study

1. Perception and
Coordination

2. Structure&Functionsofcellsinthenervoussystem
• Neurons are the basic anatomical and functional units
in the nervous system; each neuron has 3 parts:
• Neurons (nerve cells)- the most important cells in the
brain.
-They transmit chemical and electric signals that
determine thought, memory, emotion, speech, muscle
movement, sensation,
-Neurons send these signals through their nerve
fibers (axons).

3. Parts of Neuron
1. The cell body
2. Axon-carries the stimulus away from the cell body
- Axon in the PNS are covered w/ an insulating lipid layer
called myelin sheath for rapid conduction of nerve impulses
- Each axon terminates at a synapse where neurotransmitters
and other chemical substances are released
3. Dendrites- direct impulses toward the cell body

4. • Nerve cells are separated by a synaptic cleft;
neurotransmitters are secreted into the cleft by one
neuron to stimulate the dendrites of another
neuron
• Conduction of a nerve impulse is initiated when a
stimulus is sufficient to create an action potential (a
summation of impulses from the dendrites) it is
then sent down the axon by depolarization; in
myelinated nerves the action potential hops from
one node of Ranvier to the next for rapid
conduction

5. • 2. Glial cells- supportive structure of the nervous
system that nourish, support and protect the
brain neurons
4 Main Types of the Glial Cells
1. Astrocytes- star-like cells that provide nutrition
to neurons, regulate synaptic connectivity, remove
cellular debris, and control movement of molecules
in the blood-brain barrier

6. 2. Schwann cells- PNS cells that produce insulating myelin
sheaths, just as the oligodendrocytes do in the CNS, w/c
facilitates rapid conduction of impulses

7. • 3. Ependymal cells- lines the ventricular system and the
choroid plexuses they produce CSF and act as a barrier
between the fluid filled ventricles and cerebral tissue

8. 4. Microglia- small phagocytic
cells scattered in the CNS that
disintegrate and remove cellular
debris and waste products
5. Oligodendrocytes- produce the
myelin sheath w/in the CNS that
insulates the neuron allowing for
fast transmission of impulses

9. The CNS
• Consists of the brain and the spinal cord
The Brain
• Divisions of Brain (Main areas):
Cerebrum, Cerebellum and brain stem.
- responsible for planned (voluntary) muscle movements
(throwing a ball, walking, chewing, etc.) and for taking in and
interpreting sensory information such as vision, hearing,
smell, touch, and pain.

10. • The cerebrum- the largest division, composes the top of the
brain and enables individuals to reason, function intellectually,
express personality and mood, and interact with the
environment

11. The Cerebrum
• Has 2 hemispheres, each of which is divided into frontal lobe,
temporal, parietal, occipital
• Right hemisphere- generally controls the left side of the body; the
left controls the right side
• Frontal lobe performs high level cognitive function, has memory
storage, influences somatic motor control, controls
voluntary eye movements and controls motor aspect of
speech (Broca’s area)

12. • Temporal lobe-located behind the frontal and under the
parietal lobe and has a primary auditory reeptive areas
and the auditory association area (Wernicke’s area), w/c is
usually found on the dominant side and is responsible for
interpreting speech
-Interpretative area that integrates somatic, auditory and
visual data (perception, learning, memory, emotions and
intellectual abilities)

13. • Parietal lobe holds the primary sensory cortex and sensory
association areas; processes visual-spatial information and
controls spatial orientation
• Occipital lobe- the visual center for the eyes; controls both eye
reflexes and interpretation of sight

14. • Meninges: These are layers of tissue that line and protect the
brain and spinal cord. CSF travels through spaces formed by
the meninges
• Choroid plexus: The choroid plexus is the area of the brain
within the ventricles that makes CSF, which nourishes and
protects the brain.

15. • Basal ganglia: The basal
ganglia are structures deeper
within the brain that help
control our muscle
movements. Tumors or other
problems in this part of the
brain typically cause
weakness, but in rare cases
can cause tremor or other
involuntary movements.

16. The Diencephalons & Hypophysis
• Located at the bottom of the
cerebrum near the midbrain
• Includes: thalamus, pituitary gland
and other related structures
• Controls the temperature, water
metabolism, pituitary secretion,
visceral and somatic activities,
visible physical expressions in
response to emotions, sleep-wake
cycle and food-getting reflex

17. The Cerebellum
• A double-lobed area
posterior to the pons
that is responsible for
muscle energy and
coordination, and
maintains balance
through feedback loops.

18. • Cerebellum: The cerebellum lies under the
cerebrum at the back part of the brain. It helps
coordinate movement.

19. The brainstem
• Is an integration system that controls basic
functions
• 3 major divisions of the brainstem: Midbrain, Pons,
medulla
• Reticular activating system (RAS)-responsible for
alertness

20. • Brain stem: The brain stem is the lower part of the brain that
connects to the spinal cord.
- It contains bundles of very long nerve fibers that carry
signals controlling muscles and sensation or feeling between
the cerebrum and the rest the body.
-Special centers in the brain stem also help control
breathing and the beating of the heart.

22. The spinal cord
• Is an elongated mass of nerve tissue
that runs most of the length of the vertebral column
Divisions:
• Cervical area –C1 to C7
• Thoracic area - T1 to T12
• Lumbar- L1 to L5
• Sacral area- S1 to S4

23. • Spinal cord: The spinal cord has bundles of very
long nerve fibers that carry signals that control
muscles, sensation or feeling, and bladder and
bowel control.

24. • Sensory tracts (dorsal roots) carry afferent impulses from the
periphery to the dorsal root ganglia where the cell bodies of the
sensory components are located and messages send to the brain.
2 Types of Sensory Fibers
1. General somatic afferent fibers carry pain, temp, touch and
proprioception from the body wall, tendon and joints
2. General visceral fibers carry sensory input from the organs of the
body

25. • Motor tracts (ventral roots) convey efferent impulses from
the spinal cord to the body
2 Types of Fibers
1. General somatic fibers-innervates voluntary striated muscles
2. General somatic visceral afferent fiber- innervate smooth and
cardiac muscle and regulate glandular secretions

28. The peripheral nervous system
• Has 31 pairs of spinal nerves, 12 pairs of cranial nerves and
the autonomic system that is divided into the sympathetic and
parasympathetic nervous system
• Each pair of spinal nerves has dorsal and ganglion roots that
exit the spinal cord by way of an intervertebral foramina that
corresponds with the spinal level; these nerves carry input
between specific areas called dermatomes and the spine

30. • Cranial nerves: 12 pairs in the brain; 3 pure sensory
nerves, 5 pure motor nerves and 4 mixed (sensory
and motor) nerves; the olfactory nerve (CN I) and
optic nerve (CN II) arise from the cerebrum; CN III and
IV arise in the midbrain ; CN IV through VIII arise in the
pons, while CN IX to XII arise in the medulla

32. • Autonomic Nervous System- a collection of
motor nerves that regulate activities of the
viscera, smooth muscles, and glands to
maintain a stable internal environment;
• 2 parts of the ANS: sympathetic and
parasympathetic w/c work antagonistically.

