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Neuro 0411-1323
Neuro 0411-1323
Neuron Coverings
A. Myelin- white, waxy, fatty material
covering many nerve fibers (axons and
dendrites). Increases rate of transmission of
impulses and protect and insulates the fibers
B. Nodes of Ranvier- layers of myelin with
indentations
-further increases the rate of transmission
because the impulse can jump from node to
node
C. Schwann Cells- produces myelin in the
PNS
-outer memrane of the schwann cells gives
rise to neurilemma
D. Neurilemma- it is a very important layer
because it helps regenerate injured axons.
This only occur in the PNS because cells in
the CNS cannot regenerate and does not have
neurilemma, thus cells damaged in the CNS
result in permanent damage (paralysis)
2. Diencephalon
-often called interbrain
-it lies beneath the cerebrum
-contains the thalamus and the
hypothalamus
1. Cerebrum
-largest part of the brain
-divided into the left and right hemisphere
-outer portion of the brain composed of gray
matter and is called cerebral cortex
-arranged in folds called gyri, grooves are sulci 3. Cerebellum
(fissures) -lies in posterior and inferior to the
-connecting structure is the corpus collosum, cerebrumand is the second largest portion of
divides the two hemispheres into 4 lobes: the brain
frontal lobe, parietal lobe, temporal lobe,
occipital lobe -contains 2 hemispheres that is responsible
for coordination of the voluntary movement
and maintenance of balance, equilibrium and
muscle tone
-sensory messages form the semicircular
canals in the inner ear send their messages to
the cerebellum
2. Cranial Nerves
-12 pairs, attached to the posterior surface of
the brain, mainly the brainstem
-conduct impulses between the head, neck
and brain, excluding the vagus nerve (X), also
serves organs in the thoracic and abdominal
cavities.
B. Spinal Cord
-it is 17”-18” cord that extends from the brain
stem to the second lumbar vertebra
1. Spinal Nerves
-31 pairs, all mixed nerves
-they transmit sensory information to the
spinal cord through afferent neurons (afferent
is responsible for the transport of nerve
impulses from the receptor organs to the
central nervous system) and motor
3. General knowledge (such as names of
II. Assessment of the Neurological System presidents)
4. Short and long term memory
Effects of Normal Aging to the Nervous 5. Attention span
System 6. Ability to concentrate
1. Loss of weight
2. Loss of neurons (1 % a year after age 50) DOCUMENTATION
3. Reduction in cereral blood flow -is key to determining a change
4. Decrease in brain metabolism and oxygen -nurse should vary orientation questions so
utilization patient doesn’t memorize answers through
5. Decreased blood supply in the spinal cord repetition.
causes decreased reflexes
LEVEL OF CONSCIOSNESS
Prevention of Neurological Problems -it is the earliest and most sensitive indicator
1. Avoid drug and alcohol use that something is changing
2. Safe use of motor vehicles -a decerease in LOC is the earliest sign of
3. Safe swimming practices increased intracranial pressure
4. Safe handling and storing of firearms -LOC has 2 components, arousal and
5. Use hardhats in dangerous construction awareness
areas
6. Use of protective padding as needed for A. Arousal or Wakefulness is controlled by
sports the brainstem and most fundamental part of
LOC. If patient can open eyes to voice or to
HISTORY the pain, the wakefulness center in the
-comprehensive history essential for brainstem is still functioning.
diagnosing neurological disease
-be specific about symptoms experience as B. Awareness is a higher function controlled
well as patient understanding. by the reticular activating system in the
-information from the family may also be brainstem, is the ability to interact with
helpful others. It has 4 parts:
m. Electromyogram
-Used to measure the contraction of a muscle
in response to electrical stimulation
-Takes about 45-60 minutes for one muscle
study
n. Echoencephalogram
-Uses ultrasound to depict the intracranial
structures of the brain.
-Helpful in detecting ventricular dilation and
h. Magnetic Resonance Angiography major shift of midline structures in the brain
(MRA) as a result of an expanding lesion.
