Patient with Neurologic
Problems
By Linda Self
Rapid Neurologic Assessment
• Glasgow Coma Scale
• Response to painful stimuli—sternal rub,
trapezius squeeze
• Level of consciousness—even a subtle change
is the first indicator of a decline in neurologic
status
• Decortication—abnormal posturing seen in the
client with lesions that interrupt the corticospinal
pathways. The patient’s arms, wrists, and fingers
are flexed with internal rotation and plantar
flexion of the legs.
Rapid Neurologic Assessment cont.
• Decerebration-abnormal posturing and
rigidity characterized by extension of the
arms and legs,pronation of the arms,
plantar flexion and opisthotonos (kind of
spasm with head and feet bent backward
and body bowed forward). Indicates
dysfunction of the brainstem.
Rapid Neurologic Assessment cont.
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Pupillary assessment, mental exam
Cranial nerve exam
Olfactory
Optic
Oculomotor
Trochlear
Trigeminal
Abducens
Facial
Acoustic
Glossopharyngeal
Vagus
Spinal accessory
hypoglossal
Brain Disorders—Migraines
Caused by a phenomenon called “cortical
spreading depression” whereby neurological
activity is depressed over a specific area of the
cortex—formerly felt to be related to dilation of
cerebral blood vessels
Results in release of inflammatory mediators
leading to irritation of the nerve roots, especially
the trigeminal nerve
Serotonin release involved in the causation
• Diagnosis is based on H&P, neurologic exam
and imaging.
Migraines
• Triggers
1. Tyramine-containing food and beverages such
as beer, wine, aged cheeses, chocolate, yeast,
MSG, nitrates, artificial sweeteners, smoked
fish
2. Medications:estrogens, nitroglycerine,
nifedipine, cimetidine
3. Other: fatigue, hormonal fluctuations, missed
meals, sleeping problems, varying altitudes
Commonly Used Drugs for
Migraines
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NSAIDs
Beta blockers such as inderal
Calcium channel blockers-verapamil
Abortive drugs such as ASA, acetaminophen
Ergotamine preparations
Triptans
Opioids
Investigational—droperidol (Inapsine)
Seizures
• Abnormal, sudden, excessive,
uncontrolled electrical discharge of
neurons within the brain. May cause
change in LOC, motor or sensory ability,
and/or behavior.
• Epilepsy—chronic disorder characterized
by recurrent, unprovoked seizure activity
Types of Seizures
• Generalized
1. Absence—petit mal
2. Tonic-clonic—grand mal. Muscle stiffening
followed by jerking
3. Myoclonic—contractions of body muscles
4. Atonic—go “limp”, drop attacks
5. Partial—simple partial, complex partial
6. others
Antiepileptic Drugs
• Tegretol—partial or generalized seizures
• Klonopin—absence, myoclonic and akinetic
seizures
• Valium—status epilepticus
• Depakote—all types
• Zarontin-absence seizures
• Neurontin—partial seizures
• Dilantin-all types
• Topamax—for intractable partial seizures
• Keppra—adjunct in partial seizures
Common side effects of antiepileptics (AEDs)
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Teratogenic potential
Medication interactions
Blood dyscrasias
Altered liver function
Effects on renal function
Wt. gain or loss
Sometimes sedation
Surgical options
• Identify seizure area by EEG, insert
electrodes, surgically excise
• corpuscallostomy
Characteristics of Seizures
Important to observe and document:
• How often?
• Description
• Progression
• Duration
• Last time occurred
• Preceded by aura?
• What does patient do post-seizure?
• Time elapsed before returns to baseline
Seizure Precautions
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Stay with patient
O2
Airway
Suction
IV access
Siderails up, padded
Bed in lowest position
Turn patient to side
Loosen restrictive clothing
Do not force anything into the mouth
Following seizure—do neuro checks
Status Epilepticus
• Characterized by prolonged seizures
lasting more than 5 minutes or repeated
seizures over the course of 30 minutes
• Is a medical emergency. Brain damage
and death can ensue.
• Untreated can cause hypoxia,
hypotension, hypoglycemia, dysrhythmias
and lactic acidosis. Rhabdomyolysis can
occur with effects on the kidneys.
