Neurologic nursing

THE CONCEPT
OF PERCEPTION
AND COORDINATION
(NEUROLOGIC NURSING)

Perception- is defined as the perception and awareness of
sensory stimuli.
- it is a mental act involving memory and the
intellectual interpretation of new sensory data in terms of
previously encountered information.

Coordination- maybe defined as “the working together of
muscles to produce movement or of systems to
accomplish a given process.
- it implies perception of the movement or reaction that
is necessary and the subsequent completion of that
action via the appropriate bodily activity.

Management of coordination and perception within the
human body is controlled by the Central Nervous
System, the Peripheral, the Autonomic Nervous System
and the Neuro-endocrine System.

BASIC STRUCTURES

 NEURONS

 NEUROGLIA

 NEUROTRANSMITTERS

 NERVE

NEURON
 Cell body - contains
nucleus and cytoplasm
where metabolic activity
takes place. Collection
clusters of nerve cells
bodies are called ganglia
or nuclei. Ganglia with
same functions are called
centers.
 Axons- generate and
conduct impulses away
from the cell body and
release a neurotransmitter
 Dendrites- carry electrical
current towards the cell
body

NEURONS
 Types:

Based on Function (direction of impulse
transmission
1. Sensory neurons (afferent)
2. Motor neurons (efferent)
Based on Structure
1. Unipolar: most sensory neurons
2. Bipolar: sensory neurons- ear and eye
3. Multipolar: motor and association neurons

Classification
 1. Based on Function
(direction of impulse
transmission
 A. Sensory neurons
(afferent)
 B. Motor neurons
(efferent)
 2. Based on Structure
 A. Unipolar: most
sensory neurons
 B. Bipolar: sensory
neurons- ear and eye
 C. Multipolar: motor
and association
neurons

NEUROGLIA
– makes up about 85 % of the CNS cells.
They provide, nourishment, support and
protection to the neurons

 Types:

1. Astrocytes– star-shaped supportive cells
2. Oligodendrocytes
3. Microglia
4. Ependymal cells

NEUROTRANSMITTERS
– chemicals that carry messages between different nerve
cells or between nerve cells and muscles. Released by an
axon across the synaptic cleft to bind to specific receptors
in the postsynaptic bulbs of another neuron or cell.
- It acts to potentiate, terminate or modulate a specific
action.

 Types:
1. Excitatory – acetylcholine (PNS), Norepinephrine (SNS),
Gamma-aminobutyric acid, enkephalins or endorphins
2. Inhibitory – acetylcholine (Heart via vagal nerve),
Dopamine, Serotonin
 Concentration:
1. PSNS – acetylcholine
2. SNS – norepinephrine

NERVES
- bundles of neurons processes wrapped in connective tissue
coverings found outside the CNS.

MAJOR PARTS
 CNS
1. Brain
2. Spinal Cord

 PNS
1. Cranial Nerves
2. Spinal Nerves

 ANS
1. Parasympathetic
2. Sympathetic

PARTS OF BRAIN
 CEREBRUM

 CEREBELLUM

 DIENCEPHALON

 BRAIN STEM

PROTECTION OF BRAIN
 SKULL

 MENINGES

 CSF

 BLOOD BRAIN BARRIER

BLOOD-BRAIN BARRIER
 CNS is inaccessible to many
substances that circulate in the blood
plasma (dye, meds).
 Barrier is formed by the endothelial
cells of brain capillaries, which form
continuous tight junctions, creating a
barrier to macromolecules and many
compounds.
 Has an implication in the tx and
selection of meds for CNS disorders as
well as serving a protective function.

CEREBRAL CIRCULATION
 Receives 15% of cardiac output or
750ml/min.
 Brain does not store nutrients and has
high metabolic demands that require
high blood flow.
 Blood flow is against gravity as arteries
fill in below and veins drain from above.
 Can’t tolerate decreased blood flow for
it will result to irreversible tissue
damage when blood flow is occluded
even for a short period of time.

CIRCLE OF WILLIS
 Located at the base of the brain
surrounding the pituitary gland.
 It is a formed ring of arteries between
vertebral and internal carotid artery
chains (internal carotid, anterior and
middle cerebral artery, anterior and
posterior communicating artery)
 The most frequent site of aneurysm –
weakening or bulge in the arterial wall.

- reflex center and conduction
Spinal cord pathway
-located within the vertebral
canal
-extends from the foramen
magnum to L1 to L2
-has central area of gray mater
surrounded by columns of
white mater, which carry
motor and sensory tracts
from the brain.
- Serves as a connection bet.
brain and the periphery.
- About 45cm (18in) long and
about the thickness of a
finger.
- Surrounded by meninges,
dura, arachnoid and pia
layers.

SPINAL CORD PROTECTION
 MENINGES
 VERTEBRAL COLUMN
- The bones of the vertebral column surround
and protect the spinal cord.
- It consists of 7 cervical, 12 thoracic, 5 lumbar,
1 sacrum, and 1 coccyx.
- They are all separated by disks except for the
1st (atlas) and the 2nd (axis), sacral and
coccygeal.

CRANIAL NERVES (12)
- 3 Sensory (1, 2 and 8)

- 5 motor (3, 4, 6, 11 and 12)

- 4 mixed (5, 7, 9 and 10)

I. Olfactory sensory smell
II. Optic sensory visual acuity
III. Oculomotor motor muscle that
move the eye &
lid pupillary
constriction.
IV. Trochlear motor muscle that
move the eye
V. Trigeminal mixed facial sensation,
mastication,
corneal reflex

VI. Abducens motor muscle that
move the eye
VII. Facial motor facial
expression and
movement,
salvation and
tearing, ear
sensation
VIII. Acoustic sensory hearing and
equilibrium
IX. Glossopharyngeal
mixed taste, sensation in
pharynx and
tongue,
pharyngeal
muscles

X. Vagus mixed muscles of
pharynx and
larynx, soft
palate, external
ear sense,
pharynx, larynx,
thoracic,
abdominal
viscera,
parasympathetic
innervation of
thoracic and
abdominal
organs.

XI. Spinal accessory
motor
sternocleidomastoid
and trapezius muscle

XII. Hypoglossal
motor tongue movement

SPINAL NERVES
-thirty one (31) pairs of
nerves formed by the union of
the dorsal and ventral roots of
the spinal cord on each side
-splits into:
a. dorsal rami – serve the
posterior body trunk
b. ventral rami – serve the limbs
through the plexuses
(cervical, brachial , lumbar,
sacral)

ANS - regulates the activity of smooth muscles,
cardiac muscles and glands
2 divisions:
1. Sympathetic
 ”fight or flight” response; prepares the body to cope with stress
e.g. increased heart rate, blood pressure
 pre ganglionic neurons are in the sympathetic chains or in
collateral ganglia
 post ganglionic axons secrete norepinephrine
2. Parasympathetic
 ”house keeping” system; in control most of the time
 maintains homeostasis
 first motor neurons are in the brain or the sacral region of
the cord
 second motor neurons are in the terminal ganglia close to
the organ served
 post ganglionic axons secrete acetylcholine

EFFECTS OF ANS
PNS SNS
Pupil of eye constricted dilated
HR decreased increased
Heart vessels constricted dilated
Vessels in:
Skeletal mus. No effect dilated
Abd’l viscera/skin No effect constricted
BP decreased increased
Bronchioles constricted dilated
Breathing decreased increased
Digestive peristalsis increased decreased
d. Tube sphincter relaxed constricted

Secretion of glands thin, watery saliva thick, viscid saliva
Digestive secretion increased no effect
Glycogen-glucogen
Conversion of liver no effect increased
Urinary bladder wall contracted relaxed
Urinary sphincter relaxed contracted
Uterine mus. Relaxed; variable contracted;
varies in mens
& pregnancy
Ext. genitalia mus. Dilated no effect
Secretion of sweat no effect increased
Pilomotor mus. no effect contracted
(goose flesh)
Adrenal medullae no effect secretion of
epinephrine and
norepinephrine

ASSESSMENT:
NEUROLOGIC
ASSESSMENT

I. NURSING HEALTH HISTORY

 history of present illness (COLD SPA)
 review of medical history
 system by system evaluation

***are important and critical in order to
come up with to an accurate diagnosis.

II. CLINICAL MANIFESTATIONS
1. Pain - a multidimensional unpleasant experience which may
occur from neurologic disorders like:
 Acute - Spinal disk disease, Trigeminal neuralgia, Painful
neuropathies
 Chronic - Cerebral palsy
2. Seizures - results from abnormal paroxysmal discharges or
neuronal firing in the cerebral cortex, which then manifest as an
alteration in consciousness, sensation, behavior, movement or
perception. It may also be a sing of brain lesion.
3. Dizziness and Vertigo
 Dizziness - abnormal sensation of balance or movement, fairly
common in elderly and most common complaint encountered by
health professionals, can be caused by virus, hot weather, roller
coaster ride, middle ear infection, etc.
 Vertigo – specific form of dizziness, usually a manifestation of
vestibular dysfunction, can be severe as to result in spatial
disorientation, loss of equilibrium, and nausea and vomiting.

