THE
NERVOUS
SYSTEM
Divisions


Central
Peripheral

Autonomic
Sympathetic
 parasympathetic


protected by the:



skull
vertebrae
CSF- shock absorber and thus reduces the force of
impact upon it

Characteristics:








color
colorless, odorless
spec gravity
1.007
occasional lymphocyte
1-3% mml
protein
40 mg
pressure
60-180 mmH2O
total amount
125-150 ml
traces of minerals and organic material of blood
meninges



dura mater
arachnoid
pia mater

Brain

CNS
Cerebrum
2 hemispheres
 4 lobes



Cerebellum
Brainstem
Diencephalon
 mesencephalon
 rhombencephalon


Spinal cord
cerebrum
4 lobes


frontal






parietal






taste and touch
spatial orientation
receives sensory impulses from the opposite side of the body with
exception to special senses
interpretation of pain, touch, temperature and pressure
recognition of size and shape, weight, texture, consistency of object and
the ability to distinguish two object between simultaneous skin contact
temporal




personality behavior and higher intellectual functions
organization of thought
body movement
memories and emotions
autonomic functions such as respiration, GIT, cardiovascular reactions and
emotional responses
contains auditory center
important in understanding spoken words
memory
occipital


visual area
language
CEREBELLUM




located below the cerebrum
receive information from all areas of
the body
aids in coordination of voluntary
muscles, balance
maintenance of muscle tone and
maintain posture in space
Brainstem

interbrain or diencephalon




thalamus- modifies and controls primitive emotional responses
(pain, rage, love and hate)
hypothalamus- where the pituitary body is attached; influence
water, carbohydrate and fat metabolism, growth, sexual
maturity, body temperature, pulse rate, blood pressure and
sleep
midbrain or mesencephalon- includes the RAS which
control sleep, motor activity, consciousness and
awareness
hindbrain or rhombencephalon


pons – bridge the gap structurally and functionally between
hemispheres; primary motor pathway
medulla oblongata- vital center for respiratory and cardiac
function
SPINAL CORD


H-shaped gray matter (nerve cell bodies)
surrounded by white matter (thousands of
nerve fibers, descending motor and
ascending sensory tracts) all outside spinal
canal
Contains long conducting pathways for the
purpose as connecting link between brain
and periphery such as skin and muscles
PNS



Cranial nerves
Spinal nerves
Peripheral nerves


sensory (afferent) nerves- impulse to the
brain
motor (efferent) nerves- from brain down to
the muscle
mnemonics












Sexy
Secretary
Make
Money
But
My
Brother
Says
Big
Boobs
Make
More
I.
Olfactory
II. Optic
S= sensory
III. Occulomotor
M= motor
IV. Trochlear
B= both
V.
Trigeminal
VI. Abducens
VII. Facial
VIII.Acoustic
IX. Glossopharyngeal
X.
Vagus
XI. Spinal accesory
XII. Hypoglossal
Spinal Nerves

31 segments





8 cervical
12 thoracic
5 lumbar
5 sacral
1 coccygeal
Diagnostic Procedures
ELECTROENCEPHALOGRAM
(EEG)
- records electrical activity of the brain
- purpose:




detect abnormalities that may be indicative of intracranial
pathology or pathologic physiology
determine existence and type of epilepsy
nursing care:

pretest:




withhold sedatives, tranquilizers, stimulants for 2-3 days
hair shampoo
determine patient’s ability to lie still
reassure patient that electric shock will not occur
post test:


remove electrode paste with acetone and shampoo hair
LUMBAR PUNCTURE
- introduction of hollow needle with stylet into the lumbar subarachnoid
space of the spinal canal between L1/L5 and withdrawal of CSF for
diagnostic and therapeutic purposes
- purposes:






measure CSF pressure (normal opening pressure 60-150 mmH2O
obtain specimen for laboratory analysis
check color of CSF and check for blood
inject air, dye or drugs in the spinal canal
- pretest:




obtain consent
determine patient’s ability to lie still in a flexed, lateral recumbent position
have client empty bladder
- post test:









ensure labeling of CSF specimens
keep client flat in bed for 12 hours
force fluids
assess neurologic status
administer analgesics as prescribed
check puncture site for bleeding or leakage
assess sensation and movement in lower extremities
monitor vital signs
CISTERNAL PUNCTURE
Introduction of a short-beveled hollow needle
stylet in the median line below the occipital
bone into the cisterna magna
purpose:




remove CSF when impossible to obtain in lumbar
level
potential complication: respiratory distress
- nursing care:



same as for lumbar puncture
watch out for apnea, cyanosis and dyspnea
X RAY OF THE SKULL


- give radiographic picture of head
and neck bones to reveal fractures,
erosion of bone including size of
sella turcica and configuration,
density and vascular markings
-nursing care:


remove hairpins, glasses and hearing
aids
determine patient’s ability to lie still
COMPUTED TOMOGRAPHY (CT)
SCAN
- used to identify brain abnormalities; produces
a series of tomograms translated by a
computer and displayed on monitor which
represent cross sectional images of various
layers of the brain; may be performed with or
without dye
- purpose:



used to identify tumors of the brain and other
lesions
- nursing considerations:




check allergy to iodine, seafood, dyes
obtain consent
inform patient of possible throat irritation and facial
flushing if contrast die is injected
MAGNETIC RESONANCE
IMAGING (MRI)
- use of magnetic and radiowaves to create a
detailed visualization of brain and its structures
- purpose:



create a detailed visualization of brain and its
structures
- nursing considerations:





be aware that patients with pacemakers, surgical or
orthopedic clips, shrapnel should not be scanned
remove jewelry or metal objects from patient
determine patient’s ability to lie still
administer sedation as required
BRAIN SCANNING
(RADIONUCLEIDE IMAGING
STUDIES)
- intravenous scanning of radioactive
compound and the application of a scintillation
scanner in the patient’s brain – there’s an
increase uptake of radioactive compound at
the site of pathology
- purpose:



detect intracranial masses, vascular lesions, infarct
and hemorrhage
- nursing considerations:



check for allergy
keep NPO 4-6 hours before the exam
CEREBRAL ANGIOGRAM
-injection of radiopaque substance into the cerebral circulation and
visualization by means of X Ray
- purpose:



localization of tumors, abscesses, aneurysms, hematomas and occlusions
- potential complications:


anaphylactic reaction to dye, local hemorrhage, vasospasm, adverse
intracranial pressure
-pretest






check for allergies to iodine
take baseline assessment
measure neck circumference
NPO after midnight or clear liquid
explain that warm flushed feeling and salty taste in mouth may be felt during
the procedure
- during and post test









have emergency equipment available
monitor neurologic status and vital signs or shock, LOC, hemiparesis,
hemiplegia, and aphasia
monitor swelling of neck and difficulty of breathing and swallowing
administer ice collar / cap intermittently to relieve swelling and discomfort
check insertion site fro bleeding and assess pulses distal to site
maintain pressure dressing
maintain bed rest until next morning as ordered
force fluids if patient’s condition allows
Electromyography (EMG)