Treatment of Status Epilepticus
• Lorazepam is the drug of choice due to
rapid onset of action and long duration of
action
• Valium
• Phenobarbital
• Dilantin
• Supportive/safety care
Meningitis
• Inflammation of the meninges or brain covering
• Entry is via the bloodstream at the blood-brain
barrier. May be direct route or via skull fracture.
Exudate will develop.
• Viral is most common
• Fungal-Cryptococcal. Can be caused by sinusitis
• Bacterial-mortality rate+25%. Most commonly
caused by Neisseria meningitidis and
Streptococcus pneumoniae.
Meningitis—S/S
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LOC
Disorientation
Photophobia
Nystagmus
hemiparesis
CN dysfunction
Personality changes
N/V
Fever and chills
Red macular rash
Nuchal rigidity, positive Kernig’s (hamstring pain w/extension) and
Brudzinski’s (flexion of the hips when the neck is flexed)
Review of CSF findings
• Pressure <20cm of H2O
• Clear, colorless. Cloudy indicates
infection. Pink to orange==RBCs
• Cells 0-5 lymphocytes normal.
• Glucose—50-75mg/dL normal, less than
50 indicates infection
• Proteins 15-45 normal, 45-100
paraventricular tumor, 50-200 viral, more
than 500=bacterial infection
Meningitis cont.
• CSF findings:
• Bacterial—cloudy, increased WBCs,
increased protein, decreased glucose,
elevated CSF pressure >180mm h20
• Viral—clear, increased WBCs, slighly
elevated protein, normal glucose, variable
CSF pressure
Meningitis
• May display s/s of increased ICP ( see
following slide)
• Left untreated, can result in brain
herniation or damage
Meningitis
• Treatment according to causative pathogen as
found by LP (lumbar puncture)
• Bedrest
• IV fluids, analgesics for pain and fever
• Anticonvulsants
• Corticosteroids
• Pathogen specific abx—meningococcus
penicillin or cephalosporins, contacts rifampin or
cipro; pneumococcal—PCN, cephalosporins and
also vancomycin
ICP
• Pressure-volume relationship between ICP,
volume of CSF, blood, brain tissue and cerebral
perfusion pressure (Monroe-Kellie Hypothesis)
• Cranial compartment is incompressible and
cranial contents should have a fixed volume
• Equilibrium must be maintained. Increased
volume will result in downward displacement of
the brain
Key Features of Increased
Intracranial Pressure
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Lethargy to coma
Behavioral changes
Headache
N/V
Change in speech pattern
Aphasia
Pupillary changes--papilledema
Cranial nerve dysfunction
Seizures
Abnormal posturing
Cushing’s Triad—elevated BP, decreased pulse and
decreased respirations
Treatment of increased ICP
• Maintain airway
• Hyperventilate patient to “blow off” CO2 (CO2 dilates
blood vessels)
• Raise HOB to allow for venous drainage
• Decrease metabolic demands by paralyzing and
sedating patient
• Mannitol
• corticosteroids
• Pain management
• Intracranial monitoring (in ventricle)
• Craniotomies
• Decompressive craniectomy
Brain Attacks (Strokes or CVAs)
• Affects over 550, 000 Americans per year
• Two major types—ischemic and
hemorrhagic
• Caused by disruption of the normal blood
supply to the brain
• May be preventable if causes discovered
early
Risk Factors for Brain Attacks
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Obesity
Heart disease
Diabetes mellitus
Hypercholesterolemia
Hypercoagulable states
Cocaine, illicit drug use
Atrial fibrillation
Differential Features of the Types of
Stroke
Thrombotic—onset is gradual
• Usually related to ASHD and hypertension
• Intact LOC
• May have speech and visual changes
• Slight HA
• No seizures
• Deficits may be permanent
Differential of strokes
Embolic
• Abrupt
• Steady progression
• Awake
• May be associated with cardiac disease
• Maximal deficits at onset
• No seizures
• Rapid improvements
Differentials of strokes
Hemorrhagic
• Sudden onset
• Deepening stupor or coma
• May have hypertension
• Focal deficits
• Seizures possible
• Permanent deficits possible
• May result from an aneurysm, rupture of an AV
malformation or severe hypertension
Ishemic Stroke
• Caused by a blockage of a blood vessel
• Generally caused by atherosclerosis
• Early warning signs include: transient loss
of vision, transient ischemic attack (called
silent strokes)
• Risk factors: atrial fibrillation, ASHD,
cocaine use/abuse, hx of “blood clots”
• Treatment—”clot buster” TPA,
streptokinase,others
Transient ischemic attack vs.
