, L5, S1 Abduct thigh; flex leg at
difficulty the knee (hamstrings);
grasping and dorsiflex foot (tibialis
releasing. anterior); extend toes.
L5, S1, S2 Extend leg at the hip
(gluteus maximus);
plantar flex foot and flex
toes.

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 NCM 112: NGIMPEC LECTURE NOTES
Phrenic Nerve: Originates from the anterior
rami of the C3 through C5 nerve roots consists
of motor, sensory, and sympathetic nerve
fiber. This provides complete motor
innervation to the diaphragm and sensation to
the central tendon aspect of the diaphragm.
Patient cannot breathe with involvement
damage of C3-C5 or Phrenic nerve.

Thoracic cord injury

T1-T5  Paraplegia with
Conus medullaris: tapered lower end of the
diaphragmatic
breathing spinal cord near the lumbar vertebral levels 1
(L1) and 2 (L2) going down. The nerves will
 intact arm function
converse below, converging at the lower
(function of C-S
portion.
nerves), loss of leg
function, bladder,
bowel with sensation
down to nipple line
T6-T12  Paraplegia with no
abdominal reflexes at
T12
 usually spastic
paralysis of lower limbs
 at T12, sensation
Cauda equina: bundle of spinal nerves and
present down the groin
spinal nerve rootlets, consisting L2-L5 nerve
Conus  Bowel bladder
pairs, S1-S5 nerve pairs, and coccygeal
Medullaris sphincter dysfunction
nerve, arising from lumbar enlargement and
 lower leg weakness
conus medullaris.
 sacral dermatome
hyperaethesia or
anesthesia
Spinal vs neurogenic shock
 back pain
- During acute phase
Sacral Injury
Spinal Shock Neurogenic
S1-S5  Loss of bladder bowel, shock
sex function Definition Immediate Sudden loss
 Foot displacement temporary loss of the
 No paralysis of leg from of total power, sympathetic
S3-S5 sensation, and nervous
reflexes system
(hyporeflexia) signals.
below the level
of injury.

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 NCM 112: NGIMPEC LECTURE NOTES
BP Hypotension Hypotension with afferent and efferent nerves
r/t sympathetic through the pudendal nerve. Used to
dysfunction assess for presence of spinal shock.
Pulse Bradycardia r/t Bradycardia This has to be indicated if necessary,
parasympathe with physician’s order.
tic NS located - The test involves monitoring
below the level internal/external anal sphincter
of injury contraction in response to squeezing
Bulbovacerno Absent Variable the glans penis or clitoris, or tugging on
sus reflex an indwelling Foley catheter.
Motor Flaccid Variable - This reflex can also be tested electro
paralysis physiologically, by stimulating the penis
Time 48-72 hours immediately after or vulva and recording from anal
SCI sphincter.
Mechanism Peripheral Disruption of - When the reflex is absent this means
neurons autonomic that the patient is in spinal shock. The
become pathways-> anal canal sphincter will not contract
temporarily loss of when the reflex is absent.
unresponsive sympathetic Video Presentation
to brain stimuli tome and
vasodilation.

NOTE!

Spinal shock is the altered physiologic state

immediately after a spinal cord injury (SCI),
which presents as loss of spinal cord function
caudal to the level of the injury, with flaccid
paralysis, anesthesia, absent bowel, and
bladder control, and loss or reflex activity.

Neurogenic shock is a combination of both

primary and secondary injuries that lead to
loss of sympathetic tone and thus unopposed
parasympathetic response driven by the
vagus nerve. Consequently, patients suffer
from instability in blood pressure, heart rate,
and temperature regulation.

Bulbovarenosus reflex (BCR)

- Somatic reflex useful for gaining
information (use fro assessment) about
the state of the sacral spinal cord
segments indicative of intact spinal
reflex arcs (S2-S4 spinal segments)

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 NCM 112: NGIMPEC LECTURE NOTES

Diagnostic Tests:

NCM 112 NGIMPEC LECTURE NOTES 56 | P a g e

 NCM 112: NGIMPEC LECTURE NOTES
1. MRI
2. CT Scan
3. Spinal Myelography/Myelogram
- Introduction of the dye into the spinal
cord.
- To do this prepare your lumbar tap set
because they are going to insert a
needle at the space between L3 and L4
just like performing the lumbar tap.
- After the dye is introduced, they will
monitor it using the X ray to determine
the injury.
- A myelogram requires the injection of
dye into the spinal canal under the X ray
guidance. The dye is usually injected in
the lower back region (lumbar) and in
some cases, in the neck (cervical) area.
- Performed at X ray department.
4. Spinal X Ray
5. Angiography
Management
A. Pharmacological
1. Methylprednisolone (Solu-medrol)
- Steroid, it has been found out that the
administration of steroids within 8 hours
after the spinal cord injury, may prevent
secondary complications or cascade of
event after the primary injury.
- Reduce the edema below the level of
injury.
NCM 112 NGIMPEC LECTURE NOTES
2. Vasoactive inotropic agents
- For those with hypotension
3. Anxiolytics
4. Laxatives
5. Muscle relaxants (Baclofen, Lioresal,
Diazepam)
6. Analgesics
- For pain
B. Non-Surgical
1. Immobilization devices
a. Cervical collar. Use of cervical collar
to stabilize or align the cervical spine.
To support the neck and spine and limit
the head movement after the injury.
b. Stryker frame. Help move the patient
in one unit. Secures the patient in
position and permits turning in various
planes without individual motion of
parts.
c. Skeletal tractions. Halo tractions
attached to halo vests. Crutch field
tongs can be replaced of this especially
after discharge from the hospitals.
Stabilize the alignment of the cervical
spine. Worn 24 hours/day. Prevent
moisture inside by wiping, open at the
side and clean the skin to maintain the
skin integrity and return in place. Even
if asleep, this has to be used. Consists
of halo ring, bars attached to the vest.
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 NCM 112: NGIMPEC LECTURE NOTES

d. Cervical Tongs (Crutchfield gardner

wells vinke). Skeletal traction inserted 2. Spinal fusion. Designed to stop the
to the skull then attached to a weight to motion at the segment of the spine that is
maintain the alignment of the cervical the cause of the patient’s pain. Bones are
spine. used to fuse the vertebra.

e. Crutchfield tongs. Fit into the parietal

bones. A special drill point with a
shoulder is used to enable an accurate Nursing Management
depth of hole to be drilled. To maintain
the alignment of the cervical spine. A. Emergency Care
1. Assess ABC
o Do not move during assessment
o If airway obstruction exists: do not
hyperextend the neck, use jaw thrust
o Suspect always that if it not yet
established, that there is cervical
spinal injury, we will treat that patient
as with cervical spine injury because
C. Surgery we may add to the injury.
1. Laminectomy. Also known as
decompression surgery. The bone is
removed to relieve the stenosis. The entire
lamina is removed for decompression of
the cord. Creates a space by removing the
lamina- the back part of the vertebra that
covers spinal canal. Enlarges the spinal
canal to relieve the pressure on the spinal
cord or nerves. 2. Perform quick cephalocaudal assessment

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 NCM 112: NGIMPEC LECTURE NOTES
3. Immobilize in the position found until help c. IOF intake up to 3000 cc/day
arrives. d. Acid ash foods to acidify urine to
4. Once emergency help arrives: prevent UTI
a. Assist in immobilizing the head and D. Chronic Care
neck with cervical collar, 1. Spasticity
b. Place on spinal board, transfer the a. Baclofen, dantrolen, diazepam
patient as one unit (muscle relaxants)
c. Avoid any movement during transfer, b. Physical therapy; stretching
especially flexion of spine. exercises, warm tub baths (may
cause vasodilation and relax
muscles), and whirlpool. promote circulation
2. Autonomic dysreflexia
- Complication that may occur after the
spinal shock is over. Spinal shock may
occur up to days, weeks, or longer, after
that, this occurs especially when the
SCI occurred above the T6 involving
5. Evaluate respiration, observe for weak or
the cervical spine up to T6. There is the
labored breathing.
ff:
B. Acute Care
a. Sudden significant increase of BP
1. Maintain optimum respiratory function
b. Occurs in cord lesions above T6-
a. Observe for weak labored breathing
common in cervical injuries.
b. Monitor ABG
c. Reflex response to sympathetic
c. Prevent pneumonia, atelectasis
nervous system outflow when there
d. ET/Tracheostomy- MV
is already cutoff at the level of T6
2. Maintain optimal cardiovascular
d. Stimuli: distended bladder or bowel,
functioning
decubitus ulcer, chilling, pressure
a. Monitor VS
from bedclothes. Pain from the
b. Apply compression stocking
visceral glands such as ejaculation,
c. Observe for S/S of DVT such as
dysmenorrhea, and abdominal pain
swelling of LE, increased temp on the
can also trigger this
area, increase size pf LE.
e. Symptoms: severe headache,
3. Maintain fluid/electrolyte balance and
increased BP, bradycardia,
nutrition
sweating, goose bumps, nasal
4. Maintain immobilization and spinal
congestion, blurred vision,
alignment ALWAYS
convulsions.
5. Prevent complications of immobility
a. PNA
The Autonomic Nervous System
b. Atelectasis
- Part of the peripheral NS
c. Impairment of skin integrity
- Involved with involuntary motor
d. Decubitus ulcer
movement, consist of nerve pathways
e. Constipation
f. Bowel and bladder problem
6. Maintain urinary and bowel elimination
a. Stool softeners
b. Catheterization

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 NCM 112: NGIMPEC LECTURE NOTES
Parasympathetic NS has preganglionic and
postganglionic nerve pathways located at the
thoracolumbar spine. The outflow of the
sympathetic NS at side of the thoracolumbar
spine. The anatomic location of the
sympathetic outflow would be form T1-L12.
a. Preganglionic. Have neurotransmitters
involved. Acetylcholine
b. Postganglionic. Norepinephrine
Adenergic N
Sympathetic NS: Thoracolumbar location.
Fight or Flight (Exercise, Embarrassment,
Excitement)
a. Dilates the pupil
b. Inhibits the flow of saliva
c. Accelerates the heartbeat
d. Dilates bronchi
e. Inhibits peristalsis and secretion
f. Conversion of glycogen to glucose
g. Secretion of adrenaline and
noradrenaline (if understress)
h. Inhibits bladder contraction
Parasympathetic NS. Made up of nerve
pathways but only preganglionic located at the
areas they are serving at the medulla
oblongata and sacral (Cranioscaral)
(Acetylcholine neurotransmitter). Rest of
digest (Digestion, Defecation, Diuresis)
a. Constricts pupils
b. Stimulates flow of saliva (vagus nerve
is located at the medulla oblongata for
digestion)
c. Slows heartbeat
d. Constricts bronchi
e. Stimulates peristalsis and secretion
f. Stimulates release of bile
NCM 112 NGIMPEC LECTURE NOTES
g. Contracts bladder
Explanation
Pain from the visceral glands such as
ejaculation, dysmenorrhea, and abdominal
pain can also trigger the sympathetic outflow
below the level of T6. The red line marks the
cutoff communication between these areas.
So there is no regulation of sympathetic
outflow if this will be stimulated. The factors
that trigger the sympathetic outflow from the
level of T6 (SANS is sympathetic autonomic
stimulation below the level of T6) that will
cause vasoconstriction. Vasoconstriction will
elevate the BP with severe headache and
goosebumps. The vasoconstriction cannot be
regulated by the parasympathetic NS because
there is a cutoff communication form damage
of T6. However, this hypertension can be
sensed by baroreceptors by the aortic arch
and this will then signal to the medulla
oblongata at the brainstem stimulating the
function of vagus nerve so that this will cause
bradycardia (sweating, blurring of vision, and
nasal congestion).
What to do? EMERGENCY
1. Immediately after checking that the BP
is high, raise to sitting position. Above
90-degree angle to help the flow of
circulation to lower down the BP
2. Check the source of the stimulus
3. Remove offending stimulus. If its
bladder distention immediately perform
catheterization. If it is bowel distention,
do the valsalva maneuver or remove
with your fingers using gloves.
4. Monitor BP
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 NCM 112: NGIMPEC LECTURE NOTES
5. Administer antihypertensives as order
(hydralazine- aperceline)
Lesson 8: SEIZURE DISORDER
 EPILEPSY – is a disorder of the central
nervous system, characterized by
recurrent seizures unprovoked by an acute
systemic or neurologic insult
o We call the attacked as seizure
 Seizure – clinical manifestation of an
abnormal excessive, hypersynchronous
discharge of a population of cortical
neurons
o The epilepsy and the convulsion are
all under the seizure disorder
o Can be primary or secondary as a
symptoms
o Sometimes we call this also as
convulsions
*EITIOLOGY/ CATEGORY
1. Unprovoked
o Primary or idiopathic (this is usually
related to:)
 Genetic – is there a history in the
family?
 Mostly occurring in epileptic syndrome
2. Provoked
o Secondary or acute
o Symptomatic – symptoms of some
underlying problems
*PRECIPITATING FACTOR OF PROVOKED
SEIZURE
 Metabolic disturbances:
o Electrolyte imbalances – example: we
have a syndrome of inappropriate anti-
diuretic hormone. This can cause
cerebral swelling
 With cerebral swelling, this may
alter the level of consciousness
and may increase the ICP and may
cause increase metabolic demand
in the brain. This can cause the
hyper-excitability of the neurons
o Alkalosis
NCM 112 NGIMPEC LECTURE NOTES
o Hypoxia – with decrease oxygenation,
this will alter the metabolic condition
inside the brain, causing
hyper excitability
o Uremia – toxins are not excreted. This
can cause alterations in the
metabolisms inside the brain
o Hypoglycemia – supposedly, the brain
should receive a 25 % of glucose of the
body. If there is a decrease delivery of
sugar to the brain, there will be less
energy. This can lead to hyper-
excitability of the brain, that my cause
hyper-synchronization and seizure
activity. This is also the same with
hypocalcemia and alkalosis
o Hypocalcemia
o Rapid withdrawal or sedative
drugs/drug toxicity – can also trigger
seizure activity
 Fever
- some children with fever may also
manifest seizure activity. Dilated
blood vessels may increase the
cerebral blood volume and may cause
pressure changes inside the brain.
- Some children may be very sensitive,
that makes their neurons
hyperexcitable and may cause this
abnormal firing in the neurons
 CNS injuries (that may trigger seizure
activities)
 Water intoxication – as in
syndrome of inappropriate anti-
diuretic hormone causing cerebral
edema
 Meningoencephalitis – there is an
inflammation, compressing the
brain tissue inside and may
increase metabolic demand also
increasing the hyper-excitability of
the neurons
 Brain Trauma – this can cause
seizure activity
 Stroke
 Tumors
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 NCM 112: NGIMPEC LECTURE NOTES
*2 Phenomenon in the pathophysiology of is going to increase, in which it will allow
seizure the sodium to get inside the cell.
- The sodium is positively charged and
1. Hyperexcitability of a neuron
the and inside of the cell is negatively
2. Hyper synchronization charge, where you have a potassium
there. When sodium enters, the
o Means that a hyper-excitable neuron negatively charged inside the cell will
leads to excessive excitability of a large
pass the polarization. When the sodium
group of surrounding neurons
gates is filled with sodium, the amount
o Normally, the neurons can be of sodium at the inside and outside of
stimulated, these are the normal
the cell is equal, this will be the time for
properties of the neurons. Once the potassium to move out. This will
stimulated, they will conduct the
cause the depolarization.
impulses (that is conductivity).
- The moving out of the potassium will
o The third property is, it is able to
cause the calcium to get inside which
influence other neurons. Until such time
will also increase the action potential.
that the impulses will be able to reach
This will go on until the impulses will
its destination or target areas,
reach its destination.
o If the neurons become hyper excitable,
these will stimulate a group of influence
group of neurons that will hyper-
synchronized, that will cause the
abnormal firing.
 In partial cases a hyper
synchronization that a hyper-
excitable neuron leads to
excessive excitability of large
group of surrounding neurons.
This means that when a large
electrical impulse is generated in
one part of the brain from a focus
of tissues millions of neurons in
the brain fire excessively in
Neuronal Excitability
addition bringing on a seizure
Note: - Neural messages are transmitted by
The actions potentials involved the ions such electrical impulses – ACTION
as sodium, potassium and calcium. POTENTIAL
- Action potential – a net positive
inward ion flux that leads to
depolarization or voltage change in
the neural membrane (if the membrane
become permeable to sodium, sodium
will influx in to the cell and will change the
voltage there, causing depolarization)
- Ions involved: Sodium, Potassium,
Calcium and Chloride
o Sodium and Calcium are extra
cellular ions. They are present inside
the cell during the resting phase
- When a cell or a neuron is stimulated, o Potassium and chloride – are intra
the permeability inside the membrane cellular ions

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 NCM 112: NGIMPEC LECTURE NOTES
- Normally, brain tissues prevent hyper o As a presence of hyper excitability, a
excitability by several inhibitory group of neurons will be stimulated or
mechanisms involving negative ions influenced which will cause the
like CHLORIDE IONS, caused by inward currents of Na, Ca
- Disturbances in this normal and involvement of excitatory
excitability leads to hyper- excitability neurotransmitters like Glutamate and
- In this state, there is increases Aspartate (Which will modulate the
excitatory transmission of impulses influx of Na and Ca in to the cells,
and decrease inhibitory transmission causing the action potential
- In this state, there is increase o This time, a group of nerves or
excitatory transmission of impulses neurons are being stimulated.
and decreases inhibitory  Too little inhibition – which hyper
transmission excitability of the group of neurons and
- In addition, there is alteration in the too little inhibition only. With this, with
voltage gated ionic channels hyper excitability of the group of
neurons and too little inhibition by
GABA, this will result to
*Transmission
Epileptogenesis & hyperexcitability &
hypersynchronization
Two types:  Epileptogenesis & hyperexcitability &
1. Excitatory transmission – this is
hypersynchronization of neurons that
modulated by Glutamate facilitates spread, this will result to
 glutamate receptors: this will
abnormal firing of neurons (SEIZURE)
modulate Ca & Na channels &
o Epileptogenesis - is the sequence of
are responsible for fast synaptic
events that turns a normal neuronal
transmission ( the sodium and
network into a hyperexcitable network
calcium influx will be modulated
 Epileptogenesis – is the spread of
by glutamate)
the spread of the action potential
 Glutamic acid is an excitatory
neurotransmitter
o 2. Inhibitory transmission - GABA
 GABA is mediated via Chloride
and Potassium channels
 Meaning that, the excitatory
transmission is regulated by
inhibitory transmissions.
 The transmission of the impulses
is normal, this is the balance
between the excitatory and
inhibitory transmission. So that,
the one that is modulating the
inhibitory transmission is your
- Refer to the photo above.
GAMA Amino Butyric acid, which
o Under the partial or focal, we have
is medicated via chloride and
the simple partial and complex partial
potassium channels (ions inside
seizure. On the other hand, under
the cell during the resting phase
the generalized seizure, there are
of the action potential
absence or petit mal seizures,
myoclonic , tonic-clonic, tonic or
*Mechanism of seizure formation
grandmal, atonic.
 Excitation of a group of nerves
1.) SIMPLE PARTIAL seizure

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 NCM 112: NGIMPEC LECTURE NOTES
o Patient wake and aware as
uncontrol;;able jerking begins in one
part of the body, possibly spreading.
Patient experiences a distorted
environment. May see or hear things,
feel unexplained powerful emotions
and feel nausea
o Things to do:
 No first aid is necessary unless
seizure becomes convulsive
 Provide reassurance and
emotional support as necessary
 It is the first observation of the
seizure, medical evaluation
should be recommended
. French word means “never
= Signs and symptoms if Simple-Partial
seizure:
- this is common in clients with organic
brain lesions like frontal lobe tumor
o this begins with an AURA. The aura
is already part of the seizure that
precedes the actual movement or
seizure activity.
o This can be initiated by parietal lobe
manifestations like burning, tingling
or numbness sensation and crawling
feeling
o In the occipital lobe – this can be
manifested by visual
disturbances/hallucination (seeing
things with are not perceived)
o In temporal lobe manifestations – the
Déjà vu or jaimais vu are manifested.
Unusual taste or smell can also be
manifested, and feeling of fear
NCM 112 NGIMPEC LECTURE NOTES
 Déjà vu –is from a French word
means “already seen”
 In déjà vu, the patient is
feeling familiar with the
environment which are not
before familiar to him.
 It describes the fascinating
& strange experience
where you feel that
something is very familiar
but you also know that this
feeling of familiarity should
not be as strong as it is.
 Jaimais vu – also from the
seen”
 This is the opposite of the
déjà vu
 The patient is unfamiliar to
the environment/ person in
which he was familiar
before.
 Jamais vu is the
experience of being
unfamiliar with a person or
situation that is actually
very familiar.
o Frontal lobe manifestation – motor
signs including twitching or stiffness.
This may start in one part of the body
(this is focal) and may spreads or
march in to the other parts of the
body. You call this march as
JACKSONIAN EPILEPTIC MARCH.
 Starting from the distal part of
the body going to the ipsilateral
phase
 Jacksonian march or
Jacksonian seizure - is a
phenomenon where a simple
partial seizure spreads from the
distal part of the limb toward the
ipsilateral face
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2. COMPLEX PARTIAL SEIZURES

