Module 6: Neurological Emergencies

Learning Outcomes Notes

Recall the anatomy and  Acetylcholine is present at neuromuscular junctions and in the autonomic nervous system, the peripheral
physiology related to the NS, and less commonly the CNS
nervous system  Catecholamines, including norepi, epi, and dopamine, are present in the brain
 Norepinephrine is a neurotransmitter in the sympathetic NS
 Both norepi and epo, when released from the adrenal medulla in response to SNS stimulation, circulate in
the blood and interstitial fluid, ultimately diffusing into the synaptic cleft and stimulating the appropriate
receptors in the SNS
 Serotonin is involved in mood, emotions, and sleep
 Histamine is involved in emotions, regulation of body temp, and water balance
 Gamma-aminobutyric acid (GABA) is the most common inhibitory neurotransmitter in the brain
 Glycine is the most common inhibitory neurotransmitter in the spinal cord
Describe the following as it
relates to pain:
1. Pain Pathways
2. Signs and Symptoms of
Pain
3. Factors that alter pain
perception
4. Pain Control and
Management
Describe common diagnostic
tests for disorders of the
nervous system, including CT
imaging and MRIs.
Describe the general effects of Local (focal) Effects: related to the specific area of the brain or spinal cord in which the lesion or trauma is located.
neurologic dysfunction Ex: Paresis or paralysis of the right arm that results from damage to a section of the left front lobe.

Supratentorial and Infratentorial Lesions: Supratentorial lesions happen in the cerebral hemispheres and lead to
specific dysfunction in a discrete area. Ex: numbness to the hand. Infratentorial lesions are located in the brain
stem and a small lesion may affect many motor and sensory fiber, resulting in widespread impairment, because the
nerves are bundled together, when passing through the brain stem. Also, respiratory and circulatory function and
the level of consciousness may be impaired by a small lesion in this area

Left and Right Hemispheres: Either side can have different effects, in addition to focal effects. Left-sided damage
can less to a loss of logical thinking ability, analytic skills, other intellectual abilities, and communication skills.
Right-sided damage impairs appreciation for music and art and causes behavioral problems. Spatial orientation and
recognition of relationships may be deficient, resulting in interference with mobility and “neglect” of the
contralateral side of the body (which is not recognized as “self”)

Level of Consciousness: Various levels of reduced consciousness may present as lethargy, confusion,
disorientation, memory less, unresponsiveness to verbal stimuli, or difficulty in arousal. Coma is the most serious
level in loss of consciousness (although some reflexes may still be present). A Vegetative State is a loss of
awareness and mental capabilities, resulting from diffuse brain damage, although brain stem function continues,
supporting respiratory, cardiovascular, and autonomic functions. Person is unresponsive to external stimuli.
Locked-in Syndrome refers to a condition in which an individual with brain damage is aware and capable of
thinking but is paralyzed and cannot communicate. A diagnosis of Brain Death is often required to terminate
medical intervention. The criteria for brain death include: 1. Cessation of brain function, including function of the
cortex and brain stem (ex: a flat or inactive EEG). 2. Absence of brain stem reflexes or responses. 3. Absence of
spontaneous respirations when ventilator assistance is withdrawn. 4. Establishment of the certainty of irreversible
brain damage by confirmation of the cause of dysfunction.

Motor Dysfunction: Damage to the cerebral cortex or corticospinal tracts interfere with the opposite side of the
body (contralateral), causing weakness or paralysis. Damage to the lower motor neurons in the spinal cord can
cause weakness or paralysis on the same side of the body (ipsilateral). Hyperflexia; increased muscle tone, can be
caused because the intact spinal cord (below injury) continues to conduct impulses with no moderating or
inhibiting influences sent by the brain (also known as spastic paralysis). Flaccid Paralysis can occur at the area of
damage to the spinal cord and below. If the cord distal to the injury is still in tact some reflexes may still be present
or hyperactive (hyperflexia). Two involuntary motor responses that occur in persons with severe brain trauma
include posturing. Decorticate responses include rigid flexion in the upper limbs, with adducted arms and internal
rotation of the hands: the lower limbs extended. This may occur in severe damage of the cerebral hemispheres.
Decerebrate responses occur in patients with brain stem lesions and CNS depression caused by systemic effects.
Upper limbs are extended, head is extended and body is arched.

