CCN NERVOUS SYSTEM

CENTRAL NERVOUS SYSTEM (CNS)

• Skull: Frontal, Parietal, Temporal, Occipital bones
• Meninges: Dura Mater, Arachnoid layer, Pia Mater
• Cerebrospinal Fluid (CSF): clear, colorless fluid, fluid shock absorber
• Cerebral Vasculature: receives 20% of the cardiac output approx. 750ml/min
• Brain: cerebrum, pons, medulla and cerebellum
• Spinal Cord: 33 vertebrae (7 Cervical, 12 Thoracic, 5 Lumbar, 5 Sacral fused into one, 4
Coccygeal fused into one)

PERIPHERAL NERVOUS SYSTEM

• SPINAL NERVES
• 31 Pairs
• 8 Cervical
• 12 Thoracic
• 5 Lumbar
• 5 Sacral
• 1 Coccygeal
 PERIPHERAL NERVES
CRANIAL NERVE TRACT FUNCTION LOCATION OF ORIGIN
I. OLFACTORY SENSORY • SENSE OF SMELL DIENCEPHALON
II. OPTIC SENSORY • VISION DIENCEPHALON
III. OCULOMOTOR PARASYMPATHETIC • PUPILLARY CONSTRICTION MIDBRAIN
• ELEVATION OF UPPER EYELID AND
MOTOR 4 OF 6 EXTRAOCULAR
• MOVEMENTS
IV. TROCHLEAR MOTOR • DOWNWARD, INWARD MOVEMENT MIDBRAIN
OF THE EYE
• (SUPERIOR OBLIQUE)
V. TRIGEMINAL MOTOR • MUSCLES OF MASTICATION AND PONS
OPENING JAW
SENSORY • TACTILE SENSATION TO CORNEA,
NASAL, ORAL MUCOSA AND
• FACIAL SKIN
VI. ABDUCENS MOTOR LATERAL DEVIATION OF EYE PONS
VII. FACIAL Vestibular branch: Equilibrium • SECRETORY FOR SALIVATIONS AND PONS
TEARS
Cochlear: Hearing • MOVEMENT FACIAL EXPRESSIONS,
CLOSE EYE
• SENSATION OF EXT EAR, AUDITORY
CANAL, TYMPHANIC
• MEMBRANE
• TASTE SENSATION ANTERIOR 2/3
OF TONGUE
VIII. VESTIBULOCOCHLEAR SENSORY • Vestibular branch: Equilibrium PONS
(ACOUSTIC/COCHLEAR) • Cochlear: Hearing
IX. GLOSSOPHARYNGEAL PARASYMPATHETIC • SALIVATION MEDULLA
• VOLUNTARY MUSCLES FOR
MOTOR SWALLOWING AND PHONATION
• SENSATION TO PHARYNX, SOFT
SENSORY PALATE, AND POSTERIOR 1/3 OF
TONGUE
• STIMULATION ELICITS GAG REFLEX
X. VAGUS PARASYMPATHETIC • AUTONOMIC ACTIVITY OF VISCERA MEDULLA
OF THORAX AND
MOTOR • ABDOMEN
• INVOLUNTARY ACTIVITY OF
SENSORY VISCERAL MUSCLES OF
• HEART, LUNGS AND DIGESTIVE
TRACT
• INNERVATION OF STRIATED
MUSCLES OF SOFT
• PALATE, PHARYNX, LARYNX FOR
VOLUNTARY
• SWALLOWING
• SENSATION TO THE AUDITORY
CANAL, PHARYNX,
• LARYNX, AND VISCERA OF THORAX
AND ABDOMEN
XI. SPINAL MOTOR • STERNOCLEIDOMASTOID AND MEDULLA
TRAPEZIUS MUSCLE
• MOVEMENTS
XII. HYPOGLOSSAL MOTOR • TONGUE MOVEMENTS MEDULLA
PAIN
NOCICEPTORS
o pain receptors that are stimulated and send impulses back to the spinal cord then to the
brain as a result of damaged tissue
o stimulation of nociceptors is caused by the release of substances from damaged tissue
and activation of inflammatory response
o damaged cells release potassium and hydrogen ion, both of which can stimulate
nociceptors
o Inflammatory cells: macrophages, neutrophils, other WBCs
o Platelets participating in clot formation release serotonin, also
o stimulates nociceptors

