NEUROLOGIC DISORDER

PATHOPHYSIOLOGY

ASSESSMENT FINDINGS

INTERVENTIONS

MEDICATIONS

ENCEPHALITIS
- a severe inflammation of the brain
- an acute inflammatory process of the
brain tissue. HSV is the most common
cause of acute encephalitis
HERPES SIMPLEX VIRUS
ENCEPHALITIS

There are two possible modes of HSV-1

infection. In most cases primary HSV-1
infection of the buccal mucosa occurs,
followed by retrograde spread along the
trigeminal nerve to the brain. It is also
believed that latent virus in brain tissue
may reactivate and result encephalitis.
HSV-2 most commonly affects neonates.
Clinical manifestations
fever
headache
confusion
behavioral abnormalities
focal seizures
dysphasia
hemiparesis
altered level of consciousness

ARTHROPOD-BORNE VIRUS
ENCEPHALITIS
Arthoropod vectors transmit
several types of viruses that cause
encephalitis.

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Viral replication occurs at the site of the

mosquito bite. If adequate virus is
inoculated, a viremia ensues. The virus
gains access to the CNS via the cerebral
capillaries. It spreads from neuron to
neuron, predominantly affecting the
cortical gray matter, the brain stem, and
the thalamus. Meningeal exudates
compound the clinical presentation by
irritating and increasing ICP
Clinical manifestations
begins with flu-like symptoms

Neuroimaging studies:
EEG : demonstrates a specific
wave pattern
CSF examination : reveals a high
opening pressure and low
glucose and high protein
levels
MRI : dx choice
PCR : identify the DNA bands of
the HSV specifically

CT scan and MRI : reveal lesions

CSF analysis : shows a normal
glucose level, protein level,
polymorphonuclear leukocytic
pleocytosis

Pharmacologic Management
Acyclovir
Nursing Management
Assessment of neurologic
function key to monitor
progression of disease
Comfort measures reduce
headache
Nursing care addressing
patient and family anxiety

Medical Management
No specific medication for
arboviral encephalitis
Nursing Management
Assessment of neurologic
status
Injury prevention
Public education
Mosquito control

Acyclovir (Zovirax) - medication of

choice in HSV treatment. The
mode of actioin is the inhibition of
viral DNA replication.
Opioid Analgesic medication
pain and comfort

None

FUNGAL ENCEPHALITIS

The fungal spores enter the body via

inhalation. They initially infect the lungs,
causing vague respiratory symptoms. In
some cases, the fungi may enter the
bloodstream, causing a fungemia. If the
fungemia overcomes the persons
immune system, the fungus may spread
to the CNS. The initial presentation is
meningitis followed by encephalitis and
brain abscesses. In addition to infecting
the brain, the fungi may infect the spinal
cord, producing an abscess .The
abscess will produce symptoms of spinal
cord compression.

CREUTZFELDT-JAKOB DISEASE
& NEW-VARIANT CREUTZFELDTJAKOB DISEASE
- disease belong to a group of degenerative,
infectious neurologic disorders called
transmissible spongiform encephalopathies

Although still debated, the causative

agent appears to be a prion, a
proteinaceous, infectious particle smaller
than a virus. The prion converts a
normal cellular protein to an abnormal
form, thus destroying neurons and glial
cells. The gray matter takes on a
spongy appearance..
Transmission is frequently unknown;
however, direct transmission(by contact
of infected animals) of the prion to
humans may initiate the degenerative
neurologic process.
Disease is also heritable

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Laboratory evaluation: blood

shows an white cell count and
anemia
CSF: elevated white cell count and
protein levels
Neuroimaging
MRI and CT scan: indicate lesions

EEG: sharp waves and spikes; only

features available to support the
diagnosis of CJD.
CSF analysis: detection of polyclonal
antibody, protein with presence of
enzymes indicative of neuronal loss
MRI: to identify lesions
Biopsy and Autopsy: definitive
diagnosis

Medical Management
Directed at the causative fungus
and the neurologic consequences
of infection
Nursing Management
Early identification
Providing patients comfort
Monitoring serum creatinine and
blood urea nitrogen levels:
development of renal insufficiency
Providing support

Anti-seizure
Ampothericin B : treat fungi,
standard antifungal agent
Fluconazole (Diflucan) or
Flucytosine (5-FC, 5fluorocytosine, Ancobon) may be
administered in conjunction with
Ampothericin B
Diphenhydramine (Benadryl) and
acetaminophen (Tylenol) : to
prevent Amphotericin B side-effects

none
Medical Management
No effective treatment of CJD
or nvCJD
Nursing Management
Supportive and palliative care
Psychosocial and emotional
support of patients and families
throughout the course of the
illness is needed
Prevention of transmission
Aseptic technique

NEUROLOGIC DISORDER

PATHOPHYSIOLOGY

ASSESSMENT FINDINGS

INTERVENTIONS

MEDICATIONS

Assessment
Impaired neural function LOC
changes
Slowing of speech & delay in
response to verbal suggestions
Abnormal respiratory & vasomotor
response
Restlessness, confusion, increasing
drowsiness
Comatose, dilated & fixed pupils,
impaired respirations, death
Cerebral angiography, CT, MRI,
PET, transcranial doppler

Management
Monitor ICP through
ventriculostomy, subarachnoid bolt,
epidural monitor, fiberoptic monitor
Decrease cerebral edema using
osmotic diuretics
Corticosteroids for patients with
brain tumors
Fluid restriction
Maintain cerebral perfusion by fluid
volume & inotropic agents
CSF drainage
Hyperventilation for patients whose
ICP is unresponsive to conventional
therapies
Control fever by administering
antipyretic & muscle relaxants.
Prevent shivering.
Reduce metabolic demands using
high doses of barbiturates for
patients who are unresponsive to
conventional treatments
Measure venous oxygen saturation
in jugular bulb (SjO2)
Nursing interventions:
o Suction to maintain airway
o Avoid coughing, straining
o Auscultate lung fields q8h
o Elevate HOB 30 to 60 degrees
o Keep head in a neutral (midline)
position, with cervical collar to
promote venous drainage

Osmotic & loop diuretics &

corticosteroids

NEUROLOGIC DYSFUNCTION
INCREASED INTRACRANIAL
PRESSURE

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Head Injury, brain tumors

subarachnoid hemorrhage, toxic & viral
encephalitis cerebral perfusion
Cerebral edema Herniation

o Prevent infection

SEIZURES

EPILEPSIES

1.) Idiopathic: genetic & developmental

defects 2.) Acquired: hypoxemia,
vascular insufficiency, fever, head injury,
HPN, CNS infections, metabolic & toxic
conditions, brain tumor, drug & alcohol
withdrawal, allergies, cerebrovascular
(leading cause) Electrical disturbance
in nerve cells Sudden excessive
electrical discharges