Sensory Deficits: Loss may involve touch, pain, tempature and position senses, as well as the special senses of
vision, hearing, taste and smell. Specific damage to the somatosensory cortex in the parietal lobe can map specific
regions. Mapping of dermatomes can assist in the evaluation of sites of spinal cord lesions.

Visual Loss: Hemianopia: Visual pathways are unique, so location of damage determines the loss of visual field. In
the optic chiasm the fibres in each optic nerve come together and then divide. If the chiasm is injured you will lose
sight in both eyes. Fibers from the medial half of each retina cross to the other hemisphere, whereas the fibers of
the lateral half of the retina stay on the same side. If the right occipital lobe is damaged it will mean loss in site of
the “left” side of both eyes (left eye lateral, right eye medial), known as homonymous hemianopia. Remember that
the “right” side of the eye receives input from the left visual field because the light crosses over in the cornea.

Diplopia is double vision.

Language Disorders:
Type Site of Damage Effect
Expressive (motor) Broca area, left frontal lobe Cannot speak or write fluently or
appropriately. Non-fluent
aphasia with short phrases;
omitting small words
Receptive (sensory) Werincke area, left temporal Unable to understand written or
 lobe, prefrontal spoken language. Fluent aphasia
with relatively normal speech
but made up words or sentences
that do not make sense
Global Both areas and connecting fibers Cannot express self or
comprehend other’s language
Dysarthria- words cannot be articulated clearly resulting from motor dysfunction or cranial nerve damage
Agraphia- impaired writing ability
Alexia- impaired reading ability
Agnosia- loss of recognition or association. Inability to recognize objects.

Seizures: spontaneous or excessive discharge of neurons in the brain, often precipitated by inflammation, hypoxia,
or bleeding of the brain.

Increased Intracranial Pressure: Because the brain is encapsulated in a rigid, non-expandable skull, any increase in
fluid, such as blood or inflammatory exudate, causes an increased pressure in the brain. The result is that less
blood can enter the “high pressure” area in the brain, and eventually brain tissue itself is compressed, decreasing
function of neurons. Pressure happens throughout the CNS by means of continuous flow of CSF, leading to
widespread function.
1) Early Signs: body initially tries to compensate by shifting more CSF to spine, and increasing venous return
from the brain. Unfortunately, this causes hypoxia and arteries vasodilate in order to improve blood
supply to the brain, causing more fluid buildup. If the increased pressure has not been relieved, the first
sign is a decreasing level of consciousness. Other signs are severe headache (stretching of dura), Vomiting
(pressure stimulating emetic center of medulla), and papilledema (swelling of optic disk)
2) Vital Signs:
a) Cushing Reflex: increased systolic BP, increased pulse pressure, bradycardia
b) Systemic vasoconstriction to push blood into brain and reduce ischemia
c) Baroreceptors in carotid respond to increased BP by slowing heart rate
d) Chemoreceptors respond to low C02 levels by reducing respiratory rate (cheyne-stokes resps or
apnea)
e) Improved circulation relieves ischemia temporarily but then cycle continues as ICP increases
3) Visual Signs: Pressure on the oculomotor nerve affects pupil size and response. One or more pupils become
fixed and dilated as PNS in the oculomotor nerve become nonfunctional. Giving the “blown” pupil. Ptosis
or “droopy eyelid” is another effect of pressure on the oculomotor nerve affecting muscle innervation of

