Neurologic Care Nursing

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General functions of the neurologic system include:
° Cognition, emotion, and memory.
° Sensation, perception, and the integration of sensoryperceptual
experience.
° Regulation of homeostasis, consciousness, temperature, BP, and
other bodily processes.
phere are two types of nerve cells:
(1) neuroglia and
(2) neurons

Ñ ÿ
a. act as supportive tissue, nourishing and protecting the
neurons
b. maintain homeostasis in the interstitial fluid around the
neurons and account for about 50 percent of the central
nervous system (CNS) volume
c. have the ability to regenerate and respond to injury by
filling spaces left by damaged neurons.
Nervous pissue: Support Cells
Ñ Support cells in the CNS are grouped together as
ńeurogliaµ
Ñ Function: to support, insulate, and protect neurons
Ñ Astrocytes
° Abundant, star-shaped cells
° Brace neurons
° Form barrier between capillaries and neurons
° Control the chemical environment of

the brain
Ñ Microglia
° Spiderlike phagocytes
° Dispose of debris
Ñ Ependymal cells
° Ôine cavities of the brain and spinal cord
° Circulate cerebrospinal fluid
Ñ Oligodendrocytes
° Îrap around nerve fibers in the central nervous system
° Produce myelin sheaths
Ñ Satellite cells
° Protect neuron cell bodies
Ñ Schwann cells
° Form myelin sheath in the peripheral nervous system
ÿ

ÿ
a. have the ability to
produce action potentials
or impulses (excitability or
irritability) and
b. to transmit impulses
(conductivity).
Nervous pissue: Neurons
Ñ Neurons = nerve cells
° Cells
specialized to transmit messages
° Major regions of neurons
M Cell body³nucleus and metabolic center of the cell
M Processes³fibers that extend from the cell body
Ñ Cell body
° Nissl substance
M Specialized rough endoplasmic reticulum
° Neurofibrils
M ntermediate cytoskeleton
M Maintains cell shape
Ñ Cell body
° Nucleus
° Ôarge nucleolus
Ñ Processes outside the cell body
° Dendrites³conductimpulses toward the cell body
° Axons³conduct impulses away from the cell body
Ñ Axons end in axonal terminals
Ñ Axonal terminals contain vesicles with
neurotransmitters
Ñ Axonal terminals are separated from the next
neuron by a gap
° Synaptic
cleft³gap between adjacent neurons
° Synapse³junction between nerves
Ñ Myelin sheath³whitish, fatty material covering
axons
Ñ Schwann cells³produce myelin sheaths in jelly roll²
like fashion
Ñ Nodes of Ranvier³gaps in myelin sheath along the
axon
Neuron Cell Body Ôocation
Ñ Most neuron cell bodies are found in the central
nervous system
° Gray matter³cell bodies and unmyelinated fibers
° Nuclei³clusters of cell bodies within the white matter of
the central nervous system
Ñ Ganglia³collections of cell bodies outside the
central nervous system
Functional Classification of Neurons
Ñ Sensory (afferent) neurons
° Carry impulses from the sensory receptors to the CNS
M Cutaneous sense organs
M Proprioceptors³detect stretch or tension
Ñ Motor (efferent) neurons

° Carry impulses from the central nervous system to
viscera, muscles, or glands
Functional Classification of Neurons
Ñ nterneurons (association neurons)
° Foundin neural pathways in the central nervous system
° Connect sensory and motor neurons
Neuron Classification
Structural Classification of Neurons
Ñ Multipolar neurons³many extensions from the cell
body
Ñ Bipolar neurons³one axon and one dendrite
Ñ Unipolar neurons³have a short single process
leaving the cell body
ÿ
Functional Properties of Neurons

Ñ rritability
° Ability to respond to stimuli
Ñ Conductivity
° Ability to transmit an impulse
Nerve mpulses
Ñ Resting neuron
° phe plasma membrane at rest is polarized
° Fewer positive ions are inside the cell than outside the cell
Ñ Depolarization
° A stimulus depolarizes the neuron·s membrane
° A depolarized membrane allows sodium (Na+) to flow
inside the membrane
Ñ phe exchange of ions initiates an action potential in the
neuron
Nerve mpulses
Ñ Action potential
° fthe action potential (nerve impulse) starts, it is
propagated over the entire axon
° mpulses travel faster when fibers have a myelin sheath
Nerve mpulses
Ñ Repolarization
° Potassium ions rush out of the neuron after sodium ions
rush in, which repolarizes the membrane
° phe sodium-potassium pump, using ApP, restores the
original configuration
pransmission of a Signal at Synapses
Ñ mpulses are able to cross the synapse to another
nerve
° Neurotransmitter is released from a nerve·s axon
terminal
° phe dendrite of the next neuron has receptors that are
stimulated by the neurotransmitter
° An action potential is started in the dendrite
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Ñ Neurons band together into
- peripheral nerves,
- spinal nerves,
- spinal cord, and
- tissues of the brain.
Ñ phese structures make up the neurologic system, which is
divided into
- the CNS and
- the peripheral nervous system (PNS).
CENpRAÔ NERVOUS SYSpEM
consists of the:
4
Regions of the Brain: Cerebrum
Ñ Cerebral Hemispheres (Cerebrum)
° Paired (left and right) superior parts of the brain
° ncludes more than half of the brain mass
° phe surface is made of ridges (gyri) and grooves (sulci)

Ñ Ôobes of the cerebrum
° Fissures(deep grooves) divide the cerebrum into lobes
° Surface lobes of the cerebrum
M Frontal lobe
M Parietal lobe
M Occipital lobe
M pemporal lobe
Ñ Specialized areas of the cerebrum
° Primary somatic sensory area
M Receives impulses from the body·s sensory receptors
M Ôocated in parietal lobe
° Primary motor area
M Sends impulses to skeletal muscles
M Ôocated in frontal lobe
° Broca·s area
M nvolved in our ability to speak
ÿ
Ñ Cerebral areas involved in special senses
° Gustatory area (taste)
° Visual area
° Auditory area
° Olfactory area
Ñ nterpretation areas of the cerebrum
° Speech/language region
° Ôanguage comprehension region
° General interpretation area

Ñ Ôayers of the cerebrum
° Gray matter³outer layer in the cerebral cortex
composed mostly of neuron cell bodies
° Îhite matter³fiber tracts deep to the gray matter
M Corpus callosum connects hemispheres
Ñ Basal nuclei³islands of gray matter buried within
the white matter
Regions of the Brain: Diencephalon
Ñ Sits on top of the brain stem
Ñ Enclosed by the cerebral hemispheres
Ñ Made of three parts
° phalamus
° Hypothalamus
° Epithalamus
phe
Diencephalon
is the seat of
the control
system for
impulse
transmission to
different
parts of the
brain
Ñ phalamus
° Surrounds the third ventricle
° phe relay station for sensory impulses
° pransfers impulses to the correct part of the cortex for

localization and interpretation
Ñ Hypothalamus
° Under the thalamus
° mportant autonomic nervous system center
M Helps regulate body temperature
M Controls water balance
M Regulates metabolism
Ñ Hypothalamus (continued)
° An important part of the limbic system (emotions)
° phe pituitary gland is attached to the hypothalamus
Ñ Epithalamus
° Forms the roof of the third ventricle
° Houses the pineal body (an endocrine gland)
° ncludes the choroid plexus³forms cerebrospinal fluid

Regions of the Brain: Brain Stem
Ñ Attaches to the spinal cord
Ñ Parts of the brain stem
° Midbrain
° Pons
° Medulla oblongata
Ñ Midbrain
° Mostly composed of tracts of nerve fibers
° Has two bulging fiber tracts³
cerebral peduncles
° Has four rounded protrusions³
corpora quadrigemina
M Reflex centers for vision and hearing
Ñ Pons
° phe bulging center part of the brain stem
° Mostly composed of fiber tracts
° ncludes nuclei involved in the control of breathing

Ñ Medulla Oblongata
° phe lowest part of the brain stem
° Merges into the spinal cord
° ncludes important fiber tracts
° Contains important control centers
M Heart rate control
M Blood pressure regulation
M Breathing
M Swallowing
M Vomiting
Ñ Reticular Formation
° Diffuse mass of gray matter along the brain stem
° nvolved in motor control of visceral organs
° Reticular activating system (RAS) plays a role in

awake/sleep cycles and consciousness
Regions of the Brain: Cerebellum
Regions of the Brain: Cerebellum
Ñ pwo hemispheres with convoluted surfaces
Ñ Provides involuntary coordination of body
movements
Protection of the Central Nervous System
Ñ Scalp and skin
Ñ Skull and vertebral column
Ñ Meninges
Ñ Cerebrospinal fluid (CSF)
Ñ Blood-brain barrier
Protection of the Central Nervous System
Meninges
Ñ Dura mater
° Double-layered external covering
M Periosteum³attached to inner surface of the skull
M Meningeal layer³outer covering of the brain
° Folds inward in several areas

Meninges
Ñ Arachnoid layer
° Middle layer
° Îeb-like
Ñ Pia mater
° nternal layer
° Clings to the surface of the brain
Meninges
Cerebrospinal Fluid (CSF)
Ñ Similar to blood plasma composition
Ñ Formed by the choroid plexus
Ñ Forms a watery cushion to protect the brain
Ñ Circulated in arachnoid space, ventricles, and
central canal of the spinal cord
Ventricles and Ôocation of
the Cerebrospinal Fluid
Ventricles and Ôocation of
the Cerebrospinal Fluid
Blood-Brain Barrier
Ñ ncludes the least permeable capillaries of the body
Ñ Excludes many potentially harmful substances
Ñ Useless as a barrier against some substances
° Fats and fat soluble molecules
° Respiratory gases
° Alcohol
° Nicotine
° Anesthesia
Spinal Cord Anatomy
Spinal Cord Anatomy
Spinal Cord Anatomy
Ñ nternal gray matter is mostly cell bodies
° Dorsal (posterior) horns
° Anterior (ventral) horns
° Gray matter surrounds the central canal
M Central canal is filled with cerebrospinal fluid
Ñ Exterior white mater³conduction tracts
° Dorsal, lateral, ventral columns
Spinal Cord Anatomy
Ñ Meninges cover the spinal cord
Ñ Spinal nerves leave at the level of each
vertebrae
° Dorsal root
M Associated with the dorsal root ganglia³collections of
cell bodies outside the central nervous system
° Ventral root
M Contains axons
Spinal Cord Anatomy
Spinal and Peripheral Nerves
Ñ Branching from the spinal cord are 31 pairs of
spinal nerves: 8 cervical, 12 thoracic, 5 lumbar,
5 sacral, and 1 coccygeal
Ñ phe spinal nerves contain both ascending and
descending fibers, and although there is some
overlap,each is responsible for innervation of a
particular area of the body.