-differential signal characteristic of flowing
blood to evaluate extracranial and intracranial
blood vessels
-provides anatomic and hemodynamic
information
-with or without contrast
-rapidly replacing cerebral angiography for
use in dx cerebrovascular accident (CVA)
Nausea, vomiting, light sensitivity,
chilliness, fatigue, irritability, diaphoresis,
edema
IV. Common Disorders of the Neurological MANAGEMENT
System
Pharmacological management
1. H E A D A C H E S Migraine headaches
-Common neurological complaint; has many Aspirin, acetaminophen, ibuprofen
different causes Ergotamine tartrate
Codeine; Inderal
ETIOLOGY/PATHOPHYSIOLOGY Dietary recommendations
-Skull and brain tissues are not able to feel Limit MSG, vinegar, chocolate, yogurt,
sensory pain alcohol, fermented or marinated foods,
ripened cheese, cured sandwich meat,
A. Vascular headaches caffeine, and pork
Psychotherapy
i. Migraine
Cluster headaches
Pre-Migraine: visual field defects, unusual Narcotic analgesics
smells or sounds, disorientation, paresthesias Tension headaches
During Migraine: nausea, vomiting, Non-narcotic analgesics
sensitivity to light, chills, fatigue, irritability, Traction-inflammatory headaches
diaphoresis, edema Treat cause
-Cause includes abnormal metabolism of Comfort measures
serotonin, a vasoactive neurotransmitter Cold packs to forehead or base of skull
found in platelets and cells of the brain, plays Pressure to temporal arteries
a major role. Dark room; limit auditory stimulation
5. E P I L E P S Y O R S E I Z U R E S
MANAGEMENT -Seizures affect both men and women of all
-Treat cause if possible races and ages.
-Identify some potential causes of seizures.
Pharmacological management
Corticosteroids (dexmethasone) ETIOLOGY/PATHOPHYSIOLOGY
Antacids; histamine-receptor blockers -Transitory disturbance in consciousness or
Anticonvulsants (dilantin, cerebyx(short- in motor, sensory, or autonomic function due
term IV or IM use)) to sudden, excessive, and disorderly
AVOID opioids and other drugs that cause discharges in the neurons of the brain; results
respiratory depression in sudden, violent, involuntary contraction of
Mechanical decompression a group of muscles
Craniotomy (surgical operation in which a
bone flap is temporarily removed from the Types:
skull to access the brain) a. Grand mal- A grand mal seizure causes a
Craniectomy (Surgical removal of a loss of consciousness and violent muscle
portion of the cranium) contractions.
Internal monitoring devices Grand mal seizures have two stages:
Ventricular pressure monitoring – catheter Tonic phase. Loss of consciousness occurs,
inserted through a burr hole into the and the muscles suddenly contract and cause
lateral ventricle and attached to a the person to fall down. This phase tends to
transducer and oscilloscope to monitor last about 10 to 20 seconds.
ICP Clonic phase. The muscles go into rhythmic
Subarachnoid screw – inserted through a contractions, alternately flexing and relaxing.
burr hole in skull and attached to a Convulsions usually last one to two minutes
transducer and oscilloscope for or less.
continuous monitoring b. Petit mal- cause a short lapse in
awareness. This can involve staring into
space and rapid blinking. They start and
4. D I S T U R B A N C E S I N end quickly, lasting only a few seconds.
MUSCLE TONE AND There are two subtypes of petit mal seizures:
MOTOR FUNCTION typical and atypical.
-Patients experiencing neurological system Typical seizures are sudden and last under
disorders can present with a variety of signs 10 seconds. Atypical seizures have a slower
and symptoms. The assessment will be key in onset and can last up to 20 seconds or longer.
making a determination of the exact problem c. Psychomotor- A psychomotor seizure is a
and developing a plan of care. form of epilepsy that is typically limited to
the temporal lobe of the brain and results Avoid alcohol
in impairment of responsiveness and Avoid driving, operating machinery, and
awareness to ones surroundings. Patients swimming until seizures are controlled
may act out in a variety of ways while Good oral hygiene
experiencing the seizure but have not Medic Alert tag
recall of it.
