NeurologicalAlterations-ModuleC.ppt

NEUROLOGICAL
ALTERATIONS
NUR 203
Module C

Terms
• Define Terms associated with neurological
alterations:
– Headaches-
• Tension, migraines, cluster
– Tumors – benign, cancerous
– Infections-meningitis, encephalitis
– Head injury – contusions, concussions,
fractures, intracranial hemorrhage

Terms (cont)
• Transient ischemic attacks
• Cerebrovascular accidents
– Thrombotic
– Hemorrhagic
– Embolic
• Spinal Cord dysfunctions
– Spinal cord injuries
– Herniated disc

Terms
– Spinal Shock
• Paralysis
– Quadriplegic (tetraplegia)
– Paraplegic
• Autonomic Dysreflexia
• Spasticity
• Neurogenic bladder/bowel

Terms
– Respiratory
– Sexual
– Infection
• Neuromuscular dysfunction
– Multiple Sclerosis
– Parkinson’s
– Guillian-Barre
– Amyotrophic Lateral Sclerosis

Neuromuscular Dysfunctions
• Myasthenia Gravis
• Trigeminal Neuralgia
• Bell’s Palsy
• Muscular Dystrophy
• Cerebral Palsy
• Neural tube defects

VASCULAR HEADACHES
• Tension Headache
– Results from muscle contraction
– Tight, band-like discomfort that is unrelenting
– Pain builds slowly in severity
– Triggered by fatigue and stress
– Diagnosis confirmed when they occur more
than 15 days a month

• Treatment:
– Stress reduction techniques (bio-feedback,
psychotherapy and other methods of stress
reduction). Also, correction of poor posture.

Cluster Headaches
(sometimes classified as a form of
migraine)
• Cyclical pattern of periorbital pain lasting
form 4 – 8 weeks and usually occurring in
the spring or fall
– Headache lasts from 15 minutes to hours and
may occur several times a day and may awaken
from sleep. Unilateral in nature.

• Pain is described as deep, boring, intense
pain of such severity that the patient has
trouble staying still.
• May develop Horner’s syndrome
– Constricted pupils
– Unilateral lacrimation
– Rhinorrhea
• Triggered by consumption of alcohol
• Treated with 100% oxygen via mask
• Intranasal Lidocaine may be used

Migraine Headache
– Typically a “true vascular headache”
– Pain results from vasospasm and ischemia of
intracranial vessels.
– Unilateral pain, but may alternate sides
– Throbbing, pulsatile pain
– Photophobia, phonophobia, anorexia, nausea,
vomiting and focal neurogenic signs may be
present

– Aura may precede the event –scintillating
scotoma (flashing lights), euphoria, fatigue,
yawning, and/or craving for sweets
– Can be triggered by relief of intense stress,
missing meals, or tyramine rich foods
– Patient tries to find relief in a quiet, dark
environment
– Treatment: avoid precipitating factors
– Meds: propranolol, amitriptyline, valporate,
verapamil, phenelzine and methysergide taken
daily

• If medical treatment is sought at the time of
the event:
– Ergotamine
– Dihydroergotamine
– Sumatriptan
– Chlorpromazine
– Prochlorperazine

• Patient teaching for migraines:
– Identify triggers
– Avoid alcohol
– Avoid tyramine rich foods
– Avoid low blood sugars
– Reduce stress

INFECTIOUS /
INFLAMMATORY
DISORDERS

MENINGITIS
• Inflammation of the meninges of the brain
and spinal cord
– Bacterial
– Aseptic (other infective agents—usually viral)

CLINICAL MANIFESTATIONS
• Classic symptoms:
– Nuchal rigidity
– Brudzinski’s sign
– Kernig’s sign
– Photophobia
• Other: fever, tachycardia, h/a, prostration, chills,
nausea, vomiting
• May be irritable at first with progression to
confusion, stupor, and semiconsciousness

• Seizures may occur
• Petechial or hemorrhagic rash may develop
• CSF is cloudy with bacterial

DIAGNOSIS
• Lumbar puncture:
– Bacterial: increased protein, decreased glucose,
cloudy, increased leukocytes
– Viral: increased protein, normal glucose, clear,
increased lymphocytes
• May culture other areas: blood, wounds,
sinuses, etc.

TREATMENT
• Isolate until results of CSF analysis are
obtained.
– Bacterial is very contagious
• ABX
• Anticonvulsants
• Fluid and electrolyte replacement
• Monitor for increased ICP
• Provide quiet environment
• Analgesics may be avoided if they have CNS
depressant actions—will mask CNS changes

ENCEPHALITIS
• Inflammation of the parenchyma of the
brain and spinal cord. Usually caused by a
virus.
– Arbovirus encephalitis (transmitted by ticks and
mosquitoes)
– Herpes simplex virus encephalitis may occur as
a complication of measles, chickenpox, or
mumps.

• Fever
• Headache
• Seizures
• Nuchal rigidity
• Altered LOC
• Disorientation
• Agitation
• Restlessness or lethargy
• Drowsiness
• Photophobia
• N/V

BRAIN ABSCESS
• A collection of either encapsulated or free
pus within brain tissue arising from a
primary focus elsewhere (ear, mastoid
process, sinuses, heart, distal bones, lungs,
bacteremia, etc).

MANIFESTATIONS
• Headache
• Lethargy
• Drowsiness
• Confusion
• Depressed mental status
• Symptoms of infection
– Fever
– Chills

Traumatic Brain Injuries
• Over 2 million traumatic brain injuries occur each
year with approximately 500,000 injuries severe
enough to cause hospitalization.
• Approximately 50% of all trauma deaths
associated with head injury
• More than 60% of all vehicular trauma deaths are
a result of heat injury

Traumatic Brain Injury -Mechanism
of Injury
• Penetrating trauma
• Blunt trauma
– Acceleration
– Deceleration
– Rotational forces

Traumatic brain Injury – Patho
• Primary injury
• Secondary injury
• Goals of care include efforts to reduce morbidity &
mortality from primary & secondary injuries

Traumatic Brain Injury –
Patho. – Primary Injury
• Occurs at moment of impact
• May be mild or severe
• Types of primary injuries:
– Contusion, laceration, shearing injuries, and hemorrhage

Traumatic Brain Injury –
Patho. – Secondary Injury
• The biochemical & cellular response to the initial
trauma
– Can exacerbate the primary injury & cause loss of brain
tissue not originally damaged
• Ischemia is the primary culprit in secondary brain
injury

Traumatic Brain Injury - Patho –
Secondary Injury (cont.)
• Hypercapnia is a powerful vasodilator
– Results in cerebral vasodilatation & increased cerebral
blood volume & ICP
• Significant hypotension causes inadequate perfusion
to neural tissue
– *Not typical to be hypotensive with TBI
– If hypotensive, need to rule out internal injuries

Traumatic Brain Injury - Patho –
Secondary Injury (cont.)
• Cerebral edema
• Initial hypertension with severe TBI is common
• Must control HTN to prevent secondary injury
caused by increased ICP
• Effects of increases in intracranial pressure may be
varied.

BRAIN INJURY –
CEREBRAL HEMATOMAS
• Extravasation of blood produces a space-
occupying lesion on the brain and leads to
increased ICP
• Epidural & subdural
– Extraparenchymal (outside of brain tissue)
• Produce injury by pressure effect and displacement
of intracranial contents.

Epidural Hematoma
• A collection of blood between the inner table of the
skull & the outermost layer of the dura
• Most often associated with:
– Skull fractures
– Middle meningeal artery laceration

Epidural Hematoma
• Incidence relatively low
• Can occur as a result of low-impact injuries (falls)
or high-impact injuries (MVAs)
• Occurs from trauma to the skull & meninges rather
than from the acceleration-deceleration forces seen
in other types of head trauma

Epidural Hematoma (cont.)
• Clinical manifestations:
– Brief loss of consciousness followed by period of lucidity
– This lucid period is followed by a rapid deterioration in
LOC
– Dilated, fixed pupil on the same side as the impact area is
a hallmark of EDH
– May c/o severe, localized H/A & may be sleepy

Epidural Hematoma (cont.)
• Diagnosis:
– Based on clinical symptoms &
– evidence of a collection of epidural blood identified on
CT scan
• Treatment:
– Involves surgical intervention to remove the blood and to
cauterize the bleeding vessels

Subdural Hematoma
• The accumulation of blood between the dura and
underlying arachnoid membrane.
• Most often is related to a rupture in the bridging
veins between the brain and the dura.
• Acceleration-deceleration & rotational forces are
the major causes.
• Often associated with cerebral contusions &
intracerebral hemorrhage

Subdural Hematoma (cont.)
• Three types:
– Acute,
– subacute, and
– chronic
• Based on the time frame from injury to clinical
symptoms:

Subdural Hematoma - ACUTE
• Hematoma that occurs after a severe blow to the
head.
• Clinical presentation determined by
– the severity of injury to the underlying brain at the time
of impact &
– the rate of blood accumulation in the subdural space.