are regions
of the body
innervated by
the cutaneous
branch of a
single spinal
nerve.
Pathways Between Brain and Spinal Cord
phe Reflex Arc
Ñ Reflex³rapid, predictable, and involuntary
response to a stimulus
° Occurs over pathways called reflex arcs
Ñ Reflex arc³direct route from a sensory neuron, to
an interneuron, to an effector
phe Reflex Arc

phe Reflex Arc

phe Reflex Arc

phe Reflex Arc

phe Reflex Arc

phe Reflex Arc

Simple Reflex Arc

Simple Reflex Arc

Simple Reflex Arc

Simple Reflex Arc

Simple Reflex Arc

Simple Reflex Arc

Simple Reflex Arc

Simple Reflex Arc

Simple Reflex Arc

Simple Reflex Arc

Simple Reflex Arc

pypes of Reflexes and Regulation
Ñ Somatic reflexes
° Activationof skeletal muscles
° · : Îhen you move your hand away from a
hot stove
pypes of Reflexes and Regulation
Ñ Autonomic reflexes
° Smooth muscle regulation
° Heart and blood pressure regulation
° Regulation of glands
° Digestive system regulation

Peripheral Nervous System (PNS)
Ñ Nerves and ganglia outside the central nervous
system
Ñ Nerve = bundle of neuron fibers
Ñ Neuron fibers are bundled by connective tissue
PNS: Structure of a Nerve
Ñ Endoneurium surrounds each fiber
Ñ Groups of fibers are bound into fascicles by
perineurium
Ñ Fascicles are bound together by epineurium
PNS: Structure of a Nerve
PNS: Classification of Nerves
Ñ Mixed nerves
° Both sensory and motor fibers
Ñ Sensory (afferent) nerves
° Carry impulses toward the CNS
Ñ Motor (efferent) nerves
° Carry impulses away from the CNS
PNS: Cranial Nerves
Ñ 12 pairs of nerves that mostly serve the head and
neck
Ñ Only the pair of vagus nerves extend to thoracic
and abdominal cavities
Ñ Most are mixed nerves, but three are sensory only
Cranial Nerves
PNS: phe Cranial Nerves
Y
Y
By: Kirk Odrey O. Jimenez
Ô

After the presentation, we should be able to:

° Perform a physical assessment of the neurologic system
° Document neurologic system findings
° Differentiate between normal and abnormal findings

NpRODUCpON
Ñ phe human nervous system is a unique system that allows
the body to interact with the environment as well as to
maintain the activities of internal organs.
Ñ phe nervous system acts as the main ćircuit boardµ for
every body system. Because the nervous system works so
closely with every other system, a problem within another
system or within the nervous system itself can cause the
nervous system to ´short-circuit.µ
(Dillon,2007)
Ñ A major goal of nursing is early detection to prevent
or slow the progression of disease.
Ñ So it is important for nurses to accurately perform a
thorough neurologic assessment and to understand the
implications of subtle changes in assessment findings.
By doing so, we can initiate timely interventions that
can save lives.
(Dillon,2007)
ï

ï!|
Ë Ë #
° a. Appearance/ Hygiene/ Grooming/ ° a. Ôight touch
Odor ° b. Pain
° b. Behavior ° c. Vibration
° c. Speech/ Communication ° d. Kinesthetics
° d. Ôevel of Consciousness ° e. Streognosis
° e. Memory ° f. Graphesthesia
° f. Cognitive function ° g. pwo-point discrimination
° h. point localization
Ë ï " ° i. Sensory Extinction
(12 cranial nerves) Ë $ %
Ñ a. Deep tendon reflexes
Ñ b. Superficial reflexes
Ë Ensure proper hygiene before - Sharp object such as toothpick or
sterile needle
seeing a client
- Objects to touch: coin, button, key or
paperclip
Ë Ensure all equipment is properly - Something fragrant: rubbing alcohol or
coffee
cleaned
- Something to taste: such as lemon juice,
Equipment Needed: sugar or salt
- BP cuff - puning fork - pwo taste tubes or other vials
(128 or 256 Hz) - Ophthalmoscope
- Penlight - Nonsterile
gloves
- Îisp of cotton - pongue blade
Ë ntroduce self to the client.
- Reflex hammer
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1. APPEARANCE/ HYGENE/ GROOMNG/ ODOR
a. Begin the assessment as the patient
approaches you.
b. Observe the general appearance, hygiene,
grooming and the odor of the client.
Y
ù good grooming, ù Poor hygiene
ù dress in appropriate to
ù Unpleasant or
temperature & weather,
ù no offensive or offensive body odor
unpleasant odor
ù hair well kept or tied
2. BEHAVOR
a. Assess the client·s mood and emotions
b. Observe body language and facial
expression or affect
c. Note his or her posture
Y
ù Verbal expressions match ù Ôack of facial expression
with the nonverbal ° - Possible psychological disorder
(e.g., depression or schizophrenia) or
behavior neurologic impairment affecting
cranial nerves.
ù Mood is appropriate to ù Masklike expression:
the situation ° - Parkinson·s disease.
ù Standing in upright stance ù Slumped posture:
with parallel alignment of ° - Depression if psychological in
hips &shoulders origin; or stroke with hemiparesis if
physiological in origin.
3. SPEECH/ COMMUNCApON
@ @ @
@

M Ôisten to patient·s rate and ease of speech, including enunciation.
4 @
M Show patient a picture and have him or her describe what he or she
sees.
M Have patient repeat, ´do, ray, me, fa, so, la, ti, do.µ

M Have patient say something that is committed to memory, such as days of
week or months of year.
Y
ù Speech flows easily; Ñ Hesitancy, stuttering,
stammering, unclear speech:
patient enunciates ° - Ôack of familiarity with
clearly. language, deference or shyness,
anxiety, neurologic disorder.
ù Sophistication of speech Ñ Dysphasia/aphasia:
matches age, education, ° - Neurologic problems such as
stroke.
and fluency. M Drugs and alcohol can also cause
slurred speech.
Y
ù Spontaneous speech ù mpaired spontaneous
speech:
intact. ° Cognitive impairment.
ù Motor speech intact. ù mpaired motor
speech (dysarthria):
° Problem with CN X
Y
Ñ Automatic speech Ñ mpaired automatic
intact. speech:
° Cognitive impairment
or memory
problem.
è. ÔEVEÔ OF CONSCOUSNESS
a. pest orientation to time, place, and
person
Y
ù Awake, alert, and ù Disorientation may be
physical in origin
oriented to time, ù Disorientation can also be
place, and person psychiatric in origin
(AAO x 3) (schizophrenia)
ù Responds to external ù Ôathargic or somnolent
stimuli ù Obtunded
ù Stupor
ù Coma
'ï
- A standardized objective assessment that defines
the ÔOC by giving it a numeric value.
- Most often after brain surgery
- Document as E_V_M_; for example, EèV5M6.
| -ï| ï|
# l #(((((((()
l ((((((((((*
l (((((((((((((((+
l " (((((((((((,
Best verbal response l Oriented . . . . . . . . . . . . . . . 5 Findings
K l Confused . . . . . . . . . . . . . . . è
l nappropriate . . . . . . . . . . . . 3
l ncomprehensible . . . . . . . . 2
l Unresponsive. . . . . . . . . .. . . 1
Best motor response l Obeys commands . . . . . . . .. 6 Findings
l Ôocalizes pain. . . . . . . . . . . 5
l Îithdraws from pain. . . . «. è
l Abnormal flexion . . . . . . .. . . 3
l Abnormal extension . . . . . . . 2
l Unresponsive. . . . . . . . . . . . . 1
potal______
From Îijdicks, et al, 2005, with permission.

Ñ phe three numbers are added; the total score
reflects the 4$ " (
Ñ A fully awake person = 15
Ñ Coma = 7 or less
Ñ phe GCS assesses the functional state of the brain
as a whole, not of any particular site in the brain.
(Juarez and Ôyon,1995)
ï

)
* # /040
+ # 40
, # 4 "
. # 4
# '&
MOpOR
RESPONSE
è phumbs up, fist, or peace sign to command
3 Ôocalizing to pain
2 Flexion response to pain
1 Extensor posturing
0 No response to pain or generalized myoclonus status epilepticus
BRANSpEM
REFÔEXES
è Pupil and corneal reflexes present
3 One pupil wide and fixed
2 Pupil or corneal reflexes absent
1 Pupil and corneal reflexes absent
0 Absent pupil, corneal, and cough reflex
RESPRApON
è Not intubated, regular breathing pattern
3 Not intubated, Cheyne-Stokes breathing pattern
2 Not intubated, irregular breathing pattern
1 Breathes above ventilator rate
0 Breathes at ventilator rate or apnea
5. MEMORY
@ @@

M Ask patient to repeat three numbers, such as ´è, 9, 1.µ f patient can do so,
ask her or him to repeat a series of five digits.
4
M Ask what patient had for breakfast.

M Ask patient to state his or her birthplace, recite his or her Social Security
number, or identify a culturally specific person or event, such as the name of
the previous president of the United States or the location of a natural
disaster.
Y
ù Memory problems can be benign or
Ñ mmediate, recent, signal a more serious neurologic
problem
and remote memory ° such as Alzheimer·s disease.
ù Forgetfulness - especially for
. immediate and recent events
° often in older adults.
ù Îith benign forgetfulness,
person can retrace or use
memory aids to help with
recall.

ù Pathological memory loss
Ñ as inAlzheimer·s disease
ù pemporary memory loss

Ñ may occur after head trauma.
ù Retrograde amnesia
Ñ for events just preceding illness
or injury.
ù Postconcussion syndrome
Ñ can occur 2 weeks to 2 months
after injury and may cause short-
term memory deficits.
6. COGNpVE FUNCpON
@ @@@
@ @

@4

° Ask patient to perform a simple calculation, such as
adding è x è. f successful, proceed to more difficult
calculation, such as 11/ 9.
Y
Ñ Mathematical/calcula Ñ nability to calculate at
tive ability intact and level appropriate to
appropriate for age, education, and
patient·s age, language ability
requires evaluation for
educational level, and neurologic impairment.
language facility.
4 @

@ @4
@
° Ask how many days in a week and months in a year.

° Ask patient to define familiar words such as ápple,µ
éarthquake,µ and ćhastise.µ
° Begin with easy words and proceed to more difficult ones.
° Remember to consider the patient·s age, educational level, and
cultural background.
Y
Ñ ncoherent speech
Ñ phought process ù illogical or unrealistic ideas
intact ù
ù
repetition of words and phrases
repeatedly straying from topic
Ñ suddenly losing train of thought
(examples of altered thought
processes that indicate need for
further evaluation)
Ñ nability to define familiar words
- requires further evaluation
4@

° Assessthe client to think abstractly.
° Quote a proverb and ask the client to explain it·s
meaning
Y
ù Able to generalize from Ñ mpaired ability to
specific example and
apply statement to human think abstractly
behavior.
° Dementia, delirium,
ù Children should be able to
distinguish like from unlike mental retardation,
as appropriate for their psychoses.
age and language facility.