d. Jacksonian-focal- -A Jacksonian seizure V Degenerative Diseases
is a type of focal partial seizure, also
known as a simple partial seizure. This 1. M U L T I P L E S C L E R O S I S
means the seizure is caused by unusual -Multiple sclerosis is a chronic, progressive
electrical activity that affects only a small neurological disease.
area of the brain. The person maintains -The disease initially begins between the ages
awareness during the seizure.Jacksonian of 15 and 50 years.
seizures are also known as a Jacksonian -Women are affected more than men.
march. This is because the tingling or
twitching begins in a small area and then ETIOLOGY/PATHOPHYSIOLOGY
"marches" or spreads to a larger area of -Degenerative neurological disorder with
the body. demyelination of the brain stem, spinal cord,
e. Myoclonic-Myoclonic seizures are a type optic nerves, and cerebrum
of seizure that causes sharp,
uncontrollable muscle movements.
They’re usually minor and brief, but can
happen with very severe seizure disorders.
They’re most common with childhood
seizure conditions, but can also happen in
adults.
f. Akinetic- An atonic seizure (also called
drop seizure, akinetic seizure, astatic
seizure, or drop attack) is a type of seizure
that consists of partial or complete loss of
muscle tone that is caused by temporary
alterations in brain function. These
seizures are brief – usually less than
fifteen seconds.
g. Status epilepticus- Recurrent generalized
seizures will result in status epilepticus.
Sudden withdrawal from the prescribed
anticonvulsant therapies is the #1 cause
of its occurrence.Status epilepticus is a
“9-1-1” event. Emergency intervention is
needed to prevent brain damage or death
CLINICAL MANIFESTATIONS
Depends on type of seizure
Aura
Postictal period- Seizures have predictable
In multiple sclerosis, the myelin sheath becomes
stages. The seizure might begin with an
damaged. This loss of myelin integrity results in
aura (the predictor of the seizure),
impaired transmission of nerve impulses.
followed by the ictal phase (seizure), and
ending with the postictal period. CLINICAL MANIFESTATIONS
Visual problems
MANAGEMENT Urinary incontinence
During seizure: Protect from aspiration Fatigue
and injury Weakness
Anticonvulsant medications Incoordination
Surgery Sexual problems
Removal of brain tissue where seizure occurs Swallowing difficulties
Adequate rest
Good nutrition
Elimination may feel urgency and hesitancy
in voiding
Should be on a high fiber diet to help
MANAGEMENT prevent chronic constipation
-No specific treatment Encourage fluids and take a stool
Pharmacological management softener, suppositories, prune juice, or
Adrenocorticotropic hormone (ACTH) milk of magnesia
Steroids
Valium Nursing Diagnosis:
Betaseron (interferon beta-1b) Impaired physical mobility, related to
Avonex (interferon beta-1a)
rigidity, bradykineia, and akinesia
Pro-banthine; urecholine
Risk for aspiration related to disease
Bactrim, Septra, and Macrodantin
process
Nutrition
Patient Teaching:
Skin care Important to take medication as
Activity prescribed
Environmental controls Good skin care
Patient teaching Proper ambulation and positioning
Proper feeding and eating technique to
2. P A R K I N S O N’ S D I S E A S E reduce risk of aspiration
-Parkinson’s disease is a chronic neurological Prognosis
disorder. It occurs most frequently in middle- Chronic degenerative disorder with no
aged and older adults. acute exacerbations
-There is no known cure. If pt compliant with treatment, signs and
symptoms can be managed for a long
ETIOLOGY/PATHOPHYSIOLOGY period of time.
-Deficiency of dopamine
3. A L Z H E I M E R S’ DISEASE
CLINICAL MANIFESTATIONS
Muscular tremors; bradykinesia (slow ETIOLOGY/PATHOPHYSIOLOGY
movement) -Is a chronic, progressive, degenerative
Rigidity; propulsive gait (a stooped, stiff disorder
posture with the head and neck bent -Impaired intellectual functioning
forward) -Common cause of dementia in the older
Emotional instability person and affects men and women equally.