REFERRED PAIN
o pain perceived as arising from a site that is different from its true point of origin
o the “true point of origin” is from visceral organ or deep somatic structure
o the “point of reference” is some area of the body surface
o the most generally accepted theory for referred pain is that the 2 sensory neurons, one
from the region of the true point of origin and one from the point of reference, enter
the same segment of the spinal cord and synapse with the same projection neuron
o Referring pain from SEVERE CARDIAC ISCHEMIA to the left arm or the
o referring of DIAPHRAGMATIC PAIN to the neck and shoulder

PATIENT ASSESSMENT
MENTAL STATUS
o Alert (full consciousness): normal
o Awake: fully oriented when aroused
o Lethargic: drowsy but follows simple commands when stimulated
o Obtunded (somnolent): arousable with stimulation; responds verbally with a word or
two; follows simple commands; otherwise, drowsy
o Stuporous: very hard to arouse; inconsistently may follow simple commands or speak
single words or short phrases; limited spontaneous movement
o Semi-comatose: movements are purposeful when stimulated; does not follow
commands or speak coherently
o Comatose: may respond with reflexive posturing when stimulated or may have no
response to any stimulus

Neuro Assessment:
1. Mental Status
o Assess orientation and memory
o Orientation involves people, time and lace
o Memory includes: short term, recent and remote memory
 2. Level of Consciousness:
o is the single most sensitive indicator of changes in the neurologic status
- Level I: Conscious, coherent, cognitive
- Level II: Confused, drowsy, lethargic, somnolent, obtunded
- Level III: Stuporous (e.g. sternal pressure, trapezius pinch, pressure at the base
- of the nail, or supraorbital area; very strong or loud sound)
- Level IV:
- Light Coma: grimace or withdrawing limp from pain
- Deep Coma: absence of response to even the most painful stimuli

GCS: Objective mesure to describe LOC; EMV

AVPU: Alert, Verbal, Pain, Unconscious

MOTOR FUNCTION
Motor responses to Pain

PUPILLARY CHANGES
PERRLA, Pupils Equal, Round, Reactive to Light and Accommodation
o in millimeter (mm)
o pupils size and shape
o Anisocoria
Pinpoint pupils: Drugs (opiates), Drops (meds for glaucoma), “Nearly dead” (damage in the
pons area of the brain stem)
Dilated Pupils: Fear (panic attack, extreme anxiety), “Fits” (seizure), “Fast
Living” (cocaine, crack, phencyclidine)
Finger to Nose Test
- is performed by having the patient touch one finger to the examiner’s finger, then
touch his or her own nose; assess coordination
- overshooting or past-pointing the mark is called DYSMETRIA.
- Both sides are tested individually
- FTNT (Foot to Nose Test), HKT (Head to Knee to Toe test), Heel to Shin Test

Pronator Drift
- have the patient hold the arms straight out with palms upward and eyes closed and
observe for any untoward drift or pronation of the forearms

Oculocephalic Reflex
- indicates an intact brainstem
- this maneuver must not be performed in a person with possible cervical spine injury

Romberg Test
- to assess cerebellar function (receives information from the sensory systems, the
spinal cord, and other parts of the brain and then regulates motor movements)
- done by asking the client to stand with the feet together & the eyes closed or
asked to walk in an imaginary line
- if the client falls or experiences uncoordinated movement (ataxia), this is positive
Romberg that indicates cerebellar function impairment