33. a. The sympathetic nervous system (SNS) is active during
times of stress, such as the fright, flight or fight response;
- it increases heart rate and blood pressure and
vasoconstricts the peripheral blood vessels
b. The parasympathetic system is a conservation,
restoration, and maintenance system;
- it decreases heart rate and increases
gastrointestinal (GI) activity

37. • The spinal cord and cranial nerves help carry messages
between the brain and the rest of the body. These messages
tell our muscles how to move, transmit information gathered
by our senses, and help coordinate the functions of our
internal organs.

38. Blood Supply
• The brain is unique in that it can only use glucose
for its energy supply; a lack of glucose for 5 minutes
results in irreversible brain damage
• the brain receives 750mL/min of blood or 15 to
20% of the resting cardiac output;
• blood flow rates for specific sites correspond
directly with the rate of metabolism

39. • The cerebral arteries are thinner, have more internal elasticity
and less smooth muscle than the arteries in the rest of the
body
• the brain is supplied with blood by two sets of arteries that
divide it into anterior and posterior circulation

40. • The anterior circulation, fed by the internal and external
carotids, delivers blood to the base of the cerebrum
called the circle of Willis; from there it feeds the anterior
cerebrum via anterior cerebral, the middle of the
cerebrum via the middle cerebral artery, and the
posterior cerebrum via posterior cerebral artery; the
tissues that are at the terminal areas fed by the two
circulations are called watershedzones because they are
subject to marginally adequate blood supply
• The first affected if there is hypoperfusion

41. • The posterior circulation from the vertebral arteries, delivers
blood to the posterior fossa; at the bottom of the posterior fossa,
blood flows together into one basilar artery and delivers it to the
cerebellum, midbrain, pons, and medulla
• The meninges are supplied with blood from branches of the
external carotid arteries that ascend into the brain at the base of
the skull

42. • The venous system of the brain is unique
a. Vessel walls are thinner than other veins of the body
b. They do not follow the path of arteries but follow their
own course
c. There are no valves in the brain’s venous system and
therefore drainage depends on venous pressure and
gravity
d. Dural sinuses collect blood from the brain and empty it
into the jugular veins

43. THE BLOOD-BRAIN
BARRIER
• It refers to a network of endothelial cells in the
wall of the capillaries and astrocyte projections in
close proximity that do not have pores between
them

44. • This tight junction does not allow the normal
nonspecific filtering process that occurs in the rest of
the body; therefore, molecules must enter the brain
by active transport, endocytosis and exocytosis which
creates a highly selective barrier that guards the
entrance to the neurons

45. • The movement of substances across this barrier
depends on particle size, lipid solubility, chemical
dissociation and protein-binding potential
• The barrier is very permeable to water, oxygen,
carbon dioxide, other gases, glucose and lipid
soluble compounds

46. Protective structures
• Meninges: cover the brain and spinal cord to protect and
support; it is divided into 3 layers from outer to inner (dura
mater, arachnoid, and pia mater)
a. dura - a tough membranous tissue that surrounds and
extends into the brain tissue that provides important
landmarks, such as the falx cerebri and the tentorium cerebelli,
which is an important structure to note because nursing care
differs based whether an injury is supratentorial (above the
tentorium) or infratentorial (below the tentorium)

47. b. arachnoid membrane- lies below the dura and is a
network of delicate, elastic tissue that contains
blood vessels of varying sizes
c. pia mater- a vascular membrane that covers the
entire brain with tiny vesssels that extend into the
gray matter of the brain
d. Within the meninges, there are important potential
spaces (epidural, subdural, subarachnoid) where
bleeding can occur

48. • Skull- includes 8 fused cranial bones and 14 facial bones; the
cranium encloses the brain in a protective vault;
• Foramen magnum is the large hole at the base of the skull through
which the spinal cord runs
• Spine- a flexible column that encloses the spinal cord, formed from
the stacking of 33 vertebrae

49. Cerebrospinalfluidand
ventricularsystem
a. CSF is a clear colorless, odorless solution that
surrounds the brain and spinal cord;
-it acts as a shock absorber to cushion the brain
from injuries caused by movement;

50. • Cerebrospinal fluid is made by the choroid plexus, which
is located in spaces within the brain called ventricles.
• The ventricles and the spaces around the
brain and spinal cord are filled with CSF.

51. • CSF has electrolytes, glucose protein, oxygen and carbon
dioxide
• Ventricular system - is composed of 2 lateral ventricles (one
in each hemisphere of the cerebrum), a third ventricular that
lies midline in the thalamic area, and a fourth ventricle that
lies below the third, anterior to the cerebellum and the
subarachnoid space

52. • The flow of CSF starts in the choroid plexus in each lateral
ventricle and travels to the third ventricle via the Foramina of
Monro; from the third ventricle the CSF flows into the fourth
ventricle via the aqueduct of Sylvius, through lateral foramen
of Luschka, midline through the foramen of Mafendie into the
subarachnoid space, down to the spinal cord and up again to
the subarachnoid space on the top of the brain, where it is
absorbed by arachnoid villi

54. • Meninges: These are layers of tissue that line and protect the
brain and spinal cord. CSF travels through spaces formed by
the meninges
• Choroid plexus: The choroid plexus is the area of the brain
within the ventricles that makes CSF, which nourishes and
protects the brain.

55. • Pituitary gland and hypothalamus
Pituitary gland is a small gland at the base of the
brain connected to the hypothalamus.
• They help regulate the activity of glands in the body.
• they control the amount of thyroid hormone made by the
thyroid gland
• the production and release of milk by the breasts
• and the amount of male or female hormones made by the
testicles or ovaries.
• Secretes growth hormone, which stimulates body growth
• Secretes vasopressin, which regulates water balance by the
kidneys.

