MS 2
NEUROLOGY -also called neuroglial
Care of the Patient with Neurologic
Disorder
I. Anatomy and Physiology of the Nervous
System
The nervous system has 2 main structural
divisions: the Central Nervous System and
the Peripheral Nervous System
Central Nervous System
a. Brain
b. Spinal Cord
Peripheral nervous system
a. Somatic Nervous System - sends messages
from the CNS to the skeletal muscles
(voluntary)
b. Autonomic Nervous System - sends
messages from the CNS to the smooth muscle,
cardiac muscle, certain glands (involuntary)
The nervous system has two main categories
of cells: the Neurons and Glial Cells
Neurons
-transmitter cells
-the space between each neuron is called a
synapse
-it has 3 main structures: the cell body, axon
and dendrites
A. Cell Body- contains a nucleus surrounded
by cytoplasm
B. Axon- cylindric extension of the nerve cell
that conducts impulses away from the neuron
cell body
C. Dendrites- branching structures that
extend from a cell body and receive impulses
Glial cells
-support cells
Neuromuscular Junction
-the area of contact between the ends of a
large myelinated nerve fiber of skeletal muscle
- the neurotransmitter act to make sure that
the neurological impulse passes from the
nerve to the muscle
Neurotransmitters
-chemicals that modify or result in
transmission of impulses between synapses
A. Acetylcholine- role in nerve impulse
transmission, spills into the synapses area
and speeds up transmission of impulse.
Enzyme cholinesterase is then released to
deactivate acetylcholine once the message or
impulse has been sent
B. Norepinephrine- has an effect on
maintaining arousal or awakening from a
deep sleep, dreaming and regulation of mood
(happiness or sadness)
C. Dopamine- affects motor function (gross
subconscious movements of the skeletal
muscles), also plays a role in emotional
response. Parkinson’s disease there is a
decrease in dopamine levels. This causes
tremors, or involuntary, trembling muscles.
D. Serotonin- induces sleep, affects sensory
perception, controls temperature, and helps
regulate mood.
Neuron Coverings
A. Myelin- white, waxy, fatty material
covering many nerve fibers (axons and
dendrites). Increases rate of transmission of
impulses and protect and insulates the fibers
B. Nodes of Ranvier- layers of myelin with
indentations
-further increases the rate of transmission
because the impulse can jump from node to
node
C. Schwann Cells- produces myelin in the
PNS
-outer memrane of the schwann cells gives
rise to neurilemma
D. Neurilemma- it is a very important layer
because it helps regenerate injured axons.
This only occur in the PNS because cells in
the CNS cannot regenerate and does not have
neurilemma, thus cells damaged in the CNS
result in permanent damage (paralysis)

2. Diencephalon
-often called interbrain
-it lies beneath the cerebrum
-contains the thalamus and the
hypothalamus

Thalamus- serves as the relay station for

Central Nervous System
-one of the two main divisions of the nervous
system
-composed of the brain and the spinal cord
-cranium protects the brain
-vertebral column protects the spinal cord
A. Brain
- specialized cells in the brain’s mass of
convoluted, soft gray or white tissue
coordinate and regulate the functions of the
CNS
-one of the largest organs weighing
approximately 3 pounds (6.6 kg)
-it is divide into 4 principal parts: the
cerebrum, diencephalon, cerebellum, and
the brain stem
some sensory impulses while interpreting
other sensory messages such as pain, light
touch and pressure
Hypothalamus- lies beneath the thalamus,
plays a vital role in controlling the body
temperature, fluid balance, appetite, and
certain emotions, such as fear, pleasure and
pain.
-both the sympathetic and parasympathetic
divisions are under the control of the
hypothalamus
-the hypothalamus influences heartbeat,
contraction and relaxation of the walls of the
blood vessels, hormone secretion and other
vital body functions.

1. Cerebrum
-largest part of the brain
-divided into the left and right hemisphere
-outer portion of the brain composed of gray
matter and is called cerebral cortex
-arranged in folds called gyri, grooves are sulci 3. Cerebellum
(fissures) -lies in posterior and inferior to the
-connecting structure is the corpus collosum, cerebrumand is the second largest portion of
divides the two hemispheres into 4 lobes: the brain
frontal lobe, parietal lobe, temporal lobe,
occipital lobe -contains 2 hemispheres that is responsible
for coordination of the voluntary movement
and maintenance of balance, equilibrium and
muscle tone
-sensory messages form the semicircular
canals in the inner ear send their messages to
the cerebellum

Brain and Spinal Cord Coverings

4. Brain Stem 1. Dura mater -outer layer
-located at the base of the brain and contains 2. Arachnoid membrane- second layer
the midbrain, pons and the medulla 3. Pia mater- inner most layer
oblongata -provides oxygen and nourishment to
the nervous tissue.
Midbrain- forms the superior portion of the
brainstem
-responsible for motor movement, relay of
impulses and auditory and visual reflexes
-it is the origin of cranial nerve III and IV
Pons- connects to he midbrain to the medulla
oblongata
-the origin of the cranial nerves V-VIII
-compsosed of myelinated nerve fibers and is
responsible for sending impulses to the
structures that are inferior and superior to it
-also contains the respiratory center and
compliments the respiratory center in the
medulla
Medulla Oblongata- distal portion of the
brain stem
-origin of the cranial nerves IX and XII
-controls the heartbeat, rhythm of breathing,
Ventricles
swallowing, coughing, sneezing, vomiting and
-there are 4 ventricles
hiccups (singultus)
-are spaces located in the brain
-a vasomotor center regulates the diameter of
-the cerebrospinal fluid,which is clear and
the blood vessels, which aids in the control of
resembles plasma, flows into the
the blood pressure
subarachnoid spaces around the brain and
the spinal cord and cushions them. Contains
proteins, glucose, urea and salts
-it also contains certain substances that form
a protective barrier that prevents harmful
substances from entering the brain and the
spinal cord

B. Spinal Cord
-it is 17”-18” cord that extends from the brain
stem to the second lumbar vertebra
2 Main Functions of Spinal Cord
1. Conducting impulses to and from the brain
and serving as center for reflex actions.
Responsible for reflex activities such as knee
jerks.
2. Sensory neurons sends information to the
cord, a central neuron interprets the impulse,
and motoneuron sends the message back to
the muscle or organ involved. Thus message
is sent, interpreted and acted upon without
traveling to the brain.
Peripheral Nervous System
-it is comprised of the motor nerves, sensory
nerves, and ganglia outside the brain and the
spinal cord.
1. Spinal Nerves
-31 pairs, all mixed nerves
-they transmit sensory information to the
spinal cord through afferent neurons (afferent
is responsible for the transport of nerve
impulses from the receptor organs to the
central nervous system) and motor
information from the CNS to the various areas
of the body through efferent neurons ( efferent
neurons carry nerve impulses out of the CNS)
-spinal nerves are named according to the
corresponding vertebrae
2. Cranial Nerves
-12 pairs, attached to the posterior surface of
the brain, mainly the brainstem
-conduct impulses between the head, neck
and brain, excluding the vagus nerve (X), also
serves organs in the thoracic and abdominal
cavities.
A. Autonomic Nervous System
-controls the activities of the smooth muscle,
cardiac muscle, and all the glands
-it is a subdivision of the peripheral nervous
system
-primary function is to maintain homeostasis
for example, maintain a normal heartbeat,
constant body temperature, and a normal
respiratory rate
-it has 2 divisions: the sympathetic and the
parasympathetic nervous system
i. Sympathetic Nervous System- prepares
the body for “fight or flight”
ii. Parasympathetic Nervous System-
calms the body after a crisis