reversible ischemic neurologic
deficit
• Ischemic strokes are often preceded by
warning signs such as TIAs or RINDs
• Both cause transient focal neurologic
dysfunction from a brief interruption in
cerebral blood flow
• TIAs last minutes to <24h
• RINDs last >24h but less than a week
Hemorrhagic strokes
• If survive event, recovery from
hemorrhagic stroke better than ischemic
• Caused by vascular disruption e.g.
aneurysms, AVM
• Surgical decompression
Assessment of patient with brain
attack
• Neurologic exam
• Motor exam—hemiplegia vs. hemiparesis
• Sensory changes-neglect syndrome (most
notable in right cerebral hemispheric injuries)
• Amaurosis fugax—temporary loss of vision in
one eye
• Hemianopsia—blindness in one half of visual
field
• Cranial nerve function
• Cardiovascular assessment—abrupt reduction
of BP not advised
Assessment
• Baseline CT, MRI even better (want to
ensure that the stroke is not
hemorrhagic)
• ECG
• Echocardiogram
• Cardiac enzymes
Interventions
Depending of type of brain attack:
• Anticoagulants (assuming not a bleed)
• Catheter directed thrombolytic therapy—may
use if systemic tx not effective
• Endarterectomy
• Craniotomy
• Systemic thrombolytic tx—must meet strict
criteria. Must give within 3hours of onset of s/s
• Wire coils in aneurysms—seals the area
Key considerations
• Impaired physical mobility; self care deficit
• Disturbed sensory perception
• Unilateral neglect—in rt cerebral stroke.
May have lack of proprioception and
failure to recognize their impairment
• Impaired verbal communication—
expressive aphasia (Broca’s), receptive
aphasia (Wernicke’s)
Parkinson’s disease
• Genetic and environmental contributors
• Associated with four cardinal s/s: tremor,
rigidity, akinesia (slow movements), and
postural instability
• Degeneration of substantia nigra—
decreased dopamine. Acetylcholine will
predominate. Also with norepinephrine
loss thus the postural hypotension.
Parkinson’s Key Features
• Stooped posture
• Slow and shuffling gait
• Pill-rolling, mask-like facies, uncontrolled
drooling, rare arm swinging with walking
• Change in voice, dysarthria and echolalia
• Labile and depressed, sleep disturbances
• Oily skin, excessive perspiration,
orthostatic hypotension
Parkinson’s Disease
Stages
• Initial-hand and arm trembling,
weakness, unilateral involvement
• Mild-masklike facies, shuffling, bilateral
involvement
• Moderate—increased gait disturbances
• Severe—akinesia, rigidity
• Complete dependence
Interventions
• Eldepryl (MAO inhibitor which decreases
the breakdown of dopamine)
• Dopamine agonists—stimulate dopamine
receptors but have side effects such as
nausea, drowsiness, postural hypotension
and hallucinations. Mirapex and Requip
mimic the actions of dopamine.
Interventions cont.
• Levodopa/carbidopa. Used as disease
progresses. “Wearing off” phenomenon.
• Amantadine—used to treat the “wearing
off” s/s.
• Stavelo—
(carbidopa/levodopa/entacapone). Dopadecarboxylase inhibitor/dopamine
precursor/COMT inhibitor. Useful in endstage disease.
Drug toxicity/tolerance in PD
1. Reduce medication dosage
2. Change of medications or in the
frequency of administration
3. Drug holiday up to 10 days
Nursing considerations
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Maintain mobility and flexibility by ROM
Encourage self-care as much as possible
Monitor sleep patterns to avoid injury
Nutrition-may need soft or thickened foods.
Constipation
Speech therapy may be needed
Psychosocial support—impaired memory
cognition
Surgical Management in PD
• Stereotactic pallidotomy
• Deep brain stimulation when meds no
longer work. Electrode is implanted and
connected to a “pacemaker” in chest.
• Fetal tissue transplantation using fetal
substantia nigra (implanted in the caudate
nucleus of the brain).