56. • Pineal gland-is not really part of the brain, it is a small
endocrine gland that sits between the cerebral
hemispheres.
• It makes melatonin, a hormone that regulates sleep, in
response to changes in light

57. Nursing Process
• Assessment of the Nervous System
• Assess chief complaint
A- any associated symptoms w/ chief complaint
P- what provokes (makes worse) or palliates makes
better) symptoms
Q- quality of pain
R- region and radiation
S- severity of pain on a scale of 1-10
T- timing (when did it stop and start, intermittent or
constant, duration

58. • Health information: including past medical
hx, current meds, recent surgeries or other
treatments

59. Physical Assessment of the
Neurologic System
Mental status
• Includes orientation to person, place, time, appearance
and behavior, mood, speech pattern and thought and
perception including insight, thought, content and
judgment
• Considerations in conducting assessment: The client
must be awake, alert and able to understand and
respond to questions

60. • Assign: Research on Level of consciousness

61. Description of LOC
• Full consciousness- alert oriented to person,place, time,
comprehend written & spoken words
• Confusion- disoriented to person, place, time; misterpret
environment, has poor judgement; unable to think clearly
• Lethargic- oriented but slow & sluggish in speech, mental
processes & motor activity

62. • Obtundation- readily arousable to stimuli; responds w/ one or
2 words; follows simple commands, but quickly drifts back to
sleep
• Stupor- lies quietly w/ minimal movement; responds w/ a
groan or eye opening only to vigorous and repeated verbal w/
tactile stimuli

63. Coma- unarousable to stimuli; nonverbal; may exhibit
nonpurposeful response to stimuli
• Light coma- unarousable; withdraws nonpurposefully to pain;
may decerebrate or decorticate; brainstem reflexes intact
• Deep coma- unarousable; unresponsive to painful stimuli;
brainstem reflexes usually absent; decerebrate posturing
usually noted.

64. • Delirium- rapid in onset; brief impairment of cognition
including a clouding of consciousness and difficulty sustaining
and shifting attention
• Dementia- a generalized. Long term decline in cognitive
abilities such as memory, language, and clear consciousness

65. Cranial Nerve Assessment

66. Nurses Cranial Nerves Assessment
Cranial
Nerve
Function Method Normal Findings
I Olfact
ory
Smell reception
and
interpretation
Ask client to
close eyes and
identify different
mild aromas
such alcohol,
powder and
vinegar.
Client should be
able to distinguish
different smells
II Optic Visual acuity
and fields
Ask client to
read newsprint
and determine
objects about 20
ft. away
Client should be
able to read
newsprint and
determine far
objects

67. III Oculomot
or
Extraocular eye
movements, lid
elevation,
papillary
constrictions
lens shape
Assess ocular
movements and
pupil reaction
Client should be able
to exhibit normal
EOM and normal
reaction of pupils to
light and
accommodation
IV Trochlear Downward and
inward eye
movement
Ask client to move
eyeballs obliquely
Client should be able
to move eyeballs
obliquely

68. V Trigeminal Sensation of face,
scalp, cornea, and oral
and nasal mucous
membranes. Chewing
movements of the jaw
Elicit blink reflex by lightly
touching lateral sclera; to
test sensation, wipe a wisp
of cotton over client’s
forehead for light
sensation and use
alternating blunt and sharp
ends of safety pin to test
deep sensation
Assess skin sensation as of
ophthalmic branch above
Ask client to clench teeth

69. VI Abducens Lateral eye
movement
Ask client to move
eyeball laterally
Client should be able
to move eyeballs
laterally
VII Facial Taste on
anterior 2/3 of
the tongue
Facial
movement, eye
closure, labial
speech
Ask client to do
different facial
expressions such as
smiling, frowning
and raising of
eyebrows; ask
client to identify
various tastes
placed on the tip
and sides of the
mouth: sugar, salt
and coffee
Client should be able
to do different facial
expressions such as
smiling, frowning and
raising of eyebrows;
able to identify
different tastes such
as sweet, salty and
bitter taste

70. VIII Acoustic Hearing and
balance
Assess client’s
ability to hear
loud and soft
spoken words;
do the watch
tick test
Client should be
able to hear loud
and soft spoken
words; able to
hear ticking of
watch on both
ears

71. IX Glossoph
aryngeal
Taste on
posterior 1/3 of
tongue,
pharyngeal gag
reflex,
sensation from
the eardrum
and ear canal.
Swallowing and
phonation
muscles of the
pharynx
Apply taste on
posterior tongue
for identification
(sugar, salt and
coffee); ask client
to move tongue
from side to side
and up and down;
ask client to
swallow and elicit
gag reflex through
sticking a clean
tongue depressor
into client’s mouth
Client should be able
to identify different
tastes such as sweet,
salty and bitter
taste; able to move
tongue from side to
side and up and
down; able to
swallow without
difficulty, with (+)
gag reflex

72. X Vagus Sensation
from
pharynx,
viscera,
carotid body
and carotid
sinus
Ask client to
swallow; assess
client’s speech
for hoarseness
Client should be
able to swallow
without
difficulty; has
absence of
hoarseness in
speech
XI Spinal
accessor
y
Trapezius and
sternocledom
astoid muscle
movement
Ask client to
shrug shoulders
and turn head
from side to
side against
resistance from
nurse’s hands
Client should be
able to shrug
shoulders and
turn head from
side to side
against resistance
from nurse’s
hands

73. XII Hypog
lossal
Tongue
movemen
t for
speech,
sound
articulati
on and
swallowin
g
Ask client
to protrude
tongue at
midline,
then move
it side to
side
Client should
be able to
protrude
tongue at
midline and
move it side
to side

74. Cerebellar Function Assessment
• Balance & Coordination
• To assess gait: let the client walk normally and then on on heels and
toes and assess coordination; perform a Romberg’s test by having
the client stand w/ feet together & eyes closed while you stand close
by to prevent falling; there should be minimal swaying for 20seconds

75. • To assess coordination, observe the client’s ability to touch own
nose and then touch one of your fingers, then his or her nose again;
next observe the client’s ability to touch each finger to the thumb of
the same hand; finally, observe the client’s ability to run the heel
down the shin on each side while lying in the supine position.

76. Assessment of the Sensory
Function
• Have the client close the eyes while you touch the client on all
dermatomes w/ objects that are sharp, dull, light to touch.
And that vibrate (over bony prominence); the client should be
able to discriminate the location and type of touch
• To assess a client’s sense of position (kinesthesia) have the
client close the eyes and move the client’s finger or toe up or
down and ask the client to describe the movement

77. • To assess for stereognosis, have the client identify an object in
his/her hand w/ the eyes closed.
• To assess for graphesthesia have the client identify a number
or letter traced on the palm of the hand
• Test two-point discrimination by touching a client w/ 2
simultaneous pinpricks and asking how many pinpricks there
were; use dull points on a caliper and begin on finger pads

78. Assessment of the Motor Function
• Inspect all muscles for size,tone, movement and strength
• Compare left and right side for symmetry and equality
• Assess for tremors (rhythmic movements) and fasciculations
(twitching)

79. Terminologies Used to describe
Motor Function
• Strong- normal strength
• Weak- moves against resistance
• Unable to lift
• Withdraws
• Decorticate- to painful stimuli, flexes arms, wrist, fingers w/
adduction of the upper extremities and extension, internal
rotation and plantar flexion of lower extremities

80. • Decerebrate- to painful stimuli, extends, adducts, and
hyperpronates arms and stiffly extends legs and plantar flexes
feet
• Flaccid- No response to pain; no muscle tone
• Ataxia-Incoordination of voluntary muscle groups