4. Visual disturbances - visual effects that cause people to seek
health care, can range from decreased visual acuity
associated with aging to sudden blindness caused by
glaucoma, normal vision depends upon functioning visual
pathways through the retina and optic chiasm and the
radiations into the visual cortex in the occipital lobe, lesions of
the eye itself (cataract), lesion along the pathway (tumor),
lesion in the visual cortex (from stroke) interfere with normal
visual acuity, abnormality of eye movement (nystagmus
associated with multiple sclerosis) can compromise vision by
causing diplopia or double vision.
5. Weakness - especially muscle weakness is a common
manifestation of neurologic disorder. Frequently coexists with
other symptoms of disease and can affect variety of muscles
causing a wide range of disability. It can be sudden or
permanent as in stroke, or progressive as in amyotrophic
lateral sclerosis.

6. Abnormal Sensation - numbness, abnormal or loss
of sensation is a neurologic manifestation of both
central & peripheral nervous system disease. It can
significantly affect balance and coordination.

7. Impact on lifestyle - limitations imposed to the
patient by any deficit & the patient’s role in society
including family & community roles. Plan of care that
the nurse develops to address & support adaptation
to the neurologic deficit & continued function to the
extent possible within patient’s support system.

III. CEREBRAL FUNCTIONS
1. Mental status – Assess patient’s appearance, behavior,
dressing, grooming, personal hygiene, posture, gesture,
movements, facial expressions and motor activity. Assess
orientation to time, place and person.

2. Intellectual Function – Assess IQ, serial 7 test (100 minus 7),
capacity to interpret well – known proverbs, ability to recognize
similarities and make judgments. Check also for the memory
(remote and recent).

3. Thought content – Assess if thought are spontaneous,
natural, clear, relevant and coherent. Assess for presence of
fixed ideas, illusions, hallucinations, preoccupations with
morbid and paranoid ideation.

4. Emotional status – Assess the affect or the external
manifestation of mood: natural and even, irritable or angry,
anxious, apathetic, flat, euphoric, jumping of ideas, and
consistency between verbal and non verbal cues.

III. CEREBRAL FUNCTIONS
5. Perception – having an insight into the patient’s cortical ability
 Agnosia – inability to interpret or recognize objects seen through the
special senses.
Types of agnosia Affected cortical area
Visual (show pencil) occipital lobe
Auditory temporal (lateral/superior)
Tactile (hold coin) parietal
Body parts/relationship parietal (postero-inferior)

6. Motor Ability - asking the patient to perform a skilled act (throw a ball,
move a chair), failure means cerebral dysfunction

7. Language Ability- person with normal neurologic function can
understand and communicate in written & spoken language.
 Aphasia – a deficiency in language function
Types of aphasia Brain area involved
Auditory-receptive temporal lobe
Visual-receptive parietal-occipital lobe
Expressive speaking inferior posterior frontal areas
Expressive writing posterior frontal areas

IV. CRANIAL NERVE FUNCTION
Cranial Nerve Clinical Exam
I. Olfactory - with eyes closed, the pt. identifies
familiar odor (coffee, tobacco).
Each nostril is tested separately
II. Optic - Snellen eye chart; visual fields,
opthalmoscopic exam
III. Oculomotor - for CNs 3, 4 & 6; tests for ocular
IV. Trochlear rotations, conjugate mov’ts.,
VI. Abducens nystagmus. Test for pupillary
reflexes & inspect eyelids for ptosis
V. Trigeminal - have pt. close the eyes. Touch a
wisp of cotton to forehead, cheeks
& jaw. Sensitivity to superficial pain
is tested the sharp & dull ends of
a broken tongue blade.

V. Trigeminal - alternate bet. the sharp & dull end
- patient reports dull & sharp with
each mov’t. If reports are incorrect,
test for temp sensation.
- while the patient looks up, lightly
touch a wisp of cotton against the
temporal surface of each cornea. A
blink and tearing are normal
responses.
- have the patient clench & move
the jaw from side to side. Palpate
the masseter & temporal muscles,
noting strength & equality.
VII. Facial - observe symmetry while patient
performs facial mov’t.; smiles,
whistles, elevates eyebrows,
frowns, tightly closes eyes
(examiner opens them); flaccidity

VIII. Acoustic - whisper or watch-tick technique;
test for lateralization (weber); test
for air & bone conduction (Rinne)
IX. Glossopharyngeal
- assess patient’s ability to
discriminate bet. Sugar & salt on
posterior 3rd of the tongue
X. Vagus - depress a tongue blade on
posterior tongue or stimulate
posterior pharynx to elicit gag reflex
note any harshness in voice. Have
pt. say “ah”, observe for symmetric
rise of uvula & soft palate.
XI. Spinal Accessory
- palpate & note strength of
trapezius muscle on shrugging &
sternocleidomastoid muscle as pt.
turns head against pressure

XII. Hypoglossal - while pt. protrudes tongue, any
deviation or tremors are noted.
Strength of the tongue is tested by
having the protruded tongue move
from side to side against a tongue
depressor.

V. REFLEXES
 Involuntary contractions of muscle in response to abrupt
stretching or striking with a reflex or percussion hammer near
the site of muscle insertion. Valid findings depend on proper use
of reflex hammer, proper positioning of extremities & a relax
patient.
 2 TYPES: Superficial, Deep Tendon Reflexes

1. Superficial or Cutaneous Reflexes - graded as (+) or (-)
 Corneal reflex – cotton wisp is touched to outer sclera of each
eye. Normal response is a blink.
 Gag reflex – tongue depressor is touched to uvula. Normal
response is gag.
 Cremasteric reflex – inner thigh of male client is stroked. Normal
response is penile erection.
 Plantar or Babinski reflex – lateral sole is stroked with tongue
blade, normal response is toe flexion or negative babinski.

V. REFLEXES
 2 TYPES: Superficial, Deep Tendon Reflexes

2. Deep tendon reflex – graded as:
+4 -hyperactive
+3 -more brisk than avg. maybe normal or indicative of a dse.
+2 -average or normal response
+1 -hypoactive or diminished
0 -No response

 Biceps reflex (C5C6) -Arm is slightly flexed at the elbow with the
palm down. The examiners thumb is placed on the biceps tendon
and a blow is stuck over the thumb. The biceps muscles should
contact and flexion of the forearm at the elbow should occur.

 Brachioradialis reflex (C5C6) - The forearm should rest in the
person’s lap. The hand is supported in a semi prone position and
the tendon over the radius is struck about 1 to 2 inches above the
wrist. The result should be flexion and supination of the forearm.

V. REFLEXES
 Triceps reflex (C7C8) - The client’s arm is flexed at the
elbow with forearm held across the abdomen. The hand
of that arm is supported with the palm toward the body
and a blow is struck over the triceps tendon. The triceps
muscle should extend at the elbow.
 Patellar reflex (L2L3L4)

 Ankle reflex (S1S2) - With the person’s leg somewhat
flexed at the knees and the foot supported with the
examiner’s hand the Achilles tendon is struck above the
heel. Normal response is plantar flexion.

 Clonus – very hyperactive reflexes which may indicate
CNS disease abd require further evaluation

VI. MOTOR FUNCTIONS
1. Muscle Strength
2. Balance and coordination

1. Muscle Strength- Patient is asked to walk across the room while
examiner observes for posture & gait. Muscles are palpated for
size & symmetry. Any evidence of atrophy or involuntary mov’t.
(tremors, tic), muscle tone (tension present in a muscle at rest) is
evaluated by palpating various muscle groups @ rest & during
passive mov’t. Abnormalities include spasticity (inc. Muscle tone),
rigidity (resistance to passive stretch) & flaccidity. Strength is
assessed to know the ability to flex or extend against resistance.
Graded as:
 0- no contractility
 1- some contractility but no joint motion
 2- complete ROM without gravity
 3- complete ROM with gravity
 4- complete ROM with some resistance
 5- normal function against full resistance

VI. MOTOR FUNCTIONS
2. Balance & Coordination - Cerebellar influence on the motor system
is reflected in balance, control & coordination. Hand & extremity
coordination is tested by having the pt. perform alternating mov’ts &
point to point testing (thigh patting with alternate hands, pronate &
supinate, thumb with each fingers). Speed, symmetry & degree of
difficulty are noted. Patient’s finger then examiner’s finger touching)
 Check for Ataxia - incoordination of voluntary muscle action,
particularly of muscle group used in activity (rhythmic, involuntary
mov’ts)
 Check for maintenance of standing position: (Romberg’s test)-
screening test for balance.
 Patient stands with feet together with arms @ the side, with eyes open
first then both eyes closed for 20-30 seconds. Loss of balance means
(+) Romberg test.
 Ask the person to stand erect with both heels together and both eyes
open. Note any swaying or loss of balance.
 Ask the person to maintain that position but to close both eyes. Note
any abnormal swaying or tendency to fall.