II. Assessment of the Neurological System
Effects of Normal Aging to the Nervous
System
1. Loss of weight
2. Loss of neurons (1 % a year after age 50)
3. Reduction in cereral blood flow
4. Decrease in brain metabolism and oxygen
utilization
5. Decreased blood supply in the spinal cord
causes decreased reflexes
Prevention of Neurological Problems
1. Avoid drug and alcohol use
2. Safe use of motor vehicles
3. Safe swimming practices
4. Safe handling and storing of firearms
5. Use hardhats in dangerous construction
areas
6. Use of protective padding as needed for
sports
HISTORY
-comprehensive history essential for
diagnosing neurological disease
-be specific about symptoms experience as
well as patient understanding.
-information from the family may also be
helpful
a. Symptoms and Subjective data may
include:
1. Headaches- especially those that first
occur after middle age or those that
change in character; headaches are worse
in the morning or awaken a person that is
asleep is significant
2. Clumsiness or loss of function in an
extremity
3. Change in visual acuity
4. Any new or worsened seizure activity
5. Numbness or tingling in one or more
extremities
6. Pain in an extremity or other part of the
body
7. Personality changes or mood swings
8. Extreme fatigue or tiredness
MENTAL STATUS
-assessment of the neurological of the
patient’s mental status is important and is
done with every assessment. It generally
includes:
1. Orientation to person, place, time and
purpose
2. Mood behavior
3. General knowledge (such as names of
presidents)
4. Short and long term memory
5. Attention span
6. Ability to concentrate
DOCUMENTATION
-is key to determining a change
-nurse should vary orientation questions so
patient doesn’t memorize answers through
repetition.
LEVEL OF CONSCIOSNESS
-it is the earliest and most sensitive indicator
that something is changing
-a decerease in LOC is the earliest sign of
increased intracranial pressure
-LOC has 2 components, arousal and
awareness
A. Arousal or Wakefulness is controlled by
the brainstem and most fundamental part of
LOC. If patient can open eyes to voice or to
the pain, the wakefulness center in the
brainstem is still functioning.
B. Awareness is a higher function controlled
by the reticular activating system in the
brainstem, is the ability to interact with
others. It has 4 parts:
1. Orientation-person, place, time and
purpose
2. Memory- assess short term memory; do
not ask yer or no questions
3. Calculation- example “if you had $2 and
your apple is $1.25, how many quarter
would you get back?”
4. Fund a knowledge- ask the patient to
name the president and to tell you what is
on the national news
Restlessness, disorientation and lethargy may
be seen first
Glasgow Coma Scale
-it is a quick, practical and standardized
system for assessing the degree of
consciousness impairment in the critically ill
and for predicting the duration and ultimate
outcome of coma, particularly with head
injuries.
LANGUAGE AND SPEECH

Speech is a function of the dominant

hemisphere, on the left side of the brain for all
right handed people and most left-handed
people.

Aphasia is an abnormal neurological

condition in which the language function is
defective or absent due to injury of certain
areas of the cerebral cortex
-aphasia includes all areas of language, CRANIAL NERVES
including speech, reading, writing, and -12 pairs of nerves emerge from the cranial
understanding. Aphasia has been subdivided activity through opening in the skull
as follows:

1. Sensory Aphasia or Receptive Aphasia is

the inability to comprehend the spoken word
or written word
2. Motor Aphasia or Expressive Aphasia
is the inability to use symbols of speech
3. Global Aphasia is the inability to
understand the spoken word or to speak

Anomia is a form of aphasia characterized by

inability to name objects

Dysarthria is defined as difficult, poorly

articulated speech that usually results from
interference in the control over the muscles of
speech caused by damage to a central or
peripheral nerve

Broca’s Area in the frontal lobe is responsible

for speech production

Wernicke’s Area in the posterior part of the

temporal lobe responsible for understanding
speech MOTOR FUNCTION
-will detect abnormalities in the normal
functioning of nerves and muscles. Motor
status exam includes:

1. Gait and stance

2. Muscle tone -spinal fluid protein is elevated when
3. Coordination degenerative diseases or a brain tumor is
4. Involuntary movements present
5. Muscle stretch reflexes (push-pull) -blood in the spinal fluid indicates
hemorrhage from somewhere in the ventricle
Paralysis is a loss of function system
Paresis is a lesser degree of movement deficit -protein electrophoresis evaluation may give
from partial or incomplete paralysis evidentneurological disease such as multiple
Flaccid is weak, soft, flabby and lacking sclerosis (MS)
normal muscle with absent deep tendon
reflexes
Spastic is the involuntary, sudden movement
or muscular contraction with increased
reflexes
Fasciculation is a small, localized,
spontaneous and involuntary contractions

SENSORY AND PERCEPTUAL

STATUS
-it is the most difficult part of the neurological
examination
-alterations in sensation should be assessed
include: pain, touch, temperature and
proprioception ( the sensation pertaining to
spatial-position and muscular-activity stimuli
originating from within the body or to the
sensory receptors that those stimuli activate.