81. Assessment of the Reflexes
• The deep tendon reflexes (patellar, biceps, brachioradialis, triceps and
achilles)
Standard Criteria for Grading Reflexes
0- no response
1= hypoactive; weaker than normal (+)
2= normal (++)
3= stronger than normal (+++)
4= hyperactive (++++)

82. • The superficial abdominal reflex is assessed by lightly stroking the
abdomen from the side to the midline; normally the side stroked will
contract
• The cremasteric reflex is assessed by lightly stroking the inside of the
thigh on a male client to raise the testicle on that side

83. • Babinski reflex- stroke the foot laterally from the heel to ball of foot
(+)- dorsiflexion of the big toe and fanning of other toes
(-)- normal response- curling of the toes

84. Assessment of Speech
• Normal: clear normal fluent speech
• Dysarthria-ineffective articulation of speech; maybe a motor deficit
of the tongue and speech muscles
• Aphasia- a language disorder classified as:
• Expressive, motor or nonfluent aphasia ( also called Broca’s
aphasia)- inability to express one’s self using motor aspects of
speech

85. • Receptive, fluent or sensory aphasia
(Wernicke’s aphasia)- inability to comprehend
spoken words
• Global aphasia- can neither express nor
comprehend language ( mixed receptive and
expressive)

86. Diagnostic Studies/Lab
Examinations
• Cerebrospinal fluid analysis via lumbar puncture-it is studied
for color, clarity, glucose, protein, blood or bacteria
Nrsg considerations:
• Assess for CSF leakage and sign of infection at the site after
the procedure
• Position the head higher than the body for water based
contrast
• Flat position with oil-based contrast

87. Radiological studies
• Cerebral angiography- to view the vascular structure of the
brain; can be used to find arterio-venous malformations and/or
aneurysms; use standard measures asso w/ use of contrast
medium
Assess for allergy to iodine or shellfish; force fluids to aid in
its excretion after the procedure
• CT scan-detects bleeding, hydocephalus & ischemic stroke
• MRI: detects soft tissue changes(necrosis,tumor, edema,
disorders)
assess client for implanted sources of metal that would
contradict use MRI use

88. Electrographic Studies
• Electroencephalography (EEG)- measures brain waves w/
multiple scalp elctrodes; its patterns may suggest epilepsy,
herpes simplex, encephalitis and dementia, also determines
brain death
Shampoo the hair before for hygiene and after to remove residual
electrode gel
Withold anticonvulsnat and other meds as ordered for 12-24 hrs
prior
Have the client eat regular meals to avoid hypoglycemia that could
affect results

89. • Electromyography (EMG) and nerve conduction studies: these tests
are used to differentiate between peripheral nerve and muscle
disorders; conduction velocity of muscles is measured between 2
points and recording/measurements are taken at rest, w/
movement, and w/ electrical stimulation

90. Ultrasound
• Carotid doppler scan- a noninvasive ultrasound of the carotids that
detects occlusions and stenosis; ultrasound procedures cause no
discomfort
• Transcranial doppler ultrasonography (TCD)- a portable non-invasive
technique used to assess intracranial circulation by measuring blood
flow velocity; it is used to assess vasospasm, TIA, headache,
subarachnoid hemorrhage (SAH), head injury and arteriovenous
malformations (AVM)

91. Planning for Health Promotion,
Maintenance and Restoration

94. COMMON HEALTH PROBLEMS
A. Disturbances in Cerebral Function

95. Acute Disorders of the Nervous
System
• Altered level of Consciousness
Is a change in arousal or alertness and/or a change in cognition or
solving complex problems (thought process , memory, perception,
problem solving and emotion); it is often the first sign of a change in
neurologic status

96. Etiology & Pathophysiology
• Causes for unconsciousness vary from primary CNS disorders
(such as damage to the reticular activating system or the
cerebrum) to dysfunction of other organ systems
• Metabolic disorders may alter the cellular environment
enough to inhibit neuronal activity
• Is reserve for those who have long periods of
unconsciousness, lasting from hours to months

97. • Neurological origin of coma results from damage to both
hemisphere of the brain, damage to the brain stem, or both

98. Assessment
• Clinical Manifestations
• Except for case where there is damage to the brainstem, brain
function deterioration and changes in LOC follow a predictable
pattern
• Confusion, forgetfulness, disorientation to time, person, place,
agitation, poor problem solving abilities.
• Any change in behavior may be an early change in cerebrum
function.

99. • Lethargy, obtundation and stupor result from greater cerebral
deterioration
• Decorticate posturing, small reactive pupils, positive doll’s
eyes
• manifest midbrain deterioration
• Decerebrate posturing, fixed pupils and positive cold caloric
tests show deterioration at the pons

100. • Fixed pupils, flaccidity and negative cold caloric tests indicate
involvement at the medulla level
• Glasgow coma scale assessment includes components of eye
opening (scored from 1 to 4), best verbal response (scored
from 1 to 5), and best motor response ( scored from 1 to 6);
total score ranges from 3 to 15; a score of 8 or lower usually
indicates coma.

101. Diagnostic & Laboratory Test
Findings
• CT and MRI detects hemorrhage, tumor, cysts, edema or brain
atrophy
• ECG evaluate unrecognized seizures as a cause for an altered
LOC
• Cerebral angiography evaluates cerebral circulation for
aneurysm and arterial-venous malformations
• Transcranial doppler- study blood flow

102. • Lumbar puncture w/ CSF analysis for analysis of infection
• Lab Test to rule out metabolic, toxic or drug-induced
disorders: glucose, serum elect., osmolarity, creatinine, liver
funcion, CBC, ABG and toxicology

103. Therapeutic Management
• Treat the cause of the problem
• Airway maintenance
• Skin integrity
• Preventing contractures
• Maintaining nutrition

104. Priority Nrg Dx
• Ineffective airway clearance
• Risk for aspiration
• Risk for impaired skin integrity
• Impaired physical mobility
• Risk for imbalance nutrition: less than body requirements

105. Planning & Implementation
• Assess for ability to clear secretions, breath sounds
• Maintain potent airway for unconscious client
• Maintain in side-lying position
• For clients who have tracheostomy, provide tracheostomy care
every 4 hours
• Asess swaloowing and gag reflex; prevent aspiration
• Monitor and report possible aspiration

106. • Assess skin integrity every shift, reposition every 2 hrs
• Prevent skin breakdown: keep linens clean, dry and wrinkle-
free
• Prevent contractures and perform passive ROM regularly

107. Increased ICP
• A prolonged pressure greater than 15 mmHg or 180mmH2O
measured in the lateral ventricles
• Can increased ICP but does not cause significant tissue ischemia:
Coughing, sneezing, straining and bending
• Cushing’s triad/response: involves 3 classic signs or responses to
increased ICP (increasd systolic BP while diastolic remains the same,
widening pulse pressure and reflex bradycardia from stimulation of
the carotid bodies