- This known as the temporal lobe seizure
= MANIFESTATION AFTER THE POST
or psychomotor seizures
ICTAL PHASE (after seizures) OF
- In here, there may be impairment of
COMPLEX PARTIAL SEIZURE
consciousness, cognitive and affective
symptoms - CONFUSE – confuse in time, place and
- The patient may appear to be dreamy person
(dreamy state) with blank vacant - Hallucination & illusion
expression, déjà vu, jamais vu or fear - Déjà vu or jamais vu may be present
- The patient may also have a formed (either of the two)
auditory hallucination, hear music, etc. or - Overwhelming fear
other things that is not present that they - Feeling of detachment,
seen or heard. depersonalization
- They also may have a formed visual - Uncontrolled forced thinking or
hallucination. Sees houses, tress that are flood of ideas- on which this,
not there manifestation,
- Bad or unusual smell can also be - the patient is sometimes
manifested by the patient misinterpreted as having a
- For the psychomotor phenomena: psychiatric problems
o The patient may be with chewing Note:
movements, wetting lips,
automatisms (picking at clothing - Post ictal – means after the seizure
repeatedly) - Pre-ictal means – before the seizure
o The patient may have a dysphasia - Ictal phase – during the seizure
(un able to speak)
o This may lasts for 1-3 minute only 3. GENERALIZED SEIZURES
- Different types:
o Akinetic/ Atonic
o Myoclonic
o . Tonic-Clonic/Grandmal
o Absence/Petit Mal
- In generalized form of seizure, there
are abnormal brain discharges begin at
the center of the brain & take root in the
deepest tissues and simultaneous
spread of the discharges to both sides
of the brain and causing symptoms that
affect both sides of the body
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 NCM 112: NGIMPEC LECTURE NOTES
= Manifestation for generalized type of
seizure
- (refer to the picture above)
o The blue colored part is the
motor stripped, located in the
frontal lobe, responsible for the
voluntary motor movements. the
post central gyrus
o The red colored part is the
sensory that is located at the
parietal lobe. This is the pre
central gyrus.
o The abnormal discharges will
come from the center of the
brain and then will spread in the
both sides of the brain and then
to the both sides of the body.
- For somatosensory synptoms:
o There is a tingling of
contralateral limb, face or side of
the body
- For visual in the occipital lobe
manifestation:
o Hallucinations can be observed
like Seeing flashes of light,
scotomas (dark spots in front of
the eye), unilateral or bilateral
blurring of visions
- Auditory
o Auditory hallucinations may also
be present. Hears ringing,
hissing or noises
- Autonomic manifestations:
o Sweating, flushing or pallor, and/
or epigastric sensation
- Contraversive:
o You can also see the
contraversion of the head.
NCM 112 NGIMPEC LECTURE NOTES
Where the head and eyes turned
to opposite side
- Focal motor:
o May include tonic-clonic
movements of upper (or lower
limb)
= TYPES OF GENERALIZED TYPE OF
SEIZURES:
3.A) Absence seizure or Petit Mal
- Non convulsive
- Common among children
- There is a short period of “blanking out”
or staring into space
- This is very short, only few seconds and
may disappear after. This may occurs
many times a day.
- This may disappear when the child is
growing up
- 2 types:
o Typical
o Atypical
- Manifestation of the Typical type of
petit mal:
o Hx of school failure
o Blank stare
o Motionless
o Unresponsiveness
o Automatism (where there is
some repetitive movements)
- Manifestation for the Atypical type of
petit mal:
o Same with typical
o Alteration in muscle tone
o Differentiated by EEG
3.B. Atonic seizures or Drop attack
- Sudden split – second loss of muscle
tone
- Slackening of the jaw Drooping of the
limbs Falling to the ground
o the patient is high risk for brain
injury because immediately, the
patient will fall to the ground
- common in children, associated with
complete loss of consciousness &
muscle tone.
- this may disappear after the age to 18-
20 years old. But the management of
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the doctor is needed so that this can be
treated early or properly managed
- the child or adults suddenly falls. After
10 seconds to minute, they recover,
regain consciousness, and can stand
and walk again
- things to do:
o no first aid is necessary (unless
injured)
o provide reassurance
emotional support as necessary
o if it is the first observation of the
seizure, medical evaluation
should be recommended.
3.C. Myoclonic Seizure
- generalized type of seizure
- this is described as a “sudden or
momentary electrical shock” because it
is manifested by a sudden jerky
movements
- Non-rhythmic jerks resulting from
involuntary muscle twitching that
normally target the upper extremities,
and after an episode, patients may
describe the perceived sensation as
momentary electrical shocks
- Symptoms:
o Quick, uncontrolled muscle jerks
o Jerky or rhythmic movements
o Unusual clumsiness
- Myoclonic seizure affect:
o Neck, shoulders, upper arms
3.D. Tonic -Clonic type (GRAND MAL)
NCM 112 NGIMPEC LECTURE NOTES
- Tonic seizures - this is the tonic phase
and in the grand mal type of seizure
o Rigid, violent contraction of
muscles fixing the limb in
strained position
o The body becomes stiff with
violent contractions of the
muscles
- Clonic seizures – this is the clonic
phase in the grand mal type of seizures
o consist of repeated contractions
and relaxations
- The tonic-clonic or grand mal type of
seizure generalized tonic- clonic
seizure. loss of consciousness & violent
muscle contractions
- The patient may fall in the ground
-
o This is the picture of the tonic
phase (A) where in there is a
rigidity and violent contractions
of the muscles. This will be
followed by the clonic phase (B)
where you have the repeated
contractions and relaxations of
the muscles. This is followed by
the postictal phase (C) – the
patient is really exhausted
o This can be preceded by an aura
= PHASES
1. AURA - Flashing lights, smells, spots
before eyes, dizziness
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o This is in the pre-actual seizure
or pre-ictal phase but the aura is
already part of the seizure
o The patient may have Flashing
lights, abnormal smells, spots
before eyes, dizziness
2. Shout/cry – the aura may be followed
by a loud cry or shouts
3. Fall – then the patient may fall on the
ground
4. Tonic-clonic phase – after the patient
fall on the ground it will be followed by
this phase,
o Alternate contraction and
relaxation of the muscles
o Accompanied by dyspnea,
drooling of saliva, urinary
incontinence
o This movements may last up to
60-90 seconds
5. Post ictal phase – after the seizure, this
phase will follow
o There is a Cessation of tonic-
clonic movements
o The patient will have an
Exhaustion, headache,
drowsiness, deep sleep 1-2h,
disorientation
 The patient may be
disoriented, which is why
you have to reorient the
patient to the
environment after the ictal
phase
 Allow the patient to sleep
because they will feel
tired and exhausted
* COMPLICATIONS
- patient may not die of epilepsy, but
their lives would be at risk with the physical
injuries especially if the patient will fall. The
patient may not die with epilepsy, but they
might die with complication
 Physical
1. Status epilepticus - Continuous
seizure Seizure in rapid succession w/o
return to consciousness in between of
the seizures with ↑ utilization of
the energy, exhaustion will follow.
NCM 112 NGIMPEC LECTURE NOTES
the patient may die if not
controlled
2. Hypoxia/ Anoxia – decrease
oxygenation to the brain with seizure
activity
3. Traumatic Brain Injury – happened if
the patient will fall to the ground and hit
his/her head
4. Brain Damage- are physical
complications that may out the patient
die at risk
 B. Psychosocial.
1. Depression & Anxiety
* DIAGNOSTICS
this diagnostic tests will help to diagnose the
cause of the epilepsy
 Blood tests
 ECG – electroencephalogram to
measure the electrical activity
 EEG – there are electrodes that is
attached to the scalp and is
attached to a monitor. There is also
a graph in the monitor in which the
neurologists interpret it.
 MEG – Magnetoencephalography
uses sensors to form an image of
magnetic fields produced within the
brain to pinpoint areas of brain
activity that indicate epilepsy.
 CT scan / MRI
 Imaging tests
*MANAGEMENT
A. PHARMACOLOGICAL (anti-convulsant
drugs)
 Phenytoin sodium (e.g. Dilantin)
 Barbiturates (e.g. Phenobarbital for
long term use)
 Valproic Acid (e.g. Depakote)
 Thiamine
 GABA Enhancers (e.g., Pregabalin
and Gabapentin) to increase the
inhibition of the hyper excitable
neurons
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 NCM 112: NGIMPEC LECTURE NOTES
 Benzodiazepines (e.g., DIAZEPAM,
Trazepam and Valium for short term
therapy)
B. SURGICAL
- Some surgical procedures may be
performed, like if there is a tumor.
1. Lobectomy- removal of the cause
of tumor
2. Hemispherectomy - removal of the
tumor at the cerebral hemisphere
3. Corpus Callosotomy - opening in
the corpus callosom
4. Vagus Nerve Stimulation – to
interfere with the abnormal seizure
activity, which is stimulated by the
vagus nerve
C. Diet
- 1. Ketogenic diet – high fat diet. This
is used because it lowers the
carbohydrate content of the patient’s
diet. Since carbo can trigger seizure
activity. It triggers hyper excitability
inside the brain.
o to give the patient a keto diet,
this is a high fat diet with
adequate protein and decrease
carbohydrate content
o the fat is converted into ketones.
If there is less carbo, there is
less energy coming from carbo
is used. So that., the body is
going to use the fat, by breaking
down the fats, creasing the fatty
acids, and then convert this into
energy forms called “ketones”
o these ketones will be used as
energy, especially by the brain.
- 2. Omega 9
- 3. Avoid Foods/ Herbs that may
lower Seizure Threshold (e.g.
ginseng, ginko-biloba, caffeine,
theophylline)
o ginko-biloba are said to be
enhaced the memory
o caffeine – this lowers the
seizure threshold
NCM 112 NGIMPEC LECTURE NOTES
o Theophylline – anti-asthma. Its
side effects is palpitation
*Nursing Management:
A. Seizure Assessment Data:
 Time: Onset, Duration, Frequency,
Interval – while the patient is having a
seizure, we have to get these datas
 Presence of Aura – document if there is
a presence of auras, such as the
crawling sensation, abnormal smells,
and loud cries
 Behavior during Pre-ictal, Ictal, Post-
Ictal – behaviors during these phases
should be noted
 Types of Body Movement – such as the
tonic- clonic movements
 Consciousness – this is important
because this will tell us what kind of
seizure is manifested by the client. Like
in simple seizure, consciousness is not
impaired. The patient remain conscious
all throughout the activity
B. During Seizure:
 Provide privacy – because the patient
may feel uncomfortable or ashamed
because of their seizure
 Ease patient down to the floor, if
possible – to prevent head injury
 Protect head with pad to prevent injury
– because the attack may occur
anytime of the day and it may attack
frequently
 Loosen constrictive clothing – to
facilitate oxygen delivery to the brain
 Push furniture aside – because this
may cause injury
 If in bed, remove pillows, raise side rails
(which are padded)
 If aura precedes the seizure, insert oral
airway to reduce possibility of biting the
tongue or cheek (do this if the patient
doesn’t have an actual seizure yet, just
auras).
o During seizure, do not attempt to
open the jaw that are clench its
spasm, or to insert anything
because it may cause injury
o The only time that you may
insert an oral airway is before
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the tonic-clonic phases of the
seizure
 Do not attempt to try open jaws that are
clenched in a spasm or to insert
anything
 Do not restrain during seizure because
muscular contractions are strong –may
cause injury
 If possible, place patient on one side
with head flexed forward, which allows
the tongue to fall forward & facilitates
drainage of saliva & mucus. Suction to
clear secretions
C. After Seizure
 Keep on one side. Keep airway patent
– open the mouth of the patient and
position him/her in the recovery position
 After grand mal, a period of confusion
occurs – we need to reorient the patient
back to his environment to time, place
and person
 A short apneic period occurs during or
after a generalized seizure – insert a
nasal canula to assist with the oxygen
delivery in the body of the patient
 Reorient to environment after
o since there is confusion
 If agitated after, use calm persuasion &
gentle restraint
* PATIENT EDUCATION
 TAKE MEDS AT REGULAR BASIS –
otherwise, when the patient stops, this
may cause an attack of the seizure
 AVOID ALCOHOL – LOWERS
SEIZURE THRESHOLD
 ADEQUATE REST – if the patient lacks
rest, this may trigger an attack. The
patient may become restless if unable
to rest well.
 WELL-BALANCED Diet
 AVOID DRIVING, SWIMMING,
o Driving because the patient may
have an attack while driving and
this may cause an accident
o Swimming because the attack
may occur while the patient is
NCM 112 NGIMPEC LECTURE NOTES
swimming and the patient may
drawn
 OPERATING MACHINES UNTIL
SEIZURES ARE WELL CONTROLLED
Lesson 9: MULTIPLE SCLEROSIS (MS)
− Immune-mediated progressive
demyelinating disease of the CNS
− Strongly autoimmune disorder but the
actual cause is unknown. It can be related
to infections such as slow growing virus or
due to a familial predisposition/ with
genetic tendency
Factors Contributing for MS
A. Genetic Factors
a) Gender: women are 2 to 3 times more
likely to get the disease, and the age
group would be 20-40 years old
b) Family history of MS: A family history
increases the risk of developing MS
c) Race: MS appears more commonly in
Caucasians than in groups
B. Environmental Factors: MS occurs most
commonly in those living in northern
climates
a) Infections: researchers believe that
many autoimmune diseases are
provoked by some kind of infection
that strikes people who have a certain
genetic makeup; meaning that if they
already have this familial tendency
and if ever infections may be present,
they would likely get MS
b) Socioeconomic status: least common
in rural and lower class
c) Migration: the age at which you may
move may also be an important factor.
“if you move before the age of 15, your
risk is that of the people in the country
you move to. If you move after the 15,
your risk stays fixed at that of the
country you grew up in” (Ref:
O’Connor)
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In multiple sclerosis, this involves the myelin
sheath that covers the axon.
− Dendrite: carries impulses towards the cell
− Axons: carry impulses away from the cell
▪ In CNS, the large neurons with large
axons are myelinated, most of them.
▪ There are supporting cells that forms
the myelin sheath insulating the axon
− Myelin sheath: whitish in color and lipid
that coats the axons in jelly-roll fashion
which speeds the velocity of nerve impulse
conductions; when this wraps the axon in
jelly-roll fashion, it creates this segments
called the nodes of ranvier.
− Nodes of Ranvier: this is where the action
potential takes place in which the impulses
will jump from one node to another. This
type of impulse is called saltatory type of
transmission. It is very fast if myelinated;
for unmyelinated or small neurons, it just
travels all along the axon.
− Oligodendrocytes: forms myelin sheath to
insulate the axons, also gives nutrition to
the axon. This is the segmental wrapping
of the oligodendrocytes creating the nodes
of Ranvier, where impulses will jump from
NCM 112 NGIMPEC LECTURE NOTES
one node to another so the transmission is
very rapid.
− In peripheral nerves, the axons are
myelinated by the Schwann’s cells; in CNS
it is myelinated by the oligodendrocytes.
What Happens in Multiple Sclerosis?
− The T lymphocytes would come and go
into the CNS to check the environmental
milieu and they will leave BUT in MS, the
T lymphocytes doesn’t leave anymore
instead they will damage the myelin
sheath that they cannot recognize the
normal cells anymore. This is why it’s
called auto-immune because there is self
destruction of the normal cells resulting to
inflammation and scarring (2
consequence of damaged mylein
sheath)
1. Sequential Development of small
inflammatory patches as the T cells attack the
myelin. The neuron gets demyelinated and
this will resort to distortion of transmission of
impulses or it may slowed or blocked. It is
multiple because the damaged axons as well
as the scarring and inflammation is multiple.
2. Lesions extends and consolidate
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− These small inflammatory patches will
extend in size and will consolidate making
the edges hard and irregular.This
consolidation is called scarring or
sclerosis.
Areas Affected:
− Optic: There are so many tracts that may
be damaged in MS especially, the initial
manifestation will be visual because it has
a predilection on the Optic nerve which will
cause visual disturbances.
− Corticobulbar: those which innervates the
face, the tongue, is the pyramid tract that
is coming from the cerebral cortex and
then will go down to the brainstem and
before innervating/ synapsing the cranial
nerves at the level of the medulla
oblongata, this tract will cross at the level
of the pons
▪ Corticobulbar tract descending
pyramidal pathway innervating CN at
the medulla oblongata. Innervates
muscles of the face, tongue, jaw, and
pharynx, via CN located in your
brainstem.
− Corticospinal: those carrying the motor
movements to the muscles from the
cerebral cortex to the spinal cord, then will
synapse with the neurons there at the
spinal cord (anterior and lateral) are your
2 corticospinal tracts from the left and the
right which will cross at the medulla
oblongata and descend down to the
cervical, thoracic, and lumbar spines
laterally and anteriorly. Damage to this will
cause weakness or paralysis in the
muscles
▪ Corticospinal pyramidal tract carry
movement-related from the cerebral
cortex to the spinal cord.
− Cerebellar: these cerebellar tracts
descends to the spinal cord uncross
(meaning this is not a pyramidal tract)
NCM 112 NGIMPEC LECTURE NOTES
which is responsible for balance and
coordination
▪ The cerebellum is for making postural
adjustments to maintain balance.
− Spinocerebellar: from the spine and
cerebellum
▪ Spinocerebellar tracts carry
unconscious proprioceptive
information gleaned from muscles
spindles, Golgi tendon organs, and
joint capsules to the cerebellum.
− Medial Longitudinal Fasciculus
▪ Medial longitudinal fasciculus- found
in brainstem is a set of crossed fibers
with ascending and descending fibers,
links the 3 CN which control EOM and
CN VIII
− Posterior Column Pathway
− Posteriorly located: DCML pathway,
fasciculus gracillis, fasciculus cuneatus
and spinocerebellar tracts
▪ Posterior spinocerebellar tracts will
ascend to the cerebellum
− Anterior spinocerebellar tract: carries the
unconscious proprioceptive information
− Anterior and Lateral spinothalamic tract:
carries pain and temperature sensation,
these tracts will cross on the other side of
the spinal cord and ascend to the
brainstem to the thalamus
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− Dorsal Column Pathway: carries fine − Speech
touch, vibration and conscious ▪ Dysarthia: problem in the coordination
proprioception signals (deep sensations) of the tongue muscles; there is a
▪ Three-order problem in coordination but no
neuron: problem with interpretation and
· 1st order neuron expression of the language
enters spinal cord · One of the cardinal sign of the
through dorsal root; Charcot’s triad
ascends to medulla − Throat
(brain stem) ▪ Dysphagia: difficulty in swallowing
· 2nd order neuron related to cranial dysfunctions
crosses over in medulla; responsible for swallowing CN IX and
ascends to thalamus X
· 3rd order neuron − Musculoskeletal
projects to ▪ Weakness/paralysis and spams
somatosensory cortex related to damage to the
cortiocospinal tract
▪ Ataxia: related to cerebellar
functioning or damage
− Sensation: related to damage of tracts
carrying sensation such as Posterior
Column Pathway and spinothalamic tract
CLINICAL MANIFESTATIONS ▪ Pain: Lhermitte’s symptom- when the
patient flexes his neck, this will cause
an electrical-like sensation from the
neck to spine and the lower
extremities: very annoying
▪ Hypoesthesias
▪ Paraesthesias
− Bowel
▪ Incontinence
▪ Diarrhea or constipation
− Urinary
▪ Incontinence
▪ Frequency of retention
▪ Sexual impotence in male is common
− Initially, it would be visual disturbances
related to damage of the optic nerve like: Charcot’s Triad: Cardinal signs of MS
▪ Nystagmus: rapid jerky movement − Coined by Dr. Jean Martin Charcot
▪ Optic neuritis: inflammation of the ▪ Nystagmus in MS related to nerve
optic disc damage to the cerebellum or
▪ Diplopia: double vision related to the brainstem, regions of the brain which
weakness of the ocular muscles co-ordinate balance, muscle
▪ Scotoma (blind spot): presence of movements (CN III, IV and VI) and
dark spots in front of the eyes vision.

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 NCM 112: NGIMPEC LECTURE NOTES
· May arise from damage to CN II so
that visual information is not
interpreted correctly.
▪ Intentional tremor: when the patient
moves, the tremor occurs and is
perpendicular to the movement where
he is intending to do, related to
cerebellar damage
▪ Scanning speech: a type of ataxic
dysarthia
· Spoken words are broken up into
separate syllables, often
separated by a noticeable pause,
and spoken with varying force.
· Weakness and/or incoordination
of the muscles of the tongue, lips,
cheeks and moth
MS CLINICAL COURSE
1. Benign MS- no disability but may return to
normal between attacks; MS is
characterized by acute exacerbation of
symptoms then there will be some
remissions
2. Relapsing + Remitting MS- no new
disability between attacks; meaning that
there are acute exacerbation followed by
remission, then acute exacerbation again
followed by remission again
3. Secondary Progressive MS- no new
disability between attacks followed by
steady increase in disability; happens
when Relapsing + Remitting MS
progresses
NCM 112 NGIMPEC LECTURE NOTES
4. Primary progression MS- steady increase
in disability without attacks; this may
account for shorter lifespan of people with
because usually their lifespan ranges from
5-20 years; more in women
DIAGNOSTIC TESTS
Preferred diagnostic test is MRI because this
can demonstrate the extent of the sclerotic
plaques
− MRI (Magnetic resonance imaging) is
used to detect the presence of multiple
plaques
− CT scan can demonstrate increased
density of white matter of the brain where
axons are plenty, these axons can be
demyelinated
− Protein electrophoresis CSF (examination
of the CSF) uses an electrical current on a
CSF sample to separate out types of
protein called immunoglobulins
▪ meaning if you have plenty of
immunoglobulins present in the CSF,
you also have plenty of antibodies that
damage the myelin
− EEG (Electroencephalogram) determines
visual evoked response
▪ 3 electrodes are applied on the
patient’s scalp and then they are
allowed to focus on an object in the
screen
▪ Visual evoked potential (VEP)
measures electrical response of the
brain’s primary visual cortex to a visual
stimulus.
▪ If the response is delayed, this
confirms the diagnosis of MS
TREATMENT
− Treatment is possible and this will include
immune enhancers because this is an
auto-immune disorder, to prevent the
damage of the myelin.
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I. Disease-modifying
Pharmacologic therapy
→ immune enhancers; displayed that
after the treatment using these
enhancers, the sclerotic plaques
diminished in size
□ Avonex (Beta Interferon 1a, IM)
□ Betaseron (Beta Interferon 1b)
□ Copaxone (Glatiramer Acetate)
▪ Not an interferon but also an
enhancer
□ Rebif (Beta Interferon 1a)
II. For acute exacerbations:
Mentioned in the pathophysiology, there
are development of inflammatory patches
that later on will go into scarring by
consolidations
For inflammation medications given are:
□ Corticosteroids
(Methylprednisolone)
□ ACTH (Adrenocorticotropic
hormone)
□ Plasmapheresis- plasma is being
exchanged
▪ Plasma is separated from the
blood cells.
• Plasma is replaced with
another solution such as
saline or albumin, or the
plasma is treated and
returned to body
▪ The immunoglobulins that can
damage the normal myelin
sheath will be removed and then
the plasma will be returned to the
patient.
▪ There is a device that filters the
plasma.
III. For treatment of Symptoms
a) For spasticity related to damage in the
corticospinal tract
→ Muscle relaxants that ma be
administered
□ Baclofen (Lioresal)
□ Benzodiazepine (Valium)
▪ Ex: Ativan
NCM 112 NGIMPEC LECTURE NOTES
□ Dantrolene (Dantrium)
□ Tizanidine (Zanaflex)
b) For fatigue
→ Cause is unknown; but if we go back
to the pathophysiology, if its is
myelinated the transmission would be
rapid.
→ Theory why there is fatigue in MS: If it
is demyelinated, it requires a lot of
energy to be able to transmit the
impulses to the myelinated axons
□ Amantadine (Symmetryl)
▪ it is an antibiotic but it found out
the it has dopamine agonist
▪ Also used for patient with
parkinsonism that experiences
tremor
□ Fluoxetine (Prozac)
▪ Antidepressant
c) For ataxia (speech or walking ataxia)
□ Beta adrenergic blockers- Inderal
□ Antiseizure agents- Neurontin
□ Benzodiazepines- Klonopin
d) For bladder problems:
□ Ascorbic acid (vit C)
▪ To acidify the urine to prevent
UTI
□ Anticholinergics
▪ Urinary incontinence: there is
spasm of the bladder,
continuously contracts making
you pee frequently
IV. For secondary progressive:
□ Novantrone- reduces frequency of
relapses
NURSING INTERVENTION
I. Promote optimum mobility
→ The patient can spastic or can be with
ataxia, with weakness or paralysis
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→ This is an important intervention to
increase the circulation
A. Muscle-stretching & Strengthening
exercises
● As recommended by the physiotherapist
B. Walking exercises to improve gait
● Use wide-based gait to balance their self
and to avoid falling
C. Assistive devices: canes, walker, rails,
wheelchair as needed
● To assist with ambulation of the patient
D. Minimize spasticity and contractures
● Administer medication as ordered
◦ Muscle relaxants like Baclofen and
Benzodiazepines
● Exercises
E. Activity and rest
● Frequent rest periods
◦ Because fatigue exacerbates
symptoms
F. Encourage independence in self care
● Very important because this is a long
term chronic disorder so we have to the
teach the patient to perform activities of
daily living especially during remissions
● During acute exacerbation,they have to
be assisted with self-care activities but
during remission, we need to encourage
them to perform self-care activities
G. Prevent complications of immobility
● Such as pressure sores and any
impairment of skin integrity
II. Prevent injury
→ The patient have problems with
sensation
● Test bath water with thermometer
● Avoid heating pads, hot water bottles
◦ Because you may not be able to
control the temperature of this, so
the patient may be burnt because
they won’t feel it if it is too hot
● Frequent position changes
◦ Necessary to prevent injury
● Inspect body parts for injury related to
problems in sensation
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III. Enhance bladder and bowel control
● For urinary retention: the bladder is
relaxed
◦ Force fluids 3000 ml/day
◦ Use of acid-ash foods (cranberry,
grape juice): to acidify the urine
● Urinary retention
◦ intermittent catheterization
▪ The straight catheterization
when the patient cannot pee and
their bladder is distended
▪ In Bruner’s: it was stated that we
may teach the patient self-
catheterization if ever there is
bladder distention
▫ Can be done as often as
every 4 hours if bladder
distentions is still present
because the bladder isn’t
contracted
◦ bethanecol chloride: will contract the
bladder
● Urinary incontinence: bladder always
contracts
◦ Establish voiding schedule
▪ Give water and every 2 hours:
bring bed pan/commode, bring
patient to the comfort room
◦ Anticholinergic: to prevent
contractions of the bladder
▪ Propantheline bromide,
tolterodine (Detrol)
IV. Establish Bowel Elimination Pattern
→ Recommended time is after breakfast
because after sleeping, when the
patient is awake, their stomach is
empty and peristaltic movement may
still be delayed or slow.
→ After eating breakfast, this will
increase the peristaltic movement. Let
the patient sit on the toilet bowl to
stimulate defecation
● Adequate fluids
● Dietary fiber- to stimulate defecation
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● Bowel training program
V. Enhance communication and managing
swallowing difficulties
● Referral to speech therapy/ swallowing
problems to prevent aspiration
VI. Improve sensory and cognitive function
● Vision:
▪ Diplopia- use eye patch to avoid
fatigue
▪ Prism glasses if in supine position
that will enable the patient to read in
this position
▪ Large print or audio books
● Provide psychological support
▪ Encourage positive attitude, assist in
setting realistic goals in between
remissions
▫ If there is remission, the
realistic goal would be the
patient is able to perform
activities of daily living
▪ Provide compassion in adapting to
changes in body image and self
concept
▪ Provide no false hope
▪ Refer to MS societies and
community agencies that will help or
support the patient
▫ In Philippines, there are no
support groups in MS
because we have less cases
but in other countries,
especially in cold countries,
there are lost of agencies/
support groups
VII. Promoting sexual functioning
● Use of alternative methods for sexual
gratification
◦ Because MS occurs usually among
ages 20-40 years old so there are
needs to be satisfied
● Refer for sexual counselling
◦ The best choice would be OB gyn
NCM 112 NGIMPEC LECTURE NOTES
VIII. Provide teaching and discharge
planning
● Balance between activity and rest
◦ Because fatigue can exacerbate
symptoms
● Regular exercises- walking, swimming,
biking
◦ Swimming is good for patient with
MS
● Use of energy conservation techniques
● Well-balance diet
● Fresh air and sunshine
● Avoid fatigue, overheating, chilling,
stress, infection
◦ These are factors that can
exacerbate the symptoms
Lesson 10: AMYOTROPHIC LATERAL
SCLEROSIS
I. Description
Amyotrophic lateral sclerosis (ALS),
sometimes called Lou Gehrig's disease or
classical motor neuron disease, is a rapidly
progressive, invariably fatal neurological
disease that attacks the nerve cells (neurons)
responsible for controlling voluntary muscles.
In ALS, both the upper motor neurons and the
lower motor neurons degenerate or die,
ceasing to send messages to muscles. Unable
to function, the muscles gradually weaken,
waste away, and twitch. Eventually the ability
of the brain to start and control voluntary
movement is lost. Symptoms are usually first
noticed in the arms and hands, legs, or
swallowing muscles. Muscle weakness and
atrophy occur on both sides of the body.
Individuals with ALS lose their strength and the
ability to move their arms and legs, and to hold
the body upright. When muscles in the
diaphragm and chest wall fail to function
properly, individuals lose the ability to breathe
without ventilatory support. The disease does
not affect a person's ability to see, smell, taste,
hear, or recognize touch. Although the
disease does not usually impair a person's
mind or personality, several recent studies
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suggest that some people with ALS may
develop cognitive problems involving word
fluency, decision-making, and memory.

II. Causes/predisposing factors/

Incidence
The cause of ALS is not known, and scientists
do not yet know why ALS strikes some people
and not others. However, scientific evidence
suggests that both genetics and environment
play a role in motor neuron degeneration and
the development of ALS.
Genetics
- Gene mutations suggest that changes
in the processing of RNA molecules
may lead to ALS-related motor neuron
degeneration. RNA molecules are
involved with the production of
molecules in the cell and with gene
activity.
- Other gene mutations indicate there
may be defects in protein recycling—a
naturally occurring process in which
malfunctioning proteins are broken
down and used to build new working
ones. Still others point to possible
defects in the structure and shape of
motor neurons, as well as increased
susceptibility to environmental toxins.
Environmental factors
Amyotrophic lateral sclerosis (ALS) attacks
motor neurons (a type of nerve cell) in the
brain and spinal cord. There are two types of
motor neurons: upper motor neurons (UMNs)
that send nerve fibers down the from the motor
cortex in the brain (part of the brain that
controls movement) to the spinal cord; lower
motor neurons (LMNs) send nerve fibers from
the spinal cord to the muscles throughout the
body. The progressive degeneration of the
motor neurons in ALS eventually leads to their
death. When the motor neurons die, the ability
of the brain to initiate and control muscle
movement is lost. With voluntary muscle
action progressively affected, patients in the
later stages of the disease may become totally
paralyzed.
Other cell types in the central nervous system
that support motor neurons, called glia,
including astrocytes and oligodendrocytes are
also involved in ALS disease.

- Environmental factors, such as Axon Structure and Dynamics:

exposure to toxic or infectious agents,
viruses, physical trauma, diet, and
behavioral and occupational factors.
For example, exposure to toxins during
warfare, or strenuous physical activity,
is possible reasons for why some
veterans and athletes may be at
increased risk of developing ALS.
Ongoing research may show that some
Transport of materials up and down the length
factors are involved in the development
of the motor neuron is an important cellular
or progression of the disease.
process that may play into the damage seen in
ALS. Neurons normally move cellular
III. Anatomy & physiology
materials along their axons, to keep nerve cell
messages flowing and to maintain the health
of the whole nerve cell itself. Active transport
along the extensive axons of motor neurons

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conveys newly made materials to even the the growing animal, or later, in an adult, if cells
farthest-reaching nerve endings and needed are not working properly.
nutrients back to the cell body. Motor neurons
In ALS, evidence is building that actions on or
may be particularly vulnerable to any genetic
originating in the mitochondria may be an
defect or cellular insult that impedes axon
important part of the disease. Interestingly,
transport. Studies of the proteins within nerve
changes in the mitochondria can be detected
fibers have highlighted their importance in
before one can find a physical change, such
maintaining motor neurons and point to the
as hind limb weakness in mice. In addition,
possible role of these axon proteins in ALS.
mitochondria show damage early in the ALS
Cell Death: Apoptosis and Necrosis: disease process, a finding that is leading
researchers to study this cell component
Cells that do not receive the proper supplies
intensively.
will die, through a step-wise process called
apoptosis (or programmed cell death). This is Glutamate:
a normal physiologic phenomenon and in fact
apoptosis is crucial to the normal development
of the nervous system. In contrast to
apoptosis, necrosis is a type of cell death that
results from a direct injury to the nervous
system, or acute infection. Necrosis produces
an explosion of cell contents accompanied by
inflammation and immune activation. Unlike
the messy death of infected or traumatized Nerve cells pass signals to each other and to
cells in necrosis, apoptosis is a process of their target organs by releasing messenger
carefully choreographed steps to self- molecules, called neurotransmitters. Many are
destruction. But halting apoptosis when it is simple amino acids such as the one called
producing degenerative change in the nervous glutamate. The message is intended to tell the
system is now a prime goal for researchers recipient neuron whether to fire off its own
trying to design effective treatments for ALS as neurotransmitters. As with all
well as for other neurological disorders. neurotransmitters, glutamate docks at specific
recognition molecules on the receiving
Mitochondria:
neuron. Glutamate is then swiftly cleared from
Mitochondria, a type of cell organelle (little the nerve cell junctions to keep the message
organ) is the power plants of all animal cells brief.
and has many roles. In the case of motor
Prolonged excitation of the nerve cell can
neurons, they must sustain the amazing
occur from too much glutamate, which is toxic.
energetic capacity of a single cell to span from
Neurobiologists recognize that glutamate can
the spinal cord all the way to a person’s fingers
cause harm when the messages are
and toes. Mitochondria move charged
overwhelming, as in stroke or epilepsy.
particles across its membrane to produce
Molecules called transporters aid in keeping
cellular fuel, called adenosine triphosphate
glutamate in proper concentrations around
(ATP). Mitochondria also control the cellular
nerve cells.
content of calcium ions. In nerve cells, calcium
is particularly important in producing the Inflammation:
signals that contract muscles and produce
Inflammation is part of the immune system’s
thoughts. It is also the umpire of apoptosis (i.e.
protective reaction to tissue damage or
programmed cell death) in that it can call the
invasion by microbes. It is a process that
play into action or delay it using specialized
should help heal. But sometimes the
enzymes. Mitochondria also play a role in
inflammation that accompanies illness or
removing cells when they are not needed in
injury is counterproductive. Inflammation can

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turn into an unnecessary attack on the body’s Anterior horns
own tissues, as in arthritis or autoimmune
 Progressive weakness
disease.
 Muscle atrophy (arms, trunk, legs)
Inflammation in the central nervous system is  Spasticity
called neuroinflammation. There is increasing  Brisk or overreactive muscle reflexes
evidence that neuroinflammation
Cranial nerves
accompanies the death of motor neurons in
ALS. However, evidence so far does not  Muscle weakness
support that ALS is an autoimmune disease.  Difficulty talking
The inflammatory process apparently is a  Difficulty swallowing
reaction to the death of the cells, and not the  Difficulty breathing
instigator.  Soft palate and upper esophageal
weakness
IV. Pathophysiology
 Weakness on the posterior tongue
Bulbar muscles
 Progressive difficulty in speaking
 Difficulty in swallowing
 Articulation and speech effects
 Compromised respiratory function

VI. Diagnostic tests

There is no single test that provides a definitive
diagnosis of ALS. It is primarily diagnosed
based on a detailed history of the symptoms
observed by a physician during physical
examination, along with a review of the
individual’s full medical history and a series of
tests to rule out other diseases. A neurologic
examination at regular intervals can assess
whether symptoms such as muscle weakness,
muscle wasting, and spasticity are
progressively getting worse.
Muscle and imaging tests
 Electromyography (EMG) is a
recording technique that detects
V. Clinical manifestations electrical activity of muscle fibers and
The signs and symptoms presented depend can help diagnose ALS.
on the location of the affected neuron.  A nerve conduction study (NCS)
Generally, the following presentations are measures the electrical activity of the
evident: nerves and muscles by assessing the
nerve’s ability to send a signal along the
 Fatigue nerve or to the muscle.
 Progressive muscle weakness  Magnetic resonance imaging (MRI) is
 Cramps a noninvasive procedure that uses a
 Twitching magnetic field and radio waves to
 Incoordination