Unilateral neglect is a condition in which the

individual is perceptually unaware and
c. Computed Tomography (CT Scan)
inattentive to oneside of the body
-detect pathological conditions of the
cerebrum and spinal cord using a technique
Hemianopia pis characterized by defective
of scanning without radioisotopes
vision or blindness in half of the visual field
-takes 20-30 mins w/o contrast and up to 60
mins with contrast and is painless (except
III. Laboratory and Diagnostic Procedures
with some discomfort with the injection of dye)
Note: check allergies to shellfish, seafood,
a. Blood and Urine
and/or iodine
 Culture- may rule out infection
 Drug screens- rule out use of drugs with
d. Brain Scan
lethargy to identify specific drugs ingested
-detecting pathologic conditions of the
 Arterial Blood Gases- used in monitoring
cerebrum. Uses radioactive isotopes and a
O2 levels of the blood. Gases may be
scanner. Takes about 45-60 mins.
altered with neurological diseases such as
-if mercury is used as the isotope indicator, a
Guillaine- Barre syndrome ( a rare
mercurial diuretic Meralluride (aka
disorder in which your body's immune
Mercuhydrin) is administered several hours
system attacks your nerves), in which
before the procedure to allow a greater
breathing pattern are altered.
concentration of the mercury to circulate to
brain tissue because meralluride minimizes
b. Cerebrospinal Fluid
the uptake of mercury by the kidneys
-normally up to 10 lymphocytes/ml of spinal
-used less often because CT’s and MRI’s give
fluid. An increase number of lymphocytes can
excellent results
indicate infection such as tuberculosis,
meningitis or viral infection.
e. Magnetic Resonance Imaging (MRI
Scan)
-bacterial infections often lower the glucose
-uses magnetic forces to image body
level as well as the chloride levels. A culture is
structures
done to determine the causative organism for
meningitis
-relevance in the nervous system as a way to
detect pathologic conditions of the cerebrum
and spinal cord
-used to detect stroke, multiple sclerosis,
tumors, trauma, herniation and seizures
-greater contrast of soft-tissue vs CT scan
-diagnostic choice for neurological diseases
-caution: remove watches, credit cards, and
any metal from clothing and body before
entering the scanning room
-takes about 30-60 mins
f. Positron Emission Tomography Scan
(PET Scan)
-uses magnetic forces of deoxyglucose with
radioactive fluorine
-gives color composite of question area.
Shades of color give an indication of the level
of glucose metabolism
-used for patients with stroke, Alzheimer’s
disease, tumors, epilepsy, and Parkinson’s
disease
-take about 40-60 mins
g. Lumbar Puncture
-to obtain CSF for examination, to relieve
pressure, or introduce dye or medication
-takes about 10-15 mins at the bed side
-Caution: sharp shooting pain down one leg
may occur caused by the needle coming close
to a nerve
-usually done between L4-L5 or L5-S1
-post procedure patient lays flat for several
hours. Headaches may occur (opioids are
usually not helpful)
h. Magnetic Resonance Angiography
(MRA)
-differential signal characteristic of flowing
blood to evaluate extracranial and intracranial
blood vessels
-provides anatomic and hemodynamic
information
-with or without contrast
-rapidly replacing cerebral angiography for
use in dx cerebrovascular accident (CVA)
i. Electroencephalogram (EEG)
-To provide function by measuring the
electrical activity of the brain.
-Disease assessed by EEG: epilepsy, mass
lesions (tumors, abscess, hematoma),
cerebrovascular lesions, and brain injury.
j. Myelogram
-Used to identify lesions in the intradural or
extradural compartments of the spinal canal
by observing the flow of radiopaque dye
through the subarachnoid space
-Most common use is dx of herniated or
protruding intervertebral disk. Other lesions
include spinal tumors, adhesions, bony
deformations, and arteriovenous
malformations.
-Water soluble iodine dyes are more often
used because they are absorbed into the
bloodstream and excreted by the kidneys
-Site of puncture to be monitored for leakage
of CSF
k. Angiogram
-Used to visualize the cerbral arterial system
by injecting radiopaque material. For
detection of arterial aneurysms, vessel
anomalies, ruptured vessels and displacement
of vessels by tumors or masses
-Takes about 2-3 hours
l. Carotid Duplex
-Uses ultrasound and pulsed doppler
technology
-Noninvasive procedure that evaluates carotid
occlusive disease
m. Electromyogram
-Used to measure the contraction of a muscle
in response to electrical stimulation
-Takes about 45-60 minutes for one muscle
study
n. Echoencephalogram
-Uses ultrasound to depict the intracranial
structures of the brain.
-Helpful in detecting ventricular dilation and
major shift of midline structures in the brain
as a result of an expanding lesion.
  Nausea, vomiting, light sensitivity,
chilliness, fatigue, irritability, diaphoresis,
edema
IV. Common Disorders of the Neurological MANAGEMENT
System
Pharmacological management
1. H E A D A C H E S  Migraine headaches
-Common neurological complaint; has many  Aspirin, acetaminophen, ibuprofen
different causes  Ergotamine tartrate
 Codeine; Inderal
ETIOLOGY/PATHOPHYSIOLOGY Dietary recommendations
-Skull and brain tissues are not able to feel  Limit MSG, vinegar, chocolate, yogurt,
sensory pain alcohol, fermented or marinated foods,
ripened cheese, cured sandwich meat,
A. Vascular headaches caffeine, and pork
Psychotherapy
i. Migraine
Cluster headaches
Pre-Migraine: visual field defects, unusual  Narcotic analgesics
smells or sounds, disorientation, paresthesias Tension headaches
During Migraine: nausea, vomiting,  Non-narcotic analgesics
sensitivity to light, chills, fatigue, irritability, Traction-inflammatory headaches
diaphoresis, edema  Treat cause
-Cause includes abnormal metabolism of Comfort measures
serotonin, a vasoactive neurotransmitter  Cold packs to forehead or base of skull
found in platelets and cells of the brain, plays  Pressure to temporal arteries
a major role.  Dark room; limit auditory stimulation

ii. Cluster 2. N E U R O P A T H I C PAIN

-Aka alarm clock headache : known to wake
up pt in the middle of the night with intense
pain in or around the eye on one side of your
head
-Pain is described as sharp, penetrating or
burning.
-A cluster period generally lasts from six to 12
weeks
-Risk factors include: Gender (men) Age (late
20’s) Smoking/Alcohol use, family history
ETIOLOGY/PATHOPHYSIOLOGY
-May arise from several occurrences
The pain transmission is not fully understood
CLINICAL MANIFESTATIONS
-Ranges from mild to excruciating
Changes in ability to carry out ADLs
MANAGEMENT

iii. Hypertensive Pharmacological management

-Elevated blood pressure cause increased
pressure
B. Tension headaches – caused by tension,
stress, or cervical arthritis
C. Traction-inflammation headaches-
caused by an infection, intracranial causes,
occlusive vascular structures and temporal
arthritis
CLINICAL MANIFESTATIONS
 Head pain
 Migraine headaches
Prodromal (early sign/symptom)
 Visual field defects, unusual smells or
sounds, disorientation, paresthesias
During headache
 Anticonvulsants; nonopioid analgesics;
antidepressants
Comfort measures
 Cold packs to forehead or base of skull
 Pressure to temporal arteries
 Dark room; limit auditory stimulation
3. I N C R E A S E D I CP
-The structure of the cranium does not allow
for expansion as it is housed within the rigid
skull. Any increase in the contents will result
in an increase in intracranial pressure.
ETIOLOGY/PATHOPHYSIOLOGY
-Increase in any content of the cranium
-Space-occupying lesions, cerebrospinal
problems, cerebral edema