- uses electrodes to graphically record
the electrical activity of muscle at rest
and at contraction
- nursing considerations:



explain that patient must flex and relax the
muscles during the procedure
explain that discomfort might be felt but not
pain
administer analgesics after the procedure
ENCEPHALOGRAM
-visualization of the distribution of hydrogen molecules
in the body in 3 dimensions
- characteristics





non invasive
does not use harmful ionizing radiation
superior imaging of body’s soft tissues
- purpose



differentiate types of tissues in normal and abnormal states
clinical applications include: brain, both tumors and vascular
abnormalities, cardiac and respiratory conditions, cardiac
anomalies, blood vessels, liver disease, renal abnormalities,
gall bladder
- nursing care:




remove all metallic objects and let patient lie on platform that
will be moved into a table containing the magnet
explain that nothing will be felt during the procedure but
sound of magnetic coil as the magnetic field being pushed will
be heard
closely monitor client with potential respiratory or cardiac
collapse
VENTRICULOGRAPHY
- introduction of air directly in the lateral ventricles by
ventricular puncture thru opening made in the frontal,
post, parietal or occipital regions for special X-ray
study of brain
- purpose



to visualize ventricles, localize tumors
- potential complications:





headache
nausea and vomiting
meningitis
increased intracranial pressure
- nursing considerations:




monitor vital signs
check neurologic status
elevate head of bed (15-20 degrees)
PNEUMOENCEPHALOGRAPHY
-introduction of air or oxygen into the
subarachnoid space by lumbar or cisternal
puncture to outline the ventricular system and
intracranial subarachnoid space for special xray study
- demonstrates intracranial subarachnoid space
and ventricular system
-purpose:




localize intracranial lesion
MYELOGRAPHY
- injection of radiopaque dye by lumbar
puncture followed by fluoroscopy
- purpose:



visualize subarachnoid space, spinal cord and
vertebrae
- pretest:



obtain consent
tell patient of possible throat irritation and facial
flushing
- post test:




have patient flat on bed
assess puncture site
force fluids
NEUROLOGIC ASSESSMENT
LEVELS OF CONSCIOUSNESS




orientation to time, place and person
speech
ability to follow commands, comprehension and
action
levels





Hyperactive
Conscious
lethargy, drowsiness, obtundation
Stupor
Coma
LEVELS OF CONSCIOUSNESS


Mood
Memory



confabulation
circumlocation
Complex functions



Reading
Writing
Abstract reasoning and speech
VITAL SIGNS
Respiratory Patterns


Cheyne - Stokes Respiration



Central Neurogenic Hyperventilation





cluster of irregular breathing, irregularly followed by periods of apnea
lesion in upper medulla and lower pons
Ataxic Breathing


prolonged inspiratory phase followed by a 2-3 sec pause
pons dysfunction
Cluster Breathing


sustained rapid regular respirations (rate 25/min) with normal blood
oxygen levels
usually due to brainstem dysfunctions
Apneustic Breathing


regular rhythmic, altering between hyperventilation and apnea
maybe caused by structural cerebral dysfunction of metabolic problems
such as diabetic coma
breathing pattern completely irregular, indicates damage to respiratory
centers of the medulla
Biots Respiration

irregular and random deep and shallow breathing
PUPILS





affected pupil is usually on the same side
(ipsilateral) as the brain lesion whereas the
motor and sensory deficits are on the opposite
side (contralateral)
size, shape, equality of pupils
reaction to light
corneal reflex- blink reflex
occulocephalic reflex (doll’s eyes)- present in
patient with intact brainstem
MOTOR FUNCTIONS
muscle size
muscle strength











5/5- normal full strength
4/5- muscle is able to move actively thru full ROM against
gravity with weakness to applied resistance
3/5- muscle able to move actively against gravity alone
2/5- muscle able to move with support against gravity
1/5- muscle contraction is palpable and visible, trace or flicker
of movement occurs
0/5- undetectable
muscle tone- flabby or rigid
muscle coordination – point to point maneuvers
gait and station- stand still and walk in tandem
SENSORY FUNCTIONS
Pain






touch











Localization- pushes stimuli away
Flexion- pulls away from stimuli
Decorticate (abnormal flexion)- indicates damage to convex of brain
Decerebrate (abnormal extension) – indicates damage to cerebellum
No response- no visible movement to pain stimuli
dysenthesia- localized irritating sensation, warmth, cold, itching,
tickling, prickling, crawling, tingling
paresthesia- distortions of sensory stimuli (light touch may be
experienced as burning or painful)
anesthesia- absent sense of touch
hyposthesia- reduced sense of touch
hyperthesia- overperception of touch
hypalgesia- reduced sensation to pain
hyperalgesia- increased sensation to pain
analgesia- absence of pain perception
heat and cold
vibration
REFLEXES












papillary
corneal
biceps
brachial
triceps
patellar
Achilles
plantar
abdominal
cremasteric
anal
gag
CEREBRAL DYSFUNCTION

aphasia- loss of language ability




agnosia- inability to recognize objects (parietal
lobe lesion)



expressive- inability to send message (damaged
Broca’s area)
receptive- inability to perceive message (damaged
posterior or temporal portion of dominant
hemisphere)
global- loss of all speech function
visual
tactile
apraxia- loss of previously acquired ability to
perform simple skills
CEREBELLAR SYSTEM

arms





legs



finger-nose test
finger-finger test
pronation-supination
patting test
heel-knee test
heel-toe test
trunk

gait
BRAINSTEM

spontaneous motion of each eye

occulocephalic reflex (Doll’s Eye)




doll’s phenomenon- normal response if eyes move opposite
to the direction of head turning
occulovestibular test- done by slowly injecting ice
water into the external auditory canal until eye
deviation and nystagmus occurs
implications: slow conjugate deviation of eyes
towards the irrigated ear where they remain 30120 seconds is considered a response of
comatose patient with intact brainstem
abnormal movement such as skewing or jerky
movement indicates brain stem lesion
DISTURBANCES IN THE
NERVOUS SYSTEM
TRAUMATIC BRAIN
INJURY (TBI)
Traumatic Brain Injury (TBI)
“Occurs as a result of an external force that
produces a diminished or altered state of
consciousness” (Iggy, p. 989)
Can:
 Cause cognitive impairment
 Cause behavioral/emotional disturbances
 Be temporary or permanent
 Cause partial or total functional disability
or psychosocial maladjustment
Traumatic Brain Injury (TBI)


Primary brain injury
Two classifications:

Open head injury
Linear fracture
 Depressed fracture
 Open fracture
 Comminuted fracture
 Basilar skull fracture
 Penetrating injury

Traumatic Brain injury

Closed head injury
Concussion
 Contusion
 Laceration


Secondary brain injuries

Any neurological damage that occurs after the
initial injury
TBI: Secondary Brain Injury








Increased intracranial
pressure (ICP)
Hemorrhage
Epidural hemorrhage
Subdural hematoma
Intracerebral
hemorrhage
Loss of autoregulation
Hydrocephalus
Herniation
Epidural Hematoma
Subdural Hematoma
Subarachnoid
Hemorrhage
1. Hematoma (accumulated blood)
1.Cerebrum
2.Skull
3.Cerebellum
4.Herniation
of Brain into
Spinal
Column
Increased Intracranial
Pressure


Description:
Intracranial Pressure:




The normal ICP depends on the position of the client
and is 15 mmHg or less
Increased ICP is more than 15 mmHg
Untreated increased ICP can lead to displacement of the
brain tissue