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produce detailed images of the brain
and spinal cord.
 Blood and urine tests may be
performed based on the person’s
symptoms, test results, and findings
from the examination. A physician may
order these tests to eliminate the
possibility of other diseases.
 A muscle biopsy may be performed to
determine whether a physician believes
an individual has a muscle disease
other than ALS. Under local
anesthesia, a small sample of muscle is
removed and sent to the lab for
analysis.
VII. Medical /Surgical management
No specific therapy exists for ALS. The main
focus of medical and nursing management is
on interventions to maintain or improve
function, well-being and quality of life.
 Symptomatic treatment and
rehabilitative measures are employed
to support the patient and improve the
quality of life.
 Baclofen (Lioresal), dantrolene sodium
(Dantrium), or diazepam (Valium) may
be useful for patients troubled by
spasticity, which causes pain and
interferes with self-care.
 A patient experiencing problems with
aspiration and swallowing may require
enteral feeding.
 Mechanical ventilation (using negative-
pressure ventilators) is an option if
alveolar hypoventilation develops.
 Patients are encouraged to complete
an advance directive or “living will” to
preserve their autonomy in decision
making.
VIII. Nursing management
1. Provide intellectual stimulating
activities, because the client typically
experiences no cognitive deficits and
retains mental abilities.
2. Provide client and family teaching.
3. Promote measures to enhance body
image.
4. Promote client and family coping as the
client and his family deal with the poor
prognosis and the grieving process
NCM 112 NGIMPEC LECTURE NOTES
5. Maximize functional abilities
 Prevent complications of immobility
 Promote self-care
 Maximize effective communication
6. Ensure adequate nutrition
7. Prevent respiratory complications
 Promote measures to maintain
adequate airway
 Promote measures to enhance gas
exchange, such as oxygen therapy
and ventilator assistance.
 Promote measures to prevent
respiratory infection
Lesson 11: GUILLAIN BARRE SYNDROME
I. Description
Guillain-Barré Syndrome (GBS), also
known as acute idiopathic polyneuritis, is a
rare demyelinating disorder caused by a
humoral and cell-mediated immunologic
reaction directed at the peripheral nerves, and
sometimes, the cranial nerves. Due to such
demyelination, it can cause acute,
symmetrical, and ascending weakness, along
with dyskinesia, hyporeflexia, parasthesia,
and sometimes progresses to complete
paralysis. It is usually triggered by the
campylobacter jejuni, cytomegalovirus,
Epstein-Barr virus, Mycoplasma pneumoniae,
H. influenzae, and HIV.
Types of GBS:
 Acute inflammatory demyelinating
polyradiculoneuropathy (AIDP)
This type of GBS predominantly affects
the myelin sheath. It is the most common form
in North America and Europe. The most well-
known type, the patient experiences
weakness in the lower extremities, which
progresses upward and has the potential for
respiratory failure.
 Miller Fisher syndrome (MFS)
The Miller Fisher syndrome is the rarest
type of GBS, as it involves the cranial nerves
which extend from the brain to various areas
of the head and neck. It is less common in
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United States, but more common in Asia. This
form is associated with unsteady gait or ataxia,
areflexia, and opthalmoplegia, wherein there
is paralysis of the extraocular muscles that
control the movement of the eye. People with
this condition can also have other signs and
symptoms in Guillain-Barré syndrome, such
as muscle weakness.
 Acute motor axonal neuropathy
(AMAN)
This type of GBS affects the axons of
the nerves going to the muscles. It is the most
common form in some Asian countries. In this
type, only the axons of motor neurons are
damaged, hence, there is no altered
sensation.
 Acute motor and sensory axonal
neuropathy (AMSAN)
This type of GBS affects the axons of
both the motor and sensory neurons. Due to
sensory nerve damage, symptoms such as
losing proprioception or the ability to sense the
position of their limbs, as well as areflexia can
be manifested by affected individuals.
II. Causes/predisposing factors/ Incidence
Cause:
The precise cause of Guillain-Barré
syndrome is unknown. However, according to
Hinkle and Cheever (2018), the best accepted
theory of cause is molecular mimicry, in which
an infectious organism contains an amino acid
that mimics the peripheral nerve myelin
protein. The immune system cannot
distinguish between the two proteins, so as a
result, it attacks the peripheral nerve myelin as
well. In more severely affected people, this
also affects the central conducting core of the
nerve, which is the axon.
Predisposing Factors:
 Gender (Men)
Based on CDC (2019), anyone can
develop GBS; however, in the United States, it
is more common in men. Specifically, GBS has
NCM 112 NGIMPEC LECTURE NOTES
a male-to-female ratio of 1.5:1, according to
Andary (2021).
 Age (> 50 years)
People of all ages can be affected with
GBS, however, in accordance with CDC, it is
more frequent in those older than 50 years.
Moreover, Guillain-Barré syndrome in the very
old (> 80 years of age) results in more severe
disease with poorer activity.
Other Risk Factors:
There are several factors known to
trigger Guillain-Barré Syndrome. The following
are among the triggers of an autoimmune
response:
Bacteria
 Campylobacter jejuni
Campylobacter jejuni infection is the
most common risk factor for Guillain-Barré
Syndrome. The Campylobacter is a bacterium
which causes diarrhea, and is often found in
undercooked food, especially poultry. Based
on the study of Nachamkin et al., this
bacterium is thought to cause GBS through
molecular mimicry, whereby Campylobacter
contains ganglioside-like epitopes in the
lipopolysaccharide moiety that elicit
autoantibodies reacting with peripheral nerve
targets. As many as 40% of GBS cases in the
United States are thought to be triggered by
Campylobacter infection, and about 1 in every
1,000 reported such illness that leads to GBS.
 Haemophilus influenzae
Haemophilus influenzae is a major
pathogen of community acquired respiratory
infection, and is considered as a causative
agent of GBS and Fisher syndrome. However,
the frequency of this infection in GBS is
controversial. It is hypothesized that
ganglioside epitopes on H influenzae lipo-
oligosaccharide (LOS) induce autoantibodies
against GM1 and GQ1b, thereby resulting in
neuropathy.
 Mycoplasma pneumoniae
M. pneumoniae infection is an atypical
pneumonia with symptoms of dry cough, fever,
and mild shortness of breath. According to the
study of Sauteur et al. (2016), M. pneumoniae
infection is associated with GBS, more
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frequently in children than adults, and elicits
anti-galactocerebroside (GalC) antibodies, of
which specifically anti-GalC IgG may
contribute to the pathogenesis of GBS.
Viruses
 Cytomegalovirus (CMV)
Cytomegalovirus (CMV) is a strain of
the herpes virus, which causes chest infection
or glandular fever. These are the second most
commonly reported infections preceding GBS,
with CMV being the most common viral trigger
of GBS. Based on a Dutch GBS study, they
found CMV to be present in 13% of patients.
 Epstein Barr Virus (EBV)
EBV is a herpes virus which causes
glandular fever. The pathophysiology of EBV-
associated GBS is not clearly understood.
However, EBV has been known to have a
predilection for B lymphocytes, resulting in
polyclonal B cell activation and an increase of
Ig production. EBV-induced GBS results in the
demyelinating subtype of GBS.
 Mononucleosis, which is typically
caused by EBV
Infectious mononucleosis is a clinical
syndrome characterized by fever,
lymphadenopathy, and pharyngitis. Guillain-
Barré syndrome occurring in patients with
infectious mononucleosis are rarely reported
and usually present late in the course of the
disease.
 Hepatitis E virus (HEV)
Hepatitis E virus (HEV) is the most
common cause of acute viral hepatitis
worldwide, and this usually leads to jaundice.
Concerning GBS, studies from other countries
found an acute HEV infection in 5-11% of
cases. Based on the study of Liu and Ma
(2019), HEV infection may trigger GBS by
activating autoimmune response to destroy
myelin or axon mistakenly.
 Zika virus
Zika virus often spread to people
through mosquito bites, and symptoms include
fever, rash, and joint pain. Current CDC
research states that GBS is strongly
NCM 112 NGIMPEC LECTURE NOTES
associated with Zika. However, only a small
proportion of people with recent Zika virus
infection get GBS.
 HIV or AIDS
Human immunodeficiency virus-
associated Guillan-Barré syndrome (HIV-
GBS) occurs in early and late stages of HIV
infection, and may follow the onset of AIDS
(Brannagan & Zhou, 2003).
 SARS-Cov-2
SARS-Cov-2 is the cause of the current
COVID-19 pandemic. GBS has occurred after
COVID-19 but it is not yet clear whether this is
a coincidence. However, on a study of
Finsterer and Scorza (2021), they stated that
SC2-GBS is most likely secondary due to an
immune reaction against SARS-CoV-2 since
the virus has not been found in the CSF of any
SC2-GBS patients so far.
 Influenza
Influeza viruses cause flu, which is a
contagious respiratory illness that infects the
nose, throat, and sometimes the lungs.
Studies over the years have shown an
increased risk of GBS following influenza
infection, and the magnitude of risk is several
times greater than that following influenza
vaccination.
Vaccines
 Flu vaccine
People can also develop Guillain-Barré
syndrome days or weeks after receiving a flu
vaccine. However, this only happens in
extremely rare cases. In addition, occurrence
varies by flu season. The CDC states that for
every 1 million flu shots that are administered,
1 or 2 people tend to develop the condition.
Contrastingly, their research also indicates
that a person is more likely to develop Guillain-
Barré syndrome from the flu itself rather than
the flu vaccine.
 Johnson & Johnson COVID-19 Vaccine
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Guillain-Barré syndrome has also been
associated with the Johnson & Johnson
COVID-19 vaccine. In accordance with an
FDA statement, as of July 13, 2021, 100
people in the United States have reported
Guillain-Barré syndrome after vaccination. At
that time, around 12.5 million people have
received the J&J vaccine overall, which means
there were about 8 cases of Guillain-Barré
syndrome for every 1 million vaccines
administered. Additionally, the FDA also
issued a warning that there is an increased risk
of Guillain-Barré syndrome within 42 days of
vaccination. However, GBS remains very rare,
and so health experts widely agree that the
benefits of receiving the J&J vaccine still far
outweigh the risks.
Incidence:
Guillain-Barré syndrome is a rare
disorder. According to CDC, each year, about
3,000 to 6,000 people in the United States
develop GBS whether or not they received a
vaccination. On the other hand, based on
Hinkle and Cheever (2018), the annual global
incidence of GBS is 1 to 2 cases per 100,000
people. Furthermore, it is more frequent in
males between 16 and 25 years of age, and
those older than 55 years (Bader et al., 2016).
As for prognosis, 80% of the cases fully
recover, 15% remains to have some
neurological disability, and 5% leads to death,
resulting from respiratory failure, autonomic
dysfunction, sepsis, or pulmonary embolism.
III. Anatomy & physiology
Anatomy & Physiology of Nervous System
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The nervous system consists of two major
parts: the central nervous system (CNS),
including the brain and spinal cord and the
peripheral nervous system, which includes the
cranial nerves, spinal nerves, and autonomic
nervous system. The function of the nervous
system is to control motor, sensory,
autonomic, cognitive, and behavioral
activities. The brain itself contains more than
100 billion cells that link the motor and sensory
pathways, monitor the body's processes,
respond to the internal and external
environment, maintain homeostasis, and
direct all psychological, biologic, and physical
activity through complex chemical and
electrical messages.
Cells of the Nervous System
The basic functional unit of the brain is the
neuron. It is composed of dendrites, a cell
body, and an axon.
 The dendrites are branch-type
structures for receiving electrochemical
messages.
 The axon is a long projection that
carries electrical impulses away from
the cell body. Some axons have a
myelinated sheath that increases
speed of conduction.
 Nerve cell bodies occurring in clusters
are called ganglia or nuclei. A cluster of
cell bodies with the same function is
called a center (e.g., the respiratory
center). Neurons are supported,
protected, and nourished by glial cells,
which are 50 times greater in number
than neurons.
The nerve communicates by sending
signals down a long, thin extension called an
axon. These axons transmit signals from the
body of the nerve cell to muscles in order to
make muscles contract and send signals from
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sensory receptors to the cell body in order to  Satellite cells. Satellite cells act as
allow humans to feel. Myelin is made by glial protective, cushioning cells.
support cells that surround the axon of the
nerve. These glial cells protect and nourish the
axon, as well as helping speed up the traveling Neurons
electrical signal.

Nervous Tissue: Structure and Function

Even though it is complex, nervous tissue is
made up of just two principal types of cells-
supporting cells and neurons.

Supporting Cells
Supporting cells in the CNS are “lumped
together” as neuroglia, literally mean “nerve
glue”.
 Neuroglia. Neuroglia include many Neurons, also called nerve cells, are highly
types of cells that generally support, specialized to transmit messages (nerve
insulate, and protect the delicate impulses) from one part of the body to another.
neurons; in addition, each of the
 Cell body. The cell body is the
different types of neuroglia, also simply
metabolic center of the neuron; it has a
called either glia or glial cells,has
transparent nucleus with a conspicuous
special functions.
nucleolus; the rough ER, called Nissl
 Astrocytes. These are abundant, star-
substance, and neurofibrils are
shaped cells that account for nearly half
particularly abundant in the cell body.
of the neural tissue; astrocytes form a
 Processes. The armlike processes, or
living barrier between the capillaries
fibers, vary in length from microscopic
and neurons and play a role in making
exchanges between the two so they to 3 to 4 feet; dendrons convey
incoming messages toward the cell
could help protect neurons from
body, while axons generate nerve
harmful substances that might be in the
blood. impulses and typically conduct them
away from the cell body.
 Microglia. These are spiderlike
phagocytes that dispose of debris,  Axon hillock. Neurons may have
hundreds of the branching dendrites,
including dead brain cells and bacteria.
depending on the neuron type, but each
 Ependymal cells. Ependymal cells are
neuron has only one axon, which arises
glial cells that line the central cavities of
from a conelike region of the cell body
the brain and the spinal cord; the
called the axon hillock.
beating of their cilia helps to circulate
 Axon terminals.These terminals
the cerebrospinal fluid that fills those
contain hundreds of tiny vesicles, or
cavities and forms a protective cushion
membranous sacs that contain
around the CNS.
neurotransmitters.
 Oligodendrocytes. These are glia that
 Synaptic cleft. Each axon terminal is
wrap their flat extensions tightly around
separated from the next neuron by a
the nerve fibers, producing fatty
tiny gap called synaptic cleft.
insulating coverings called myelin
sheaths.  Myelin sheaths. Myelin is made of fat
and protein and it's wrapped in
 Schwann cells. Schwann cells form
the myelin sheaths around nerve fibers numerous layers around many of the
nerves in the central nervous system
that are found in the PNS.
(CNS), which includes your brain,

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spinal cord, and the optic (eye) nerves,
as well as in the peripheral nervous
system (PNS), which contains all the
nerves outside of the CNS. Myelin is
created by specific types of glial cells.
In the CNS, glial cells are
oligodendrocytes; in the PNS, they are
Schwann cells.
 Nodes of Ranvier. Because the myelin
sheath is formed by many individual
Schwann cells, it has gaps, or
indentations, called nodes of Ranvier.
Peripheral Nervous System
The peripheral nervous system includes the
cranial nerves, the spinal nerves, and the
autonomic nervous system.
Cranial Nerves
Twelve pairs of cranial nerves emerge from
the lower surface of the brain and pass
through openings in the base of the skull.
Three cranial nerves are entirely sensory (I, II,
VIII), five are motor (III, IV, VI, XI, and XII), and
four are mixed sensory and motor (V, VII, IX,
and X). The cranial nerves are numbered in
the order in which they arise from the brain.
The cranial nerves innervate the head, neck,
and special sense structures.
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Spinal Nerves
The spinal cord is composed of 31 pairs of
spinal nerves: 8 cervical, 12 thoracic, 5
lumbar, 5 sacral, and 1 coccygeal. Each spinal
nerve has a ventral root and a dorsal root. The
dorsal roots are sensory and transmit sensory
impulses from specific areas of the body
known as dermatomes to the dorsal horn
ganglia. The sensory fiber may be somatic,
carrying information about pain, temperature,
touch, and position sense (proprioception)
from the tendons, joints, and body surfaces; or
visceral, carrying information from the internal
organs. The ventral roots are motor and
transmit impulses from the spinal cord to the
body; these fibers are also either somatic or
visceral. The visceral fibers include autonomic
fibers that control the cardiac muscles and
glandular secretions.
Autonomic Nervous System
The autonomic nervous system (ANS) is the
motor subdivision of the PNS that controls
body activities automatically.
 Composition. It is composed of a
specialized group of neurons that
regulate cardiac muscle, smooth
muscles, and glands.
 Function. At every moment, signals
flood from the visceral organs into the
CNS, and the automatic nerves make
adjustments as necessary to best
support body activities.
 Divisions. The ANS has two arms: the
sympathetic division and the
parasympathetic division.
Anatomy & Physiology of the Immune
System
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The immune system is composed of an
integrated collection of various cell types, each
with a designated function in defending
against infection and invasion by other
organisms. Supporting this system are
molecules that are responsible for the
interactions, modulations, and regulation of
the system. These molecules and cells
participate in specific interactions with
immunogenic epitopes (antigenic
determinants) present on foreign materials,
initiating a series of actions in a host, including
the inflammatory response, the lysis of
microbial agents, and the disposal of foreign
toxins. The major components of the immune
system include central and peripheral organs,
tissues, and cells.
The basic function of the immune
system is to remove foreign antigens such as
viruses and bacteria to maintain homeostasis.
There are two general types of immunity:
natural (innate) and acquired (adaptive).
Natural immunity or nonspecific immunity is
present at birth. Acquired or specific immunity
develops after birth. Each type of immunity has
a distinct role in defending the body against
harmful invaders, but the various components
are usually interdependent.
IV. Pathophysiology
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V. Clinical manifestations
 Muscle weakness
 Diminished reflexes of the lower
extremities
o Hyporeflexia
o May progress to tetraplegia
 Neuromuscular respiratory failure-
Demyelination of the nerves that
innervate the diaphragm and intercostal
muscles
 Paresthesias of the hands and feet
o May also feel pain due to
demyelination of sensory fibers
 Blindness- due to optic nerve
demyelination
 Inability to swallow or clear secretions
due to bulbar muscle weakness related
to demyelination of the
glossopharyngeal and vagus nerves
VI. Diagnostic tests
Guillain-Barré syndrome can be difficult to
diagnose because several other conditions
can cause similar symptoms.
A GP will refer you to a hospital specialist if
they think you might have it or are not sure
what's causing your symptoms.
Examination
A GP or specialist may:
 ask about your symptoms, such as how
long they've lasted and whether they're
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getting worse – muscle weakness that's
getting worse over time is a common
sign of Guillain-Barré syndrome
 examine your hands, feet or limbs to
check for symptoms such as numbness
 ask if you've recently been ill – Guillain-
Barré syndrome often follows an
infection such as food poisoning or flu
 check your reflexes, such as whether
your leg twitches when your knee is
tapped in a particular place – people
with Guillain-Barré syndrome usually
have no or reduced reflexes
Nerve tests
In hospital, 2 tests may be carried out to see
how well your nerves are working.
These are:
 electromyography (EMG) – tiny
needles are inserted into your muscles
and electrical recordings are taken to
see how they react when nearby nerves
are activated
 nerve conduction studies – small discs
(electrodes) are stuck on your skin and
minor electric shocks are used to
activate the nerves and measure how
quickly these signals travel along them
In people with Guillain-Barré syndrome, these
tests will usually show that signals are not
travelling along the nerves properly.
Lumbar puncture
A lumbar puncture is a procedure to remove
some fluid from around the spinal cord (the
nerves running up the spine) using a needle
inserted into the lower part of the spine.
The sample of fluid will be checked for signs of
problems that can cause similar symptoms to
Guillain-Barré syndrome, such as an infection.
Guillain-Barre syndrome can be difficult to
diagnose in its earliest stages. Its signs and
symptoms are similar to those of other
neurological disorders and may vary from
person to person.
Your doctor is likely to start with a medical
history and thorough physical examination.
Your doctor may then recommend:
NCM 112 NGIMPEC LECTURE NOTES
 Spinal tap (lumbar puncture). A small
amount of fluid is withdrawn from the
spinal canal in your lower back. The
fluid is tested for a type of change that
commonly occurs in people who have
Guillain-Barre syndrome.
 Electromyography. Thin-needle
electrodes are inserted into the
muscles your doctor wants to study.
The electrodes measure nerve activity
in the muscles.
 Nerve conduction studies. Electrodes
are taped to the skin above your
nerves. A small shock is passed
through the nerve to measure the
speed of nerve signals.
VII. Medical /Surgical management
Treatment
There's no cure for Guillain-Barre syndrome.
But two types of treatments can speed
recovery and reduce the severity of the illness:
 Plasma exchange (plasmapheresis).
The liquid portion of part of your blood
(plasma) is removed and separated
from your blood cells. The blood cells
are then put back into your body, which
manufactures more plasma to make up
for what was removed. Plasmapheresis
may work by ridding plasma of certain
antibodies that contribute to the
immune system's attack on the
peripheral nerves.
 Immunoglobulin therapy.
Immunoglobulin containing healthy
antibodies from blood donors is given
through a vein (intravenously). High
doses of immunoglobulin can block the
damaging antibodies that may
contribute to Guillain-Barre syndrome.
These treatments are equally effective. Mixing
them or administering one after the other is no
more effective than using either method alone.
You are also likely to be given medication to:
 Relieve pain, which can be severe
 Prevent blood clots, which can develop
while you're immobile
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People with Guillain-Barre syndrome need
physical help and therapy before and during
recovery. Your care may include:
 Movement of your arms and legs by
caregivers before recovery, to help
keep your muscles flexible and strong
 Physical therapy during recovery to
help you cope with fatigue and regain
strength and proper movement
 Training with adaptive devices, such as
a wheelchair or braces, to give you
mobility and self-care skills
Recovery
Although some people can take months and
even years to recover, most people with
Guillain-Barre syndrome experience this
general timeline:
 After the first signs and symptoms, the
condition tends to progressively worsen
for about two weeks
 Symptoms reach a plateau within four
weeks
 Recovery begins, usually lasting six to
12 months, though for some people it
could take as long as three years
Among adults recovering from Guillain-Barre
syndrome:
 About 80% can walk independently six
months after diagnosis
 About 60% fully recover motor strength
one year after diagnosis
 About 5% to 10% have very delayed
and incomplete recovery
Children, who rarely develop Guillain-Barre
syndrome, generally recover more completely
than adults.
Treatment for Guillain-Barré syndrome can
help reduce the symptoms and speed up
recovery.
Most people are treated in hospital and usually
need to stay in hospital for a few weeks to a
few months.
NCM 112 NGIMPEC LECTURE NOTES
Intravenous immunoglobulin (IVIG)
The most commonly used treatment for
Guillain-Barré syndrome is intravenous
immunoglobulin (IVIG).
When you have Guillain-Barré syndrome, the
immune system (the body's natural defences)
produces harmful antibodies that attack the
nerves.
IVIG is a treatment made from donated blood
that contains healthy antibodies. These are
given to help stop the harmful antibodies
damaging your nerves.
IVIG is given directly into a vein.
Plasma exchange (plasmapheresis)
A plasma exchange, also called
plasmapheresis, is sometimes used instead of
IVIG.
This involves being attached to a machine that
removes blood from a vein and filters out the
harmful antibodies that are attacking your
nerves before returning the blood to your
body.
Most people need treatment over the course
of around 5 days.
Other treatments
While in hospital, you'll be closely monitored to
check for any problems with your lungs, heart
or other body functions.
You'll also be given treatment to relieve your
symptoms and reduce the risk of further
problems. This may include:
 a breathing machine (ventilator) if
you're having difficulty breathing
 a feeding tube if you have swallowing
problems
 painkillers if you're in pain
 being gently moved around on a regular
basis to avoid bed sores and keep your
joints healthy
 a thin tube called a catheter in your
urethra (the tube that carries urine out
of the body) if you have difficulty peeing
 laxatives if you have constipation
 medicine and/or special leg stockings
to prevent blood clots
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VIII. Nursing management
Nursing management for identified nursing
diagnoses includes:
1. Impaired respiratory function
The nurse will need to carefully monitor
vital signs for changes in respiratory rate,
quality of respirations, and decreasing vital
capacity. Respiratory assessment for
ascending paralysis and impending
respiratory failure due to weakness of
intercostal muscles and diaphragm along with
shallow and irregular breathing, the use of
accessory muscles, and difficulty in clearing
secretions. If the patient is intubated, the nurse
will need to work with the physician and
respiratory therapist to manage all aspects of
mechanical ventilation. During the course of
GBS, the nurse will need to assess and
monitor the patient for respiratory infections
including pneumonia.
2. Immobility
The nurse will need to assess problems
associated with immobility related to muscle
weakness and paralysis. The nurse should
support and maintain paralyzed extremities in
function positions, perform passive ROM
exercises at least twice daily, ensure that the
patient has position changes every two hours
or ensure the patient is positioned on a foam,
air, water, or gel support surface bed. Skin
assessment for skin breakdown, assessment
of bowel function through monitoring of bowel
sounds and frequency of bowel movements,
use of anti-embolism stockings and
compression boots to prevent DVT and PE,
and maintenance of adequate hydration to
decrease the risks of pressure ulcers are
important nursing management
considerations for the immobility related to
GBS.
3. Nutritional imbalance
The nurse will need to work carefully to
assist in the maintenance of optimal nutrition
in the patient with GBS. The patient with
impaired swallowing due to muscle weakness
should be carefully assessed for aspiration.
The nurse will need to manage gastrostomy
NCM 112 NGIMPEC LECTURE NOTES
tube feedings, IV fluid administration, or the
administration of parenteral nutrition as
needed to ensure that the patient receives
necessary nutrients.
4. Communication impairments
The nurse will need to provide
strategies for adequate communication with
the patient who is unable to verbally
communicate due to paralysis associated with
GBS. Management of adequate patient
communication may include the use of
strategies such as eye blinks, use of pictures,
or the use of computer graphics. The nurse
should also consider discussing the use of
communication strategies with family
members and friends. Referrals to a speech
therapist may also assist to address
communication impairments due to GBS.
5. Pain
The nurse will need to carefully assess the
patient for pain related to GBS related muscle
changes. If the patient is unable to
communicate verbally, the nurse should use
assessment strategies including pictures or
pain management scales to obtain an
adequate understanding of the patient's pain
level. Non-verbal signs of pain including
restlessness, facial grimaces, or restlessness
should also be noted in this assessment.
Adequate pain management is essential,
especially in the acute stages of GBS.
6. Psychological problems
The nurse will need to carefully assess and
manage the GBS patient for potential
psychological problems. The sudden onset of
loss of control in the acute phase of a
potentially life-threatening illness may result in
anxiety, fear, and feelings of helplessness.
Patients and family members may also
confront uncertainty, helplessness, and
loneliness when dealing with GBS. The impact
of GBS on family members may be influenced
by the role of the patient in the family. Social
and economic issues may be exacerbated if
the patient is the primary breadwinner or major
source of family support. Patients and family
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members may experience fear and
helplessness, especially within the ICU or
acute care setting. The nurse will need to
educate the patient and family members,
providing information about GBS and the
equipment, medications, and therapies used
to treat GBS. The nurse may also suggest
patient education materials, referrals to
support groups, social workers, or
psychologists as strategies to improve patient
and family coping with GBS.

Lesson 12: BELL’S PALSY

I. Description
 Bell palsy (facial paralysis) is caused by
unilateral inflammation of the seventh
cranial nerve, which results in II. Causes/predisposing factors/
weakness or paralysis of the facial Incidence
muscles on the affected side. Bell palsy is a type of facial nerve palsy, which
 Although the cause is unknown, was originally thought to have no identifiable
theories include vascular ischemia, cause (idiopathic facial nerve palsy). However,
viral disease (herpes simplex, herpes current evidence suggests that in some cases,
zoster), autoimmune disease, or a Bell palsy can be caused by a viral infection or
combination of all of these factors. Most another disorder.
adults with Bell palsy are younger than
45 years (Hickey, 2014). Evidence suggest that common causes of Bell
 Bell palsy may be a type of pressure palsy include:
paralysis. The inflamed, edematous
1. Infections and autoimmune disorders.
nerve becomes compressed to the
The cause may be a viral infection or an
point of damage, or its blood supply is
immune disorder that causes the facial
occluded, producing ischemic necrosis
nerve to swell. As the facial nerve swells
of the nerve.
and becomes inflamed in reaction to the
 The face is distorted from paralysis of
infection, it causes pressure within the
the facial muscles; decreased
Fallopian canal (a bony canal through
lacrimation (tearing) occurs; and the
which the nerve travels to the side of the
patient experiences painful sensations
face), leading to the restriction of blood and
in the face, behind the ear, and in the
oxygen to the nerve cells (ischemia). In
eye.
some mild cases where recovery is rapid,
 The patient may also experience
there is damage only to the myelin sheath
speech difficulties and may be unable
(the fatty covering that act as insulation of
to eat on the affected side because of
nerve fibers). Infection causes the nerve to
weakness or paralysis of the facial
swell. When the nerve is swollen, it is
muscles. The majority of patients
squeezed (compressed) by the narrow
recover completely and Bell palsy
passageways in the skull that it passes
rarely recurs (Hickey, 2014).
through. Other viruses, such as
coxsackievirus, cytomegalovirus, and the
viruses that cause mumps, rubella,

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mononucleosis, or influenza, may also
cause Bell palsy.
2. Trauma. Trauma to the facial nerve is the
second most common cause of facial
paralysis. This includes blunt force trauma
that causes temporal bone skull fractures,
sharp penetrating trauma (stab or gunshot
wounds), and iatrogenic forms (those that
occur during surgery). Fractures of the
temporal bone are the number one
traumatic cause of facial nerve injury. If the
fracture involves the bone surrounding the
facial nerve, the nerve can undergo
swelling or may get cut.
3. Genetics. There may also be an inherited
tendency toward developing Bell’s palsy. A
family history of Bell palsy has been
reported in approximately 4% of cases.
Inheritance in such cases may be
autosomal dominant with low penetration;
however, which predisposing factors are
inherited is unclear.
4. Pregnant women. The apparent
predisposition of pregnant women to Bell
palsy has been attributed to the high
extracellular fluid content, viral
inflammation, and immunosuppression
characteristic of pregnancy, but findings
are controversial. Most cases of Bell palsy
occur in the third trimester or the
puerperium. Some authors suggest that
Bell palsy increases the risk of
hypertension and toxemia of pregnancy,
whereas the pregnant state, in turn, may
affect the course and severity of disease.
5. Diabetic patients. Research in the adult
population with diabetes shows a
correlation between poor glycemic control
and the development of Bell palsy. The
more elevated the glycated hemoglobin
level, the more severe the facial nerve
palsy. It is suggested that Bell's palsy is a
syndrome resulting from ischemia of the
facial nerve, in many cases due to diabetic
angiopathy. Diabetes makes the blood
more viscous, decreasing the flow of blood
and oxygen to the 7th cranial nerve.
NCM 112 NGIMPEC LECTURE NOTES
6. Old age. The onset of disease usually
occurs in the median age which is 40 years
old.
7. Exposure to cold winds. Medical
practitioners believe that exposure of one
side of the face to cold wind has the
potential of numbing the 7th cranial nerve.
8. Other disorders can cause facial nerve
palsy. Lyme disease can cause facial
nerve palsy that, unlike Bell palsy, may
affect both sides of the face. In African
Americans, sarcoidosis is a common
cause of facial nerve palsy.
III. Anatomy and Physiology of Cranial
Nerve VII- Facial Nerve
Anatomically, the course of the facial nerve
can be divided into two parts:
A. Intracranial
Intracranially, the seventh cranial nerve or
the facial nerve arises from the pons, an area
of the brainstem. From there, it roots into large
motor root and a small root (the part of the
facial nerve that arises from the sensory root
is sometimes known as the intermediate
nerve). Thus, its function is considered as both
motor and sensory.
The two roots travel through the internal
acoustic meatus, a 1 cm long opening in the
petrous part of the temporal bone wherein they
are proximal to the inner ear.
Still within the temporal bone, the roots
leave the internal acoustic meatus, and enter
into the facial canal. The canal is a ‘Z’ shaped
structure. Within the facial canal, three
important events occur:
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1. Firstly, the two roots fuse to form the facial
nerve.
2. Next, the nerve forms the geniculate
ganglion (a ganglion is a collection of nerve
cell bodies).
3. Lastly, the nerve gives rise to:
a. Greater petrosal nerve
- Carries mixed sensory and
parasympathetic fibers to mucous
glands and lacrimal gland.
- The greater petrosal nerve arises
immediately distal to the geniculate
ganglion within the facial canal. It then
moves in anteromedial direction, exiting
the temporal bone into the middle
cranial fossa. From here, its travels
across (but not through) the foramen
lacerum, combining with the deep
petrosal nerve to form the nerve of the
pterygoid canal.
- The nerve of pterygoid canal then
passes through the pterygoid canal
(Vidian canal) to enter the
pterygopalatine fossa, and synapses
with the pterygopalatine ganglion.
Branches from this ganglion then go on
to provide parasympathetic innervation
to the mucous glands of the oral cavity,
nose and pharynx, and the lacrimal
gland.
- The primary functions of this nerve are
taste and secretomotor (dealing with
secretions from glands).
a. Nerve to stapedius
- Motor fibres to stapedius muscle of the
middle ear.
b. Chorda tympani
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- Special sensory fibers to the anterior
2/3 tongue and parasympathetic fibers
to the submandibular and sublingual
glands.
Sensory: Innervates at the anterior 2/3
of the tongue responsible for the
special sense of taste. The nerve arises
in the facial canal, and travels across
the bones of the middle ear, exiting via
the petrotympanic fissure, and entering
the infratemporal fossa. Here, the
chorda tympani travel with the lingual
nerve. The parasympathetic fibers of
the chorda tympani stay with the lingual
nerve, but the main body of the nerve
leaves to innervate the anterior 2/3 of
the tongue.
Parasympathetic: The chorda tympani
also carry some parasympathetic
fibers. These combine with the lingual
nerve (a branch of the trigeminal nerve)
in the infratemporal fossa and form the
submandibular ganglion. Branches
from this ganglion travel to the
submandibular and sublingual salivary
glands.
The facial nerve then exits the facial canal
(and the cranium) via the stylomastoid
foramen. This is an exit located just posterior
to the styloid process of the temporal bone.
B. Extracranial
The nerve will exit the skull, to continue to
branch outside the cranium, through the face
going down to the neck. The facial nerve will
branch out the cranium superiorly to run just
anterior to the outer ear.
After it exits the skull, innervating between the
stylomastoid foramen, and the parotid gland,
three more motor branches are given off three
branches will arise.
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1. Posterior auricular nerve.
- It provides motor innervation to the
some of the muscles around the ear.
- First extracranial branch of the facial
nerve that ascends in front of the
mastoid process, and innervates the
intrinsic and extrinsic muscles of the
outer ear. It also supplies the occipital
part of the occipitofrontalis muscle.
2. Nerve to the posterior belly of the
digastric muscle
- Branches immediately distal to
posterior auricle nerve, where motor
branches continue to the digastric
muscle.
- Innervates the posterior belly of the
digastric muscle (a suprahyoid muscle
of the neck).
- It is responsible for raising the hyoid
bone.
3. Nerve to the stylohyoid muscle.
- Innervates the stylohyoid muscle (a
suprahyoid muscle of the neck). It is
responsible for raising the hyoid bone.
The motor root of the facial nerve, known as
the main trunk of CN VII, continues to branch
anteriorly and inferiorly into the parotid gland
(note – the facial nerve does not contribute
towards the innervation of the parotid gland,
which is innervated by the glossopharyngeal
nerve).
Within the parotid gland, the nerve terminates
by splitting into five branches which are
responsible for innervating the muscles of
facial expression namely:
1. Temporal branch
- Innervates the frontalis, orbicularis oculi
and corrugator supercilii.
- The frontalis muscle plays a role in
elevating the eyebrows, while the
corrugator supercilii, orbicularis oculi,
and procerus is responsible for its
depression.
3. Buccal branch
- Innervates the orbicularis oris,
buccinator and zygomaticus.
- Orbicularis oris is called the “kissing
muscle” and allows a person to close,
elevate, depress, and protracts the lips.
- Buccinator muscles assists in chewing
and hold the teeth.
- Zygomaticus is a major muscle for
facial expression which helps a person
to draw mouth in an upward and
downward angle.
4. Marginal mandibular branch
- Innervates and responsible for the
motor function of the depressor anguli
oris (pulls the angle of the mouth
inferolaterally), the depressor labii
inferioris (pulls lower lip down or to the
side), the inferior fibers of the
orbicularis oris and the mentalis
muscles (stabilizes lower lips and allow
pouting).
5. Cervical branch
- Innervates the platysma and is
responsible for depression of mandible
and angle of mouth, tenses skin of
lower face and anterior neck.