CLINICAL MANIFESTATIONS
 Diplopia
 Headache
 Decreased level of consciousness
 Pupillary signs
 Widening pulse pressure (increased
systolic/decreased diastolic)
 Bradycardia (pulse less than 60)
 Respiratory problems (poss. Cheyne
stoking)
 High, uncontrolled temperatures
 Positive Babinski’s reflex (extension of the
big toe while fanning the other toes.)
 Seizures
 Posturing (Decorticate, Decerebrate, or
both)
 Vomiting
 Singultus (ordinary hiccup)
MANAGEMENT
-Treat cause if possible
Pharmacological management
 Corticosteroids (dexmethasone)
 Antacids; histamine-receptor blockers
 Anticonvulsants (dilantin, cerebyx(short-
term IV or IM use))
AVOID opioids and other drugs that cause
respiratory depression
Mechanical decompression
 Craniotomy (surgical operation in which a
bone flap is temporarily removed from the
skull to access the brain)
 Craniectomy (Surgical removal of a
portion of the cranium)
Internal monitoring devices
 Ventricular pressure monitoring – catheter
inserted through a burr hole into the
lateral ventricle and attached to a
transducer and oscilloscope to monitor
ICP
 Subarachnoid screw – inserted through a
burr hole in skull and attached to a
transducer and oscilloscope for
continuous monitoring
4. D I S T U R B A N C E S I N
MUSCLE TONE AND
MOTOR FUNCTION
-Patients experiencing neurological system
disorders can present with a variety of signs
and symptoms. The assessment will be key in
making a determination of the exact problem
and developing a plan of care.
-Review the assessments that will be
performed.
ETIOLOGY/PATHOPHYSIOLOGY
-Damage to the nervous system causes
serious problems in mobility
CLINICAL MANIFESTATIONS
 Flaccid or hyperreflexic muscle tone
 Clumsiness or incoordination
 Abnormal gait
MANAGEMENT
 Muscle relaxants
 Protect from falls
 Assess skin integrity
 Positioning
 Sit up and tuck chin when eating
 Encourage patient to assist with ADLs
 Emotional support
5. E P I L E P S Y O R S E I Z U R E S
-Seizures affect both men and women of all
races and ages.
-Identify some potential causes of seizures.
ETIOLOGY/PATHOPHYSIOLOGY
-Transitory disturbance in consciousness or
in motor, sensory, or autonomic function due
to sudden, excessive, and disorderly
discharges in the neurons of the brain; results
in sudden, violent, involuntary contraction of
a group of muscles
Types:
a. Grand mal- A grand mal seizure causes a
loss of consciousness and violent muscle
contractions.
Grand mal seizures have two stages:
Tonic phase. Loss of consciousness occurs,
and the muscles suddenly contract and cause
the person to fall down. This phase tends to
last about 10 to 20 seconds.
Clonic phase. The muscles go into rhythmic
contractions, alternately flexing and relaxing.
Convulsions usually last one to two minutes
or less.
b. Petit mal- cause a short lapse in
awareness. This can involve staring into
space and rapid blinking. They start and
end quickly, lasting only a few seconds.
There are two subtypes of petit mal seizures:
typical and atypical.
Typical seizures are sudden and last under
10 seconds. Atypical seizures have a slower
onset and can last up to 20 seconds or longer.
c. Psychomotor- A psychomotor seizure is a
form of epilepsy that is typically limited to
 the temporal lobe of the brain and results  Avoid alcohol
in impairment of responsiveness and  Avoid driving, operating machinery, and
awareness to ones surroundings. Patients swimming until seizures are controlled
may act out in a variety of ways while  Good oral hygiene
experiencing the seizure but have not  Medic Alert tag
recall of it.
d. Jacksonian-focal- -A Jacksonian seizure V Degenerative Diseases
is a type of focal partial seizure, also
known as a simple partial seizure. This 1. M U L T I P L E S C L E R O S I S
means the seizure is caused by unusual -Multiple sclerosis is a chronic, progressive
electrical activity that affects only a small neurological disease.
area of the brain. The person maintains -The disease initially begins between the ages
awareness during the seizure.Jacksonian of 15 and 50 years.
seizures are also known as a Jacksonian -Women are affected more than men.
march. This is because the tingling or
twitching begins in a small area and then ETIOLOGY/PATHOPHYSIOLOGY
"marches" or spreads to a larger area of -Degenerative neurological disorder with
the body. demyelination of the brain stem, spinal cord,
e. Myoclonic-Myoclonic seizures are a type optic nerves, and cerebrum
of seizure that causes sharp,
uncontrollable muscle movements.
They’re usually minor and brief, but can
happen with very severe seizure disorders.
They’re most common with childhood
seizure conditions, but can also happen in
adults.
f. Akinetic- An atonic seizure (also called
drop seizure, akinetic seizure, astatic
seizure, or drop attack) is a type of seizure
that consists of partial or complete loss of
muscle tone that is caused by temporary
alterations in brain function. These
seizures are brief – usually less than
fifteen seconds.
g. Status epilepticus- Recurrent generalized
seizures will result in status epilepticus.
Sudden withdrawal from the prescribed
anticonvulsant therapies is the #1 cause
of its occurrence.Status epilepticus is a
“9-1-1” event. Emergency intervention is
needed to prevent brain damage or death