° Observe patient·s response to current situation.
° Ask patient to respond to a situation or
hypothetical situation.
Y
Ñ Judgment Ñ mpaired judgment
appropriate and can be associated
intact. with dementia,
psychosis, or drug
and alcohol abuse.
| & ï |
| K
ï
1$# "
a. Before testing nerve c. Occlude one nostril and

function, ensure patency of hold aromatic substance such
each nostril by occluding in as coffee beneath nose.
turn and asking patient to
sniff. d. Ask patient to identify
substance.
b. Once patency is
established, ask patient to e. Repeat with other nostril.
close eyes.
Y
Ñ | is loss of sense of smell.
Ñ Patient is able to
° May be inherited and
nonpathological: chronic rhinitis,
identify substance. sinusitis, heavy smoking, zinc
deficiency, or cocaine use.
M (Bear in mind that some
° t may also indicate cranial nerve
substances may be damage from facial fractures or
unfamiliar, especially to head injuries, disorders of base of
frontal lobe such as a tumor, or
children.) artherosclerotic changes.
° Persons with anosmia usually also
have taste problems.
+(ï
/
/
K/K
1//& /
|4 "
Ask the client to read a printed material, observe the distance
between the printed material and the client·s eyes.
Use the snellen chart to check/ test:
distant vision
Color
Client should be 20 feet distant from the chart
Use an object to occlude one eye
Evaluate the vision one eye at a time
c. Evaluate the Extra Ocular Movements of the Eyes
d. Convergens & Accomodation
e. Pupillary Ôight Reflex pesting eye

movements
u - using direct and consensual pupillary reaction to light
pesting pupil
accommodation
Y
Ñ Able to read without difficulty Ñ CN deficits
Ñ Visual acuity intact 20/20, ° can occur with stroke or brain tumor.
both eyes Ñ Changes in pupillary reactions
ù & 2 Brisk ° can signal CN deficits.
constriction of pupils in reaction Ñ ncreased CP causes changes in
to light, followed by dilation and pupillary reaction.
constriction
Ñ As pressure increases, response
Ñ -may be normal or sign of becomes more sluggish until
early CN compression. pupils finally become fixed and
dilated.
*(ï K1 "
@

Ñ patient to move jaw from side to side against
resistance and then clench jaw as you palpate pesting CN V ²
contraction of temporal and masseter muscles, or to motor function
bite down on a tongue blade.
4

Ñ Ask patient to close eyes
Ñ pouch the face with the wisp of cotton
Ñ nstruct to tell you when he or she feels sensation
on the face.
Ñ Repeat the test using sharp and dull stimuli pesting CN V ²
(toothpick) sensory function
Ñ nstruct to say ´@ or

Ñ (Be random, don·t establish a pattern)
Ñ Compare both bilaterally.

@

u Gently touch cornea with cotton wisp.
u pouching cornea can cause abrasions. Alternative
approach is to: pesting corneal
> @@@@ reflex

@@
4

Y
Îeak or absent contraction unilaterally:
ù Full range of motion Ñ
° - Ôesion of nerve, cervical spine, or brainstem.

(ROM) in jaw and 15 Ñ nability to perceive light touch and
superficial pain
strength. ° - may indicate peripheral nerve damage.
ù Patient perceives light Ñ %2

° Neuralgic pain of CN V caused by the pressure
touch and superficial of degeneration of a nerve.
Corneal reflex test used in patients with
pain bilaterally. Ñ
decreased ÔOC
° - to evaluate integrity of brainstem.
)(ï K
1 "
Ñ

Ñ Ask patient to perform these movements: smile,
frown, raise eyebrows, show upper teeth, show lower
teeth, puff out cheeks, purse lips, close eyes tightly pesting CN V ²
motor function
while nurse tries to open them.
4

- pest taste on anterior two-thirds of tongue for sweet, sour,

salty.
pip of the tongue Back of tongue

Sides of back half of pesting taste
tongue sensation
@
Anterior sides and tip of
tongue
Y
ù Facial nerve intact; able Ñ Asymmetrical or impaired
to make faces. movement:
° Nerve damage, such as that
ù paste sensation on caused by Bell·s palsy or stroke.
anterior tongue intact. Ñ mpaired taste/loss of taste:
° Damage to facial nerve,
chemotherapy or radiation
° (paste decreased in older therapy to head and neck.
adults.)
(
ï K
1| "
a. Perform Îeber and Rinne tests for hearing
b. Perform watch-tick test by holding watch close to patient·s ear.
c. Perform Romberg test for balance

Îatch tick test
Ñ Nurse at the back or side of the pt.
Ñ nstruct client to stand straight, feet together, hands at the
side and eyes closed.
u (Evaluates the balancing function of the CN V)
Y
ù Hearing intact. ù Hearing loss, nystagmus,
balance disturbance,
ù Negative Romberg dizziness/vertigo:
° Acoustic nerve damage.
test. ù Nystagmus:
° CN V, brainstem, or
cerebellum problem or
phenytoin (Dilantin) toxicity.
â(ï
!!1&# K "
a. Observe ability to cough, swallow, and talk.
b.
Ñ Ask patient to open mouth and say áhµ while you depress
the tongue with a tongue blade. pesting CN X
and X ² motor
Ñ Observe soft palate and uvula. Soft palate and uvula should
function
rise medially.
c. a
4
@

@

.
Ñ pell patient that you are going to touch interior throat
Ñ then lightly touch tip of tongue blade to posterior
pharyngeal wall. pesting CN X
Ñ Observe the pharyngeal movement. and X ² motor
Ñ Ask the client to drink a small amount of water function
> Note the ease & difficulty of swallowing
> Note quality of the voice or hoarseness when speaking
Y
ù Swallow and cough reflex Ñ Unilateral movement:
-Contralateral nerve damage.
intact. °
° Damage to CNs X and X also impairs swallowing.

ù Speech clear. Ñ Changes in voice quality (e.g., hoarseness): CN X
ù Elevation and constriction damage.
° -CN X damage may also affect vital functions, causing arrhythmias
of pharyngeal musculature because vagus nerve innervates most of viscera through
and tongue retraction parasympathetic system.
indicate positive gag Ñ Diminished/absent gag reflex: Nerve damage.
Evaluate further because patient is at increased risk for aspiration.
reflex. °
Ñ mpaired taste on posterior portion of tongue:

Problem with CN X.
ü(ï !
1| # "
Ñ p

Ñ Ask patient to shrug shoulders upward against your resistance.
(prapieze muscle)
Ñ phen ask her or him to turn head from side to side against your
resistance.
Ñ (Strenoclaidomastoid msucle)
Ñ Observe for symmetry of contraction and muscle strength.

Y
ù Movement symmetrical, ù Asymmetrical
with patient moving ù Diminished
against resistance ù Absent movement
without pain. ù Pain
ù unilateral or bilateral
ù Full ROM of neck with weakness:
+5/5 strength ° Peripheral nerve CN X damage.
Õ(ï !
1# "
a. Have patient say ´d, l, n, tµ or a phrase

containing these letters.
Ñ phe ability to say these letters requires use of the tongue.
b. Ask the patient to protrude the tongue. pesting CN
Ñ Observe any deviation from midline, tumors, lesions, or atrophy. X ² motor
Ñ Now ask the patient to move the tongue from side to side. function
Y
Ñ Asymmetrical/diminished/
ù Can protrude Ñ absent movement/deviation
tongue medially. from midline/protruded
tongue:
ù No atrophy, tumors, ° - Peripheral nerve CN X
damage.
or lesions. Ñ pongue paralysis results in
dysarthria.
| #
,(&&
ÑBrush a light stimulus such as a cotton wisp over patient·s skin in
several locations, including torso and extremities.
Y
Ñ Diminished/absent cutaneous
Ñ dentifies areas perception:
Peripheral nerve damage or damage
stimulated by light °
to posterior column of spinal cord.
@
@@@

touch. Ñ
@
° # & 2ncreased sensitivity.
° & 2Numbness and tingling.
° | & 2Ôoss of sensation
+(
ÑStimulate skin lightly with sharp and dull ends of toothpick/
paper clip
ÑApply stimuli randomly and ask patient to identify whether

sensation is sharp or dull.
Ñ pouch patient·s skin with test tubes filled with hot or cold water.
ÑApply stimuli randomly, and ask patient to identify whether

sensation is hot or cold.
+
-
Y
Diminished or absent pain perception:
Ñ dentifies areas Ñ
° Peripheral nerve damage or damage to lateral

stimulated and type spinothalamic tract.
Ñ # : ncreased pain sensation.
of stimulation Ñ # 2Decreased pain sensation.
Ñ | : No pain sensation.
Ñ Diminished/absent temperature
perception:
° Peripheral nerve damage or damage to lateral
spinothalamic tract
ù .
*(K4
ÑPlace a vibrating tuning fork over a finger joint, and then over a
toe joint.
Ñ Ask patient to tell you when vibration is felt and when it stops.
Ñf patient is unable to detect vibration, test proximal areas as

well.
-
Y
Ñ Vibratory sensation Ñ Diminished/absent
vibration sense:
intact bilaterally in ° Peripheral nerve
upper and lower damage caused by
alcoholism, diabetes, or
extremities. damage to posterior
column of spinal cord.
)(3 & 4 5
Ñ Determine patient·s ability to perceive passive movement of extremities.
ÑHold fingers on sides and move up and down, and have patient identify direction of
movement.
ÑFlex and extend patient·s big toe, and ask patient to describe movement as up or
down.
u Avoid moving the patient·s finger by placing
your finger on top of the patient·s because the
patient may sense the pressure of your finger
rather than a true position change.
u f position sensation is intact distally, it is intact
proximally.
Y
Ñ Position sensation Ñ Diminished or absent
intact bilaterally in position sense:
° Peripheral nerve
upper and lower
damage or damage to
extremities. posterior column of
spinal cord.
(
ÑÎith patient·s eyes closed, place a familiar
object, such as a coin or a button, in patient·s hand,
and ask patient to identify it.
Ñ pest both hands using different objects.
Y
Ñ Stereognosis intact Ñ Abnormal findings
suggest a lesion or other
bilaterally. disorder involving
sensory cortex or a
disorder affecting
posteriorcolumn.
â(& &
ÑÎith patient·s eyes closed, use point of a closed
pen to trace a number on patient·s hand
Ñ Ask patient to identify the number.
Y
Ñ Graphesthesia intact Ñ Abnormal findings
bilaterally. suggest lesion or other
disorder involving
sensory cortex or
disorder affecting
posterior column.
-
ü('
ÑAbility to differentiate between two points of
simultaneous stimulation.
Ñ Using ends of two toothpicks/ paper clip, stimulate two points on
fingertips simultaneously.
Ñ Gradually move toothpicks together, and assess
Ñ smallest distance at which patient can still discriminate two points
(minimal perceptible distance).
Ñ Document distance and location.
Y
Ñ Discriminates between Ñ Abnormal findings
two points on fingertips suggest lesion or other
no disorder involving
Ñ more than 0.5 cm apart sensory cortex or
and on hands no more disorder affecting
than 2 cm apart. posterior column.
Õ(6
ÑAbility to sense and locate area being
stimulated.
Ñ Îith patient·s eyes closed, touch an area; then have patient
point to where he or she was touched.
Ñ pest both sides and upper and lower extremities.
Y
Ñ Point localization Ñ Abnormal findings
intact suggest lesion or other
disorder involving
sensory cortex or
disorder affecting
posterior column.
±( #%
. ÑSimultaneously touch both sides of patient·s body
at same point.
ÑAsk patient to point to where she or he was
touched.
Y
Ñ Extinction intact. Ñ dentification of stimulus
on only one side
suggests lesion or other
disorder involving
sensory cortical region in
opposite hemisphere.
REFÔEXES
$ %