Alzheimer’s Disease
• Chronic progressive degenerative disease
usually seen in individuals older than 65
• Characterized by loss of memory,
judgment, and visuospatial perception and
by a change in personality
• Progressively physically and cognitively
impaired resulting ultimately in death
AD
• Increased amount of beta amyloid
• Neurofibrillary tangles throughout the
neurons
• Neuritic plaques
• Granulovascular degeneration
• Reduced levels of acetylcholine
• ? Increased levels of glutamate
Key Features of AD
• Early-forgets names, misplaces household
items, mild memory loss, short attention span,
subtle changes in personality, wanders, impaired
judgment
• Middle—cognition vitally impaired; disoriented to
time, place and event; agitated; unable to care
for self, incontinent
• Severe-incapacitated; motor and verbal skills
lost
Physical Assessment of AD
• Observe for stage of progression
• Observe for changes in cognition—attention,
judgment, learning and memory,
communication/language
• Observe for changes in behavior
• Changes in self-care skills
• Psychosocial assessment
• Dx of exclusion. Check CMP, CBC, B12, folate,
TSH, RPR, drug toxicities and levels, alcohol
screening
• PET or MRI to r/o pathology
• Mini-mental state examination—
orientation, registration (repeat three
words), naming, reading and following
directions.
• Good one is to have them draw a clock
with an indicated time
Interventions for AD
• Provide environmental stimulation through
contact with people, provide a clock and
calendar, present change gradually, allow
for rest periods, use repetition
• Be concrete
• Limit information
• Prevent overstimulation and provide
structure
Interventions cont.
• Promote independence in ADL
• Be consistent
• Promote bowel and bladder contenence fy
offering rest room breaks q2h daytime,
limit fluids at hs
• Administer cholinesterase inhibitors such
as Aricept, Reminyl and Exelon. Maintains
functionality for a few more months.
Interventions cont.
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Provide ID band
Monitor to ensure safety from wandering
Walk patient to reduce restlessness
Involve in activities
Restraints only as last resort
Multiple Sclerosis (MS)
• Also called disseminated sclerosis or
encephalomyelitis disseminata
• Chronic, inflammatory disease of CNS
• Causes gradual destruction of myelin sheath of
neurons. Results in scars or sclerosis on the
myelin sheaths.
• Results from autoimmune process
• Between attacks, s/s may resolve but permanent
injury occurs as disease progresses
MS
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Usually affects adults 20-40 years of age
More common in women than men
Occurs in more temperate climates
No cure
MS signs and symptoms
• Changes in sensation*
• Muscle weakness
• Incoordination, loss of balance*
• Dysarthria
• Dysphagia
• Visual problems (diplopia)*
• Fatigue
• Bladder and bowel problems
• Cognitive impairment
• Heat intolerance
*indicates initial or presenting symptoms
Diagnosis of MS
• MRI
• CSF testing will show oligoclonal bands
• Visual evoked potentials and somatosensory
evoked potentials (sensory and visual nerves
respond less actively in MS)
• Antibody testing for myelin oligodendrocyte
glycoprotein and myelin basic protein—in
formative stages for testing at this time
Types
• Relapsing-remitting--charac. by remissions
and relapses
• Secondary progressive
• Primary progressive—no remissions,
gradual decline
• Progressive relapsing—steady decline
with superimposed attacks
• ---Copaxone (immunomodulator that
targets T-cells, decreases inflammation),
Avonex (interferon beta), Betaseron
(interferon beta), Tysabri (immunotherapy)
• Avoidance of over-heating (Uththoff’s
phenomenon)
Spinal Cord Injury
• Force applied to spinal cord will result in
neurologic deficits
• Injury may be direct insult to the spinal
cord or may be secondary to a contusion,
compression or to a concussion (loss of
function resulting from a blow)
Primary mechanisms of injury
• Hyperflexion injury occurs when the head
is suddenly and forcefully accelerated
forward, causing extreme flexion of the
neck. Often occurs in head-on collisions
and diving accidents
Primary mechanisms of Injury
• Hyperextension injuries occur most often
in automobile accidents in which the
client’s vehicle is struck from behind or
during falls when the client’s chin is struck.
The head is accelerated and decelerated.
Results in stretching or tearing longitudinal
ligament, fractures or subluxates vertebrae
and may rupture the disc.
Primary mechanisms of injury cont.