VII. SENSORY FUNCTIONS

GENERAL TYPES OF SENSATION:
1. Superficial - concerned with touch, pain, temperature

2. Deep sensation - concerned with muscle and joint
sense

3. Combined – superficial and deep sensory mechanism
combined in steriognosis (recognition and naming of
familiar objects placed on hand) and in the ability to
localize cutaneous stimuli

1. Tactile Sensation – lightly touch a cotton wisp to a body part.
Compare proximal to distal sensation.

2. Vibration Sensation - Ask the client to close both eyes. Vibrate a
tuning fork by knocking it against the palm of the hand. Apply the
tuning fork to the bony prominences to ensure that the person is
responding to vibration and not sound both eats should be blocked
from receiving sound. Ask the client to report the feeling of a
“buzz” and to say when the “buzz” stop

3. Pain and Temperature Sensation

3. Position Sensation or Proprioception – moves toes up, down,
side to side

5. Integration of Sensation
 Two point discrimination - Ask the client to close both eyes. Hold
one pin in each hand and apply them so that the fingers of the
examiner slide down the pin. Simultaneously apply the two pins to
the same body part. Ask the person to report when one or two pins
is/are felt

 Test for stereognosis – the ability to recognize an object of touch

 Test for extinction phenomenon - Ask the client to close both eyes
and to report where he or she is touched. The answer should not
just state “on the side” but should state which side it is.

VIII. BOWEL FUNCTIONS

IX. BLADDER FUNCTIONS

ASSESSMENT:
KEY SYMPTOMS
OF NEUROLOGIC
DISORDERS

1. Altered Level of Consciousness
2. Altered memory, orientation, concentration
3. Speech difficulties
4. Altered movement and coordination (weakness,
paralysis)
5. Pain
6. Seizures
7. Dizziness (Vertigo)
8. Visual disturbances
9. Taste & Smell alterations
10. Abnormal Sensation (numbness, paresthesia)
11. Altered temp regulation
12. Altered pain perception
13. Altered bowel and bladder elimination

DIAGNOSIS:
DIAGNOSTIC
TESTS

I. GLASGOW COMA SCALE
1. Verbal response
Oriented 5
Confused 4
Inappropriate words 3
Incomprehensible sounds 2
None 1

2. Eye opening
Spontaneous 4
To voice 3
To pain 2
None 1

3. Best motor response
Obeys command 6
Localizes pain 5
Withdraws from pain 4
Abnormal flexion (decorticate) 3
Abnormal extension 2
None 1

Levels of consciousness
Deep coma 3 -5
Coma 6 -8
Lethargic 9 - 11
Stuporous 12 -14
Normal 15

Coma – a clinical state of unconsciousness in
which the patient is unaware of self or the
environment for prolonged periods (days to
months or even years)

Persistent vegetative state – condition in
which the patient is described as wakeful but
devoid of conscious content, without cognitive
or affective mental function

Brain Death – irreversible loss of all functions
of the entire brain, including the brain stem

II. LUMBAR PUNCTURE AND CSF
ANALYSIS
 Carried out by inserting a needle into the lumbar SA
space to withdraw CSF.
 Done to obtain CSF for examination, measure &
reduce CSF pressure, determine the presence or
absence, detect spinal SAB & administer medications
intrathecally.
 Needle is inserted into the SA space between 3rd & 4th
or 4th & 5th lumbar vertebrae.
 Specimens are obtained for cell count, culture &
glucose & protein testing.
 Specimen should be sent to lab immediately because
changes will take place & alter result if allowed to
stand.
 Other form include Queckenstedt’s test.

ANALYSIS
 RESULT:
a. 70-200mmH20- normal CSF pressure with the pt in lateral
recumbent
b. Should be clear & colorless
c. Pink, blood-tinged or grossly bloody CSF may indicate a cerebral
contusion, laceration or SA hemorrhage
 COMPLICATIONS:
a. Herniation of intracranial contents
b. Spinal epidural abscess/hematoma
c. Meningitis
d. Temporary voiding problems
e. Slight increase of temperature
f. Backache or spasms
g. Stiffness of neck
h. Post lumbar puncture headache

ANALYSIS
 POST LUMBAR PUNCTURE HEADACHE :

 Caused by CSF leakage @ the puncture site. The fluid continues
to escape into the tissues by way of the needle track, from the
spinal canal. It is then absorbed promptly by the lymphatics.

 As a result, the supply of CSF in the cranium is depleted @ point
@ which it is insufficient to maintain proper mechanical
stabilization of the brain.

 This leakage of CSF allows settling of the brain when the patient
assumes an upright position, producing tension & stretching the
venous sinuses & pain-sensitive structures.

 Both traction & pain are lessened & the leakage is reduced when
the pt lies down.

ANALYSIS
 NURSING INTERVENTIONS:

1. Signed consent and void before the procedure. Use small gauged
needles
2. Instruct to relax to avoid traumatic or bloody tap, fetal position. A
local anesthetic will be used.
3. Patient remains on prone position 2 – 3 hours post procedure
4. Headache is managed by rest, analgesics & hydration
5. Assist with EPIDURAL BLOOD PATCH – blood is withdrawn from
antecubital area & injected into the epidural space, usually @ the
site of previous spinal puncture

 *** Blood acts as gelatinous plug to seal the hole in the dura,
preventing further loss of CSF

III. CT SCAN
- a non-invasive & painless procedure & has a high
degree of sensitivity for detecting lesions.
- makes use of a narrow x-ray beam to scan the head
in successive layers. The images provide cross
sectional views of the brain or other organs.
- performed first without contrast then with IV contrast
enhancement.

- patient lies in adjustable table with the head in fixed
position while the scan system rotates around the
head & produces cross-sectional images. The patient
must stay still because motion will distort the image

III. CT SCAN

1. teaching the pt about the need to lie quietly & still
throughout the procedure
2. sedation can be used if agitation, restlessness or
confusion will interfere with a successful study
3. instruct pt to be on NPO for at least 4 hours
4. monitoring pt for allergic reaction of contrast agent &
other side effects
5. increase hydration to flush out contrast

IV. POSITRON EMISSION TOMOGRAPHY
 Computerized nuclear imaging technique that produces images of
actual organ functioning.
 Patient either inhales radioactive gas or injected, that emits
positively charged particles.
 It is useful in showing metabolic changes in the brain (Alzheimer’s
dse), locating lesion (tumor, epileptogenic lesion), identifying blood
flow & O2 metabolism in pts with strokes, evaluating new therapies
for brain tumors & revealing biochemical abnormalities associated
with mental illness.

1. Patient preparation; explanation of the test & teaching patient of
inhalation techniques & sensation (dizziness, lightheadedness,
headache)

V. ELECTROENCEPHALOGRAPHY
 Represents a record of the electrical activity generated in the brain.
Obtained through electrodes applied in the scalp or through electrodes
applied within the brain tissue.
 Provides a physiologic assessment of cerebral activity.
 Useful test for diagnosing & evaluating seizure disorders, coma, or
organic brain syndromes. Tumors brain abscesses, blood clots, &
infection may cause abnormal patterns in electrical activity

1. Patient is deprived of sleep
2. Anti-seizures, tranquilizers, stimulants, depressants are withheld 24-48
hours (can alter/mask abnormal wave patterns of seizure disorders.
3. No coffee, tea, chocolate & cola (all stimulants)
4. Meal should NOT be omitted - altered blood glucose change brain
wave
5. Patient is informed that it would take 45-60 minutes for awake & 12
hours for sleep EEG.

VI. MYELOGRAPHY
 An x-ray of the spinal subarachnoid space taken after the injection
of contrast agent into the spinal subarachnoid space through a
lumbar puncture.
 Shows any distortion of the spinal cord or spinal dural sac caused
by tumors, cysts, herniated vertebral disks or other lesions

1. Information of the procedure; meal prior to procedure is omitted;
sedative may be given
2. After procedure, pt may lie in bed with HOB @ 30-45 degrees for 3
hours

VII. ELECTROMYELOGRAPHY
 Obtained by introducing needle electrodes into the skeletal
muscles to measure changes in the electrical potential of the
muscle & the nerves leading to them.
 Useful in determining the presence of neuromuscular disorders &
myopathies and help distinguish weakness due to neuropathy from
weakness due to other causes

1. Explanation of the procedure & patient is warned to expect a
sensation similar to that of an IM injection as the needle is inserted
into the muscle
2. Inform that muscles examined may ache for a short of time after
the procedure

VIII. MAGNETIC RESONANCE IMAGING
 Helps identify cerebral abnormality more early and clearly than
other test by using a highly magnetic field.
 The test may be done with or without a contrast.
 The magnet causes hydrogen ions in the body (protons) to align
like small magnets and emit signals which are converted into
images.

 NURSING REPONSIBILITIES:
1. Remove all metal objects from the patient and inside the
examination room.
2. Instruct patient that it is painless but he may hear loud thumping
3. Inform that he or she may communicate to the staff via a
microphone inside the scanner.
4. For claustrophobic patients, sedation may be used.