Continuous firing of neurons Body

parts controlled perform erratically
Body parts controlled perform
erratically Mild to incapacitating
dysfunction & loss of consciousness

Loss of consciousness
Excessive movement
Loss of muscle tone or movement
Disturbance of behavior, moos,
sensation & perception

Staring episode
Prolonged convulsive movement
with loss of consciousness
Simple partial: shaking of hand &
finger, jerking of mouth, talk
unintelligibly, dizziness, unusual &
unpleasant sights, sounds, odors,
tastes
Complex: motionless or moves
automatically, excessive emotions of
fear, anger, elation, irritability,
doesnt remember episode
Generalized: intense rigidity of
entire body followed by alternating
muscle relaxation & contraction,
simultaneous contractions of the
diaphragm & chest muscles
produces epileptic cry, tongue is
chewed, urinary & bowel

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During a seizure
Keep airway patent
o Observe & record the sequence
of symptoms
o Prevent injury & support patient
physically & psychologically
o Do not restrain
o Loosen clothing
After a seizure
o Document events leading to &
occurring during the seizure & to
prevent complications (eg,
aspiration & injury)
o Side lying position
o Suction
o Bed is placed in a low position
with side rails up & padded

Surgical management for those with

intracranial tumors, abscess, cysts,
vascular anomalies
Prevent injury by placing patient on
floor appropriately, never be forced
in a position
Pad siderails
Ensure proper compliance with
medications
Wear dark 4eurolo or cover one eye
if photic stimulation brings about
seizure
Avoid alcohol
Stress management classes

IV Diazepam
Dilantin
Phenobarbital
Tegretol

STATUS EPILEPTICUS

Withdrawal of antiseizure medication,

fever, concurrent infection
Generalized seizures Vigorous
muscle contractions Possible
respiratory arrest, cerebral anoxia &
edema

incontinence
ECG & SPECT
Clinical or electrical seizures lasting
at least 30 minutes
IV diazepam, lorazepam or
fosphenytoin

CEREBROVASCULAR
DISORDERS
ISCHEMIC STROKE

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Ischemic brain attack disruption of

blood flow due to obstruction of a
blood vessel
Disruption initiates a complex series
of cellular metabolic events called
ISCHEMIC CASCADE
ISCHEMIC CASCADE
o Cerebral blood flow falls to less
than 25 mL/100g/min (at this pt
neurons can no longer maintain
aerobic respiration.
o Mitochondria then switch to
anaerobic respiration which 1.)

Airway & adequate oxygenation

IV line is established
Blood samples to monitor serum
electrolytes, glucose & phenytoin
levels
EEG
Nursing management:
o Assess & monitor respiratory &
cardiac function brought about
by medications & sedatives
o Document seizure activity &
patients responsiveness
o Side lying position to assist in
draining pharyngeal secretions
o Suction as necessary
o Prevent injury

Motor loss
Because of a lesion of the upper
motor neurons
Hemiplegia paralysis of one side
of the body due to a lesion of the
opposite side of the brain
Hemiparesis weakness of one
side of the body
Early stage of stroke: flaccid
paralysis, loss or decrease in the

ACUTE PHASE:
Maintain patent airway
Maintain BP at 150/100 for cerebral
perfusion
Suction as Rx but not nasally for no
longer than 10 seconds
Monitor for increased ICP during
first 72 hrs.

Thrombolytic therapy dissolving

the blood clot that is blocking the
blood flow to the brain.
-recombinant t-PA a genetically
engineered form of t-PA, a
thrombolytic subs made
naturally by the body. Works
by: binds to fibrin ? converts
plasminogen to plasmin ?
fibrinolysis stimulated
-max dose: 90 mg min dose: 0.9
mg/kg

generates large amts. of lactic

acid causing a change in pH
level 2.)renders the neuron
incapable of producing sufficient
quantities of ATP to fuel the
depolarization process
o The membrane pumps that maintain
electrolyte balances begin to fail
and the cells cease to fxn.
o A penumbra region (ischemic brain
tissue that can be salvaged with
timely intervention; an area of
low cerebral region) exists
around the area of infarction.
o The ischemic cascade threatens the
cells in the penumbra because
membrane depolarization of the
cell wall leads to an increase in
intracellular calcium and the
release of glutamate.
o The penumbra area can be
revitalized by the administration
of tissue plasminogen activator
(t-PA); The influx of calcium can
be limited with the use of calcium
channel blockers.
o The continued influx of calcium and
release of glutamate activate
a number of damaging pathways
destruction of the cell
membrane release of more
calcium and glutamate
vasoconstriction generation of
free radicals enlarge the area
of infarction into the penumbra
extension of stroke

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deep tendon reflexes.

When deep tendon reflexes
reappear (usually by 48 hrs),
increased tone is observed along
with spasticity (abnormal increase
in muscle tone) of the extremities
on the affected side.
Communication loss
Dysarthria difficulty in speaking;
caused by paralysis of the muscles
responsible for producing speech.
Dysphasia or aphasia defective or
loss of speech
apraxia inability to perform a
previously learned action.
Perceptual disturbances
a. visual perceptual
due to disturbances of the
primary sensory pathways
between the eye and visual
cortex.
Homonymous hemianopsia
loss of half of the visual field
b. visual spatial
perceiving the relation of two
or more objects in spatial areas
seen in patients with right
hemispheric damage
c. sensory loss
slight impairment of touch
loss of proprioreception
ability to perceive the position
and motion of the body parts
difficulty in interpreting visual,
tactile and auditory stimuli.
Cognitive impairment and

Position at the side with head of

bed elevated 15-30 degrees as Rx
Perform neuro checks
POST-ACUTE PHASE
Position on the unaffected side for
two hrs and 20 mins on the affected
side.
Skin & eye care
Provide anti-embolic stockings
Monitor gag & swallowing reflexes
Feeding: when able to swallow, give
semi-soft & soft foods rather than
liquids; upright position for feeding
with head and neck slightly forward
& flexed; place foods on the
unaffected side
If patient is recovering from ischemic
stroke:
-improving mobility and
preventing joint deformities
arms tend to adduct and to
rotate internally, elbows and
wrist tend to flex, affected leg
tend to to rotate externally at
the hip joint and flex at the
knee, foot at the ankle joint
supinates and tends towards
plantar flexion.
Correct positioning
Posterior splint applied at night
to the affected part prevent
flexion and maintain correct
positioning during sleep
Preventing shoulder adduction
pillow placed under the arm.
Elbow positioned higher than
the shoulder and the wrist
higher than the elbow (prevent
edema and joint fibrosis)