2. Zygomatic branch
- Innervates the orbicularis oculi which is
responsible for closing the eyelids. In
addition, it assists in pumping the tears
from the eye into the nasolacrimal duct
system

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IV. Pathophysiology

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V. Clinical Manifestations
1. Pain behind the ear – usually the first
symptom that occur.
2. Weakening of the facial muscles –
occurs suddenly, usually within hours.
The effect ranges from mild weakness
to complete paralysis. By 48 to 72
hours, the weakness is as severe as it
will be. Only one side of the face is
affected.
3. Difficulty in wrinkling the forehead,
blinking, and grimacing on the affected
side – For most people, the face feels
numb or heavy, even though sensation
remains normal.
4. Production of tearing impaired – closing
the eye on the affected side may be
difficult and therefore people may be
unable to close the eye completely, and
they blink less frequently.
5. Eye damage – Because fewer tears are
produced and the eye blinks less often,
the eye becomes dry, resulting in pain
and eye damage.
6. Loss of sense of taste – people may be
unable to taste with the front part (about
2/3) of the tongue on the affected side.
7. Hyperacusis – wherein the ear on the
affected side may be hypersensitive
because the muscle that stretches the
eardrum is paralyzed.
VI. Diagnostic tests
Bell’s palsy can normally be diagnosed by
simply looking at the symptoms as there are
no specific tests used to diagnose Bell’s palsy.
However, a healthcare provider may order
tests to rule out other conditions that can
cause similar symptoms and to determine the
extent of nerve involvement or damage. These
tests may include:
 Electromyography (EMG). This test can
confirm the presence of nerve damage
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and determine its severity. An EMG
measures the electrical activity of a
muscle in response to stimulation and
the nature and speed of the conduction
of electrical impulses along a nerve.
 Blood tests to determine if another
condition such as diabetes or Lyme
disease is present. Diabetes and Lyme
disease both can cause Bell’s Palsy or
show symptoms similar to Bell’s Palsy.
Diabetes due to a diabetic patient being
more prone than the non-diabetic
person to nerve degeneration. And
Lyme disease due to the bacteria linked
to it, a blacklegged tick infected with
Borrelia burgdorferi or Borrelia mayonii
bacteria, having the ability to cause
joint and nerve system damage. It can
also impact the facial nerve and lead to
facial paralysis symptoms.
 Imaging scans. Magnetic resonance
imaging (MRI) or computerized
tomography (CT) may be needed on
occasion to rule out other possible
sources of pressure on the facial nerve,
such as a tumor or skull fracture.
It is important to rule out the presence of a
stroke or tumor that may cause symptoms
similar to Bell’s palsy. Other conditions — such
as a stroke, infections, Lyme disease and
tumors — can cause facial muscle weakness
that mimics Bell's palsy.
VII. Medical /Surgical management
Medications
Commonly used medications to treat Bell's
palsy include:
 Corticosteroids, such as prednisone,
are powerful anti-inflammatory agents.
If they can reduce the swelling of the
facial nerve, it will fit more comfortably
within the bony corridor that surrounds
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it. Corticosteroids may work best if
they're started within several days of
when the symptoms started.
 Antiviral drugs. The role of antivirals
remains unsettled. Antivirals alone
have shown no benefit compared with
placebo. Antivirals added to steroids
are possibly beneficial for some people
with Bell's palsy, but this is still
unproven.
However, despite this, valacyclovir (Valtrex) or
acyclovir (Zovirax) is sometimes given in
combination with prednisone in people with
severe facial palsy.
Physical therapy
Paralyzed muscles can shrink and shorten,
causing permanent contractures. A physical
therapist can teach you how to massage and
exercise your facial muscles to help prevent
this from occurring.
Surgery
In the past, decompression surgery was used
to relieve the pressure on the facial nerve by
opening the bony passage that the nerve
passes through. Today, decompression
surgery isn't recommended. Facial nerve
injury and permanent hearing loss are
possible risks associated with this surgery.
Rarely, plastic surgery may be needed to
correct lasting facial nerve problems. Facial
reanimation helps to make the face look more
even and may restore facial movement.
Examples of this type of surgery include
eyebrow lift, eyelid lift, facial implants, and
nerve grafts. Some procedures, such as an
eyebrow lift, may need to be repeated after
several years.
VIII. Nursing Management
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Patients need reassurance that a stroke has
not occurred and that spontaneous recovery
occurs within 3 to 5 weeks in most patients.
Teaching patients with Bell’s palsy to care for
themselves at home is an important nursing
priority.
Teaching Eye Care
Because the eye usually does not close
completely, the blink reflex is diminished, so
the eye is vulnerable to injury from dust and
foreign particles. Corneal irritation and
ulceration may occur. Distortion of the lower lid
alters the proper drainage of tears. Key
teaching points include the following:
 Cover the eye with a protective shield
at night.
 Apply eye ointment to keep eyelids
closed during sleep.
 Close the paralyzed eyelid manually
before going to sleep.
 Wear wraparound sunglasses or
goggles to decrease normal
evaporation from the eye.
Teaching About Maintaining Muscle Tone
 Show patient how to perform facial
massage with gentle
 upward motion several times daily
when the patient can tolerate the
massage.
 Demonstrate facial exercises, such as
wrinkling the forehead,
 blowing out the cheeks, and whistling,
in an effort to prevent muscle atrophy.
 Instruct patient to avoid exposing the
face to cold and drafts.
Diet & Nutrition
 Instruct patient to chew on the
unaffected side of his mouth.
 Provide soft and nutritionally balanced
diet. Eliminate hot fluids and foods.
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 Give frequent mouth care, being
particularly careful to remove residues
of food that collects between the
cheeks and gums.

While paralysis is present, nursing care

involves protection of the eye from injury.
Frequently, the eyelid does not close
completely and the blink reflex is diminished,
so the eye is vulnerable to injury from dust and
foreign particles. Corneal irritation and
ulceration may occur. Distortion of the lower lid
alters the proper drainage of tears. To prevent - At the terminal end of the neuron, there
injury, the eye should be covered with a is electrical stimulation of calcium to
protective shield at night. The eye patch may stimulate the release of
abrade the cornea, however, because there is neurotransmitter acetylcholine. Once
some difficulty in keeping the partially released, this will bind with the
paralyzed eyelids closed. Moisturizing eye receptors of the muscles to cause
drops during the day and eye ointment at muscular contraction.
bedtime may help prevent injury (Hickey, - Myasthenia gravis is a chronic
2014). The patient can be educated to close autoimmune disorder in which
the paralyzed eyelid manually before going to antibodies destroy the communication
sleep. Wraparound sunglasses or goggles between nerves and muscles that is
may be worn during the day to decrease going to result to weakness of skeletal
evaporation from the eye. After the sensitivity muscles.
of the nerve to touch decreases and the Incidence: Common among women than man
patient can tolerate touching the face, the in the 2nd or 3rd decades of life (20-30 years
nurse can suggest massaging the face several old).
times daily, using a gentle upward motion, to Neuromascular joint
maintain muscle tone. Facial exercises, such
as wrinkling the forehead, blowing out the
cheeks, and whistling, may be performed with
the aid of a mirror to prevent muscle atrophy.
Exposure of the face to cold and drafts is
avoided.
Lesson 13: MYASTHENIA GRAVIS

 Junction point between the nervous and

Myasthenia Gravis muscular system. In which, once
- Autoimmune disorder that affects the stimulated, the calcium or electrical
myoneural junction. impulse travelling to the neuron, once
reaches the terminal it will synapse and
release neurotransmitter.
 A chemical neurotransmitter is released
(Ach or acetylcholine)

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 Detected by receptors on surface of
muscle of muscle fiber.
 Results in muscle contraction.
 In myasthenia gravis, the normal
antibodies that is responsible for fighting
off infection (autoimmune) are the one who
damage the normal receptors so there is
no binding of Ach with the receptors at the
muscles. If there is no binding, this would
result to muscular weakness (no muscular
contraction).

Video Presentation

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Note!
This disease is strongly autoimmune
Pathophysiology
1. Normal neuromascular transmission
begins with action potential travelling down
the motor neuron.
2. Action potential reaches the nerve terminal
and activates Calcium channels (electrical
impulse).
3. The increase in calcium causes synaptic
vesicles (open) containing Ach to be
released into synaptic cleft.
4. UNKNOWN initiating event
Associated risk factors include:
a. Autoimmune disease
b. Thymus abnormalities (Thymus is
responsible for the production of T
lymphocytes necessary for fighting
against infection. When we are still
small, our thymus is enlarged about 70
grams but as we grow older (18 yo), the
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thymus will involute or atrophy about 3
grams. In clients with MG, the thymus is
enlarged, when the gland is enlarged,
there is an overproduction of T
lymphocytes that will cause damage to
the neuromuscular junction, possible
cause of MG)
c. Genetic link (familial tendency)
5. T cell process produces Ach receptor
antibodies which reduce normal
neurotransmission: Myasthenia Gravis
6. 3 Mechanisms:
a. Directly alters function of the receptor
by blocking Ach binding and Ach
receptor activation.
b. Promote endocytosis of Ach resulting to
degradation of Ach R
c. Destroys post synaptic surface leading
to decrease number of Ach R
7. Decrease neurotransmission to skeletal
muscles.
8. Muscle weakness and fatigue with
repetitive use= myasthenic fatigue due to
continuous muscle contraction.
9. Clinical presentation of MG:
a. Diplopia
o Double vision r/t eom innervated
by CN III, IV, and VI
b. Ptosis
o Drooping of the eyelids
innervated by CN III
c. Snarling Expression
o r/t CN VII dysfunction or
responsible for expression
d. Dysphagia
o Difficulty in swallowing
innervated by CN IX and X
e. Nasal Speech
o Weakness of muscles for
communication or speech.
f. Proximal Limb Weakness
g. Respiratory Muscle Weakness
o Muscles of respiration if affected
in MG this becomes medical
emergency. MG is not that grave
but whenever the respiratory
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muscles is affected this will b. Sweating
cause respiratory failure and c. Cramping
patient should be in ICU and this ANTIDOTE: ATROPINE SULFATE
usually is the cause of mortality
3. Electromyography
in MG.
- The muscle is stimulated and the result
Assessment Findings
will be recorded through a monitor.
1. Muscle weakness - Detects the delay or failed
neuromuscular transmission in muscle
fiber supplied by a single nerve fiber.

4. Blood Test
a. Diplopia - Check for the presence of
b. Ptosis immunoglobulins or the
c. Masklike expression antiacetylcholine receptor antibodies in
d. Speech impairment the serum.
e. Dysphagia
NOTE: Extreme muscle weakness
increased with activity and reduced with
rest. With repetitive use of muscles
Diagnostic Tests
1. Arms raised to fatigue the muscles.
- Observe when the hands fall just like in
pronator drift. Extremity that will fall first
is the one that is weak. Medical Management
2. Tensilon Test or endrophonium
- Anticholinesterase inhibitor medication A. Drug Therapy
is administered then we observe if there 1. Anticholinesterase drugs:
is relief of the muscle weakness the a. neostigmine (Prostigmin)
strength will be increased, then if so, it b. pyridostigmine (Mestinon) most
is MG. This medication is used when popular
we are suspecting MG. This provides c. ambenomium (Metylase)
spontaneous relief of symptoms (lasts MOA: block the action of
5-10 minutes) cholinesterase and increase levels of
- Before the test we have to observe for acetylcholine and NMJ
the side effects of the drug such as:
REMEMBER!!!
a. Bradycardia
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Once a neurotransmitter is released
from the vesicle there are enzyme that
will breakdown the neurotransmitters
for reuptake to the vesicles for reuse.
The anticholinesterase drug will
prevent the enzyme cholinesterase
from breaking down the acetylcholine
into its parts for reuptake back to its
vesicles so that acetylcholine will be
available for muscle contraction.
2. Corticosteroid
a. Prednisone
MOA: suppress the autoimmune
response. Serves as anti-inflammatory
B. Surgery
1. Thymectomy
o There can be presence of
enlargement of thymus which
can increase the production of T
lymphocytes which will damage
the neuromuscular junction.
o Removal of thymus thought to
be involved in production of
acetylcholine receptor
antibodies.
o The effect of the removal of
thymus is good and the
guarantee for this is 10 year or
more.
C. Plasmapheresis
- Works like hemodialysis where we
withdraw the blood from the body, then
will be filtered through the device. In
here, the plasma is removed from the
body through a device, removed with its
Ig’s or filtered, then the plasma will then
be put back into the body.
- Removes circulating acetylcholine
receptor antibodies. After which, the
plasma is returned back to the body.
Anatomy and Physiology od the Thymus
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Anatomy: upper mediastinum. Large in infants
(70g), atrophied in adult (3g), 2 lobed organ
Hormones: thymosin (for maturation of t
lymphocytes)
Target: T lymphocytes (WBC)
Hormone function: promote production and
maturation of T lymphocytes.
Nursing Management
1. Administer the anticholinesterase
drugs as ordered
a. Give on time- 30 minutes before the
time because the peak effect is 30
minute after, so the effect is to improve
the strength to relieve muscular
strength to avoid aspiration with
increase muscle strength.
b. With milk and crackers to reduce GI
upset
c. Monitor effectiveness: muscle strength,
vital capacity (measure the strength
and score the muscle) Done frequently
to check if MS is improved to adjust also
the dose. If ever we can see
fasciculation or fine muscular twitches
instead of muscle strength this could
mean that there is an overdose of the
medicine. To regulate the dose of this
drug monitor muscle strength q2h in
first 2 weeks of the drugs
administration.
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d. Avoid use of the following drugs: fasciculation). Discontinue and
aminoglycosides (gentamycin-potent resume after the acute phase is
antibiotics which can cause stabilized.
neuroblocking), morphine and strong o Cause: Overmedication with
sedatives (can cause muscular anticholinesterase drugs
relaxation that can contradict the o ET/Tracheostomy to mech vent.
anticholinesterase drug effect) o ABG Monitoring
2. Promotes optimal nutrition o d.c. (after meals) use of
a. Mealtime should coincide with the peak acetylcholinesterase
effects of the drug; give meds at 30
mins a.c. (before meals). Lesson 14: TRIGEMINAL NEUROGLIA
b. Check the gag and swallowing reflex I. Description
c. Provide soft diet because of dysphagia
d. Stay with client at mealtimes or instruct
significant others. Neuralgia
e. Keep suction, airway nearby
I. a stabbing, burning, and often
3. Monitor respiratory status frequently
severe pain due to an irritated or
4. Assess muscle strength frequently
- As often as q2h or q4h especially when damaged nerve. The nerve may be
patient is on anticholinesterase anywhere in the body, and the damage
medication. may be caused by several things,
5. Observe for signs of myasthenia or including aging, diseases such as
cholinergic crisis diabetes or multiple sclerosis, and an
a. Myasthenia crisis infection such as shingles.
o Symptoms: Abrupt onset of
severe generalized muscle
weakness with inability to Classifications:
swallow, speak or maintain Under the general heading of Neuralgia are:
respiration
o Cause: under-medication, 1. Trigeminal Neuralgia
stress, infection. 2. Occipital Neuralgia
o Symptoms will improve 3. Glossopharyngeal Neuralgia
temporarily with tensilon test 4. Postherpetic Neuralgia
o ET/Tracheostomy (prolong) to 5. Intercostal Neuralgia
Mech Vent.
o ABG monitoring (continuous for
O2) Trigeminal Neuralgia
o Increased dose of
acetylcholinesterase
b. Cholinergic crisis
o Symptoms similar to
myasthenia crisis and side
effects of anticholinesterase
drugs (increased salivation,
abdominal cramps, nausea and
vomiting, diarrhea, and

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Trigeminal neuralgia is a condition of the
fifth cranial nerve that is characterized
by paroxysms of sudden pain in the area
innervated by any of the three branches of
the nerve (Bader et al., 2016). The pain
ends as abruptly as it starts and is
described as a unilateral shooting and
stabbing or burning sensation. The
unilateral nature of the pain is an important
feature. Associated involuntary contraction
of the facial muscles can cause sudden
closing of the eye or twitching of the mouth,
hence the former name tic douloureux
(painful twitch). Although the cause is not
certain, it is thought to be demyelination of
axons in the ganglion, root, and nerve
(Grossman & Porth, 2014).
Tic douloureux
II. Painful jerking
III. In which a patient may clutch the hand
over the face and experience severe,
lancinating pain associated with
spasmodic contractions of the facial
muscles during attacks.
Types of Trigeminal Neuralgia
1. Typical Trigeminal Neuralgia:
- most common form, previously termed
classical, idiopathic, and essential
trigeminal neuralgia. Nearly all cases
of typical trigeminal neuralgia is
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caused by blood vessel
compressing the trigeminal nerve
root.
o Pulsation of vessels upon the
trigeminal nerve root do not
visibly damage the nerve.
However irritation from repeated
pulsations may lead to changes
of nerve function, delivery of
abnormal signals to the
trigeminal nerve nucleus, this
causes
hyperactivity of trigeminal nerve
root leading to trigeminal nerve
pain.
2. Atypical Trigeminal Neuralgia:
- It t is characterized by a unilateral,
prominent constant, and severe
aching and burning pain
superimposed upon otherwise typical
symptom.
- Some believe that atypical trigeminal
neuralgia is due to vascular
compression upon specific part of the
trigeminal nerve( the portio minor) while
other theorize atypical trigeminal
neuralgia as more severe progression
of typical trigeminal neuralgia.
Others:
3. Pre-Trigeminal Neuralgia:
- Days to years before the first attack of
trigeminal neuralgia pain, some patient
experience odd sensations of pain,(
such as toothache) or discomfort(
parasthesia).
4. Multiple Sclerosis Related:
- Trigeminal Neuralgia symptoms of
Multiple Sclerosis related Trigeminal
Neuralgia are identical to typical
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trigeminal neuralgia. Bilateral
Trigeminal Neuralgia is more
commonly seen in people with
Multiple Sclerosis. Multiple Sclerosis
involves formation of demyelinating
plaques within the brain.
5. Secondary or Tumor Related Trigeminal
Neuralgia:
- Trigeminal neuralgia pain caused by a
lesion, such as a tumor. Tumor that
severely compresses or distorts the
trigeminal nerve may cause numbness,
weakness of chewing muscles or
constant aching pain
6. Failed Trigeminal Neuralgia:
- In a very small proportion of patients, all
medications, surgical procedures
prove ineffective in controlling
trigeminal neuralgia pain such
individual also suffer from additional
trigeminal neuropathy as a result of
destructive intervention they underwent
II. Causes
The following are the causes of
Trigeminal Neuralgia:
• Blood Vessel Pressing On The
Trigeminal Nerve As It Exits
Brainstem
- (Superior Cerebellar Artery)
• Demyelination And Indentation Of
The Nerve Results In Hyperactivity
Of The Nerve
- also hinders nerves ability to shut
off signal
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• Multiple Sclerosis: a disease that can
cause deterioration of the trigeminal
nerve's myelin sheath.
- Leukocytes are driven to white
matter causing inflammation and
pressure to myelin
• Nerve Compression From A Tumor
(Rare)
• Arteriovenous Malformation: tangle
of arteries and veins. (Rare)
• Scleroderma: a very rare chronic
connective tissue disorder that is
classified as an autoimmune condition.
Among other symptoms, trigeminal
pain can occur in later stages.
• Shingles (herpes zoster): is a viral
infection of the nerves. Common
symptoms include a raised, painful
rash and, less typically, trigeminal
neuralgia pain. Trigeminal pain
generally occurs when the shingles
rash in located near or on the head,
face, or neck.
• Deformity In The Arteries And
Veins: arteries and veins that become
swollen with blood can compress the
trigeminal nerve.
• Injury To The Trigeminal Nerve due
to result of sinus surgery, oral surgery,
stroke, or facial trauma
• Are sometimes associated with facial
trauma or dental procedures
III. Predisposing Factors
The following are considered as
predisposing factors of Trigeminal Neuralgia:
• Hypertension
• Arteriosclerotic vascular changes
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• Aging
• Individual sensitivity
• Familial history
• Race
Additional Notes:
- Age and gender are primary risk
factors, as women over the age of 50
are most likely to develop this condition.
- Hypertension (high blood pressure) is
also a risk factor, as is the occurrence
of a stroke.
- Trigeminal neuralgia occurs most often
as people age, most commonly
between the fifth and sixth decade of
life.
- It is more common in women and in
people with MS compared to the
general population (Bader et al., 2016).
- Patients who develop trigeminal
neuralgia before age 50 years should
be evaluated for the coexistence of MS,
because trigeminal neuralgia occurs in
approximately 5% of patients with MS
(Bader et al., 2016).
- Pain-free intervals may be measured in
terms of minutes, hours, days, or
longer. With advancing years, the
painful episodes tend to become more
frequent and agonizing. The patient
lives in constant fear of attacks.
- Paroxysms can occur with any
stimulation of the terminals of the
affected nerve branches, such as
washing the face, shaving, brushing the
teeth, eating, and drinking. A draft of
cold air or direct pressure against the
nerve trunk may also cause pain.
Certain areas are called trigger points
because the slightest touch
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immediately starts a paroxysm or
episode.
- To avoid stimulating these areas,
patients with trigeminal neuralgia try not
to touch or wash their faces, shave,
chew, or do anything else that might
cause an attack. These behaviors are a
clue to the diagnosis.
Some common trigeminal neuralgia
triggers include:
 Shaving
 Touching your face
 Eating
 Drinking
 Brushing your teeth
 Talking
 Putting on makeup
 A breeze on the face
 Rising or falling barometer
 Showering
 Smiling (or frowning)
 Increase in blood pressure
 Cold weather
 Drinking alcohol
 Stress
 Washing your face
IV. Incidence
It is reported that 150,000 people are
diagnosed with trigeminal neuralgia (TN)
every year. While the disorder can occur at
any age, it is most common in people over the
age of 50. The National Institute of
Neurological Disorders and Stroke (NINDS)
notes that trigeminal neuralgia is twice as
common in women than in men. A form of
Trigeminal Neuralgia is associated with
multiple sclerosis (MS).
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Structural Classification
V. Anatomy & Physiology: Nervous
System

Functions
It uses millions of sensory receptors to
monitor changes occurring both inside and
outside the body. These changes are called
stimuli, and gathered information is called
sensory input. It process and interprets the
sensory input and decide what should be
done at each moment – a process called
integration. It then causes a response, or
effect, by activating muscles or glands
(effectors) via motor output.

The nervous system’s functions:

• Monitor changes occurring both
inside and outside the body
• Process and interpret the sensory
input and decide what should be done
at each moment
• Cause a response or effect
The structural classification, which includes all
nervous system organs, has two
Organization of the Nervous System
subdivisions – the CNS and the PNS.

The Central Nervous System consist of the

brain and spinal cord, which occupy the
dorsal body cavity and act as the integrating
and command centers of the nervous system.
They interpret incoming sensory
information and issue instructions based
on past experience and current conditions.

The Peripheral Nervous System includes all

parts of the nervous system outside the CNS.
It consists mainly of the nerves that extend
from the spinal
cord and brain. Spinal nerves carry impulses
to and from the spinal cord. Cranial nerves
carry impulses to and from the brain. These
nerves serve as communication lines. They
link all parts of the body by carrying impulses

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from the sensory receptors to the CNS and
from the CNS to the appropriate glands or
muscles.
Functional Classification
The functional classification scheme is
concerned only with PNS structures. It
divides them into two principal
subdivisions.
The sensory division or afferent “to
go toward” division, consist of nerves
(composed of many individual nerve
fibers) that convey impulses to the
central nervous system from sensory
receptors located in various parts of the
body. The sensory divisions keeps the
CNS constantly informed of events
going on both inside and outside the
body. Sensory fibers delivering
impulses from the skin, skeletal
muscles, and joints are called somatic
(soma-body) sensory (afferent) fibers,
whereas those transmitting impulses
from the visceral organs are called
visceral sensory (afferent) fibers.
The motor division, or efferent
division, carries impulses from the
CNS to effector organs, the muscles
and glands. These impulses activate
muscles and glands; that is, they effect
(bring about or cause) a motor
response.
The Motor Division In Turn Has Two
Subdivisions
• The Somatic nervous system allows
us to consciously, or voluntarily,
control our skeletal muscles. Hence, we
often refer to this subdivision as the
voluntary nervous. However, not all
skeletal muscle activity controlled by
this motor division is voluntary. Skeletal
110 | P a g e
muscles reflexes, such as the stretch
reflex, are initiated involuntarily by
these same fibers.
• The autonomic nervous system
regulates events that are autonomic, or
involuntary,
such as the activity of smooth muscles,
cardiac muscles, and glands. This
subdivisions, commonly called the
involuntary nervous system, itself has
two parts, the sympathetic and
parasympathetic, which typically bring
about opposite effects. What one
stimulates, the other inhibits.
Nervous System Tissue Structure And
Function
Nervous tissue is made up of just two
principal types of cells – supporting
cells and neurons.
Supporting cells – in the CNS are
“lumped together” as neuroglia.
Supporting Cells
• Astrocytes: abundant star-shaped
cells that account for nearly half of
neural tissue recapturing chemicals
released for communication purpose.
• Microglia: spider-like phagocytes that
monitor the health of nearby neurons
and dispose of debris, such as dead
brain cells and bacteria
• Ependymal cells: neuroglia that line
the central cavities of the brain and
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spinal cord. The beating of their cilia
helps to circulate the CSF that fills
those cavities and forms a protective
watery cushion around the CNS. Classification of Neurons
• Oligodendrocytes: neuroglia that
wrap their flat extension (processes)
tightly around the nerve fibers,
producing fatty insulating coverings
called myelin sheath.
• Schwann Cells: form myelin sheath
around nerve fibers in the PNS
• Satellite Cells: act as protective,
cushioning cells for peripheral neuron
cell bodies.