• Axial loading (vertical compression) occurs
from diving accidents, falls on the
buttocks, or a jump in which a person
landed on their feet. The blow may cause
the vertebrae to shatter. Pieves of bone
enter the spinal canal and damage the
cord.
Secondary Injury
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Neurogenic shock
Vascular insult
Hemorrhage
Ischemia
Fluid and electrolyte imbalance
Extent of Injury
• Most spinal cord injuries are incomplete
lesions
• Specific syndrome result from incomplete
lesions
Cervical Injuries
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May produce:
Anterior cord syndrome
Posterior cord syndrome
Brown-Sequard syndrome
Central cord syndrome
Cauda equina syndromes are associated
with injuries to the lumbar and sacral
cord
Cervical Injuries
• Anterior cord syndrome results from
damage to the anterior portion of both gray
and white matter of the spinal cord,
generally 2ndary to decreased blood
supply. Motor function, pain and
temperature sensation are lost below the
level of injury but touch, position and
vibration remain intact.
• Posterior cord lesion—rare. Results from
damage to the posterior gray and white
matter of the spinal cord. Motor function
remains intact but the patient loses the
sense of position sensation, of crude touch
and of vibration.
• Brown-Sequard—results from a
penetrating injury that causes hemisection
of the spinal cord or injuries that affect half
of the spinal cord. Motor function,
proprioception, vibration and deep touch
sensations are lost on the same side of
the body as the lesion. On the opposite of
the lesion, the sensations of pain,
temperature and light touch are affected.
• Central cord syndrome—results from a
lesion of the central portion of the sc. Loss
of motor function is more pronounced in
the upper extremities than in the lower
extremities. Sensation varies.
• Lumbosacral Injuries—damage to the
cauda equina or conus medullaris
produces a variable pattern of motor or
sensory loss as the peripheral nerves
have the potential for recovery and
regrowth. This injury generally results in a
neurogenic bowel and bladder.
Vital statistics of spinal cord injuries
• Primary cause is trauma secondary to
MVA
• Unmarried male between 16-30
• Generally are Causcasian
• Most injuries are cervical
Assessment
• Thorough history including mechanism of
injury, any changes since initial responder,
previous medical history, hx of
osteoporosis, osteomyelitis or previous
neck or back injuries or surgeries
Assessment
• First priority for the client with a SCI is
assessment of the respiratory pattern and airway
• Ensure neck is stabilized
• Assess for evidence of abdominal hemorrhage
or other sites of injury/hemorrhage
• Glasgow Coma Scale
• Detailed assessment of the client’s motor and
sensory status
Spinal Shock
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Occurs immediately after injury as a result of disruption
of pathways between upper motor neurons (lie in
cerebral cortex) and lower motor neurons (lie in spinal
cord).
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Characterized by:
1. Flaccid paralysis
2. Loss of reflex activity below level of lesion
3. Bradycardia
4. Possible paralytic ileus
5. Hypotension.
May last days to weeks; reversal indicated by return of
reflex activity
Assessment
Sensory function
• C4-5 can shrug
• C5-6 can pull up arms against resistance
• C7 can overcome resistance with arms flexed
• C8 can grasp objects
• L2-4 can raise legs straight up against
resistance
• L5 apply resistance when patient dorsiflexes
• S1apply resistance while the client plantar flexes
his feet
Cardiovascular
• Dysfunction r/t disruption of the autonomic
nervous system, especially if above T-6
• Bradycardia, hypotension and
hypothermia may result from disruption of
sympathetic input
• BP < 90 torr requires intervention to
ensure satisfactory perfusion of the spinal
ccord
Respiratory
• Can develop from both immobility and
from interruption of spinal innervation to
the respiratory muscles
• C3-5 innervate the diaphragm
Gastrointestinal and Genitourinary
assessment
• Must assess the patient’s abdomen for
indications of hemorrhage, distention or
paralytic ileus
• Ileus may develop within 72h of the injury.
Can cause areflexic bladder which can
lead to urinary retention and a neurogenic
bladder.
Musculoskeletal Assessment
• Assess muscle tone and size
• Muscle wasting is 2ndary to long-term
flaccid paralysis seen in lower motor
neuron lesions (cell body lies in ant. gray
column of spinal cord. Innervates striated
muscles).
• Upper motor neuron lesions (neuron body
lies in cortex, axon synapses with lower
motor neuron). Causes spasticity.