Subdural Hematoma – ACUTE
• Observe for deterioration in level of
consciousness or lateralizing signs,
– such as inequality of pupils or motor movements.
• Deterioration may be rapid
• Surgical intervention may include
– craniectomy,
– craniotomy, or
– burr hole evacuation

Subdural Hematoma -SUBACUTE
• Develop symptomatically 2 days to 2 weeks after
trauma.
• Expansion of the hematoma occurs at a rate slower
than that in acute SDH.
• Takes longer for symptoms to become obvious.
• Clinical deterioration with subacute SDH usually is
slower than that with acute SDH
• Surgical intervention, when appropriate, is the same

Subdural Hematoma – CHRONIC
• This term is used when symptoms appear days or
months after injury.
• Most patients usually are elderly or in late middle
age.
• Patients at risk include:
– Patients with coordination/balance disturbances,
– Elderly,
– Those receiving anticoagulation therapy

Subdural Hematoma –CHRONIC
• Clinical manifestations are insidious
• Patient may report a variety of symptoms:
– Lethargy, absent-mindedness, headache, vomiting, stiff
neck, and photophobia, and show signs of TIA, seizures,
pupillary changes, or hemiparesis
• Often not seen as initial diagnosis
• CT scan can confirm diagnosis of SDH

Subdural Hematoma – CHRONIC
• If surgical intervention required, evacuation of the
chronic SDH may occur by:
– Craniotomy, burr holes, or catheter drainage
• Outcome variable
• Return of neurologic status variable
• Recovery slow
• Recurrence frequent

Subarachnoid Hemorrhage (SAH)
• Described as bleeding into the subarachnoid space
• Usually caused by rupture of a cerebral aneurysm or
arteriovenous malformation (AVM).
• Accounts for 6% to 7% of all strokes
– Non-traumatic SAH affects more than 30,000 people in
US each year
– Incidence > in women & increases with age

Subarachnoid Hemorrhage
(cont.)
• Overall mortality rate is 25% with most patients
dying on first day after injury.
• Approximately 2 million people in the US are
believed to have an unruptured cerebral aneurysm,
the congenital anomaly responsible for most cases of
SAH.

Subarachnoid hemorrhage (cont.)
• Known risk factors include:
• **Hypertension,
• Smoking,
• Alcohol use, and
• Stimulant use

SAH – Patho
• Pathophysiology of two most common causes is
distinctly different:
– Cerebral Aneurysm
– Arteriovenous (AV)Malformation

SAH – CEREBRAL ANEURYSM
• As individual with a congenital cerebral aneurysm
matures,
– BP rises &
– more stress placed on vessel wall
• Saccular or berry-like & most occur at the
bifurcation of blood vessels

SAH – CEREBRAL ANEURYSM
• Vessel wall becomes thin & ruptures,
– Sending arterial blood at a high pressure into the
subarachnoid space.
• In other situations, the unruptured aneurysm
expands and
– places pressure on surrounding structures.

SAH – ARTERIOVENOUS
MALFORMATION
• Pathologic features related to the size & location of
the malformation.
• One or more cerebral arteries, known as “feeders”
feed an AVM
• Feeder arteries enlarge and increase the volume of
blood shunted through the malformation.
• Large, dilated, tortuous draining veins develop

SAH –ARTERIOVENOUS
MALFORMATION
• The enlarged veins rupture easily
• Cerebral atrophy is sometimes also present.
– It is the result of chronic ischemia because of the
shunting of blood through the AVM and away from
normal cerebral circulation

SAH – ASSESSMENT
• Characteristically has an abrupt onset of pain,
described as the “worst headache of my life.”
• Brief loss of consciousness, nausea, vomiting,
focal neurologic deficits, and a stiff neck may
accompany the headache.
• The SAH may result in coma or death.

SAH – ASSESSMENT
• May have “warning leaks” which go undetected.
• Symptoms of unruptured AVM may be found in the
history
– Headaches with dizziness or
– Syncope or
– Fleeting neurologic deficits

SAH - DIAGNOSIS
• Based on:
– Clinical presentation,
– CT scan,
• **Noncontrast CT is the cornerstone of definitive SAH
diagnosis
– Lumbar puncture

SAH – DIAGNOSIS (cont.)
• CT
– In 92% of cases, CT can demonstrate a clot in the
subarachnoid space, if performed within 24 hours of the
onset of the hemorrhage
• Lumbar puncture if initial CT negative
– CSF after SAH bloody in appearance with a RBC >
1000/mm3.

SAH – Cerebral Angiography
• Cerebral angiography necessary once SAH has been
documented
– To identify exact cause of the SAH
• If a cerebral aneurysm rupture is the cause,
– angiography essential for identifying exact location of
aneurysm in prep. for surgery.
• If AVM rupture the cause,
– angiography necessary to identify the feeding arteries &
draining veins

SAH – Medical Management
• Is a medical emergency!
• Preservation of neurologic function is the goal
• Initial treatment must always support vital
functions
• Early diagnosis is essential
• Ventriculostomy is performed to control ICP if
the patient’s LOC is depressed.

SAH – Medical Management
• Factors attributing to deaths:
• 19% - related to direct effects of the initial
hemorrhage
• 22% - rebleeding
• 23% - cerebral vasospasm
• 23% – non-neurologic medical complications

SAH – Re-bleeding
• The occurrence of a second SAH in an unsecured
aneurysm
• With conservative therapy, 20 – 30% likelihood of
re-bleeding in first month, with highest occurrence
on first day after initial bleed
• Mortality with aneurysmal re-bleeding is 48% to
78%

SAH – Rebleeding
CONS. MEASURES FOR PREV
• BP control:
– Maintain SBP no greater than 150 mm Hg
(individualized based on previous values):
– Nitroprusside, metoprolol, Hydralazine
– *Rebleeding more associated with variations in BP
• Prophylactic anticonvulsant therapy

SAH – Rebleeding –
Surgical Aneurysm Clipping
• Definitive treatment is surgical clipping
w/complete obliteration of aneurysm.
• Timing is key issue
• Usually within first 48 hours of rupture
• Eliminates risk of rebleeding
• Allows more aggressive therapy post-op
• Allows for flushing out excess blood & clots to
reduce risk of vasospasm

SAH – Rebleeding –
Surgical Aneurysm Clipping
• Classification of Subarachnoid Hemorrhage
• Early surgery recommended for patients with Grade
I or Grade II SAH & some patients with Grade III
• Careful consideration of patient’s clinical situation is
necessary in determining if candidate for surgery &
optimal time

SAH - Rebleeding
• Surgical procedure involves a craniotomy
• Requires skill of an experienced neurosurgeon
• Complications

SAH – Rebleeding
Surgical AVM Excision
• Decision for surgical excision depends on the
location & size of the AVM
• Surgical excision of large AVMs includes risk of
reperfusion bleeding
• Postop – low BP maintained to prevent further
reperfusion bleeding
• In large AVMs, 2 – 4 stages of surgery may be
required over 6 to 12 months

SAH – Rebleeding Embolization
• Used to secure a cerebral aneurysm or AVM that is
surgically inaccessible because of size, location, or
medical instability of the patient.
• Several techniques available – All use a
percutaneous transfemoral approach in a manner
similar to an angiogram

SAH – Rebleeding
Pharmacologic Therapy
• In the Past,
– antifibrinolytic agents were suggested (aminocaproic
acid)
• TODAY,
– Antifibrinolytic agents are NOT recommended for
routine use in SAH

SAH –
CEREBRAL VASOSPASM
• Presence or absence of cerebral vasospasm
significantly affects the outcome of aneurysmal
SAH
• Estimated that 50% of all SAH patients develop
vasospasm
– 32% resulting in symptomatic vasospasm &
– 15% - 20% result in ischemic stroke or death

SAH –
CEREBRAL VASOSPASM
• Onset usually 3 – 5 days after initial bleed & can
last for 3 to 4 weeks.
• Treatment:
– Induced hypertensive, hypervolemic, hemodilution
therapy
– Oral nimodipine; and
– Transluminal cerebral angioplasty

TRANSIENT ISCHEMIC
ATTACKS (TIA)
• Sudden, brief episodes of neurologic
dysfunction caused by temporary, focal
cerebral ischemia
• Lasts less than 24 hours, often as little as 5
– 20 minutes
• Warning sign of impending CVA

• Carotid artery occlusion: weakness or
numbness in an arm or leg, aphasia, and
visual field cuts
• Vertebrobasilar circulation: vertigo,
diplopia, dysphagia, dysarthria, and ataxia

DIAGNOSIS
• Carotid bruit
• CT
• Doppler
• Cerebral angiogram
• ECG (looking for A fib if site of emboli
formation
• TEE (looking for site of emboli formation)

TREATMENT
• Antihypertensives
• Antiplatelet drugs
• Surgery

CEREBROVASCULAR ACCIDENT
(CVA OR STROKE)
• Neurological deficits occur as a result of
decreased blood flow to a localized area of the
brain.
• Risk factors:
– Hypertension
– Diabetes Mellitus
– CV disease, a-fib
– Hyperlipidemia
– Cigarette smoking, alcohol consumption, cocaine use
– Obesity

ISCHEMIC CVA
• Occurs when blood supply to a part of the
brain is interrupted or occluded. Causes:
– Spasm: caused by irritation
– Thrombosis: platelets adhere to irregular
plaque surfaces
– Embolism: traveling clot which becomes
lodged in a narrow lumen

HEMORRHAGIC CVA
• Occurs in only 10 % of cases, usually
women
• Results from rupture of a cerebral blood
vessel that results in bleeding into the brain
tissue or the subarachnoid space

• H/A
• Vomiting
• Seizures
• AMS
• Fever
• ECG changes
• Manifestations related to area of injury

• Motor deficits:
– Hemiplegia
– Hemiparesis
– Flaccidity
– Spasticity
– Rigidity
– Dysphagia
• Elimination disorders
– Bowel
– bladder

• Sensory perceptual deficits
– Hemianopia
– Agnosia
– Apraxia
• Language disorders
– Aphasia
– Dysarthria
• Cognitive and behavioral changes
• Intellectual: memory and judgment changes

• Right sided CVA
– Impulsive
– Over estimate their abilities
– Have decreased attention span
– Left sided weakness

• Left sided CVA
– Slow, cautious, and disorganized
– Right sided weakness
• Spatial perceptual defects: denial of illness
or non functioning body parts; erroneous
perception of self; agnosia; apraxia