Neurons

Neurons: also called nerve cells, are highly
specialized to transmit messages (nerve
impulses) from one part of the body to another.
Although neurons differ structurally from one
another, they have many common features. All
have a cell body, which contains the nucleus
and one or more slender processes extending
from the cell body.
Cell body: the cell body is the metabolic
center of the neuron. Processes – axons and
dendrites
Myelin sheath: whitish, fatty material that
protects and insulates the fibers and increases
the transmission rate of nerve impulses.
• Functional classification
Sensory/ Afferent Neurons: carry
impulses from sensory receptors to
the CNS.
Motor/ Efferent Neurons: carry
impulses from the CNS to the viscera
and/ or muscles and glands.
Interneurons/ Association
Neurons: connect the motor and
sensory neurons in neural pathways.
• Structural Classification
Unipolar Neurons: contain single
axon; sensory neurons.
Bipolar Neurons: one axon and one
dendrite; found in special sense
organs.
Multipolar Neurons: one axon and
multiple dendrites; motor and
association neurons; the most
common structural type.
REFLEXES
• Rapid, predictable and involuntary
responses to stimuli

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• Occur over neural pathways called
reflex arcs and involve both CNS and
PNS structures.
• Classifies as either somatic or
autonomic reflexes
• Somatic reflexes: include all reflexes
that stimulate the skeletal muscles
• Autonomic reflex: regulate the activity
of the smooth muscles, heart and
glands.
• 5 elements of reflex arcs - receptor
- effector
- sensory neuron
- motor neuron
- integration center
• patellar or knee-jerk reflex
• flexor or withdrawal reflex
• reflex testing is an important tool in
evaluating the condition of the NS.
Central Nervous System
Brain
• is protected by the cranium
• largest and most complex
mass of nervous tissue in the
body
• four major regions: cerebrum,
brainstem, diencephalon and
cerebellum
Cerebrum
• the largest and most superior
part of the brain, divided into left
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and right cerebral hemisphere
by the median longitudinal
fissure and connected by
commisures.
• The entire surface of the
cerebrum exhibits elevated
ridges of tissue called gyri,
separated by shallow grooves
called sulci.
• Each cerebral hemisphere has
three basic regions: superficial
cortex of gray matter, an internal
area of white matter and the
basal nuclei.
Lobes Of Cerebrum
• Frontal Lobe: control of
voluntary motor functions,
motivations, aggression, mood,
and olfactory reception
• Parietal Lobe: principal center
for the reception and conscious
perception of most sensory
information such as touch, pain,
temperature, balance
and taste.
• Occipital Lobe: reception and
perception of visual input.
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• Temporal Lobe: olfactory and
auditory sensations and plays an
important role in memory.
Diencephalon
• Or interbrain, sits atop the brain
stem and is enclosed by the
cerebral hemispheres.
• Major structures: thalamus,
hypothalamus and epithalamus
• Thalamus:
- enclose the third
ventricles
- relay station for sensory
impulses passing upward
to the sensory cortex
• Hypothalamus:
- makes up the floor of
diencephalon
- plays role in regulating
body temperature, water
balance and metabolism
- center for many drives
and emotions - regulates
the pituitary gland
• Epithalamus:
- forms the roof of the
third ventricle
- important parts: pineal
body and choroid plexus
Brainstem
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provides pathway for ascending and
descending tracts structures: midbrain, pons
and medulla oblongata
Midbrain
- superior to the pons; the smallest
region of brainstem
- the dorsal part consist of four colliculi
- contains nuclei involved in the
coordination of eye movement and in
the control of the pupil diameter and
lens shape
- contains substantia nigra involved in
the regulation of regulation of general
body movements
- consist largely of ascending tracts from
the spinal cord to cerebrum and
descending tracts from the cerebrum to
the spinal cord or cerebellum
Pons
- superior to the medulla oblongata
- contains ascending and descending
nerve tracts as well as several nuclei
- relay information between cerebrum
and the cerebellum
- breathing, swallowing and balance are
controlled in the lower pons
Medulla Oblongata
- the most inferior portion of the
brainstem and is continuous with
thespinal cord
- contains ascending and descending
nerve
- contains nuclei that regulate the heart
rate, blood vessel diameter, breathing,
swallowing, vomiting, coughing,
sneezing, balance and coordination
Reticular Formation
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• Connective tissue membranes covering and

• a group of nuclei scattered throughout the
protecting CNS structures
brainstem
• Outer: dura mater
• plays an important regulatory functions in the
• Middle layer: arachnoid mater
brain
• Inner layer: pia mater
• involved in regulating cyclical motor functions
such as respiration, walking and chewing
Cerebrospinal Fluid (CSF)
• major component of reticular activating
• Watery with components similar to
system
blood plasma, contains less protein and
• damage to cells of the reticular formation can
more vitamin C.
result in coma
• Forms watery cushion that protects
the nervous tissue from mechanical
injury
• Choroid plexus form CSF from the
Cerebellum
blood
• Little brain
• Attached to the brainstem by several
large connections called cerebellar
penducles
• Involved in balance, maintenance of
muscle tone, and coordination of fine
motor movement.

Meninges

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• Endoneurium, perineurium, fascicles,
epineurium
• Sensory (afferent) nerves, motor
(efferent) nerves and mixed nerves
• 12 pairs of cranial nerves primarily
serve the head and neck
• 31 pairs of spinal nerves are formed
by the combination of the ventral and
dorsal roots
of the spinal cord.

Cranial Nerves

Spinal Cord
• Extends from the foramen magnum at
the base of the skull to the second
lumbar vertebra
• Transmits signal to and from the brain
and is the integrating center for the Autonomic Nervous System
spinal cord reflexes • Motor subdivision of PNS that controls
• Protected by the vertebral column and body activities automatically
meninges from mechanical injury • Composed of a specialized group of
• Spinal nerves communicate between neurons that regulate the cardiac
the spinal cord and the body muscle, smooth muscles and glands
• 2 main functions • Contribute to maintaining the stability
- center for many reflex actions of the body’s internal environment
- provides means of • Two arms: sympathetic and
communication between the parasympathetic nervous system.
brain and the spinal nerves.
Trigeminal Nerve
Peripheral Nervous System
• Consist of nerves and scattered
ganglia
• Nerve: bundle of neuron fibers found
outside the CNS

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The trigeminal nerve is the part of the nervous
system responsible for sending pain, touch
and temperature sensations from your face to
your brain. It’s a large, three part nerve in your
head that provides sensation.
• Largest cranial nerve
• Fifth cranial nerve
• Mixed nerve (sensory and motor)
• Sensory to skin of face
• Motor to muscles of mastication
The trigeminal nerve primarily helps you feel
(sensory), although the mandibular nerve
branch has both sensory and motor functions.
The trigeminal nerve helps with:
• Biting, chewing and swallowing
• Facial sensation
The trigeminal nerve, also called the Cranial V
(CV), is the fifth of 12 cranial nerve. Every
person have two trigeminal nerve, one on
each side of the body. They start in the brain
and travel throughout the head.
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Like a tree extending from the brain
throughout the face, the trigeminal nerves
have roots and branches:
1. Trigeminal nerves begin within four
nuclei – or collections of nerve cell
bodies – the brain. Three of these
nuclei control the functioning of the
senses. The fourth controls motor
function (or the movements).
2. These three sensory nuclei merge to
become one sensory root near the
pons, which is the largest, central part
of the brainstem.
3. This sensory root becomes the
trigeminal ganglion as it leaves the
brainstem on each side. Each
trigeminal ganglion is located near the
temple at the side of the head, in front
of the ear.
4. The trigeminal ganglion splits into
three trigeminal nerves branches.
These branches travel along each side
of the head to different part of the face.
Trigeminal Nerve Branches
The trigeminal nerve has three branches that
performs distinct functions:
• Ophthalmic: this branch send nerve
impulses from the upper part of the
face and scalp to the brain. Ophthalmic
refers to the eye. The ophthalmic nerve
relates to the eyes, upper eyelids and
forehead.
Superior division of the V nerve
Entirely sensory
Has 3 branches. All 3 of them
pass through the sup. Orbital
fissure into the orbit. They are;
1. Lacrimal nerve: smallest,
sensory, supplies: lacrimal gland
and the
conjunctiva, skin of the upper
eyelid.
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2. Frontal nerve: largest 1. internal nasal
branch, it enters the orbit branch: medial and
through the lateral mucosa of
superior orbital fissure divides nose
into 2 branches. 2. external nasal
- The supra orbital branch: lower
branch: it is larger, arises border of the nasal
from the orbit bone.
through the supraorbital V. infra trochlear nerve:
foramen. Supplies: the medial end of eyelid,
skin of the forehead an conjunctiva, lacrimal sacs
scalp and mucous and upper half of nose
membrane of the frontal • Maxillary: this nerve branch is
sinus. responsible for sensations in the middle
- The supra trochlear part of the face. Maxillary refers to
branch: it is smaller and upper jaw. The maxillary nerves
from the orbit above the extends to the cheeks, nose, lower
trochlea. Supplies: skin of eyelids and upper lip and gums.
the upper eyelid and Second division of trigeminal nerve
lower part of the Pure sensory
forehead. Supplies: derivatives of maxillary
3. Nasocilliary nerve: it enters process and frontonasal process
the orbit through middle of Branches:
superior orbital fissure and ends 3. in the cranium:
in anterior ethmoidal foramen. meningeal
Branches: 4. in the
I. Communicating branch pterygopalatine
to cilliary ganglion: fossa: ganglionic,
sensory zygomatic, post.
II. Long cilliary nerve: iris Superior alveolar
and cornea 5. in the intra orbital
III. Posterios enthmoidal canal: middle sup,
nerve: mucous alveolar, anterior
membrane lining of the superior/ greater
post etmoidal and alveolar
sphenoidal paranasal 6. on the face:
sinus. palpebral, nasal,
IV. Anterior ethmoidal superior labial
nerve: ant. Ethmoidal and
frontal paranasal air cells. In the cranium: meningeal branch:
In the upper part of the it given off near the foramen
nasal cavity, further rotundum. Supplies: dura mater of
divides: the anterior and middle cranial
fossae.
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In the pterygopalatine fossa: the
gangalionic branches: connect the
maxillary nerve to the
pterygopalatine ganglion. Contain
secretomotor fibers to the lacrimal
gland and provide sensory fibers to
the orbital periosteum and mucous
membrane of the nose, palate and
pharynx
• Mandibular: the mandibular (lower
jaw) branch aids sensation to the lower
part of the face, such as jaws, lower lip
and gum. These nerves also have
motor function (biting, chewing and
swallowing).
Third and largest division
Large sensory root – foramen
ovale
Small motor root which passess
deep to the ganglion, and unites
with
sensory root in the infratemporal
fossa.
Branches:
1. Anterior division: undivided nerve and
divided nerve
2. Undivided nerve: meningeal branch,
nerve to the medial pterygoid Divided
nerve: buccal nerve, masseteric nerve,
deep temporal nerve and nerve to the
lateral pterygoid. Posterior divisions:
auriculotemporal nerve, lingual nerve
and inferior alveolar nerve.
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VI. Pathophysiology of Trigeminal
Neuralgia
Compression of the Trigeminal Nerve
- It is estimated that compression of the
trigeminal nerve is responsible for 80 to
90% of cases of trigeminal neuralgia,
this means that the trigeminal nerve is
compressed by nearby arteries and or
veins, vasculature in the nearby area of
the face may press or compress on that
nerve which leads to the compression
of a specific artery.
Tumors
- Tumors in that area of the head may also
lead to the compression of the trigeminal
nerve that leads to trigeminal neuralgia as
well.
Atherosclerosis of the Superior Cerebellar
Artery, Anterior Inferior Cerebellar Artery,
Vertebral Artery, and Petrosal Vein
- Amongst them the most common artery that
is implicated in compression of the
trigeminal nerve is the “superior cerebellar
artery” this artery is the common cause of
the compression of the trigeminal nerve.
Compression leads to “Demyelination of
the Trigeminal Nerve”
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- What happens here is the
compression of some of those arteries
or veins leads to
demyelination of the trigeminal nerve,
demyelination is where the fatty
insulation on the nerve is destroyed or
removed.
Hyperexcitability of nerve fibers
- Hyperexcitability means they become
excitable or firing pain which causes
brief episodes of intense pain in patient
with Trigeminal Neuralgia.
VII. Clinical Manifestations
Trigeminal neuralgia is a condition where
there is a problem in trigeminal nerve (CN 5)
which is composed of three (3) branches
(ophthalmic, maxillary, and mandibular
branches). These three (3) branches is
typically affected and patient tend to present
some clinical manifestation in these specific
areas. The following are the three major
clinical manifestation:
Facial Pain
Patient usually experienced a paroxysms of
sudden pain lasting for a seconds to 2
minutes. But attack may repeat rapidly as
often as 100 times a day. Pain is characterized
as shooting and stabbing or burning
sensation. Usually, only one side (unilateral) of
the face affected. With advancing years,
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painful episode tend to be one more frequent
and agonizing for the patient. Pain can happen
when there is stimulation of the affected nerve
branches such as washing of face, shaving,
brushing , eating and drinking. These trigger
points must not be stimulated even with
slightest touch because it can start a paroxysm
episode.
Diminished or Loss of Corneal Reflex
Due to pain associated with involuntary
contraction of facial muscle, sudden closing of
the eye can happen. Diminished or loss of
corneal reflex is present due to damage of the
ophthalmic branch. Patient may experience
sudden, sporadic, shock-like pain around the
eye.
Chewing Dysfunction & Mouth Twitching
Involuntary facial muscle contraction can lead
to twitching of mouth. Patient may find that
pain worsens upon chewing. Because
mandibular branch is affected which gives
sensation to the jaw and lower lip and also
provides movement of the muscles involved in
biting, chewing, and swallowing, patient may
experience chewing dysfunction.
VIII. Diagnostic Tests
There is no specific diagnostic test fro
Trigeminal Neuralgia. Diagnosis is based on
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patient's description of the symptoms,
including the type of pain, it's frequency and
intensity and where the pain is located. The
following test may be used to have the most
accurate diagnosis of the condition.
• Neurological Examination: a detailed
medical history and neurological
examination is needed to assess and
evaluate patient's mental status, motor
strength, vision, and reflex testing. It permits
healthcare provider to assess the cranial
nerve affected by testing the sensation of
the face, checking of eye movements and
hearing, observing how patient swallow and
test the ability of the head, neck and
shoulder to move.
• Computed Tomography (CT) Scan: a test
used to rule out etiologies like tumor,
multiple sclerosis, or stroke regarding the
manifestation of facial pain. But CT scan is
limited in evaluating the brainstem and
cisterns. That is why, MRI is the imaging
modality of choice and considered as the
initial screening procedure to assess
Trigeminal Neuralgia.
• Magnetic Resonance Imaging (MRI) : This
test uses strong magnetic fields and radio
120 | P a g e
waves to create a two or three dimensional
image for proper viewing of the brain, head,
and neck. It permits physician to determine
the area where blood vessels might be
compressing one of the trigeminal nerve. It
also look for other conditions such as
sinusitis, multiple sclerosis, tumors or nerve
damage that can lead to facial pain.
• Panoramic Radiograph: Trigeminal
Neuralgia affects one of the branches,
specifically, the mandibular and maxillary
branches which causes some clinical
manifestation like chewing dysfunction and
jaw pain. This test is used to rule out
temporomandibular joint disorder.
• Positron Emission Tomography (PET)
Scan: an imaging test that uses a dye. This
tests is used to detect neuropathic pain due
to nerve injury. It is also used to rule out
brain tumor.
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• Electromyography: used to assess muscle

response and electrical activity in response
to nerve stimulation of the muscle. EMG
recordings of trigeminal reflexes can be
utilized to rule out structural lesions in client
with symptoms related to the trigeminal
nerve. Medication: oxcarbazepine (Trileptal)
Drug Class: Anticonvulsant
IX. Medical Management
Indications: It is used to treat the symptoms
of seizures.
Side Effects: dizziness, drowsiness,
tiredness, balance or coordination problems,
vomiting, nausea, tremors or shaking, double
vision, and rash
Medication: carbamazepine (Tegretol)
Nursing Considerations:
Drug Class: Anticonvulsants
1. Monitor signs of allergic and
Indications: It is used by reducing the hypersensitivity reactions, including
abnormal electrical activity in the brain. pulmonary symptoms (tightness in the
throat and chest, wheezing, cough,
Side Effects: ataxia, nystagmus, diplopia,
dyspnea) or skin reactions (rash,
dizziness, vertigo, sedation, confusion, pruritus, urticaria).
impaired concentration 2. Monitor daytime drowsiness, agitation,
Nursing Considerations: confusion, or other cognitive
impairments. Repeated or excessive
1. Monitor CBC and platelet count. symptoms may require change in dose
2. Monitor serum blood levels of or medication.
medication often. 3. Monitor signs of low sodium levels
3. Assess for trigeminal neuralgia: facial (hyponatremia), including headache,
pain including location, duration, confusion, lethargy, irritability,
intensity, and character, activity, that decreased consciousness, and
stimulates pain. neuromuscular abnormalities (muscle
4. Advise patient to avoid driving and weakness and cramps).
other activities requiring alertness the 4. Assess vertigo or dizziness that might
first 3 days. affect gait, balance, and other
5. Advise patient to avoid with alcohol, functional activities.
and CNS depressant while taking 5. Assess any gait disturbances, tremor,
carbamazepine. or ataxia.
6. Advise patient to take with food or milk 6. Document the number, duration, and
to decrease GI upset. severity of seizures to help determine if
7. Advise patient do not consume this drug is effective in reducing seizure
grapefruit juice while taking activity.
carbamazepine.

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Medication: phenytoin (Dilantin)
Drug Class: Anticonvulsants
Indications: Used to treat grand mal
seizures, complex partial seizures, and to
prevent and treat seizures during or following
neurosurgery.
Side Effects: drowsiness, confusion, slurred
speech, abnormal eye movement, and
problems with balance or muscle movement
Nursing Considerations:
1. Observe patient closely for neurologic
adverse effects following IV
administration. Have on hand oxygen,
atropine, vasopressor, assisted
ventilation, seizure precaution equipment
(mouth gag, nonmetal airway, suction
apparatus).
2. Observe for symptoms of folic acid
deficiency: neuropathy, mental
dysfunction.
3. Monitor vital signs and symptoms during
IV infusion and for an hour afterward.
Watch for respiratory depression.
4. Monitor for signs of gingival hyperplasia
appears most commonly in children and
adolescents and never occurs in patients
without teeth.
5. Monitor for decrease in serum calcium
levels.
6. Ensure the patients on prolonged therapy
have adequate intake of vitamin D-
containing foods and sufficient exposure
to sunlight.
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Medication: baclofen (Lioresal)
Drug Class: Skeletal muscle relaxants
Indications: promotes segmental inhibition at
the nucleus oralis of trigeminal brainstorm
complex
Side Effects: dizziness weakness, confusion,
headache, nausea, constipation, difficulty
falling asleep or staying asleep, tiredness,
frequent urination
Nursing Considerations:
1. Monitor sudden changes in spasticity,
muscle strength, or CNS symptoms
(confusion, somnolence, agitation,
hallucinations) that might indicate pump
malfunction.
2. Monitor signs of hypersensitivity
reactions, including pulmonary
symptoms (tightness in the throat and
chest, wheezing, cough, dyspnea) or
skin reactions (rash, pruritus, urticaria).
3. Assess dizziness, drowsiness, and
ataxia that might affect gait, balance,
transfers, and other functional
activities.
4. Assess patient's spasticity, ROM,
functional ability, and posture.
5. Assess blood pressure periodically and
compare to normal values.
6. Assess peripheral edema using girth
measurements, volume displacement,
and measurement of pitting edema.
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Medication: gabapentin (Apo-Gabapentin
(CAN))
Drug Class: Antiepileptic
Indications: It is used to treat the type of
nerve pain (neuralgia) that results from nerve
damage
Side Effects: drowsiness, dizziness, ataxia,
headache, and tremor. • Microvascular Decompression (MVD)
- Microvascular Decompression is a surgical
Nursing Considerations:
procedure to relieve the symptoms (pain,
1. Instruct the patient/family that muscle twitching) caused by compression of a
extended-release tablet should not be nerve by an artery or vein. It provides the
cut, crushed, or chewed. If swallowing longest duration of relief from trigeminal
the gabapentin capsule is difficult, neuralgia pain, and the lowest rate of
sprinkle its content over soft food or permanent numbness of the face after
juice just before consumption. surgery.
2. Educate the patient/family to take
gabapentin at least 2 hours after taking
an antacid.
3. Educate the patient about CNS
depressive such as ataxia, dizziness, Ablative Treatments
drowsiness, and blurred vision effects
of gabapentin and instruct the patient to
refrain from engaging in high-risk
activities until the drug’s CNS effects
are known.
4. Explain the importance of follow-up with
physician to assess therapeutic
effectiveness of the therapy
(gabapentin serum level: therapeutic
level 5.9-21 mcg/mL, toxic level more ▪ Radiofrequency Thermocoagulation
than 85 mcg/mL). (RFT)
5. Explain the patient that alcohol - Used to treat trigeminal neuralgia (TN) with a
consumption may cause ataxia and satisfactory pain relief but a high recurrence
impaired psychomotor function. rate.

X. Surgical Management

Gasserian ganglion – level procedures

▪ Glycerol Rhizotomy (GR)

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- Used to treat trigeminal neuralgia (TN), with
satisfactory pain relief lasting 2 to 3 years in • Peripheral neurectomy
most patients after the first intervention. - the simplest, most economical, and safest
surgical treatment for Trigeminal Neuroglia. It
is one of the oldest and least invasive surgical
options, is well tolerated by patients, and can
be done under local anesthesia, if necessary.

• Cryotherapy (cryonanlgesia)
- Cryotherapy in neuralgia works by freezing
▪ Balloon compression (BC)
nerve cells and thus, blocking transmission of
- Balloon compression is a minimally invasive
pain. The mechanism of action of Cryotherapy
procedure that seems to be comparably
can be divided into three parts: 1. Heat
successful for idiopathic and secondary
transfer/heat exchange: The heat between
Trigeminal Neurglia, as well as TAC. However,
target area and cryogenic agent is exchanged
further studies are deemed necessary to
due to temperature gradient between the two.
establish it as the first-line treatment in
medically resistant trigeminal pain.

• Alcohol block
- Trigeminal Nerve Block with alcohol for the
pain management of Trigeminal Neuroglia can
▪ Stereotactic radiosurgery (SRS)
provide considerably long-lasting pain relief.
- Stereotactic radiosurgery (SRS) has been a
Repeated Trigeminal Nerve Block with alcohol
viable treatment option for TN. SRS is an
has pain relief duration as long as the first
outpatient, non-invasive alternative to
block, and seems to produce less complication
rhizotomies or MVD following the failure of
as well. Trigeminal Nerve Block with alcohol is
medical pain management or surgery with a
a valuable treatment modality or Trigeminal
lower risk of concurrent side effects
Neuroglia as a percutaneous procedure.
Peripheral Procedures
XI. Nursing Management

Nursing Management
1. Assess for pain and triggering mechanism
for pain
2. Assess for difficulty in chewing
3. Educate the patient about trigger zones
and pain precipitants with patient
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4. Educate the patient about medication
regimen
5. Ensure the patient to have a good oral
hygiene
6. Instruct the patient to protect cornea from
abrasion
7. Instruct the patient not to touch or wash
their faces, shave ,chew, or do anything
else that might cause an attack.
Preventing Pain
1. Monitor for anxiety, depression, and
insomnia that often accompany chronic
painful conditions.
2. Instruct the patient to take food and fluids
at room temperature, to chew on the
unaffected side, and to ingest soft foods.
3. Instruct the patient to rinse with
mouthwash after eating if toothbrushing
causes pain
4. Assist the patient in preventing or
reducing this pain by providing
instructions about preventive strategies.
5. Provide cotton pads and room
temperature water for washing the face,
6. Perform personal hygiene during pain-
free intervals are all effective strategies.
Providing Postoperative Care
1. Observe the patient carefully for presence
of difficulty in eating or swallowing foods of
different consistencies
2. Assess the eye for presence of irritation or
redness.
3. Artificial tears may be prescribed to
prevent dryness in the affected eye.
4. Instruct the patient not to chew on the
affected side until numbness has
diminished.
5. Instruct the patient not to rub the eye
because the pain of a resulting injury will
not be detected.
6. Evaluate the patient for facial motor and
sensory deficits in each of the three
branches of the trigeminal nerve.
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Lesson 15: RETINAL DETTACHMENT
I. Description:
Retinal detachment is an eye problem that
happens when your retina (a light-sensitive
layer of tissue in the back of your eye) is pulled
away from its normal position at the back of
your eye.
Separation of 2 primitive layers of the epithelial
pigment & rods & cones layer, or separation of
the entire retina from the choroid r/t presence
of a tumor
II. CAUSES
A retinal detachment is when the retina starts
to peel off the wall of the eye.
There are main causes of retinal detachment.
1. Shrinkage or contraction of the vitreous
 Vitreous is the gel-like substance that fill
the inside of the eye. This can create
tugging on the retina and the retinal tear,
leading to a retinal detachment.
2. Injury
 Blunt eye trauma and injury can cause
bruises and scarring of the retina.
3. Advance diabetes
 These new blood vessels are fragile
and can leak into the clear, jellylike
substance that fills the center of your
eye (vitreous). Eventually, scar tissue
from the growth of new blood vessels
can cause the retina to detach from the
back of the eye.
4. Inflammation eye disorder
 This kind happens when fluid builds up
behind the retina, but there's no tear.
The fluid pushes the retina away from
the tissue behind it. Common causes
include leaking blood vessels and
swelling because of conditions such as
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an injury, inflammation, or age-related Allow liquid vitreous to seep thru sensory
macular degeneration. retina
Causes of Retinal Detachment: ▼
Detach it from RPE
 Myopic degeneration
 Trauma
 Hemorrhage
 Exudates in front or behind retina
 Aphakia
 Sudden & severe physical exertion in
debilitated clients

Traction Retinal Detachment

eyeball elongates excessive growth

▼
cornea curving too steeply
▼
walls of the eye stretch causing the sclera and
retina to thin
▼
increasing risk of retinal holes, tears,
detachment
Proliferative membranes on the surface of
the retina or vitreous
▼
can pull on the neurosensory retina
▼
separation between the neurosensory retina
& retinal pigment epithelium