The result of the amount of brain tissue, intracranial blood
volume, and CSF within the skull at any time.
Herniation
Presents life – threatening situation because of pressure
on vital structures in the brain stem, nerve tracts and
cranial nerves
Increased Intracranial Pressure

Etiology:





Head injury
stroke
inflammatory lesions
brain tumor
intracranial surgery




any type of injury to the head may increase the ICP
Cerebral edema
Inflammation or abscesses
Hemorrhage
Increased Intracranial Pressure

Pathophysiology:




The only thing in the skull is brain tissue, blood and CSF
If any abnormality occurs in the adult skull there is no room for
expansion, which results in neurologic deficits because of the
increased pressure in the closed cavity.
The body compensate for this increased pressure or
decompensate
Compensatory mechanisms for maintaining ICP within normal
limits include:




Increased CSF absorption
Shunting of blood to the spinal arachnoid space
Decreased CSF production
Failure of these compensatory mechanisms results in
decompensation with the following sequence of events:




Decreased cerebral blood flow with inadequate perfusion
Increased PCO2 and decreased PO2 leading to hypoxia
Vasodilation and cerebral edema
Further increases in ICP
↑ ICP
↓ cerebral blood flow
↓ serum pH and ↑ CO2
cerebral vasodilation
Edema
↑ ICP
brain herniation
irreversible brain damage
death
Increased Intracranial Pressure

Clinical Manifestations:

Earliest Signs:



Headache


Caused by the tension and displacement of pain sensitive structure such as
intracerebral vessels (basal arteries, large venous sinuses and dura)
Projectile vomiting



Decreased LOC
Progresses from restlessness to confusion and disorientation to lethargy and
coma
Recurrent and may be projectile
Due to irritation of vagal nuclei in the floor of 4th ventricle
Pupillary changes


Unilateral dilatation of pupils which results from Truncal herniation and
lateral brainstem compression
Ipsilateral



Same side dilation of pupil with sluggish reaction to light from compression of
cranial nerve III
Pupil eventually becomes fixed and dilated
Papilledema


Edema of the optic disc
Increased in pressure thus optic disc becomes swollen and pushed forward above
level of retina (Chorea disc)
Increased Intracranial Pressure

Changes in vital signs


Maybe a late sign
Decreased respiration


Increased temperature






Widening of pulse pressure
Abnormal respiratory patterns


Slow and bounding due to ischemia of Vasomotor center to medulla
Increased blood pressure
Increased pulse pressure
Systolic blood pressure rises while diastolic pressure remains the same


Due to compression of hypothalamus
May also indicate other infection or dehydration
Fever
 Increased metabolism in brain leads to increased oxygen consumption,
which is detrimental to an ischemic and insulated brain.
Decreased pulse


Due to pressure and anoxia in respiratory center in medulla
Cheyne – stoke respiration
Motor abnormalities

Contralateral


Opposite side Hemiparesis from compression of corticospinal tracts
Decorticate or Decerebrate rigidity
Increased Intracranial Pressure

Laboratory and Diagnostic Study
findings:


ICP monitoring reveals an ICP greater than 15
mmHg
MRI scans, radiographs, and CT scans may
identify the cause of the increased pressure

Tumor, ischemic area
Increased Intracranial Pressure

Medical Management of Increased
ICP

Remove basic cause


Drain a hematoma, treat if surgical removal is
impossible use of temporary measures such as:
Medications
Promote diuresis thus decrease cerebral edema
 Furosemide (Lasix), Mannitol (Osmitrol)


Mechanical decompression

Removal of CSF or surgically providing for brain
expansion.
Nursing Management









Maintain patent airway and adequate ventilation
Limit suctioning to 15 minutes
Produces hypocarbia
Monitor vital sign and neuro check frequently to detect
rises in ICP
Maintain fluid balance:
Position client with head of bed elevated to 30 to 45
degrees and neck in neutral position unless
contraindicated
Improves venous drainage from brain
Prevent further increase in ICP
Administer stool softeners and mild laxatives as
ordered
Nursing Management
Administer antiemetics as ordered
Prevent complications of immobility
Administer medications as ordered




Hyperosmotic agents




Corticosteroids







Phenytoin (Dilantin)
To prevent seizures
Analgesics for headache as needed
Assist with ICP monitoring when indicated


Furosemide (Lasix)
To reduce cerebral edema
Anticonvulsants


Dexamethasone (Decadron)
Anti-inflammatory effect reduces cerebral edema
Diuretics


Mannitol (Osmitrol)
To reduce cerebral edema
Monitor urine output every hour
Normal ICP reading is 15 mm Hg
Provide intensive nursing care for client treated with barbiturate
therapy or administration of paralyzing agent
Observe for hyperthermia secondary to hypothalamus damage
DEGENERATIVE CONDITIONS
Multiple Sclerosis
Myasthenia Gravis
Parkinson’s Disease
Guillain Barre Syndrome
Amyotrophic Lateral Sclerosis
MULTIPLE
SCLEROSIS

Description:

A progressively disabling demyelinating
disease affecting nerve fibers of the brain and
spinal cord




Marked by periodic exacerbations and remissions
Incidence is greater for women than men and
is highest in temperate climate
Age of onset is typically between 20 to 40
years old
Etiology:



Unknown cause
Theories suggest that myelin damage is the
primary event and that it results from a viral
infection early in life that becomes apparent
as a autoimmune process later in life
It is believed that a defective immune
response has a major role in the pathogenesis
Pathophysiology:

Produces patches of demyelination throughout the
central nervous system


The plaques in the involved area become





Resulting in myelin being lost form the axis cylinders and
degeneration of the axons themselves
Sclerosed
Interrupting the flow of nerve impulses
Variety of manifestations depending on which nerves are
affected
Periodic an unpredictable exacerbations and remissions
mark the course of MS
Prognosis varies

MS can cause rapid, sometimes fatal, disability, but about 70%
of clients lead active, productive lives with long periods of
remission
1. Nerve cell body
2. Axon with myelin sheath
3. Neuromuscular junctions
4. Muscle fibers
Clinical Manifestations:

Vary widely but may include:

Visual problems




Motor dysfunction such as:









Diplopia
Blurred vision
Nystagmus
Muscle weakness that typically worsens throughout the day
Paralysis
Spasticity
Hyperreflexia
Tremors
Gait ataxia
Fatigue
Bladder or bowel incontinence
Mental changes such as:



Mood swings
Irritability
Depression
Laboratory and Diagnostic
Study findings:


Lumbar puncture
CSF analysis


Reveal elevated CSF gamma globulins
MRI

Confirm the presence of demyelinating plaques
Nursing management:

Administer prescribed medications

Which may include:



Hormones such as corticotropin (ACTH) maybe prescribed to
stimulate release of adrenal cortex hormones


Corticosteroids
Muscle relaxants
Helps to improve nerve conduction
Instruct the client to notify a physician if serious side effects
such as:




Fluid retention
Muscle weakness
Abdominal pain
Headache

Promote measures to avoid fatigue





Assess the clients sleep and rest patterns
Encourage adequate rest
Assist the client in planning lifestyle modifications to
decrease stress and fatigue and maximize functional
abilities
Encourage relaxation and coordination exercises to
improve muscle efficiency
Maximize functional abilities