DIAGNOSIS
• CT
• MRI
• Doppler ultrasound
• Cerebral angiogram
• Lumbar puncture if not contraindicated

TREATMENT
• Acute phase (first 12 – 72 hours):
– If not hemorrhagic: anticoagulant
– Thrombolytics, if not hemorrhagic
– Calcium channel blockers
– Hyperosmolar solutions
– Diuretics
– Anticonvulsants
– Decadron
– Antipyretics

NURSING DIAGNOSIS
• ALTERED CEREBRAL TISSUE PERFUSION
– Monitor respiratory and airway patency
• Suction only as needed
• Lateral low Fowler’s position ( HOB 30 to 
cerebral edema, head in neutral position –
improves venous drainage)
• If risk for hemorrhage or IICP, no coughing, deep
breathing
• If no risk of hemorrhage, cough and deep breathe
• Oxygen as ordered

• Monitor Neurologic Status
– LOC
– Pupilary response
– Movement, strength of extremities
– Babinski
– Decorticate/decerebrate posturing
– Changes in LOC

• Monitor CV status
– Assess for fluid overload (rales, SOB, dyspnea)
– Fluid restriction (if CO is low, increase fluid
based on ADH and aldosterone levels)
– Prevent thrombosis of lower extremities (ROM,
antiembolic hose, pneumatic compression
sleeves
• Monitor Neuro status
– Monitor temp (risk for hyperthermia
– Monitor for seizures (place on precautions)

• Impaired mobility:
– Prevent contractures
• Passive/active ROM
• TQ2H
• Prone position 15 – 30 minutes several times
daily
• Monitor for thrombophlebitis
• Self Care deficit
– Encourage use of unaffected side
– Teach to dress affected side first

• Sensory perceptual
– Keep environment clutter free
– Well lighted environment
– Bed in low position
– Wheels locked
– Side rails up
– Keep needed objects of the unaffected side

• Elimination
Bladder
– Offer bedpan/urinal every 2 hours
– Encourage bladder training
– Teach Kegel exercises
– Use positive reinforcement
Bowel
– Encourage fluids (2000 cc/day unless CI)
– High fiber diet
– Stool softeners
– Establish bowel evacuation routine

• Swallowing
– Sit upright when eating and for 30 minutes after
– Make sure neck is slightly flexed
– Pureed or soft diet initially
– Place food/drink on unaffected side
– When finished eating, assess mouth for absence
of food
– Maintain suction at bedside
– Minimize distractions so they can concentrate

PROGNOSIS
• Assessment
– Neurologic
– Urinary
– Orthopedic
– Bowel

Acute Spinal Cord Injury
• Diagnosis begins with:
– a detailed history of events surrounding incident,
– precise evaluation of sensory & motor function, &
– radiographic studies of the spine
• Majority occurs in males between 16 & 30

Mechanism of injury
• Hyperflexion
• Hyperextension
• Rotation
• Axial loading
• Penetrating injuries

Mechanism of injury
• Hyperflexion
– Most often seen cervical area at level of C5 to C6.
– Sudden deceleration motions
• Hyperextension
– Involve backward & downward motion of the head
– Often seen in rear-end collisions or diving accidents

Mechanism of Injury
• Rotation
• Often occur in conjunction with a flexion or
extension injury
• Axial loading
– Vertical compression
– Falls & lands on feet
• Penetrating injuries
– Bullet, knife, etc.
– Cause permanent damage by anatomical transection

SCI – Patho
• Result of a mechanical force that disrupts
neurologic tissue or its vascular supply or both.
• Injury process includes both primary & secondary
injury mechanism

SCI – Patho
• Primary injury
– The neurologic damage that occurs at moment of impact
• Secondary Injury
– The complex biochemical processes affecting cellular
function
– Can occur within minutes of injury and can last for days
to weeks

SCI – Patho
• Several events after a spinal cord injury lead to
spinal cord ischemia & loss of neurologic function
• Leads to:
– Ischemia,
– elevated intracellular calcium
– Inflammatory changes
• Current research focused on inhibiting secondary
processes & preserving functional neurons.

SCI
• Functional Injury of the spinal Cord
– The degree of disruption of normal spinal cord function
– Depends on what specific sensory & motor structures
within the cord are damaged
• Classified as:
– Complete or Incomplete

SCI
• Complete Injury
– Results in a total loss of sensory & motor function
below the level of injury
• Incomplete Injury
– Results in a mixed loss of voluntary motor activity &
sensation below the level of the lesion

SCI - Complete Injury
• Quadriplegia
– Injury occurs from the C1 to T1 level
– Also known as Tetraplegia
• Paraplegia
– Injury occurs in the thoracolumbar region (T2 to L1)
– May have full use of arms

SCI – Incomplete Injury
• Brown-Sequard Syndrome
– Damage to one side of the cord
– Loss of voluntary motor movement on same side as
injury, with loss of pain, temperature & sensation on
opposite side
• Central Cord Syndrome
– Motor & sensory deficit more pronounced in upper
extremities than in lower.

SCI – Incomplete Injury
• Anterior Cord Syndrome
– Loss of motor function, as well as loss of sensations of
pain & temperature below level of injury
– Below injury, position sense & sensations of pressure &
vibrations remain intact.
• Posterior cord Syndrome
– Loss of position sense, pressure & vibration below the
level of the injury.
– Motor function & sensation of pain & temperature
remain intact

Spinal Shock
• The complete loss of all normal reflex activity
below the level of injury.
• Manifestations include:
– Bradycardia & hypotension
• Intensity is influenced by level of injury &
• duration of this shock state can persist for up to 1
month after surgery
• *Be careful with positioning

Assessment for SCI
• Airway
• Breathing
• Circulation
• Neurologic
• Diagnostic Procedures

AUTONOMIC DYSREFLEXIA
• A life threatening complication that may occur
with SCI.
• Caused by a massive sympathetic response to a
noxious stimuli such as:
– Full bladder, line insertions, fecal impaction
• Results in:
– Bradycardia, hypertension, facial flushing, and
headache

• Treatment aimed at alleviating noxious stimuli
• If symptoms persist, anti-hypertensive agents can
be administered to reduce blood pressure
• Prevention is imperative and can be accomplished
through use of a good B & B program

• Clinical algorithm for treatment of autonomic
dysreflexia
– Positioning
– Constrictive devices
– Look for cause
– BP
– Catheter/Bowel

Medical Management
• Primary treatment is to preserve remaining
neurologic function
• Interventions Divided into:
– Pharmacologic
– Surgical
– nonsurgical

Medical Management
• Pharmacologic Management
• Methylprednisolone
– Bolus followed by continuous infusion for at least 24
hrs & preferably 48 hrs.
• Prevents post-traumatic spinal cord ischemia
• Improves energy metabolism
• Restores extracellular calcium
• Improves nerve impulse conduction

Surgical Management
• Laminectomy
• Spinal fusion
• Rodding

Non-surgical Management
• Cervical Injury
– Gardner-Wells and Crutchfield tongs
– Halo Vest
• Thoracolumbar

Nursing Management
• CV
• Astute assessment of fluid volume
• Inotropic or vasopressor support
• Hypotension/hypertension
• Bradycardia
• DVT
• Loss of thermoregulation (poikilothermy)

Nursing Management
• Pulmonary complications are most common cause
of mortality
• Observe rate, rhythm, pattern
• ABGs
• Watch for paralysis/weakness of respiratory muscles
• airway

Nursing management
• Musculosketal
– ROM, PT, OT
– Splints
• Integumentary
• Elimination

Rehabilitation & Maximizing
Psychosocial Adaptation
• Provide dedicated emotional support
• “four D syndrome”
– Dependency, depression, drug addiction, and, if married,
divorce.
• Further support given by:
– Social workers, occupational therapists, psychiatric
clinical nurse specialists, pastors, physical therapists,
long-term rehab, support groups.

Disc Herniation
• An intervertebral disc is a pad composed of three
parts that rests between the centers of two
adjacent vertebrae.
• Discs provide cushions for spinal movement.
• Strenuous activity or degeneration of the disc or
vertebrae can allow the disc to move from its
normal location.

Disc Herniation –(cont.)
• Displacement of intervertebral disc material may
be referred to as:
– Prolapse,
– herniation,
– rupture, or
– extrusion

Disc Herniation (cont.)
• Ruptured intervertebral discs may occur at any
level of the spine.
• Lumbar discs are more likely to rupture than
cervical discs because of the:
– Force of gravity;
– continual movement in this region; and
– improper movements of the spine, as with lifting or
turning

Description
• Thoracic disc disorders are the least common
• More than half of patients give a hx of a previous
back injury.
• Heavy physical labor, strenuous exercise, & weak
abdominal and back muscles increase risk
• Repeated stress progressively weakens the disc,
resulting in bulging and herniation

Clinical Manifestations
• Lower back pain that radiates down the sciatic nerve
into the posterior thigh.
• Typically begins in the buttocks & extends down the
back of the thigh and leg to the ankle.
• Can also lead to groin pain
• Muscle spasms & hyperesthesia (numbness &
tingling) in areas of distribution of affected nerve
roots

Clinical Manifestations (cont.)
• Pain exacerbated by
– straining (coughing, sneezing, defecation, bending,
lifting, & straight-leg raising) or
– prolonged sitting &
• Is relieved by
– side-lying with the knees flexed.