Rhegmatogenous
(break)
▼
Hole or tear develops in sensory retina
▼
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Exudative Retinal Detachment
- Or serous detachments are r/t associated
problem that produce subretinal fluid without
retinal break
- usually involves the choroid as a tumor or an
inflammatory disorder
normally, water flows from vitreous cavity to
choroid.
▼ potential space known as subretinal space.
direction of flow is influenced by the relative
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hyperosmolarity of the choroid with respect to
the vitreous and the RPE that actively pumps
ions and water from the vitreous into the
choroid.
▼
↑ inflow of fluid or ↓outflow of fluid from
vitreous cavity that overwhelms the normal
compensatory mechanisms,
▼
fluid accumulates in subretinal space
▼
exudative retinal detachment.
III. Anatomy and Physiology
o Rods - dim light
o Cones - bright, daylight, color vision
o Melanin epithelial pigment - absorbs
light that enters eyes
Photosensitive cells in the retina: rods &
cones
▼
convert incident light energy into signals
▼
carried to the brain by the optic nerve.
▼
visual recognition
Retina consists of two primary layers: an
inner neurosensory retina and retinal
pigment epithelium (RPE).
Sensory retina develops from the inner layer
of the neuroectoderm, whereas RPE is
derived from the outer layer of the
neuroectoderm. The RPE is continuous
anteriorly with the pigment epithelium of the
ciliary body. Sensory retina extends from the
optic disc to ora serrata, where it is continuous
with non-pigmented ciliary epithelium.
Between the neural retina and RPE, there is a
The adhesion between neural retina and RPE
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is relatively weak. The neural retina is firmly
attached at its anterior termination, the ora
serrata, and at the margins of the optic nerve
head. The ora serrata is located 4-6 mm
behind ciliary epithelium and corresponds to
the insertion of medial and lateral rectus
muscles. Ora serrata has a smooth
appearance temporally but serrated nasally.
The retina is divided into two distinct regions
which are the posterior pole and the peripheral
retina, and this 2 regions also separated by the
so called retinal equator. So the retinal equator
is an imaginary line which is considered to lie
in line with the exit of the four Vortex veins.
A. Area centralis (commonly known as the
posterior pole or central retina)
 Area centralis is about 5–6 mm
diameter circular zone of the retina. It is
situated between the superior and
inferior temporal arteries and contain
two distinct areas, the maculla lutea
and optic disc
1. Macula lutea
 Also called the yellow spot, it is about
5.5 mm diameter area situated in area
centralis, 3 mm lateral to the optic disk.
It is partly yellow as a result of yellow
xanthophyll carotenoid pigments
(zeaxanthin and lutein) in the cone
axons. This pigment is believed to act
as a short wave-length filter protecting
against UV irradiation. The macula is
responsible for photopic vision & color
vision.
2. Optic Disc
 The optic disc lies a 3 mm medial to the
center of the macula (fovea). This pale
pink/whitish area is about 1.8 mm (1.86
× 1.75 mm) in diameter with a slightly
raised rim. The central retinal vessels
emerge at the center of the optic disk,
pass over the rim, and radiate out to
supply the retina.
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B. Peripheral Retina
The peripheral retina is the remainder of the
retina. The distance from the optic disk to the
ora serrata is 23–24 mm on the temporal
aspect and approximately 18.5 mm on the
nasal aspect. The peripheral retina is the
thinnest (110–140 µm in thickness) and the
retina becomes thicker as it progresses
towards the posterior pole.
 Peripheral retina can be divided into four
regions.
1. Near periphery- about 1.5 mm around
the macula
2. Mid periphery- for about 3 mm around
the near periphery
3. Far periphery- extend 9-10 mm from
optic disc on the temporal side and 16
mm on the nasal side in the horizontal
Meridian.
4. Ora serrata- It's about 5mm anterior to
the equator of the eye. Ora serrata is
serrated peripheral margin where the
retina ends.
Cellular Structures in Retina:
The neurosensory retina is mainly made up of
three groups of neurons: which are the
photoreceptors, bipolar cells, and ganglion
cells. Other important neurons like amacrine
cells, horizontal cells have supporting roles.
The photoreceptor cells, bipolar cells, and
ganglion cells carry the neural signal in a
three-step pathway through the retina.
Photoreceptors are sensory receptors. Bipolar
cells are first-order cells and ganglion cells
form second-order neurons.
Photoreceptors:
Photoreceptors are the special sense cells
which contain photopigments and can absorb
photons of light. There are two types of
photoreceptors, the rods, and the cones.
Rods are responsible for vision in dim light or
dark, sensing contrast, brightness, motion and
usually produce images of black and white
shades. Cones are responsible for vision in
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bright light, fine resolution, spatial resolution,
and color vision. The density of rods and
cones varies in different parts of the retina.
Rods are absent at fovea, increases in number
towards the periphery and then again
decreasing in number towards the extreme
periphery. The density of cone increases
nearer the macula and the foveal region
contains only cones.
Bipolar Cells
A bipolar cell is a second-order neuron in the
visual pathway which transmits signals from
photoreceptors to ganglion cells. Their cell
bodies lie in the inner nuclear layer and lie
parallel to the photoreceptors. Their single or
multiple dendrites synapse principally with
photoreceptors (and also with horizontal cells),
while their single axon synapses with ganglion
and amacrine cells. Bipolar cells have been
subdivided into nine morphological subtypes.
Principal types of bipolar cells are:
 Rod Bipolar Cells: connect several rods
to one to four ganglion cells.
 Flat or Diffuse Bipolar Cells: connect
many cones with many ganglion cells
 Midget Bipolar Cells: connect a single
cone with a single ganglion cells
Ganglion Cells
Ganglion cell is the third-order neurons in the
visual pathway. The reason for the name "
ganglion cell" is their resemblance to cells in
nervous ganglia. Usually, they form a single
layer in peripheral retina and form as many as
10 layers in the macula.
The dendrites of ganglion cells synapse with
the axons of bipolar cells and amacrine cells.
Each ganglion cell has a single axon and these
nonmyelinated axons form the nerve fiber
layer on the innermost surface of the retina.
These axons make 90 degrees turn to reach
the inner surface of the retina and leave the
eye as the optic nerve. While coming out from
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the eye through the lamina cribrosa, these
axons become myelinated with
oligodendrocytes.
Layers of Retina:
The retina consists of 10 layers which include;
1. Retinal pigment epithelium
 This is a single cell layer made up of
hexagonal shaped RPE cells and lies
between Bruch's membrane and the
neurosensory retina. There is a potential
space between RPE and sensory retina,
known as subretinal space. Absence of
specialized molecules like laminin and
fibronectin, lack of junctional complexes
between RPE cells and photoreceptors
are responsible for this loose attachment
of RPE cells to the photoreceptors. The
RPE extends from the optic nerve to the
ora serrata and is continuous with the
ciliary body pigment epithelium.
2. Layer of Rods & Cones
 Photoreceptors Layer (Layer of rods and
cones):
 The photoreceptor layer contains only
photosensitive part of rods and cones
whereas cell bodies and inner
processes of them lies in outer nuclear
and outer plexiform layers. The central
fovea has no rods and foveal region is
densely packed with cones (2, 00,000
cones per square millimeter). Outside
the fovea, this density of cones gradually
decreases. This structural variation
results from the centripetal migration of
the first order & centrifugal lateral
displacement of second & third-order
neurons during fetal maturation which
occurs 3 months before & 3 months after
term.
3. External limiting membrane
 The external limiting membrane is not a
true membrane, but a discrete “wire
netting” layer. It is composed of zonula
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adherens junctions between
photoreceptor cells and between
photoreceptors and Müller cells.
Through the fenestrations of the band
formed by zonula adherens processes
of the rods and cones pass.
4. Outer nuclear layer
 The outer nuclear layer consists of rod
and cone nuclei. In the peripheral retina,
the outer nuclear layer consists of 3 to 4
layers of rod nuclei and a single layer of
cone nuclei. It is thickest in the fovea,
where it contains approximately 10
layers of cone nuclei
5. Outer plexiform layer
 The word “plexiform” means something
related to plexus. The outer plexiform
layer is the layer of processes and
synapses, which lies in between two
nuclear layers (nuclei of various retinal
cells). This layer contains synapse and
network of branching processes of
horizontal cells and bipolar cells along
with inner fibers of photoreceptors.
6. Inner nuclear layer
 This layer contains nuclei of horizontal
cells, various types of bipolar cells,
amacrine cells and Müller cells
7. Inner plexiform layer
 This layer contains processes and
synapse of the bipolar, amacrine and
ganglion cells. Another unique feature of
this layer is that it contains the synapse
between the second-order and third-
order neuron in the visual pathway
8. Ganglion cell layer
 This is the innermost layer of cell nuclei.
In peripheral retina, the ganglion cell
layer consists of only a single layer of
cells whereas in central retina they form
a layer comprise of up to 10 cells. The
ganglion cells send a single axon which
eventually forms the optic nerve. Thus,
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ganglion cell is the only layer that is
continuous across the optic nerve head.
9. Nerve fiber layer
 This layer contains axons of the
ganglion cells which run parallel to the
surface of the retina and emerge out as
the optic nerve. These axons or fibers
have been grouped according to the
area. The group of axons that radiate to
the disc from the macular area is called
the papillomacular bundle. The temporal
retinal raphe is a horizontal boundary
separating the superior and inferior
retinal nerve fiber bundles in the
temporal retina. The retinal vessels are
located mainly in the nerve fiber layer
(and in the inner nuclear layer). Müller
cells play an important role in
ensheathing vessels and nerve fibers.
10. Internal limiting membrane.
 The inner limiting membrane is the
innermost layer of the retina. This layer
is made up of extensions of Müller cells
covered by a basement membrane.
IV. Retinal Detachment
 RD is an ophthalmological or eye
condition involving tearing or separation
of the multilayer neurosensory retina
from the RPE (retinal pigment
epithelium).
 Basically, detachment happens if there
is no blood supply to the neurons.
Detachment could be happen passive and
active.
 Passive- when there is accumulation of
fluid between the two layers, which is the
retina and retinal pigment epithelium. Or
it could happen
 Actively- in which actively pulling the
retina off, which could be the vitreous
traction of the retina.
 These may results in ischemia because
the retina is pulled away from the retinal
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pigment epithelium and there's rapid Trauma also one manifestation of
progressive photoreceptor generation. rhegmatogenous detachment.
So basically, without the blood, just like 2. Traction retinal detachment
any other part of the body, these cells or
neurons will die.  Tension or pulling force of the retina.
What causes the detachment of the retina?  Patients with this condition have
developed fibrous scar tissue from
One cause of the retinal detachment if there is conditions such as diabetic retinopathy,
a tear or hole develops in the retina This allows vitreous hemorrhage, or the retinopathy
for fluid in the eye to seep through that break of prematurity. The hemorrhage and
and peel the retina off the wall of the eye. This fibrous proliferations associated with this
fluid is clear jelly like substance or what we condition exert a pulling force on the
vitreous, as a person age, the vitreous delicate retina.
becomes less like Jelly and more like liquid.
Usually, the vitreous is only loosely attached
to the retina, so as the eye moves, the vitreous 3. Exudative retinal detachment
moves away from the retina without causing
problems. Sometimes, though, the vitreous  Are the result of the production of the
pulls hard enough to tear the retina. Fluid serious fluid under the retina from the
passes through that air and lift through the choroid. Conditions such as uveitis and
better off the back of the eye. macular degenaration may cause the
production of the serious fluid.
 Exudative also caused by underlying
Three types of Retinal Detachment inflammatory process. It's inflammation
underneath the retina, and that
1. Rhegmatogenous detachment inflammations leads to swelling and
 Is the most common form or the most essentially allows the retina to be pulled
common type of detachment. away from the underlying layers.
 And in this condition involved a Rip  Another thing for the retina to pull away
leading to break or hole in retina. So with disrupted, and this inflammatory
there is a ripping or tearing of the retina process can be due to tumor or lesions.
and this Rip in the retina allowing some
liquid vitreous to seep through the
sensory retina and detach it from the
RPE.
 Vitreous humor (which is the clear gel
like fluid that essentially fills the space of
the eyeball) flows through disruption
V. PATHOPHYSIOLOGY
underneath the retina, leading to
separation of retina and other layers
 People at risk for this type of detachment
include those with high myopia
(nearsightedness). Or those who have
Aphakia (Absence of natural lens) after
cataract surgery.

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VII. Diagnostic Test:
Your doctor may use the following tests,
instruments and procedures to diagnose
retinal detachment:

 Retinal examination. The doctor may

use an instrument with a bright light and
special lenses to examine the back of
your eye, including the retina. This type
of device provides a highly detailed view
of your whole eye, allowing the doctor to
see any retinal holes, tears or
detachments.
 Ultrasound imaging. Your doctor may
use this test if bleeding has occurred in
the eye, making it difficult to see your
retina.

VIII. Medical & Surgical Management:

Surgical Methods:
EARLY SYRGERY
Scleral buckle surgery
- Scleral buckling is a type of eye
surgery to correct a detached retina
and restore vision.
- The buckle is designed to repair
retinal detachment by pushing the
sclera toward the retinal tear or
break.
- Scleral buckle can be used to
close the retinal break - moves the
wall of the eye closer to the
VI. CLINICAL MANIFESTATIONS detached retina
Signs & Symptoms
 seeing flashes of light.
 the sudden appearance of floaters.
 changes in vision.
 blurry vision or a loss of vision in some
areas of the visual field.
 reduced central or side (peripheral)
vision.
 a sudden loss of vision.
 changes in color perception.

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1. Cryopexy and laser photocoagulation
 Cryotherapy is an outpatient surgical
procedure that uses extreme cold
therapy or freezing to treat retinal tears
and other retinal conditions.
 Laser photocoagulation is type of
laser surgery for the eyes. It is done to
treat age related macular degeneration,
a condition that can lead to loss of vision.
2. Pneumatic retinopexy
 Pneumatic retinopexy is a procedure to
repair a detached retina and restore
vision. Unlike other procedures to treat
a detached retina, it often takes place in
an office setting.
3. Vitrectomy
 A vitrectomy is a type of eye surgery to
treat various problems with the retina
and vitreous.
 The vitreous is a gel-like substance that
fills the middle portion of your eye.
Postoperative Care
 Apply pressure patch over eye
 Position: area affected should be upper
part of the eye
 Ambulation/activity as prescribed
 Activity/occupation heavy physical
exertion after 6 weeks
 Sedentary activities, resumed after 3
weeks
Nursing Management
This is postoperative care:
1. Monitor the status of the eye dressing
 Assess dressings for the presence of
bleeding or drainage from the eye, as
either could indicate a surgical
complication.
2. Maintain the eye patch or eye shield in
place.
133 | P a g e
 Bed rest, cover the eyes
To prevent further detachment
 The eye patch or shield helps prevent
inadvertent injury to the operative site.
4. 3. Place the client in a semi-Fowler’s or
Fowler’s position, having the client lie
on the unaffected side. Position head so
that retinal hole is in lowest part of eye
(dependent position)
 These positions reduce intraocular
pressure in the affected eye.
4. After surgery for a detached retina, the
client is positioned so that the detachment
is dependent or inferior.
 For example, if the outer portion of the
left retina is detached, the client is
positioned on the left side.
 Positioning so that the detachment is
inferior maintains pressure on that area
of the retina, improving its contact with
the choroid.
5. Assess the client, and medicate or assist
to avoid vomiting, coughing, sneezing, or
straining as needed.
 These activities may increase
intraocular pressure.
6. Assess comfort and medicate as
necessary for complaints of an aching or
scratchy sensation in affected eye.
Immediately report any complaint of
sudden, sharp eye pain to the physician.
 An abrupt increase in or onset of eye
pain may indicate hemorrhage or other
ocular emergency that require
immediate intervention
7. Assess for potential surgical
complications:
 a. Pain in or drainage from the affected
eye
 b. Hemorrhage with blood in the anterior
chamber of the eye
 c. Flashes of light, floaters, or the
sensation of a curtain being drawn over
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the eye (indicators of retinal
detachment)
 d. Cloudy appearance to the cornea
(corneal edema)
 Evidence of any of the above
manifestations or unusual complaints by
the client should be reported to the
physician at once. Early intervention is
often necessary to preserve sight.
8. Administer antibiotic, anti-inflammatory,
and other systemic and eye medications as
prescribed.

Medications are prescribed
postoperatively to prevent infection or
inflammation of the operative site,
maintain pupil constriction, and control
intraocular pressure.
9. Administer antiemetic medication as
needed.
 this medication helps to prevent
vomiting to maintain normal intraocular
pressures.
Lesson 16: GLAUCOMA
I. Description
- the silent thief of vision
- characterized by optic neuropathy with
gradual loss of peripheral vision, increased
intraocular pressure
Glaucoma is a group of eye diseases that can
cause vision loss and blindness by damaging
a nerve in the back of your eye called the optic
nerve.
The symptoms can start so slowly that you
may not notice them. The only way to find out
if you have glaucoma is to get a
comprehensive dilated eye exam.
There’s no cure for glaucoma, but early
treatment can often stop the damage and
protect your vision.
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Glaucoma is defined as a group of eye
diseases characterized by damage to the optic
nerve usually due to excessively high
intraocular pressure (IOP). This increased
pressure within the eye, if untreated, can lead
to optic nerve damage resulting in
progressive, permanent vision loss usually
starting with unnoticeable blind spots at the
edges of the field of vision, progressing to
tunnel vision, and then to blindness.
There are no symptoms in the early stage of
glaucoma. This disease is often called “the
sneak thief of sight.” Often, by the time the
patient notices vision loss, glaucoma can only
be halted, not reversed.
II. Causes
As this nerve gradually deteriorates, blind
spots develop in the visual field. This nerve
damage is usually related to increased
pressure in the eye.
Elevated eye pressure is due to a buildup of a
fluid (aqueous humor) that flows throughout
the inside of the eye. This internal fluid
normally drains out through a tissue called the
trabecular meshwork at the angle where the
iris and cornea meet. When fluid is
overproduced or the drainage system doesn't
work properly, the fluid can't flow out at its
normal rate and eye pressure increases.
Glaucoma tends to run in families. In some
people, scientists have identified genes
related to high eye pressure and optic nerve
damage.
III. Risk factors/ predisposing factors
Because chronic forms of glaucoma can
destroy vision before any signs or symptoms
are apparent, be aware of these risk factors:
 Having high internal eye pressure
(intraocular pressure)
 Being over age 60 (The amount of
aqueous humor produced tends to
decrease with age, in systemic
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diseases such as diabetes, and in V. Anatomy & Physiology
ocular inflammatory conditions.)
What’s intraocular pressure?
 Being black, Asian or Hispanic
 Having a family history of glaucoma
 Having certain medical conditions, such
as diabetes, heart disease, high blood
pressure and sickle cell anemia
 Having corneas that are thin in the
center
 Being extremely nearsighted or
farsighted
 Having had an eye injury or certain
types of eye surgery
 Taking corticosteroid medications,
especially eyedrops, for a long time
 intraocular conditions such as uveitis Intra means within and ocular means eye…so
and retinal detachment have been intraocular pressure is the fluid pressure within
associated with elevated IOP. the eye, and the fluid we’re talking about is
called aqueous humour. IOP is calculated by
IV. Incidence the production and drainage rate of aqueous
humour in the eye. The production and
Glaucoma is a leading cause of irreversible drainage rate should be equal or increased
blindness in the United States and the world. intraocular pressure will occur.

• Age - > 40 years old

• Race - African Americans; Hispanics A tonometer is used to measure the intraocular
pressure. A normal intraocular pressure is
More than three million Americans are living about 10-21 mmHg.
with glaucoma, 2.7 million of whom—aged 40
and older—are affected by its most common
form, open-angle glaucoma.
Blindness or low vision affects 3.3 million
Americans age 40 and over.
In 2020, about 80 million people have
glaucoma worldwide, and this number is
expected to increase to over 111 million by
2040.
Primary Causes:
 Genetics
 Ageing
Secondary Causes: What’s Aqueous Humour?
 Infection
 Injury

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It’s the fluid within the eye that has many roles,
but it plays a significant role with maintaining
intraocular pressure.
Structures of the eye
Choroid
Layer containing blood vessels that lines the
back of the eye and is located between the
retina (the inner light-sensitive layer) and the
sclera (the outer white eye wall).
Ciliary Body
Structure containing muscle and is located
behind the iris, which focuses the lens.
Cornea
The clear front window of the eye which
transmits and focuses (i.e., sharpness or
clarity) light into the eye. Corrective laser
surgery reshapes the cornea, changing the
focus.
Fovea
The center of the macula which provides the
sharp vision.
Iris
The colored part of the eye which helps
regulate the amount of light entering the eye.
When there is bright light, the iris closes the
pupil to let in less light. And when there is low
light, the iris opens up the pupil to let in more
light.
Lens
Focuses light rays onto the retina. The lens is
transparent, and can be replaced if necessary.
Our lens deteriorates as we age, resulting in
the need for reading glasses. Intraocular
lenses are used to replace lenses clouded by
cataracts.
Macula
The area in the retina that contains special
light-sensitive cells. In the macula these light-
136 | P a g e
sensitive cells allow us to see fine details
clearly in the center of our visual field. The
deterioration of the macula is a common
condition as we get older (age related macular
degeneration or ARMD).
Optic Nerve
A bundle of more than a million nerve fibers
carrying visual messages from the retina to the
brain. (In order to see, we must have light and
our eyes must be connected to the brain.) Your
brain actually controls what you see, since it
combines images. The retina sees images
upside down but the brain turns images right
side up. This reversal of the images that we
see is much like a mirror in a camera.
Glaucoma is one of the most common eye
conditions related to optic nerve damage.
Pupil
The dark center opening in the middle of the
iris. The pupil changes size to adjust for the
amount of light available (smaller for bright
light and larger for low light). This opening and
closing of light into the eye is much like the
aperture in most 35 mm cameras which lets in
more or less light depending upon the
conditions.
Retina
The nerve layer lining the back of the eye. The
retina senses light and creates electrical
impulses that are sent through the optic nerve
to the brain.
Sclera
The white outer coat of the eye, surrounding
the iris.
Vitreous Humor
The, clear, gelatinous substance filling the
central cavity of the eye.
How aqueous humour is produced and flows
through the eye helps us understand
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 NCM 112: NGIMPEC LECTURE NOTES
glaucoma. Therefore, first let’s discuss the
normal flow of aqueous humour in the eye
without glaucoma presenting:
Ciliary body produces aqueous humour-> the
aqueous humour first goes through the
posterior chamber of the eye which is found
between the lens and iris-> then it goes
through the pupil’s opening and makes its way
to the anterior chamber, which is found
between the iris and cornea -> then it drains
out via the drainage angle into the trabecular
meshwork (which is permeable and like a
strainer) -> then into Schlemm’s canal and
eventually into the episcleral veins of the eyes.
**An important area I want to talk about is the
drainage angle. This area is where an angle is
formed at the front of the eyes between the iris
(the colored part of the eye) and
cornea….hence this area forms an angle.
This angle is where aqueous humour drains
out into the trabecular meshwork. It’s the angle
we are talking about when we refer to either
open or closed angle glaucoma. An
ophthalmologist can check the patient’s
drainage angle with a gonioscope.
body into the suprachoroidal space and then
drains into the venous circulation of the ciliary
body, choroid, and sclera. Unimpeded outflow
of aqueous fluid depends on an intact
drainage system and an open angle (about 45
degrees) between the iris and the cornea. A
narrower angle places the iris closer to the
trabecular meshwork, diminishing the angle.
The amount of aqueous humor produced
tends to decrease with age, in systemic
diseases such as diabetes, and in ocular
inflammatory conditions.
IOP is determined by the rate of aqueous
production, the resistance encountered by the
aqueous humor as it flows out of the
passages, and the venous pressure of the
episcleral veins that drain into the anterior
ciliary vein. When aque ous fluid production
and drainage are in balance, the IOP is
between 10 and 21 mmHg, When aqueous
fluid is inhibited from flowing out, pressure
builds up within the eye. Fluctuations in IOP
occur with time of day, exertion, diet, and
medications. IOP tends to increase with
blinking, tight lid squeezing, and upward
gazing. Systemic conditions such as diabetes
and intraocular conditions such as uveitis and
retinal detachment have been associated with
elevated IOP.
Glaucoma may not be recognized in people
with thin corneas because measurement of
the IOP may be falsely low as a result of this
thinness.

VI. Pathophysiology
Aqueous humor flows between the iris and the
lens, nourishing the cornea and lens. Most
(90%) of the fluid then flows out of the anterior
chamber, draining through the spongy
trabecular meshwork into the canal of
Schlemm and the episcleral veins. About 10%
of the aqueous fluid exits through the ciliary

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Aqueous Humor
- crystal clear fluid
- fills anterior posterior of the eye
- refraction medium
- provides nutrition to lens & cornea
- maintains IOP
Normal IOP: 10 – 21 mmHg

↓ OUTFLOW OR ABSORPTION OF
AQUEOUS HUMOR
▼
DISRUPTED BALANCE BETWEEN
PRODUCTION & OUTFLOW OF AQUEOUS
HUMOR
▼
INCREASED INTRAOCULAR PRESSURE

Anterior Chamber – extends from cornea to

iris
Trabecular meshwork – base of cornea, near
ciliary body
Lens – posterior chamber extends from iris to
lens
Ciliary body – produces aqueous humor;
changes shape of lens when focusing on near
object

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Vision in Glaucoma:

Acute Glaucoma (Narrow Angle or Close

Angle)
Abnormal displacement of iris against the
angle of the anterior chamber
↓
Imbalance in production and excretion of
aqueous humor
↓
Intraocular tension
↓
Sudden impaired
vision

Rim of Optic Disk shrinks and the normal

depression at the center becomes larger and
deeper.
Chronic Glaucoma (Simple, Wide Angle or
Open Angle)
Hereditary thickening of trabecular meshwork
or deliberative narrowing of Canal of Schlemm
↓
Develops slowly, asymptomatic
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↓ consistent Rapid
increase increase in
Actual obstruction in excretion of aqueous
usually IOP
humor
bilateral usually
↓ unilateral
Manifest No initial Abrupt of
Intraocular tension ations s/s pain,
↓ Frequent headache
changes in Decreased
Permanent loss of vision occur before the eyeglasses visual acuity
client is aware Impaired Nausea/vomi
dark ting
adaptation Reddened
Halos conjunctiva
around Cloudy
lights cornea
Gradual Fixed pupil
reduction Rapid
of visual significant ↑
fields with IOP
preservatio
n of central
vision until
late in the
disease
Manage Topical Topical
ment medication miotics or
Open Angle :beta beta blockers
Angle Closure blockers, Systemic
adrenergic osmotic
Incidenc Common Uncommon
s, agents,
e 90% of all
prostaglan carbonic
cases
din analog anhydrase
Risk Age 35 Narrow
Carbonic inhibitors
Factors Genetics anterior
anhydrase Laser
African angle
inhibitors iridotomy or
Americans Aging
Laser peripheral
Asian
trabeculopl iridectomy
ancestry
asty,
Pathoph Impaired Pupil dilation
trabeculect
ysiology Aqueous or lens
omy
Outflow Accommodat
thru Canal ion causes
of already VII. Clinical manifestations
Schlemm narrowed
angle to Tunnel vision:
Cause: close,
unknown blocking
gradual aqueous
outflow

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the eyes and the forehead. The
type of glaucoma that usually
causes headaches and eye pain
is angle-closure glaucoma
6. Nausea and vomiting
 This may be related to the
oculocardiac reflex, which is a
decrease in pulse rate
1. Muscle eye pain or pressure
associated with traction applied
 Due to the elevated IOP
to the extraocular muscles
2. Red eyes
and/or compression of the
 The most common cause of red
eyeball. Perhaps in acute
eyes in patients with glaucoma is
glaucoma, where the pressure
medication, it is until proven
rise can be as high as 1
otherwise. It can also be due to
mmhg/minute, it is sufficient to
an infection but is a less
activate secondary stimulation of
common cause. It can also be
the vagus nerve which results in
due to the poorly controlled
abdominal symptoms.
glaucoma wherein the pressure
VIII. Diagnostic tests
is very high or there is already an
intraocular inflammation. Early detection, through regular and complete
3. Corneal edema eye exams, is the key to protecting your vision
 Cell degeneration or damage from damage caused by glaucoma. A
may cause the endothelial cells complete eye exam includes five common
to be unable to pump excess tests to detect glaucoma.
fluid out of the cornea.
If you have high risk factors for glaucoma,
 The accumulation of fluid
diabetes, high blood pressure, or a family
disrupts corneal transparency,
history of glaucoma, you should see an eye
which increases light scatter that
doctor now to determine how often to have eye
may cause a rainbow halo in the
exams.
vision.
4. Changes in vision
 Due to optic nerve damage, it
may cause low vision, blurring of
vision, and even vision loss if left
unattended for too long.
 Tunnel vision: open-angle Testing visual fields
glaucoma, gradual loss of vision;
- degree of central visual field narrowing
loss of peripheral vision.
and peripheral vision loss
5. Headaches
 Excessive use of the muscles Confrontation Test
involved in focusing the eyes o measures peripheral vision compared
may cause visual fatigue and, to examiner (assuming examiner’s
subsequently, headache. vision is normal)
 Headaches due to glaucoma o both examiner and patient cover one
can most usually be felt around eye with a card, stand about 2 feet
away, and maintain eye contact
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o advance finger, starting from periphery,
and ask patient to say “now” when the
finger is first visible
o inability to see when the examiner sees
suggests peripheral field loss
Fundoscopy
o an exam that uses a magnifying lens
and a light to check the fundus of the
eye (back of the inside of the eye,
including the retina and optic nerve)
Abnormal results: Pallor, ↑ size depth of optic
cup
Tonometry
Tonometry measures the pressure within your
eye. During tonometry, eye drops are used to
numb the eye. Then a doctor or technician
uses a device called a tonometer to measure
the inner pressure of the eye. A small amount
of pressure is applied to the eye by a tiny
device or by a warm puff of air.
The range for normal pressure is 12-22 mm Hg
(“mm Hg” refers to millimeters of mercury, a
scale used to record eye pressure). Most
glaucoma cases are diagnosed with pressure
exceeding 20mm Hg. However, some people
can have glaucoma at pressures between 12 -
22mm Hg. Eye pressure is unique to each
person.
142 | P a g e
Ophthalmoscopy
This diagnostic procedure helps the doctor
examine your optic nerve for glaucoma
damage. Eye drops are used to dilate the pupil
so that the doctor can see through your eye to
examine the shape and color of the optic
nerve.
The doctor will then use a small device with a
light on the end to light and magnify the optic
nerve. If your intraocular pressure (IOP) is not
within the normal range or if the optic nerve
looks unusual, your doctor may ask you to
have one or two more glaucoma exams:
perimetry and gonioscopy.
Perimetry
Perimetry is a visual field test that produces a
map of your complete field of vision. This test
will help a doctor determine whether your
vision has been affected by glaucoma. During
this test, you will be asked to look straight
ahead as a light spot is repeatedly presented
in different areas of your peripheral vision. This
helps draw a "map" of your vision.
Do not be concerned if there is a delay in
seeing the light as it moves in or around your
blind spot. This is perfectly normal and does
not necessarily mean that your field of vision
is damaged. Try to relax and respond as
accurately as possible during the test.
Your doctor may want you to repeat the test to
see if the results are the same the next time
you take it. After glaucoma has been
diagnosed, visual field tests are usually done
one to two times a year to check for any
changes in your vision.
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Gonioscopy IX. Medical Management
This diagnostic exam helps determine whether
the angle where the iris meets the cornea is 1. Objective of treatment is to prevent
open and wide or narrow and closed. During optic nerve damage by lowering the
the exam, eye drops are used to numb the IOP to a level consistent with retaining
eye. A hand-held contact lens is gently placed vision. Treatment is almost always
on the eye. This contact lens has a mirror that lifelong. Treatment also focuses on
shows the doctor if the angle between the iris achieving the greatest benefit at the
and cornea is closed and blocked (a possible least risk, cost and inconvenience to
sign of angle-closure or acute glaucoma) or the patient.
wide and open (a possible sign of open-angle, 2. Pharmacologic therapy is the initial and
chronic glaucoma). principal treatment for glaucoma. Acute
angle-closure glaucoma is treated with
medication (including miotics) to reduce
Pachymetry IOP before laser or incisional
iridectomy. Commonly used agents
Pachymetry is a simple, painless test to include:
measure the thickness of your cornea -- the
 Beta-adrenergic
clear window at the front of the eye. A probe
blockers/antagonists are the
called a pachymeter is gently placed on the
most widely used hypotensive
front of the eye (the cornea) to measure its
agents. They are effective in
thickness. Pachymetry can help your
many types of glaucoma.
diagnosis, because corneal thickness has the
 Cholinergic agents (topical) are
potential to influence eye pressure readings.
miotics (cause papillary
With this measurement, your doctor can better
constriction) and are used in
understand your IOP reading and develop a
short-term management of
treatment plan that is right for you. The
glaucoma with papillary block.
procedure takes only about a minute to
 Alpha-2-adrenergic
measure both eyes.
agonists(topical) reduce IOP by
increasing aqueous humor
outflow.
Why Are There So Many Diagnostic
 Carbonic anhydrase inhibitors
Exams?
(systemic) and prostaglandins
Diagnosing glaucoma is not always easy, and lower IOP by reducing aqueous
careful evaluation of the optic nerve continues humor formation.
to be essential to diagnosis and treatment.  Osmotic diuretics reduce IOP by
The most important concern is protecting your increasing the osmolality of the
sight. Doctors look at many factors before plasma to draw water from the
making decisions about your treatment. If your eye into the vascular circulation.
condition is particularly difficult to diagnose or
DRUGS MOA
treat, you may be referred to a glaucoma
Beta adrenergic Decrease AQH
specialist. A second opinion is always wise if
blockers production
you or your doctor become concerned about
betaxolol,
your diagnosis or your progress. carteolol,
levobunolol,

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metipranolol, 4. Avoid drinking large quantities of fluid
timolol
5. Surgery
Alpha Decrease AQH
Adrenergic production, enhance o provide a permanent fistula from a
Agonists outflow facility chamber to subconjunctival space
dipivefrin, o sclerotomy, iridectomy,
epinephrine, trabeculectomy, trephine operations
latanoprost, Acute Glaucoma Collaborative
praclomidine, Management
brimonidine
Cholinergic Parasympathomimetics 1. Maintain bed rest in quiet dark room, elevate
Agents (miotics) causing constriction of head 30 degrees.
carbachol, pupils, opening of 2. Miotics, Acetazolamide, Glycerol,
pilocarpine trabecular meshwork, Antiemetics as ordered
facilitating AQH
Carbonic Decrease AQH 3. Assess ability to see. Assist according to
Anhydrase production degree of visual impairment.
Inhibitors 4. Diet as tolerated.
A. Systemic:
acetazolamide, 5. Monitor vital signs.
dichlorphenamide
6. Provide emotional support.
methazolamine
B. topical 7. No ABC
brinzolamide,
dorsolamide o A – tropine
Combination timolol & dorzolamide o B – enadryl
therapy o C – ogentin
Hyperosmolar ↑ extracellular o Rationale: dilate pupils, iris is brought
Agents osmolarity, so that closer to angle of outflow of AQH ->
glycerin liquid, intracellular fluid moves further obstruction
isosorbide sol, to extracellular & 8. Prepare for surgery
mannitol sol vascular spaces X. Surgical Management
reducing IOP

 Ophthalmic laser surgery is indicated

Chronic Glaucoma Collaborative as the primary treatment for glaucoma
Management
or is required when medication therapy
Objective: ↓ IOP, keep it at a safe level
is poorly tolerated or ineffective in
1. Miotics lowering IOP.
o constrict pupils; draw smooth muscles  Conventional surgery procedures are
of iris away from canal of Schlemm – performed when laser techniques are
allow AQH to drain unsuccessful or when patient is not a
o Alert: Warn decreased visual acuity good candidate for laser surgery (eg.
especially in daylight Patient cannot sit still or follow
o Ex. Miotic drops: pilocarpine (Ocusert) instructions)
2. Acetazolamide (Diamox)  Filtering procedures: an opening or a
o reduce formation of AQH fistula in the trabecular meshwork
3. Avoid fatigue or stress (trabeculectomy) is made to allow

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drainage implant or shunt surgery may immediate surgical opening of
be performed. the eye chamber.
b. Prepare to administer carbonic
Post Operative Care in Eye Surgery
anhydrase inhibitors IV or IM, to
Goals: To Prevent or Relieve the ff: restrict production of aqueous
humor.
 ↑ IOP
c. Prepare to administer osmotic
 Stress On Suture Line
agents.
 Hemorrhage Into Anterior Chamber
d. Discuss and prepare the client
 Infection
for surgical or laser peripheral
 Pain
iridectomy after the acute
1. Position supine or turn to unaffected site. episode is relieved.
2. Provide information about laser
2. Eye patch 5-7 days. Eye shield at night 4 trabeculoplasty, if medication therapy
weeks. proves ineffective.
3. Report sensation of pressure, sharp pain 3. Teach the client about specific safety
within eye – bleeding precautions.
a. Instruct the client to avoid
4. Miotics – constrict pupils
mydriatics such as atropine,
o Carbachol which may precipitate acute
o Pilocarpine glaucoma in a client with closed-
o Isoflurophate angle glaucoma.
5. Consider: Burning is felt 1 hour after surgery b. Instruct the client to carry
– anesthesia is wearing off prescribed medications at all
6. Consider: Feeling of “something in the eye” times.
4-5 days post op r/t sutures
c. Instruct the client to carry a
medical identification card or
wear a bracelet stating his type
Avoid the ff to prevent ↑ IOP:
of glaucoma and need for

Rubbing the eyes medication.