Heat intolerance -Chronic, progressive degeneration of the cells
Decreased blinking of the brain
“Pill-rolling” motions of fingers -Brain changes include plaques in the cortex,
neurofibrillary tangles, and the loss of
MANAGEMENT connections between cells and cell death.
Pharmacological management -Decrease in brain size
Levodopa 10% age 65 or older and 50% age 85 and
Sinemet older have AD
Artane -Genetic link
Cogentin -Increased plasma levels of homocysteine are
Symmetrol associated with a significantly increased risk
Surgery – ablation of affected area vs deep of AD or dementia
brain stimulator -Blood homocysteine levels can be lowered by
Activity – posture is important, best to not eating foods rich in folic acid, such as fruits
use a pillow and green leafy vegetables.
Should walk with hands behind back to
maintain erect spine and decrease CLINICAL MANIFESTATIONS
incidence of falling Stage 1
Nutrition – malnutrition and constipation can Mild memory lapses; decreased attention
be severe span
Need foods that are appetizing and easily Difficulty in using the correct word
chewed and swallowed Disinterest in surroundings and possibly
Encourage 5-6 small meals a day depression
No impairment (normal function) should be able to detect clear-cut
The person does not experience any symptoms in several areas: Forgetfulness
memory problems. An interview with a of recent events
medical professional does not show any Impaired ability to perform challenging
evidence of symptoms of dementia. mental arithmetic — for example,
Stage 2 counting backward from 100 by 7s
Obvious memory lapses, especially short- Greater difficulty performing complex
term memory tasks, such as planning dinner for guests,
Disoriented to time paying bills or managing finances
Loss of personal objects Forgetfulness about one's own personal
Loss of impulse control , behavioral history
manifestations of AD result from changes Becoming moody or withdrawn, especially
in brain (agitation) in socially or mentally challenging
Some pts develop psychotic situations
manifestations
Decrease in sleep Stage 5
Very mild cognitive decline (may be Moderately severe cognitive decline
normal age-related changes or earliest (Moderate or mid-stage Alzheimer's
signs of Alzheimer's disease) disease)
The person may feel as if he or she is Gaps in memory and thinking are
having memory lapses — forgetting noticeable, and individuals begin to need
familiar words or the location of everyday help with day-to-day activities. At this
objects. But no symptoms of dementia can stage, those with Alzheimer's may: Be
be detected during a medical examination unable to recall their own address or
or by friends, family or co-workers. telephone number or the high school or
college from which they graduated
Stage 3 Become confused about where they are or
Total disorientation to person, place, and what day it is
time Have trouble with less challenging mental
Apraxia ( impairment in the ability to arithmetic; such as counting backward
perform purposeful acts or to use objects from 40 by subtracting 4s or from 20 by
properly ); visual agnosia (inability to 2s
recognize objects by sight); dysgraphia Need help choosing proper clothing for the
(difficulty communicating via writing); season or the occasion
wandering Still remember significant details about
Awake most of the night themselves and their family
Mild cognitive decline (early-stage Still require no assistance with eating or
Alzheimer's can be diagnosed in some, but using the toilet
not all, individuals with these symptoms)
Friends, family or co-workers begin to Stage 6
notice difficulties. During a detailed Severe cognitive decline
medical interview, doctors may be able to (Moderately severe or mid-stage
detect problems in memory or Alzheimer's disease)
concentration. Common stage 3 Memory continues to worsen, personality
difficulties include: Noticeable problems changes may take place and individuals
coming up with the right word or name need extensive help with daily activities.