Determine what is appropriate
pupil size and reactivity for a
patient with a neurological
condition and adapt findings with
a patient’s history, age or gender
Describe the etiology,
pathophysiology, and
manifestations relating to
convulsive disorders
1. Febrile Seizure
2. Generalized Seizures
3. Partial Seizures (focal)
the upper eyelid.
4) Changes in CSF: With lumbar puncture you can see an increase in CSF pressure (20mmHg). The colour can
also indicate what is wrong. Pinkish= hemorrhage. Cloudy or yellow=infection. Abnormal protein levels=
neoplasm.
CPP=MAP-ICP
Normal MAP=80-90mmHg
Normal ICP=1-10mmHg
Normal CCP= 70-80mmHg
CCP below 50= Brain ischemic (aim to keep BP at least 100-120 systolic)
Anisocoria- unequal pupils. Sign of increased ICP. Many people have slight inquality in pupil size normally, so
anything over 1mm should be worth noting.
Nystagmus- Involuntary rhythmic movement of the eyes, that can be caused by seizures, vertigo, and MS.
All Seizures: Pathophysiology: result from a sudden, spontaneous, uncontrolled depolarization of neurons, which
causes abnormal motor or sensory activity and possibly loss of consciousness. The neurons on the epileptogenic
focus are hyperexcitable and have a lowered threshold for stimulation. Any physiological change such as alkalosis,
temperature changes, or sensory stimulus can activate irritable neurons.
Febrile Seizure:
1. Etiology:
2. Pathophysiology: Initiated by a rapid rise in body temperature of an infant or young child.
3. Manifestations: Can shows as any generalized seizure (tonic-clonic, absence, spasms, etc)
Generalized Seizure:
1. Etiology: Have multiple foci or origins in the deep structures of both cerebral hemispheres and the brain
stem.
2. Pathophysiology:
3. Manifestations:
a. Absence (Petit Mal)- seizure lasts for about 5 to 10 seconds and may occur many times a day. A
brief loss in awareness and sometimes transient facial movements such as twitches of the eyelids
or lip smacking. No memory of the epidose is retained.
b. Tonic-Clonic (Grand Mal)- May occur spontaneously or after simple seizures. General follows a
pattern:
 i. Prodromal signs occur in some individuals such as nausea, irritability, depression, or
muscle twitching some hours before the seizure
ii. An Aura, such a peculiar visual or auditory sensation, immediately preceding the seizure
iii. Loss of consciousness
iv. Strong tonic muscle contraction
v. A cry escapes as the abdominal and thoracic muscles contract. Jaw clenches tightly and
respiration ceases
vi. Clonic stage follows in which the muscles alternatively contract and relax, resulting in a
series of forceful movement that involve the whole body (increased salivation and bladder
incontinence)
vii. Contractions gradually subside; the body goes limp and consciousness slowly returns
viii. The person is confused and fatigued, which aching muscles, and falls into deep sleep in the
postictal period
Partial (focal) Seizure:
1. Etiology: Have a single focal origin, often in the cerebral cortex.
2. Pathophysiology:
3. Manifestations: repeated motor activity, such as jerking or turning of the head or eye aside, jerking
movements of a leg, or by sensation such as tingling that begins in one area and may spread. Auditory or
visual manifestations can appear. Jacksonian seizures are when clonic contractions begin in a specific area
and spread progressively (arm up into face)
Describe the etiology, Infection (sinus): Inflammation or infection within the sinus cavities of the face. The pain is located in the superior
pathophysiology, and portions of the face and increase with bending the head forward. The patient may have postnasal drip, a sore
manifestations relating to throat, and nasal discharge.
headache and facial pain: Migraine: Are thought to be caused by changed in blood vessel size within the base of the brain. The patient may
1. Infection experience an aura (seeing bright lights) and unilateral, focused pain that spreads over time. The pain is throbbing,
2. Migraine pounding, and pulsating in nature. Nausea or vomiting may be present. Patients refer dark, quiet environments.
3. Tension Migraines can last several days.
4. Intracranial Hemorrhage Tension: The most common types of headaches, caused by life stress that results in muscle tension within the face
5. Cerebral Vascular and head. Pain tends to be on both sides of the head, and travels from back to front; it is a dull ache or squeezing
Malformation in nature. The jaw, neck, or shoulders may be stiff or sore.
Cluster: rare, vascular headaches that start in the face. They last only 30-45mins but pt may have several a day and
it can recur for days. The pattern consists of minor pain around the eye, pain that quickly intensifies and spreads to
one side of the face, and a feeling of anxiety.
Describe etiology, Ischemic Stroke
pathophysiology, and
manifestations relating to
cerebrovascular disorders
including the use of the
cinncinati stroke scale AEIOU-
TIPS
1. Ischemic Stroke
(thrombotic vs
embolitic)
2. Hemorrhagic Stroke
3. TIA
4. Syncope
5. Epilepsy
6. Cerebral Vascular
Accidents (CVAs)
Describe etiology,
pathophysiology, and
manifestations relating to
Chronic neurologic disorders:
1. Alzheimers
2. Amyotrophic lateral
Etiology: 75% of strokes. A blood vessel is blocked, so the tissue distal to the blockage becomes ischemic.
Pathophysiology: Only the tissue beyond the blockage is affected, so the areas of the brain involved are limited.