IX. CEREBRAL ANGIOGRAPHY
 X- ray study of cerebral circulation after injection of a dye to a
selected artery (usually femoral artery) under local anesthesia and
heparinized saline.
 Valuable for detection of aneurysm, AV malformations and other
vascular diseases.

 NURSING RESPONSIBILITIES:
1. Ensure well hydration and clear liquids before the test
2. Instruct to void before the test
3. Location of peripheral pulses are marked with a felt – tip pen
4. Shave the are (groin)
5. Instruct to remain immobile during the test, brief feeling of warmth
behind the eyes, face, jaw, teeth, tongue and lips and a metallic
taste after dye injection.
6. After the test, monitor VS, affected extremity for s/s of occlusion,
apply cold compress to relive hematoma.

X. NON – INVASIVE CAROTID FLOW
STUDIES & TRANSCRANIAL DOPPLER
 Uses UTZ imagery and Doppler measurements of arterial
blood flow to assess carotid and deep orbital circulation and
presence of Stenosis or obstruction.
 Transcranial Doppler assesses flow velocities in deep cranial
arteries and helpful in detection of vasospasm.

1. Inform that it is non – invasive, hand held transducer is
placed over the neck and orbits of the eyes with water
soluble jelly.
2. It is done at bedside.

XI. CHEST X - RAY
 Makes images of the heart, lungs, airway, blood vessels and
the bones of the spine and chest.
 An x-ray (radiograph) is a painless medical test that helps
physicians diagnose and treat medical conditions.
 Radiography involves exposing a part of the body to a small
dose of ionizing radiation to produce pictures of the inside of
the body.
 X-rays are the oldest and most frequently used form of
medical imaging.
1. Check the doctor’s order.
2. Inform the patient about the procedure.
3. Provide privacy.
4. Instruct the patient to remove clothing’s and jewelries.
5. Instruct the patient to take full inspiration during the procedure.

1. Altered Cerebral Tissue Perfusion
2. Impaired Physical Mobility
3. Ineffective Breathing Pattern
4. Ineffective Airway Clearance
5. Impaired Gas Exchange
6. Pain
7. Self – Care Deficit
8. Activity Intolerance
9. Impaired Urinary / Bowel Elimination, Incontinence, Retention
10. Altered Nutrition Less than Body Requirement
11. Impaired / Risk for Impaired Skin Integrity
12. Risk for Injury
13. Impaired Verbal Communication
14. Disturbed Sensory Perception
15. Altered Thought Process
16. Confusion: Acute / Chronic
17. Anxiety
18. Low Self Esteem
19. Ineffective Individual Coping
20. Risk for Ineffective Family coping
21. Sexual Dysfunction

MANAGEMENT
OF
NEUROLOGIC
DISORDERS

INTRACRANIAL SURGERIES
 LAYERS OF SCALP & MENINGES: (SCALP – SKULL - DAP)
1. Skin
2. Connective tissue
3. Aponeurosis
4. Loose Connective Tissue (vascular layers)
5. Pericranium (skull)
6. Dura, Arachnoid, Pia matter

 TYPES OF SURGERIES:
1. Supratentorial
2. Infratentorial
3. Transphenoidal
4. Burr Holes

I. UNCONSCIOUSNESS & COMA
 TERMS:
1. Altered LOC – disorientation, difficulty in following commands and
needs persistent stimuli to achieve a state of alertness.
2. Coma – state of unarousable unconsciousness wherein
purposeful response to external and internal stimuli are absent
except for involuntary responses to painful stimuli and brain stem
reflexes.
3. Akinetic mutism – unresponsiveness to the environment in which
the patient makes no voluntary movements.
4. Persistent vegetative state - condition in which the unresponsive
patient is described as wakeful or resumes sleep – wake cycles
after coma but is devoid of conscious content, without cognitive
or affective mental function.
5. Locked-in syndrome - inability to speak, tetraplegia but with
intact vertical eye movements and eyelid elevation . Results from
lesions in Pons.

 S/S:
1. Glasgow coma scale result below 15
2. Presence of multiple pathophysiologic phenomenon
3. Comatose w/ localized abnormal pupillary & motor response –
neurologic problem
4. Comatose but w/ pupillary light reflexes – toxic or metabolic
disorder

 COMPLICATIONS:
1. Respiratory failure
2. Pneumonia
3. Pressure ulcers
4. Venous stasis
5. Musculoskeletal deterioration
6. Disturbed GI Functions
7. Aspiration

 MEDICAL/SURGICAL/NURSING MGT:
1. Maintain patent airway
 Semi – Fowler’s position, lateral or semi-prone position, suction
secretions with hyper-oxygenation, monitor breath sounds,
prepare intubation set.
2. Protect the client
 Side rails: 2 @ day, 3 @ night, privacy during nursing activities
3. Maintain fluid balance and proper nutrition
 IV (slow), NGT, gastrostomy
4. Mouth care
 Cleanse, rinse, remove secretions, apply thin petrolatum on lips,
move ET tube to side regularly
5. Maintain skin and joint integrity
 Regular turning, proper moving in bed, passive ROM, assistive
devices, proper positioning, fluidized or low – air loss bed

 MEDICAL/SURGICAL/NURSING MGT:
6. Preserve corneal integrity
 Cleanse with cotton moistened w/ NSS, artificial tears every 2
hours, cold compress for periorbital edema, proper eye patching
7. Maintain Body temperature
 Proper ventilation, clothes, TSB, IV hydration, antipyretics,
monitor temperature
8. Prevent urinary retention
 Regular palpation of bladder, IFC, bladder training
9. Promote bowel function
 Monitor bowel sounds and movements, rectal exam, fecal
collection bags, stool softeners; glycerin suppositories, enema.
10. Provide sensory stimulation
 Orientation, patience
11. Meet family’s needs
12. Monitor and manage complications

II. INCREASED ICP
 PREDISPOSING FACTORS:
1. Cerebral edema
2. Head injury
3. Hydrocephalus
4. Inflammatory conditions
5. Tumor

 SITUATION:
 Imbalance among the 3 major determinants of ICP.

 ICP exceeds 20 mmHg (normal is 10 – 20 mmHg
,measured at the lateral ventricles)

II. INCREASED ICP
3 major determinants of ICP:
1. Brain tissue – 1,400 grams (increased by space
occupying lesions/tumor, abscess, edema)

2. Blood supply – 75 ml (affected by thrombosis,
embolism, aneurysm, AV malformation)

3. CSF – 75 ml (increased by obstruction to flow or
overproduction d/t a tumor in choroid plexuses)

**** CSF and Blood supply undergo constant minor
changes due to increase in the intra-thoracic pressure
when the person sneezes, coughs, strains; posture,
BP, systemic oxygen and CO2 levels.

II. INCREASED ICP
 CEREBRAL RESPONSE TO INCREASED ICP:
1. Monro – Kellie Hypothesis
2. Autoregulation
3. Cushing’s Reflex

 EFFECTS:
1. Ischemia – cell death
2. Cerebral edema
3. Fatal complication - Herniation of brain tissue (brain
stem)
4. Secondary complications – SIADH, Diabetes insipidus
(> 250ml urine/hour in 2 consecutive hours)

II. INCREASED ICP
 Early Signs:
1. Change in LOC – earliest sign, restlessness to confusion
2. Slowing of speech – delayed response to verbal suggestions
3. Pupillary changes – anisocuria
4. Constant Headache

 Late Signs:
1. Change in VS – Cushing’s triad plus hyperthermia
2. Deterioration of LOC - disorientation to lethargy, stupor to coma
3. Cheyne-stokes breathing
4. Ataxic breathing – irregular with random sequence of deep and
shallow respiration
5. Projectile vomiting
6. Decorticate and Decebrate posture, flaccidity, hemiplegia
7. Loss of brainstem reflexes – pupillary (fixed, dilated pupils),
corneal reflex, gag, swallowing reflex

II. INCREASED ICP
Medical Nursing
1. Monitoring ICP and Cerebral
Oxygenation
a. Ventriculostomy a. Evaluate ICP as ordered
b. Subarachnoid screw or bolt b. Perform regular neurologic
ICP check
c. Epidural monitor c. Prompt referral of
d. Fiberoptic monitor significant abnormal
e. Jugular Venous Bulb (SjvO2) findings
f. LICOX - measures O2 and

II. INCREASED ICP
Medical Nursing
2. Decreasing cerebral edema

a. Osmotic diuretics – mannitol a. Administer meds ad ordered
b. Loop diuretics – furosemide b. Monitor for electrolyte
c. Potassium sparing diuretics – imbalance with use of
spironolactone diuretics especially
d. For Hypokalemia – KCL Potassium
e. For Hyperklaemia – Insulin, c. Record I and O
kayexalate, Na CHO3, Calcium d. Emphasize fluid restriction
Gluconate to patient and SO
f. Corticosteroids e. Position properly to facilitate
g. Negative fluid balance - Fluid drainage – HOPB elevated
restrictions by 30 degrees
h. Ventriculostomy f. Regulate IVF properly
i. IFC g. Oral care during fluid
restrictions