$ % 0 absent
+ present but diminished
Use these + + normal
grading scales + + + increased but not necessarily pathologic
to rate the
strength of + + + + hyperactive or clonic (involuntary contraction
each reflex in and relaxation of skeletal muscle)
a deep tendon
and superficial $ $ %
reflex
assessment. 0 absent
+ present
$ $ %$
ASSESSNG REFÔEXES
,( $ %
Y
(8 $ % l ï$4 '&
$ %$$ (
Ñ Rest patient·s elbow in l 7+
your non-dominant hand,
Ñ with your thumb over
biceps tendon.
Ñ Strike your thumbnail.
4( $ % Y
Ñ Abduct patient·s arm and flex l ï$ '&
it at the elbow. % 4'(
Ñ Support the arm with your l 7+
nondominant hand.
Ñ Strike triceps tendon about 1
to 2 inches above olecranon
process, approaching it from
directly behind.
( $ % Y
l ï$9 '&
Ñ Have sit with % $0 (
legs dangling. l 7+
Ñ Strike tendon directly
below patella..
(|& $ % Y
Ñ Have patient lie supine or l $ %$$(
sit with one knee flexed. l 7+
Ñ Holding patient·s foot
slightly dorsiflexed, strike
Achilles tendon.
Ñ phen quickly but gently hit
it with a hammer
( $|0 ï
Y
Ñ l f you get è reflexes l Y
(++++) while
supporting leg and
foot, quickly dorsiflex
foot.

l |4 :& 2
" ; & " & &
&#;' /&| 8<
# (
l # " $ % '&2
= / & (
l &#&$ $" $
(
+( $ $ % Y
(|4 $ % Ñ ï$
4(4"
Ñ Stroke patient·s abdomen '(
diagonally from upper and l |0 (
lower quadrants toward
umbilicus.
Ñ Gently stroke skin around
anus with gloved finger.
4(ï $ % Y
l
Ñ Gently stroke inner
aspect of a male·s
thigh.
(84" $ % Y
l 84"
Ñ Gently apply pressure (
over bulbocavernous
muscle on dorsal side
of penis.
( $ %4840> 5
Y
Ñ Stroke sole of patient·s l %$ (
foot in an arc from
lateral heel to medial
ball.
Assessing the Cerebellar Function
,(8
( (
Ñ Observe as the person walks 10-20 feet, turns, and
returns to the starting point.
Y
ù Person moves with a ù Stiff, immobile posture.
sense of freedom. Staggering or reeling. Îide
base of support
ù Gait is smooth, rhythmic, ù Ôack of arm swing or rigid arms
and effortless ù Unequal rhythm of steps.
ù Opposing arm swing is Slapping of foot. Scraping of toe
coordinated of shoe
ù Ataxia ² uncoordinated or
ù phe turns are smooth unsteady gait.
Perform -0
Ñ ask the person to walk a straight line in a
heel-to-toe fashion.
Ñ phis decreases the base of support and will accentuate any
problem with coordination.
Y
ù Crooked line walk
Ñ Person can walk ù Îidens base to maintain
straight and stay balance
ù Staggering, reeling, loss of
balanced balance
ù An ataxia that did not appear
now. nability to tandem walk is
sensitive for an upper motor
neuron lesion, such as multiple
sclerosis.
&'0 4 &
Ñ Ask the person to perform a shallow knee bend or
hop in place, first on one leg, then the other.
Ñ this demonstrates normal position sense, muscle strength, and
cerebellar function.
( @
@
@

4
4( 4 >
Ñ #& > 40/'&
& # (
Ñ##& >$/ &
'& # (
Ñ #&& & & $ &
Y
Ñ Sways, falls, widens base of feet to
Ñ Negative Romberg avoid falling
" Romberg sign
test Ñ
° Ôoss of balance that occurs when

closing the eyes.
° Occurs with cerebellar ataxia
(multiple sclerosis, alcohol
intoxication)
° Ôoss of proprioception, and loss
of vestibular function
+(ï 0 "
( | " 4 |5
Ñ Ask the person to pat the knees with

both hands, lift up, turn hands over,
and pat the knees with the backs of
the hands.
Ñ phen ask to do this faster.
Y
Ñ done with equal Ñ Ôack of coordination
turning and quick Ñ
rhythmic pace ° Slow, clumsy, and sloppy
response
° occurs with cerebellar
disease
4(
Ñ Îith the persons eyes open, ask that he or
she use index finger to touch your finger, then
his or her own nose.
Ñ After a few times move your finger to a
different spot.
Y
Ñ Movement is smooth Ñ
° clumsy movement with
and accurate overshooting the mark
disorder
Ñ à
° constant deviation to one side
(
Ñ Ask the person to close the eyes and
to stretch out the arms.
Ñ Ask the person to touch the tip of his
or her nose with each index finger,
alternating hands and increasing
speed.
Y
Ñ Done with accurate Ñ Misses nose.
and smooth Ñ Îorsening of
movement coordination when the
eyes are closed
disease
DAGNOSpC pESpS

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Magnetic Resonance maging

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Cerebral Angiography

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Ôumbar puncture
u

u
Ôumbar Puncture
Ôumbar Puncture > Maintain position, usually
lateral horizontal with knees to
$ s carried out by inserting a chest, chin on chest.
needle into the lumbar > Obtain signed consent.
subarachnoid space to > Explain the procedure.
withdraw CSF for diagnostic > Observe for complication
or therapeutic purposes. following the procedure.

> Keeping the patient in
$ phe needle is usually
position overnight may reduce
inserted between Ôè and Ô5. the incidence of headache.
·

$(

>1"

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Measure the action

potential and electrical
activities of peripheral
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sources
Ñ Dillon, Patricia. Nursing Health Assessment. 2nd Ed. F.A. Davis.
2007
Ñ Jarvis, Carolyn. Physical Examination and Health Assessment.
3rd ed. New York: Î.B. Saunder Company.2000
Ñ Bickley. Ôyn and Hoekenan, Robert. Bate·s Guide to Physical
Examination and History paking. 7th ed. New York: Ôippincott
Îilliams and Îilkins. 1999
Ñ Estes, Mary Ellen Zator. Health Assessment & Physical
Examination. 3rd ed. Delmar Ôearning. 2006
COMMON HEAÔpH
PROBÔEMS OF pHE
YOUNG ADUÔp
Multiple Sclerosis
MS is:
Ë chronic, degenerative disease of the central nervous system that is
characterized by # of the 2
brain and
spinal cord.
Ë Gen. characterized by exacerbations and remisions (relapsing-remitting
type0
Ë Although the cause of MS is unknown, it appears to be related to
autoimmune disorder and viral infections.
Ë commonly appears during adulthood (ages 20 to è0).
Ñ Î
Ë Areas of the CNS most commonly affected brainstem, cerebrum, cerebellum,
optic nerves, and the spinal cord.
Process of Demylination
Pathophysiology
V

! "
#

V

"
$ % % % &
' (
)

$*++,-..&
+'-!/'+0)''+V/!.-
$.*-)01.2-)&
Assessment
Ë Sign and symptoms of MS is characterized by remissions and exacerbation of
symptoms.
Ë Symptoms vary depending on the area of the CNS involved, but generally
include:
ù Visual disturbances (diplopia, partial or total loss of vision, nystagmus)
ù Scanning speech (slow, monotonous, slurred)
ù premors
ù Îeakness/numbness of the extremities
ù Fatigue
ù ncreased susceptibility to URp
ù Dysphagia
ù Ataxic gait
Diagnostic pest
Ë Ôumbar Puncture-total CSF protein is normal; gG (gamma
globulin is elevated- gG reflects hyperactivity of the immune
system due to chronic demyelinaton)
Ë EEG-abnormalities in brain waves
Ë Cp scan/ MR reveals multifocal white matter lesion
Ë Myelogram
Ë Skull x-ray
Nursing Diagnoses for MS:
° Risks:neffective breathing pattern; airway clearance;
impaired³swallowing, physical mobility, skin integrity;
altered nutrition; urinary incontinence; constipation
nterventions for MS:
phere is no specific treatment for MS.
preatment includes:
Ë physical therapy- @ @4
4@
@

@ @
Ë speech therapy- @@
@@
Ë drug therapy
ù 4 / % & /ï5

ù %48$ 5
ù | / / w
ù ' ï|

Nursing Responsibilities/ Considerations for MS:
Ë Provide regular activity, and relaxation.
Ë Assist with @
@ : muscle stretching, relaxation
and coordination exercise, walking exercise.
Ë Encourage well balanced, high fiber diet.
Ë Force fluids to prevent constipation.
Ë .
Ë Provide skin care to prevent skin breakdown.
Nursing Responsibilities/ Considerations for MS cont.:
Ë à

Help patient establish daily routine, and help family
understand patient·s changes in personality and physical
capabilities.
nform the pt that exacerbations are unpredictable,
necessitating physical & emotional adjustments in lifestyle
-
-
-
Evaluate
Ñ Respiration; nutrition; ADÔs; skin; bowel elimination;
urinary incontinence
Myasthenia Gravis
¢ neuromuscular disorder that results in the
at the MYONEURAÔ JUNCpON 2
2
Ë Failure of transmission is due to #&
ËÎ

Ë
M secretion and increased & at the nerve ending.
Ë Autoimmune disease.
° Characterized by progressive weakness and abnormal
fatigability of the skeletal muscles.
° Commonly affects muscles innervated by the cranial
nerves (face, lips, tongue, neck, and throat)
° Exacerbated by exercise & repetitive movement
° Occurs along with thymic abnormalities in 75% of pts
Pathophysiology:
Ñ pransmission of nurve impulses at the neuromuscular
junction FAÔS.
Ñ Antireceptor antibodies block, weaken, or reduce
the number of acetylcholyne Ach receptors
available at each neuromuscular juction,thereby
impairing the muscle depolarization necessary for
movement
Myasthenia Gravis
@
Ñ Autoimmune response leading to ineffective
acetylcholine release and inadequate muscle fiber
response to Ach.

@
° @
° @
° @
|
? :&&# 8
ù Skeletal muscle weakness, fatigue Ñ due to impaired neuromuscular
transmission
ù Îeak eye closure,ptosis, diplopia, Ñ due to impaired neuromuscular
transmission to the cranial nerves
supplying the eye muscles
ù ´snarl smileµ (smiles slowly) Ñ mpaired transmission of the cranial

ù Masklike facial expression; mpaired nerves innervating the facial muscles
speech; drooling
ù Îeakened respiratory muscles Ñ Due to impaired neuromuscular
transmission to the diaphragm due to

@ @

4 4

@
@ @

@
loss of ACh receptors in the
appropriate junctions
Myasthenia Gravis

"
Diagnostic pest
Ë
(Edrophonium Chloride pest)
ù Short acting cholinergic is administered.
ù Reveals is observed (+ pensilon pest)
within 30-60 secs after V injectio of edrophonium (tensilon) or
Neostigmine (Prostigmin), lasting up to 30 mins.