-loading dose: 10% of the

calculated dose administered
over 1 minute
-remaining dose: administered 1
hr via an infusion pump
-after infusion completed: line
flushed with 20 ml of NSS-to
ensure all med is administered
-continuous cardiac monitoring
required
-SE: bleeding
Therapy for those not receiving t-PA
-anticoagulant administration,
maintenance of cerebral
hemodynamics to maintain
cerebral perfusion
-elevate HOB to promote
venous drainage and to lower
increased ICP
-intubation with ET ensure
patent airway
-continuous hemodynamic
monitoring systolic pressure
should be maintained at less
than 180 mm Hg, diastolic
pressure at less than 100 mm
Hg (reduces the potential for
addtl bleeding or further
ischemic damage.
-neurologic assessment to
determine whether the stroke
is evolving or other
complications have developed
Platelet inhibiting meds (aspirin,
dipyridamole [Persantine],
clopidogrel [Plavix], ticlopidine
[Ticlid]) decrease incidence of
cerebral infarction in pts who have
experienced TIA

psychologoical effects
frontal lobe damage: impaired
learning capacity, memory,
intellectual fxns.
Limited attention span,
difficulties in comprehension,
forgetfulness, lack of
motivation, depression,
emotional lability, hostility,
frustration, resentment, lack of
cooperation.

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Intracerebral hemorrhage

Positioning the hands and the

shoulders slight supination
(palms faced upwards); upper
extremity spastic: dont use
hand roll because it stimulates
grasp reflex.
Changing positions every 2
hrs; when side lying, place
pillow in between legs before
pt is turned. Upper thigh
shouldnt be acutely flexed bec
can cause edema; Prone
position for 15-30 min several
times a day. Small pillow under
the pelvis from the level of
umbilicus to upper 3rd of thigh
to promote hyperextension of
the hip joints essential for
normal gait, draining
secretions. Reduce pressure,
position frequently to prevent
pressure ulcers.
Establishing an exercise
program passive exercises,
full ROM 4-5 times a day
Preparing for ambulation
taught to maintain balance
when sitting then standing; use
of tilt tables.
Preventing shoulder pain
never lift the pt by the flaccid
shoulder because dislocation
could occur; admin of Lamictal
to treat post stoke pain;
properly worn sling; ROM
exercises; elevation of arms
and hands to prevent
peripheral edema

HEMORRHAGIC STROKE

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- bleeding into the brain substance

- common in pts with HPN, cerebral
atherosclerosis (cause rupture of
vessel)
- may be due to arterial pathology,
brain tumor and use of meds
(oral anticoagulants,
amphetamines, and illicit drugs
such as crackles and codeine)
- occur commonly in the cerebral
lobes, basal ganglia, thalamus,
brain stem, cerebellum
- bleeding ? ruptures wall of lateral
ventricle ? intraventricular
hemorrhage
intracranial (cerebral) aneurysm
- weakness in the arterial wall ?
dilation of the walls of a cerebral
artery
- may be due to atherosclerosis,
congenital defect of the vessel
wall, HPN, advancing age
- usually occurs at the bifurcation of
the large arteries at the Circle of
Willis
- most commonly affected: internal
carotid artery (ICA), anterior
cerebral artery (ACA), anterior
communicating artery (ACoA),
posterior communicating artery
(PCoA), posterior cerebral artery
(PCA) and middle cerebral artery
(MCA)
- multiple aneurysms are uncommon
arteriovenous malformations (AVM)
- due to an abnormality in embryonal
devt ? Tangle of arteries & veins
in the brain w/o a capillary bed ?
absence of capillary bed ?
dilation of arteries and veins ?

Manifestations:
neurologic deficits
rupture of AVM: sudden,
severe headache, loss of
consciousness, pain and
rigidity of the back of the neck
(nuchal rigidity) and spine due
to meningeal irritation, tinnitus,
dizziness, hemiparesis, severe
bleeding

CT scan and cerebral

angiography dx of aneurysm
or AVM; location, size of lesion,
affected arteries, veins
adjoining vessels and vascular
branches

Lumbar puncture if there is

no evidence of increased ICP,
the CT scan results are (-).
Shouldnt be done with an
increased ICP because it can
result to brain stem herniation
or bleeding. If pt younger than
40, obtain a toxicology screen
for elicit drug use.
Hunt-Hess classification
system dx of the severity of
subarachnoid hemorrhage
after an aneurismal bleed.

MEDICAL
To allow the brain to recover from the
initial insult, to minimize the risk for
rebleeding, top prevent or treat
complications
Bedrest with sedation to prevent
agitation and stress, mgt of vasospasm,
analgesics for pain, elastic compression
stockings to prevent deep vein
thrombosis.
Complications and mgt:
Cerebral hypoxia and
decreased blood flow
adequate hydration to reduce
blood viscosity and improve
cerebral blood flow; avoid
extremes of HPN or
hypotension to prevent
changes in cerebral blood flow
and potential bleeding; admin
of 02 as ordered
Vasospasm- narrowing of the
lumen; clipping of aneurysm;
removal of blood from the
basal cisterns around the
major arteries; IV admin of
Nimodipine (ca channel
blocker) or fluid volume
expanders to prevent ischemic
deterioration
Increased ICP CSF drainage

rupture
- most common in young people
subarachnoid hemorrhage
- as a result of an AVM, intracranial
aneurysm, trauma or HPN
- most common cause: leaking
aneurysm in the area of the
Circle of Willis or a congenital
AVM of the brain

by lumbar puncture; mannitol

to reduce ICP; monitor for
dehydration due to Mannitol
Seizures maintain airway;
prevent injury; antiseizure
Dilantin
Hydrocephalus
venticuloperitoneal shunt
Rebleeding antifibrinolytic
meds (epsilon aminocaproic
acid) to delay the lysis of the
clot surrounding the rupture

SURGICAL MGT

Ligation or clipping of
aneurysm to exclude
aneurysm from cerebral
circulation
Extracranial-intracranial
bypass to establish collateral
blood supply to allow surgery
on the aneurysm
Endovascular tx occlusion of
the parent artery
Aneurysm coiling obstruction
of the aneurysm site with a coil
Postop complications:
disorientation, amnesia,
Korsakoffs syndrome,
personality changes,
injtraoperative embolism,
internal artery occlusion FE
imbalance, GI bleeding

NURSING

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Optimizing cerebral tissue

perfusion VS, LOC, papillary

ISTIONKO/USTCON/05

INFECTIOUS
MENINGITIS- inflammation of the
meninges, the protective membrane lining the
brain and spinal cord.