Clinical Manifestations (cont.)
• Any movement of lower extremities that stretches
the nerve causes pain & involuntary resistance
• Straight-leg raising on the affected side is limited
• Complete extension of the leg is not possible when
the thigh is flexed on the abdomen.
• May have depression of deep tendon reflexes

Diagnostic Findings
• X-Ray Studies
– May show spinal degenerative changes
– Usually do not show a ruptured disc
• Magnetic resonance imaging (MRI)
– May show extrusion of disc material into the spinal
canal and impingement of a spinal nerve root

Diagnostic Findings
• Discography
– Injection of a water-soluble imaging material into the
nucleus pulposus
– Used to determine internal changes in the disc.
• Electromyography of the peripheral nerves
– To localize the site of the ruptured disc

Outcome Management
• Goals include:
– Reducing pain & spasms
– Improving mobility
– Repairing any structural problems in the spine or discs

Control Pain & Spasms
• Pain usually managed with
– Non-steroidal anti-inflammatory drugs (NSAIDS),
– muscle relaxants, and at times,
– narcotics
– Ice may be used for the first 48 hrs
– After that heat may be used

Control Pain & Spasms- Positioning
• Semi-sitting position (in a recliner chair)
– More comfortable, reduces back strain
– promotes forward lumbar spine flexion
• Supine with pillows under the legs
• Lateral with thin pillow between knees with
painful leg flexed
• AVOID:
– prone position
– sleeping w/thick pillows under the head

Control Pain & Spasms
• Physical Therapists
– may be able to relieve pain & spasm with stretching
exercises & ultrasonic heat treatments
• Spinal manipulation
– Use of the hands on the spine to stretch, mobilize, or
manipulate the spine
• Work space or equipment modifications may be
necessary
• Progressive muscle relaxation exercises
• For severe lumbar disc problems with leg pain
– 2 to 4 days of bed rest on a firm mattress

Improve Mobility
• Most clients do not require bed rest
– > 4 days of BR can be debilitating & slow recovery
• Client taught use of proper body mechanics
• If have to sit, should change positions often
• Aerobic activities prescribed to help avoid
debilitation
• Walking, stationary bicycling, & back strengthening
– Begin within first 2 weeks after injury (perform for 20 to
30 minutes, 2 or 3 times per week)

Improve Mobility
• Work activities individualized
• Back brace or corset may be prescribed
– Usually not recommended once clinical manifestations
are relieved
• Exercise to strengthen the back and abdominal
muscles
– helps prevent further problems if the exercises are done
daily throughout life

Surgical Management
• Surgery indicated in clients with spinal disc
problems when
– Sciatica is severe & disabling
– Manifestations of sciatica persist without improvement or
worsen, and
– Physiologic evidence of specific nerve root dysfunction
• Also used to stabilize spinal fractures

Surgical Management (cont.)
• Chemonucleolysis
– Chymopapain - a proteolytic enzyme isolated from
papaya latex - is used as a meat tenderizer.
– Injected into the disc, it digests the protein in the disc &
shrinks it.
– Contraindicated in people with multiple allergies & in
people allergic to papaya.
– Immediate & delayed (after 15 days) allergic responses
– Use abandoned by most practitioners

Percutaneous Disectomy
• Herniated disc material can be excised with a
trocar to remove the center of the disc.
• The laser also is used to destroy the damaged
disc.

Microdisectomy
• The use of microsurgical instruments to remove the
herniated fragment of disc.
• Results in less trauma to the surgical site compared
with stand surgery & more tissue integrity is
preserved.

Decompressive Laminectomy
• Term laminectomy is confusing & is used loosely.
• Laminectomy
– Describes complete removal of the bone between the
spinous process & the facet;
– This is seldom necessary.
• Laminotomy
– More correct term for what is usually done
– Describes the creation of a hole in the lamina.

Decompressive Laminectomy (cont.)
• Surgical removal of the posterior arch, of a
vertebra, exposing the spinal cord.
• This procedure gives access to the spinal canal for
– Removing a spinal cord tumor
– Removing portions of the facets
– Decompressing bone infringement on the spinal cord

Decompressive Laminectomy (cont.)
• Foraminotomy
– Sometimes is performed to enlarge the intervertebral
foramen if it is narrowed & osteophytic processes
(overgrowth of bone) entrap the nerve root & impinge on
neural structures

Spinal Fusion/Arthrodesis
• Spinal fusion
– Describes the placement of bone grafts (bone chips)
between vertebrae
– New bone that grows fuses the two vertebrae &
immobilizes them to reduce the pain.
– Usually no more than 5 vertebrae are fused
• Fusing more than five vertebrae causes considerable loss of
movement in the spine

Spinal Fusion/Arthrodesis (cont.)
• Bone graft may be obtained from a bone bank or the
anterior-superior iliac crest.
• During healing, the graft gradually grows into the
vertebrae & forms a bone union
• This bone union causes permanent stiffness in the
area.

Spinal Fusion/Arthrodesis
• Lumbar Fusion
– Stiffness hardly noticed in the lumbar area after a while
• Cervical Fusion
– Stiffness usually noticeable in the cervical area
• The client cannot be guaranteed that back pain will
be relieved permanently or that further surgery will
not be required.

Spinal Fusion with Instrumentation
• Metal rods may be used to straighten & fuse the
spine in disorders such as scoliosis or multiple
vertebral fractures.
• Other devices also can be used to provide
additional support while the bones heal in a fused
manner

Complications
• General potential complications after spinal disc
surgery at any level include:
– Infection and inflammation,
– injury to nerve roots,
– dural tears, and
– hematoma

Complications (cont.)
• Non-union of the surgical area also is a risk
– Is associated with smoking
• Some surgeons assess serum nicotine levels prior to surgery to
reduce risk of non-union &
• validate statements of smoking cessation

Prognosis
• Patients with severe and disabling leg pain:
– Lumbar disectomy often relieves manifestations of pain
faster than continued medical management
• Patients w/o leg pain,
– little difference in medical vs surgical relief of
symptoms
• Client preference plays a big role in the technique
chosen

Preoperative Nursing Care
• Explain post op limitations, positioning, etc.
• If fusion is to be done:
– Encourage clients who smoke to stop.
– Clients need to be evaluated for autologeous blood
donation.
• 2 – 3 units should be donated, the last one at least 1 week
before the surgery
– Inform client of bone graft site & the additional pain
associated it.

Post Op
• Assess:
– Dressings, drains
– Level of pain & response to analgesia
– Neurologic function – compare to baseline

Post Op
• BR for post fusion -Risk for DVT
– Compression devices
– Observe for & report S/S
• Assess Wound Site:
– Bulging or clear drainage
• May indicate cerebrospinal fluid leakage
– Anterior approach
• Usual care for abdominal surgery is required

Positioning
• After lumbar fusion
– Bed is generally kept flat
• Log-rolling
– Usually beginning about 4 hrs after surgery, then q 2 –
4 hrs thereafter
– Ensure safety
– Common to have spasms & pain w/turning
• Analgesics & anti-spasmodics

Post–Op – Urinary Retention
• Common after spinal surgery –
– because of pain & spasms &
– as a side effect of narcotics.
• Assess for retention –
– Cath prn as ordered

Post Op – Paralytic Ileus
• Most common bowel problem after laminectomy & spinal
fusion
– Due to lack of peristalsis from a sudden loss of parasympathetic
function innervating the bowels &
– manipulation of the intestines in anterior approaches
• Assessment findings
– N & V,
– hard abdomen,
– absence of bowel sounds

Paralytic Ileus - Intervention
• NGT to low intermittent suction
• NPO
• Assess at least q 4 hrs

HERNIATION SYNDROMES
• **TO PREVENT HERNIATION:
– The goal of neurologic evaluation, ICP monitoring, and
treatment of increased ICP

Herniation Syndromes
• Herniation results in shifting of tissue
• Places pressure on cerebral vessels & vital function
centers of the brain.
• If unchecked, herniation rapidly causes death as a
result of the cessation of cerebral blood flow &
respirations

HERNIATION SYNDROMES –
(cont.)
• Supratentorial Herniation
– Uncal
– Central, or Transtentorial
– Cingulate
– Transcalvarial
• Infratentorial Herniation
– Upward transtentorial herniation
– Downward cerebellar herniation

Herniation Syndromes –
UNCAL
• Most often noted herniation syndrome
• Unilateral, expanding mass, usually of the
temporal lobe, increases ICP, causing lateral
displacement of the tip of the temporal lobe.
• Clinical S/S:
– Ipsilateral pupil dilation, decreased LOC, respiratory
pattern changes/arrest, contralateral hemiplegia
(decorticate/decerebrate)

Herniation Syndromes -
CENTRAL
• Often preceded by uncal and cingulate herniation
• Expanding mass lesion of the midline, frontal,
parietal, or occipital lobes
• S/S
– Similar to Uncal in late stages

CINGULATE
• Occurs often
• Not in itself life-threatening, but if the expanding
mass lesion is not controlled, uncal or central
herniation will follow.

Transcalvarial
• The extrusion of cerebral tissue through the
cranium
• In the presence of severe cerebral edema,
transcalvarial herniation occurs through an opening
from a skull fx or craniotomy site

Upward Transtentorial Herniation
• Deterioration progresses rapidly
• Compression of 3rd cranial nerve & diencephalon
occurs
• Blockage of central aqueduct
• Distortion of 3rd ventricle obstruct CSF flow

Downward Cerebellar Herniation
• Compression & displacement of the medulla
oblongata occur
• Rapidly results in respiratory & cardiac arrest

AMYOTROPHIC LATERAL
SCLEROSIS (ALS)
• Also known as Lou Gehrig’s Disease
• A progressive degenerative neurologic disease
characterized by weakness and wasting of the
involved muscles, without any accompanying
sensory or cognitive changes.
• Unknown cause
• Affects men more than women, usually between
the ages of 40 – 60.