Assess the nature and degree of neuromuscular
deficits and their effect on the client’s routine
activities
Prevent complications of immobility
Promote self – care
Maximize effective communication


Encourage use of eye patch if Diplopia
occurs
Provide adequate care during
exacerbations






Provide measures to maintain adequate
airway
Provide client and family teaching
Promote measure to enhance body image
Promote client and family coping


Help the client establish bladder and bowel control
Prevent and treat muscle spasticity
Maybe compromised because of the chronic,
progressive disease process
Provide referrals
PARKINSON’S
DISEASE
Description:




A progressive neurologic disorder resulting from
degeneration of basal ganglia in the cerebrum
The second most common neurologic disorder in
the elderly
Affects about 1 of 100 persons older than 60
years
The incidence is higher among men than women
Etiology:



Cause is unknown
Predominantly idiopathic
Suspected causes include:




Viral infection
Chemical toxicity
Cerebrovascular disease
Effects of such drugs as major tranquilizers




Reserpine
Methyldopa (Aldomet)
Haloperidol (Haldol)
Phenothiazines
Pathophysiology:


Dopamine, a neurotransmitter secreted by the basal
ganglia, is essential to extra pyramidal function.
Depletion of dopamine diminishes normal neuromuscular
inhibiting mechanisms leading to the characteristic
neurologic deficits associated with parkinsonism such as:





Bradykinesia
Muscle rigidity
Resting tremor
Progressive deterioration continues for about 10 years
Death commonly results from pneumonia or another
infection
Clinical Manifestations:

Most common initial symptoms:





Rigidity: Cogwheel type
Bradykinesia











Tremor: mainly of the upper limb
“Pill rolling”
Resting tremor
Slowness of movement
Fatigue
Stooped posture
Shuffling, propulsive gait
Difficulty rising from a sitting position
Mask – like face with decreased blinking of eyes
Quiet, monotone speech
emotional lability, depression
Increased salivation, drooling
Cramped, small handwriting
Autonomic symptoms:





Excessive sweating
Seborrhea
Lacrimation
Constipation
Decreased sexual capacity
Nursing management:
Administer medication as ordered


Levodopa (L – dopa)

Increases level of dopamine in the brain


relieves tremor, rigidity and bradykinesia
Side effects:






anorexia
nausea and vomiting
postural hypotension
mental changes such as:

confusion

agitation

hallucinations
cardiac arrhythmias
dyskinesia

Contraindications:






Narrow angle glaucoma
clients taking

MAOI

Reserpine

guanithidine

methyldopa

antipsychotics
acute psychoses
Be aware of any worsening of symptoms with
prolonged high – dose therapy
administer with food or snack to decrease GI
irritation
inform client that urine and sweat may be
darkened

Carbidopa – Levodopa (Sinemet)


Amantadine (Symmetrel)


prevents breakdown of dopamine in the
periphery and causes fewer side effects
used in mild cases or in combination with L –
dopa to reduce rigidity, tremor and bradykinesia
Anticholinergic drugs:



benzotropine mesylate (Cogentin)
procyclidine (Kemadrin)
trihexphenidyl (Artane)



Inhibit action of acetylcholine
Used in mild cases or in combination with L – dopa
Relieve tremor and rigidity

Side effects:








antihistamines:



stimulates release of dopamine in the substantia nigra
often employed when L – dopa loses effectiveness
Eldepryl (Selegilene)


diphenhydramine (benadryl)

decrease tremor and anxiety

side effect:

drowsiness
Bromocriptine (Parlodel)


dry mouth
blurred vision
constipation
urinary retention
confusion
hallucinations
tachycardia
MAO Inhibitor

inhibits dopamine breakdown and slows progression of disease
Tricyclic antidepressants

given to treat depression commonly seen in Parkinson’s disease
Provide safe environment

Side rails on bed



Rails and handlebars in toilet, bathtub and hallways
No scatter rugs
Hard – back or spring – loaded chair to make getting up easier

Provide measures to increase mobility

Physical therapy:






Active and passive ROM exercises
Stretching exercises
Warm baths
Assistive devices
If client “freezes” suggest thinking of something to walk over
Encourage independence in self – care activities:




Alter clothing for ease in dressing
Use assistive devices
Do no rush client
Improve communication abilities:




Instruct client to practice reading aloud
to listen to own voice
enunciate each syllable clearly
Refer for speech therapy when indicated
Maintain adequate nutrition





Cut food into bite – sized pieces
Provide small, frequent feedings
Allow sufficient time for meals, use warming tray
Avoid constipation and maintain adequate bowel
elimination
Provide psychologic support to client/significant others
depression is common due to changes in body image
and self – concept
Provide client teaching and discharge planning
concerning:




Nature of disease
Use of prescribed medications and side effects
Importance of daily exercise:






Activities/methods to limit postural deformities:






Walking swimming
Gardening as tolerated
Balanced activity and rest
Firm of mattress with a small pillow
Keep head and neck as erect as possible
Use broad – based gait
Raise feet while walking
Promotion of active participation in self – care activities
MYASTHENIA
GRAVIS

Description:





A progressive disorder affecting
neuromuscular transmission of impulses in
voluntary muscles
The incidence is 1 per 25,000
Higher among women than men
Initial symptoms typically occur between the
ages of 20 and 40 years old
Etiology:

Thought to result from an autoimmune
response
Pathophysiology:

The acetylcholine receptor (ACHR) antibodies
interfere with impulse transmission across
myoneural junctions

Causes



abnormal weakness and fatigability of the skeletal muscle
particularly of the eyes, face, jaw and neck
may involve muscles of upper extremities and respiratory
muscles
The disorder follows an unpredictable course of
periodic exacerbations and remissions


Drug therapy allows many clients to lead normal lives
Progressive weakness of respiratory muscles may
cause life – threatening respiratory distress or
myasthenic crisis
Clinical Manifestations:

Abnormal weakness of any striated muscle

Particularly of the:









Face
Neck
Arms
hands
Sever fatigue
Drooping facial muscles and ptosis
Diplopia
Impaired chewing and swallowing
Breathing difficulty because of weak respiratory
muscles
Laboratory and Diagnostic
Study findings:

Positive Tensilon test result confirms the diagnosis

Tensilon Test:




Description:
 Performed to diagnose myasthenia gravis and to differentiate
between myasthenic and cholinergic crisis
To diagnose myasthenia gravis:
 Tensilon injection is injected into the client
 Positive for myasthenia gravis:
 Client shows improvement in muscle strength after the
administration of Tensilon
 Negative for myasthenia gravis:
 Client shows improvement in muscle strength and strength may
even deteriorate after injection of Tensilon
To differentiate crisis:
 Myasthenic Crisis:
 Tensilon is administered and if strength improves the client needs
more medication
 Cholinergic Crisis:
 Tensilon is administered and if weakness is more severe, the client
is overmedicated, administer Atropine Sulfate
Serum anti – ACHR bodies are present
Nursing management:










Monitor Respiratory status and ability to cough
Monitor respiratory failure
Maintain suctioning and emergency equipment at the
bedside
Monitor vital signs
Monitor speech and swallowing abilities to prevent
aspiration
Encourage client to sit up when eating
Assess muscle status
Instruct the client to conserve strength
Plan short activities that coincide with times of maximal
muscle strength
Monitor for Myasthenic and cholinergic crisis
Myasthenic Crisis