Trouble remembering names when At this stage, individuals may:
introduced to new people Lose awareness of recent experiences as
Having noticeably greater difficulty well as of their surroundings
performing tasks in social or work settings Remember their own name but have
Forgetting material that one has just read difficulty with their personal history
Losing or misplacing a valuable object Distinguish familiar and unfamiliar faces
Increasing trouble with planning or but have trouble remembering the name
organizing of a spouse or caregiver
Need help dressing properly and may,
Stage 4 without supervision, make mistakes such
Moderate cognitive decline as putting pajamas over daytime clothes
(Mild or early-stage Alzheimer's disease) or shoes on the wrong feet
At this point, a careful medical interview
Experience major changes in sleep Increase foods high in folic acid and
patterns — sleeping during the day and vitamin B12 to reduce homocysteine
becoming restless at night levels
Need help handling details of toileting (for
example, flushing the toilet, wiping or Safety
disposing of tissue properly) Remove burner controls at night
Have increasingly frequent trouble Double-lock all doors and windows
controlling their bladder or bowels Constant supervision
Experience major personality and Prognosis
behavioral changes, including NO effective treatment to stop progression
suspiciousness and delusions (such as Lifespan w/ disease 5-20 yrs; cost is
believing that their caregiver is an approximately $19,000 annually
impostor)or compulsive, repetitive Most pt die from complications related to
behavior like hand-wringing or tissue the disease such as pneumonia,
shredding malnutrition, or dehydration
Tend to wander or become lost
4. M Y E S T H E N I A GRAVIS
Stage 7 (Terminal stage)
Severe mental and physical deterioration ETIOLOGY/PATHOPHYSIOLOGY
Hospice appropriate -Autoimmune disease of the neuromuscular
Very severe cognitive decline junction
(Severe or late-stage Alzheimer's disease) -Neuromuscular disorder; nerve impulses fail
In the final stage of this disease, to pass at the myoneural junction; causes
individuals lose the ability to respond to muscular weakness
their environment, to carry on a -Can occur at any age but common between
conversation and, eventually, to control ages 10 to 65. Peak in women age 20 – 30.
movement. They may still say words or -Women more affected than men in young but
phrases. equals out at older age
At this stage, individuals need help with -Infants of mothers with MG may be
much of their daily personal care, symptomatic at birth
including eating or using the toilet. They -25% patient have Thymoma (cancer of the
may also lose the ability to smile, to sit thymus)
without support and to hold their heads -80% have cellular structure of the thymus
up. Reflexes become abnormal. Muscles gland
grow rigid. Swallowing impaired.
CLINICAL MANIFESTATIONS
Assessment Ptosis (eyelid drooping); diplopia (double
Memory loss initial sign combined w/ vision); 15% of cases confined to the eye
inability to carry out normal activities. muscles
Skeletal weakness; ataxia (lack of
Diagnostic Tests voluntary coordination of muscle
No specific test for AD movements)
CT, EEG, MRI, and PET may be used to Dysarthria (difficulty w/ speech);
rule out other pathologic conditions dysphagia (difficulty swallowing)
At times only confirmation is at autopsy Bowel and bladder incontinence
Exacerbations may be initiated by upper
respiratory infections, emotional tension,
MANAGEMENT and menstuation
Pharmacological management
Agitation: Lorazepam; Haldol MANAGEMENT
Dementia: Cognex ; Aricept (short-term Pharmacological management
benefit for mild cognitive impairment Anticholinesterase drugs (promote nerve
(MCI) , slows progression by up to 3 yrs) impulse transmission and quite effective
Namenda used for moderate to sever (only of alleviating symptoms)
slows symptoms not MCI) Prostigmin
Nutrition Mestinon
Finger foods; frequent feedings; encourage Corticosteroids (adjunct therapy d/t
fluids (2000 ml/day) immune component)