• Musculoskeletal:
– weakness and fatigue
– “heaviness” of the legs
– fasciculations (focal muscle twitching)
– Uncoordinated movements
– Loss of motor control in the hands
– Spasticity
– Paresis

– Hyperreflexia
– Atrophy
– Problems with articulation
• Respiratory
– Dyspnea
– Difficulty clearing the airway
• Nutrition
– Difficulty chewing
– Dysphagia

• Emotion
– Loss of control, liability
• Cognitive
– Intellect is not affected
– Remains alert and mentally intact throughout
the course of the disease
• Death is usually resultant from pneumonia
• Diagnosis is made with an EMG

TREATMENT
• Supportive
• Riluzole (Rilutek): drug which extends the
life by a few months
• Respiratory compromise usually results
within 2 – 5 years of diagnosis

INTERVENTIONS
• Mobility
– ROM
– Stretching exercises
– Splints
– Ankle boots
– Wheelchair
– Frequent rest periods to decrease fatigue

• Nutrition
– Suction at bedside
– Rest before meals
– Upright to eat and 30 minutes after
– Semisolid food
– Frequent meals
– Soft cervical collar to keep head upright
– Enteral feedings
– Syringe with short, small bore tubing (placed
on anterior aspect of tongue, used for giving
liquids)

• Breathing
– Mechanical ventilation as necessary
– Elevate HOB
– TQ2H
– Oxygen
– Breathing exercises
– Incentive spirometry
– Suctioning as needed

• Communication
– Speech therapy
– Hand held computers
– Pointer held with teeth and use of a picture
board
– Word charts
– Eye blinks

MULTIPLE SCLEROSIS
• Chronic, progressive disorder of the CNS.
• Weakness
• Remission
• Progression
• Glial scar tissue (hard, sclerotic plaque)
• Loss of function

• musculoskeletal
– Fatigue (most common and often most disabling)
– Limb weakness ( loss of muscle strength)
– Ataxia
– Intention tremors
– Spasticity
– Muscular atrophy
– Dragging of the foot
– Foot drop

• Urinary
– Hesitancy
– Frequency
– Retention
– Recurrent UTI’s
– Incontinence

• Gastrointestinal
– Difficulty chewing
– Dysphagia
– Diminished or absent sphincter control
– Bowel incontinence
– Constipation
• Respiratory
– Diminished cough reflex
– Respiratory infections

• Sensory
– Blurred vision
– Optic neuritis
– Diplopia
– Nystagmus
– Eye pain
– Visual field defects
– Vertigo/ loss of balance and coordination
– Nausea
– Numbness
– Parasthesias (numbness or tingling)
– Diminished sense of temperature/ desensitized touch
sensation

• Neurologic
– Emotional lability/ mood changes/ depression
– Forgetfulness
– Apathy
– Irritability
– Impaired judgment
– Dysarthria (speech problems)
• Diagnosis
– History
– CSF evaluation
– MRI
– Optic/Auditory testing (shows slowed nerve
conduction)

TREATMENT
• Corticosteroids
• Interferon
• Plasmapheresis
• Surgery
• Diet therapy

INTERVENTIONS
• Respiratory
– CDB Q 2 – 4 H
– Elevate HOB 90o to eat
• Immobility
– PT for walking and hydrotherapy
• Gastrointestinal
– Stool softeners
– Encourage activity
– Maintain fluid intake

• Skin
– Assess every shift
– TQ2H
– Keep linen clean and dry
– Massage around bony prominences
• Vision
– Assess acuity
– SR elevated, bed in low position, wheels locked
– Eye patch with diplopia

• Urinary
– Administer appropriate meds
– Intermittent catheterization
– Assess for infection
– Increase fluids to 3000 cc/day if allowed
• Teaching
– Factors which cause exacerbation
• Hyperthermia
• Stress
• Infection
• pregnancy

MUSCULAR DYSTROPHY
• A group of genetic disorders involving gradual
degeneration of muscle fibers
• Progressive weakness and skeletal muscle
wasting, accompanied by disability and
deformity
• Types:
1. Pseudohypertrophic MD (Duchene MD)
2. Facioscapulohumeral MD (Landouzy-
Dejerine)

• Evidence of muscle weakness usually
appears at 3-4 yrs
• May have history of delayed motor
development, especially walking
• First symptom may be : difficulties in
running, riding a bike
• Develop characteristic rising from squatting
or sitting position on floor (Gower’s sign)

TREATMENT
• Supportive measures
– Physical therapy
– Orthopedic procedures
– Use of braces for spine and lower extremities
– Breathing exercises

MYASTHENIA GRAVIS
• A chronic, progressive autoimmune disease
characterized by fatigue and severe muscle
weakness of the skeletal muscles, that
worsens with exercise and improves with
rest
• Manifestations result from a loss of Ach
receptors in the postsynaptic neurons of the
neuromuscular junction

• Primary feature: increasing weakness with
sustained muscle contraction
• Ptosis (drooping of upper eyelid)
• Diplopia (double vision)
• Facial weakness (snarls when smiling)
• Dysphagia
• dysarthria

• Weakness and fatigue
• Decreased function of hands, arms, legs,
and neck muscles
• Weakening of intercostals
• Decreased diaphragmatic movement
• Breathlessness and dyspnea
• Poor gas exchange
• Inability to chew and swallow
• Decreased ability to move tongue

DIAGNOSIS
• Based on clinical presentation and response
to anticholinesterase drugs
• TENSILON TEST

TREATMENT
• Anticholinesterase drugs
– Pyridostigmine (mestinon)
– Neostigmine (Prostigmine)
• Immunosuppressive therapy
(corticosteroids)
• Plasmaphoresis
• Thymectomy

COMPLICATIONS
• Myasthenic crisis: caused by
undermedication
– Sudden marked rise in B/P due to hypoxia
– Increased heart rate
– Severe respiratory distress and cyanosis
– Absent cough and swallow reflex
– Increased secretions, increased diaphoresis,
increased lacrimation
– Restlessness, dysarthria
– Bowel and bladder incontinence

• Cholinergic Crisis: caused by excessive
medication
– Weakness with difficulty swallowing, chewing,
speaking and breathing
– Apprehension
– N/V/D/abdominal cramps
– Increased secretions and saliva
– Sweating, lacrimation, fasciculations, and
blurred vision

NURSING CARE
• Airway management
• Suction at bedside
• ABGs
• Endotracheal intubation if ventilatory support is
needed
• Administer edrophonium chloride (Tensilon) to
determine type of crisis
• Monitor electrolytes, I&O, daily weight
• Tube feeding if unable to eat

CEREBRAL PALSY
• Impaired muscular control due to abnormality in
the brain resulting in abnormal muscle tone and
coordination. Physical signs:
– Poor head control after 3 months
– Stiff or rigid arms or legs
– Pushing away or arching back
– Floppy or limp body posture
– Cannot sit up without support by 8 months
– Use of only one side of body, or only the arms to
crawl
– Clenched fists after 3 months

BEHAVIORAL SIGNS
• Extreme irritability or crying
• Failure to smile by 3 months
• Feeding difficulties
– Persistent gagging or choking when fed
– After 6 months of age, persistent tongue
thrusting

• Delayed gross motor movement (universal
manifestation)
• Abnormal motor performance
• Altered muscle tone
• Abnormal posture
• Abnormal reflexes
• Associated disabilities and problems

INTERVENTIONS
• Mobilizing devices
• Surgery
• Speech therapy
• Dental care
• Hearing aids
• Physical therapy

PARKINSON’S DISEASE
• Progressive, degenerative disease
characterized by disability from tremor and
rigidity
– Depletion of dopamine

CARDINAL FEATURES
• Tremor at rest
• Rigidity
• Bradykinesia (slow movement)
• Flexed posture of neck, trunk, and limbs
• Loss of postural reflexes
• Freezing movement

OTHER CLINICAL
MANIFESTATIONS
• Skin problems
• Heat intolerance
• Postural hypotension
• Constipation
• Dementia
• Anxiety
• Depression

TREATMENT
• Dopaminergics
– Levodopa
– Carbidopa-levodopa (Sinemet)
• Anticholinergics
– Trihexphenidyl (Artane)
– Benztropine (Cogentin)
• Dopamine Agonists
– Bromocriptine (Parlodel
– Pergolide (Permax)

• Surgery:
– Pallidotomy
– Sterotaxic thalamotomy
– Autologous adrenal medullary transplant
(doesn’t work well)
– Fetal tissue transplant (better results)

INTERVENTIONS
• Mobility
– ROM
– PT (individualized)
– Ambulate qid
– Assistive devices
– Provide for safety

• Communication
– Allow time to speak
– Encourage deep breathing before speaking
– Speech therapy
– Alternative methods of communication
• Sleep
– Quiet environment
– Position of comfort
– ROM to decrease rigidity
– Stay awake during day
(meds may interrupt normal sleep cycle)

• Nutrition
– Calorie count/weekly weight
– Assess swallowing ability
– Soft, solid food appropriate for the individual
– Massage facial and neck muscles before eating
– Sit upright for feeding and 30 minutes after
– Suction at bedside
– Adequate roughage/fiber
– Small, frequent meals

• Elimination
– Drink 3000 cc/day if possible
– Increased fiber
– Increase mobility to stimulate peristalsis
– Stool softeners/suppositories
• Self care:
– Encourage independence but set time limits
– Keep items in reach
– Give a time frame to allow the patient to do
their own care

Bell’s Palsy –Patho & Etiology
• Affects motor aspects of the facial nerve, (7th
cranial nerve).
• Most common type of peripheral facial paralysis.
• Affects women & men in all age groups
• Most common between ages 20 & 40 yrs.
• Results in a unilateral paralysis of the facial
muscles of expression.