108. • A prolonged increase in ICP causes tissue ischemia because
cerebral blood flow and perfusion are compromised
• Autoregulation, a compensatory mechanism to maintain
cerebral blood flow, is disrupted and can lead to cellular
hypoxia and ischemia
• Untreated ↑ ICP leads to herniation and
ultimately death

109. Etiology & Pathophysiology
• Because the brain is encased in a closed cavity, expansion of
any of the contents of the cavity can cause increased ICP

110. • Cerebral edema- is an increase in volume of brain tissue due
to alterations in capillary permeability (vasogenic edema),
changes in functional or the structural integrity of the cell
membrane (cytotoxic edema) or an increase in interstitial
fluids (interstitial cerebral edema);

111. • Hydrocephalus- is an 9ncrease in the volume of CSF w/in the
ventricular system
• Noncommunicating hydrocephalus- the drainage from the
ventricular system is impaired (as when a mass blocks the flow of
CSF)
• Communicating hydrocephalus-when blood blocks the arachnoid
villi from absorbing CSF in a subarachnoid hemorrhage

112. Assessment
• Clinical Manifestations:
• Earliest sign of ↑ICP: blurred vision, ↓ visual acuity, diplopia
because of pressure on the visual pathways; headache,
papilledema or swelling of the optic disk
• Vomiting
• Most significant sign: change in LOC,

113. Diagnostic and Lab Test
• To identify and treat underlying cause of ↑ ICP
• CT and MRI scanning
• Lab Test: serum osmolality monitors hydration status and
ABGs measure pH, oxygen, and carbon dioxide
(hydrogen ions)

114. Therapeutic Management
• Increased ICP is a medical emergency with little time for lengthy
diagnostic studies; it centers on restoring normal pressure and can be
accomplished through medications, surgery, and drainage of CSF from
the ventricular system
• A drainage catheter, inserted via ventriculostomy into the lateral
ventricle, can be done o monitor ICP and to drain CSF to maintain
normal pressure; if used, the system is calibrated with the trasducer is
leveled 1 inch above the ear (height of foramen of Munro); sterile
technique is of utmost importance)

115. Priority Nursing Diagnosis
Planning and Implementation
• Assess neurological status every 1 to 2 hours and report any
deterioration; assessment areas include LOC, behavior,
motor/sensory function, pupil size and response vital signs with
temperature
• Maintain airway; elevate head of bed 30 degree or keep flat as
prescribed; maintain head and neck in neutral position to promote
venous drainage

116. • Assess bladder distention and bowel constipation; assist client
when necessary to prevent valsalva maneuver
• Avoid prolonged activity, it may increased ICP; provide quiet
environment (lights kept low) and limit noxious stimuli; limit
stimulants such as radio, TV, and newspaper
• Avoid ingesting stimulants; coffee, tea, cola and cigarette smokes
• Maintain fluid restriction

117. • Keep dressings over catheter dry and change dressings as
prescribed; monitor insertion site for CSF leakage or infection;
monitor clients for signs and symptoms of infection; used aseptic
technique when in contact with ICP monitor

118. Medication Therapy
• Osmotic diuretics such as mannitol (Osmitrol) and loop
diuretics such as furosemide (Lasix) are used to decreased ICP;
they work by drawing water from edematous tissues and into
the vascular system; they can also disturb glucose and
electrolytes, so it is necessary to monitor their effect
• Corticosteroids decreases ICP esp. with tumors

119. Client Education
• Teach the client at risk for increased ICP to avoid coughing,
blowing the nose, straining for bowel movements, pushing
against the bed side rails, or performing isometric exercises
• Advise the client to maintain neutral head and neck alignment
• Encourage the family to maintain a quiet environment and
minimize stimuli

120. Head Trauma; Skull Fractures
• Is a break in the skull that occurs with/without intracranial
trauma; the force of the impact significantly increases the risk
of hematoma formation; the disruption of the skull can lead to
infection and cranial nerve injury

121. Etiology and Pathophysiology
• Skull fractures occur from trauma
• 4 Classifications of Fracture;
1. Linear fractures; infection and CSF
leakage is minimal because the dura remains intact; hematoma
formation is possible

122. • Comminuted and depressed; skull fractures have a higher risk of
brain tissue damage and infection especially if the overlying skin
and dura is torn or damaged; the risk of secondary brain injury is
reduced because, impact energy caused bone fracture instead of
being transferred to brain tissue
• Basilar; skull fractures involve the base of the skull and are usually
secondary injuries; most are uncomplicated, but those that disrupt
the sinuses and middle ear bones can lead to infection and CSF
leakage

123. Assessment
• Clinical manifestations of basilar skull fracture
1. Battle’s sign, ecchymosis over the mastoid process
2. Hemoytmpanum, blood visible behind the tympanic
membrane
3. Raccoon eyes, bilateral periorbital ecchymosis
4. Rhinorrhea, CSF leakage through the nose
5. Otorrhea, CSF leakage through the ear

124. • Diagnostic and laboratory test findings: diagnosis of skull fractures
may be done with plain x-ray films and ICT or MRI scans; basilar
skull fractures may be difficult to identify on plain x-ray

125. Therapeutic Management
• Linear skull fractures generally require bed rest and observation for
underlying brain injury; no specific treatment is necessary
• Commuted and depressed skull fractures require surgical
intervention within 24 hours
• Basilar skull fractures do not require surgery unless there is
persistent CSF leakage; regular neurological assessments and
observations for meningitis are required

126. Priority Nrsg Dx
• Risk for infection
• Risk for injury

127. Planning & Implementation
• Observe for otorrhea or rhinorrhea
• Test clear ear and sinus drainage for glucose; only CSF has
glucose; mucous secretions do not
• Observe blood tinged drainage for halo sign: glucose-
containing CSF dries in concentric rings on gauze or tissues
• Keep nasopharynx and external ear clean; use sterile
technique and supplies when cleaning drainage from nose
and/or ears

128. • Instruct client not to blow nose, cough or inhibit sneeze and to
sneeze through an open mouth
• Use aseptic technique when changing head dressings

129. Medication Therapy
• Dexamethasone to decrease cerebral edema
• Antibiotics for risk of infection

130. Client Education
• Is an escape of blood into the cranium, most commonly
associated with blunt trauma: hemorrhage may cause a very
slow to very rapid neurological deterioration
• Etiology and pathophysiology: intracranial hemorrhage results
directly from trauma or from the shearing forces on cerebral
arteries and veins from acceleration-deceleration injuries;
they are classified by location

131. Epidural Hematoma
• Develops between the dura and the skull
• As the hematoma forms, it strips the dura away from the skull
• Epidural hematoma usually develop from a tear in the
meningeal artery
• Because this is an arterial blood, it rapidly expands, leading to
a rapid deterioration in neurological status

132. Subdural hematoma
• Forms between the dura mater and the arachnoid-pia mater
layers of the meninges
• Usually involves veins but may involve small arteries as well
• As blood collects, pressure is applied to the underlying brain
tissue
• Subdural hematoma may be acute (developing within 48
hours after an acute injury), subacute (developing 2 days to 3
weeks after lesser injury), or they may develop spontaneously