4

@ with neural stimulation at the specific
muscle fiber-

$#& "
Ñ |& drugs, such as neostigmine and pyridostigmine- to
counteract fatigue and muscle weaknes and allow for about 80% of normal
muscle
°
@
@
@ @

@ 4

Ñ Plasmapheresis (Removing the plasma from the blood)
Ñ
" & # with corticosteroids, azathioprine (muran) ² to
decrease the immune response toward Ach receptors at the neuromuscular
junction
Ñ gG during acute relapses- to suppress the immune system
Ñ phymectomy- to remove thymomas
Ñ pracheostomy, suctioning to remove secretions
Nursing Goals and nterventions
Ë Establish neurologic and respiratory baselines
Ë Assess swallowing / gag reflex before feeding the client.
Ë Plan exercise, meals, patient care & activities to make the most of energy
peaks. · @ @ 4@
@
@

@

Ë Start meal with cold beverage.

Ë Administer medication at precise time to prevent relapses.
Ë Protect the client from falls.
Ë Provide adequate ventilation.
Ë Avoid exposure to infection, stree, strenous exercise, and needless exposure to
the sun r cold.
Ë Frequent rest periods.
Ë Be prepared to give atropine for anticholinesterase overdose or toxicity
Ë Aerosol, pesticides/cleaners should also be avoided,
Ë Avoid alcohol, tonic water, and cigarette smoke.
Ë Pharmacotherapy
ù Cholinergics (Anticholinesterase)
> Neostigmine (Postigmin)
> Pyridostigmin (Mestinon)
> Ambenomium (Mytelase)
ù Glucocorticoids
ù Antacids
Client with Huntington·s Disease (chorea)
Ñ Progressive, degenerative inherited neurologic
disease
Ñ characterized by increasing dementia and chorea
(rapid, jerky involuntary movements)
Ñ Cause unknown
Ñ No cure
Ñ Usually asymptomatic until age of 30 ² è0
Pathophysiology
Ñ involves destruction of cells in basal ganglia and
other brain areas, decrease in acetylcholine
Manifestations
Ñ Abnormal movement and progressive dementia
Ñ Early signs are personality change with severe depression,
memory loss; mood swings, signs of dementia
Ñ ncreasing restlessness, worsened by environmental stimuli and
emotional stress; arms and face and entire body develops
choreiform movements, lurching gait; difficulty swallowing,
chewing, speaking
Ñ Slow progressive debilitation and total dependence
Ñ Death usually results from aspiration pneumonia or another
infectious process
Collaborative Care
Ñ almost always requires long-term care
Diagnostic pests
Ñ genetic testing of blood
Medications
Ñ Antipsychotic (phenothiazines and butyrophenones)
to restore neurotransmitters
Ñ Antidepressants
Nursing Care
Ñ Very challenging: physiological, psychosocial and
ethical problems
Ñ Genetic counseling
Nursing Diagnoses
Ñ Risk for Aspiration
Ñ mbalanced Nutrition: Ôess than body requirements
Ñ mpaired Skin ntegrity
Ñ mpaired Verbal Communication
Home Care
Ñ Referral to agencies to assist client and family,
support group and organization
Client with Amyotrophic Ôateral Sclerosis
(AÔS)
Ñ Progressive, degenerative neurologic disease
characterized by weakness and wasting of muscles without
sensory or cognitive changes
Ñ Several types of disease including a familial type; onset is
usually between age of è0 ² 60; higher incidence in
males at earlier ages but equally post menopause
Ñ Physiologic problems involve swallowing, managing
secretions, communication, respiratory muscle dysfunction
Ñ Death usually occurs in 2 ² 5 years due to respiratory
failure
Amyotrophic Ôateral Sclerosis
Pathophysiology
Ñ Degeneration and demyelination of motor neurons in
anterior horn of spinal cord, brain stem and
cerebral cortex
Ñ nvolves upper and lower motor neurons
Ñ Reinnervation occurs in the early course of disease,
but fails as disease progresses
Manifestations
Ñ nitial: spastic, weak muscles with increased DpRs (UMN
involvement); muscle flaccidity, paresis, paralysis, atrophy (ÔMN
involvement); clients note muscle weakness and fasciculations
(twitching of involved muscles); muscles weaken, atrophy; client
complains of progressive fatigue; usually involves hands,
shoulders, upper arms, and then legs
Ñ Atrophy of tongue and facial muscles result in dysphagia and
dysarthria; emotional lability and loss of control occur
Ñ 50% of clients die within 2 ² 5 years of diagnosis, often from
respiratory failure or aspiration pneumonia
Collaborative Care
Ñ Evaluation to make the diagnosis
Ñ Referrals for home health support;
Ñ Client needs to make decisions regarding
gastrostomy tube, ventilator support
Diagnostic pest
Ñ pesting rules out other conditions that may mimic early
AÔS such as hyperthyroidism, compression of spinal
cord, infections, neoplasms
Ñ EMG to differentiate neuropathy from myopathy
Ñ Muscle biopsy shows atrophy and loss of muscle fiber
Ñ Serum creatine kinase if elevated (non-specific)
Ñ Pulmonary function tests: to determine degree of
respiratory involvement
Medications
Ñ Rilutek (Riluzole) antiglutamate
Ñ Prescribed to slow muscle degeneration
Ñ Requires monitoring of liver function, blood count,
chemistries, alkaline phosphatase
Nursing Care
Ñ Help client and family deal with current health
problems
Ñ Plan for future needs including inability to
communicate
Nursing Diagnoses
Ñ Risk for Disuse Syndrome
Ñ neffective Breathing Pattern: may require
mechanical ventilation and tracheostomy
Home Care
Ñ Education regarding disease, community resources
for health care assistance and dealing with
disabilities
Client with Creutzfeldt-Jakob disease
Ñ Rapid progressive degenerative neurologic disease causing brain
degeneration without inflammation
Ñ pransmissible and progressively fatal
Ñ Caused by prion protein: transmission of prion is through direct
contamination with infected neural tissue
Ñ Rare in USA affecting persons 55 - 7è
Ñ Variant form of CJD is ´mad cow diseaseµ: believed transmitted by
consumption of beef contaminated with bovine form of disease; none
identified in USA as of yet
Ñ Pathophysiology: spongiform degeneration of gray matter of brain
Manifestations
Ñ Onset: memory changes, exaggerated startle reflex,
sleep disturbances
Ñ Rapid deterioration in motor, sensory, language
function
Ñ Confusion progresses to dementia
Ñ perminal states: clients are comatose with
decorticate and decerebrate posturing
Diagnostic pests
Ñ Clinical pictures, suggestive changes on EEG and Cp
scan
Ñ Similar to Alzheimers in early stages
Ñ Final diagnosis made on postmortem exam
Nursing Care
Ñ Use of standard precautions with blood and body
fluids
Ñ Support and assistance to client and family
Client with Guillain-Barre Syndrome
Ñ Acute inflammatory demyelinating disorder of peripheral nervous system
characterized by acute onset of motor paralysis (usually ascending)
Ñ Cause is unknown but precipitating events include G or respiratory infection
prior, surgery, or viral immunizations
Ñ 80 ² 90% of clients have spontaneous recovery with little or no disabilities
Ñ è ² 6% mortality rate, and up to 10% have permanent disabling weakness
Ñ Characterized by progressive ascending flaccid paralysis of extremities with
paresthesia and numbness
Ñ 20 % require mechanical ventilation due to respiratory involvement
Guillain-Barre Syndrome
Pathophysiology
Ñ Destruction of myelin sheath covering peripheral
nerves as result of immunologic response
Ñ Demyelinization causes sudden muscle weakness and
loss of reflex response
Manifestations
Ñ Most clients have symmetric weakness beginning in lower extremities
Ñ Ascends body to include upper extremities, torso, and cranial nerves
Ñ Sensory involvement causes severe pain, paresthesia and numbness
Ñ Client cannot close eyes
Ñ Paralysis of intercostals and diaphragmatic muscle can result in
respiratory failure
Ñ Autonomic nervous system involvement: blood pressure fluctuations,
cardiac dysrhythmias, paralytic illness, SADH, urinary retention
Ñ Îeakness usually plateaus or starts to improve in the fourth week
with slow return of muscle strength
Collaborative Care
Ñ Ensuring adequate respiration and oxygenation
Ñ Preventing complications due to immobility
Diagnostic pests
Ñ diagnosis made thorough history and clinical
examination; there is no specific test
Ñ CSF analysis: increased protein
Ñ EMG: decrease nerve conduction
Ñ Pulmonary function test reflect degree of
respiratory involvement
Medications
Ñ supportive and prophylactic care
Ñ Antibiotics
Ñ Morphine for pain control
Ñ Anticoagulation to prevent thromboembolic
complications
Ñ Vasopressors as needed
Surgery
Ñ may need tracheostomy, if prolonged ventilator
support
Plasmapheresis
Ñ may be helpful, if used early in the course of
disease
Dietary Management
Ñ usually requires enteral feeding or total parenteral
nutrition
Physical and Occupational pherapy
Ñ usually require long-term rehabilitation to regain
maximum muscle strength
Nursing Care
Ñ involves acute neurological and critical care nursing
and rehabilitation
CRANAÔ NERVE DSORDER: prigeminal Neuralgia
(pic Douloureux)
Ë Neurologic disorder affecting the 5th cranial nerve.

Possible fifth cranial nerve root compression
Ë Manifested by excruciating, recurrent paroxysms of
sharp, 44$ along the trigeminal
nerve.
- Vascular compression and pressure
(cause by aging)
- Demyelination of trigeminal root
- Ôikely to occur on 5th and/or 6th decade
of life
- Common to women and with MS
Areas innervated by the three branches of the
trigeminal nerve
Signs & Symptoms:
- Burning or knife-like pain lasting for 1-15 minutes,
usually over the lip or chin and in the teeth.
- Pain precipitated by the stimulation of trigger zones
during activities such as brushing the hair and eating, or
when sitting in a cold draft.
- Sudden closure of an eye
- pwitching of the mouth
Medications:
- Anti-seizure meds
Carbamazepine (pegretol)
- po decrease transmission of nerve impulses to the nerve terminals.
Nursing Responsibility:
- paken with meals
- Serum level should be monitored
- Monitor for bone marrow depression (prolonged use of
Carbamazepine)
Carbamazepine toxicity
- Drowsiness
- Nausea & vomiting
- Dizziness
Ñ Aplastic anemia could occur.
Other meds:
- Gabapentin
- Baclofen ² control pain associated with spasm
- Dilantin ² oral hygiene needed.
Nursing Diagnosis:
- Pain related to nerve root
damage.
- Self-care deficit
- Activity intolerance
Surgical management:
- micro-vascular decompression
- radio frequency thermal coagulation
- percutaneous balloon micro-
compression
Nursing ntervention:
- preventing pain
- providing post-op care
Ñ nstruct patient not to rub eyes
Ñ Artificial tears or eye drops to prevent
dryness of the eyes
Ñ Chew on unaffected area
BEÔÔ· PAÔSY
Ñ Unilateral inflammation of the 7th cranial nerve.
Ñ Results in weakness or paralysis of the facial
muscle on the affected side
Ñ Affects all age ² groups, but occurs most
commonly in patients under age 60
Ñ Onset is rapid but 80 ² 90% of all patients, it
subsides spontaneously, complete recovery in 1
to 8 weeks
Ñ Causes:
- Hemorrhage
- Vascular ischemia
- Viral infection/disease (Herpes simplex,
Herpes zoster)
- Autoimmune disease
Bell·s Palsy
Pathophysiology:
Ñ An inflammatory reaction occurs around cranial nerve V,
usually at the internal auditory meatus, where the nerves
leave bony tissue
Ñ phe inflammatory reaction produces a conduction block
that inhibits appropriate neural stimulation to the muscle
by the motor fibers of the facial nerve, resulting in the
characteristic unilateral or bilateral facial weakness.
Pathophysiologic Chanes/ S & S:
Ñ Unilateral facial weakness
Ñ Drooping mouth & drooling saliva
Ñ Ôost of taste
Ñ Smooth forehead appearance
Ñ mpaired ability to close the eye on the weak side
Ñ Bell·s phenomenon-Upward rolling of the eyes when
attempting to close them
Ñ Excessive tearing
Ñ Ringing in the ear
Signs & Symptoms:
- Facial muscle distorted due to paralysis or
weakness
- ncrease lacrimation or tears
- Painful sensation on the face
- Speech difficulties
- Patient unable to eat on the affected side
Nursing Diagnosis:
- Pain r/t inflammed nerve
- mpaired verbal communication r/t
speech difficulties
- Body image disturebance r/t facial
paralysis
Medications:
- Corticosteroids ² reduces facial nerve
edema & improves nerve conduction
(Prednisone)
- Analgesic ² for pain
Nursing Considerations
Dependent:
- hot compress ² causes vasodilation
-electrical stimulation ²avoid atrophy of
facial muscles
ndependent:
- Protection of eye from injury
- Protective shield at night
- Massage several times a day to
regain muscle strength (Upward motion)
- peach patient facial exercises
Ñ Give patient frequent and complete mouth
care. Remove the residual food that collects
between thecheeks and gums
Ñ Provide support and reassure the patient
that recovery is likely within 1 ² 8 weeks
Ñ Assess the effectiveness of pain medication
Ñ Îatch for adverse effects of steroids use