II. INCREASED ICP
Medical Nursing
3. Maintaining Cerebral
Perfusion and oxygenation
a. Inotropic agents - a. Administer meds as
Dobutamine HCL (dobutrex) ordered
and Norepi. bitartrate b. Proper positioning,
(Levophed) use of cervical collar
b. Oxygenation administration c. Maintain oxygen as
mechanical ventilation ordered
c. CPP monitoring
d. ABG, Hgb, Pulse oximetry

II. INCREASED ICP
Medical Nursing
4. Reducing CSF and
Intracranial Blood Volume

a. CSF drainage a. Proper positioning
b. Promoting mild cerebral b. Maintain integrity of
vasoconstriction – PaCO2 at intraventricular
30 – 35 mmHg catheter for CSF
drainage

II. INCREASED ICP
Medical Nursing
5. Preventing further
increase in ICP
a. Cough suppressants a. Proper positioning, use
(dextrometorphan) of cervical collar,
b. Antivomiting (plasil) preventing hip flexion
c. Stool softeners (dulcolax) b. Instruct to conscious
d. Surgery – burr hole client to avoid valsalva
maneuver, bending,
stooping, lifting heavy
objects
c. Prevent vomiting and
coughing

II. INCREASED ICP
Medical Nursing
6. Controlling Fever and
reducing metabolic demands

a. Antipyretics a. Monitor VS esp. Temperature
b. Hypothermic blanket – use rectal or tympanic
c. High doses of barbiturates – thermometer
Pentobarbital (nembutal), b. Provide adequate ventilation
Thiopental (pentothal) c. Administer meds as ordered
d. Paralyzing agents – propofol d. Monitor for adverse effects of
(Diprivan) with analgesia and paralyzing agents and
sedation barbiturates
e. Induced hypothermia e. Assist in induction of
hypothermia

II. INCREASED ICP
Medical Nursing
7. Maintaining a patent
airway
a. Suction secretions as needed –
a. Intubation with oxygenation
b. Monitor breath sounds

8. Preventing Infection

a. Prophylactic antibiotics a. Maintain aseptic technique when
especially if with caring for tubes and
intraventricular catheter intraventricular catheter
b. Monitor for signs and symptoms
of meningitis and other infections

II. INCREASED ICP
Medical Nursing

9. Monitoring and managing
complications

a. Diabetes Insipidus – a. Perform frequent and regular
electrolyte replacement, neurologic assessments
vasopressin b. Monitor urine and record output
b. SIADH – fluid restriction, c. Proper use of monitoring devices
monitoring F & E status d. Educate family regarding
monitoring technology/equipment
and their purposes.

III. HEADACHE/CEPHALGIA
 DEFINITION:
A symptom rather than a disease which may indicate organic
disease, stress response, vasodilatation, skeletal muscle tension,
or combination of factors.

 TYPES:
1. PRIMARY HEADACHE – no organic cause is identified.
Includes:
 Migraine
 Tension – type headache
 Cluster headaches
 Cranial arteritis
 Other primary headaches

2. SECONDARY HEADACHE - associated with organic cause such
as brain tumor or aneurysm.

 ASSESSMENT:
1. Migraine
a. Prodrome
b. Aura Phase
c. Headache Phase
d. Recovery and Postdrome

2. Other headache types
a. Tension headache
b. Cluster headaches
c. Cranial arteritis

Medical Nursing
1. Prevention
Migraine:
a. Educate patients
1. Beta blockers – propanolol,
regarding causes and
metoprolol
predisposing factors
2. Calcium channel blockers for clients
and the need to avoid
with asthma, DM, bradycardia –
them.
verapamil
b. Teach relaxation
3. Amitriptyline HCL (elavil)
techniques
c. Administer meds as
4. Divalproex (valproate)
ordered
5. Flunarizine
6. Serotonin antagonist (pizotyline)
Others:
a. Ergotamine tartrate
b. Lithium naproxen (naprosyn)
c. Methysergide (sansert)

Medical Nursing
2. Relieve Pain

a. 100 % oxygen via face a. Provide comfort
mask for 15 minutes measures, quiet, dark
b. Ergotamine tartrate environment
c. Corticosteroids b. Assist with comfortable
d. Other analgesics positioning – usually
HOB elevated by 30
degrees
c. Apply warm compress
and massage to area
with muscle tension
d. Administer meds as
ordered

IV. SEIZURE DISORDER
Convulsion Seizure Epilepsy
- can be best described as - includes clinical - when seizures
a sudden, excessive, manifestation such become recurrent or
disorderly discharge of as disturbances in chronic in nature
neurons in either a sensation, alteration - a paroxysmal
structurally normal or in perception and or disturbance in
diseases cortex which coordination, LOC, consciousness with
arises from an instability convulsive autonomic, sensory
of the neuronal movements or a and /or motor
membrane caused by an combination of any dysfunction
excess of excitation or a or all of the - a manifestation of
deficiency of normal aforementioned. excessive
inhibitory mechanism. neurological
-refers only to those discharge in the brain.
violent, involuntary
muscular contraction of
voluntary muscle.

 CAUSES:
1. Idiopathic
2. Acquired
a. Cerebrovascular disease
b. Hypoxemia of any cause
c. Fever (childhood)
d. Head injury
e. Hypertension
f. CNs infections
g. Brain tumor
h. Drug and alcohol withdrawal
i. Agents - (INH) isoniazid
j. Allergies
k. Metabolic and toxic conditions – hypoglycaemia, hypocalcemia,
hyponatremia, renal failure, pesticides

 PATHOPHYSIOLOGY:
1. Depletion of K+ and a gain of Na+ in the neuronal cell produce seizure
2. Alteration in the blood brain barrier system can precipitate a shift in K+
concentration lowering the convulsive threshold
3. An altered O2 and glucose concentration – produce rapid marked
potassium loss and a sodium accumulation within the cells depolarizing
the membrane and producing those paroxysmal discharges.
4. Infectious process – as a result of cell destruction, fever, inflammation and
possible bacterial toxicity.
5. Vitamin B6 deficiency whether dietary or drug antagonized. Since Vit B6 is
involved in the metabolism of GABA, a shift of the normal excitatory
inhibitory balance occur with excitation prevailing and a results to seizure.
6. The duration of a seizure varies greatly. It may last a few seconds or
persists for several minutes. Although investigators do not know why
seizure stops at a given time. It is thought to be related to exhaustion of
the neurons involved and to certain unknown factor which inhibits further
electrochemical transmission. Some individuals may experience them
once or twice a year, while others may have 2 or 3 episodes in a single
day. It is unpredictable which is especially frightening to the individual.

 CLASSIFICATION:
1. Generalized seizure
 Grand mal or major motor
 Petit mal
 Myoclonic seizure
 Infantile spasms
 Atoning seizure
 Tonic seizure
 Febrile seizures
 Status epilepticus
2. Partial seizure
 Localized motor seizures
or Jacksonian seizure
 Psychomotor
(complex partial seizure)
 Partial seizure with secondary generalization
3. Unilateral
4. Unclassified epileptic seizures

 MEDICAL MANAGEMENT:
1. Prevention – removal of precipitating factors
2. Anticonvulsant Therapy
 Phenytoin (Dilantin) – DOC
 Phenobarbital (Luminal)
 Mephobarbital (Mebaral)
 Primidone (Mysoline)
 Succinamides
 Ethosiximide (Zarontin)
 Methsuximide (Celontin)
 Others
 Diazepam (Valium)
 Clonazepam (Clonopin)
 Valproic Acid (Depakene)
 Acetazolamide (Diamox)
 Carbamazepine (Tegretol)
3. Surgery

 NURSING MANAGEMENT:

1. General – C-A-E-S-A-R

2. During the Seizure

3. After the Seizure

V. CEREBROVASCULAR ACCIDENT
(STROKE)
 SITUATION:
 Sudden loss of brain function resulting from a
disruption of blood supply to part of the brain causing
temporary or permanent dysfunction.
 May be caused by thrombosis, embolism,
hemorrhage.
 Also known as Ischemic stroke and brain attack

 MAJOR CAUSES:
1. Ischemic
2. Hemorrhagic

V. CVA/STROKE
 RISK FACTORS:
1. HPN
2. DM
3. MI
4. Aortic valve disease
5. CHF
6. Arterio/Atherosclerosis

 TYPES ACCORDING TO TIME:
1. Transient Ischemic Attack (TIA)
2. Reversible ischemic Neurologic deficit
3. Stroke in Evolution
4. Completed Stroke

 TYPES ACCORDING TO CAUSE:
1. Ischemic
2. Hemorrhagic

STROKE CLASSIFICATION
ACCORDING TO TIME
1. Transient Ischemic Attack (TIA)
- temporary episode of neurologic dysfunction (loss of
motor, sensory & visual dysfunction)
Management: Anticoagulant therapy heparin, coumadin,
aspirin
2. Reversible ischemic Neurologic deficit
- signs & symptoms are consistent with but more
pronounced than TIA. S/Sx resolve in days without
neurologic deficit
3. Stroke in Evolution
- worsening of neurologic S/Sx over several minutes or
hours. Also called Progressing stroke
4. Completed Stroke
- stabilization of neurologic S/Sx. No further progression
of hypoxic insult to the brain.