CLINICAL MANIFESTATIONS
Depends on type of seizure
 Aura
 Postictal period- Seizures have predictable
In multiple sclerosis, the myelin sheath becomes
stages. The seizure might begin with an
damaged. This loss of myelin integrity results in
aura (the predictor of the seizure),
impaired transmission of nerve impulses.
followed by the ictal phase (seizure), and
ending with the postictal period. CLINICAL MANIFESTATIONS
 Visual problems
MANAGEMENT  Urinary incontinence
 During seizure: Protect from aspiration  Fatigue
and injury  Weakness
 Anticonvulsant medications  Incoordination
 Surgery  Sexual problems
Removal of brain tissue where seizure occurs  Swallowing difficulties
 Adequate rest
 Good nutrition
 Elimination may feel urgency and hesitancy
in voiding
 Should be on a high fiber diet to help
MANAGEMENT prevent chronic constipation
-No specific treatment  Encourage fluids and take a stool
Pharmacological management softener, suppositories, prune juice, or
 Adrenocorticotropic hormone (ACTH) milk of magnesia
 Steroids
 Valium Nursing Diagnosis:
 Betaseron (interferon beta-1b)  Impaired physical mobility, related to
 Avonex (interferon beta-1a)
rigidity, bradykineia, and akinesia
 Pro-banthine; urecholine
 Risk for aspiration related to disease
 Bactrim, Septra, and Macrodantin
process
 Nutrition
Patient Teaching:
 Skin care  Important to take medication as
 Activity prescribed
 Environmental controls  Good skin care
 Patient teaching  Proper ambulation and positioning
 Proper feeding and eating technique to
2. P A R K I N S O N’ S D I S E A S E reduce risk of aspiration
-Parkinson’s disease is a chronic neurological Prognosis
disorder. It occurs most frequently in middle-  Chronic degenerative disorder with no
aged and older adults. acute exacerbations
-There is no known cure.  If pt compliant with treatment, signs and
symptoms can be managed for a long
ETIOLOGY/PATHOPHYSIOLOGY period of time.
-Deficiency of dopamine
3. A L Z H E I M E R S’ DISEASE
CLINICAL MANIFESTATIONS
 Muscular tremors; bradykinesia (slow ETIOLOGY/PATHOPHYSIOLOGY
movement) -Is a chronic, progressive, degenerative
 Rigidity; propulsive gait (a stooped, stiff disorder
posture with the head and neck bent -Impaired intellectual functioning
forward) -Common cause of dementia in the older
 Emotional instability person and affects men and women equally.
 Heat intolerance -Chronic, progressive degeneration of the cells
 Decreased blinking of the brain
 “Pill-rolling” motions of fingers -Brain changes include plaques in the cortex,
neurofibrillary tangles, and the loss of
MANAGEMENT connections between cells and cell death.
Pharmacological management -Decrease in brain size
 Levodopa 10% age 65 or older and 50% age 85 and
 Sinemet older have AD
 Artane -Genetic link
 Cogentin -Increased plasma levels of homocysteine are
 Symmetrol associated with a significantly increased risk
Surgery – ablation of affected area vs deep of AD or dementia
brain stimulator -Blood homocysteine levels can be lowered by
Activity – posture is important, best to not eating foods rich in folic acid, such as fruits
use a pillow and green leafy vegetables.
 Should walk with hands behind back to
maintain erect spine and decrease CLINICAL MANIFESTATIONS
incidence of falling Stage 1
Nutrition – malnutrition and constipation can  Mild memory lapses; decreased attention
be severe span
 Need foods that are appetizing and easily  Difficulty in using the correct word
chewed and swallowed  Disinterest in surroundings and possibly
 Encourage 5-6 small meals a day depression
 No impairment (normal function)
The person does not experience any
memory problems. An interview with a
medical professional does not show any
evidence of symptoms of dementia.
Stage 2
 Obvious memory lapses, especially short-
term memory
 Disoriented to time
 Loss of personal objects
 Loss of impulse control , behavioral
manifestations of AD result from changes
in brain (agitation)
 Some pts develop psychotic
manifestations
 Decrease in sleep
 Very mild cognitive decline (may be
normal age-related changes or earliest
signs of Alzheimer's disease)
The person may feel as if he or she is
having memory lapses — forgetting
familiar words or the location of everyday
objects. But no symptoms of dementia can
be detected during a medical examination
or by friends, family or co-workers.
Stage 3
 Total disorientation to person, place, and
time
 Apraxia ( impairment in the ability to
perform purposeful acts or to use objects
properly ); visual agnosia (inability to
recognize objects by sight); dysgraphia
(difficulty communicating via writing);
wandering
 Awake most of the night
 Mild cognitive decline (early-stage
Alzheimer's can be diagnosed in some, but
not all, individuals with these symptoms)
Friends, family or co-workers begin to
notice difficulties. During a detailed
medical interview, doctors may be able to
detect problems in memory or
concentration. Common stage 3
difficulties include: Noticeable problems
coming up with the right word or name
 Trouble remembering names when
introduced to new people
 Having noticeably greater difficulty
performing tasks in social or work settings
Forgetting material that one has just read
 Losing or misplacing a valuable object
 Increasing trouble with planning or
organizing
Stage 4
 Moderate cognitive decline
(Mild or early-stage Alzheimer's disease)
At this point, a careful medical interview
should be able to detect clear-cut
symptoms in several areas: Forgetfulness
of recent events
 Impaired ability to perform challenging
mental arithmetic — for example,
counting backward from 100 by 7s
 Greater difficulty performing complex
tasks, such as planning dinner for guests,
paying bills or managing finances
 Forgetfulness about one's own personal
history
 Becoming moody or withdrawn, especially
in socially or mentally challenging
situations
Stage 5
 Moderately severe cognitive decline
(Moderate or mid-stage Alzheimer's
disease)
Gaps in memory and thinking are
noticeable, and individuals begin to need
help with day-to-day activities. At this
stage, those with Alzheimer's may: Be
unable to recall their own address or
telephone number or the high school or
college from which they graduated
 Become confused about where they are or
what day it is
 Have trouble with less challenging mental
arithmetic; such as counting backward
from 40 by subtracting 4s or from 20 by
2s
 Need help choosing proper clothing for the
season or the occasion
 Still remember significant details about
themselves and their family
 Still require no assistance with eating or
using the toilet
Stage 6
 Severe cognitive decline
(Moderately severe or mid-stage
Alzheimer's disease)
Memory continues to worsen, personality
changes may take place and individuals
need extensive help with daily activities.
At this stage, individuals may:
 Lose awareness of recent experiences as
well as of their surroundings
 Remember their own name but have
difficulty with their personal history
 Distinguish familiar and unfamiliar faces
but have trouble remembering the name
of a spouse or caregiver
 Need help dressing properly and may,
without supervision, make mistakes such
as putting pajamas over daytime clothes
or shoes on the wrong feet
 Experience major changes in sleep
patterns — sleeping during the day and
becoming restless at night
 Need help handling details of toileting (for
example, flushing the toilet, wiping or
disposing of tissue properly)
 Have increasingly frequent trouble
controlling their bladder or bowels
 Experience major personality and
behavioral changes, including
suspiciousness and delusions (such as
believing that their caregiver is an
impostor)or compulsive, repetitive
behavior like hand-wringing or tissue
shredding
 Tend to wander or become lost
Stage 7 (Terminal stage)
 Severe mental and physical deterioration
 Hospice appropriate
 Very severe cognitive decline