Apraxia - inability to perform fine (learned) motor activities like whistle, singing, smacking
Agraphia is inability to write
Ataxia - uncoordinated movement, characterized by wide – base stance and swaying manner
of walking

Cortical Sensory Function

Graphesthesia is tested by having the patient identify numbers traced on the palm of the
hands while the eyes are closed
Stereognosis is ability to perceive the form and nature of objects
Agnosia is the inability to perceive sensory stimuli

Language and Speech:

Global Aphasia – inability to use and understand language. Impairment of both Broca’s and
Wernicke’s areas
Broca’s aphasia (left frontal lobe) - impairment to expressive or motor aphasia. Inability to
speak and make gestures
Wernicke’s aphasia (temporal lobes) – receptive or auditory aphasia, which is inability to
understand sounds or language
REFLEXES:
Deep Tendon Reflex – 1 to 5 scale (2+ is Normal)
- hypoactive; normal; brisk but not pathological; hyperactive, pathological
Plantar Reflex – Babinski’s sign is abnormal; lesion in pyramidal tract
- but normal in children under the age of 2
Hyperreflexia is associated with upper motor neuron disease
Areflexia or absence of reflexes is associated with lower motor neuron dysfunction
Clonus – an abnormal response, is a continued rhythmic contraction of the muscle

SENSATION
Proprioception is tested by asking the patient, with eyes closed to identify
the direction of the movement of finger in both extremities
Agnosia is the inability to recognize objects by touch, sight, or sound
Stereognosis is the ability to recognize and identify objects by touch
- is a function of the parietal lobe
Graphesthesia is the ability to recognize numbers or letters traced lightly on
the skin
VITAL SIGNS
Respirations:
Cheyne-Stokes respirations
- (Crescendo-decrescendo respirations alternating with periods of apnea)
Hypoventilation
- can lead to respiratory acidosis
Hyperventilation
- after cerebral trauma produces respiratory alkalosis with decreased blood CO2
levels
Shallow, rapid respirations
- can indicate a problem with maintenance of a patent airway or the need for
suctioning
Snoring respirations or stridor
- can indicate a partially obstructed airway

VITAL SIGNS
Temperature (hypothalamus)

HYPOTHERMIA
- occurs with metabolic causes, pituitary damage and spinal cord injuries
CNS
- fevers may be very high and differentiate themselves from other causes of fever by
their resistance to antipyretic therapy
Pulse –
- Tachycardia in increased ICP, alterations in ECG pattern such as atrial or ventricular
dysrhythmias
-
Blood Pressure (medulla)
Hypertension is common due to increase in ICP
Hypotension must be avoided in the post-injury stage because it can lead to decreased
cerebral perfusion, hypoxia and extension of the initial injury

Signs of Trauma and Infection

Battle’s sign (bruising over the mastoid areas) suggests a basilar skull fracture
Raccoon’s eye (periorbital edema and bruising) suggests a frontobasilar fracture
Rhinorrhea (drainage of CSF from the nose) suggest fracture of the cribriform plate with
herniation of a fragment of the dura and arachnoid through the fracture
Otorrhea (drainage of CSF from the ear) usually is associated with fracture of the petrous
portion of the temporal bone
Signs of Meningeal Irritation:
NUCHAL RIGIDITY (pain and resistance to neck flexion)
- fever, headache and photophobia
KERNIG’S SIGN
- pain in the neck when the thigh is flexed on the abdomen and the leg is extended at
the knee; meningitis inflammation
BRUDZINSKI’S SIGN
- involuntary flexion of the hips when the neck is flexed toward the chest; meningitis
inflammation

Signs of Increased Intracranial Pressure (ICP):