Imuran
Cyclosporine Tests may be done to rule out other
Caution with certain drugs: causes (i.e. blood, CT or MRI,
Anesthetics, antidysrhythimics, Electromyography, spinal tap, swallow
antibiotics, quinine, antipsychotics, studies, nerve conduction)
barbituates, sedatives, hypnotics, opioids,
tranquilizers, and thyroid prep NO CURE
Plasmapheresis removes antibodies produced Pharmacological management
by the autoimmune response…short term fix Rilutec (Riluzole): slows the progression of
Thymectomy if thymoma is present ALS and prolongs life. Helps protect
Intravenous immune globulin to reduce motoneurons damaged by the disease
production of acetylcholine antibodies used Baclofen or diazepam: used to control
only in severe relapse of MG spasticity that interferes with daily
May require mechanical ventilation activities
Prognosis: chronic disease Trihexyphenidyl or amitriptyline: used for
people w/ problems of swallowing their
5. A M Y O T R O P H I C L A T E R A L own saliva
SCLEROSIS
G-Tube placement due to choking
ETIOLOGY/PATHOPHYSIOLOGY Complications:
Motor neurons in the brain stem and Aspiration
spinal cord gradually degenerate Loss of abilty to care for self
Electrical and chemical messages Lung failure (ARDS)
originating in the brain do not reach the Pneumonia
muscles to activate them Pressure sores
Lou Gehrig’s disease famous baseball Weight loss
player stricken in early 1940’s Multidisciplinary ALS teams; emotional
Onset between ages 40-70 (2:1 support;
men:women) Part of the Muscular Dystrophy
10% of cases is genetic defect Foundation
Effects 5 out of every 100,000 people ALS Associan
worldwide Prognosis
Death. Lifespan post diagnosis typically
CLINICAL MANIFESTATIONS ranges 2-6 years. Approximately 25%
Weakness of the upper extremities patients live for more than 5 years (up to
Head drop due to weak neck muscles 7 years)
Muscle cramps
Muscle contractions called fasciculations 6. H U N T I N G T O N’S DISEASE
Dysarthria (speech difficulty)
Dysphagia (difficulty swallowing) ETIOLOGY/PATHOPHYSIOLOGY
Choking easily Like Parkinson’s disease involves the
Drooling basal ganglia and the extrapyramidal
Gagging motor system
Muscle wasting Overactivity of the dopamine pathways
paralysis Genetically transmitted autosomal
Compromised respiratory function dominant disorder that affects both men
Difficulty breathing and women of all races. Defect on
Weight loss chromosome 4
DOES NOT AFFECT THE SENSES (sight, Offspring of person w/ disease has 50%
smell, taste, hearing, touch) chance of developing disease
Two forms:
MANAGEMENT Adult-onset (most common) symptoms in
Diagnostics mid 30s-40s
Medical Hx. w/ strength and endurance Early-onset symptoms occur during
eval (muscle tremors , spasms, twitching, childhood or adolescence
or loss of muscle tissue (atrophy),
twitching of tongue is common) CLINICAL MANIFESTATIONS
Abnormal reflexes, stiffness and Behavioral
clumsiness Hallucinations
Emotional incontinence Irritability
Moodiness Loss of ability to interact
Restlessness or fidgeting Injury to self or others
Paranoia Increased risk for infection
psychosis Depression
Abnormal and excessive involuntary death
movements (chorea) Prognosis
Facial movements, including grimaces Causes disability that gets worse overtime
Head turning to shift eye position Average lifespan from onset of symptoms
Wild jerking of extremities face and other is 15-20 years.
body parts Cause of death is often infection or suicide
Slow, uncontrolled movement
Abnormal reflexes VI Vascular Problems
Hesitant speech or poor enunciation
Ataxia to immobility 1. S T R O K E (CEREOBROVASCULAR
Unsteady gait ACCIDENT)
“Prancing” and wide walk
ETIOLOGY/PATHOPHYSIOLOGY
Deterioration in mental functions Brain attack
Dementia -Abnormal condition of the blood vessels of
Disorientation or confusion the brain: 2 types
Loss of judgment 85% thrombosis & embolism = ischemic
Loss of memory stroke
Personality changes 15% hemorrhage = hemorrhagic stroke
Speech changes (weak and bursts open, aneurysm,
Symptoms in children arteriovenous malformation)