Interventions for Patients with
Spinal Cord Injuries
• Immobilization for cervical injuries—fixed
skeletal traction such as halo fixation or tongs
• Maintain proper alignment of head, neck and
body
• Turn using the log roll technique
• Monitor skin integrity
• Traction pin insertion site care
• If thoracic or lumbosacral injury—immobilize with
corset or brace
• Medications—supportive, may use steroids,
baclofen, other meds under investigation
Interventions for patients with SCIs
• Surgical decompression and
stabilization—spinal fusion, insertion of
Harrington rods, laminectomy (excision of
a posterior vertebral arch)
• Prevent complications of immobility
• Promote self-care
• Bladder retraining—spastic (UMN) or
flaccid (LMN) may be able to initiate
voiding or may need I&O catherterizations
Interventions cont.
• Bowel retraining—LMN may have to have
manual disimpactions, see p. 993.
• Rehab, involve community resources
• Home care management
• Psychosocial implications
Autonomic Dysreflexia or
Hyperreflexia
• Commonly seen in patients with injury to the
upper spinal cord (T5 and above). Caused by
massive sympathetic discharge of stimuli from
the autonomic nervous system.
• Stimulus sends nerve impulses to sc, travel
upward until blocked by lesion at level of injury.
Can’t reach brain so reflex is activated that
increases activity of sympaathetic portion of
ANS.
Autonomic dysreflexia cont.
• Increased activity of sympathetic portion
of ANS results in spasms and a narrowing
of blood vessels with resultant rise in BP.
Brain perceives elevated BP, sends
message to heart which slows down and
dilates vessels above level of injury to
dilate. Brain cannot send messages below
level of injury so BP cannot be regulated.
Autonomic Dysreflexia
• Precipitated by distension of the bladder or
colon; catheterization of or irrigation of the
bladder
• Is a medical emergency
Key Features of Autonomic
Dysreflexia
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Sudden onset of severe, throbbing headache
Severe, rapidly occurring hypertension
Bradycardia
Flushing above the level of the lesion
Pale extremities below the lesion
Nausea
Blurred vision
Piloerection
Feeling of apprehension
Care of Patient experiencing
Autonomic Dysreflexia
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Place in sitting position
Notify physician
Loosen tight clothing
Assess for cause
Check foley cath
If no cath, check bladder for distention
Place anesthetic ointment on tip of
catheter before insertion
Care of Patient with Autonomic
Dysreflexia cont.
• Check for fecal impaction, disimpact with
anesthetic ointment if present
• Check room to ensure not too cool
• Monitor BP q15 minutes
• Give nitrates or hydralazine as ordered
Myasthenia Gravis (MG)
• Autoimmune disease of neuromuscular
junction. Characterized by flare-ups and
remissions. Caused by auto antibody
attack on the acetylcholine receptors. May
be related to hyperplasia of the thymus.
• Presents with muscle weakness that
improves with rest, poor posture, ocular
palsies, ptosis, diplopia, respiratory
compromise, bowel and bladder problems
MG
• Diagnosis based on H&P, labs which
include thyroid studies, tests to R/O
inflammatory illnesses, (RA, SLE,
polymyositis), acetylcholine receptor
antibodies (positive confirms but negative
does not rule out)
MG
• Testing with cholinesterase inhibitors
(Tensilon). Baseline muscle strength
tested then injection given. Within 30-40
seconds, most myasthenic patients show
a marked improvement in muscle tone that
lasts several minutes.
• May be used to distinguish between
myasthenic crisis and cholinergic crisis.
Myasthenic Crisis
• Undermedicated with anticholinesterase
drugs.
• Increased pulse and respirations
• Rise in BP
• Anoxia
• Cyanosis
• Bowel and bladder incontinence
• Absence of cough and swallowing reflex
Cholinergic crisis
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Like being tx with chemical weapons
Too much acetylcholine
Nausea, vomiting, diarrhea
Abdominal cramps
Muscle twitching
Hypotension
Blurred vision
Treatment of MG
• Immunosuppression with steroids, Imuran or
Cytoxan
• Plasmapheresis
• Resp. support
• Nutritional support
• Eye protection if unable to close eyes completely
• Thymectomy
• Maintanance—cholinesterase inhibitor drugs
such as Mestinon