1. Decreased level of consciousness (LOC)
- restlessness, confusion and combativeness
- from lethargy, obtundation to coma
2. Pupillary reactions begin to diminish, with sluggishly reactive pupils and eventually
fixed, dilated pupils
- Frequently, because of the potential for injury to be ipsilateral, one pupil dilates
before the other one does, resulting in unequal pupils
3. Abnormal motor activity – from localized to painful stimuli to either abnormal flexion
or extension
4. Changes in vital signs

CUSHING’S TRIAD
1. increased systolic pressure (resulting in an increased pulse pressure)
2. bradycardia
3. irregular respirations
4. pupillary changes - a sign of impending herniation

NEURODIAGNOSTIC STUDIES
Computed Tomography or CT scan (Invasive and Noninvasive)
- a scanner takes a series of radiographic images all around the same axial plane. A
computer hen creates a composite picture of various tissue densities visualized. The
images may be enhanced with the use of IV contrast dye
- Instruct the patient to lie flat on a table with the machine surrounding
❖ Patient must remain immobile as possible

Magnetic Resonance Imaging (MRI)

- a selected area of the patient’s body is placed inside a powerful magnetic field
- it gives a more defined image of anatomical details and may diagnose small tumors
or early infarction syndromes
 - is contraindicated in patients with previous surgeries where hemostatic or
aneurysm clips were implanted
- also contraindicated to cardiac pacemakers, prosthetic valves, bullet fragments,
and orthopedic pins
- procedure is very noisy
- must remove all metal objects
- use caution if patient is claustrophobic

Positron Emission Tomography (PET); Single-Photon Emission Computed Tomography

(SPECT)
- the patient either inhales or receives by injection radioactively tagged substances,
such as oxygen or glucose. A gamma scanner measures the radioactive uptake of
these substances and computer produces a composite image, indicating where the
radioactive material is located, corresponding to areas of cellular metabolism
- help diagnose abnormalities and behavioral disturbances, such as dementia and
schizophrenia, that may have a physiological basis
- the patient receives only minimal radiation exposure because the half-life of
radionuclides used is from a few minutes to 2 hours
- testing may take a few hours
- very expensive
- instruct the patient that remaining very still and immobile will produce best test
results

Cerebral Angiography (invasive)

- is a radiographic contrast study in which radiopaque contrast medium is injected by
a catheter into the patient’s cerebral arterial circulation.
- the contrast medium is directed into each common carotid artery and each
vertebral artery, and serial radiographs are then taken
- the contrast medium illuminates the structure of the cerebral circulation
- the vessel pathways are examined for patency, narrowing and occlusion
- the femoral artery is a common insertion site. Local anesthesia will be used
- a warm, flushed feeling will occur when the contrast medium is injected
- after the procedure, assess the puncture site for swelling, redness and bleeding.
Also, check the skin color, temperature, and peripheral pulses of the extremity
distal to the site for signs of arterial insufficiency (CTP)

Electroencephalogram, or EEG (noninvasive)

- is a recording of electrical impulses generated by the brain cortex that are sensed by
electrodes on the surface of the scalp
- helps detect and localize abnormal electrical activity occurring in the cerebral cortex
 - it aids in seizure focus detection, localization of a source of irritation such as a tumor
or abscess and diagnosis of metabolic disturbances and sleep disorders
- the patient’s scalp and hair should be free of dirt, creams, and sprays because they
can cause electrical interference and thus, an inaccurate recording (shampoo
patient’s hair)

LUMBAR PUNCTURE – fetal position

- a hollow needle is positioned in the subarachnoid space at L3-L4 or L4-L5 level, and
CSF is sampled
- the pressure of the CSF also is measured (45mm H2O in full term newborns – 120
mm H2O in adults)
- the CSF is examined for blood and for alterations in appearance, cell count, protein
and glucose
- the test is contraindicated in patients with suspected increased ICP because a
sudden reduction in pressure from below may cause brain structures to herniate,
leading to death
- in preparation for this test, position the patient on side with knees, and head flexed.
- Explain to the patient that some pressure may be felt as the needle is inserted and
not To move suddenly or cough
- After this procedure, keep the patient flat for 8-10 hours to prevent headache.
❖ Encourage liberal fluid intake
- Complications from CSF leak include a post procedure headache, nuchal rigidity,
fever and difficulty voiding. Treatment involves the injection of blood into the dura,
called a Blood Patch, to stop the leak