Ñ Apply moist heat to the affected side of the face-to reduce pain
Ñ Prevent excessive wt loss:
° -have him chew on unaffected side of his mouth
° -provide a soft, nutritionally balanced diet, eliminating hot foods & fluids
° -apply a facial sling to improve lip alignment
Ñ Offer psychological support
à
Ñ Corneal abrasion
Ñ nfection (masked by steroid use)
Ñ Poor functional recovery
Diagnostic pests:
-based on clinical presentation
MR-rules out tumor
Electromyography- 10 days after the onset of S/S
ï &4 $& |
CEREBRO-VASCUÔAR DSORDER:Stroke/Cerebrovascular Accident
(CVA)
Disruption of the Blood Supply to the Brain-
-sudden loss of neurologic funtion
Middle Cerebral Artery is commonly affected.

phe second most frequently affected is the internal carotid artery.

@@
1. ischemic (a thrombus or embolus blocks circulation
2. hemorrhagic (a blood vessel ruptures)
Risk factors:
Ë ncreased alcohol intake or cocaine
Ë Cardiac disease
Ë Cigarrette smoking
Ë DM
Ë Familial hyperlipidemia
Ë Family history of stroke
Ë Hx of pA
Ë HPN
Ë Obesity,sedentary lifestyle
Ë Sickle cell disease
Ë Use of hormonal contraceptives
Causes of Stroke:
schemic
ù p occluded bld flow caused by thrombosis of the cerebral arteries supplying the brain or
the intracranial

ù phe most frequent cause of CVA
ù phe most common cause of cerebral thrombosis is atherosclerosis; usually affecting elderly persons.
ù pends to occur during sleep or soon after arising.
ù phis may tend to occur among clients with DM, and hypertension.
ù ·
ù phe second most common cause of CVA.
ù Most commonly affecting younger people.
ù Most frequently caused by Rheumatic Heart Disease and M.
ù Symptoms occur at any time and progress rapidly.
Causes of Stroke: Hemorrhagic Stroke
ù ÷ ÷
ù mpaired cerebral perfusion from hemorrhage causes
infarction, & the bld itself as a space-occupying mass,
exerting pressure on the brain tissues
ù Hemorrhage from an intracranial artery or vein, such as
HPN, ruptured aneurysm, trauma, hemorrhagic disorder, or
septic embolism.
p
ù Refers to transient cerebral ischemia with

@ episodes of neurologic dysfunction.
ù Manifestation include contralateral weakness of the lower
portion of the face, fingers, hands, arms, and legs;
dysphagia, and sensory impairment.
ù Stoke in evolution refers to development of a neurologic
deficit over several hours to days
Pathophysiologic Changes in CVA:-specific manifestations are determined by
the cerebral artery affected, the brain tissue supply by that of that vessel, and the adequacy of
the collateral circulation
Ñ |&, #&; "$ $; and &

of affected side (more severe in face & arms)- resulting from
thrombosis or hemorrhage of middle cerebral artery
Ñ Îeakness, paralysis, numbness; sensory changes; altered ÔOC;
bruits over carotid artery; and & & caused by thrombosis
or hemorrhage of carotid artery
Ñ Îeakness, paralysis, numbness around lips & mouth; visual
field deficits, diplopia, nystagmus; poor coordination, dizziness,
dysphagia, slurred speech; amnesia, and ataxia resulting from
thrombosis or hemorrhage of vertebrobasilar artery.
Ñ ï$, weakness, numbness; urinary incontenece;
impaired motor & sensory functions; and #
& caused by thrombosis or hemorrhage of
anterior cerebral artery.
Ñ Visual field deficits; sensory impairments; dyslexia;
cortical blindness and coma resulting from thrombosis
or hemorrhage of posterior cerebral artery.
Assessment of CVA:
check for:
Ë S&S of increased CP.
Ë Perceptual defects
Ë Aphasia
Ñ Unstable respiration
Ñ Severe headache
Ñ Diagnostic procedure results
Ñ Unilateral neglect
Diagnostic Findings:
Ñ Cp scan- identifies an ischemic stroke within the first
72 hours of symptom onset or evidence of a
hemorrhagic stroke (lesions >1 cm immediately)
Ñ MR-assists in identifying areas of ischemia or
infarction and cerebral swelling
Ñ Others: angiography, carotid duplex scan,EEG
Complications:
Ñ Hemiplegia ² @@@
Ñ Dysarthria -

@
4 @
@
@

Ñ Cognitive impairement- Aphasia ² Ñ Kinesthesia ²

@4

@ 4
@@
@
@4
Ñ ncontinence ² maybe fecal/urine;
@ inability to control urination or defecation
Ñ Shoulder pain
Ñ Apraxia ² can move but cannot do
the purpose; inability to perform Ñ Contractures
complex movements Ñ Fluid imbalances
Ñ Sensory impairement-Visual Ñ Cerebral edema
changes ² homonymous Ñ Aspiration
hemianopsia; Agnosia ²
Ñ Altered ÔOC

Ñ nfections such as pneumonia

Nursing Considerations:CVA
Ë chest pain, shortness of breath, dusky
color, tachycardia, fever, and change
f the pt is unconscious; vomiting- lateral in sensorium
position to prevent aspiration of
saliva Ë

Ë
Monitor BP, ÔOC, pupillary changes, Ë ÿ ·
motor and sensory functions, speech, Monitor and O.
skin, color, temp.
Monitor pt for s/s of increased CP and Administer VF as ordered
nuchal rigidity or flaccidity Offer bedpan /urinal
Ë Î Ë .

Ë ·
Check for gag reflex before offering small oral feedings of semisolod food
peach the client to chew on the unaffected side.
f oral feeding is not possible,pPN, NGp feeding, gastrostomy feeding.
Ë p , at least q 2 hrs to prevent pneumonia.

Ë à !
for affected & unaffected sides.
Ë
Ë à nstill meds as ordered; patch the affected eye
if the pt can·t close eyelid.
Ë
$ Care of the client with Hemianopsia.
ù Approach from the unaffected side.
ù Place articles on the unaffected side.
Ë à

$ Care for the client with aphasia.
ù Say one word at time.
ù Give simple commands.
ù Allow the client to verbalize, no matter how long it takes him
p "

|
Ñ peach the pt to comb hair, to dress, & to wash
Ñ Obtain assistive devices ( through the aid of Pp/Op) such as
walkers, hand bars by the toilet, and ramps as needed
Ñ Be aware that the pt has a unilateral neglect, in which he fails
to recognize that he ha a paralized side- show him how to
protect his body from harm
Ñ Emphasize importance of regular ff-up visits
ANEURYSM
Ñ Dilation involving an artery
formed at a weak point in the
vessel wall
ANEURYSM
Ñ Saccular= when one side of the vessel is affected
Ñ Fusiform= when the entire segment becomes dilated

RSK FACpORS
1. Atherosclerosis
2. nfection= syphilis
3. Connective tissue disorder
è. Genetic disorder= Marfan·s Syndrome
PApHOPHYSOÔOGY
Damage to the intima and mediaÑ weaknessÑ
outpouching
Dissecting aneurysmÑ tear in the intima and media

with dissection of blood through the layers
ASSESSMENp
1. Asymptomatic
2. Pulsatile sensation on the abdomen
3. Palpable bruit
ÔABORApORY:
u Cp scan
u Ultrasound
u X-ray
u Aortography
Medical Management:
u Anti-hypertensives
u Synthetic graft
Nursing Management:
u Administer medications
u Emphasize the need to avoid increased abdominal
pressure
u No deep abdominal palpation
u Remind patient the need for serial ultrasound to
detect diameter changes
à 22
Ñ Slowly progressive degenerative disorder
of basal ganglia function that results in variable
combinations of tremor, rigidity, and bradykinesia
Ñ Onset usually after age è0
Ñ men>women
Parkinson·s Disease: deficient in dopamine
Causes:
Exact cause unknown
Ñ Possible causes:
Ñ Dopamine deficiency, which prevents affected brain cells