Description:



Assessment:






Acute exacerbation of the disease
Caused by a rapid, unrecognized progression of the
disease, an inadequate amount of medication, infection,
fatigue or stress
Restlessness
Weakness
Dyspnea
Dysphagia
Difficulty speaking
Implementation:


Assess for signs of myasthenic crisis
Increase anticholinesterase medications
Cholinergic Crisis

Description:



Assessment:










Depolarization of motor end plates
Caused by overmedication with anticholinesterase
Restlessness
Weakness
Dyspnea
Dysphagia
Nausea, vomiting and diarrhea
Fasciculations
Sweating
Salivation
Increased bronchial secretions
Implementation:


Hold anticholinesterase medications
Prepare to administer the antidote
 Atropine sulfate if prescribed

Administer prescribed medications

May include anticholinesterase agents

Action:


Medications:









Sweating
Salivation
Nausea
Diarrhea and abdominal cramps
Bradycardia
Hypotension
Implementation:





Neostigmine bromide (Prostigmin)
Pyridostigmine bromide (Mestinon, Regonol)
Edrophonium chloride (Tensilon)
Side effects:


Increase the levels of acetylcholine at the myoneural junction
Administer medications on time
Administer 30 minutes before meals with milk and crackers to reduce
gastrointestinal upsets
Monitor and record muscle strength
Note that excessive does lead to cholinergic crisis
Instruct the client to avoid stress, infection, fatigue, and over the
counter medications
AMYOTROPHIC LATERAL
SCLEROSIS
(Lou Gehrig’s Disease)

Description:





A progressively debilitating and eventually
fatal disease involving degeneration of motor
neurons
Affects 2 to 7 every 100,000 persons
Affecting men more than women
Onset typically occurs between the ages 40
and 70 years
Etiology:

Unknown
Pathophysiology:

ALS is marked by destruction mo motor cells in
the anterior gray horns and pyramidal tract


As motor neurons die, the muscle cells they
supply undergo atrophic changes


Upper and lower motor neurons are affected
Progressive paralysis results
Prognosis varies

Most ALS clients die within 3 to 10 years of onset,
usually from secondary causes such as pneumonia
Clinical Manifestations:

Vary with the location of affected motor neurons
and disease stage and may include:






Progressive weakness, atrophy, spasticity and tremors
of the upper extremities, followed by involvement of
lower extremities and then respiratory muscles
Fatigue
Impaired speech, chewing and swallowing
Breathing difficulty
Depression
Laboratory and Diagnostic study findings:

Electromyograpic (EMG) studies of the affected
muscles indicate reduction in the number of
functioning motor units
Nursing Management:


Because no treatment is available to slow disease progression, provide supportive
care
Maximize functional abilities





Ensure adequate nutrition
Prevent respiratory complications




Encourage the client to verbalize feelings about body image and self – concept changes
Promote client and family coping


Provide explanations for the cause, treatment, and expected course of the neurologic
disorder
Promote measures to enhance body image


Because the client typically experiences no cognitive deficits and retains mental abilities
Provide client and family teaching


Promote measures to maintain adequate airway
Promote measures to enhance gas exchange such as oxygen therapy and ventilatory
assistance
Promote measures to prevent respiratory infection
Provide intellectually stimulating activities


Prevent complications of immobility
Promote self – care
Maximize effective communication
Encourage the client and family to verbalize feelings and refer to appropriate resources as
needed
Provide referrals
GUILLIAN –
BARRE SYNDROME
Description:




An acute, rapidly progressing motor neuropathy
involving segmental demyelination of nerve
roots in the spinal cord and medulla
Demyelination causes inflammation, leading to
edema, nerve root compression, decreased
nerve conduction and rapidly ascending paralysis
Both sensory and motor impairment occur
Also called Landry’s paralysis

Etiology:


A postinfectious polyneuritis of unknown
origin that commonly follows febrile illness
Pathophysiology:


Segmental demyelination of peripheral nerves
causes inflammation and degeneration in
sensory and motor nerve roots
Most clients experience spontaneous and
complete recovery, although mild deficits may
persist
normal
Damaged myelin
neuron
nerve
Myelin sheath
Clinical Manifestations:


Progressive weakness and paralysis begin in the lower
extremities and ascend bilaterally
Paralysis ascends the body symmetrically






Paralysis of respiratory muscles
Cranial nerve involvement, most often facial nerve, produces
difficulty talking and swallowing
Loss of sensation and function of bowel and bladder
Manifestations may progress rapidly over hours or may
occur over 2 to 4 weeks
Muscle atrophy is minimal
Paralysis decreases as the client begins recovery; most
often, there are no residual effects

Partial or total paralysis
Laboratory and diagnostic
studies:


Based primarily on the clinical
manifestations
Lumbar puncture and CSF analysis


Checks for elevated protein concentration
Electromyogram
Treatment (Supportive)




Respiratory support, possibly mechanical
ventilation
Corticosteroids
Immunosuppressive and immunoglobulins
Plasmapheresis: plasma exchange
Nursing management:

Goal is to evaluate progress of paralysis and initiate
actions to prevent complications


Evaluate rate of progress of paralysis; carefully assess changes
in respiratory pattern
Frequent evaluation of cough and swallow reflexes





Remain with client while client is eating; have suction available
Maintain NPO status if reflexes are involved
If paralysis is rapid, prepare for endotracheal intubation and
respiratory assistance
Prevent complications of immobility during period of paralysis
Assess for involvement of the ANS




Orthostatic hypotension
Hypertension
Cardica dysrhythmias
Urinary retention and paralytic ileus

Goal is to prevent complications of hypoxia if
respiratory muscles become involved

Position client to maintain patent airway







Elevate head of bed and may position on side as well
Encourage coughing and deep breathing
Suction client as needed and as indicated by amount
of sputum and ability to cough
Maintain adequate fluid intake to keep secretions
liquified
Encourage exercises and ambulation as indicated by
condition
Administer Oxygen if dyspnea is present
Goal is to maintain psychological homeostasis




Simple explanation of procedures
Completer recovery is anticipated
Provide psychological support during period of
assisted ventilation
Keep client and family aware of progress of disease
…..
COGNITIVE IMPAIRMENT
DISORDERS
Alzheimer’s Diseases
Multi – infarct dementia
Description:


CID are a group of chronic, progressive,
organic mental disorders resulting in
deterioration of the cognitive processes
Most common are Alzheimer disease and
Multi – infarct dementia

Alzheimer disease accounts for more than
50% of dementias and affects 2% to 4% of
persons older than age 65


Increases with age, particularly after age of 75
Multi – infarct dementia accounts for about
15% of cases of dementia
Incidence is greater among men than women
 Onset generally is earlier than in Alzheimer's
Disease

Etiology:

Alzheimer's Disease


Cause is unknown
Many theory exist such as:
Toxic chemical excess
 Autoimmune mechanism
 Slow virus mechanism
 One or more faulty genes


Multi – infarct Dementia

results from Cerebrovascular disease
producing multiple small cerebral infarctions
Pathophysiology

Alzheimer's Disease:

chronic and irreversible disease characterized by
specific neurologic and biochemical changes
including:






Neurofibrillary tangles, granulovacuolar degeneration of
neurons ad senile or neuritic plaques
primarily in the cerebral cortex
Brain atrophy
with widened cortical sulci and enlarged cerebral ventricles
decreased acetylcholine production
Multi – infarct Dementia