Normal CSF Values:

Color colorless, clear
WBC 0-5 mm3, all mononuclear
RBC none
Chloride 120-130 mEq/L
Glucose 50-75 mg/100 ml
Pressure 70-180
Protein 14-45 mg/100 ml
CLINICAL MANAGEMENT
HYPEROSMOLAR THERAPY
Hypertonic Agents
Hypertonic Saline
- induced hypernatremia has been demonstrated to increase cerebral perfusion
pressures and decrease intracerebral pressure in multiple pathologies (stroke,
subarachnoid hemorrhage, mass lesions)
- bolus dosing vs. continuous infusion
- 2% to 23.4%

Mannitol Administration –
- a hypertonic crystalloid solution that decerease
- cerebral edema, is also used as first-tier therapy for reducing ICP after brain injury
- monotherapy, if combined with Furosemide, there is a risk for excessive diuresis,
causing depletion of intravascular urine and electrolytes
- foley catheter must be inserted
- BP precaution

RESPIRATORY SUPPORT
- Normocapnia is essential for maintaining stable ICP because CO2 directly affects
the degree of vasodilation in the cerebral blood vessels
- limit the duration of passes of suction catheter to no more than 5-10 seconds avoids
hypoxia
- limiting the number of passes to 1 or 2 avoids overstimulation of the cough reflex
and decreases the incidence of intrathoracic pressure and ICP

PHARMACOLOGICAL THERAPY
Analgesics, Sedatives and Paralytics
In patients with severe brain injury, GCS Score < 8:
- reduce agitation, discomfort and pain
- facilitate mechanical ventilation by suppressing coughing
- limit responses to stimuli, such as suctioning
Analgesics – Opioid narcotics primarily affect the CNS
Fentanyl and morphine
- Limit pain caused by injuries and nursing interventions
- Facilitate mechanical ventilation
- Potentiate the effect of sedatives
- adverse effects: respiratory depression, depression of the cough reflex, mood
changes, nausea and vomiting
Naloxone (Narcan) reverses CNS depression (narco toxicity)
SEDATIVES
- Benzodiazepines
- Midazolam, Diazepam (Valium), Lorazepam before ICU procedures and as needed
to treat anxiety
- Lorazepam for alcohol withdrawal and anticonvulsant therapy
- Midazolam with Fentanyl is most often used before procedures

ANESTHETICS
- Propofol is administered as continuous infusion to decrease agitation in the
critically ill patient
- common side effect is Hypotension
BP Management
- MAP greater than 110 mm Hg must be avoided
- ACE inhibitors: Lisinopril
- B blockers:

SEIZURE PROPHYLAXIS
- 7 days use to decrease the incidence of early seizure
- Phenytoin, Levetiracetam and Carbamazepine (Tegretol)
- Levetiracetam is more convenient to administer as no blood drug levels need to be followed

HEADACHES
Migraine Headache
- caused by inflammation and dilatation of blood vessels in the brain.
- one side of the head is more affected than the other
- stress or life crisis
- last for hours to days. Pain is throbbing or pulsatile
- Aura of acute attacks includes visual field defects, confusion, paresthesia, paralysis
in extreme cases
- Associated symptoms are as follows: nausea and vomiting, chills, fatigue,
irritability, sweating, edema, photophobia, phonophobia (sound sensitivity)
Management:
- provide quiet environment, stress therapy and relaxation techniques
Diet: small, frequent meals
Avoid the ff: chocolate, nuts, onions, food seasoning, cheese, citrus fruits, coffee, pork, dairy
products, red wine
Pharma:
1. Beta-adrenergic blockers: Inderal (propranolol), Tenormin (Atenolol)
2. Calcium channel blockers: Calan (Verapamil)
3. Tricyclic antidepressants: Elavil (Amitriptyline)
4. Ergotamine tartrate
5. NSAIDS
6. Opioids: Demerol (Meperidine), Butorphanol nasal spray
7. Triptans (Selective Serotonin Receptor Agonists)
- Imtrex (Sumatriptan)
- Amerge (Naratriptan)