Manifestations: Signs and symptoms eventually stop increasing and plateau, indicating that the area of the brain
involved is no longer working. Extent and severity is dictated by which artery is involved and which part of the
brain is denied oxygen.
Hemorrhagic Stroke
Etiology: 25% of strokes.
Pathophysiology: Bleeding in the brain vs a clot, so tissues distal can still become ischemic due to lack of proper
blood flow.
Manifestations: Tends to worsen over time (vs ischemic) due to the bleeding in the cranium. Bleeding may lead to
ICP and herniation. Hallmark of hemorrhagic CVA is “the worst headache of my life”, followed by not being able to
speak, then difficulty to arouse, then signs of increased ICP/herniation.
Transient Ischemic Attack (TIA)
Etiology: “ministrokes” that are serious vascular problems. More than 1/3 of patients with TIA will suffer a CVA
shortly after.
Pathophysiology:
Manifestations: any of the typical symptoms of a CVA, that resolve within minutes to 24 hours without any
residual damage to brain tissue.
Cincinnati Prehospital Stroke Scale
Assessment Normal Abnormal
Facial Droop Both sides of the face move One side of the face does not
equally well move as well as the other
Arm Drift Both arms move the same, or One arm does not move, or the
both arms do not move one arm drifts down compared
to the other
Abnormal Speech The patient uses the correct The patient slurs words, uses
words with no slurring inappropriate words, or is unable
to speak.
Alzheimer's
1. Etiology: Specific cause is unknown. At least four defective genes located on different chromosomes have
been associated with Alzheimer’s disease (AD). Three gene mutations on chromosomes 1, 14, and 21 are
inherited as autosomal dominant traits resulting in early onset AD. High incidence in older people with
down syndrome.
2. Pathophysiology: Changes in AD include progressive cortical atrophy, which leads to dilated ventricles, and
 sclerosis (ALS) widening of the sulci. Neurofibrillary tangles in the neurons and senile plaques are found in large numbers
3. Bell’s Palsy in the affected parts of the brain. The plaques, which disrupt neural conduction, contain fragments from
4. Cerebral Palsy beta-amyloid precursor protein (BAPP). Some neurofibrils and plaques have been found in the brains of
5. Multiple Sclerosis elderly people whose cognitive function is not impaired, and therefore it appears that the number and
6. Muscular dystrophy distribution of plaques plays a factor. A deficit of th Acetylcholine also occurs in the affected brain.
7. Parkinson’s 3. Manifestations: Course of disease can progress over 10-20 years. Early stage is gradual loss of memory
8. Poliomyelitis and lack of concentration. Ability to learn new information and to reason is impaired and behavioral
9. Neoplasm changed, such as irritability, hostility and mood swings are common. Cognitive function, memory, and
10. Dystonia language skills continue to decline. Problem solving, math abiilty, and judgement become poor. Apathy,
11. Trigeminal Neuralgia indifference and confusion become more marked. Managing activities of daily living becomes difficult.
12. Spina Bifida Wandering is common, and the person may become confused or lost, even in familiar territory. In late
13. Myasthenia Gravis stages, the person does not recognize his or her family, lacks awareness or interest in the environment, is
14. Peripheral Neuropathy incontinent, and is unable to function in any way. Degenerative changes may gradually interfere with
motor function.
Amyotrophic Lateral Sclerosis (ALS) (ALA Lou Gehrig Disease)
1. Etiology: Amyotrophic means “muscle wasting”, and sclerosis means “hardening.” Cause has not been
confirmed. Primarily affects men between the ages of 40 and 60. There is so far no means of preventing
continuous and rapid decline of motor and respiratory function, whereas cognitive function remains intact.
Has been a major focus of debate with talks considering euthanasia.
2. Pathophysiology: Progressive degenerative disease affecting both upper motor neurons in the cerebral
cortex and lower motor neurons in the brain stem and spinal cord. Supportive glial cells called astrocytes
secrete neurotoxin leading to the death of motor neurons. Loss of upper motor neurons leads to spastic
paralysis and hyperreflexia; damage to the lower motor neurons result in flaccid paralysis, with decreased
muscle tone and reflexes. Sensory neurons, cognitive function, and cranial nerves III (oculomotor), IV
(Trochlear), and VI (Abducens) are NOT affected. Progressive muscle weakness eventually effects
respiratory function.
3. Manifestations: Upper extremities, particularly the hands, manifest weakness and muscle atrophy, with
the loss of fine motor coordination commencing with distal fibers. Stumbles and falls are common. Muscle
cramps and twitching. Weakness and paralysis progress throughout the body. Dysarthia develops as cranial
nerves involving speech are lost. Eventually swallowing and respiration are impaired, and a ventilator is
required.
Bell’s Palsy
1. Etiology: Is a temporary paralysis of the facial nerve (VII). Patients typically experience a minor infection
before Bell’s palsy appears. The attack is very sudden and can be confused with stroke (so make sure you
 do a proper stroke screen to rule out stroke)
2. Pathophysiology: The facial nerve controls the muscles on each side of the face, including those used in
eye blinking and facial expressions such as smiling and frowning. It also controls the tear glands and saliva