Bell’s Palsy –Patho & etiology
• No evidence of a pathologic cause.
• Facial paralysis central or peripheral in origin.
• Central facial palsy is an upper motor neuron
paralysis or paresis.
– Client cannot voluntarily show teeth on paralyzed side
but can show them with emotional stimulation.
• Called voluntary emotional dissociation

Bell’s Palsy –
• Typical findings on affected side include:
– Upward movement of the eyeball on closing the eye
(Bell’s phenomenon)
– Drooping of the mouth
– Flattening of the nasolabial fold
– Widening of the palpebral fissure
– Slight lag in closing the eye
• Eating may be difficult

Bell’s Palsy –
Outcome Management
• No known cure.
• Palliative measures include:
– Analgesics if discomfort occurs from herpetic lesions
– Corticosteroids to decrease nerve tissue edema
– Physiotherapy, moist heat, gentle massage, &
stimulation of the facial nerve
– Corneal protection w/artificial tears, sunglasses, eye
patch

Neurological Clinical Assessment
• History
• Physical examination components
– Level of consciousness (LOC)
– Motor function
– Pupillary function & eye movement
– Respiratory patterns
– Vital signs

Bell’s Palsy – Recovery/Prognosis
• Clients experiencing Bell’s Palsy often think they
have had a stroke.
– Reassure client
• Prognosis
– Most clients recover within a few weeks w/o residual
manifestations.
• If permanent facial paralysis occurs, surgery may
be necessary.
– Anastomosis of the peripheral end of the facial nerve
with the spinal accessory or hypoglossal nerve may
allow closure of the eye & restore tone to face

Trigeminal Neuralgia
• Chronic irritation of the fifth cranial nerve
• Trigeminal nerve has 3 division & neuralgia may
occur in any one or more of these divisions
– Opthalmic,
– maxillary, &
– mandibular

Trigeminal Neuralgia – Etiology
• Causes can be intrinsic or extrinsic lesions within
the nerve itself
– Ex: multiple sclerosis
• Extrinsic lesions are outside the trigeminal root &
include mechanical compression by
– Tumors, vascular anomalies, dental abscesses, or jaw
malformation

Trigeminal Neuralgia –
• Characterized by intermittent episodes of intense
pain of sudden onset.
• Pain is rarely relieved by analgesics
• Tactile stimulation, such as touch & facial hygiene,
& talking may trigger an attack
• More prevalent in the maxillary and mandibular
distributions & on the right side of the face.
• Bilateral trigeminal neuralgia is rare

Trigeminal Neuralgia –Diagnosis
• None of the current diagnostic studies identify
trigeminal neuralgia
• CT scan, MRI, & angiography can identify a
causative lesion.
• Diagnosis made on basis of in-depth history,
w/attention paid to triggering stimuli & nature &
site of the pain.

Nursing Considerations
• Careful history is obtained regarding triggering
stimuli
• Dental hygiene & nutritional intake are evaluated

Trigeminal Neuralgia–Outcome Mgt
• Anticonvulsant agents often prescribed as initial treatment
– Carbamazepine (Tegretol)
– phenytoin
• These drugs may dampen the reactivity of the neurons
within the trigeminal nerve
• For some clients, these medications are all the treatment that
is needed
• Monitor liver enzymes before & during therapy
• Use caution if hx of alcohol abuse

• Baclofen (Lioresal)
– An antispasmodic that may be used alone or in
conjunction with anticonvulsants.
• Narcotics are not particularly effective
• Help client use & improve any pain control strategy
they have developed.
• Provide emotional support

• Surgery includes
– Nerve blocks with alcohol & glycerol
– Peripheral neurectomy &
– Percutaneous radio-frequency wave forms
• Relief obtained not always permanent
• 0ften better tolerated by elderly or debilitated clients
– Therefore, present later with symptoms

Outcome Mgt
• More invasive techniques involve major surgical
procedures (craniotomy):
• Microvascular decompression
– Removing the vessel from the posterior trigeminal root
• Rhizotomy
– Actual resection of the root of the nerve

TN – Outcome Mgt –
Surgical Complications
• Same as with any surgical procedure
• Facial weakness & paresthesias
• If facial anesthesia present after surgery
– Test food before placing in mouth
– Assess for aspiration & advance diet slowly
– Water jet device instead of toothbrush
– Visit dentist soon
• If corneal reflex impaired
– Eye care

Guillian-Barre’ Syndrome (GBS)
• Once thought to be single entity characterized by
inflammatory peripheral neuropathy
• Now understood to be a combination of clinical
features with varying forms of presentation &
multiple pathologic processes.

GBS (cont.)
• Most cases do not require admission to CCU
• Prototype of GBS, known as acute inflammatory
demyelinating polyradiculoneuropathy (AIDP)
involves rapidly progressive, ascending peripheral
nerve dysfunction leading to paralysis & maybe
respiratory failure

GBS (AIDP)
• Because of the need for ventilatory support, AIDP is
one of the few peripheral neurologic diseases that
necessitate a critical care environment.
• Annual incidence of GBS is 1.6 – 1.9 per 100,000
persons.
• Occurs more often in males
• Most commonly acquired demyelinating neuropathy.
• Clusters of cases reported following 1977 swine flu
vaccinations

GBS - Etiology
• Precise cause unknown
• Syndrome involves an immune-mediated response
• Most patients report a viral infection 1 to 3 weeks
before the onset of clinical manifestations, usually
involving upper respiratory tract.

GBS - Etiology
• Numerous triggering events include:
– Viral infections
– Bacterial infections
– Vaccines
– Lymphoma
– Surgery
– Trauma

GBS - Pathology
• Affects:
– motor & sensory pathways of the peripheral nervous system,
– as well as the autonomic nervous system functions of the cranial
nerves.
• Believed to be an autoimmune response to antibodies
formed in response to a recent physiologic event.
• Once temporary inflammatory reaction stops, myelin-
producing cells begin the process of re-insulating
demyelinated portions of PNS.
• Degree of axonal damage is responsible for the degree of
neurologic dysfunction.

GBS – Assessment & DX
• Symptoms include:
– Motor weakness
– Paresthesias & other sensory changes
– Cranial nerve dysfunction
• (especially oculomotor, facial, glossopharyngeal, vagal, spinal
accessory, and hypoglossal); and
– Some autonomic dysfunction

• Abrupt onset of lower extremity weakness that
progresses to flaccidity and ascends over a period
of hours to days.
• Motor loss usually symmetric, bilateral, and
ascending
• In the most severe cases, complete flaccidity of all
peripheral nerves, including spinal and cranial
nerves, occurs.

• Admitted to hospital when lower extremity
weakness prevents mobility
• Admitted to CCU when progression of weakness
threatens respiratory muscles.
• DX based on clinical findings plus CSF analysis &
nerve conduction studies.
• Diagnostic finding is elevated CSF protein with
normal cell count

• Frequent assessment of respiratory system
• Most common cause of death is from
RESPIRATORY ARREST
• As disease progresses & respiratory effort
weakens, intubation & MV are necessary
• Continued, frequent assessment of neurologic
deterioration is required until the patient reaches
the peak of the disease & plateau occurs.

GBS – Medical Mgt
• No curative treatment available
• Disease must run its course, which is characterized
by ascending paralysis that advances over 1 to 3
weeks & then remains at a plateau for 2 to 4
weeks.
• Plateau stage followed by descending paralysis &
return to normal or near-normal function.

GBS – Medical Mgt
• Main focus is the support of bodily functions &
prevention of complications
• Plasmapheresis often used in attempt to limit
severity & duration
– Contraindicated if hemodynamically unstable
• IV imunoglobulin may be used
• Steroids may be used

GBS – Nursing Mgt (cont.)
• Support all normal body functions until the patient
can do so on his or her own
• Requires extensive long-term care,
– recovery can be a long process

GBS – Nursing Mgt (cont.)
• Focuses on:
– Maintaining surveillance for complications
– Initiating rehabilitation
– Facilitating nutritional support,
– Providing comfort & emotional support

GBS –Monitor for Complications
• Once intubated and on MV
– Observe for pulmonary complications
• (ie: atelectasis, pneumonia, pneumothorax
• Autonomic dysfunction, dysautonomia
– Can produce variations in HR & BP
– Hypertension and tachycardia may require beta-blocker
therapy

GBS – Initiating Rehabilitation
• Immobility may last for months
• Usual course of GBS involves:
– average of 10 days of symptom progression
– 10 days of maximal level of dysfunction
– Followed by 2 to 48 weeks of recovery
• Patient requires physical & occupational
rehabilitation because of the problems of long-term
immobility.

GBS – Rehab (cont.)
• Facilitating Nutritional Support
– Usually accomplished through use of enteral feeding
• Patient education
• Participation in a neurologic rehabilitation program
(if necessary)

GBS – Providing Comfort & Emotional
Support
• Pain control
– A safe, effective, long-term solution to pain
management must be identified.
• Extensive psychologic support
• *GBS does not affect the LOC or cerebral function
– Patient interaction & communication are essential
elements of the nursing management plan.