- Triptans cause vasoconstriction, reduce inflammation, and relieve migraine

❖ Imitrex is contraindicated in hypertension, renal and hepatic impairment. It should be

taken with full glass of water

CLUSTER HEADACHE:
- episodes clustered together in quick succession for few days or weeks with
- remission that lasts for months
- intense, throbbing, deep and often unilateral
- begins in infraorbital and spread to head and neck
- it is precipitated by alcohol or nitrate
Associated symptoms: flushing, tearing of eyes, nasal stuffiness and swelling of temporal
vessels
Treatment includes narcotic analgesic during acute phase

TENSION HEADACHE:
- relate to tension and muscle contraction
- episodic and vary with stress
- usually bilateral, involves neck and shoulders
- associated symptoms includes sustained contraction of head and neck muscles
Treatment:
1. Non-narcotic analgesics: Acetaminophen, ASA
2. Elavil (Amitriptyline)
3. Relaxation techniques
NEUROLOGICAL DISORDERS
CEREBROVASCULAR DISEASE (STROKE)
Causes: Thrombosis, Embolism, Hemorrhage
- damage to a focal area of the brain
- occurs when there is a disruption of blood flow to a region of the brain
- “Brain attack”

Clinical Management
4 Goals:
1. Reperfusion
2. Prevention of recurrent thrombosis
3. Neuroprotection
4. Supportive care – emotional and behavioral modification, communication,
rehabilitation

STROKE
Thrombus or Embolus:
- oxygen and substrate deprivation of the cerebral tissue begins
Deprivation for 1 minute – reversible symptoms, such as LOC
O2 deprivation for longer periods – microscopic necrosis of the neurons (infarcted)

Clinical Manifestations:
• weakness,
• numbness,
• visual changes,
• dysarthria,
• dysphagia or aphasia
Transient Ischemic Attack (TIA)
- neurological deficit lasting less than 24 hours that is attributed to focal or retinal
ischemia
- if symptoms resolve in less than 24 hours

Initial treatment for Ischemia:

1. Oxygen – ABGs, Pulse oximetry
2. Glucose – serials checks of blood glucose levels, insulin sliding scale regimen or
continuous insulin infusion
3. Reperfusion (adequate blood flow) – IV t-PA or thrombolytic medications

Thrombolytic Drugs
IV t-PA (streptokinase) –
- dissolves the clot and permits reperfusion of brain tissue
- should be initiated as quickly as possible; 4.5 hours or less from the onset of neuro
symptoms
- activates plasminogen

Anticoagulation
- dipyridamole, ticlopidine, clopidogrel (Plavix), aspirin (ASA)
- moderate consumption of leafy green vegetables containing vitamin K
- monitor prothrombin time and INR (bleeding); wof signs of bleeding

Control of Hypertension and Increased Intracranial Pressure

HTN
- Diastolic BP 105 mmHg – lowered gradually
ICP elevations
- short-term hyperventilation, fluid restriction, head elevation, avoidance of neck flexion
or severe head rotation, use of osmotic diuretics (mannitol) to decrease cerebral edema

Surgical Management
• Carotid endarterectomy to prevent stroke
• Hemicraniectomy
• Extracranial-intracranial bypass surgery

Nonsurgical Management
• Carotid artery stenting
Emotional and Behavioral Modification
- controlling stimuli in the environment, providing rest periods, giving positive feedback,
providing repetition, reduce stress