ASEPTIC/ VIRAL MENINGITIS- the

cause is viral (mumps virusor one of the
picornaviruses) or secondary to lymphoma,
leukemia, or brain abscess.

SEPTIC MENINGITIS- caused by bacteria,

most commonly Neisseria meningitides, also
Haemophilus influenzae and Streptococcus
pneumoniae are also causative agents.

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1.) Bloodstream (as a consequence of

other infections) 2.) Direct extension
(such as might occur after a traumatic
injury to the facial bones or secondary to
invasive procedures)
Causative Organism enters the
bloodstream Causative organism
crosses the blood-brain barrier
Causes inflammatory reaction in the
meninges Inflammation of SAS and
pia mater ICP and
CSF cell count

Initial Manifestations:
- headache
- fever
Classical Manifestations:
- nuchal rigidity
- (+) Kernigs sign
- (+) Brudzinskis sign
- photophobia
Others:
- rash; skin lesions (ranging from
petechial rash with purpuric lesions
to large areas of ecchymosis)
- disorientation and memory
impairment
- behavioral manifestations
- lethargy, unresponsiveness and
coma may develop as the illness
progresses
- seizures (sec. to focal areas of
cortical irritability )
- Increased ICP (sec. to

responses and motor

responses checked hourly
Implementing aneurysm
precautions bedrest; HOB
elevated 15 to 30 degrees to
promote venous drainage and
decrease ICP; avoid activities
requiring exertion; no enemas;
stool softeners and laxatives;
dim lighting because of
photophobia; avoid coffee and
tea; thigh high elastic
compression stocking to
prevent deep vein thrombosis.
Relieving sensory deprivation
and anxiety reduce pts
sense of isolation; pt
reassurance; keep pt and
family informed of procedures

Prevention: vaccination
Nursing. Mgt.:
- Neurologic status and VS
continually assessed
- Monitoring of body wt. serum
electrolytes and urine volume,
specific gravity and osmolality
- Protect client from injury (seizure
or altered LOC)
- Preventing complications
- Instituting droplet precaution until
24 hrs. after the initiation
Early administration of antibiotic
( penicillin e.g. ampicillin and piperacillin;
cephalosporin e.g. ceftriaxone
sodium and cefotaxime sodium,)
( Vancomycin HCL)

accumulation of purulent
exudates); as manifested by
decrease LOC and focal motor
deficits)
- Fulminating infection

BRAIN ABSCESS
is a collection of either encapsulated or free
pus within brain tissue arising from a primary
focus elsewhere(e.g. ear, mastoid sinuses,
nasal sinuses, heart, distal bones, lungs, or
primary bacteremia) or is a collection of
infectious material within the tissue of the
brain.
- relatively rare but it is a
complication encountered
increasingly in patients whose
immune system have been
suppressed
- The frontal lobe is the most

Brain abscess may occur by

- direct invasion of the brain
from intracranial trauma or
surgery
- by spread of infection from
nearby sites such as sinuses,
ears and teeth (paranasal
sinus infections, otitis media,
dental sepsis)
- by spread of infection from
other organs (lung abscess,
infective endocarditis)
The abscess produces inflammation,
necrotic tissue and surrounding edema.
Within several days, the center of the
abscess is purulent, and a wall of
granulation tissue forms, encapsulating
the abscess. Infection may spread
through thin places in the wall of the
capsule, resulting in development of
additional abscesses.

Diagnostic evaluation:
- CBC with differential
( Increased WBC especially
polymorphonuclear leukocytes)
- Blood culture (to indicate the
organism)
- Lumbar puncture with CSF
examination
(moderately elevated CSF pressure
leukocytes; decrease glucose level;
increase protein level; (+) gram
stain)

Headache (usually worse in the

morning, is the most prevailing
symptom)
Vomiting
Focal neurologic signs
(weakness of an extremity,
decreasing vision, seizures
Change in mental status
(lethargic, confused, irritable or
disoriented behavior)
Fever may or may not be

Med. Mgt.:
- Antimicrobial therapy
- Surgical incision or aspiration
(CT-guided needle aspiration
under local anesthesia)
- Penicillin G and
chloramphenicol
- Corticosteroids
- Antiseizure meds

Adjunctive therapy
(Dexamethasone)
Dehydration and shock are treated
with fluid volume expanders.
Seizures are controlled with
phenytoin (Dilantin)

common site of a brain abscess

Toxoplasma is the usual agent found in
clients with HIV infection

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present
Frontal Lobe
- Hemiparesis
- Aphasia (expressive)
- Seizures
- Frontal headache
Temporal Lobe
- Localized headache
- Changes in vision
- Facial weakness
- Aphasia
Cerebellar Abscess
- Occipital headache
- Ataxia (inability to coordinate
movements)
- Nystagmus (rhythmic, involuntary
movements of the eye)
Diagnostic Evaluation:
- Repeated neurologic examinations
- MRI

Nsg. Mgt.:
- Ongoing assessment of
12eurologic status
- Administering meds
- Assessing the response to
treatment
- Providing supportive care

Antimicrobial therapy

NEUROLOGIC DISORDER
AUTOIMMUNE
MYASTHENIA GRAVIS

PATHOPHYSIOLOGY
Autoantibodies directed at the acetyl
choline receptor sites impair
transmission of impulses across the
myoneural junction. Therefore fewer
receptors are available for stimulation,
resulting in voluntary muscle weakness
that escalates with continued activity.