133. Intracerebral hemorrhage
• Is bleeding into the brain tissue
• It can occur anywhere in the brain but is most common in the
frontal or temporal lobes
• It may be the result of closed head trauma, where shearing
forces are applied deep in the brain;

134. Assessment
• Clinical manifestation
1. Epidural hematoma: loss consciouness then have a short
periods of lucidness followed rapidly by deterioration from
drowsiness to coma; headache, fixed dilated pupil on affected
side, hemiparesis, hemiplegia and possible seizures

135. 2. Subdural hematoma- the manifestations develop slowly and
maybe mistaken as dementia: slow thinking, confusion,
drowsiness, lethargy, headaches, ipsilateral pupil dilation and
sluggishness and possible seizures

136. 3. Intracerebral hematoma- headache; as the hematoma
progresses, a decreased LOC, hemiplegia and ipsilateral pupil
dilation occurs; an expanding clots may lead to herniation

137. Diagnostic and Lab Test
• CT scan, MRI scan

138. Therapeutic Mgt
• Small hematomas will reabsorb spontaneously
• Surgery- needed for epidural hematomas and larger subdural
hematomas

139. Planning & Intervention
• Assess neurological signs on a regular schedule: clear the
client’s nose and mouth of secretions; suction airway as
needed
• Monitor respiratory for rate, depth and rhythm, prep for
oxygen admin and endotracheal intubation for resp. distress

140. • Prep for surgery for deteriorating neurological condition
• Preop and postop care
• Manage increased in ICP

141. Medication Therapy
• Anticonvulsants and steroids to treat seizures and increased
ICP

142. Inflammatory Conditions:
Meningitis
• An inflammation of the meninges of the brain and spinal cord
due to exposure to infectious disease, skull fructure (basilar),
otitis media, sinusitis, mastoiditis, neurosurgery or other
invasive procedures, systemic sepsis and impaired immune
function

143. Etiology and Pathophysiology
• Commonly due to infection of the meninges and CSF
(bacterial, viral, fungal, parasitic or chemicals) causes an
inflammatory response in the meninges.

144. Assessment
Clinical Manifestations
• Restlessness, agitation, irritablity
• Abdominal and back pain
• Nausea and vomiting
• Severe headaches
• Chills and fever
• Seizures
• Confusion and altered LOC
• s/s of increased ICP

145. • Signs of meningeal irritation: nuchal rigidity (stiff neck),
positive Brudzinski’s sign (pain, resistance and hip and knee
flexion occur when the neck is flexed to the chest while lying
supine) and positive Kernig’s sign (pain and/or resistance
occurs w/ flexion of the knee and hip and straightening of the
knee in the supine position) and photophobia

146. Diagnostic and Lab Test
• Lumbar puncture w/ CSF analysis gram stain and cultures
(definitive diagnostic measure for meningitis), cultures of
blood, urine, throat and nose are collected to identify possible
source of infection

147. Therapeutic Mgt
• Bacterial meningitis (a medical emergency if not treated it is
fatal): antibiotics
• Intrathecal (into the subarachnoid space) Ommaya reservoir
to allow administration of antibiotics

148. Planning and Implementation
• Assess neuro status and VS regularly
• Assess and report changes in neuro status or presence of cranial
nerve dysfunction
• Assess, prepare and report any seizure activity
• Assess for signs of increased ICP
• Maintain fluidrestrictions
• Assess for fluid volume deficits, MIO, weight, skin turgor, lab values
and urine concentration.

149. Medication Therapy
• High-dose broad-spectrum antibiotics initially (bacterial
meningitis) to cross the blood-brain barrier; anticonvulsants
(usually phenytoin [Dilantin]) are prescribed to prevent or
control seizures; antipyretic, antiemetic and analgesic
medications are used for symptom relief; IV fluid replacement
is continued until client can resume oral intake

150. Client Education
• Teach the client the name and purpose of prescribed
antibiotics and to take them until they are gone; teach client
about other ordered medications as well
• Teach the client and family to recognize and report signs and
symptoms of ear, throat, and upper respiratory infections so
they can be assessed for meningitis

151. Cerebrovascular Accident (CVA,
brain attack, stroke)
• Description: a CVA is a condition where neurological deficits
occur as a result of decreased blood flow to a localized area of
the brain; hypertension, diabetes mellitus, sickle cell disease,
substance abuse, and atherosclerosis are risk factors for
stroke;

152. Etiology & pathophysiology
• Ischemia followed by cell death is the result of severe and
prolonged cerebral blood flow obstruction

153. 4 Types of Brain Attacks
1. Transient ischemic attack (TIA) – is a brief period of
neurological deficits that resolve w/in 24 hrs; are usually
precursors to permanent CVA; the causes maybe inflammatory
arterial disorders, sickle cell anemia, atherosclerotic changes in
cerebral vessels, thrombosis and emboli

154. 2. Thrombotic CVA- caused by a thrombus occluding a cerebral
vessel thrombi tend to form on atherosclerotic plaque in the
larger arteries while the BP is lower ( during sleep or rest)
-the thrombosis occurs quickly but deficits progress slowly

155. 3. Embolic CVA – is caused by traveling blood clot from other
parts of the body; the CVA has sudden onset w/ immediate
symptoms; if the embolus is not absorbed deficits will be
persistent

156. 4. Hemorrhagic CVA or intracranial hemorrhage occurs when a
blood vessel ruptures, this often occurs in long term poorly
controlled HPN, a ruptured intracranial aneurysm, embolic CVA,
tumors, arteriovenous malformations, anticoagulant therapy,
liver disease and blood disorders
- Fatal because of rapidly increasijg ICP
- Onset is rapid

157. Assessment
A. Clinical Manifestations: vary according to cerebral vessel involved
1. Internal carotid: contralateral motor and sensory deficits of the
arm, leg and face
In dominant hemispheric CVA: aphasia (loss of ability to use language)
In nondominant hemispheric CVA:
• apraxia (inability to perform known tasks)
• agnosia (inability to recognize)
• hemianopsia ( loss of one half of the visual field in each eye)

158. 2. Middle cerebral artery: drowsiness, stupor, coma, contralateral
hemiplegia and sensory deficits of arm and face, aphasia and
homonymous hemianopsia
3. Anterior cerebral artery: contralateral weakness or paralyisis
and sensory loss of the foot and leg, loss of decision making and
voluntary action abilities and urinary incontinence

159. 4. Vertebral artery: pain in face, nose, eye, numbness or
weakness of face on ipsilateral side, problems with gait,
dysphagia (difficulty swallowing) and dysarthria (difficulty
speaking)