Using the Glasgow Coma Scale
Coma, Persistent Vegetative State
Other Complications

Glasgow Coma Scale (GCS) –
A tool for assessment
• For LOC only
• Not a complete neurological exam
• Evaluation of 3 categories
– Eye opening
– Verbal response
– Motor response

Rapid Neurologic Examination
• Organized, thorough, & simple.
• Performed accurately & easily at each assessment
point
• Conscious Patient
• Unconscious Patient

Rapid Neurologic Assessment –
Conscious Patient
• Exam should take less than 4 minutes
• LOC
• Facial Movements
• Pupillary function & eye movements
• Motor assessment
• Sensory
• VS
• Change in status

Rapid Neurologic Assessment –
Unconscious Patient
• Assessment takes 3 to 4 minutes
• Initial efforts are directed at achieving maximal
arousal of the patient
• LOC
• Pupillary assessment
• Motor examination
• Respiratory pattern
• VS

Neurologic changes Associated with
Intracranial Hypertension
• Increasing ICP can be identified by changes in:
• LOC (*1st Sign of deterioration in a conscious
patient)
– Increased restlessness, confusion, agitation, decreased
responsiveness
• Pupillary Reaction
• Motor Response
• Vital Signs
• Respiratory Patterns

Diagnostic Procedures
• Computerized tomograpy (CT Scan)
• Magnetic resonance imaging (MRI)
• Cerebral Angiography
• Myelography
• Cerebral Blood Flow Studies
• Electrophysiology Studies
• Lumbar Puncture

COMA
• A state of unconsciousness in which both
wakefulness and awareness are lacking
• A symptom, rather than a disease
– Occurs as a result of some underlying process
• Can be produced by a wide variety of both
neurologic & non-neurologic conditions
• Comprises a continuum of many levels

COMA - Etiology
• Structural neurologic lesions
• Metabolic and toxic conditions
• Psychiatric disorders

COMA – Structural Lesions
• Vascular lesions
– Ischemic & hemorrhagic strokes
• Trauma
– Loss of consciousness may occur immediately or may
develop several days–weeks after injury
• Brain tumors and brain abscesses
– Compression of neurologic structures
– Often accompanied by motor paralysis

COMA –
Metabolic & Toxic Conditions
• Accounts for more than half of all cases of
coma

COMA –
Cardiopulmonary Decompensation
Any cardiopulmonary condition can precipitate a state
of coma by threatening the state of oxygenation of
cerebral tissue

COMA – Poisoning & Alcohol
• May occur as the result of self-administration,
accidental ingestion, industrial exposure, or
homicidal administration
• Drug overdose – 30% of cases in ED
• Symptoms depend on substance ingested
• Alcohol may not be cause of coma in inebriated
patient
– Trauma, cerebral hemorrhage, subdural hematoma
• Thiamine deficiency

COMA – Hypertensive
Encephalopathy/HTN Crisis
• Sudden onset, usually following hx of kidney
disease, severe HTN, or both

COMA - Meningitis
• Common cause of coma
• Fever or signs of meningeal irritation
• Abrupt onset, severe HA followed by loss of
consciousness
• Hx of infectious process affecting middle ear or
paranasal sinuses should raise suspicion of
meningitis.

• Classic symptoms:
– Nuchal rigidity
– Brudzinski’s sign
– Kernig’s sign
– Photophobia
• Other: fever, tachycardia, h/a, chills, nausea,
vomiting, seizures
• May be irritable at first with progression to
confusion, stupor, and semiconsciousness

COMA
• Encephalitis
• Post-convulsion
• Other Metabolic Disturbances
• Hyper/hypoglycemia
• Hepatic coma
• Pneumonia
• Ecclampsia, various endocrine disorders;
hyperthermia, & electrolyte, acid-base, or water
imbalance.

COMA – Patho.
• Slight or moderate cortical depression
• Complete cortical suppression
• Midbrain depression
• Brain stem depression

COMA –Assessment & DX
• Detailed serial neurologic examinations
• CT or MRI
– Usually readily identify structural causes
• Lumbar Puncture (unless contraindicated by signs of
increased ICP)
– Analysis of CSF pressure & content
– **CT precedes Lumbar Puncture to identify patients
at risk for brain herniation
• Laboratory studies to identify metabolic or
endocrine abnormalities

Medical Management
• Identification & tx of underlying cause
• Emergency measures to support vital functions &
prevent further neurologic deterioration
• Protection of airway & ventilatory assist
• If cause not known
– Thiamine (at least 100 mg), glucose, & a narcotic
antagonist suggested

Medical Mgt (cont.)
• Prognosis depends on
– cause of the coma &
– length of time unconsciousness persists.
• Best prognosis is associated with early arousal
• Metabolic coma - better prognosis than coma caused
by a structural lesion
• Traumatic coma - better outcome than non-traumatic

COMA
• Clinical Manifestations of Metabolically &
Structurally Induced Coma

COMA – Nursing Mgt
• **Patient is totally dependent on the health care
team
• Interventions directed toward:
– Assessment
• changes in neurologic status &
• clues to the origin of the coma
– Supporting all body functions
– Maintain surveillance for complications
– Providing comforting and emotional support
– Initiating rehabilitation measures

COMA – Eye Care
• Blink reflex is often diminished or absent
– Results in drying & ulceration of the cornea
• Interventions to protect the eyes
– Instill saline or methyl cellulose lubricating drops &
taping eyelids shut
– Instilling saline drops q 2 hr & applying a polyethylene
film over the eyes

Coma Stimulation Therapy
• Based on the belief that structured brain
stimulation fosters brain recovery

PERSISTENT VEGETATIVE STATE
(PVS)
• State of unconsciousness in which wakefulness is
present but awareness is lacking
• Absence of any ascertainable cerebral cortical
function
• Complete or partial hypothalmic & brain stem
autonomic functions are present,
• Sleep-wake cycles are present
• There is complete unawareness of self & the
surrounding environment

Diagnostic Criteria for PVS
• No evidence of awareness of self or environment
• Inability to interact with others
• No evidence of sustained, reproducible,
purposeful, or voluntary behavioral response to
visual, auditory, tactile, or noxious stimuli
• No evidence of language comprehension or
expression

Diagnostic Criteria for PVS(cont.)
• Intermittent wakefulness manifested by presence
of sleep-wake cycles
• Sufficiently preserved hypothalmic & brain stem
autonomic functions to permit survival with
medical & nursing management
• Bowel & bladder incontinence
• Variably preserved cranial nerve reflexes and
spinal reflexes

PVS - Assessment & DX
• Differentiating feature between PVS & coma is the
wakefulness of the PVS patient
• Most difficult differential diagnosis is between PVS
& a locked-in state
– Locked-in state patient is conscious but unable to
communicate because of severe paralysis
Differentiating characteristics of PVS & other related
conditions

PVS - Assessment & DX
• Diagnosis must be made by a specialist with
expertise in this area.
• Moral, ethical & legal issues pertaining to PVS are
the subject of much debate
• Positron-emission tomography (PET) &
electroencephalography (EEG) are used to support
diagnosis

PVS - Medical Mgt
• No treatment to reverse PVS is known
• Coma sensory stimulation is being studied
• Prognosis depends on the cause of the underlying
brain disease
• For patient in a PVS that resulted from
degenerative or metabolic brain disease
– No chance for recovery is possible
• Average life expectancy is 2 to 5 years

PVS - Medical Mgt
• Collaboration between physicians & family to
determine appropriate level of medical
management
• Decisions must be made regarding:
– Resuscitation status
– Medications (including antibiotics & O2)
– Hydration, nutrition, and
– Long-term placement

PVS - Nursing Management
• Primarily comprised of:
– Performing a detailed neurologic assessment
– Providing supportive & hygienic measures, and
– Preventing complications of immobility
– Psychosocial & informational support of the family

REYE SYNDROME (RS)
• A disorder defined as toxic encephalopathy
associated with other characteristic organ
involvement.
• Very uncommon now- review from PEDS

ASSESSMENT OF
INTRACRANIAL PRESSURE

• Intracranial space comprises 3 components:
– brain substance (80%),
– cerebrospinal fluid (CSF) (10%),
– and blood (10%).
• Under normal conditions, the ICP is maintained
below 15 mm Hg mean pressure

• Monroe-Kellie hypothesis proposes that
– an increase in volume of one intracranial component
must be compensated by a decrease in one or more of
the other components so that total volume remains
fixed

ICP
• As ICP rises, small increases in volume may
cause major elevations in ICP.
• Cerebral blood flow (CBF) corresponds to the
metabolic demands of the brain & is normally 50
ml/100 g of brain tissue/minute.
• Brain requires 15% to 20% of the resting cardiac
output & 15% of the body’s O2 demands

ICP
• MAP of 50 – 150 does not alter CBF when
autoregulation is present
• Acidosis (causes cerebrovascular dilation)
– Hypoxia, hypercapnia, ishcmia
• Alkalosis (causes cerebrovascular constr.)
– hypocapnia
• Changes in metabolic rate
– Increases increase CBF
– Decreases decrease CBF

Operative Terms
Burr hole
Craniotomy
Craniectomy
Cranioplasty
Supratentorial
Intratentorialy

Mgt of Intracranial Hypertension
• Once identified, therapy must be prompt
• Most current evidence suggests that ICP generally
must be treated when it exceeds 20 mmHg
• All therapies are directed toward reducing the
volume of one or more of the components (blood,
brain, CSF) that lie within the intracranial vault.

ICP
• Major goal of therapy is to determine the cause of
the elevated pressure, and if possible, to remove the
cause
• In absence of a surgically treatable mass lesion,
intracranial hypertension is treated medically.

ICP – Nsg Interventions for intracr.
HTN
• Patient positioning
• Maintaining normothermia
• Controlled ventilation to ensure normal PaCO2
• Administering meds
– Keep CPP near 80 mmHg to provide adequate blood
supply to the brain
– CPP = MAP – ICP
• Performing ventricular drainage

ICP – Nursing Interventions
POSITIONING
• Head elevation increases venous return
– May place some patients at risk for intracranial HTN &
cerebral ischemia caused by increases of CPP
• Recent trend is to individualize head position to
maximize CPP & minimize ICP measurements

POSITIONING
• Obstruction of jugular veins or an increase in
intrathoracic or intrabdominal pressure is seen as
increased pressure through the open venous system,
– impeding drainage from the brain and increasing ICP.