ASSESSMENT FINDINGS

Muscle weakness: dyspnea,

dysphagia, decreased physical
activity
Fatigue
Ptosis
Diplopia
Impaired speech
Strabismus
snarl smile
mask-like facial expression
drooling
respiratory difficulty, diminished
breath sounds

TENSILON TEST dx of MG and

differential for cholinergic & myasthenic
crisis

INTERVENTIONS
MEDICAL AND NURSING
MANAGEMENT

monitor respiratory status,

speech & swallowing abilities,
VS
assess gag reflex before
feeding the client
administer medications before
meals to prevent aspiration
protect from falls
aspiration precaution
start meal with cold beverages
adequate ventilation
avoid exposure to infection
adequate rest with activity
plasmapheresis
thymectomy
Observe for myasthenic &
cholinergic crisis
Myasthenic Crisis: acute
exacerbation due to
underdosage of meds, ifection,
stress & fatigue
TX: increase
anticholinesterase dose
Cholinergic crisis: due to
overmedication
Sx: restlessness, weakness,
Dysphagia, dyspnea, nausea
vomiting

MEDICATIONS

Cholinergic/
anticholinesterase::
neostiogmine, pyridostigmine,
endrophonium chloride
- adm. Meds on time
- give 30 mins before meals
with milk & crackers
- note for over- & underdosage
SE: sweating, salivation,
nausea, salivation, abdominal
cramps, bradycardia &
hypotension
glucocorticoids
antacids

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MULTIPLE SCLEROSIS

TX: Atropine SO4

Causes: idiopathic, viral infection,
autoimmune
multiple foci of demyelination in the
white matter (brain stem, spinal
cord, optic nerves, cerebrum then
later the gray matter)
destruction of the myelin sheath
(schwanns cell)
interruption / distortion of impulse
(slowed / blocked) conduction

GUILLIAN BARRE SYNDROME

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Myelin which provides insulation and

speeding the conduction of impulses
from the cell body to the dendrites. The
cell that produces myelin in the PNS is
the schwann cell. In guillain-barre the
schwann cell is spared, allowing for the
remyelination in the recovery phase of
the disease.It is a result of a cell
mediated immune attack on the
peripheral nerve myelin proteins. With
the autoimmune attack there is an influx
of macrophages and other immunemediated agents that attack myelin,
cause inflammation and destruction, and
leave the axon unable to support nerve
conduction

diplopia
scotoma
blindness
muscle spasm
weakness
numbness
fatigue
increase susceptibility to infection
emotional instability
euphoria during remissions
Charcots triad : scanning speech,
intention tremors, nystagmus
lhermittes sign: sudden electric
shock sensation experienced on
passive flexion of the neck
dysphagia
ataxic gait
LP- increased levels of IgG & IgM

muscle weakness
diminished reflexes of the
lower extremities
quadriplegia
neuromuscular respiratory
failure
paresthesias of the hand and
feet
pain related to the
demyelination of the sensory
fibers
blindness
bulbar muscle weakness
inability to swallow or clear
secretions
instability of the cardiovascular

MEDICAL AND NURSING

MANAGEMENT

eye patch for diplopia

well balanced diet, high in fiber
to prevent constipation
maintain optimal function
Promote ADLs
physical therapy
force fluids
avoid hot baths
plasmapheresis
speech therapy

medical emergency: ICU mgt.

assess changes in motor
weakness and respiratory
function
respiratory therapy /
mechanical ventilation
prevent the complications of
immobility: elastic stockings,
plasmapheresis
IVIG
Continuous ECG monitoring

muscle relaxants: baclofen

glucocortisoids: prednisone,
dexamethasone, corticotrophin
Amantadine (Symmetrel): Tx of
fatigue
Methylphenidate (Ritalin): CNS
stimulant that reduces fatigue
Fluoxetine (Prozac); Elavil:
antidepressant
Tegretol: anticonvulsant
***Steroids: prevent edema
formation at the sclerotic
plaques. Most effective Tx fro
acute exacerbations.
Vit B: supports cell replication;
enhances metabolic functions
Immunomodulating agents:
ABC: Avonex, Betaseron,
Copaxone
anticoagulant
alpha adrenergic blockers
steroids

DEGENERATIVE DISORDERS
PARKINSONS DISEASE

There is destruction of dopaminergic

neuronal cells in the substantia nigra in
the basal ganglia leading to depletion of
dopamine stores resulting then in the
degeneration of dopaminergic
nigrostriatal pathway and imbalance of
acetylcholine and dopamine
neurotransmitters in the corpus striatum
which is responsible for the impairment
of extrapyramidal tracts controlling
complex bodily movements thus there is
the occurrence of tremors, bradykinesia
and rigidity

system
CSF increased CHON

tremors pill rolling, involuntary

movement noticeable when the
extremities are at rest, walking,
feeling anxious and concentrating
rigidity resistance to passive limb
movement
bradykinesia most common sign,
has difficulty in initiating movement
hypokinesia abnormally
diminished movement
microphagia shrinking, slow hand
writing
dysphonia soft slurred, lowpitched, less audible speech
postural and gait problems
difficulty in pivoting and loss of
balance
diaphoresis, paroxysmal flushing
orthostatic hypotension
may have dementia
sleep disturbances and
hallucinations

Laboratory Test
PET scanning in evaluating
levels of levodopa uptake and
conversion
Laboratory and imaging studies are not
helpful in the diagnosis of parkinsons
ISTIONKO/USTCON/05

Medical Management
- Treatment is directed in controlling
symptoms and maintaining
functional independence because
there are no medical or surgical
that prevents disease progression.
- Care is individualized for each
patient
- Pharmacologic management is the
mainstay of treatment
- Patients are usually cared at home
and admitted to hospital when
complication arises
Surgical Management
Thalamotomy and
pallidotomyive in treating the
symptoms of parkinsons
disease
Neural transplantation of
adrenal medullary tissue is
performed in effort to restore
normal dopamine release
Deep brain stimulation
pacemaker like brain implants
It is not always practiced but it
is done if the condition is
serious
It does not produce permanent
improvement
Nursing Management
Improve mobility through daily
exercise
Enhance self care activities

Pharmacologic Management
Drugs act by:
Increasing striatal
dopaminergic activity
Reducing excessive excitatory
cholinergic neurons on the
extrapyramidal tract
Acting on neurotransmitter
pathway other than the
dopaminergic pathway.
Antiparkinsonian medications
Levodopa is the most effective
agent and mainstay of
treatment
Levodopa is converted to
dopamine in the basal ganglia
promoting relief
Prolong use could lead to
dyskinesia (abnormal
involuntary movements)
Patient may also experience
on-off syndrome
Anticholinergic therapy
Effective in controlling tremor
and rigidity
May be combined with
levodopa
Counteract neurotransmitter
acetylcholine
IOP must be monitored
Poorly tolerated by elderly
Patients with hyperplasia are
monitored for signs of urinary
retention.
Antiviral therapy

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Improve bowel elimination

Improve nutrition by
maintaining normal weight
Diet: hi CHON, hi caloric, hi
fiber, soft; fluids 2L/day
Enhance ability to swallow
Avoid foods high in Vit B6
since they block the effects of
anti-parkinson meds
Encourage the use of assistive
device
Improve communication
Promote PT & rehabilitation.
Provide emotional and
psychological support