Lifting head or hips d. Instruct the client to take extra

Sneezing, coughing (follow through precautions at night (e.g. use of
with open mouth if cannot be avoided) handrails, provide extra lighting
 Nausea & vomiting ( keep eyelids open to compensate for impaired pupil
if vomiting occurs) dilation from miotic use).
 Straining at stool
 Bending, stooping Lesson 17: OTITIS MEDIA
 Heavy lifting > 5 lbs
 Reading for few days I. Description
 Watching fast moving objects Otitis Media: Inflammation of the middle ear
Sudden jerky head movement
Types
XI. Nursing management
1. Acute otitis media: Acute otitis media
1. Provide information regarding
(AOM) is an acute infection of the
management of glaucoma
middle ear, lasting less than 6 weeks.
a. Discuss preoperative and
Ear infections can occur at any age;
postoperative teaching for
however, they are most commonly
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seen in children (3 months to 3 years
old). Acute otitis media is the second
most common pediatric diagnosis in the
emergency department following upper
respiratory infections.
2. Serous Otitis Media. Middle ear
effusion, or serous otitis media,
involves the presence of fluid, without
evidence of active infection, in the
middle ear. In theory, this fluid results
from a negative pressure in the middle
ear caused by Eustachian tube
obstruction. When this condition occurs
in adults, an underlying cause for the
eustachian tube dysfunction must be
sought. Middle ear effusion is
frequently seen in patients after
radiation therapy or barotrauma and in
patients with eustachian tube
dysfunction from a concurrent upper
respiratory infection or allergy.
Barotrauma results from sudden
pressure changes in the middle ear
caused by changes in barometric
pressure, as in scuba diving or airplane
descent. A carcinoma (e.g.,
nasopharyngeal cancer) obstructing
the eustachian tube should be ruled out
in adults with persistent unilateral
serous otitis media.
3. Chronic otitis media: repeated
episodes of acute otitis media causing
irreversible tissue damage.Chronic
otitis media is recurrent AOM that
causes irreversible tissue pathology.
Chronic infections of the middle ear
damage the tympanic membrane,
destroy the ossicles, and involve the
mastoid but are rare in developed
countries.
II. Anatomy and Physiology of the Ear
146 | P a g e
Ears are paired organs used for hearing.
These are organs that are externally seen on
each side of the head and the structures
continue internally for the sound signals to be
brought inside for hearing and transfer of
information to the brain. Anatomically, ears are
divided into three, namely the outer, middle,
and inner ear.
Outer Ear
1. Auricle
- A pair of cartilaginous structure that is
visibly found on each side of the head.
All part of the auricle is made up of
cartilage except for the lobule which is
not. Thus, the auricle can be folded.
- It functions to capture, trap, and deliver
sound waves towards the external
acoustic meatus. The cartilaginous part
of the auricle forms an outer curvature,
known as the helix. A second innermost
curvature runs in parallel with the helix
– the antihelix.
- Immediately anterior to the beginning of
the external acoustic meatus is an
elevation of cartilaginous tissue – the
tragus. Opposite the tragus is the
antitragus.
- In the midline portion of the auricle, is a
hollow depression called the concha
that structurally continues internally to
the skull into the external meatus for the
sound to be directed internally.
2. External acoustic meatus
- A sigmoid shape tube, approximately 2-
5cm in length that extends from the
deep part of the concha and continues
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to the tympanic membrane. The outer
1/3 is composed of cartilage and the
inner 2/3 is composed of the temporal
lobe.
- Normally grayish in color and is ciliated.
These layers of cilia help propel sound
waves into the tympanic membrane.
More importantly, it is responsible in the
secretion of earwax.
- Functions as an entryway for sound
waves which gets propelled directly to
the tympanic membrane.
- The external acoustic meatus is not a
straight path. Rather, it travels an S
shaped curve. Thus, the shape,
sigmoid. It travels in a superioanterior
direction and continuously turns slight
superoposteriorly until it finishes its
direction in inferoanteriorly.
3. Tympanic membrane
- A translucent connective tissue
structure, covered with skin on the
outside and a mucous membrane on
the inside found lying at the distal end
of the external acoustic meatus. The
membrane is connected to the
surrounding temporal bone by a
fibrocartilaginous ring.
- This vibrates when sound waves
passes through the external auditory
canal and reaches the ear drum.
- It is responsible for propelling sound to
the inner ear specifically the three
smallest bones.
Middle ear
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The middle ear is an air filled space connected
to the back of the nose by a long, thin tube
called the Eustachian tube. It lies within the
temporal bone, and extends from the tympanic
membrane to the lateral wall of inner ear. The
middle ear is composed of three ossicles
which conduct sound from the tympanic
membrane to the inner ear namely:
1. Malleus (hammer)
o The malleus is shaped like a
club; its handle is embedded in
the tympanic membrane,
running from its center upwards.
2. Incus (anvil)
o Its head is articulated with the
head of the malleus incus which
is cone shaped, with the base of
the cone articulating with the
head of the malleus, also in the
attic.
o Incus runs backwards from the
malleus and has sticking down
from it a very little thin projection
known as its long process which
hangs freely in the middle ear.
3. Stapes (stirrup)
o Attached to the bended right
angle of the incus and is shaped
with an arch and a foot plate.
o Oval window: located at the
footplate of the stapes; when the
footplate vibrates, the cochlear
fluid is set into motion.
o Round window: functions as the
pressure relief port for the fluid
set into motion initially by the
movement of the stapes in the
oval window.
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muscle. Contracture of muscle actively opens
the tube and allows the air pressure in the
middle ear and the nose to equalize.
As air enters, the pressure builds up in
the middle ear, the Eustachian tube will open
when a person swallows. By this opening, the
air pressure inside equalizes.

Eustachian tube
The middle ear is part of a functional system
composed of the nasopharynx and the
Eustachian tube (anteriorly) and the mastoid
air cells (posteriorly). The middle ear is an
extension of the respiratory air spaces of the
nose and the sinuses and is lined with
respiratory membrane, thick near the
Eustachian tube and thin as it passes into the
mastoid. One can think of the middle ear
space shaped rather like a frying pan on its
side with a handle pointing downwards and
forwards (the Eustachian tube) but with a hole
in the back wall leading to a piece of spongy
bone with many air cells, the mastoid air cells.
It opens intermittently to equalize the
intratympanic air pressure with the pressure in
the external auditory canal. At the front end of
the middle ear lies the opening of the
Eustachian tube and at its posterior end is a
passageway to a group of air cells within the
temporal bone known as the mastoid air cells.
It is an air-filled tube that balances the
pressure inside the ears. It also removes
secretion and epithelial debris from the middle Muscles of the Eustachian tube
ear by ciliary motion and gravity. The tube has The only active muscle that opens the
an elongated hourglass shape with a Eustachian tube is the tensor veli palatini,
constricted area known as the isthmus located which promotes ventilation of the middle ear.
near the junction of the osseous and The eustachian tube also functions to protect
pharyngeal zones. It can secret mucus. The the middle ear from excessive sound
Eustachian tube is bony as it leaves the ear pressure, and nasopharyngeal secretions.
but as it nears the back end of the nose, in the The levator veli palatini and tensor veli palatini
nasopharynx, consists of cartilage and muscles insert to some extent on the
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eustachian tube. Both probably are
responsible for competence of the tube in Inner Ear
preventing reflux from the nasopharynx into
the eustachian tube as well as for opening the The inner ear is made up of two parts, the
tube to equalize pressure in the middle ear. cochlea and the vestibular system
The levator veli palatini (levator) muscle is
considered to be the primary muscle
responsible for velar elevation. As its name
implies, it functions to elevate the velum to
create closure between the oral and nasal
cavities (Moon and Kuehn, 2004). Velum or
soft palate acts as the "gatekeeper" to the
nasal cavity.

1. Cochlea: Fluid filled sensory organ that

resembles a snail. Contains the organ of
Corti, the organ for hearing. The organ of
Corti inside the cochlea is lined with hair
cells where neurons that process the
sound waves and convert them to
electrical impulses to be processed to the
brain and transmitted by CN VIII-
vestibulocochlear.
2. Vestibular system: Also known as the
semicircular canals where the vestibule is
located. It is filled with endolymph that is
responsible for maintaining our balance.
The membrane labyrinth contains a fluid
endolymph which plays a role in
excitation of hair cells responsible for
sound and vestibular transmission. Made
up of cells called the utricle and saccule
that can register the position of the head
when it is not moving.
Vestibulocochlear nerve
- Cranial nerve number VIII which
innervates from the Pons at the
brainstem.
- Composed for two nerves:
a. Cochlear nerve: found at the
cochlear and is responsible for
hearing

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b. Vestibular nerve: found at the
semicircular canals which is
responsible for balance.
III. Cause
Viral or bacterial infection. The etiology of
acute otitis media may be viral or bacterial.
Viral infections are often complicated by
secondary bacterial infection. In neonates,
gram-negative enteric bacilli, particularly
Escherichia coli, and Staphylococcus aureus
cause acute otitis media. Viral pathogens such
as respiratory syncytial virus, influenza virus,
parainfluenza virus, rhinovirus, and
adenovirus. Pathogens that cause AOM are
usually bacterial or viral and enter the middle
ear after eustachian tube dysfunction caused
by obstruction related to upper respiratory
infections, inflammation of surrounding
structures (e.g., rhinosinusitis, adenoid
hypertrophy), or allergic reactions (e.g.,
allergic rhinitis) (Grossman & Porth, 2014).
Bacteria can enter the eustachian tube from
contaminated secretions in the nasopharynx
and the middle ear from a tympanic membrane
perforation. A purulent exudate is usually
present in the middle ear, resulting in a
conductive hearing loss.
IV. Predisposing factors/ Incidence
1. Age. Although acute otitis media can
occur at any age, it is most commonly
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seen in children (3 months to 3 years
old)..
2. Genetic predisposition. Mucins
(mucoglycoproteins) which include
abnormalities of this gene expression.
Mucins, such as mucin gene 5AC
(MUC5AC), participate in protecting the
underlying ME epithelium from
pathogen invasion, pathogen damage
and assist with pathogen clearance.
However, over production of these
same mucins can lead to increased
viscosity of ME fluids, limiting
mucociliary clearance in the ME, and
eventual accumulation within the ME
leading to hearing loss. Mucin gene
5AC (MUC5AC) has been identified as
a major secretory mucin in the middle
ear (ME). MUC5AC is fundamentally
important in the development of ME
mucoid effusions, hearing loss and also
provides ME mucosal protection and
bacterial clearance.
The secreted or gel-forming mucins are of
particular interest in middle ear pathogenesis
as they are the primary mucins determining
the viscoelastic properties of fluid overlying
respiratory epithelium like that found in the
middle ear. This is especially important in
chronic disease states such as chronic
bronchitis, asthma and chronic otitis media.
3. Low socioeconomic income. Living in a
low resource or high air-pollution
region. Lack of access to medical care
are all major risk factors for otitis media.
Indigenous children in both remote and
urban settings tend to suffer otitis
media earlier, more frequently and
severely, and with more serious
complications than non-Indigenous
children.
4. Family history. A strong family history of
otitis media. The tendency to get ear
infections can run in the family.
5. Decreased immunity. Due to human
immunodeficiency virus (HIV),
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diabetes, and other immuno-
deficiencies. Deficiencies in secretory
IgA, which is implicated in bacterial and
viral adherence and has been shown to
reduce bacterial colonization of the
nasopharynx.
6. Environmental factors. The same
factors hold for overcrowding in homes
and families with several older siblings.

Pathophysiology

Serous Otitis Media

- otitis media with effusion, secretory
otitis media
cold, sore throat or upper respiratory infection
↓
a collection of non-infected fluid in the middle
ear space

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URTI / EUSTACHIAN TUBE DYFUNCTION/ perforation or therapeutic incision of the
ALLERGIES tympanic membrane. Other symptoms may
↓ include drainage from the ear, fever, and
Edema of tube lining hearing loss.
↓
Obstruction of eustachian tube Conducive Hearing Loss
↓ Feeling fullness within the ear
Impairment of air pressure equalization Otalgia
↓ Otorrhea, (ear discharges) from the ear
Air within middle ear is trapped & gradually that may be foul smelling
absorbed  Bulging or perforation of the eardrum.
↓ Acute Otitis Media Manifestations:
Creating negative pressure in this space
↓ 1. Otorrhea
Prevents more air from entering middle ear - Drainage of liquid from the ear. Present
↓
if tympanic membrane perforates;
Sterile serous fluid moves from capillaries
into the space discharge is profuse.
↓ 3. Otalgia
Forming sterile effusion of middle ear - Ear pain. Relieved if tympanic
membrane ruptures.
Acute Otitis Media 4. Aural tenderness
- Usually absent
URTI
5. Systemic Symptoms
↓
Oronasophayngeal entry of pathogens - Fever, upper respiratory infection and
↓ rhinitis.
Via eustachian tube 6. Tympanic membrane
↓ - Erythema, bulging, may be perforated.
Edema of eustachian tube 7. Hearing loss
↓ - Conductive type.
Impairment of drainage of middle ear
8. Dizziness
↓
9. Tinnitus
Mucus and serous fluid accumulation
10. Mastoid tenderness r/t pus within
↓
mastoid air cells
Good medium for growth of bacteria or virus
11. TM – red, inflamed, or dull & bulging
↓
12. Purulent discharge if TM ruptures
Pus formation – accumulation
↓
Increase middle pressure
Serious Otitis Media Manifestations:
↓
Rupture of tympanic membrane 1. ↓ Hearing in affected ear
2. ‘snapping’ or ‘popping’ sound in the ear
3. Tm bulging, ↓ mobility on examination
V. Clinical manifestations: 4. Fluid or air bubbles visible behind drum
Symptoms of otitis media vary with the severity 5. Rupture of tm
of the infection. The condition, usually 6. Rupture of round window
unilateral in adults, may be accompanied by 7. Pain r/t ↑ pressure
otalgia. The pain is relieved after spontaneous 8. Bleeding in middle ear
9. Sensory hearing loss
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10. Vertigo

Chronic Otitis Media Symptoms may be

minimal:
1. With varying degrees of hearing loss
2. persistent or intermittent, foul-smelling
otorrhea
3. Pain is not usually experienced, except in
cases of acute mastoiditis, when the  The Culture and Sensitivity Ear Swab is
postauricular area is tender and may be
a test that is performed on a sample of
erythematous and edematous.
swab taken from the ear. The test helps
4. Otoscopic examination may show a
in determining and measuring the level
perforation
of Culture of the pathogenic organism
in the ear swab. The test helps to detect
VI. Diagnostic tests:
ear infection and during and after the
Otoscopy
treatment of Ear Infection. Your doctor
may ask you to undergo the test if your
ear infection is not healing or getting
better with treatment, you have an
infection in your outer ear canal, or if
you have an ear infection with drainage
or ruptured eardrum.

Tympanocentesis

 Otoscopic Examination is the

visualization of the external canal and
tympanum. The ear canal is observed
for size, shape, color, amount and type
of cerumen. The tympanum is observed
for color, contour, intactness, and
presence of impacted cerumen. The
external auditory canal is examined for  Rarely, a doctor may use a tiny tube
discharge, inflammation or foreign that pierces the eardrum to drain fluid
body. from the middle ear. A procedure called
Ear Culture Sensitivity Test tympanocentesis. The fluid is tested for
viruses and bacteria. This can be
helpful if an infection hasn't responded
well to previous treatments.
Tympanometry

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 This test measures the movement of
the eardrum. The device, which seals
off the ear canal, adjusts air pressure in
the canal, which causes the eardrum to
move. The device measures how well
the eardrum moves and provides an
indirect measure of pressure within the
middle ear.
Acoustic reflectometry
 This test measures how much sound is
reflected back from the eardrum. An
indirect measure of fluids in the middle
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ear. Normally, the eardrum absorbs
most of the sound. However, the more
pressure there is from fluid in the middle
ear, the more sound the eardrum will
reflect.
VII. Medical /Surgical management
MEDICAL MANAGEMENT
The FDA has approved more than a dozen
antibiotics to treat otitis media.
Antibiotic Therapy.
Antimicrobial agents such as amoxicillin and
azithromycin. These agents remove
pathogenic bacteria from the middle ear fluid.
Amoxicillin at a dosage of 80 to 90 mg per day
should be the first-line antibiotic for most
children with acute otitis media.
Treat patients with mild to moderate infections
for five to seven days, and those with more
severe infections (significant hearing loss,
severe pain, and/or marked tympanic
membrane erythema) with a 10-day course of
antibiotics.
Patients with otitis media who fail to respond
to the initial treatment option within 48 to 72
hours should be reassessed to confirm the
diagnosis.
Antihistamines may help with nasal allergies,
but they may prolong middle ear effusion. Oral
decongestants may be used to relieve nasal
congestion. However, neither antihistamines
nor decongestants improve healing or
minimize complications of acute otitis media,
and they are not routinely recommended.
Corticosteroid use has no benefit in acute otitis
media. (not proven effective)
Most beneficial in children younger than two
years with bilateral acute otitis media and in
children with acute otitis media and otorrhea.
Antibiotics are recommended for all children
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younger than six months, for those six months
to two years of age when the diagnosis is
certain, and for all children older than two
years with severe infection (defined as
moderate to severe otalgia or temperature
greater than 102.2° F [39° C]). Antibiotics may
be deferred in otherwise healthy children six
months to two years of age with mild otitis in
whom the diagnosis is uncertain, and in
children older than two years with mild
symptoms or in whom the diagnosis is
uncertain.
ACUTE OTITIS MEDIA
MEDICAL:
The outcome of AOM depends on the
efficacy of therapy (the prescribed dose
of an oral antibiotic and the duration of
therapy), the virulence of the bacteria,
and the physical status of the patient.
With early and appropriate broad-
spectrum antibiotic therapy, otitis media
may resolve with no serious sequelae.
If drainage occurs, an antibiotic otic
preparation is usually prescribed.
SURGICAL:
 A myringotomy (i.e., tympanotomy) is
an incision in the tympanic membrane.
Under microscopic guidance, an
incision is made through the tympanic
membrane to relieve pressure and to
drain serous or purulent fluid from the
middle ear. Normally, this procedure is
unnecessary for treating AOM, but it
may be performed if pain persists. If
AOM recurs and there is no
contraindication, a ventilating, or
pressure-equalizing, tube may be
inserted.
SEROUS OTITIS MEDIA (MIDDLE EAR
EFFUSION/OTITIS MEDIA W/EFFUSION)
MANAGEMENT:
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Serous otitis media need not be treated
medically unless infection (i.e., AOM)
occurs. If the hearing loss associated
with middle ear effusion is significant, a
myringotomy can be performed, and a
tube may be placed to keep the middle
ear ventilated. Corticosteroids in small
doses may decrease the edema of the
eustachian tube in cases of
barotrauma. Decongestants have not
proved to be effective.
 A Valsalva maneuver, which forcibly
opens the eustachian tube by
increasing nasopharyngeal pressure,
may be cautiously performed; this
maneuver may cause worsening pain
or perforation of the tympanic
membrane. The Valsalva maneuver is
a breathing technique that can be used
to unclog ears. Procedure: close your
mouth, pinch your nose shut and press
the air out like you are blowing up a
balloon.
CHRONIC OTITIS MEDIA
MEDICAL:
Local treatment for chronic otitis media
consists of careful suctioning of the ear
under otoscopic guidance. Instillation of
antibiotic drops, or application of
antibiotic powder is used to treat
purulent discharge. Systemic antibiotic
agents are prescribed only in cases of
acute infection.
SURGICAL:
 Tympanoplasty - The most common
surgical procedure for chronic otitis
media, it is a surgical reconstruction of
the tympanic membrane.
Reconstruction of the ossicles may also
be required. The purposes of a
tympanoplasty are to reestablish
middle ear function, close the
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perforation, prevent recurrent infection,  Monitoring hearing loss. Assess
and improve hearing. hearing ability frequently.
 Ossiculoplasty - is the surgical ACUTE MASTOIDITIS
reconstruction of the middle ear bones - is a bacterial infection of the mastoid air
to restore hearing. Prostheses made of cells surrounding the inner and middle ear.
materials such as Teflon, stainless
steel, and hydroxyapatite are used to
reconnect the ossicles, thereby
reestablishing the sound conduction
mechanism. However, the greater the
damage, the lower the success rate for
restoring normal hearing.
 Mastoidectomy - The objectives of
mastoid surgery are to remove the
cholesteatoma, gain access to
acute otitis media
diseased structures, and create a dry ↓
(noninfected) and healthy ear. If middle ear effusion
possible, the ossicles are reconstructed ↓
during the initial surgical procedure. ... Because the mastoid air cells are
Occasionally, extensive disease or contiguous with the middle ear via the aditus
to the mastoid antrum,
damage dictates that this be performed
↓
as part of a two-stage operation. A fluid will enter the mastoid air cells during
mastoidectomy is usually performed episodes of otitis media with effusion.
through a postauricular incision.
Clinical Manifestations:
VIII. Nursing management
Most infants and children/patients with otitis  Pain
media are cared for at home; therefore, a  Hearing loss
primary responsibility of the nurse is to teach  Tenderness over mastoid process
the family, and/or caregivers about prevention  Red & inflamed
and the care of the child/patient.  Fever
 Headache
 Positioning. Have the child sit up,  Tinnitus
raise head on pillows, or lie on  Drainage from affected ear
unaffected ear.
 Heat application. Apply heating pad or Management:
a warm hot water bottle.
 Diet. Encourage breastfeeding of 1. Antibiotic therapy
infants as breastfeeding affords natural o IV Ticarcillin-clavulanate & gentamicin
immunity to infectious agents; position x 14 days
bole-fed infants upright when feeding. 2. Surgery
 Hygiene. Teach family members to o Mastoidectomy
cover mouths and noses when o Tympanoplasty
sneezing or coughing and to wash
hands frequently.
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↓
Erosion adjacent bones

Rx: Surgery
o Mastoidectomy
o Tympanoplasty

OSTEOCLEROSIS
growth in the bones of the middle ear
interfering
Sound transmission
↓
Progressive conductive hearing loss
↓
Begins in adolescence or early adulthood

CHOLESTEATOMA

o formed from in pouching of upper

segment of TM into middle ear cavity
o cyst lined by squamous epithelium &
filled with layers of epithelial cells

Initially, epithelial cells escape to external ear Risk Factors:

↓
o Genetics
narrowing of pouch,
↓ o Common in Caucasians & female
Manifestations:
Accumulate
↓ o Reddish or pinkish orange TM r/t ↑
remains infected vascularity of ME
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o Bony growth causes footplate of the window is some 20 times higher than on the
stapes to become fixed in oval window eardrum.
↘ conductive hearing loss
o Rinne’s test shows > bone conduction Pressure is ↑ due to the difference in size
than air conduction between the relatively large surface of the
Management: eardrum and the smaller surface of the oval
window.
 Hearing aid
 Na Fluoride to slow bone resorption &
overgrowth The round window in the middle ear vibrates
in opposite phase to vibrations entering the
inner ear through the oval window. In doing
so, it allows fluid in the cochlea to move.
INNER EAR

Oval window - membrane covering the Cochlea

entrance to the cochlea in the inner ear.
When the eardrum vibrates, - sensory organ of hearing
↓ - fluid-filled snail-like structure that
the sound waves travel via the hammer and contains the organ of Corti, the organ
anvil to the stirrup and then on to the oval for hearing
window.
↓ Organ of Corti
When the sound waves are transmitted from
the eardrum to the oval window, the middle organ for hearing consists of tiny hair cells
ear is functioning as an acoustic transformer that line the cochlea
amplifying the sound waves before they move
on into the inner ear. ▼
The pressure of the sound waves on the oval translate vibrations into electrical impulses
158 | P a g e NCM 112: NGIMPEC Lecture Notes
▼
carried to the brain by sensory nerves
 NCM 112: NGIMPEC LECTURE NOTES

Vestibular System
- regulate balance and sense head
position.
Endolymph
- produced continuously by specialized
epithelial cells - stria vascularis in one
wall of the cochlear duct and in several
other locations in the membranous
labyrinth, using an active pumping
mechanism that results in a positive
electrical potential inside the
membranous labyrinth.
Saccule & utricle system, can register the
position of the head when it is not moving

Membranous labyrinth contains a fluid -

endolymph, which plays a vital role in the
excitation of hair cells responsible for sound
and vestibular transmission.