(Severe or late-stage Alzheimer's disease)
In the final stage of this disease,
individuals lose the ability to respond to
their environment, to carry on a
conversation and, eventually, to control
movement. They may still say words or
phrases.
 At this stage, individuals need help with
much of their daily personal care,
including eating or using the toilet. They
may also lose the ability to smile, to sit
without support and to hold their heads
up. Reflexes become abnormal. Muscles
grow rigid. Swallowing impaired.
Assessment
 Memory loss initial sign combined w/
inability to carry out normal activities.
Diagnostic Tests
 No specific test for AD
 CT, EEG, MRI, and PET may be used to
rule out other pathologic conditions
 At times only confirmation is at autopsy
MANAGEMENT
Pharmacological management
 Agitation: Lorazepam; Haldol
 Dementia: Cognex ; Aricept (short-term
benefit for mild cognitive impairment
(MCI) , slows progression by up to 3 yrs)
 Namenda used for moderate to sever (only
slows symptoms not MCI)
Nutrition
 Finger foods; frequent feedings; encourage
fluids (2000 ml/day)
 Increase foods high in folic acid and
vitamin B12 to reduce homocysteine
levels
Safety
 Remove burner controls at night
 Double-lock all doors and windows
 Constant supervision
Prognosis
 NO effective treatment to stop progression
 Lifespan w/ disease 5-20 yrs; cost is
approximately $19,000 annually
 Most pt die from complications related to
the disease such as pneumonia,
malnutrition, or dehydration
4. M Y E S T H E N I A GRAVIS
ETIOLOGY/PATHOPHYSIOLOGY
-Autoimmune disease of the neuromuscular
junction
-Neuromuscular disorder; nerve impulses fail
to pass at the myoneural junction; causes
muscular weakness
-Can occur at any age but common between
ages 10 to 65. Peak in women age 20 – 30.
-Women more affected than men in young but
equals out at older age
-Infants of mothers with MG may be
symptomatic at birth
-25% patient have Thymoma (cancer of the
thymus)
-80% have cellular structure of the thymus
gland
CLINICAL MANIFESTATIONS
 Ptosis (eyelid drooping); diplopia (double
vision); 15% of cases confined to the eye
muscles
 Skeletal weakness; ataxia (lack of
voluntary coordination of muscle
movements)
 Dysarthria (difficulty w/ speech);
dysphagia (difficulty swallowing)
 Bowel and bladder incontinence
 Exacerbations may be initiated by upper
respiratory infections, emotional tension,
and menstuation
MANAGEMENT
Pharmacological management
 Anticholinesterase drugs (promote nerve
impulse transmission and quite effective
of alleviating symptoms)
 Prostigmin
 Mestinon
 Corticosteroids (adjunct therapy d/t
immune component)
 Imuran
 Cyclosporine
Caution with certain drugs:
 Anesthetics, antidysrhythimics,
antibiotics, quinine, antipsychotics,
barbituates, sedatives, hypnotics, opioids,
tranquilizers, and thyroid prep
Plasmapheresis removes antibodies produced
by the autoimmune response…short term fix
Thymectomy if thymoma is present
Intravenous immune globulin to reduce
production of acetylcholine antibodies used
only in severe relapse of MG
May require mechanical ventilation
Prognosis: chronic disease
5. A M Y O T R O P H I C L A T E R A L
SCLEROSIS
ETIOLOGY/PATHOPHYSIOLOGY
 Motor neurons in the brain stem and
spinal cord gradually degenerate
 Electrical and chemical messages
originating in the brain do not reach the
muscles to activate them
 Lou Gehrig’s disease famous baseball
player stricken in early 1940’s
 Onset between ages 40-70 (2:1
men:women)
 10% of cases is genetic defect
 Effects 5 out of every 100,000 people
worldwide
CLINICAL MANIFESTATIONS
 Weakness of the upper extremities
 Head drop due to weak neck muscles
 Muscle cramps
 Muscle contractions called fasciculations
 Dysarthria (speech difficulty)
 Dysphagia (difficulty swallowing)
 Choking easily
 Drooling
 Gagging
 Muscle wasting
 paralysis
 Compromised respiratory function
 Difficulty breathing
 Weight loss
 DOES NOT AFFECT THE SENSES (sight,
smell, taste, hearing, touch)
MANAGEMENT
Diagnostics
 Medical Hx. w/ strength and endurance
eval (muscle tremors , spasms, twitching,
or loss of muscle tissue (atrophy),
twitching of tongue is common)
 Abnormal reflexes, stiffness and
clumsiness
 Emotional incontinence
 Tests may be done to rule out other
causes (i.e. blood, CT or MRI,
Electromyography, spinal tap, swallow
studies, nerve conduction)
NO CURE
Pharmacological management
 Rilutec (Riluzole): slows the progression of
ALS and prolongs life. Helps protect
motoneurons damaged by the disease
 Baclofen or diazepam: used to control
spasticity that interferes with daily
activities
 Trihexyphenidyl or amitriptyline: used for
people w/ problems of swallowing their
own saliva
 G-Tube placement due to choking
Complications:
 Aspiration
 Loss of abilty to care for self
 Lung failure (ARDS)
 Pneumonia
 Pressure sores
 Weight loss
Multidisciplinary ALS teams; emotional
support;
 Part of the Muscular Dystrophy
Foundation
 ALS Associan
Prognosis
 Death. Lifespan post diagnosis typically
ranges 2-6 years. Approximately 25%
patients live for more than 5 years (up to
7 years)
6. H U N T I N G T O N’S DISEASE
ETIOLOGY/PATHOPHYSIOLOGY
 Like Parkinson’s disease involves the
basal ganglia and the extrapyramidal
motor system
 Overactivity of the dopamine pathways
 Genetically transmitted autosomal
dominant disorder that affects both men
and women of all races. Defect on
chromosome 4
 Offspring of person w/ disease has 50%
chance of developing disease
Two forms:
 Adult-onset (most common) symptoms in
mid 30s-40s
 Early-onset symptoms occur during
childhood or adolescence
CLINICAL MANIFESTATIONS
Behavioral
 Hallucinations
 Irritability
 Moodiness  Loss of ability to interact
 Restlessness or fidgeting  Injury to self or others
 Paranoia  Increased risk for infection
 psychosis  Depression
Abnormal and excessive involuntary  death
movements (chorea) Prognosis
 Facial movements, including grimaces  Causes disability that gets worse overtime
 Head turning to shift eye position  Average lifespan from onset of symptoms
 Wild jerking of extremities face and other is 15-20 years.
body parts  Cause of death is often infection or suicide
 Slow, uncontrolled movement
 Abnormal reflexes VI Vascular Problems
 Hesitant speech or poor enunciation
Ataxia to immobility 1. S T R O K E (CEREOBROVASCULAR
 Unsteady gait ACCIDENT)
 “Prancing” and wide walk
ETIOLOGY/PATHOPHYSIOLOGY
 Deterioration in mental functions Brain attack
 Dementia -Abnormal condition of the blood vessels of
 Disorientation or confusion the brain: 2 types
 Loss of judgment  85% thrombosis & embolism = ischemic
 Loss of memory stroke
 Personality changes  15% hemorrhage = hemorrhagic stroke
 Speech changes (weak and bursts open, aneurysm,
Symptoms in children arteriovenous malformation)
 Rigidity -Results in ischemia of the brain tissue
 Slow movements -Most common disease of nervous system
 Tremors (estimated 700,000 suffer strokes each yr. and
the cause of 158,000 deaths annually)
MANAGEMENT -All ages affected
Diagnostics -Greatest number between ages 75-85
 CT of head may show loss of brain tissue -Residual effects vary from mild deficits to
 MRI or PET of brain severe disabilities
 Genetic tests -Hemiparesis (weakness or paralysis of one
Treatment side of the body), inability to walk, complete or
 NO CURE; palliative care (treat the
symptoms)
Pharmacological management
 Antipsychotics: Dopamine blockers
may reduce abnormal behaviors
(Azilect, Clozaril, Reglan, Haloperidol)
 Antidepressants (Depression and
suicide common (assess for S&S))
 Antichoreas (Amantadine &
tetrabenzine: used to control extra partial dependence with ADL’s and aphasia
movements)
 Co-enzyme Q10: help slow down the Risk Factors
course of the disease (but not conclusive)  Atrial Fibrillation
 Diabetes
 Safe environment  Family Hx of stroke
Emotional support  High Cholesterol
 Huntington’s Disease Society of America  Increasing age >65