Amantadine hydrochloride
(Symmetrel); effective agent
against parkinsons
Reduces tremor, rigidity and
bradykinesia
Has antiglutamatergic
properties
Dopamine agonist
Bromocryptine mesylate and
pergolide (ergot derivatives)
are dopamine receptor agonist
Useful in postponing the
initiation of carbidopa or
levodopa therapy
MAO inhibitors
Eldepryl inhibits dopamine
breakdown and slows the
progression of the disease
COMT inhibitors
Entacapone (Comtess) and
tolcapone (Tasmar) have little
effect on parkinsonian
symptoms when given alone
but increases the duration of
action when given with
carbidopa or levidopa
Blocks the enzyme that
metabolizes levodopa
Antidepressants
Trycyclic antidepressants
alleviates depression that is
common in parkinsons disease
Amitriptyline is prescribed
because of its anticholinergic
and antidepressant effect
SSRI are effective in treating
depression but may aggravate
parkinsonism
Antihistamine

Benadryl and Banflex and

NEO-synephrine have mild
anticholinergic and sedative
effects and may reduce
tremors

HUNTINGTONS DISEASE
Involves premature death of cells in the
striatum of the basal ganglia involved in
the control of movement. There is also
loss of cells in the cortex, region of the
brain associated with thinking, memory,
perception and judgement, and in the
cerebellum the area that coordinates
voluntary muscle activity. Glutamine a
protein that collects inside the cells is the
one that causes cell death. The cells
destruction results in a lack of
neurotransmitter GABA and
acetylcholine which inhibit nerve action.
The disease progresses slowly and
usually strikes persons aging from 35 to
35 yrs of age

ISTIONKO/USTCON/05

Clinical manifestation
chorea
intellectual decline
emotional disturbance
constant writhing and twisting
facial movements produces tics
and grimaces
speech is affected
chewing and swallowing are
difficult
choreiform movement persist but
diminish during sleep
gait becomes disorganized
cognitive function is altered
illness results in suicidal
depression, anxiety, euphoria
and psychosis
disjointed movements
hallucinations
dementia
Laboratory tests
CT scan
MRI
Recombinant DNA

Nursing management
Use padded heel and elbow
protectors
Keep the skin clean
Encourage ambulation to
improve muscle tone
Encourage patient to wear
paddings
Secure the patient in bed or
chair
Learn the position that is best
for the patient
Talk to the patient before
meals to promote relaxation
Do not interpret stiffness or
sudden turning away of head
as a means of saying no for
sometimes it is caused by
involuntary movement
Placed bite sized foods
Wait the patient in chewing and
swallowing his food
Use blenderized meals if
patient cant chew
Learn how the patient
expresses his emotion

Pharmacologic management
Thiothixene hydrochloride
(Navane) and haloperidol
decanoate (Haldol), blocks
dopamine receptors which
improves chorea in patients
Chorea is also lessened with
tetrabenazine
Patients having parkinsons
symptoms like are given with
antiparkinson medication such
as levodopa
Patients having emotional
disturbances may be given
with antidepressants
Psychotic symptoms are
usually suppressed by giving
antipsychotics

 Speech therapy
Do not abandon the patient because the
disease is usually terminal, patients are
living until the end

AMYOTROPHIC LATERAL
SCLEROSIS (Lou Gehrigs disease)

ISTIONKO/USTCON/05

ALS is a disease having an unknown

cause in which there is a loss of motor
neurons in the anterior horns of the
spinal cord and the motor nuclei of the
lower brain stem. As these cells die, the
muscle fibers that they supply undergo
atrophic changes. Neuronal
degeneration might occur in both the
upper and lower neuron system. This
disease may actually cause death

Clinical Manifestations
fatigue
progressive muscle weakness
cramps
fasciculation
incoordination
atrophy of the muscles in arms,
trunks and legs
spasticity
deep tendon stretch reflexes
become brisk and overactive

The main focus of medical and nursing

management is to maintain or improve
function, well-being and quality of life
Medical management
Individualized therapeutic
exercise is prescribed to
prevent muscle tightness,
contractures and disuse
atrophy
Night splints and stretching
exercises to delay contracture
of joints
Wearing orthotic jacket to
improve sitting stability and
reduce trunk deformity
Genetic counseling is advised
for parents and siblings
because of the genetic nature
of disease
Nursing management
Monitor respiratory staus &
prepare to initiate any
respiratory support
The family is taught to monitor
the patient for respiratory
problems
encouraged to do range of
motion exercises to prevent

Pharmacologic management
Riluzole (Rilutek) a glutamate
antagonist that slows the
deterioration of motor neurons
Baclofen (lioresal), dantrolene
sodium (Dantrium) or
diazepam (Valium) may be
useful for patients with
spasticity

 difficulty talking and swallowing

difficulty in breathing
voice assumes a nasal sound
Laboratory test
EMG shows the reduction of
functional motor units of the
muscles
MRI may show a high signal
intensity in the corticospinal tracts
ALZHEIMERS DISEASE
Specific neuropathologic and
biochemical are found in patients having
Alzheimers disease. These include
neurofibrillary tangles and neuritic
plaques in the brain . this neuronal
damage occurs primarily in the cerebral
cortex and results in decreased brain
size. Cells that use acetylcholine are the
ones principally affected by this disease.
Biochemically the enzyme active in
producing acetylcholine, which is
specifically involve in memory
processing is decreased.