glands. Finally, it also transmits taste sensation from the tongue.
3. Manifestations: Ptosis, facial droop or weakness, drooling, and loss of the ability to taste. Will often
resolve within 2 weeks.
Cerebral Palsy
Athetoid and choreiform 1. Etiology: Single or multiple factors may be implicated. Hypoxia or ischemia is the major cause of brain
movements (below) damage; it may occur prenatally, perinatally, or postnatally. Ischemia can be caused by placental
complications, vascular occlusion, hemorrhage, aspiration, or respiratory impairment in the infant. High
bilirubin levels may cause kernicterus, in which accumulated bilirubin crosses the BBB and damages the
neurons. Other causes include infection or metabolic abnormalities, such as hypoglycemia, in either the
mother or the child.
2. Pathophysiology: The brain tissues is altered by malformation, mechanical trauma, hypoxia, hemorrhage,
hypoglycemia, hyperbilirubinemia, infection or other factors resulting in necrosis. Can cause generalized
necrosis affecting the whole brain, or localized areas.
3. Manifestations: 3 Major groups of motor disability have been identified:
1. The first and largest group included those with spastic paralysis, which results from damage to the
pyramidal tracts(diplegia) or the motor cortex(hemiparesis), or from general cortical damage
(quadriparesis). This form is characterized by hyperreflexia.
2.The second group is dyskinetic disease, which results from damage to the extrapyramidal tract, basal
nuclei, or cranial nerves. Manifested in athetoid or choreiform involuntary movements.
3.Ataxic Cerebral Palsy, common develops from damage to the cerebellum and manifests in loss of balance
and coordination.
Multiple Sclerosis
1. Etiology: Onset of symptoms occurs in individuals between 20-40 years and peaks at 30 years. More
common in women than men (2:1). Cause is unknown, but researchers believe it is an autoimmune
disorder.
2. Pathophysiology: Loss of myelin interferes with the conduction of impulses in the affected fibers. It affects
all types of nerve fibers. Lesions occur as an inflammatory response as cells that do not normally enter the
brain or spinal cord do so and attack neurons, with loss of myelin in the white matter of the brain or spinal
cord. Research has identified a protein in the body’s clotting mechanism as a potential trigger for immune
response. Larger areas of inflammation and demyelination are termed plaques. Once initial inflammation
subsides, neural function may return to normal, until another exacerbation occurs. In time neural
 degeneration becomes irriversible and additional areas of the CNS are involved. Can be a slow and
progressive, or rapid and progressive disease.
3. Manifestations: Symptoms determined by the areas that are demyelinated in each individual. Blurred
vision is a common early sign. Initial weakness in the legs often occurs. Diplopia, scotoma (spot in visual
field), or dysarthria (difficulties articulating) may occur. Chronic fatigue is common. Sensory deficits will
continue to spread causing paresthesia, and progression to paralysis and loss of bladder and bowel control.
Depression is common later in the disease.
Muscular Dystrophy
1. Etiology: Neurological condition marked by degeneration of muscle tissue.
2. Pathophysiology: Defective DNA causes an error in muscle tissue, such that the malformed muscle cells
rupture more easily. MD is diagnosed at age 2 to 5 and occurs only in men. Progression of symptoms is
over months or years.
3. Manifestations: Presents with muscle weakness, delayed development of motor skills, ptosis, drooling, and
poor muscle tone. The most common form, Duchenne, manifests itself in childhood and can include
damage to the respiratory and cardiac muscle. They have a short life expectancy (20s) and often die of
pneumonia or cardiogenic shock.
Parkinson’s
1. Etiology: Usually develops after 60yrs and occurs fairly equally in men and women. Can be a genetic
disease, but can also be a result of exposure to certain viruses and toxins. Parkinsons involved the presence
of clumps of specific substances in affected brain cells, called Lewy Bodies. Bodies contain an important
natural and widespread protein called alpha-synuclein, which researchers believe may be an important
clue in finding the cause of the disease.
2. Pathophysiology: Dysfunction of the extrapyramidal motor system occurs because of the degenerative
changes in the basal nuclei, principally in the substantia nigra. A decreased number of neurons secrete
dopamine, an inhibitory neurotransmitter, leading to an inbalance between excitation and inhibition in
basal nuclei. Many patients also have a reduced number of cortical neurons, which is a characteristic of
dementia.
3. Manifestations: Early signs include fatigue, muscle weakness, muscle aching, decreased flexibility, and less
spontaneous change in facial expression. More obvious signs are tremors in the hands at rest and a
repetitive “pin rolling” motion of the hands. Tremors eventually affect more of the body. With further
impairment muscles become rigid, with difficulty initiating movement, and slow movements (bradykinesia).
Short shuffling steps, and falls are common. Voice can become lower with minimal inflections while
talking. Chewing and swallowing become difficult, with drooling. Blank, staring faces with minimal blinking.
Autonomic dysfunction with urinary retention, constipation, and orthostatic hypertension. Dementia can
 occurs late in the disease.
Poliomyelitis