TYPES ACCORDING TO CAUSE (ISCHEMIC):
1. Large artery thrombosis
– due to atherosclerotic plaques in the large blood vessels of
the brain. Thrombus formation & occlusion @ the site of
atherosclerosis result in ischemia & infarction.
2. Small penetrating artery thrombosis
- affect one or more vessels & are the most common type of
ischemic stroke.
- also called lacunar stroke.
3. Cardiogenic Embolic stroke
- associated with cardiac dysrhytmias, usually atrial fibrillation.
Emboli originate from the heart & circulate to the cerebral
vasculature, most commonly the left middle cerebral artery,
resulting in a stroke. Embolic strokes may be prevented with
use of anticoagulants.
4. Cryptogenic
- no known cause
5. Others
- cocaine use, coagulopathies, migraine & spontaneous
dissection of the carotid or vertebral arteries.

Pathophysiology:
Obstruction of blood vessels
(of different causes)
↓
Ischemia
↓
Energy failure
Acidosis ↓
Ion imbalance
↓ inc. glutamate depolarization

Intracellular calcium increase
↓
Cell membranes & protein breakdown
Formation of free radicals;
Decrease protein production
↓
Cell injury & death

 Ischemic cascade begins when cerebral blood flow
falls to less than 25 ml/100g/min. at this point,
neurons can no longer maintain aerobe respiration.

 Mitochondria switches to anaerobic respiration
which generates large amounts of lactic acid,
causing change in Ph, also renders the neuron
incapable of producing large quantities of ATP to fuel
depolarization process. Membranes pump that
maintain electrolyte balance begin to fail & cells
cease to function.

 An area of low cerebral blood flow (penumbra region)
exists around the area of infarction. It is ischemic
brain tissue that can be salvaged with timely
intervention.

TYPES ACCORDING TO CAUSE:
(HEMORRHAGIC STROKE)

1. Intracerebral Hemorrhage
2. Intracranial/Cerebral Aneurysm
3. Subarachnoid Hemorrhage
4. Arterio-Venous Malformation

V. CVA/STROKE
RISK FACTORS
1. HPN – BP vasoconstriction pressure
in blood vessels rupture of vessels
thrombus in the blood vessel of brain
blood supply to the brain

2. DM - blood sugar levels viscosity of
blood perfusion of blood stasis of blood
flow thrombus formation blood supply to
the brain

3. MI – decrease O2 to myocardium decreased
cardiac output decreased perfusion stasis
thrombus decreased blood supply to brain
4. Aortic valve dse - decreased cardiac output
decreased perfusion stasis thrombus
decreased blood supply to brain
5. CHF – inability of heart to pump sufficient amount
of blood back to heart decreased cardiac output
decreased perfusion stasis thrombus
decreased blood supply to brain
6. Arterio/Atherosclerosis – narrowing of blood
vessels decreased cardiac output decreased
perfusion stasis thrombus decreased blood
supply to brain

V. CVA/STROKE
CLINICAL MANIFESTATIONS
 Stroke can cause a wide variety of neurologic deficits,
depending on the location of lesion, size of area of
inadequate perfusion & the amount of collateral blood
flow.
1. Ischemic
2. Hemorrhagic
3. Motor disturbances
4. Communication problems
5. Perceptual/ Sensory disturbance lesion; numbness & tingling
of extremities.
6. Cognitive deficit
7. Emotional deficits

V. CVA/STROKE

 Ischemic: Numbness or weakness of face,
arm or leg especially on one side of the body

 Hemorrhagic: “Exploding headache”,
decreased LOC, focal seizures, nuchal rigidity

V. CVA/STROKE
MOTOR
 hemiplegia – most common motor dysfunction, due
to lesion of the opposite side of the brain (paralysis of
one side of the body)
 hemiparesis – weakness of one side of the body.
Ataxia – staggering, unsteady gait; unable to keep
feet together, needs a broad base to stand
 Dysphagia – swallowing difficulty.
 apraxia – inability to perform a previously learned
action (picks up a fork but attempts to comb hair)

V. CVA/STROKE
COMMUNICATION
 dysarthria – difficulty in speaking, caused by
paralysis of muscles responsible for
producing speech

 dysphasia/aphasia – defective or loss of
speech. Could either be expressive, receptive
or mixed/global

V. CVA/STROKE
PERCEPTUAL DISTURBANCE
- Perception is the ability to interpret sensation. Disturbances
are due to disturbances of primary sensory pathways between
the eye & cerebral cortex.
 Homonymous hemianopsia – loss of half of the visual field. It
corresponds to the paralyzed side of the body.

 Loss of peripheral vision – difficulty seeing @ night.

 Diplopia – double vision, unaware of objects or borders of
objects.

 Paresthesia – occurs on side opposite to lesion; numbness &
tingling of extremities.

V. CVA/STROKE
COGNITIVE DEFICIT
 Short & long term memory loss
 Decreased attention span
 Impaired ability to concentrate
 Poor abstract reasoning
 Altered abstract reasoning

EMOTIONAL DEFICITS
 Loss of self control
 Emotional lability
 Decreased tolerance to stressful situations
 Depression
 Withdrawal
 Fear, hostility & anger
 Feelings of isolation

V. CVA/STROKE
USUAL SIGNS & SYMPTOMS
1. Headache
2. Vomiting
3. Seizures
4. Confusion
5. Decreased LOC
6. Nuchal rigidity
7. Fever
8. Hypertension
9. Slow bounding pulse
10. Cheyne-stokes respirations

V. CVA/STROKE
DIAGNOSTIC TESTS
1. CT scan show lesion – to determine if the event is
ischemic or hemorrhagic; to determine treatment
2. 12 lead ECG
3. Carotid Ultrasound
4. Cerebral arteriography shows occlusion or
malformation of vessels
5. Transcranial Doppler
6. Transthoracic or transesophageal echocardiogram
7. MRI of brain
8. Single photon emission CT

V. CVA/STROKE
MEDICAL MANAGEMENT
 Ischemic Stroke
1. Thrombolytic therapy – Recombinant t-PA
2. Anticoagulants – heparin – Coumadin (after 24 hours)
3. Antiplatelets - Aspirin
4. Statins - simvastatin
5. AntiHPN – ACE Inhibitors
6. Thiazide Diuretics
7. Intubation
8. Surgery: Carotid Endarterectomy – removal of an
atherosclerotic plaque or thrombus from carotid artery to
prevent stroke in patients with occlusive diseases of the
extracranial cerebral arteries.
9. Manage complication – pulmonary care, maintenance of patent
airway, & administration of supplemental oxygen

V. CVA/STROKE
MEDICAL MANAGEMENT

 Hemorrhagic Stroke
1. Analgesics – codeine, acetaminophen
2. Sequential compression devices – prevent DVT
3. Surgery: endovascular treatment, aneurysm coiling,
removal of aneurysm

V. CVA/STROKE
MEDICAL MANAGEMENT
COMMUNICATION:
Aphasia right hemiplegics
Receptive – inability to decode spoken word
(WERNICKE”S area affectation) give one command at a
time, simple instructions, non verbal communication
Expressive – inability to speak (BROCA’S area affected)
encourage attempts at speech – anticipate needs, allow to
verbalize, no matter how long it takes, do not finish
sentences for him

HOMONYMOUS HEMIANOPSIA AND LOSS OF HALF OF
EACH VISUAL FIELD
- approach patient on unaffected side place belongings on
unaffected side teach scanning technique (turn head to
sides)

V. CVA/STROKE
MEDICAL MANAGEMENT
MANAGING COMPLICATIONS:
- pulmonary care, maintenance of patent airway, &
administration of supplemental oxygen

ENDARTERECTOMY – removal of an atherosclerotic plaque
or thrombus from carotid artery to prevent stroke in
patients with occlusive diseases of the extracranial
cerebral arteries.