Rigidity -Results in ischemia of the brain tissue
Slow movements -Most common disease of nervous system
Tremors (estimated 700,000 suffer strokes each yr. and
the cause of 158,000 deaths annually)
MANAGEMENT -All ages affected
Diagnostics -Greatest number between ages 75-85
CT of head may show loss of brain tissue -Residual effects vary from mild deficits to
MRI or PET of brain severe disabilities
Genetic tests -Hemiparesis (weakness or paralysis of one
Treatment side of the body), inability to walk, complete or
NO CURE; palliative care (treat the
symptoms)
Pharmacological management
Antipsychotics: Dopamine blockers
may reduce abnormal behaviors
(Azilect, Clozaril, Reglan, Haloperidol)
Antidepressants (Depression and
suicide common (assess for S&S))
Antichoreas (Amantadine &
tetrabenzine: used to control extra partial dependence with ADL’s and aphasia
movements)
Co-enzyme Q10: help slow down the Risk Factors
course of the disease (but not conclusive) Atrial Fibrillation
Diabetes
Safe environment Family Hx of stroke
Emotional support High Cholesterol
Huntington’s Disease Society of America Increasing age >65
www.hdsa.org Race (black people are more likely to die of
High-calorie diet a stroke)
As much as 4000-5000 kcal/day to Unhealthy lifestyle
maintain body weight due to involuntary Overweight or obese
body movements Drinking heavily
Complications To much fat or salt in diet
Loss of ability to care for self Smoking
Illegal drugs (cocaine) American Stroke Association
Birth control pills www.strokeassociation.org
Pharmacological Management
Anti-seizure drugs (carbamazepine CLINICAL MANIFESTATIONS
(Tegratol), gabapentin, phenytoin, Facial numbness or stiffness
valproate, and pregabalin) Hard to close one eye
Muscle relaxants (baclofen, clonazepam) Problems w/ smiling, grimacing, or
Tricyclic antidepressants (amitriptyline, making facial expressions
nortriptyline) Drawing sensation of the face
Twitching
Surgical resection of the trigeminal nerve Unilateral weakness of facial muscles
Within 24 hrs of resection of 5th nerve pt Drooping of face
develops herpes simplex of the lips (cold Reduction of saliva
sores) heals in about a week (5-14 days) Drooling
Avoid stimulation of face on affected side Pain behind the ear
Comfort measures Ringing in ear or other hearing loss
Keep room free of drafts
Avoid walking briskly to bedside of patient MANAGEMENT
Place bed out of traffic area to prevent Diagnostics
jarring of bed CT scan or MRI of the head
avoid touching the patients face Electromyography (EMG) or Nerve
Don’t urge pts to wash or shave the conduction test to check nerves that
affected area or to comb the hair supply the muscles of the face
Avoid hot or cold liquids, may trigger pain Treatment
Puree food and ensure that it is Often no tx needed. Begins to resolve
lukewarm. Suggest food be taken through immediately but may take up to months
a straw to get full muscle strength
Prognosis Eye drops to lubricate if needed or an eye
Depends on cause. Pain varies and patch when sleeping
permanent relief of pain is obtained only Pharmacological management
by surgery Corticosteroids may reduce swelling
Pain can be disruptive to lifestyle. Can be around the facial nerve
total physical and psychological Antiviral medications in an attempt to
dysfunction or even suicide. fight off virus that may be causing bell’s
palsy
2. B E L L E’ S PALSY
Electrical stimulation
ETIOLOGY/PATHOPHYSIOLOGY Moist heat
-Inflammatory process involving the facial Massage of the affected area
nerve VII from the nucleus in the brain to the Facial exercises
periphery Prognosis
-Damage to this nerve causes weakness or Usually resolve on own
paralysis of these muscles Long term changes in taste
-Evidence the reactivated herpes simplex Spasms of muscles or eyelids
(HSV) may be involved. Causing inflammation, Weakness that remains in facial muscles
edema, ischemia, and demyelination of the Complications
facial nerve. Excess drying of the eye surface, leading
-Can be unilateral (one side) or bilateral (both to eye ulcer or infections
sides)
Causes, Incidence, and risk factors