ISTIONKO/USTCON/05

Clinical manifestations
1. forgetfulness
and
subtle
memory loss
2. depression
3. loses the ability to recognize
familiar faces, places and
objects
4. they may repeat similar stories
because they forget that they
have already told them
5. conversation becomes difficult
6. the ability to formulate
concepts disappears
7. changes in personality
8. becomes anxious, combative,
suspicious and paranoid
9. patient may wander at night
10. has
dysphagia
and
incontinence
Laboratory test

contractures
The patient and family are
encourage to join in decision
making including end to life
decisions
The knowledge of the family
regarding handling the
condition are assessed and
modifications are done by the
nurse
The nurse may need to help
boost the confidence of an
adolescent and older adult
patient by encouraging them to
pursue job training to become
economically independent
Guidance in accessing adult health care
and finding appropriate programs in sex
education

Nursing management
Provide
a
predictable
environment that helps the
person
interpret
his
surroundings and activities
Use pleasant manner of
speaking
Use simple instructions
Use simple explanations
Always display clocks and
calendars
Colorcoding the doorway may
help the patient in recognizing
his room
Removed
all
hazardous
objects
Patients intake of food and
medications are monitored

Pharmacologic management
Tacrine hydrochloride (Cognex)
an agent that enhances
acetylcholine uptake in the
brain,
thus
maintaining
memory skills for a period of
time
Donepezil
(Aricept)
acetylcholinesterase inhibitor
Rivastigmine (Exelon

health history, family history,

social and cultural history,
physical examination, are key
in the diagnosis of the disease
CBC
VRDL (Venereal Research
Disease Laboratory test for
syphilis
HIV testing
Chemistry profile
Vit B12 and thyroid hormone
levels
EEG
CT scan
MRI
And examination of CSF
Cerebral biopsy
Depression scale
Mini-mental state examination

MUSCULAR DYSTROPHIES

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The muscular dystrophies are a group of

chronic muscle disorders characterized
by progressive weakening and wasting
of the skeletal or voluntary muscles.
Most of these diseases are inherited.
Duchenne Muscular dystrophy is the
most common and occurs in 1 of every
3000 male births. The pathologic
features include degeneration & loss of
muscle fibers variation in muscle fiber

Signs & Symptoms

Muscle tightness

Reinforce a positive self image

Provide
a
peaceful
environment
Keep the patient independent
as possible by providing simple
activities
Visits, letters and phone call
are encourage to provide
socialization
promote balanced activity and
rest
encourage family cooperation.

Nursing Intervention
The goals of the patient & the nurse
are to maintain function at optional
levels & to enhance the quality of life.
Therefore, the patients physical
requirements which are considerable,
are addressed w/o loosing sight of
emotional & developmental needs.
The patient & the family are actively
involved in decision making including
end of life decision.
During hospitalization per treatment of
complications, the knowledge &
expertise of the patient and family
members responsible for care giving in
the home are assessed. Because the
patient & family caregivers often have
develop care giving strategies need to be
acknowledged & accepted, & provisions
must be made to ensure that they are
maintained during hospitalization.

 Muscle Contracture
Disuse Atrophy
Spinal Deformity
- Weakness of trunk muscles
- Spinal Collapse
Compromised Pulmonary Function
- Maybe due either to
progression of the disease or to
deformity of thorax secondary to
severe scoliosis
Dental & Speech Problem
- May result from weakness of
facial muscles, which make it
difficult to attend to dental
hygiene & to speak coherently.
GI Problems
- Gastric dilation
- Rectal Prolapse
- Fecal Impaction

size, phagocytosis & regeneration &

replacement of muscle tissue. The
common characteristics of these
diseases include varying degrees of
muscle wasting & weakness abnormal
elevation of blood muscle enzymes &
myopathic finding in EMG & muscle
biopsy.

DEGENERATIVE DISK DISEASE

ISTIONKO/USTCON/05

The intervertebral disk is a cartilaginous

plate that forms a cushion between the
vertebral bodies. This tough, fibrous
material is incorporated in a capsule. A
ball like cushion in the center of the disk
is called the nucleus pulposus. In
herniation of the intervebral disk. The
nucleus of the disk protrudes into the
annulus with subsequent nerve
compression. Protrusion or rupture of the
nucleus pulposus usually is preceded by
degenerative changes that occur with
aging. Loss of protein polysaccharides in
the disk decreases the water content of
the nucleus pulposus. The development
of the radiating cracks in the annulus

Cardiomyopathy
The pathologic features include:
Degeneration & loss of muscle
fibers
Variation in muscle fiber size
Phagocytosis
Regeneration & Replacement of
muscle tissue

Signs & Symptoms

Muscle tightness
Muscle Contracture
Disuse Atrophy
Spinal Deformity
- Weakness of trunk muscles

Nursing Intervention
The goals of the patient & the nurse
are to maintain function at optional
levels & to enhance the quality of life.
Therefore, the patients physical
requirements which are considerable,
are addressed w/o loosing sight of
emotional & developmental needs.
The patient & the family are actively
involved in decision making including
end of life decision.
During hospitalization per treatment of
complications, the knowledge &
expertise of the patient and family
members responsible for care giving in
the home are assessed. Because the
patient & family caregivers often have
develop care giving strategies need to be
acknowledged & accepted, & provisions
must be made to ensure that they are
maintained during hospitalization.

weakens resistance to nucleus

herniation. After trauma, the cartilage
may be injured.
For most patients immediate symptoms
of trauma are short loved and those
resulting from injury to the disk do not
appear for months or years. Then with
degeneration in the disk, the capsule
pushes back into the spinal cord or it
may rupture.

HERNIATION OF CEREBRAL
INTERVERTEBRAL DISK

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- Spinal Collapse
Compromised Pulmonary Function
- Maybe due either to
progression of the disease or to
deformity of thorax secondary to
severe scoliosis
Dental & Speech Problem
- May result from weakness of
facial muscles, which make it
difficult to attend to dental
hygiene & to speak coherently.
GI Problems
- Gastric dilation
- Rectal Prolapse
- Fecal Impaction
Cardiovascular Problem:
Cardiomyopathy
The pathologic features include:
Degeneration & loss of muscle
fibers
Variation in muscle fiber size
Phagocytosis
Regeneration & Replacement of
muscle tissue

The cervical sine is subjected to stresses

that result from disk degeneration &
spondylosis (degenerative changes
occurring in disk & adjacent vertebral
bodies). Cervical disk degeneration may
lead to lessons that can cause damage
to the spinal cord & its roots.
A cervical disk herniation usually occurs
at C5 6 & C6 7 interspaces Pain &
stiffness may occur in the neck the top of
the shoulders & the region of the
Signs & Symptoms
scapulae. Sometimes patients interpret
A herniated disk with
these signs as symptoms of heart trouble
accompanying pain may occur in
or bursitis. Pain may also occur in the
any portion of the spine: cervical,
upper extremities & head accompanied
thoracic or lumbar. The clinical
by paresthesia and numbness of the
manifestations depend on the
upper extremities. Cervical MRI usually
location, the rate of development
confirms the diagnosis
and the effect of surrounding
structure.
Low Back Pain

Medical Management
Herniation of the cervical and
the lumbar disks occur most
commonly and are usually
managed conservatively with
bed rest.
Surgical Management
Discectomy
- Removal of herniated

- Fracture
- Tumor
- Infection
Cauda Equina Syndrome
FINDINGS:
MRI

Has become the diagnostic

tool of choice for localizing even
small disk, protrusions, particularly
for lumbar spine disease. If clinical
symptoms are not consistent with
the pathology seen on MRI, CT &
myelography are then performed.
A neurologic examination is carried
out to determine if there is reflex
sensory or motor impairment from
root compression & to provide a
baseline for future assessment.
EMG

May be used to localize the

specific spinal nerve roots
involved.