Communication
Expressive or nonfluent dysphasia –
- patient understands language but is unable to use it appropriately; Left Broca’s area
(memory of motor patterns of speech is affected)
Receptive or fluent dysphasia –
- patient is unable to understand the meaning of the spoken word (and usually the
written word); left Wernicke’s area (control center for recognition of spoken language)
Global dysphasia –
- both expressive and receptive dysphasia

SEIZURES
SEIZURES
- is an episode of abnormal and excessive discharge of cerebral neurons
- it can result in altered sensory, motor or behavioral activities
- can be associated with changes in the LOC
- common sites are the frontal and temporal lobes, particularly the hippocampus in the
- medial temporal lobe
EPILEPSY –
- is a condition in which seizures are spontaneous and recurrent
STATUS EPILEPTICUS
- a condition of either continued seizure activity or repetitive seizures over a period of 30
minutes.
- Rapid succession and full consciousness is not regained between seizures
Etiology:
Idiopathic
- 50%,occur most often in children younger than 10 years of age Congenital and Genetic
causes – 10%
Causes: vascular disease, alcohol, cerebral tumors, trauma, infection or fever, metabolic
disturbances, anoxia, and degenerative diseases

Classification of Seizure types:

1. Generalized: involves both hemispheres; LOC; no local onset in the cerebrum
a. Tonic-Clonic (Grand Mal) – LOC; stiffening; forced expiration (cry); rhythmic jerking
b. Clonic – symmetrical, bilateral semirhythmic jerking
c. Tonic – sudden increased tone and forced expiration
d. Myoclonic – sudden, brief body jerks
e. Atonic (“drop attacks”) – sudden loss of tone, falls
f. Absence (petit mal) – brief staring, usually without motor involvement, not
preceded by aura, 10-20 seconds

2. Partial: involves one hemisphere

a. Simple partial seizure – no change in LOC, Jacksonian
b. Complex partial seizure – altered LOC; with or without automatisms; lip smacking,
swallowing, aimless walking, verbalizations
c. Partial with secondary generalization

Jacksonian (Focal seizure)

- common among patients with organic brain lesion like frontal lobe tumor
- aura is present like numbness, tingling, crawling feeling.
- tonic-clonic movements of group of muscles e.g., hands, foot or face then proceeds to
grand mal seizure
Febrile Seizure
- common among children under 5 years of age, when body temperature is rising

Psychomotor seizure
- psychiatric component, aura is present (hallucinations or illusions)
- mental clouding (being out of touch of the environment), appears intoxicated
MANAGEMENT:
1. Stay with the patient
2. Protect the client from injury – padded siderails, no restraints, do not insert tongue
blade, ease patient on floor with pillow n head or place on lap
3. Promote patent airway
Diagnostic Tests:
• EEG, MRI, CT Scan
• Epilepsy monitoring unit

DRUG THERAPY:
• Carbamazepine (Tegretol)
• Gabapentin (Neurontin)
• Levitiracetam (Keppra)
• Phenobarbital – potential CNS toxicity; taper slowly
• Phenytoin (Dilantin) – dose guided by blood levels (10-20 mcg/ml); less expensive
a. parenteral DILANTIN should be diluted in normal saline
• Valproate (Depakote)

The symptoms of a Dilantin overdose vary. They may include:

1. Coma
2. Confusion
3. Fever
4. Involuntary, jerky, repeated movement of the eyeballs (nystagmus)
5. Lethargy
6. Low blood pressure
7. Nausea and vomiting
8. Sleepiness
9. Slow or slurred speech
10. Staggering gait or walk
11. Swollen gums
12. Seizures
13. Tremor (uncontrollable, repeated shaking of the arms or legs)
14. Unsteadiness, uncoordinated movements
Guillain-Barre Syndrome
- also known as acute inflammatory demyelinating polyneuropathy
- is a rapidly evolving illness
- commonly presents as symmetrical weakness, sensory loss and areflexia
- is an inflammatory peripheral neuropathy in which lymphocytes and macrophages strip
myelin from axons
- it a referred as a syndrome, because of the combination of signs and symptoms