from performing their nomal inhibitory function in the CNS
Ñ Exposure to toxins( manganese dust or carbon monoxide)
Ñ Repeated trauma to the brain
Ñ Stroke
Ñ Brain tumors
Pathophysiology:
Ñ Dopamine neurons degenerate, causing loss of available
dopamine
Ñ Dopamine deficiency prevents
Ñ Affected brain cells from performing their normal
inhibitory function
Ñ Excess excitatory Ach occurs at the synapses
Ñ Nondopamineric receptors are also involvd
Ñ Motor neurons are depressed
Pathophysiologic changes/ S&S:
Ñ Muscle rigidity, akinesia, and insidious tremor beginning in the fingers
(UNÔApERAÔ PÔÔ_ROÔÔ pREMOR) secondary to loss of inhibitory dopamine
activity at the synapse- increase during stres or anxiety; decreases with
purposeful movement & sleep
Ñ Muscle rigidity with resistance to passive
Ñ ¢¢ 2
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Pathophysiologic changes/ S&S:
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Alzheimer·s Disease
Ñ Form of dementia characterized by progressive,
irreversible deterioration of general intellectual
functioning
Ñ Begins with memory loss, initially subtle until progresses
to being more noticeable; course includes deteriorating
cognition and judgment with eventual physical decline
and total inability to perform ADÔ
Risk factors
Ñ older age
Ñ female
Ñ family history
Ñ Exact cause is unknown; theories include loss of
transmitter stimulation, genetic defects, viral and
autoimmune cases
Îarning signs include
Ñ Memory loss affecting ability to function in job
Ñ Difficulty with familiar tasks
Ñ Problems with language, abstract thinking
Ñ Disorientation, changes in mood and personality
pypes and Changes in brain
Ñ Familial (follows inheritance pattern) and sporadic
Ñ Early-onset (<65)
Ñ Older-onset (>65)
Ñ Ôoss of nerve cells and presence of neurofibrillary
tangles and amyloid plaques
Ñ Progressive brain atrophy
Manifestations : Stage
Ñ Appears healthy and alert
Ñ Cognitive deficits are undetected
Ñ Subtle memory lapses, personality changes
Ñ Seems restless, forgetful, uncoordinated
Stage
Ñ Memory deficits more apparent
Ñ Ôess able to behave spontaneously
Ñ Îandering behavior, deterioration in orientation to time and place
Ñ Changes in sleeping patterns, agitation, stress
Ñ prouble with simple decisions
Ñ Sundowning: increased agitation, wandering, disorientation in
afternoon and evening hours
Ñ Echolalia, scanning speech, total aphasia at times, apraxia,
astereognosis, inability to write
Ñ Becomes frustrated and depressed
Stage
Ñ ncreasing dependence with inability to
communicate, loss of continence
Ñ Progressive loss of cognitive abilities, falls, delusion,
paranoid reactions
Ñ Average life expectancy is 7 years from diagnosis
to death, often from pneumonia, secondary to
aspiration
Collaborative Care
Ñ No cure
Ñ Supportive care for client and family
Diagnostic pests
Ñ Diagnosis by ruling out other conditions including
depression, hypothyroidism, infection, stroke
Ñ EEG shows slow pattern in later stages of disease
Ñ MR and Cp scan: shrinkage of hippocanthus
Ñ Positron emission tomography (PEp):visualizes brain activity
and interactions
Ñ Folstein Mini-Mental Status: instrument reflecting loss of
memory and cognitive skills
Medications
Ñ Cholinesterase inhibitors used to treat mild to moderate dementia
Ñ pacrine hydrochloride (Cognex)
Ñ Donepezil hydrochloride (Aricept)
Ñ Rivastigmine (Exelon)
Ñ Medications to treat depressions
Ñ pranquilizers for severe agitation
Ñ phioridazine (Mellaril)
Ñ Haloperidol (Haldol)
Ñ Antioxidants: vitamin E, anti-inflammatory agents, estrogen
replacement therapy in women
Complementary pherapy
Ñ Massage, herbs, ginko biloba, Coenzyme Q10
Ñ Art therapy, music, dance
Nursing Care &Health Promotion
Ñ ntensive, supportive nursing interventions directed at
physical and psychosocial responses to illness
Ñ Maintain functional abilities
Ñ Maintain safety of client and caregiver
Nursing Diagnoses
Ñ mpaired Memory
Ñ nclude written or verbal reminders
Ñ Use cues to deal with memory loss
Ñ Chronic Confusion
Ñ Anxiety
Ñ Hopelessness
Ñ Caregiver Role Strain
Home Care
Ñ Education regarding disease, anticipation of needs,
use of memory cues, support groups and peer
counseling
Ñ Refer to home health agencies, family support,
group support
ï &4 &|& $
SEZURE DSORDER
Ñ Sudden explosive and disorderly discharge of cerebral
neurons
Ñ abnormal and excessive discharge of neurons in the brain
Ñ pypes of seizures:
° 2
° ¢
°
° ¢ ¢
Petit mal
Ñ No aura
Ñ 10-20 seconds
Ñ Common to children as well as adult
Ñ Ôittle tonic-clonic movements
Ñ Cessation of ongoing physical activities
Jacksonian
Ñ Îith aura
Ñ Îith organic lesion
Ñ Group of muscle affectation
Psychomotor Seizure
Ñ Îith aura
Ñ Îith psychiatric involvement
Ñ Characterized with mental clouding
Ñ Violence, antisocial acts
Febrile Seizure
Ñ Related to temperature
Ñ Present among children
Status epilepticus
Ñ Prolonged seizure state
Ñ Can occur in any type of sizure
Ñ Rapid successions with no full consciousness in between
Ñ Brain damage can occur; most life threatening in tonic-
clonic seizures
Ñ Common to clients who are in coma
Ñ Related to medication
à "·
Ñ diopathic
Ñ No apparent structural changes in the brain
·
Ñ Characterized by structural changes or metabolic
alterations of the neuronal membranes that caused
increased automacity
Causes of Seizures:
Ñ diopathic- two-thirds of all seisure disorders
Ñ Anoxia
Ñ Birth trauma (inadequate supply of O2 supply to the brain, bld incompatibility,
hemorrhage)
Ñ Brain tumors
Ñ Drug or alcohol abuse or rapid withrawal from abused drugs
Ñ Febrile illness
Ñ Genetic predisposition
Ñ Head injury or trauma
Ñ nfectious diseases
Ñ ngestions of toxins( lead, mercury, or carbon monoxide)
Ñ Metabolic disorders, such as hypoglycemia or hypoparathyroidism
Ñ Perinatal infections
Pathophysiology:
Ñ Some neurons of the brain may depolarize easily or
hyperexcitable.
Ñ On stimulation, these neurons fires locally or throughout the
cerebrum and spreads electric current to surrounding cells.
Ñ Cells fire in turn and the impulses cascades to one side of
the brain ( a partial seizure), both sides of the brain (a
generalized seizure), or the cortical, subcortical, and brain
stem areas.
Pathophysiologic changes:
Ñ Recurring seizures, possibly of more than one type ( hallmark
of epilepsy)
Ñ Visual, olfactory, or auditory hallucinations; sweating or
flushing; dream states; anger, or fear reactions resulting from
simple partial seizures
Ñ Altered consciousness , such as amnesia for events around the
time of the seizure, resulting from complex partial seizures
Ñ Movement and muscle involvement resulting from tonic-clonic or
myoclonic seizures
Ñ Brief changes in ÔOC without motor involvement due to
absence sizures
Complications:
Ñ Hypoxia or anoxia from airway occlusion
Ñ praumatic injury
Ñ Brain damage
Ñ Depression and anxiety
Diagnostic pests:
Ñ Cp scan or MR- reveals abnormalities
Ñ EEG- reveals paroxysmal abnormalities
in tonic-clonic seizures, high, fast voltagespikes are
present in all leads
n absence seizures, rounded spike wave complexes are
present
Note: a negative EEG doesn·t rule out epilepsy because the
abnormalities occur intermittently
Ñ Skull x-ray may show evidence of fractures or
shifting of the pineal gland, bony erosion, or
separated sutures
Ñ Serum chemistry bld studies may reveal
hypoglycemia, electrolyte imbalances, and
elvated liver enzyme & alcohol level
preatment
Ñ Drug pherapy-
Ñ Ex. Phenytoin (Dilantin) carbamazepine
(pegretol), phenobarbital (Barbita, Ôuminal) ²
for generalized tonic clonic seizures and
complex partial seizures
Ñ Valproic acid (Depakene), clonazepam
(Klonopin) for absence seizures
Ñ f drug therapy is inefective, surgery to remove
a demonsrated focal lesion, or to remove the
underlying cause (tumor, abscess)
Ñ .V. diazepam ( valium), lorazepam (Ativan)
phenytooin, or phenobarbital for status
epilepticus
Ñ Dextrose- for hypoglycemia
Ñ phiamine-for chronic alcoholism or withdrawal
Ñ Patent airway
Ñ Oxygenate as needed
Ñ Raise siderails
Ñ Ensure safety-during seizure:
° Avoid restraining the pt
° Help the pt to a lying position
° Ôoosen any tight clothing
° Clear the area of hard objects
° Don·t place anything into the pt·s mouth to prevent lascerating the mouth & lips
or displace teeth
° f vomiting occurs, turn the head to provide an open airway
Ñ After the seizure subsides, reorient the patient
to time & place; inform him that he had a
seizure
Ñ Companion at bedside
Ñ Meds as ordered
ncreased ntracranial Pressure
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Major pypes of Herniation
ncreased ntracranial Pressure
"
Ñ ncreased HA
Ñ Nausea &Vomoting
Ñ Cushing·s triad
Ñ Restlessness
Ñ Eye involvement
Ñ Altered ÔOC
Ñ Sensory dysfunction
Ñ Elimination problem
Ñ Decorticate/decerebrate
NURSNG MANAGEMENp OF NCREASED CP:
Ñ Determine airway patency
Ñ Elevate HOB
Ñ Check VS/neuro assessment
Ñ Record &O
Ñ Enema restriction
Ñ Avoid coughing,vomiting, restraints, stress ulcer,suctioning
Ñ Seizure precaution
Ñ Edema reduction
Ñ Diuretics
Craniocerebral prauma (Head njury)
Ë nvolves injury to the scalp, skull, and/or brain tissues.
Ë pypes of Brain njury
Ë Jarring of the brain and its sudden, forceful contact
with the rigid skull. phere is transient period of unconsciousness.
Ë (bruising). A structural alteration characterized by
extravasion of blood cells.
Ë Ô . pearing of tissue caused by sharp fragment or object
or shearing force.
Ë . Result from depressed fracture causing
edema and hemorrhage.
Assessment
Ë Sign and symptoms of increased CP.
Ë CSF leakage from ears and nose.
Ë Battle·s sign (hematoma at the mastoid process) in basilar head trauma.
Management
Ë Care for the client with increased CP.
Ë Monitor drainage from ears and nose.
Ë Monitor for signs and symptoms of meningitis, atelectasis, pneumonia, Up.
ntracranial pumors
Ë ntracranial tumors may be classified as: gliomas,
meningiomas, neuromas, hemangiomas.
Ë Gliomas account for about 50% of all brain tumors.
Assessment
Ë Frontal lobe
Ë Personality disturbance
Ë nappropriate affect
Ë ndifference of bodily functions
Ë Precental gyrus
Ë Jacksonian seizures
Ë Occipital lobe
Ë Visual disturbances preceeding convulsions.
Ë pemporal lobe
Ë Olfactory,
visual or gustatory hallucinations.
Ë Psychomotor seizures with automatic behavior.
Ë Parietal lobe
Ë nability to replicate pictures.
Ë Ôoss of right-left discrimination
Management
Ë Care for the client with increase CP.
Ë Surgery
Ë Supratentorial craniotomy (post-op)
Ë Semi-fowler·s position
Ë nfratentorial craniotomy
Ë Flat position; turn to sides, avoid supine position for the first è8 hours. Avoid
neck flexion.
Ë Report immediately for presence of yellowish drainage on the head dressing.
Ë An increase in urine output may herald onset of 4 .
Ë pest the urine for glucose and acetone when steroids are administered.
Spinal Cord njury
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°
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Nursing Asessment:
° njury; treatment given at scene
° Neurologic assessment: Document findings
° Vital signs; respiratory status
° Movement and sensation below injury level
° Signs
M Îorsening neurologic damage
M Respiratory distress
M Spinal shock
Nursing Diagnoses:
° neffective breathing pattern
° neffective airway clearance
° Neuropathic pain
° mpaired physical mobility
° Anxiety
° Risks
M mpaired gas exchange
M Disuse syndrome
M neffective coping
Ñ Medical Management
° Cervical collar; cast or brace; traction; turning frame
° V; stabilization of vital signs
° Corticosteroids
° Surgical intervention
Ñ Surgical Management
° Surgery to
M Remove bone fragments
M Repair dislocated vertebrae
M Stabilize the spine
Management
Ñ 2 2 ¢ 2
Ñ
Ñ 2à
Ñ à 2
Ñ 2
Ñ ( 2 2
2
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Evaluation:
° Adequate breathing
° Painrelief
° Mobility using minimal assistive devices
° Reduced complications from inactivity
° Coping with the challenge of rehabilitation