NURSING MANAGEMENT POST OP
1. Close cardiac monitoring
2. Maintenance of adequate BP

V. CVA/STROKE
NURSING MANAGEMENT
1. Maintain Patent airway
2. Monitor VS , neurological checks
3. Promote Bed rest
4. Perform GI decompression (NGT)as ordered
5. Maintain Fluid electrolyte balance
6. Reposition q2h
7. Promote Skin integrity
8. Improve mobility
9. Support Elimination – offer bed pan every 2 hours –
catheterize if necessary – stool softeners and
suppositories
10. Ensure safety
11. Facilitate Communication
12. Administer drugs as ordered

VI. NEUROLOGIC TRAUMA
 CLASSIFICATION:
1. Brain Trauma
 Primary trauma –is the direct result of some force applied to the
skull resulting in a fracture, hemorrhage, contusion, or concussion.
 Secondary trauma - is one in which some other medical condition
causes a person to fall or otherwise to sustain a blow to the head.
These conditions include diabetic, cardiac, epileptic or hysterical
problems and situations following drug and/or alcohol ingestion in
which the person falls, strikes the head and loses consciousness.
a. Fracture
b. Hemorrhage
c. Contussion
d. Concussion

2. Spinal Cord Injury

BRAIN TRAUMA: FRACTURES
1. Linear fracture- are those in which there is a simple
break in the continuity of the bone/skull
2. Comminuted fracture- are fragmented interruptions of
the skull from multiple linear fractures

3. Depressed fracture - comminuted bone fragments
penetrate the brain tissue

4. Compound fracture- any of the preceding which also
has an opening through the sinuses, eardrums or scalp.

BRAIN TRAUMA: HEMORRHAGE
1. Linear fracture- are those in which there is a simple
break in the continuity of the bone/skull
2. Comminuted fracture- are fragmented interruptions of
the skull from multiple linear fractures

3. Depressed fracture - comminuted bone fragments
penetrate the brain tissue

4. Compound fracture- any of the preceding which also
has an opening through the sinuses, eardrums or scalp.

BRAIN TRAUMA: HEMORRHAGE
1. Epidural Hematoma

2. Subdural Hematoma

3. Intra-cerebral Hematoma

BRAIN TRAUMA: CONCUSSION
Concussion
- It is essentially a disruption of normal activity among some of
the synapses of the neurons. It is a temporary disarrangement
of normal neurons activity. Muscular activity and mental clarity
usually return within a few minutes after trauma, although there
may be residual amnesia for the event.

BRAIN TRAUMA: CONTUSION
Contusions
- Resemble bruises. There is only slight injury to small vessels
with a small amount of bleeding into the surrounding tissues.
The resulting effects of increased ICP are dependent upon the
amount of contused brain tissue.

SPINAL CORD INJURY
 Primary Injury
- results from initial insult or trauma and produces
permanent damage

 Secondary Injury
– results from contusion or tear injury in which nerve fibers
begin to swell and disintegrate. Damage is reversible up to
4 – 6 hours after the injury.

 Effects:
1. Central Cord Syndrome
2. Anterior Cord Syndrome
3. Brown Sequard Syndrome

SPINAL CORD INJURY
 COMPLICATIONS:
1. Spinal and Neurogenic shock “areflexia”

2. Autonomic Dysreflexia “hyperreflexia”

3. Tetraplegia and Paraplegia

4. Deep Vein Thrombosis and Thrombophlebitis

5. Orthostatic Hypotension

SPINAL CORD INJURY
 MANAGEMENT:
1. Cord Damage – immobilize
2. Respiration – stabilize, intubation
3. Urinary and bowel function – training, IFC, enema,
suppositories, don’t allow bladder to distend
4. Thrombosis – anticoagulants, elastic compression
stockings
5. Cardiovascular stability
6. Help assess meurologic status
7. Encourage adequate fluid, nutrition
8. Support skin to prevent breakdown, watch out for Shock

VII. HYDROCEPHALUS
 DEFINITION:
 A.k.a. water on the brain
 Can be caused by impaired CSF flow and re-
absorption, or excessive CSF production.
 Flow obstruction, hindering free passage of CSF
through the Ventricular System & SA space (e.g.
stenosis of cerebral aqueduct or obstruction of
Foramen of Monro) due to tumors hemorrhages,
infection or congenital malformations.
 Overproduction of CSF (e.g. papilloma of choroid
plexus)

VII. HYDROCEPHALUS
 TYPES:
1. Congenital

2. Acquired

3. Communicating or Non – obstructive

4. Non – communicating or Obstructive

VII. HYDROCEPHALUS
1. Drugs
2. Surgical removal of obstruction
3. Surgical placement of shunting devices
a. VP shunt
b. VA shunt
c. EVD

1. Prevent Increase ICP
2. Prevent Infection
3. Promote proper nutrition
4. Educate SO
5. Post – op care

VIII. NEURAL TUBE DEFECTS
 DEFINITION:
Failure of neural tube to close or fully develop at 3 – 5 weeks of
gestation.

 CAUSE:
Genetics, heredity, drugs, radiation, chemicals or toxins, maternal
malnutrition, maternal use of antiepileptic drugs, infectious
diseases and FOLIC ACID DEFICIENCY (normal intake 0.4 - 4
mg/day).

 CLASSIFICATION:
1. Anencephaly - cerebrum
2. Encephalocele – cerebrum, meninges, glial cells
3. Spina Bifida – spinal cord, meninges, usually L5 and S1 region
a. Spina Bifida occulta
b. Spina Bifida cystic
 Meningocele
 Myelomeningocele

VIII. NEURAL TUBE DEFECTS
 GENERAL MANAGEMENT FOR NTD:
1. All – protect from LATEX allergy, NO to balloons, vinyl gloves
2. Anencephaly – no cure, support parents
3. Encephalocele – protect from infection, support perio-peratively,
and educate parents about possible intellectual impairment.
4. Spina bifida occulta - facilitate work ups, referral to surgery,
monitor for development of s/s.
5. Meningocele – protect sac from rupture, drying or infection, place
in prone position, facilitate early sac excision (24 – 48 hours of
life), complete closure of spinal column, monitor for development
of complications.
6. Myelomeningocele – cover sac with non-adhesive, sterile, moist
saline gauze, place infant in prone position, facilitate surgery
(repair and shunt placement), emphasize to parents that surgery
has its risks (lower extremities paralysis), monitor for development
of complications like increase ICP and HYDROCEPHALUS.

IX. MULTIPLE SCLEROSIS
 DEFINITION:
Immune-mediated progressive demyelination or destruction of
myelin sheath that surrounds certain nerve fibers in brain and
spinal cords resulting to impaired transmission of nerve impulses.
Affects the CNS. May be Relapsing-remitting, Primary
progressive, Secondary progressive, Progressive-relapsing.
 CAUSE:
Possibly Human Leukocyte Antigen in cell wall, presence of
sensitized T – Cells that remain within the CNS.
 DX: MRI, Electophoresis of CSF (several bands of IG G)
 MAIN S/S: FATIGUE, CHARCOAT’S TRIAD
 MGT: Analgesics, immunosuppressive agents and steroids,
GABA agonist, Benzodiazepines (valium), Symmetrel, Cylert,
Prozac, Inderal, Vitamin C, antibiotics.
 NSG. CARE: AVOID FATIGUE, AVOID PREGNANCY during
remission

MULTIPLE SCLEROSIS
A degenerative disease characterized by
demyelination of nerve fibers within the spinal cord
and brain. Destruction of an area of a myelin sheath
occurs, followed by a proliferation of neuroglial cells,
scar formation and damage to the nerve fiber with
ensuing loss of transmission of impulses.
Etiology and incidence:
The cause is unknown. At present theories
undergoing investigation are concerned with auto
immune mechanisms and viral infections as possible
etiologic factors. It most prevalent in colder climates.
It has a slightly higher incidence in females between
20 to 40 years of age.

Course and manifestations:
Characterized by remissions and relapses, and the
course is extremely variable and unpredictable.
Early symptoms:
Transient tingling sensations, numbness and muscular
weakness in one or both arms and legs and visual
disturbances (nystagmus, diplopia or blurring of vision);
emotional lability, evidenced bv alternating periods of
euphoria, depression, irritability.
Late symptoms:
With relapses and increasing damage, the patient may
develop paralysis, impaired speech, dysphagia,
increasing loss of sensation, bladder and bowel
incontinence, increasing visual difficulties, personality
changes, and intellectual impairment. Weakness of the
respiratory muscles and cough reflex may also be
present, predisposing him to pulmonary complication.

Diagnostic test:
At present there are no specific diagnostic tests. The CSF
shows an elevated gamma globulin and a positive colloidal gold
precipitation test (Lange colloidal gold curve)
Treatment and Nursing Care:
During remissions – the patient is encouraged to resume his
usual pattern of life modifying it as necessary to avoid fatigue,
emotional stress and infection. Well balanced diet adequate
rest and learning to accept what cannot be readily change are
stressed. Avoid pregnancy.
During relapses – confine to bed for a period of 2 to 3 weeks or
until symptoms begin to disappear. Warm baths, massage,
pleasant quiet surroundings, encouraging reading and listening
to radio, chat. The limbs are passively moved through the full
range of motion twice daily.
Steroid therapy:
Dexamethasone (Decadron), Adrenocorticotropin (ACTH) or
Prednisone

X. MYASTHENIA GRAVIS
 DEFINITION:
Immune-mediated varying degrees of voluntary muscle weakness.
Affects the MYONEURAL JUNCTION.