Etiology:
- half of patients have a mild febrile illness 2-3 weeks before the onset of symptoms
- respiratory or GI
- Campylobacter jejuni and cytomegalovirus are the causes of the most frequent
antecedent infections

Clinical Manifestations:
- flaccid, ascending paralysis develops quickly
- commonly affected in a symmetrical pattern
- starts as a weakness in the lower extremities
- may develop rapidly over the course of hours to days
- 3-4 weeks to develop
Acute stage: onset of symptoms and rapidly progresses until no additional deterioration
Plateau stage: symptomatic, days to weeks
Recovery Phase: can take up to 2 years; remyelination and axonal degeneration;
remyelination 1-2 mm/day

Clinical Management:
• ICU admission
• Mechanical Ventilation
• Preventive measures- PE, DVT (heparin)
• Intravenous immunoglobulin (IVIG) – adverse effect
is acute tubular necrosis
• Plasmapheresis – hemorrhage and catheter-related
infections

Patient Education and Discharge Planning

Rehabilitation – 2 years
Support groups – Guillain-Barre Syndrome International Foundation

MYASTHENIA GRAVIS
MYASTHENIA GRAVIS
- is an autoimmune disorder of the neuromuscular junction transmission
- presents with fatigue and muscle weakness in the ocular, bulbar, diaphragm or limb
muscles
- derived from the Greek words for “muscle” and “weakness” whereas gravis means
“grave” in Latin
- because of the high mortality related to diaphragmatic muscle weakness, the disorder
was called “grave muscle weakness”

Pathophysiology:
- acetylcholine binds to the AChR

Epidemiology:
- seen more often in women than in men at a ratio of 3:2

Clinical Manifestations:
- Ocular Myasthenia or Generalized Myasthenia
Diagnosis:
Electromyography EMG - needle electrode is inserted in skeletal muscle; electrical activity
Blood is drawn for AChR antibodies
Tensilon Test (edrophonium)
- 10 mg IV Tensilon is given over 1 minute
- a response is anticipated within 2-3 minutes
- Atropine should be readily available in the event of bradycardia

Clinical Management:
• Long-term immunosuppression with corticosteroids
• Mycophenolate mofetil (CellCept)
• Azathioprine (Imuran) or cyclosporine
• Cyclophosphamide (Cytoxan)
• IVIG
• Plasmapheresis
• Thymectomy

Diagnosis:
Electromyography EMG
- needle electrode is inserted in skeletal muscle; electrical activity
- Blood is drawn for AChR antibodies
Tensilon Test (edrophonium)
- 10 mg IV Tensilon is given over 1 minute
- a response is anticipated within 2-3 minutes
- Atropine should be readily available in the event of bradycardia

Pharmacological Management:
Pyridostigmine (Mestinon)
- liquid, 60 mg tablet, 180 mg time-span formula or IV neostigmine

Muscarinic s/e: diarrhea, abdominal cramping, increased salivation, blurred vision,

bradycardia, increased perspiration
Nicotinic s/e: muscle twitching, weakness and fatigue

Myasthenic crisis vs. Cholinergic crisis

Myasthenic crisis
- respiratory failure along with sudden exacerbation of weakness in other muscle groups
- caused by lack of medication or lack of responsiveness at the
- neuromuscular junction to cholinergic treatment
Cholinergic crisis
- are muscarinic or nicotinic side effects; increased perspiration, abdominal cramping
and diarrhea
- too much medication

Patient Education and Discharge Planning

Medications: purpose, schedules, side effects
Medical ID and Card

S/S of crisis
Avoid crowds – movies or concerts
Support groups – Myasthenia Gravis Foundation