1. Etiology: Is a viral infections that is transmitted by the fecal-oral route.
2. Pathophysiology: The virus attacks motor neurons in the brain and brain stem, which causes the classic
signs of weakness and paralysis. Remaining neurons try and compensate by sending out new axons, which
allows patient to regain function. These axons become overworks and break down and function can be
lost again.
3. Manifestations: Postpolio syndrome Is when someone contracted polio in the past and their compensatory
axons are breaking down. This causes weakness, fatigue, difficulty swallowing or breathing problems,
typically wherever the patient had symptoms when they were originally infected.
Neoplasm
1. Etiology: A cancer within the brain or spinal cord.
2. Pathophysiology: Primary neoplasms begin within the nervous system. Metastatic neoplasms begin in
Spasmodic Torticolli (dystonia) some other part of the body, gain access to the bloodstream or lymphatic system, and then take up
residence within the nervous system. Lung and breast cancers most common metastasize to the CNS.
3. Manifestations: headache, nausea, vomiting, seizures, changes in mental status, and stroke-like symptoms
are common in cases of neoplasm. Rate and intensity of these symptoms depend on growth rate and
location.
Dystonia
1. Etiology: Primary dystonia occurs for unknown reasons, although a defect in the body’s ability to process
neurotransmitters is thought to lie at the heart of the problem. Secondary dystonia can occur with people
who take antipsychotic meds.
2. Pathophysiology:
3. Manifestations: Severe, abnormal muscle spasms that cause bizarre contortions, repetitive motions, or
postures. Spasmodic Torticollis is when neck muscle contract, twisting the head to one side and pulling it
forward or backward. The head remains painful frozen in that position.
Trigeminal Neuralgia
1. Etiology: Inflammation of the trigeminal nerve (V). This nerve receives sensory information from the face.
2. Pathophysiology: The usual cause of trigeminal neuralgia is irradiation by an artery lying too close to the
nerve. Over time the artery will expand and contract, grating the myelin sheath off the nerve. The nerve
may “short out” causing pain without trauma to the area.
3. Manifestations: Patients receive severe shock-like stabbing pain, usually on one side of the face. These
attacks for several minutes to several months. They may be triggered by touching the face, seaking,
brushing the teeth, eating, putting on clothing, the wind—essentially any activity that stimulates the face.
 There is no loss of motor control over the face so facial droop, ptosis and difficulty controlling the airway
are very uncommon
Spina Bifida
1. Etiology: Appears to have a multifactorial basis, with a combination of genetic and environmental factors
contributing to its development. Anecephal (absence of cerebral hemispheres). Environmental factors
include radiation exposure, gestational diabetes, and deficits if vitamin A and folic acid (which is why it is
recommended during the first 6 weeks of pregnancy)
2. Pathophysiology: Neural tubes develop during the 4th week of gestation, beginning in the cervical area and
progressing to the lumbar. The problem with spina bifida is the failure of the posterior spinous processes
on the vertebrae to fuse, which may permit the meninges and spinal cord to herniate, resulting in
neurological impairment. 3 subtypes of spina bifida:
1.Occulta develops when the spinous processes don’t fuse, but herniation of the spinal cord and meninges
does not occur. Defect may not be visible, but often there is a dimple or tuft of hair. Only some
neurological signs show during growth periods due to tension on the cord.
2.Meningocele has same bony defect, and herniation of the meninges occurs through the defect, and then
meninges and CSF form a sac on the surface. Neurologic impairment is not usually present although
infection or sac rupture could lead to damage.
3.Myelomeningocele is the most serious form of spina bifida. Herniation of the spinal cord and nerves
along with the meninges and CSF occurs, resulting in considerable neurological impairment.
3. Manifestations: the 2nd and 3rd subtypes are visible as a protruding sac over the spine. In the 3rd, the extend
of neurologic deficit depends on the level of the defect and the status of the nerve tissue; sensory and
motor function below the level of the herniation are impaired. Some degree of muscle weakness or
paralysis is present. Bladder and bowel control are usually impaired. There may be fecal and urinary
incontinence.
Myasthenia Gravis
1. Etiology: Autoimmune disorder that impairs the receptor for acetylcholine at the neuromuscular junction.
Women more common than men, with an age of onset between 20-30, with men greater than 50.
2. Pathophysiology: IgG antibodies to ACh receptors form, blocking and ultimately destroying the receptor
site, preventing further stimulation in the muscle. Leads to skeletal muscle weakness and rapid fatigue of
the affected muscles. Facial and ocular muscles affected initially, followed by arm and trunk muscles.
3. Manifestations: Muscle weakness noticeable in face and eyes, and fatigue develops quickly when muscles
are used. Diplopia and ptosis impair vision. Speech becomes a nasal monotone. Face appears droop with
sadness; attempts to smile may look more like a snarl. Chewing and swallowing become difficult as the
weakness progresses and the risk of aspiration increases. Head droop as neck muscle become involved.