Pathologic changes include multiple areas of
extensive localized softening, along with various
changes in cerebral vessels
Clinical Manifestations:

Alzheimer's disease



Signs and symptoms are highly variable and may include:
Early, subtle changes such as forgetfulness, recent memory loss
and poor concentration, which the client maybe able to hide
Later more overt signs of impaired cognition







Severe memory loss and forgetfulness
Inability to hold a conversation
Think abstractly
Formulate concepts
Poor hygiene, grooming and inappropriate dress
Inability to perform instrumental ADL’s
Behavioral changes, such as








Depression
Anxiety
Wandering
Impulsive behavior
Catastrophic reaction
Imitation
Emotional lability
Withdrawal
Clinical Manifestations:

Multi – infarct dementia





Dizziness, headaches
Confusion
Patchy memory loss
Hallucinations
Focal neurologic signs
Muscle weakness
 Dysreflexia


Dysarthria
Laboratory and diagnostic
study findings:




CT scan
Electroencephalography (EEG)
Positron Emission Tomography (PET)
useful in excluding:







hematomas
brain tumors
stroke
normal pressure hydrocephalus
atrophy
not reliable in make a definitive diagnosis of
Alzheimer Disease
Autopsy is the definitive diagnosis of Alzheimer
Disease
Nursing management:
Administer prescribed medications

Tacrine HCL (Cognex)

- slows progression of Alzheimer's Disease by maintaining the availability
of dopamine but have very toxic hepatic effects
Provide initial and ongoing assessments


Record the clients usual routine as well as words and behaviors used to
communicate ADL needs


Chart words and techniques that get “through” to the client
Request that a family member or other person stay with the client if the client
wanders or cannot be sent to diagnostic tests by himself


Avoid sedation and restraints whenever possible
Assign the client to a room that maximizes the potential for observation and
is not next to an exit or stairwell


For clients who are prone to wanderer
Orient the client to the room and the unit


Mark the room and bedside area with familiar belongings
Attach an ID bracelet


Alert others to wandering


special clothing, care plan, posted notice
Determine and obtain copy if the client has a Living Will or Durable Power of
Attorney
Maximize effective communication

Use short sentences, simple words, gestures and written or pictorial
cues, if needed
explain and repeat instructions unless this increase distress
Maintain a calm demeanor and a consistent approach
Avoid excessive questioning and confrontation
Break down instructions into simple components
Support the anxious or depressed client
Attempt to analyze behavior for meaning







Maximize environmental safety

Install alarms on stairwells
Institute injury, fire and poisoning precautions
Provide adequate lighting in all rooms
Keep the bed in a low position or place the mattress on the floor





Side rails may pose as a hazard
Provide wanderer’s bracelet on the client
Intervene as necessary to manage evening agitation



“Sun – downing”
- provide night light, soft music and supervision


If indicated, create a limited – access, safe unit to obviate activity
restriction and decrease the need for supervision
Promote optimal functioning

Fit diagnostic and therapeutic procedures into the client’s usual schedule as possible
Assign consistent caregivers
Establish a daily routine for care, maintaining the client’s pre-admission sleep – wake
cycle if possible and desirable
Provide a clock, calendar and daily schedule in the room





Avoid pressuring the client for accuracy
Prompt for ADLs with memory aids and verbal cues



Encourage performance within the limits of ability
Avoiding pressuring for performance

Focus the client on simple, repetitive and purposeful activities with sequencing of skills
Monitor for adverse effects of drug therapy
Encourage ambulation and other exercise
Encourage good grooming and personal hygiene
Use distraction to alter undesirable behavior













Noise
People
Caffeine
Regularly assess the skin, gums, teeth and feet for breakdown and infection and provide
good skin and mouth care
Maximize opportunities for social interaction
Optimize nutrition and fluid balance


Break episodes of preservation or remove from harm
Intervene as necessary an agitated client
Limit stimuli


may trigger catastrophic reactions
Monitor food and fluid intake, noting;
Optimize elimination
Provide discharge planning
SEIZURES
Description:

Convulsion


Epilepsy


Involuntary contraction of muscles resulting
from abnormal cerebral stimulation
Refers to paroxysmal, uncontrolled, excessive
firing of hyperexcitable neurons in the brain
Not a disease entity in itself but rather an
indicator of underlying pathology
TYPES

Generalized



Tonic – clonic (grand mal)
Absence (petit mal)
Partial



Complex (temporal lobe; psychomotor)
Status epilepticus
Jacksonian
ETIOLOGY
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About 50% of cases of epilepsy are idiopathic, for which
no underlying pathology can be identified.
Incidence higher in those with family history of idiopathic
seizures
Possible causes:
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Birth trauma
Head trauma
Brain tumor
Meningitis, encephalitis or brain abscess
Metabolic disorders
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E.g.
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Hypoglycemia
Phenylketonuria
Cerebrovascular disorders
Pathophysiology:
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After a task is completed, nerve cell impulses
should cease.
Sometimes these nerve cell impulses continuing
firing even after the task is finished.
During the continued firing of nerve cell
impulses, the parts of the body controlled by the
errant cells may perform erratically
These erratic physical movements are called
seizures

Seizures are classified as

Partial

arising from a localized area of the brain

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Generalized

marked by widespread electrical abnormality in
the brain


e.g. complex, Jacksonian
e.g. tonic – clonic, absence
Status epilepticus refers to continued seizure
activity

a medical emergency treated with medications
Clinical Manifestations

Tonic – clonic seizures (grand mal)

Tonic
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Clonic
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Involuntary contraction and relaxation of opposing muscle groups
producing a jerky convulsive movements
A generalized seizure activity, with no focal onset and lasting
about 2 minutes
Possible prodrome of a vaguely uneasy feeling (aura)
Loss of consciousness, with falling if upright at onset
Tonic phase

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Persistent contraction of a muscle or sets of muscles due to
muscular shrinkage
muscle contraction (including jaw clenching)
possibly periods of apnea
Clonic phase
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rhythmic, forceful movement of extremities
excessive salivation
rapid pulse
Possible incontinence
Stupor for 5 to 10 minutes after the clonic phase

Absence seizures (petit mal)
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Generalized seizure activity
no focal onset
occurring primarily in children
Momentary loss of consciousness (10 to 30
second)
marked by a glassy stare
usually no falling
Complex seizures

the client exhibits altered behavior


e.g. automatisms, unusual sensations, delusions
Not aware of what is happening
Jacksonian seizures

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begin in one part of the body

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e.g. twitching of one side of the face or abnormal movements
of the hand
may progress to a generalized tonic – clonic
seizures
Status epilepticus

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Usually refers to generalized grand mal seizures
Seizures is prolonged (or there are repeated
seizures without regaining consciousness)
Unresponsive to treatment
Can result in decreased oxygen supply and possible
cardiac arrest
Medical management:

Drug therapy

Phenytoin (Dilantin)

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Often used with Phenobarbital for its potentiating effect
Inhibits spread of electrical discharge
Side effects:
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Phenobarbital

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gum hyperplasia
hirsutism
ataxia
gastric distress
Nystagmus
anemia
sedation
Elevates the seizure threshold
Inhibits the spread of electrical discharges
Surgery:

To remove the tumor, hematoma or epileptic focus
Nursing management
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During seizure activity
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Protect from injury
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Keep airway open
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Prevent falling, gently support the head
Decrease external stimuli
do not restrain
do not use tongue blades
do not add additional stimuli
loosen tight clothing
Place in side – lying position
Suction excess mucus
Observe and record seizure

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Note pre-ictal aura
affective signs:
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Fear
anxiety
Psychosensory signs:
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Hallucinations

Cognitive signs:
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“deja – vu symptoms”
note nature of ictal phase
symmetry of movement
response to stimuli; LOC
respiratory pattern
note post-ictal response
amount of time it takes child to orient to time and place
Provide client teaching and discharge planning
concerning
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Care during a seizure
Need to continue drug therapy
Safety precautions/activity limitations
Need to wear Medic – Alert identification bracelet or carry
identification card
Potential behavior changes and school problems
Availability of support groups/community agencies
How to assist child in explaining the disorders to peers
CEREBROVASCULAR
DISORDERS
Cerebrovascular
Accident
TIA
Cerebral Aneurysm
Cerebrovascular Disorders
• Destruction/infarction of brain
cells caused by a reduction in
cerebral blood flow and oxygen
• Group of disorders that involves
disruption of blood supply to the
brain
Cerebrovascular Accident
(CVA, Stroke)
Sudden loss of brain function
 Most common site is middle cerebral
artery
 Most leading cause of death in the US
which strikes 50,000 persons each
year


One half of survivors sustain permanent
neurologic deficits
Transient Ischemic Attacks
(TIA)
Transient or temporary episode of
neurologic dysfunction
 Considered
a warning sign of CVA
 Common site is bifurcation of
common carotid artery
Cerebral Aneurysm
Dilation of the walls of the cerebral
artery resulting from a weakness in the
arterial wall
 Most common type of berry aneurysm
 Most common site is the circle of Willis

 Usually
at a vessel at a junction
Cerebrovascular Disorders

Affects men more than women


Caused by:
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Incidence increases with age
Thrombosis
Embolism
Hemorrhage
Risk Factors:
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Hypertension
Diabetes mellitus
Arteriosclerosis/atherosclerosis
Cardiac disease

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Valvular disease/replacement
Chronic atrial fibrillation
Myocardial infarction
Life – style:
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Obesity
Smoking
Inactivity
Stress
Use of oral contraceptives
Etiology

CVA
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TIA
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Results from
Thrombosis
Most common
Embolism
Vessel rapture
Spasm
Result from occlusion of an intracranial or extracranial
artery
Commonly associated with atherosclerosis
CEREBRAL ANEURSYM



Results from a weakness in a vessel wall because of a
congenital defect or a degenerative process such as
Hypertension
Atherosclerosis
Pathophysiology:


Interruption of cerebral blood flow for 5 minutes
or more causes death of neurons in affected
area with irreversible loss of function
Modifying Factors:

Cerebral edema:
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Vasospasm:

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Develops around affected area causing further impairment
Constriction of cerebral blood vessel may occur, causing
further decrease in blood flow
Collateral circulation:

May help to maintain cerebral blood flow when there is
compromise of main blood supply
Stages of Development:

TIA:
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Warning sign of impending CVA
Brief period of neurologic deficit:
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May last less than 30 seconds, but not more than 24 hours
with complete resolution symptoms
Stroke in evolution:
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Visual loss
Hemiparesis
Slurred speech
Aphasia
Vertigo
Progressive development of stroke symptoms over a period
of hours or days
Completed stroke:

Neurologic deficit remains unchanged for a 2 to 3 day period
Clinical Manifestations:
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Headache
Generalized symptoms:
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Vomiting
Seizures
Confusion
Disorientation
Decreased LOC
Nuchal rigidity
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Fever
Hypertension
Slow bounding pulse
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strong and forceful pulse
Cheyne – stokes respiration
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Inability to flex the head forward due to rigidity of the neck muscles
deepening breaths, followed by shallower and shallower breaths and stops breathing for a
short period of time before starting to breathe again
Focal signs: (related to site of infarction)
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Hemiplegia
Sensory loss
Aphasia
Homonymous hemianopsia

blindness or reduction in vision in one half of the visual field
Laboratory and Diagnostic
Study findings:

CT and brain scan


EEG:
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Reveal the lesion
Abnormal changes
Cerebral arteriography:

May show occlusion or malformations of blood
vessels
Nursing Management:
Acute Stage:
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Maintain patent airway and adequate ventilation
Monitor vital signs and neuro checks
Provide complete bed rest as ordered
Maintain fluid and electrolyte balance and ensure
adequate nutrition
Maintain proper positioning and body alignment
(elevate HOB)
Promote optimum skin integrity
Maintain adequate elimination
Provide quiet, restful environment
Establish means of communicating with client

Administer medications as ordered:
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Hyperosmotic agents, corticosteroids to decrease cerebral
edema
Anticonvulsants to prevent or treat seizures
Thromboembolytics given to dissolve clot
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Anticoagulants for stroke in evolution or embolic stroke

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Rule out the possibility of hemorrhage
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Tissue Plasminogen Activator (tPA, Alteplase)
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Streptokinase, urokinase
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Must be given within 2 hours of episode
Rule out the possibility of hemorrhage

Heparin
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Warfarin (Coumadin)
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For long term therapy
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Aspirin and Dipyridamole (Persantine)
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To inhibit platelet aggregation in treating TIA’s
Anti-hypertensive if indicated for elevated blood pressure
Nursing Management