 CAUSE: Presence of ANTIBODIES directed towards Ach
receptors.

 DX: Achetylcholinesterase inhibitor test: TENSILON TEST,
Presence of Ach receptor antibodies in serum, Successive nerve
stimulation, Evaluation of Thymus gland.

 S/S: Ptosis, descending paralysis, muscle weakness in late
afternoon, risk for respiratory failure.

 COMPLICATIONS: Respiratory Failure and Crisis:
 Myasthenic crisis

 Cholinergic crisis

 Brittle Crisis – extreme under meds

Etiology: Predisposing factor:
- autoimmune - auto immune disease
- viral infection, Thymoma, rheumatoid arthritis,
- systemic lupus erythematous
│--------------------------------------------------------------------------------------│
↓
auto antibodies
↓
blocking the binding of acetylcholine
↓
destruction of ACH receptor
↓
impaired transmission of impulses across the myoneural junction

----------------------------------------------------------------------------------------------------------------------
↓ ↓ ↓
↓ ↓ ↓
facial expression limb movements laryngeal chewing & eye & eyelid
involvement swallowing movements
-myasthenic smile - unstable - dysphonia - dysphagia - diplopia
- waddling gait - dysarthria - choking - ptosis
- weak arms, - slurred speech - aspiration
legs, hands
& fingers

Diaphragm
- Shortness of breath

Complications:
- Myasthenia crisis or Brittle Crisis
- Cholinergic crisis

CRISIS: acute episodes to severe muscular weakness in
which respiratory insufficiency and the inability to
swallow are manifested.

Categories:
Myasthenic type – is attributed to a temporary
resistance to or inadequate dosage of the cholinergic
preparation being administered. Manifested by extreme
weakenss. Tensilon relieves symptoms

Cholinergic crisis – is caused by excess of
anticholinesterase medication. Patient becomes pale
and manifests diarrhea, nausea, vomiting, diaphoresis,
increased salivation and bronchial secretions,
abdominal cramps and blurred vision. Symptoms
worsen in Tensilon. Atropine as antidote.

X. MYASTHENIA GRAVIS
 MGT:
1. Drugs – ANTICHOLINESTERASE/pyridostigmine bromide
(Mestinon) and Neostigmine (Prostigmin), immunosuppressive
agents (Prednisone), cytotoxic agents NO TO MORPHINE,
CURARE, QUININE, NEOMYCIN, STREPTOMYCIN
2. IVIG, Plasmapheresis, Thymectomy, Intubation, Mechanical
Ventilation

 NSG. CARE:
1. Avoid overfatigue.
2. Support nutrition.
3. Administer meds at precise time. 20 – 30 minutes before meals.
4. Protect patient from fall.
5. Aspiration precaution.
6. Monitor respiratory status and provide adequate ventilation.
7. Avoid exposure to infection.
8. Provide eye care. “Crutches” to eyelids, patch one eye and give
artificial tears.

XI. GUILLAIN BARRE SYNDROME
 DEFINITION:
An acute inflammatory demyelinating disease of the peripheral
nervous system.
 CAUSE: Unclear. It is believed to be associated with an viral
infections 1-4 weeks before.
 DX: Spinal Tap - High Protein levels in CSF, EMG – slow
conduction of impulses to muscles
 S/S:
1. Initial phase - Bilateral muscle weakness in the lower
extremities, with an ascending pattern. Can result in potential
life-threatening respiratory compromise.
2. Plateau phase - May last days to weeks. It is an interim period
in which no changes occur.
3. Recovery phase - Synonymous with re myelination and axonal
regeneration. Paralysis resolves gradually in a descending
symmetrical pattern following a proximal to distal pattern.

 Pathophysiology:

Schwann cells, which cover the nerve axons,
form the myelin sheath.
Degeneration of these cells occurs, causing a
flaccid paralysis, which is usually in an
ascending pattern. It is primarily the motor
neurons affected. Sensory involvement is limited
and is usually confined to the hands and feet in
what is termed the glove and stocking pattern.
Spontaneous regeneration of the myelin sheath
occurs with complete recovery within 6 months to
1 year. Management is aimed at supporting body
functions and preventing complications
associated with paralysis until recovery occurs.

GB Planning and Intervention:
1. Assess for respiratory compromises - evaluate ABGs
and pulse oximetry
2. Be prepared to provide respiratory support – mech. vent
and later on, intubation
3. Perform pulmonary toilet to prevent pneumonia, suction
as necessary, hyperoxygenate/hyperventilate
4. Monitor Vital signs, ECG
5. Assess for urinary retention
6. Maintain optimal positioning
a. Elevate head of bed as tolerated to promote lung
expansion and decrease risk for aspiration
b. Turn and reposition every 2 hours
c. Assist with active and passive ROM

7. Prevent DVT & pulmonary embolism – Anti-embolic
stockings, sequential compression boots,
anticoagulants

8. Administer medications as indicated and ordered,
including:
1. IVIG – therapy of choice, followed by plasmapheresis
2. Analgesics
3. Anti-anxiety agents
4. Corticosteroids
5. Antibiotics for prophylaxis
6. Antacids to control gastric irritation
7. H2 blockers to reduce gastric acid secretion and
prevent ulcer
8. Anticoagulants
9. A short – acting alpha adrenergic blockers for HPN in
autonomic dysfunction

XII. PARKINSON’S DISEASE
 DEFINITION:
A progressive degenerative neurologic disorder affecting the brain
centers that are responsible for control and regulation of
movement (extrapyramidal) caused by deficiency of dopamine.
Occurs in the elderly.

 CAUSE:
Dopamine deficiency

 DX:
EEG, CT Scan, SPECT (PET)

 S/S:
1. Resting tremors
2. Rigidity
3. Bradykinesia
4. Postural instability

 Manifestations:
1. Tremors of the upper limbs; “Pill rolling”
2. Rigidity; “cogwheel rigidity”
3. Bradykinesia (moves slowly)to hypokinesia (diminished
movements)
4. Stooped posture, loss of postural reflexes
5. “Shuffling, propulsive gait/ festinating” gait
6. Monotone speech; “microphonia, dysphonia”
7. Mask like facial expression
8. Increased salivation, drooling, dysphagia
9. Excessive sweating, seborrhea
10. Lacrimation, constipation
11. Decreased sexual capacity
12. Alteration in handwriting; “micrographia”
13. Dementia, depression, sleep disturbances and hallucinations

XII. PARKINSON’S DISEASE
 MGT: Drugs, Surgery
1. Antiparkinsonians
2. Anticholinergics
3. Antihistamines
4. Dopamine agonist
5. Antidepressants
6. MAO Inhibitors
7. Antiviral
8. Stereotactic Procedures - Thalamotomy and Pallidotomy
9. Neural Tranplantation
10. Deep Brain Stimulation

 NSG. CARE:
1. Aspiration precaution
2. Educate on drug therapy
3. Physical therapy and gait training
4. Diet
5. Safety
6. Emotional support
7. Promote independence
8. Skin care

Drug Function Generic Name (Trade Name)
Levodopa Enhances conversion of levodopa to Levodopa (Laradopa);
dopamine in the brain. levodopa/carbidopa (Sinemet, Sineme
CR,Atamet); levodopa/benserazide
(Madopar)

Dopamine agonist Mimics the action of dopamine by Bromocriptine (Ergoset, Parlodel);
activating nerve cells in the brain. pergolide (Permax); pramipexole
(Mirapex); ropinirole (Requip)
Anticholinergic Blocks action of acetylcholine, a brain Trihexiphenidyl (Artane, Trihexy);
chemical that becomes overactive when biperidine (Akineton); benztropine
dopamine levels drop. (Congentin)

MAO-B inhibitor Blocks action of an enzyme that breaks Selegiline (Eldepryl, Movergan)
down dopamine in the brain.

COMT inhibitor Blocks action of an enzyme that breaks Tolcapone (Tasmar); entacapone
down levodopa in the body, permitting (Comtan)
more levodopa to reach the brain.

Amantadine Stimulates release of dopamine from Amantadine (Symadine, Symmetrel)
nerve cells in the brain and may block
acetylcholine action.

BELL’S PALSY
It is a lower motor neuron lesion of the 7th cranial
nerve, resulting in paralysis of one side of the face. It
is usually self-limiting to a few weeks.

Manifestations:
Facial paralysis involving the eye
Tearing of eye
Painful sensations in the face
Sagging of one side of mouth; drooling

Management:
Steroids and analgesics
Protect involved eye
Active facial exercises

CEREBRAL PALSY
- Is an umbrella term encompassing a group of
non-progressive, non-contagious neurological
disorders that cause physical disability in
human development, specifically movement &
posture.
- Neurological disability or difficulty controlling
voluntary muscles (caused by damage to some
portion of the brain, with associated sensory,
intellectual, emotional or convulsive disorders.

Neurologic nursing

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Similar to Neurologic nursing

Similar to Neurologic nursing (20)

Recently uploaded

Recently uploaded (20)

Neurologic nursing