Describe etiology,
pathophysiology, and
manifestations relating to
Infectious Disorders:
1. Encephalitis
2. Guillian Barr Syndrome
3. Menengitis
Utilize the AVPU and GCS
technique for determining the
level of consciousness
Explain the effects of herniation
Muscle fatigue increases as day progresses. Upper respiratory infections are common as it is difficult to
move secretions. Myaesthenic crisis occurs when there is added stress such as infection, trauma, or
alcohol, which can increase weakness.
Peripheral Neuropathy
1. Etiology: Can be caused by trauma, toxins, tumours, autoimmune attacks and metabolic disorders. Most
common form is diabetic neuropathy.
2. Pathophysiology: A group of conditions in which the nerves leaving the spinal cord become damaged. As a
result, the signals moving from or to the brain are distorted. In diabetic neuropathy, blood glucose levels
rise, and peripheral nerves become damaged, resulting in misfiring and shorting of signals.
3. Manifestations: Loss of sensation, numbness, burning sensations, pain, paresthesia, and muscle weakness
are common. Patients may eventually lose the ability to feel their feet or other areas.
Encephalitis
Guillian-Barre Syndrome
Etiology: Cause of the condition is unclear, although some degree of immune response appears to be present.
Pathophysiology: The theory is that an infectious agent creates a situation in which the body attacks its own
neurons. The attack damaged the myelin, thereby causing “shorting” of the signals travelling along the axon.
Manifestations: Begins with weakness and tingling senstions in the legs. The weakness moves up the legs and
begins to affect the thorax and the arms. It can quickly become severe and lead to paralysis. Transition from being
able to walk and speak to needing a ventilator can happen in a few hours. Some patients will have complete
recovery within weeks. Some have some degree of weakness after years, and some never recover from their
weakness.
Eye Opening Verbal Response Motor Response
4.Sponateous 5.Oriented to time and space 6.Obeys Commands
3.Responds to Speech 4.Confused 5.Localizes Pain
2.Responds to Pain 3.Inappropriate Words 4.Flexion to Pain (withdraw)
1.No response 2.Incomprehensible 3.Flexion (Decorticate)
1.None 2.Extension (Decerebrate)
1.None
Transtentorial (Central) Herniation: the cerebral hemispheres, diencephalon, and midbrain are displaced
downward, resulting in changes in blood flow and CSF, reticular activating system (RAS), and respiration.
Uncal Herniation: the uncus of the temporal lobe is displaced downward, creating pressure on the oculomotor
(nerve III), the posterior cerebral artery, and the RAS.
Cerebellar (Tonsillar) Herniation: cerebellar tonsils are pushed downward through the foramen magnum, which
compressed the brain stem and vital centers and caused death.