nfectious Neurologic Disorders
Ñ Meningitis
Ñ Brain Abscess
Ñ Herpes Simplex Virus Encephalitis
Ñ Arthropod-Borne Virus Encephalitis
Ñ Fungal Encephalitis
Ñ Creutzfeldt-Jakob and New-Variant Creutzfeldt-
Jakob Disease
nfectious Process
Bacterial meningitis and nfectious Enceohalitis
Ñ Pyrogenic or purulent infection that involves the pia
matter and arachnoid matter layers of the
meninges.
nfection of Meninges
Pathogens
Ñ Under 2 months :E-coli, Group B streptococcus,
Ôisteria, Haemophilus influenza type B, and
Streptococcus pneumonia
Ñ Beyond neonate: Strep, Haemophilus, Neisseria.
Contributing History
Ñ Otitis
Ñ Sinusitis
Ñ Mastoiditis
Ñ Post skull fracture
Ñ Meningiocele
Ñ PROM
Ñ Premature infant
Ñ Sepsis / bacteremia
Clinical Manifestations
Ñ Poor feeding
Ñ Hypothermia / hyperthermia
Ñ rritability
Ñ Apnea
Ñ Bulging fontanel
Ñ Ôook sick
Ñ Older Child
° High fever
° Headache
° Nuchal rigidity / stiff neck
° + Kernigs = inability to extend legs
° + Brudzinski sign = flexion of hips when neck is flexed
° Purple rash (check for blanching)
Assessment for Positive Meningitis
Kernig Sign
h

h

Brudzinski Sign
ÿ

Septic Ôooking

Purple Rash
!

Diagnostic pests
Ñ + Spinal fluid
Ñ + Blood Culture
Management
Ñ V antibiotics
Ñ Dexamethasone to decrease meningeal
inflammation and hearing loss
Ñ Monitor Gentamicin blood levels
nterventions
Ñ Droplet precautions
Ñ solation X 2è hours
Ñ Vital signs
Ñ Neuro checks / palpate fontanel
Ñ Monitor fluids to prevent fluid overload
Ñ Head circumference
Ñ Pain management / quiet environment
Droplet Protection
Ñ f patient is a rule out meningitis the nurse should
wear a mask when helping with diagnostic tests.
Outcomes
Ñ Unfavorable outcomes
° Young age
° Delay in treatment
° Coma
° Focal neurologic signs
° Poor clinical course

Follow-up
Ñ BAER hearing test in hospital and 3 to 6 months later
Ñ Developmental testing
Ñ Îatch for learning disabilities
Brain njuries
Ñ Closed (blunt) Brain Ñ ntracranial
njury Hemorrhage
° EpiduralHematoma
Ñ Open Brain njury
° Subdural Hematoma
Ñ Concussion
Ñ ntracerebral
Ñ Contusion Hemorrhage and
Ñ Diffuse Axonal njury Hematoma
Pathophysiology
Subdural Hematoma
Ñ Shear force injury created by impact can cause
tearing of bridging vessels.
Ñ Falls, assaults, MVA, Shaken Baby Syndrome.
Ñ Children under 1 year
Ñ or changes in ÔOC
Ñ Vomiting
Ñ Headache
Ñ Retinal hemorrhages
Ñ Pupil on side injury fixed and dilated
Ñ Seizures
Retinal Hemorrhages
Y
h

Subdural Hematoma
"

#!
Epidural Hematoma
Depressed Skull Fracture
a

Depressed Skull Fracture
Ñ Part of the skull is actually sunken in from trauma.
Ñ May occur with or without a cut in the scalp.
Ñ Surgical intervention is needed to correct the

deformity.
Basilar Skull Fracture
Ñ Most serious type of skull fracture.
Ñ nvolves a break in the bone at the base of the skull.
Ñ Child has bruises around their eyes and a bruise
behind the ear.
Ñ May have clear fluid draining from their nose or
ears.
Ñ Need close observation in hospital.
Battle·s Sign
Ä
a
Nursing ntervention
Ñ Secure the injured site.
Ñ Prevent further injury by imobilizing, covering, applying pressure on
bleeding sites.
Ñ Assess the extent of the injury including spinal and neurologic
involvement.
Ñ f spinal involvement is negative, place patient on a high fowler·s
position
Ñ Ôoosen clients clothing and allow optimal ventilation
Ñ Place client on NPO until vomiting is unlikely to ocure.
& $"$
%
Postpoliomyelitis Syndrome
Ñ Complication of previous poliomyelitis virus (epidemic occurred in
USA during 19è0·s and 1950·s); persons who recovered are re-
experiencing manifestation of acute illness in their advanced age
Ñ Pathophysiology: Process is unknown
Ñ Manifestations: Fatigue, muscle and joint weakness, loss of muscle
mass, respiratory difficulties, and pain
Ñ Diagnosis: By history and physical examination
Ñ preatment: nvolves physical therapy and pulmonary rehabilitation
Ñ Nursing Care: nvolves emotional support and interventions to deal
with dysfunction; ADÔ, safety are including in interventions
Rabies
Rhabovirus infection of CNS transmitted by infected
saliva that enters the body through bite or open
wound
Ñ Critical illness almost always fatal
Ñ Source often is bite of infected domestic or wild

animal
Ñ ncubation is 10 days to years
Rabies
Manifestations occur in stages
Ñ Prodromal: wound is painful, various paresthesias, general
signs of infection; increased sensitivity to light, sound, and
skin temperature changes
Ñ Excitement stage: periods of excitement and quiet;
develops laryngospasm and is afraid to drink
(hydrophobia), convulsions, muscle spasms and death
usually due to respiratory failure
Rabies
Collaborative Care
Ñ Animal that bit person is held under observation for
7 ² 10 days to detect rabies
Ñ Sick animal are killed and their brains are tests for
presence of rabies virus
Ñ Blood of client may be tested for rabies antibodies
Rabies
Post-exposure treatment
Ñ Rabies immune globulin (RG) is administered for passive
immunization
Ñ Client often has local and mild systemic reaction; treatment is over
30 days
preatment of client with rabies: involves intensive care treatment
Health Promotion
Ñ Vaccination of pets
Ñ Avoid wild animals, especially those appearing ill
Ñ Follow up care for any bites
petanus (lockjaw)
Disorder of nervous system caused by neurotoxin from

@, anaerobic bacillus present in the soil
Ñ Contract disease from open wound contaminated with dirt, debris
Ñ Has high mortality rate
ncubation is usually 8 ² 12 days
Manifestations
Ñ Stiffness of jaw and neck and dysphagia
Ñ Spasms of jaw and facial muscles
Ñ Develops generalized seizures and painful body muscle spasms
Ñ Death occurs from respiratory and cardiac complications
petanus (lockjaw)
Diagnosis is made on clinical manifestations
Clients with disease are treated in intensive care with
antibiotics, chlorpromazine (phorazine) and diazepam
(Valium ) for muscles spasms
Health Promotion
Ñ Active immunization with boosters given at time of
exposure
Ñ Passive immunization is given to persons who are not
adequately immunized
Botulism
Food poisoning caused by ingestion of food contaminated
with toxin from
4
, anaerobic bacteria
found in soil
Ñ Contracted by eating contaminated foods usually
improperly canned or cooked
Ñ Untreated death rate is high
Pathophysiology: Bacteria produce a toxin, which blocks

release of acetylcholine from nerve endings causing
respiratory failure by paralysis of muscles
Botulism
Manifestations
Ñ Visual disturbances
Ñ Gastrointestinal symptoms
Ñ Paralysis of all muscle groups
Ñ Effecting respiration
Diagnosis
Ñ Based on clinical picture
Ñ Verified by laboratory analysis of client·s serum and stool
Ñ pesting the suspected food
Botulism
preatment
Ñ Administration of antitoxin
Ñ Supportive treatment including mechanical ventilation and

systemic support in intensive care unit
Health Promotion
Ñ peaching clients to process foods properly when home canning
Ñ Boiling foods for 10 minutes which destroys the toxin
Ñ Not eating spoiled foods

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| || 

° Form barrier between capillaries and neurons

° Control the chemical environment of

Ñ Motor (efferent) neurons

Functional Properties of Neurons

 

 

 

° phe surface is made of ridges (gyri) and grooves (sulci)

° General interpretation area

° pransfers impulses to the correct part of the cortex for

° ncludes the choroid plexus³forms cerebrospinal fluid

° ncludes nuclei involved in the control of breathing

° Reticular activating system (RAS) plays a role in

° Folds inward in several areas

° Digestive system regulation

After the presentation, we should be able to:

° Differentiate between normal and abnormal findings

b. Observe body language and facial

From Îijdicks, et al, 2005, with permission.

ù pemporary memory loss

a. Before testing nerve c. Occlude one nostril and

d. Convergens & Accomodation

e. Pupillary Ôight Reflex pesting eye

° - Ôesion of nerve, cervical spine, or brainstem.

ù Patient perceives light Ñ  %2

- pest taste on anterior two-thirds of tongue for sweet, sour,

pip of the tongue  Back of tongue

b. Perform watch-tick test by holding watch close to patient·s ear.

c. Perform Romberg test for balance

a. Observe ability to cough, swallow, and talk.

b.    

° Damage to CNs X and X also impairs swallowing.

Ñ mpaired taste on posterior portion of tongue:

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Ñ Observe for symmetry of contraction and muscle strength.

a. Have patient say ´d, l, n, tµ or a phrase

ÑApply stimuli randomly and ask patient to identify whether

ÑApply stimuli randomly, and ask patient to identify whether

° Peripheral nerve damage or damage to lateral

Ñf patient is unable to detect vibration, test proximal areas as

° Ôoss of balance that occurs when

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Ñ Ask the person to pat the knees with

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subarachnoid space to > Explain the procedure.

withdraw CSF for diagnostic > Observe for complication

or therapeutic purposes. following the procedure.

Measure the action

ù ´snarl smileµ (smiles slowly) Ñ mpaired transmission of the cranial

Ë Start meal with cold beverage.

Ë Neurologic disorder affecting the 5th cranial nerve.

Ñ Îatch for adverse effects of steroids use

Ñ Poor functional recovery

 Middle Cerebral Artery is commonly affected.

ù Refers to transient cerebral ischemia with

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Ñ Cognitive impairement- Aphasia ² Ñ Kinesthesia ²

Ñ nfections such as pneumonia

Ë Î       Ë .

Ë p     , at least q 2 hrs to prevent pneumonia.

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Ñ Saccular= when one side of the vessel is affected

Ñ Fusiform= when the entire segment becomes dilated

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° ncludes nuclei involved in the control of breathing

ù Patient perceives light Ñ %2

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