160. Diagnostic and Lab Test
• CT and MRI
• Cerebral angiography to detect abnormal vessel structure,
vasospasm, stenosis of the carotid artery and loss of vessel
wall integrity; ultrasound evaluates blood flow

161. Therapeutic Management
• Drug therapy is the most common treatment for CVAs; if it is a
thrombotic stroke, medications could include thrombolytics
and/or heparin
• It is imperative not to disrupt a clot that has formed following
hemorrhagic CVA
• Surgery is not usually indicated as a treatment modality
• Rehabilitation is crucial to improve deficits

162. Priority Nursing Diagnosis
Planning and Implementation
• Encourage active range of motion on unaffected side and passive
range of motion on affected side
• Turn client every 2 hours
• Monitor lower extremities for thrombophlebitis
• Encourage use of unaffected arm for ADLs
• Teach client to put clothing on affected side first

163. • Resume diet orally only after successfully completing a swallowing
evaluation; clients may need thicken liquids, foods w/ the
consistency of oatmeal, and to chew on unaffected side of mouth
(dysphagia diet)
• Collaborate w/ PT for rehab
• Use alternate methods of communication w/ aphasia clients
• Teach client w/ homonymous hemianopsia to overcome the deficit
by turning the head side to side to be able to fully scan the visual
field.

164. Medication Therapy
• Antiplatelet to treat TIA and previous CVA clients (except hemorrhagic
CVAs)
• Acute phase of thrombotic and embolic stroke, thrombolytic therapy –
tissue plasminogen activator is admin w/in 3 hrs to dissolve the clot
• Anticoagulant therapy: heparin or oral anticoagulant
• In clients w/ cerebral edema, hyperosmolar solutions (mannitol) or
diuretics (furosemide or lasix)
• In clients w/ seizures: anticonvulsants-phenytoin (Dilantin),
barbiturates, diazepam (Valium) lorazepam (Ativan)

165. Seizures
• A seizure is an episode of excessive and abnormal electrical
activity of all part of the brain
• It is manifested by disturbances in skeletal motor activity,
sensation, autonomic dysfunction of the viscera, behavior or
consciousness
• Seizures can be due to head injury, infection, acute febrile
state, metabolic and endocrine disorders or exposure to toxins

166. Etiology and Pathophysiology
• Can occur due to metabolic needs, oxygen requirements,
metabolic by-products and compromised cerebral blood flow
• Maybe idiopathic (without identifiable cause) or may occur
secondary to birth traumaa, infection, vascular abnormalities,
trauma or tumors.

167. Seizure Classification
• Partial seizures- begin in one area of the cortex
• Generalized- involved both hemispheres and deeper brain
structures

168. Assessment
• Clinical Manifestations
• Simple partial seizures are limited to one hemisphere;
alteration in motor functions, sensory signs or autonomic or
psychic symptoms
• Complex partial seizures originate in the temporal lobe and
maybe preceded by an aura: an impaired level of
consciousness and repetitive nonpurposeful movements such
as lip-smacking, picking, aimless walking, amnesia

169. • Generalized partial seizures- has spread to both hemispheres
and deeper structures of the brain
• Advance seizure- is a generalized seizure that lasts 5 to 30
seconds; there is a sudden brief cessation of motor activity
and a blank stare; they may occur occasionally or up to a 100
per day; accompanied by eyelid fluttering or automatisms
such as lip-smacking

170. • Tonic-clonic seizures (grand mal)-most common type of
seizures
• Maybe precede by an aura but often w/o warning
• Starts w/ a loss of consciouness and sharp muscle contractions
• May have urinary and/ or bowel incontinence
• Breathing ceases and cyanosis develops during the tonic phase
(about 15 sec to 1 min)

171. • Clonic phase (60 to 90 sec) follows w/ alternating muscle
contraction and relaxation in all extremities, hyperventilation,
and eyes rolled back in the head.
• In the next phase (postictal period) the client is relaxed w/ quiet
breathing, unconscious and unresponsive; the client gradually
regains consciousness and may have transient confusion and
disorientation; clients often complain of head and muscle aches,
fatigue and may sleep several hours

172. • Clients may have amnesia of the seizures and events just prior to
the seizures
• Status epilepticus- is a life-threatening emergency that can
occur during seizure activity; it is characterized by continuous
cycles of tonic-clonic activity w/ short periods of calm
between them; this can interfere w/ respiration; the client is
in great danger of developing hypoxia, hyperthermia,
hypoglycemia and exhaustion if it is not stop

173. Diagnostic and lab Test
• Complete neurological exam, EEG, skull x-ray series, CT scan,
lumbar puncture w/ CSF analysis, blood studies,
electrocardiogram

174. Therapeutic Mgt

175. Planning & Intervention
• Maintain airway patency, turn client to side (maintain airway
and promote drainage of secretions w/o aspiration), prep
oxygen at the bedside, do not force an object into the mouth
of a client
• Do not restrain client
• Protect him from injury

176. Medication Therapy
Anticonvulsants
• Phenytoin (Dilantin)
• Divalproex sodium ( Depakote)
• Valproic acid (Depakene)
• Carbamazepine (Tegretol)
• Gabapentin (neurontin)
• Lamotrigine (lamictal)
• Diazepam (Valium)
• Lorazepam (Ativan)
• phenobarbital

177. Health Education
• Avoid stress, lack of sleep, emotional upset and alcohol use
• Avoid alcohol and limit caffeine
• Avoid tub baths to avoid drowning

178. Intracranial Aneurysm
• is a weak or thin spot on a blood vessel in the brain that
balloons out and fills with blood.
• The bulging aneurysm can put pressure on a nerve or
surrounding brain tissue.
• It may also leak or rupture, spilling blood into the surrounding
tissue (hemorrhage).
• Possible risk factors for rupture include hypertension, alcohol
abuse, drug abuse (particularly cocaine), and smoking

179. Rupture of the Aneurysm can cause:
 serious complications: hemorrhagic stroke, permanent nerve
damage, or death
subarachnoid hemorrhage— bleeding into the space between the
skull bone and the brain.
subarachnoid hemorrhage can cause hydrocephalus, in which the
excessive buildup of CSF in the skull dilates fluid pathways
(ventricles) that can swell and press on the brain tissue.
Vasospasm- other blood vessels in the brain contract and limit
blood flow to vital areas of the brain w/c can cause stroke or tissue
damage.

180. Causes
• Congenital- inborn abnormality in an artery wall.
• common in people with genetic diseases, such as connective
tissue disorders and polycystic kidney disease, and certain
circulatory disorders, such as arteriovenous malformations
(snarled tangles of arteries and veins in the brain that disrupt
blood flow).

181. • trauma or injury to the head
• high blood pressure
• infection
• tumors
• atherosclerosis and other diseases of the vascular system,
• cigarette smoking, and drug abuse.