www.hdsa.org  Race (black people are more likely to die of
 High-calorie diet a stroke)
 As much as 4000-5000 kcal/day to  Unhealthy lifestyle
maintain body weight due to involuntary  Overweight or obese
body movements  Drinking heavily
Complications  To much fat or salt in diet
 Loss of ability to care for self  Smoking
 Illegal drugs (cocaine)
 Birth control pills
CLINICAL MANIFESTATIONS
 Headache
 Sensory deficit
 Hemiparesis; hemiplegia
 Dysphasia or aphasia
MANAGEMENT
Diagnostics
 CT – primary test for diagnosis. Used to
differentiate between ischemic vs
hemmorhagic
 CT angiography (CTA) provides
visualization of vasculature
 MRI or PET used to determine extent of
damage
 Doppler, CTA, or MRA may be done to
assess cartoids
 post TIA may result in cerebral angiogram
Hemorrhagic
 Surgery to repair damage
 May cause vasospasm (narrowing of blood
vessel, decreasing perfusion)
 Occurring in 30-60% of cases post-
operatively (between days 4-12).
 Mortality rate as high as 50%
 If not tx rapidly can cause cerebral
ischemia or cerebral anoxia which leads to
severe mental and physical deficits or
death.
Thrombosis or embolism
 Thrombolytics (plasmnogen activator t-PA,
alteplase) causes lyses of clot
 Must be administered within 3 hours of
the onset of symptoms. The longer the
wait the less effective. TIME IS A FACTOR
 Heparin, Lovenox, and Coumadin (platelet
inhibitors and anticoagulants
PATIENTS MUST BE SCREENED CAREFULLY
BEFORE TX BEGINS
-Recent hx. Of GI bleed, CT or MRI to rule out
hemorrahagic stroke
 Decadron to reduce ICP
 Neurological checks at regular intervals
Q8 hrs
Nutritional interventions: tube feeding may
be necessary or TPN
 Physical, occupational, and/or speech
therapy
 Bobath approach: designed to normalize
muscle tone by providing as many
sensations of normal muscle tone,
posture, and movement as possible
Support Groups
 American Stroke Association
www.strokeassociation.org
Complications
 Aspiration
 Dementia
 Falls
 Loss of mobility
 Loss of movement or feeling in one or
more parts of the body
 Muscle spasticity
 Poor nutrition
 Pressure ulcers
 Problems speaking and understanding
(effects on Broca or Wernike’s area of
brain)
 Problems thinking and/or focusing
VII. Cranial and Peripheral Nerve Disorders
1. T R I G E M I N A L N E U R A L G I A
-Trigeminal neuralgia is a disorder of the
peripheral nervous system. It is most common
in women in middle and late adulthood.
-Patients having trigeminal neuralgia
experience severe pain when trigger points
along the trigeminal nerve are activated
ETIOLOGY/PATHOPHYSIOLOGY
-Degeneration of or pressure on the trigeminal
nerve; tic douloureux
-Occurs at any age
-Caused by
-Multiple Sclerosis
-Pressure on the trigeminal nerve from a
swollen blood vessel or tumor
CLINICAL MANIFESTATIONS
 Excruciating, burning facial pain, electric-
like spasms that last a few seconds or
minutes
 Pain usually one side of face
 May be triggered by touch or sounds
 Can be triggered by
 Brushing teeth, chewing, drinking, eating,
lightly touching the face, shaving
MANAGEMENT
Diagnostics:
 Blood tests
 MRI of the head
 Trigeminal reflex testing: electrical
stimulation of the divisions of the
trigeminal nerve and measurement of the
response with standard electromyography
apparatus. This testing is not readily
available to most physicians, and its
 indications and clinical utility are still
unclear
Pharmacological Management
 Anti-seizure drugs (carbamazepine
(Tegratol), gabapentin, phenytoin,
valproate, and pregabalin)
 Muscle relaxants (baclofen, clonazepam)
 Tricyclic antidepressants (amitriptyline,
nortriptyline)
 Surgical resection of the trigeminal nerve
 Within 24 hrs of resection of 5th nerve pt
develops herpes simplex of the lips (cold
sores) heals in about a week (5-14 days)
 Avoid stimulation of face on affected side
Comfort measures
 Keep room free of drafts
 Avoid walking briskly to bedside of patient
 Place bed out of traffic area to prevent
jarring of bed
 avoid touching the patients face
 Don’t urge pts to wash or shave the
affected area or to comb the hair
 Avoid hot or cold liquids, may trigger pain
 Puree food and ensure that it is
lukewarm. Suggest food be taken through
a straw
Prognosis
 Depends on cause. Pain varies and
permanent relief of pain is obtained only
by surgery
 Pain can be disruptive to lifestyle. Can be
total physical and psychological
dysfunction or even suicide.
2. B E L L E’ S PALSY
ETIOLOGY/PATHOPHYSIOLOGY
-Inflammatory process involving the facial
nerve VII from the nucleus in the brain to the
periphery
-Damage to this nerve causes weakness or
paralysis of these muscles
-Evidence the reactivated herpes simplex
(HSV) may be involved. Causing inflammation,
edema, ischemia, and demyelination of the
facial nerve.
-Can be unilateral (one side) or bilateral (both
sides)
Causes, Incidence, and risk factors
-Affects 30,000-40,000 people in the USA
-Cause is not clear. But may be caused by
other disease processes such as:
-Herpes simplex
-HIV infection
-Middle ear infection
-Sarcoidosis - inflammation occurs in the
lymph nodes, lungs, liver, eyes, skin, or other
tissues
CLINICAL MANIFESTATIONS
 Facial numbness or stiffness
 Hard to close one eye
 Problems w/ smiling, grimacing, or
making facial expressions
 Drawing sensation of the face
 Twitching
 Unilateral weakness of facial muscles
 Drooping of face
 Reduction of saliva
 Drooling
 Pain behind the ear
 Ringing in ear or other hearing loss
MANAGEMENT
Diagnostics
 CT scan or MRI of the head
 Electromyography (EMG) or Nerve
conduction test to check nerves that
supply the muscles of the face
Treatment
 Often no tx needed. Begins to resolve
immediately but may take up to months
to get full muscle strength
 Eye drops to lubricate if needed or an eye
patch when sleeping
Pharmacological management
 Corticosteroids may reduce swelling
around the facial nerve
 Antiviral medications in an attempt to
fight off virus that may be causing bell’s
palsy
 Electrical stimulation
 Moist heat
 Massage of the affected area
 Facial exercises
Prognosis
 Usually resolve on own
 Long term changes in taste
 Spasms of muscles or eyelids
 Weakness that remains in facial muscles
Complications
 Excess drying of the eye surface, leading
to eye ulcer or infections
3. G U I L L A I N E - B A R R E
SYNDROME
ETIOLOGY/PATHOPHYSIOLOGY
-Inflammation and demyelination of the
peripheral nervous system
-Possibly viral or autoimmune reaction
-Most common in people of both sexes
between the ages of 30-50
-Often follows a minor infection, such as lung
or GI infection
-Nerve damage causes tingling, muscle 4. M E N I N G I T I S
weakness, and paralysis. Guillian-Barre
syndrome most often affects the nerves’ ETIOLOGY/PATHOPHYSIOLOGY
covering (myelin sheath) and causes nerve -Acute infection of the meninges
signals to move more slowly or not at all. -Bacterial or aseptic
-Increased incidence in winter and fall months
CLINICAL MANIFESTATIONS
 Symptoms are progressive CLINICAL MANIFESTATIONS
 Paralysis usually starts in the lower  Headache; stiff neck
extremities and moves upward; may stop  Irritability; restlessness
at any point  Malaise
 Respiratory failure if intercostal muscles  Nausea and vomiting
are affected  Delirium
 May have difficulty swallowing, breathing,  Elevated temperature, pulse, and
and speakingSymptoms are progressive respirations
 Paralysis usually starts in the lower  Kernig’s and Brudzinski’s signs
extremities and moves upward; may stop
at any point MANAGEMENT
 Respiratory failure if intercostal muscles Pharmacological management
are affected  Antibiotics
 May have difficulty swallowing, breathing,  Massive doses
and speaking  Multiple types
 IV or intrathecal
MANAGEMENT  Corticosteroids
Diagnostics  Anticonvulsants
 Lumbar puncture  Antipyretics
 ECG
 Electroyography (EMG)  Dark, quiet room
 Nerve conduction velocity test
 Pulmonary function tests 5. E N C E P H A L I T I S