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Lesson 18: MENIERE’S DISEASE
I. DESCRIPTION
Ménière disease is an abnormality in inner
ear fluid balance caused by a malabsorption
in the endolymphatic sac or a blockage in the
endolymphatic duct. Also called as
Endolymphatic Hydrops.
o Endolymphatic hydrops (dilation of the
endolymphatic space) develops, and
either increased pressure in the system
or rupture of the inner ear membrane
occurs, producing symptoms of Ménière
disease (Hansson & Brattmo, 2013).
o Meniere’s disease is a disorder that
affects the inner ear. The inner ear is
responsible for hearing and balance.
o The condition is often associated with
severe attacks of vertigo, the sensation
of spinning. It also leads to hearing
problems and a ringing sound in the ear.
Meniere’s disease usually affects only
one ear and often accompanied with
nausea.
o It is named after Dr. Prosper Ménière,
who first reported the syndrome in a
young girl in 1861.
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IV. Causes
The exact cause of Ménière’s Disease is
unknown. Possible causes include:
 Defective absorption by endolymphatic
sac
 Allergies
 Sodium and water retentio
 Hypothyroidism
 Autoimmune and viral aetiologies
 Mumps
 Syphilis
 Head Trauma
 Previous Infection
 Hormonal (Pregnant females are more
prone)
Predisposing Factors
The following are the risk factors that can
predispose to Ménière disease:
 Smoking
 Alcohol Use
 Fatigue
 Respiratory Infection
 Circulatory Disorder??
 Stress / Emotional Factor
 Toxicity / Use of Certain medications,
including aspirin
 Genetics may also play a role
V. Incidence
o Male are more affected than Women
o Disease is mainly unilateral
o It is more common in age group of 35-60
years old
o About 50,00 – 100,000 people of world
develop Ménière’s disease in a year
o About 50% of the patients who have
Ménière’s disease have a positive
family history of this disease
VI. ANATOMY AND PHYSIOLOGY
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Anatomy & Physiology: The Ear
Internal (inner) Ear
 Oval window: located at the footplate
of the stapes; when the footplate
vibrates, the cochlear fluid is set into
motion
 Round window: functions as the
pressure relief port for the fluid set into
motion initially by the movement of the
stapes in oval window.
Inner ear is made up of 2 parts: sensory
organ for hearing and balance
1. Cochlea: looks like a snail; sensory
organ for hearing fluid filled snail like
structure that contains the organ of
corti, the organ of hearing; lined with
hair cells where neurons that process
the sound and converts it to electric
impulses to be processed to the brain
transmitted by CN 8
2. Vestibular system: filled with
endolymph to maintain balance
The internal ear is a maze of bony chambers
called the bony labyrinth, or osseous
labyrinth, located deep within the temporal
bone behind the eye socket. The three
subdivisions of the bony labyrinth are the
spiraling, pea-sized cochlea, the vestibule,
and the semicircular canals. The vestibule is
situated between the semicircular canals and
the cochlea.
The bony labyrinth is filled with a plasmalike
fluid called perilymph. Suspended in the
perilymph is a membranous labyrinth, a
system of membrane sacs that more or less
follows the shape of the bony labyrinth. The
membranous labyrinth itself contain a thicker
fluid called endolymph.
Endolymph and perilymph are fluid that
circulates; secreted by the cochlear duct and
stored in the endolypmh sac.
Equilibrium
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The equilibrium sense is not easy to describe
because it does not “see”, “hear”, or “feel”.
What it does is respond (frequently without
our awareness) to various head movement.
The equilibrium receptors of the inner ear,
collectively called the vestibular apparatus,
can be divided into two branches- one branch
is responsible for monitoring static
equilibrium, and the other monitors dynamic
equilibrium.
Hearing
Within the cochlear duct, the endolymph-
containing membranous labyrinth of the
cochlea is the spiral organ of corti, which
contain the hearing receptors, or hair cells.
The chambers (scalae) above and below the
cochlea duct contain perilymph. Sound
waves that reach the cochlea through
vibrations of the eardrum, ossicles, and oval
window set the cochlear fluids into motion. As
the sound waves are transmitted by the
ossicles from the eardrum to the oval
window, their force (amplitude) is increased
by the lever activity of the ossicles. In this
way, nearly the total force exerted on the
much larger eardrum reaches the tiny oval
window, which in turn sets the fluids of the
inner ear into motion, and these pressure
waves set up vibrations in the basilar
membrane. The receptor cells, positioned on
the basilar membrane in the spinal organ of
corti, are stimulated by the vibrating
movement of the basilar membrane against
the gel-like tectorial membrane that lies over
them. The “hairs” of the receptor cells are
embedded in the stationary tectorial
membrane such that when the basilar
membrane vibrates against it, the “hairs”
bend.
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The length of the fibers spanning the basilar
membrane “tunes” specific regions to vibrate
at specific frequency. In general, high pitched
sounds disturb the shorter, stiffer fibers of the
basilar membrane and stimulate receptor
cells close to the oval window, whereas low
pitched sounds affect longer, more floppy
fibers and activate specific hair cells further
along the cochlea.

Once stimulated, the hair cells transmit

impulses along the cochlear nerve (a division
of cranial nerve Vlll – vestibulocochlear
nerve) to the auditory cortex in the temporal
lobe, where interpretations of the sound, or
hearing, occurs. Because sound usually
reaches the two ears at different times, we
could say that we hear “in stereo”.
Functionally, this helps us to determine
where sounds are coming from in our
environment.
The cause of Meniere’s disease remains
When the same sounds, or tones, keep unclear or idiopathic, however the
reaching the ears, the auditory receptors pathophysiology is it’s going to be caused by
tend to adapt, or stop responding to those an excessive accumulation of
sounds, and we are no longer aware of them. “endolymphatic fluid” within the vestibular
This is why the drone of a continuously apparatus, so the structure which we called
running motor does not demand our attention the “endolymphatic sac” is responsible for
after first few seconds. However, hearing is manufacturing endolymphatic fluid and it also
the last sense to leave our awareness when has a variety of other functions including
we fall asleep or receive anesthesia and is drainage of the fluid from this area and also
the first to return as we awaken. phagocytosis of foreign invaders or any
debris.
VII. PATHOPHYSIOLOGY
When this endolymphatic sac produces
Impaired filtration & excretion of fluid by
endolymphatic fluid it delivers it to the
endolymphatic sac
vestibular apparatus through the duct which
↓
we called the “endolymphatic duct”. Normally
Excess of endolymph in membraous
the endolymphatic sac is able to produce an
labyrinth
amount of this fluid in accordance with what
↓
the vestibular apparatus needs at the time.
Excessive pressure
However in meniere’s disease we have an
↓
overproduction of endolymphatic fluid. So the
Degeneration of neural organs in the
sac is bulged because it’s making too much
cochlea
of the fluid, and the duct also is bulged
because it’s transporting too much of that
fluid into the vestibular apparatus and then
the result overall you have a distended
“endolymph” and end up with too much fluid

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within the membranous labyrinth walls.
The etiology is not entirely known, but there
are some conditions that can cause these
types of symptoms and if the etiology or the
underlying cause is known we would refer to
this as “Meniere’s Syndrome”, and on the
other side “Meniere’s Disease” is an inner ear
disorder that the underlying cause is not
known. Even though it’s not known the
pathophysiology behind why it occurs is due
to:
Overproduction and defective absorption
of endolymph
- The membranous labyrinth contains a
fluid known as “endolymph”, which plays a
vital role in the excitation of hair cells
responsible for sound and vestibular
transmission. If there is an overproduction
and defective absorption of endolymph it
can cause excessive accumulation of
endolymphatic fluid with increased
hydraulic pressure within the inner ear
structure (cochlea) will occur.
Excessive accumulation of
endolymphatic fluid with increased
hydraulic pressure within the inner ear
structure (cochlea) will occur.
- When there is an excessive accumulation
of endolymphatic fluid in the endolymphatic
sac it increases the hydraulic pressure (fluid
pressure in the ear) which causes the inner
ear to inflamed. On the other side the disease
is more likely to occur in individuals in their
4th to 6th decade of life and most of the
cases is “unilateral” which means it only
affects the one part of the ear. However, it
can also be “bilateral” in approximately 1/3 of
the cases.
− First sign of an acute attack of Meniere’s
Disease is a feeling of fullness in the
affected ear.
− Followed by mixture of signs and
symptoms including vertigo (dizziness
and a perception of like the room is
spinning and it is sudden and
unpredictable and often severe), nausea,
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vomiting, tinnitus (ringing in the ear), and
hearing loss.
Increases the volume and pressure within
the membranous labyrinth that leads to
misfiring of vestibular nerve
- The membranous labyrinth is a group of
ducts and chambers filled with
endolymphatic fluid. So when there is an
increased volume and as well as a pressure
it can lead to distention of the endolymph.
Also there is a misfiring of the vestibular
nerve which is the nerve that communicates
messages about head position and motion
from the inner ear to the brain. When this
nerve is damage, these messages become
jumbled and inaccurate, confusing your brain
and producing the dizziness, nausea and
movement issues which is the main signs
and symptoms of the Meniere’s Disease.
Distention (Endolymph)
- If the endolymph is distended,
endolymphatic hydrops will occur. In
endolymphatic hydrops the membranes
ruptures with mixing of endolymph and
perilymph (inner ear fluid) causing injury to
the hair cells and producing the
characteristics symptoms. This process is
called endolymphatic hydrops meaning there
is too much endolymph or there is an
increased fluid pressure within the
endolymphatic fluid compartment of the inner
ear occurs with disruption to the inner ear.
Increase Pressure
Rupture of the of the wall of the
Membranous Labyrinth and causes
fluid to leak into the Bony Labyrinth.
- Too much endolymph can cause micro
ruptures of the walls of the membraneous
labyrinth and causes that fluid to leak into
the bony labyrinth.
In some cases permanent loss of
auditory and vestibular function
- A severe episode of vertigo caused by
Meniere's disease can last for several
hours or even days. This condition causes
vertigo that can often cause vomiting,
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nausea, and hearing loss, as well as
ringing in the ear.
VIII. CLINICAL MANIFESTATIONS
Meniere’s Disease is described by a triad of
symptoms. At the onset of the disease,
patient usually manifesting only one or two of
the symptoms. The following are the three
major symptoms that usually manifested by
the patient with Meniere’s Disease.
1. Episodic vertigo
Vertigo (attacks can last anywhere from a few
minutes to 24 hours)
It is usually the most disturbing complaint
related to the disease characterized by
feeling of dizziness or spinning sensation of
the environment. This is due to
endolymphatic hydrops or the dilation of the
endolymphatic space. Episodic vertigo occur
without warning may last 20 minutes to 6
hours, but not more than 24 hours. Severe
vertigo can sometimes be incapacitating
accompanied with diaphoresis nausea and
vomiting. This manifestation range in severity
from minor nuisance to extreme disability
especially if the attacks are severe. Patient
may also experienced persistent feeling of
imbalance or disequilibrium which make
client wake at night. However, patient will feel
well between attacks.
2. Tinnitus
Described as ringing in the ears where
unwanted noises such as buzzing, roaring,
whistling or hissing sound may be heard in
the head and ear. Patient may also
experience aural pressure where feeling of
pressure or fullness in the affected ear
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occurs.
3. Fluctuating Sensorineural Hearing
Loss
This type of hearing loss is due to the
damage of the inner ear where soft
sounds may be hard to heard and
louder sounds may be unclear or
muffled. Hearing loss is usually occur in
one ear (unilateral) and may fluctuate,
accompanied by tinnitus and aural
pressure waxing and waning with changes
in hearing. This feeling may happen during
or before attacks and might be constant.
This condition must be intervened to
prevent permanent hearing loss.
Others:
1. A feeling of fullness in the affected ear.
2. Loss of balance
3. Headaches
4. Nausea, vomiting, and sweating caused
by severe vertigo
Additional Notes:
• Cochlear Meniere’s Disease:
characterized by fluctuating, progressive
sensorineural hearing loss accompanied
by tinnitus and aural pressure in the
absence of vestibular symptoms and
findings.
• Vestibular Meniere’s Disease: described
as the occurrence of episodic vertigo
accompanied
- by aural pressure but no cochlear
symptoms and findings.
• Client may encounter either cochlear or
vestibular disease symptoms, but
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eventually all of these symptoms develop.
IX. DIAGNOSTIC TESTS
A person who experienced symptoms of
Meniere’s Disease will undergo different
diagnostic test and examination to examine
both hearing and balance. Some test is
performed to rule out other causes of the
symptoms. The following are the different
diagnostic test to help identify and confirm
the disease.
Physical Examination: the examiner will
ask questions about the attacks, its severity
and frequency. Physical examination
includes checking of ears, eyes and nervous
system. Findings are usually normal except
of those of Cranial Nerve VIII. By performing
the Weber’s Test, sound from a tuning fork
may lateralize to the ear opposite the hearing
loss, the one affected by the disease.
Audiometry: assess how well the patient
determine sounds at different pitches and
volumes and how well the client distinguish
between similar-sounding words. Usually,
patient with Meniere’s Disease have
problems hearing low frequencies with
normal hearing in mid range frequency. The
audiogram shows a sensorineural hearing
loss in the affected ear. This can be in a form
of a “Pike’s Peak” pattern, that illustrates a hill
or mountain like.a sensorineural loss in the
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low frequencies occurs as the condition
progresses.
Electronystagmogram: evaluates
balance function by assessing eye
movement.An electrode are placed above
and below the eye of the patient and it will
record electrical activities of the muscles
that facilitate eye movement. . Balanced
related sensors in the inner ear are
connected to muscles that control the
movement of the eye. This relation allows
patient to moves he’d wile keeping eye
focused on one point. Result may be
normal or may show reduced vestibular
response.
Other test may include:
Rotary Chair Testing: Client is sited in a
turning chair that is controlled by a computer
that will stimulate the inner ear. This will allow
the doctor to assess how eye movement
affects the inner ear.
Vestibular Evoked Myogenic Potential
(VEMP): It will measure the patient reaction
to sudden, loud noise. It is not only used fo
diagnosing Meniere’s Disease bur also used
to monitor the disease.
Posturography: This will test patient’s
balance and how well he/she will keep it. The
client will stand on a platform that can move
in several directions. He/she will ear a
harness that allow the physician to determine
how they respond as the platform moves in
different directions.
Video Head Impulse Test (VHIT): This test
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uses video images to see how well the
patient’s eye can focus and respond to
sudden movement. While patient focus on a
point, the head is turned quickly and
unpredictably. If the eye move off the target
when the hear is moved or turned, result will
show abnormal reflex.
Electrocochleography: It assess the inner
ear in response to sounds. It might help to
identify if there is an abnormal buildup of fluid
inn the inner ear, but isn’t specific to
Meniere’s Disease.
Auditory Brainstem Response Test:
Patient is wearing a headphones and a
computer measure the brain waves as it
respond to different sounds. It’s typically only
used for people who cant have types of
hearing test like the babies or who can’t have
imaging test.
Blood Test, MRI, & CT Scan might be
requested to rule out disorders such as tumor
in the brain or multiple sclerosis that can
cause similar clinical manifestation.
X – rays & CT scans of petrous bones
o to evaluate internal auditory canal
o In Meniere’s disease vestibular
aqueduct is shorter & straighter than
normal
Glycerol test
o Administration of oral glycerol to
decrease fluid pressure in inner ear
Rinne’s Test
Normal:
o AC > BC
o tone is louder in front of ear
Conductive hearing loss:
o BC > AR
o Tone is louder behind ear
Sensorineural hearing loss:
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o same as normal
o More accurate in diagnosing
conductive hearing loss like in
otosclerosis
Weber’s Test
Normal: sound heard equally in both sides
Abnormal:
o In an affected patient,
if the defective ear hears the Weber
tuning fork louder - conductive hearing
loss in the defective ear.
o In an affected patient,
if the normal ear hears the tuning fork
sound better - sensorineural hearing
loss on the other (defective) ear.
X. Medical Management
Medication: meclizine (Antivert)
Drug Class: Antihistamine
Indications: Used to treat nausea, vomiting,
and dizziness associated with motion
sickness, and management of vertigo
Side Effects: blurred vision, dry mouth,
constipation, dizziness, drowsiness,
headache, vomiting, or tiredness.
Nursing Considerations:
 Monitor for any improvements in
symptoms such as, nausea,
vomiting, dizziness, vertigo in order
to help document the effects of this
drug.
 Instruct patient about the risk of
daytime drowsiness and decreased
attention and mental focus. These
problems can be severe in certain
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people
 Instruct patient to avoid alcohol and
other CNS depressants because of
the increased risk of sedation and
adverse effects
 Instruct patient to report other
troublesome side effects including
severe or prolonged fatigue, dry
mouth, or blurred vision
 Provide protection to patient against
falls and trauma such as, hip
fractures, head injury, and so forth
 Provide fall prevention strategies,
especially in older adults or if
balance is impaired
Medication: dyazide (Triamterene)
Drug Class: Diuretics
Indications: To relieve the inner ear fluid
build-up thereby reducing vertigo frequency
and avoiding hearing loss progression
Side Effects: blood pressure that’s lower
than normal, dizziness, headache,
weakness, tingling in hands, legs, and feet,
photosensitivity, muscle spasms, diarrhea
Nursing Considerations:
1. Monitor signs of fluid, electrolyte, or acid-
base imbalances, including dizziness,
drowsiness, blurred vision, confusion,
hypotension, or muscle cramps and
weakness.
2. Monitor signs of hyperglycemia
(drowsiness, fruity breath, increased
urination, unusual thirst). Patients with
diabetes mellitus should check blood
glucose levels frequently.
3. Assess the patient’s potassium needs
4. Assess blood pressure periodically and
compare to normal values
5. Educate patient on the disease process
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and medication regiment\
6. Instruct the patient to report concerns and
side effects
Medication: Intratympanic steroid
Drug Class: Steroids
Indications: Reduces the frequency and
severity of vertigo attacks.
Side Effects: transient dizziness, injection
pain, a burning sensation, increasing tinnitus,
tongue numbness, and a small perforation of
the eardrum
Nursing Considerations:
1. After the procedure instruct patients to lie
down flat on their back on the examining
table with head turned
2. Instruct patient to remain in position for 15
to 30 minutes
3. Place a cotton ball in the treated ear
4. Instruct patient that the ear should be kept
dry for 24 hours (no swimming or direct
shower spray to the head or ear)
5. Instruct patient to report for mild
discomfort, gurgling, popping, and
moisture in the ear canal following the
injection are common, temporary
sensations
Medication: diazepam (Valium)
Drug Class: Benzodiazepines
Indications: Help to reduce the spinning
sensation and help control nausea and
vomiting
Side Effects: drowsiness, tired feeling,
dizziness, spinning sensation, fatigue
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Nursing Considerations:
1. Monitor and assess for side effects
2. Instruct patient of avoiding intake of
alcohol beverages or other CNS depressants
3. Instruct patient, avoid sudden position
changes to prevent orthostatic hypertension
or fainting
4. Instruct patient to report for signs of severe
dizziness, weakness, drowsiness that
persists, rash or skin lesions, palpitations,
swelling of the ankles, visual or hearing
disturbances, difficulty voiding.
5. Instruct patient to take with food or milk to
avoid GI irritation
Medication: amikacin (Amikin)
Drug Class: Aminoglycosides
Indications: Used for short-term treatment
of serious infections especially in extreme
Meniere’s syndrome
Side Effects: Agitation Black, tarry stools,
Bloody or cloudy urine, Bluish lips or skin,
Blurred vision, Burning, Crawling, Itching,
Numbness, Confusion, Cough, Drowsiness,
Dry mouth
Nursing Considerations:
1. Monitor serum creatinine or creatinine
clearance (generally preferred) more
often, in the presence of impaired renal
function
2. Monitor S&S of ototoxicity (primarily
involves the cochlear and auditory)
branch
3. Monitor for auditory symptoms (tinnitus,
roaring noises, sensation of fullness in
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ears, hearing loss) and vestibular
disturbances (dizziness or vertigo,
nystagmus, ataxia).
4. Monitor for any changes in I&O, oliguria,
hematuria, or cloudy urine. Keeping
patient well hydrated reduces risk of
nephrotoxicity; consult physician
regarding optimum fluid intake
5. Instruct the patient to report immediately
any changes in hearing or unexplained
ringing/ roaring noises or dizziness, and
problems with balance or coordination.
XI. SURGICAL MANAGEMENT
Destructive Surgical Procedure
- Destructive surgeries for Meniere’s
disease. These labyrinthine surgeries
cure the patient of vertigo by
destroying the final vestibular organ.
The brain compensates for the loss of
vestibular function on one side using
the contralateral labyrinth, as long as it
is functioning properly.
- Destructive surgeries (e.g.,
labyrinthectomy, vestibular nerve
sectioning) have success rates of
about 95-98%. However, destructive
surgeries have a greater risk of
hearing impairment.
Non-Destructive Surgical Procedure
 Endolymphatic sac decompression
or shunt
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- The endolymphatic sac procedure
decreases endolymph pressure
accumulation by removing the petrous bone,
which encases the endolymph reservoir. This
procedure allows the reservoir sac to expand
more freely, thus reducing the pressure. A
drain or valve from the endolymphatic space
to either the mastoid or subarachnoid space
can be inserted as another means of further
reducing pressure. Success rates (in terms
of controlling vertigo and stabilizing hearing
acuity) with this procedure are reported at 60-
80%.
 Vestibular nerve section
- For patients with useful hearing in the
affected ear, sectioning the diseased
vestibular nerve can be the ultimate
solution.
- This anatomical separation allows
balance function to be isolated and
ablated without affecting hearing
function.
- Although the hearing and balance
functions are housed in one common
chamber within the inner ear, their
neural connections to the brain
separate into distinct nerve bundles as
they course through the internal
auditory canal.
 Labyrinthectomy
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- This management option for Meniere’s
disease has the advantage of a high cure
rate (>95%) and is useful in the patient
whose hearing on the diseased side has
been destroyed already by Meniere’s
disease.
- Labyrinthectomy involves ablation of the
diseased inner ear organs.
- This procedure is less complex than
vestibular nerve section because
labyrinthectomy does not require entry into
the cranial cavity.
- Labyrinthectomy is less invasive than
vestibular nerve section.
 Chemical labyrinthectomy
- A chemical labyrinthectomy is also known
as trans tympanic or intratympanic treatment
or gentamicin infusion.
- This is a destructive procedure used for
Meniere’s disease. An antibiotic called
gentamicin is introduced into the middle ear
and absorbed via the round window.
- The drug destroys the vestibular hair cells
so that they cannot send signals to the brain.
XII. Nursing Management
1. Provide patient a nursing care during
acute attack.
2. Provide patient a safe, quiet, dimly lit
environment and enforce bed rest
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3. Provide patient emotional support and
reassurance to alleviate anxiety
4. Instruct the patient on self-care
instructions
5. Explain to the patient about the
importance of avoiding stimulants and
vasoconstrictions
6. Educate the patient about the nature
of the disorder
7. Educate patient about the need for a
low-salt diet
8. Educate the patient about the
medications that may be prescribed to
prevent attacks or self-
9. Educate the patient about the client
with surgical options.
10. Administer a prescribed medication.
Lesson 19: CATARACT
- Opacification of the lens
- lens is transparent which is responsible
for the focusing of the light as it passes
through the transparent lens.
- Lens has proteins, transparent and
clear.
- A cataract is an opacity of the normally
clear lens which may develop as a
result of aging, metabolic disorders,
trauma or heredity.
- The lens has become milky white. With
the opacity, light cannot pass through it.
Aging: First predisposing factor. As we age,
blood vessels are hardened, decrease
elasticity decreasing the blood supply in the
eyes.
Metabolic disorders: DM, in here, the blood is
viscous plus the 50% accelerated
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atherosclerosis in DM that narrows the lumen
of the blood vessels decreasing blood supply
to the eyes.
Trauma or hereditary (of familial tendency)
Causes and Risk Factors “CATARACT”
C ongenital
A geing
T oxicity steroids, etc.
A ccidents
R adiation/Sunlight
A ltered metabolism | DM
CT igarette smoking
1. Congenital- hereditary
2. Aging- related to decrease blood supply
and narrowing of the lumen of blood
vessels later in life. Arteriosclerosis in lens
of eye, hardening. Number 1 predisposing
factor. As people age, their tendency to
develop cataracts increases.
3. Toxicity steroids
4. Accidents
5. Radiation/Sunlight- Lens damages by UV
rays due to excessive exposure to the
sunlight. Common among fishermen
because they are exposed to sun directly
at noon time when they go fishing.
6. Altered metabolism | DM- increase
viscosity of blood plus 50% atherosclerosis
will cause a decrease in blood supply to the
eyes.
7. Cigarette smoking- predispose to
hypertension and decrease circulation to
all parts of the body.
Others:
8. Alcohol excessive intake- predisposes to
atherosclerosis which causes decrease O2
delivery to the eyes. Eyes have small blood
vessel, and if they are narrowed, oxygen
delivery to the eyes will be decreased.
9. Hypertension- decrease circulation due to
increasing pressure within the blood
vessels.
10. Overweight- fat deposits inside the
arteries, narrowing them causing a
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decrease O2 delivery to the body
especially to the eyes.
Anatomy and Physiology of the Lens
Lens: transparent, biconvex structure helps to
refract light to be focused on the retina. Made
up of proteins that denatures (hardens) when
aging.
- The clear lens transmits light rays and
focuses them on the retina (this what
happened normally). But with aging,
since the lens are made up of proteins,
this will harden as the person is aging.
171 | P a g e
We called it “denature” denaturing of
the proteins in the lens, increasing the
density of the lens. With this, the lens
become opaque and yellowish-brown
coloration of the lens.
- Other factors also included such as
Blunt-force (accidents) /trauma that can
also result to the thickening and
irreversible whitening of lens. Resulting
to the cloudy lens blocks ability to
transmit and focus light rays on retina.
This result would be, blurry vision or
loss of vision
- The normal lens allows light to pass into
the eye. Images are clear
- If you have an opaque or clouded lens,
this will allow less light to pass into the
eye. Images are blurry
CLINICAL MANIFESTATION
 Clouded, blurred or dim vision
 Increasing difficulty with vision at night
 Sensitivity to light and glare
 Seeing halos around lights
 Need for brighter light for reading and
other activities
 Fading or yellowing of colors
 Frequent changes in eyeglass or
contact lens prescription
ASSESSMENT/ DIAGNOSTIC FINDINGS
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 Use of Snellen’s visual acuity test – interferes with mobility, ability to carry
(patient may have a decreased visual out normal activities
acuity)
 Ophthalmoscopy – where in the body of *Types of CATARACT EXTRACTION
the eye was examined by using an
ophthalmoscope 1. Intra Capsular Extraction (ICCE) –
 Slit-lamp Biomicroscopic examination – removal of the cataract within its
allow the examination in the inside of capsule
the eye to detect presence of cataract
or other problems of the eye like
glaucoma or refractive errors

MANAGEMENT
 Primary Prevention – intake of dietary
antioxidants prevents cataract 2. Extracapsular cataract extraction –
formation by blocking the oxidative opening is made in the capsule, lens is
modification of the lens such as the lifter without disturbing the membrane
Vitamins A, C, and E
 Vitamins A, C, and E – people who had
a regular daily doses of the antioxidants
Vitamin C and E were 32% less likely to
have developed cataracts

HOW CATARACTS TREATED?

 For early Cataracts
o Vision may improve by: 3. Phacoemulsion – in which a probe is to
 Using different eyeglasses be inserted to break up the lens and
 Magnifying lenses – to magnify flushes it out in tiny pieces
the letters or words
 Stronger lightning
o If these measures do not improve
quality of life, surgery is the only
option
 Involves the removal of the
cloudy lens and replacing it
with a substitute lens
 A cataract needs to be removed only
when vison loss interferes with
everyday activities such as driving, *IRIDOTOMY
reading, or watching TV
 Surgery is the only option to remove the
cataract

Note:
 Surgery is the only satisfactory
treatment for cataracts when it
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- Before a cataract extraction is to be
performed, usually the doctor will
perform iridectomy
- Iridectomy – is done preceding cataract
extraction to create an opening for the
flow of aqueous humor which may be
blocked after the operation – when the
vitreous humor moves forward to
prevent 2nd glaucoma (in here, we are
preventing the secondary glaucoma to
happen).
- The aqueous humor is a fluid which
should be continuously flowing form the
posterior part of the brain. This is
produced by the ciliary body. The
aqueous humor is produced there, then
it will flow through the iris, then to the
anterior portion of the eye, then it will
pass by the two canals, through the
trabecular meshwork then to the canal
of Schlemm, then into the venous
circulation. It must be continuously
flowing
- The aqueous humor is necessary for
refraction and also providing nutrition
for the eye.
- Before the cataract extraction to
perform, they would open this to create
this for a bigger opening for the out flow
of the aqueous humor. Because
possibly, the cataract extraction can
cause blocking of the aqueous humor
and eventually, may cause increase
intraocular pressure
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- If the IOP already increased, this called
the secondary glaucoma
*CRYOEXTRACTION
- CRYOEXTRACTION - Cataract is lifted
from the eye by a small probe that has
been cooled to a temp below zero and
adheres to the wet surface of the
cataract
*PREOPERATIVE CARE
- Before: the patient was admitted and
had to stay for a few days in the
hospital. They will be maintained in the
bed rest and needs to limit the mobility
of the head. But this is not applicable
today because cataract now is an
outpatient. They can just go home after
the operation
- Now:
- Before the operation the patient
should have a full bath - because after
the surgery, the patient cannot take a
full bath because the patient is not able
to bend anymore, otherwise, it may
cause IOP increase
- Orient to staff and environment
o Give mydriatics/ cyclopegics (1
drop to the affected eye) as
prescribed. Examples: Isopto
atropine, ocu-tropine, atropisol
(Atropine SO4), atropisol (atropine
SO4), Cytogyl (cyclopentolate
HCL), Scopolamine, mydriacyl,
cyclomydril (cyclopentolate and
phenylephrine)
o MOA of mydriatics . cyclopegies –
they dilate pupils (mydriasis) and
to relax ciliary muscles
(cyclopedia)
o This ciliary muscles needs to be
relaxed before he operation so
that it will not produce aqueous
humor
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o After given the drops or
medication, the patient will
proceed to the operating room
o However, this is not indicated for
the patient with GLAUCOMA –
since there is an increased IOP,
and if the flow of the aqueous
humor slows down, the IOP may
increase.
*POST OP-CARE
 Cover the eye with eye pad and eye
shield to protect the eye.
 (before)The patient can be Out of bed
day after surgery (now: after surgery,
the patient was advised to go home to
rest, and we should not wait for a day
before the patient can get out of bed)
 The patient needs to go back to the
hospital for dressing. Dressing OD
o Dressing should be done daily, but
a few hours after the operation, the
doctor will open it and will change
the dressing and give instruction to
the patient and family
o This dressing should be removed
7-10 days after surgery. This
should be the ophthalmologist who
will remove the dressing
 Eye shield should be worn at night for
1st month – to protect the eye from
injury while asleep
 Eye drops as ordered
 Temporary glasses may be prescribed
1-4 weeks after. Within 6-12 weeks
healing (the surgery is already healed)–
fitting od permanent glasses (the
patient is recommended to come back
to the clinic for the fitting of permanent
glasses
 Instruct the patient to do the ff:
o there should be no lifting above the
waist
o After the surgery, do not use the
eyes yet
o Prevent / limit the sneezing or
coughing. If the patient need to
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sneeze or cough, instruct the
patient to open the eyes and the
mouth so that there is no increase
pressure in the eyes
o No positioning on the operative
side because this may cause
tension over the operative side that
may lead to increase IOP
REMEMBER:
 Cataract glasses (aphakic) magnify so
that everything appears about ¼ closer
than it is.
o We have to inform the patient that
this type of glasses, especially for
the first few times that they are
wearing it, tell them that the things
may appear very near
o Due to this the client has a potential
for injury
 Instruct the client that it will take time to
learn to: Judge distances, climb stairs,
do simple things
 Intraocular lens implant
o After the removal of the cataract,
they are immediately implant he
new lens
 Lens (Polyethyl Methacrylate) is
implanted at the time of cataract
extraction
 Advantage: better binocular vision
NCM 112: NGIMPEC Lecture Notes