Rehabilitation:
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Hemiplegia
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
Results from injury to cells in the cerebral motor cortex or to
corticospinal tracts
 Causes contra-lateral hemiplegia since tracts cross in
medulla
 Turn every 2 hours
 20 minutes on affected side
 Use proper positioning and repositioning to prevent
deformities
 Foot drop
 External rotation of hip
 Flexion of fingers
 Wrist drop
 Abduction of shoulder and arm
 Support paralyzed arm on pillow or use sling while out of
bed to prevent sub-luxation of shoulder
 Elevate extremities to prevent dependent edema
 Provide active and passive ROM exercise every 4 hours
Susceptibility to hazards
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Keep side rails up at all times
Institute safety measures
Inspect body parts frequently for signs of injury
Dysphagia
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Check gag reflex before feeding client
Maintain a calm, unhurried approach
Place client in an upright position
Place food in unaffected side of mouth
Offer soft foods
Give mouth care before and after meals
Homonymous Hemianopsia
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Loss of half of each visual field
Approach client on unaffected side
Place personal belongings on unaffected side
Gradually teach client to compensate by scanning
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Turning the head to see things on the affected side
Emotional lability
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Mood swings, frustrations
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Create a quite restful environment with a reduction in excessive
sensory stimuli
Maintain a calm non-threatening manner
Explain to family that the clients behavior is not purposeful
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Aphasia
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Most common in right hemiplegics
Maybe receptive or expressive
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Receptive Aphasia
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Give simple slow directions
Give one command at a time
Gradually shift topics
Use non-verbal communications
Pantomime, demonstration
Expressive Aphasia
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Listen and watch very carefully when the client attempts
to speak
Anticipate client’s needs to decrease frustration and
feelings of helplessness
Allow sufficient time for client to answer
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Sensory/Perceptual Deficits
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More common in left hemiplegics
Characterized by:
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Assist with self – care
Provide safety measures
Initially arrange objects in environment on unaffected side
Gradually teach client to take care of the affected side and to turn frequently
and look at affected side
Apraxia
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Loss of ability to perform purposeful, skilled acts
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Impulsiveness
Unawareness of disabilities
Visual neglect
 Neglect of affected side and visual space on affected side
Guide client through intended movement
 Take object such as washcloth and guide client through movement of
washing
Keep repeating the movement
Generalizations about the clients with left hemiplegia versus
right hemiplegia and nursing care
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Left Hemiplegia
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Perceptual, sensory deficits, quick and impulsive behavior
Use safety measures, verbal cues, simplicity in all areas of care
Right Hemiplegia
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Speech – language deficits, slow and cautious behavior
Use of pantomime and demonstration
TIC DOULOUREUX
(Trigeminal Neuralgia)
Description:
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Disorder of cranial nerve V causing disabling and recurring attacks
of severe pain along the sensory distribution of one or more
branches of the trigeminal nerve
Trigeminal neuralgia (TN), also known as tic douloureux
pain syndrome recognizable by patient history alone.
The condition is characterized by pain often accompanied by a brief
facial spasm or tic.
Pain distribution is unilateral and follows the sensory distribution of
cranial nerve V, typically radiating to the maxillary (V2) or
mandibular (V3) area.
At times, both distributions are affected.
Physical examination eliminates alternative diagnoses.
Signs of cranial nerve dysfunction or other neurologic abnormality
exclude the diagnosis of idiopathic TN and suggest that pain may be
secondary to a structural lesion.
Incidence increase in elderly women
Cause unknown
Etiology:
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The condition has no clear – cut cause
Some experts argue that the syndrome is caused by
traumatic damage to the nerve as it passes from the
openings in the skull to the muscles and tissue of the
face.
The damage compresses the nerve, causing the nerve
cell to shed the protective and conductive coating
(demyelination)
Others believe the cause stems from biochemical change
in the nerve tissue itself
A more recent notion is that an abnormal blood vessel
compresses the nerve as it exits the brain
In all cases, though, an excessive burst of nervous
activity from a damaged nerve causes the painful
attacks.
Pathophysiology:

The mechanism of pain production remains controversial.
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One theory suggests that peripheral injury or disease of the trigeminal nerve
increases afferent firing in the nerve; failure of central inhibitory mechanisms
may be involved as well.
Pain is perceived when nociceptive neurons in a trigeminal nucleus involve
thalamic relay neurons.
Aneurysms, tumors, chronic meningeal inflammation, or other lesions may
irritate trigeminal nerve roots along the pons.
An abnormal vascular course of the superior cerebellar artery is often cited
as the cause.
In most cases, no lesion is identified, and the etiology is labeled idiopathic
by default.
Uncommonly, an area of demyelination from multiple sclerosis may be the
precipitant.
Lesions of the entry zone of the trigeminal roots within the pons may cause
a similar pain syndrome.
Thus, although TN typically is caused by a dysfunction in the peripheral
nervous system (the roots or trigeminal nerve itself), a lesion within the
central nervous system may rarely cause similar problems.
Infrequently, adjacent dental fillings composed of dissimilar metals may
trigger attacks.
Clinical Manifestations:


Sudden paroxysms of extremely severe shooting pain
in one side of the face
Attacks may be triggered by:
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During attack:
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cold breeze
foods/fluids of extreme temperature
Tooth brushing
Chewing
Talking
Touching the face
Twitching
Grimacing
Frequent blinking
Tearing of the eye
Poor eating and hygiene habits
Withdrawal from interactions with others
Laboratory and Diagnostic
Study findings:
 Diagnostic
 X-rays
Test:
of the
 Skull
 Teeth
 Sinuses
 May
identify dental or sinus infection
which may aggravate the condition
Medical management:

Anticonvulsant drugs:



Carbamazipine (tegretol)
Phenytoin (dilantin)
Nerve block:



Injection of alcohol or phenol into one or
more branches of the trigeminal nerve
Temporary effect
Last for 6 – 18 months

Surgery:

Peripheral


Avulsion of peripheral branches of trigeminal nerve
Intracranial

Retrogasserian rhizotomy:



Total severance of the sensory root of the trigeminal
nerve intracranially
Results in
 Permanent anesthesia
 Numbness
 Heaviness
 Stiffness in affected part
 Loss of corneal reflex
Microsurgery:

Uses more precise cutting and may preserve facial
sensation and corneal reflex

Percutaneous radio – frequency trigeminal
gangliolysis:





Current surgical procedure of choice
Thermally destroys the trigeminal nerve in the area of
the ganglion
Provides permanent pain relief with preservation of:
 Sense of touch
 Proprioception
 a sensory nerve ending in muscles, tendons, and
joints that provides a sense of the body’s position by
responding to stimuli from within the body
 Corneal reflex
Done under local anesthesia
Microvascular decompression of trigeminal nerve:

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Decompresses the trigeminal nerve
Craniotomy is necessary
Provides permanent pain relief
Preserves facial sensation
Nursing management:
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Assess the characteristics o pain including triggering factors, trigger
points and pain management techniques
Administer medications as ordered, monitor response
Maintain room at an even, moderate temperature, free from drafts
Provide small, frequent feedings of lukewarm water and perform
hygiene during periods when pain is decreased
Prepare the client for surgery if indicated
Provide client teaching and discharge planning concerning:


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Need to avoid outdoor activities during cold, windy or rainy weather
Importance of good nutrition and hygiene
Use of medications, side effects and signs of toxicity
Specific instructions following surgery for residual effects of anesthesia
and loss of corneal reflex
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Protective eye wear
Chew on unaffected side only
Avoid hot fluids or foods
Mouth care after meals to remove particles
Good oral hygiene; visit dentists every 6 months
Protect the face during extremes of temperature
BRAIN
TUMORS
Brain Tumors

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Primary tumors
Secondary tumors
Signs and symptoms

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Cerebral edema
Increased ICP
Focal neurologic deficits
Obstruction of flow of CSF
Brain Tumors: Complications
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Cerebral (vasogenic) edema/ ↑ ICP
Herniation of brain tissue/ischemia of
affected area
Rupture/hemorrhage into brain tissue
Seizure activity/hydrocephalus
Pituitary dysfunctions/SIADH/diabetes
insipidus
Fluid and electrolyte imbalances
Brain Tumor: Classification


Malignant/benign
Location

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Gliomas
Meningiomas
Pituitary gland
Acoustic neuromas
Brain Tumors: Symptoms
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Headaches (severe on awakening in am)
Nausea and vomiting
Visual symptoms
Seizures
Changes in mentation or personality
Papilledema (swelling of the optic disk)
Brain Tumors: Interventions
Nonsurgical
 Radiation/chemotherapy
 Blood brain barrier disruption
 Recombinant DNA
 Monoclonal antibodies
 Antineoplastic drugs
 Immunotherapy/hyperthermia
Surgical
 Biopsy
 Craniotomy
Brain Tumors: Post-op
Complications
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Increased ICP
Hematomas
Hydrocephalus
Respiratory problems
Neurogenic pulmonary edema
Wound infection
Meningitis
Fluid/electrolyte imbalance