 Adrenocortical steroids ETIOLOGY/PATHOPHYSIOLOGY

 Apheresis -Acute inflammation of the brain caused by a
 Mechanical ventilation virus
 Gastrostomy tube
 Meticulous skin care CLINICAL MANIFESTATIONS
 Range-of-motion exercises  Headache
Complications:  Fever
 Respiratory failure  Seizures
 DVT  Change in LOC
 Increased risk of infections
 Low or unstable bp MANAGEMENT
 Paralysis that is permanent  Primarily supportive
 Pneumonia
 Skin damage 6. W E S T NILE VIRUS
 aspiration
Prognosis: ETIOLOGY/PATHOPHYSIOLOGY
 Most recover completely but can take -Principal route of infection through the bite
weeks, months, or years. 30% of cases of an infected mosquito
will have some residual effects
CLINICAL MANIFESTATIONS
 Fever
 Headache
 Back pain
 Myalgia

MANAGEMENT
 Prevention

7. B R A I N ABCESS MANAGEMENT
 Surgical removal of tumor
ETIOLOGY/PATHOPHYSIOLOGY a. Craniotomy
-Accumulation of pus within the brain tissue b. Intracranial endoscopy
 Radiation
CLINICAL MANIFESTATIONS  Chemotherapy
 Headache  Combination of above
 Fever
 Drowsiness, changes in LOC VIII. Trauma
 Seizures
1. C R A N I O C E R E B R A L T R A U M A
MANAGEMENT
 Antimicrobial therapy ETIOLOGY/PATHOPHYSIOLOGY
 Supportive care -Motor vehicle and motorcycle accidents, falls,
industrial accidents, assaults, and sports
trauma
8. A C Q U I R E D -Direct trauma: Head is directly injured
IMMUNODEFICIENCY -Indirect trauma: Tension strains and
SYNDROME shearing forces
-Open head injuries
ETIOLOGY/PATHOPHYSIOLOGY -Closed head injuries
-Symptoms may develop from the infection -Hematomas
with HIV or as a result of an associated
infection CLINICAL MANIFESTATIONS
 Headache
CLINICAL MANIFESTATIONS  Nausea
 AIDS dementia complex (ADC)  Vomiting
 Memory loss  Abnormal sensations
 Global cognitive dysfunction  Loss of consciousness
 Bleeding from ears or nose
MANAGEMENT  Abnormal pupil size and/or reaction
 Antiviral, antifungal, antibacterial agents  Battle’s sign
 Anticonvulsants
 Safety MANAGEMENT
 Maintain airway
 Oxygen
9. B R A I N TUMORS  Mannitol and dexamethasone
 Analgesics
ETIOLOGY/PATHOPHYSIOLOGY  Anticonvulsants
-Benign or malignant
-Primary or metastatic
-May affect any area of the brain 2. S P I N A L CORD TRAUMA

CLINICAL MANIFESTATIONS ETIOLOGY/PATHOPHYSIOLOGY

 Headache -Automobile, motorcycle, diving, surfing, other
 Hearing loss athletic accidents, and gunshot wounds
 Motor weakness
 Ataxia
 Decreased alertness and consciousness
 Abnormal pupil response and/or unequal
size
 Seizures
 Speech abnormalities
 -Fracture
of vertebra
-Complete
cord injury
-
Incomplete
cord injury

CLINICAL

MANIFESTATIONS
 Loss of muscle function depends on level
of injury
 Spinal shock
 Autonomic dysreflexia
 Sexual dysfunction

MANAGEMENT
 Realignment of bony column for fractures
or dislocations: Immobilization; skeletal
traction
 Surgery for spinal decompression
 Methylprednisolone
 Mobility: Slowly increase sitting up
 Urinary function: Foley catheter; bladder
training
 Intermittent catheterization
 Bowel program

Nursing diagnoses
1. Autonomic dysreflexia
2. Communication, impaired
3. Coping, compromised family
4. Disuse syndrome, risk for
5. Grieving
6. Infection, risk for
7. Knowledge, deficient
8. Memory, impaired
9. Mobility, impaired physical
10. Nutrition, imbalanced: less than body
requirements
11. Pain, acute, chronic
12. Self-care deficit
13. Swallowing, impaired
14. Thought process, disturbed
15. Tissue perfusion (cerebral), ineffective