POSITIONING
• Positions that decrease venous return from the
head must be avoided if possible.
• Examples of positions to avoid:
– Trendelenburg,
– prone,
– extreme flexion of the hips,
– angulation of the neck

POSITIONING
• If have to place in Trendelburg
– Monitor ICP & VS closely
• May use mechanisms to reduce intracranial pressure
– Sedation and/or ventricular drainage

ICP – Nsg Interventions
• Associated with increased ICP:
– Use of PEEP > 20 cm H20 pressure
– Coughing, suctioning
– Tight tracheostomy tube ties
– Valsalva maneuver
– Care activities performed one after another
• Associated with decreased ICP:
– Family contact & gentle touch

ICP – BP control
• Maintenance of arterial BP in the high normal range
is essential in the brain-injured patient.
• Inadequate perfusion pressure decreases the supply
of nutrients & O2 requirements for cerebral
metabolic needs.
• A blood pressure too high increases cerebral blood
volume and may increase ICP

ICP – BP Control MEDICATIONS
• Sedatives – small, frequent doses
• Antihypertensive agents
– Avoid use of nitroprusside & NTG (potent peripheral &
cerebral vasodilators)
• To reduce vasodilating effect of anti-hypertensives,
co-treatment with beta-blockers
– Metoprolol, Labetalol

SEIZURES
• Episodes of excessive and abnormal
discharges of electrical activity within the
CNS
• Epilepsy is a syndrome of recurrent,
paroxysmal episodes of seizure activity
– Partial
– Generalized

PARTIAL (FOCAL, LOCAL)
SEIZURES
• Simple partial seizures
– Seizure activity occurs in a specific body part
• Jacksonian March
– Sensory phenomena
– Autonomic manifestations
– Psychic manifestations

GENERALIZED SEIZURES
• Absence: sudden, brief sensation of motor
activity accompanied by a blank stare and
unconsciousness
• Myoclonic:sudden, uncontrollable jerking
movements of either a single muscle group
or multiple groups, sometimes causing the
patient to fall. Patient loses consciousness
for a moment and is then confused
postictally

TONIC CLONIC SEIZURE
• May or may not have an aura
• Sudden loss of consciousness
• Tonic phase
• Clonic phase

• Clonic seizures: rhythmic muscular
contraction and relaxation lasting several
minutes
• Tonic seizures: an abrupt increase in
muscular tone and muscular contraction
• Tonic-Clonic “Grand Mal”
• Tonic-clonic phase

STATUS EPILEPTICUS
• Continuous seizing activity and may have
brief periods of calm. Because the patient is
in a constant state of seizing, they may
develop hypoxia, acidosis, hypoglycemia,
hyperthermia, and exhaustion

• Complex Partial Seizures
– With automatisms: purposeless repetitive
activities
– Complex partial evolving to secondary
generalized

PHARMACOLOGY
• Phenytoin (Dilantin)
– Therapeutic level: 10 – 20 mcg
– SE: nystagmus, diplopia, ataxia, slurred
speech, insomnia, dizziness, gingival
hyperplasia, n/v/c, measles like rash, rust
colored urine, Steven Johnson’s syndrome

• Phenobarbital
– Therapeutic range: 10 – 40 mcg/ml
– SE: drowsiness, dizziness, h/a, n/v/d, jaundice,
mild rash
– Nursing Interventions
• No abrupt withdrawal
• Use caution
• No alcohol, CNS depressants, other
barbiturates
• Medic alert identification
• No calcium products
• Deep IM

• Nursing interventions for Dilantin:
– Don’t give IM
– Incompatible with dextrose
– Not faster than 50 mg/min IV
– Monitor for hypotension, bradycardia,
bradypnea
– Do not give po with milk, calcium, antacids,
MOM
– Hold tube feeding
– Teaching

Neural Tube Defects
Neurological
Dysfunctions

HYDROCEPHALUS
• Blockage of the drainage of cerebrospinal
fluid from the ventricles of the brain or from
impaired absorption of CSF within the
subarachnoid space
• Many causes

• Bulging fontanels with or without head
enlargement
• Dilated scalp veins
• Frontal protrusion (Bodding)
• Eyes rotated downward (setting sun sign)
• Sluggish pupils, unequal response to light
• Irritability
• Poor feeding

• Lower extremity spasticity
• Difficulty swallowing, feeding
• Shrill, high pitched cry
• seizures

TREATMENT
• Preferred procedure: ventriculoperitoneal shunt
• Preoperative
– Elevate HOB
– Prevent crying which increases intracranial pressure
– Avoid jarring, bouncing or any activity that will
increase intracranial pressure
– Head measured daily
– Monitor fontanels for bulging

• Ventriculoperitoneal shunt
• Post op care
– Position flat, on unoperative side
– Monitor for increased ICP (indicates obstruction
of shunt)
– NPO restriction for 24 – 48 hours
– IV fluid caution to prevent overload
• Revised as child grows
• Complications
– Infection
– Malfunction due to obstruction

SPINA BIFIDA OCCULTA
• A neural tube defect that is not visible
externally
• Skin depression or dimple, port wine
angiomatous nevi, or dark tufts of hair may
be the only visible sign
• No treatment is necessary unless neurologic
problems develop (abnormal weight gain,
problems with bowel or bladder, etc.)

SPINA BIFIDA CYSTICA
• Neural tube defect with external sac-like
protrusion
– Meningocele: encases meninges and spinal
fluid but no neural elements
– Myelomeningocele: contains meninges, spinal
fluid and nerves

MYELOMENINGOCELE
• Located anywhere on the neural tube
• May be covered with a fine membrane, the
dura, meninges, or skin
• Most frequently occurs in the lumbar or
lumbar sacral area
• 80-85 % have associated hydrocephalus

PATHOPHYSIOLOGY
• Failure of the neural tube to close during the
first 28 days of pregnancy
• Can also occur due to splitting of the
already closed tube due to increase in
cerebrospinal fluid pressure during the first
trimester

• Usually not uniform on both sides
• Affects bowel and bladder sphincters
(constant dribbling or overflow
incontinence; lack of bowel control or rectal
prolapse – no rectal temps for these
children)
• May have lower joint deformities (from
contractures in utero)

DIAGNOSIS
• MRI
• CT
• Ultrasound
• Elevated maternal alpha fetoprotein level
(done at 16 – 18 weeks gestation)

PREOPERATIVE CARE
• Warm incubator without clothing (clothing may irritate
sac)
• Moist dressing changes every two hours (0.9% Normal
Saline)
• Cleanse carefully if soiled
• Keep prone
• Diapering is contraindicated until repaired
• ROM (restricted to foot, ankle and knee)
• Prone position when held by parents (may not be able
to do)
• Tactile stimulation (caressing, stroking, other comfort
measures)

POSTOPERATIVE CARE
• Maintain prone or side lying position
• Frequent vital signs and daily weights
• Measure head circumference daily
• Examine fontanels for signs of tension or
bulging
• Catheterization for urinary retention
• Monitor for infection

Complications
• Increased intracranial pressure
• Unconsciousness
• Systemic Infections
• Neurogenic Shock
• Seizure disorders
• Others

INCREASED ICP
• Risk factors: head injury, brain tumors,
cerebral bleeding, hydrocephalus, and
edema from surgery or injury
• Most often associated with a space
occupying lesion

PATHOPHYSIOLOGY
• The skull is a hard, bony vault filled with
brain tissue, blood, and CSF. A balance b/w
these 3 maintains the pressure w/in the
cranium
• B/C the bony skull can’t expand, when one of
the 3 components expands, the other 2 must
compensate by decreasing in volume in order
for the total brain volume to remain constant

INCREASED INTRACRANIAL
PRESSURE
• Decreased LOC is the first sign
– Alert
– Lethargic
– Obtunded
– Stuporous
– Semicomatose

MORE CLINICAL
MANIFESTATIONS
• Pupillary responses:
– Early: diplopia, blurring, decreased acuity
• Changes in motor function:
– Early: progressive muscle weakness
– Late: decorticate, decerebrate, flaccid
• Headache
– Early: vague but present
– Late: accompanied by projectile vomiting without
nausea

• B/P and Pulse:
– Early: relatively stable
– Late: increased SBP while DBP stays the same (widened
pulse pressure); bradycardia
• Temperature:
– Early: normal, then increases – hyperthermia followed
by hypothermia as CSF increases
• Respirations:
– Early: normal
– Late: decreased at first together with increased SBP and
decreased pulse. As ICP increases, the character
changes: deeply yawning, signing, Cheyenne Stokes.

DOLL’S EYES
• Unconscious patient’s only
• Hold eyes open
• Briskly turn head side to side
• If eyes move in the opposite direction than the
way the head is turned, then the patient has
positive doll’s eyes. This is normal
• If they stay fixed at midline, this is negative.
• Do not perform on a patient with a cervical
fracture

TREATMENTS
• Mannitol
• Corticosteroids
• Antipyretics
• Barbiturates to induce coma
• Anticonvulsants
• Antibiotics
• IV fluids (NS is best but ½ NS may be used)
• Surgery

ACTIONS DURING SEIZURES
• Airway
– Loosen clothing around neck
– Turn to side if possible
– Do not force anything into the mouth
– Oxygen as ordered via mask
– Suction as needed

• Injury
– Bed in low position with wheels locked
– Side rails up
– Padded side rails
– If standing, lie down; place padding under head—
protect the head from injury
– Remove potentially harmful objects
– Teaching
• Don’t smoke alone or in bed, avoid alcohol, avoid
being tired, grab the bars in the bathroom, don’t
lock doors, avoid excessive caffeine

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