TRAUMATIC
SPINAL CORD INJURY

fragments
Laminetomy
- Removal of the bone between
the spinal process.
Hemilaminectomy
- Removal of part of the lamina
Discectomy with Fusion
- A bone graft is used to fused
the vertebral spinous process.
Foraminotomy
- Removal of the Intervertebral
foramen.

methylprednisolone reduce swelling

WHIPLASH INJURY

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damage to the spinal cord that results in

a loss of function such as mobility or
feeling
Frequent causes of damage are
trauma (car accident, gunshot, falls, etc.)
or disease (polio, spina bifida,
Friedreich's Ataxia, etc.).

may cause changes in virtually every

system in the body
there is usually swelling of the spinal
cord
After days or weeks, the swelling
begins to go down and people may
regain some functioning

Currently there is no cure for SCI

Pain medications, nonsteroidal antiinflammatory drugs, antidepressants,

muscle relaxants, and a cervical collar
(usually worn for 2 to 3 weeks).

a soft tissue injury to the neck also

called neck sprain or neck strain is
characterized by a collection of
symptoms that occur following damage
to the neck, usually because of sudden
extension and flexion

PERIPHERAL NERVOUS SYSTEM

DISORDERS

STIONKO/USTCON/05

Pathophysiology: Neuropathies involve

damage to the axon or to myelin, or to
both. It is worthwhile reviewing the
changes that occur with damage to
each element.Primary demyelination
slows or halts nerve conduction.
Individual Schwann cells lose their
myelin from the underlying pathologic
process. The loss may be spotty; with
each Schwann cell covering about 1
mm of axonal length, there are many
sites for damage along a nerve fiber. If a
few Schwann cells lose their myelin,
conduction slows, and if too many

commonly occurs as the result of an

automobile accident and may include
injury to intervertebral joints, discs, and
ligaments, cervical muscles, and nerve
roots
Symptoms such as neck pain may be
present directly after the injury or may be
delayed for several days. In addition to
neck pain, other symptoms may include
neck stiffness, injuries to the muscles
and ligaments (myofascial injuries),
headache, dizziness, abnormal
sensations such as burning or prickling
(paresthesias), or shoulder or back pain
some people experience cognitive,
somatic, or psychological conditions
such as memory loss, concentration
impairment, nervousness/irritability,
sleep disturbances, fatigue, or
depression.

There are eight principle manifestations

of peripheral nervous system disorders.
These are listed below:

Impairment of muscle
function.

Range of motion exercises, physical

therapy, and cervical traction
Supplemental heat application may
relieve muscle tension.

Treatment is aimed at maximizing the

ability to use the affected body part. The
cause should be identified and treated as
appropriate. In some cases, no treatment


consecutive Schwann cells lose their
myelin, conduction slows to a halt. A
whole nerve may contain several
thousand nerve fibers. Therefore,
impulse conduction along individual
fibers may be unaffected, may be mildly
slowed, or blocked. The longer the
nerve segment, the greater chance of
detecting mild degrees of slowing

MONONEUROPATHY

Mononeuropathy is most often caused

by damage to a local area resulting from
injury or trauma, although occasionally
systemic disorders may cause isolated
nerve damage (as with mononeuritis
multiplex). The usual causes are direct
trauma, prolonged pressure on the nerve
and compression of the nerve by
swelling or injury to nearby body
structures.The damage includes
destruction of the myelin sheath
(covering) of the nerve or of part of the
nerve cell (the axon). This damage slows
or prevents conduction of impulses
through the nerve.

Impairment of deep tendon

reflexes.
Twitching, cramps, and
spasms of muscles.
Loss of sensation.
Altered sensation such as
tingling or painful burning
(termed paresthesias and
dysesthesias)
In coordination due to loss of
sense of position of the limbs
(termed Sensory ataxia).
Deformity, loss of muscle mass
and hair loss
Autonomic dysfunction (e.g.
impotence, abnormal
sweating)

Symptoms
Impairment of sensation in a body
part supplied by a specific
nerve
o Numbness, decreased
sensation
o Tingling, burning, pain,
abnormal sensations
o Loss of sensation
Impairment of movement in one
muscle supplied by a specific
nerve
o Weakness
o Paralysis (total loss of

is required and recovery is spontaneous.

Vascular lesions (injuries to an artery)
can often affect a single nerve, and in
these cases the cause of the
vasculopathy (such as high blood
pressure or diabetes) should be treated.
If there is no history of trauma to the
area, conservative treatment is indicated
if there was sudden onset, minimal
sensation changes, no difficulty in
movement, and no test results indicating
degeneration of the nerve axon.

Physical therapy exercises may be

appropriate for some people to maintain
muscle strength. Orthopedic assistance
may maximize the ability to use the
affected body part. This may include the
use of braces, splints, or other
appliances.
Vocational counseling, occupational
therapy, occupational changes, job
retraining, or similar interventions may
be recommended if appropriate.

Corticosteroids injected into the area

may reduce swelling and pressure on the
nerve in some cases. Surgical
intervention is indicated if the symptoms
are caused by entrapment of the nerve.
Surgical removal of lesions that press on
the nerve may help in some cases.
CONTROL OF SYMPTOMS:
Over-the-counter analgesics or
prescription pain medications may be
needed to control pain (neuralgia).
Various other medications may reduce
the stabbing pains that some people
experience, including gabapentin,
phenytoin, carbamazepine, or tricyclic
antidepressants such as amitriptyline.
Whenever possible, the use of these
drugs should be avoided or minimized to
reduce the risk of medication side
effects.

movement)
Note: Symptoms are isolated to one
location.
Signs and tests
Neuromuscular examination of the
affected area may indicate which nerve
is involved. Reflexes may be abnormal in
the area. Symptoms are isolated to one
nerve area.
Tests for mononeuropathy may include
the following:
EMG (a recording of electrical

activity in muscles)
Nerve conduction tests
Nerve biopsy

Testing is guided by the suspected cause

of the dysfunction, as suggested by the
history, symptoms and pattern of
symptom development. Testing may
include various blood tests, X-rays, and
scans.

ISTIONKO/USTCON/05