-Affects 30,000-40,000 people in the USA 3. G U I L L A I N E - B A R R E
-Cause is not clear. But may be caused by SYNDROME
other disease processes such as:
-Herpes simplex ETIOLOGY/PATHOPHYSIOLOGY
-HIV infection -Inflammation and demyelination of the
-Middle ear infection peripheral nervous system
-Possibly viral or autoimmune reaction
-Most common in people of both sexes
between the ages of 30-50
-Often follows a minor infection, such as lung
or GI infection
-Nerve damage causes tingling, muscle 4. M E N I N G I T I S
weakness, and paralysis. Guillian-Barre
syndrome most often affects the nerves’ ETIOLOGY/PATHOPHYSIOLOGY
covering (myelin sheath) and causes nerve -Acute infection of the meninges
signals to move more slowly or not at all. -Bacterial or aseptic
-Increased incidence in winter and fall months
CLINICAL MANIFESTATIONS
Symptoms are progressive CLINICAL MANIFESTATIONS
Paralysis usually starts in the lower Headache; stiff neck
extremities and moves upward; may stop Irritability; restlessness
at any point Malaise
Respiratory failure if intercostal muscles Nausea and vomiting
are affected Delirium
May have difficulty swallowing, breathing, Elevated temperature, pulse, and
and speakingSymptoms are progressive respirations
Paralysis usually starts in the lower Kernig’s and Brudzinski’s signs
extremities and moves upward; may stop
at any point MANAGEMENT
Respiratory failure if intercostal muscles Pharmacological management
are affected Antibiotics
May have difficulty swallowing, breathing, Massive doses
and speaking Multiple types
IV or intrathecal
MANAGEMENT Corticosteroids
Diagnostics Anticonvulsants
Lumbar puncture Antipyretics
ECG
Electroyography (EMG) Dark, quiet room
Nerve conduction velocity test
Pulmonary function tests 5. E N C E P H A L I T I S
MANAGEMENT
Prevention
7. B R A I N ABCESS MANAGEMENT
Surgical removal of tumor
ETIOLOGY/PATHOPHYSIOLOGY a. Craniotomy
-Accumulation of pus within the brain tissue b. Intracranial endoscopy
Radiation
CLINICAL MANIFESTATIONS Chemotherapy
Headache Combination of above
Fever
Drowsiness, changes in LOC VIII. Trauma
Seizures
1. C R A N I O C E R E B R A L T R A U M A
MANAGEMENT
Antimicrobial therapy ETIOLOGY/PATHOPHYSIOLOGY
Supportive care -Motor vehicle and motorcycle accidents, falls,
industrial accidents, assaults, and sports
trauma
8. A C Q U I R E D -Direct trauma: Head is directly injured
IMMUNODEFICIENCY -Indirect trauma: Tension strains and
SYNDROME shearing forces
-Open head injuries
ETIOLOGY/PATHOPHYSIOLOGY -Closed head injuries
-Symptoms may develop from the infection -Hematomas
with HIV or as a result of an associated
infection CLINICAL MANIFESTATIONS
Headache
CLINICAL MANIFESTATIONS Nausea
AIDS dementia complex (ADC) Vomiting
Memory loss Abnormal sensations
Global cognitive dysfunction Loss of consciousness
Bleeding from ears or nose
MANAGEMENT Abnormal pupil size and/or reaction
Antiviral, antifungal, antibacterial agents Battle’s sign
Anticonvulsants
Safety MANAGEMENT
Maintain airway
Oxygen
9. B R A I N TUMORS Mannitol and dexamethasone
Analgesics
ETIOLOGY/PATHOPHYSIOLOGY Anticonvulsants
-Benign or malignant
-Primary or metastatic
-May affect any area of the brain 2. S P I N A L CORD TRAUMA
CLINICAL
MANIFESTATIONS
Loss of muscle function depends on level
of injury
Spinal shock
Autonomic dysreflexia
Sexual dysfunction
MANAGEMENT
Realignment of bony column for fractures
or dislocations: Immobilization; skeletal
traction
Surgery for spinal decompression
Methylprednisolone
Mobility: Slowly increase sitting up
Urinary function: Foley catheter; bladder
training
Intermittent catheterization
Bowel program
Nursing diagnoses
1. Autonomic dysreflexia
2. Communication, impaired
3. Coping, compromised family
4. Disuse syndrome, risk for
5. Grieving
6. Infection, risk for
7. Knowledge, deficient
8. Memory, impaired
9. Mobility, impaired physical
10. Nutrition, imbalanced: less than body
requirements
11. Pain, acute, chronic
12. Self-care deficit
13. Swallowing, impaired
14. Thought process, disturbed
15. Tissue perfusion (cerebral), ineffective