182. 3 Types of Cerebral Aneurysm
• saccular aneurysm- is a rounded or pouch-like sac of blood
that is attached by a neck or stem to an artery or a branch of a
blood vessel.
• Also known as a berry aneurysm (because it resembles a berry, it
is typically found on arteries at the base of the brain.
• lateral aneurysm- appears as a bulge on one wall of the blood
vessel
• fusiform aneurysm is formed by the widening along all walls
of the vessel.

183. Assessment
Signs and Symptoms
• Small aneurysms are usually asymptomatic
• larger aneurysm that is steadily growing may press on tissues
and nerves
• pain above and behind the eye; numbness, weakness, or paralysis
on one side of the face; dilated pupils; and vision changes.

184. • When an aneurysm hemorrhages, an individual may
experience : a sudden and extremely severe headache, double
vision, nausea, vomiting, stiff neck, and/or loss of
consciousness
• Other signs that a cerebral aneurysm has burst: nausea and
vomiting associated with a severe headache, a drooping
eyelid, sensitivity to light, and change in mental status or level
of awareness, may have seizures, lose consciousness or go
into prolonged coma.

185. Diagnostic Tests
• Angiography is a dye test used to analyze the arteries or veins. intracerebral
angiogram-detects the degree of narrowing or obstruction of an artery or blood
vessel in the brain, head, or neck, identifies changes in an artery or vein such as
a weak spot like an aneurysm.
• Used to diagnose stroke and determine the location, size, and shape of a brain
tumor, aneurysm, or blood vessel that has bled.
• Following the injection of a local anesthetic, a flexible catheter is inserted into an
artery and threaded through the body to the affected artery. A small amount of
contrast dye is released into the bloodstream and a series of x-rays is taken.

186. • Computed tomography (CT) see aneurysms that have burst
and if blood has leaked into the brain. When a contrast dye is
injected into the bloodstream prior to scanning CT
angiography is done
• Magnetic resonance imaging (MRI) and Magnetic resonance
angiography (MRA)
• Cerebrospinal fluid analysis - to detect any bleeding or brain
hemorrhage.

187. Arteriovenous
Malformations
• are defects of the circulatory system that are generally believed to arise during
embryonic or fetal development or soon after birth.
• They are comprised of snarled tangles of arteries and veins.
• The absence of capillaries—small blood vessels that connect arteries to veins—
creates a short-cut for blood to pass directly from arteries to veins. The
presence of an AVM disrupts this vital cyclical process. Although AVMs can
develop in many different sites, those located in the brain or spinal cord—the
two parts of the central nervous system—can have widespread effects on the
body

188. • can form anywhere in the brain or spinal cord wherever
arteries and veins exist
• Some are formed from blood vessels located in the dura
mater (outermost) or in the pia mater (innermost) of the
three membranes surrounding the brain and spinal cord.

189. AVMs affecting the spinal cord are
of two types
• AVMs of the dura mater- affect the function of the spinal cord by transmitting excess
pressure to the venous system of the spinal cord, and AVMs of the spinal cord itself, which
affect the function of the spinal cord by hemorrhage, by reducing blood flow to the spinal
cord, or by causing excess venous pressure.
• Spinal AVMs frequently cause attacks of sudden, severe back pain, often concentrated at
the roots of nerve fibers where they exit the vertebrae; the pain is similar to that caused by
a slipped disk. These lesions also can cause sensory disturbances, muscle weakness, or
paralysis in the parts of the body served by the spinal cord or the damaged nerve fibers.
Spinal cord injury by the AVM by either of the mechanisms described above can lead to
degeneration of the nerve fibers within the spinal cord below the level of the lesion,
causing widespread paralysis in parts of the body controlled by those nerve fibers.

190. • Those located on the surface of the cerebral hemispheres—the
uppermost portions of the brain—exert pressure on the cerebral cortex,
the brain’s “gray matter.” Depending on their location, these AVMs may
damage portions of the cerebral cortex involved with thinking, speaking,
understanding language, hearing, taste, touch, or initiating and
controlling voluntary movements.
• AVMs located on the frontal lobe close to the optic nerve or on the
occipital lobe, the rear portion of the cerebrum where images are
processed, may cause a variety of visual disturbances.

191. • AVMs also can form from blood vessels located deep inside
the interior of the cerebrum. These AVMs may compromise
the functions of three vital structures: the thalamus, which
transmits nerve signals between the spinal cord and upper
regions of the brain; the basal ganglia surrounding the
thalamus, which coordinate complex movements; and the
hippocampus, which plays a major role in memory.

192. • AVMs can affect other parts of the brain besides the cerebrum. The
hindbrain is formed from two major structures: the cerebellum, which is
nestled under the rear portion of the cerebrum, and the brainstem,
which serves as the bridge linking the upper portions of the brain with
the spinal cord. These structures control finely coordinated movements,
maintain balance, and regulate some functions of internal organs,
including those of the heart and lungs. AVM damage to these parts of
the hindbrain can result in dizziness, giddiness, vomiting, a loss of the
ability to coordinate complex movements such as walking, or
uncontrollable muscle tremors

193. Assessment
Symptoms
• Seizures and headaches
• Seizures can be partial or total, involving a loss of control over
movement, convulsions, or a change in a person’s level of
consciousness.
• muscle weakness or paralysis in one part of the body
• loss of coordination (ataxia) that can lead to such problems as
gait disturbances;

194. • apraxia, or difficulties carrying out tasks that require planning;
• dizziness;
• visual disturbances such as a loss of part of the visual field;
• an inability to control eye movement;
• papilledema (swelling of a part of the optic nerve known as
the optic disk)

195. • various problems using or understanding language (aphasia);
• abnormal sensations such as numbness, tingling, or spontaneous
pain (paresthesia or dysesthesia);
• memory deficits; and mental confusion,
• hallucinations, or dementia.
• Researchers have recently uncovered evidence that AVMs may also
cause subtle learning or behavioral disorders in some people during
their childhood or adolescence, long before more obvious symptoms
become evident.

196. • Bruit- the rhythmic, whooshing sound caused by excessively rapid
blood flow through the arteries and veins of an AVM.
• vein of Galen defect – a lesion located deep inside the brain. It is
frequently associated with hydrocephalus, swollen veins visible on
the scalp, seizures, failure to thrive, and congestive heart failure.
Children born with this condition who survive past infancy often
remain developmentally impaired.

197. • AVMs become symptomatic only when the damage they
cause to the brain or spinal cord reaches a critical level
• AVMs damage the brain or spinal cord through three basic
mechanisms: by reducing the amount of oxygen reaching
neurological tissues; by causing bleeding (hemorrhage) into
surrounding tissues; and by compressing or displacing parts of
the brain or spinal cord.

198. Pathophysiology
• AVMs compromise oxygen delivery to the brain or spinal cord by altering normal
patterns of blood flow. Arteries and veins are normally interconnected by a
series of progressively smaller blood vessels that control and slow the rate of
blood flow. Oxygen delivery to surrounding tissues takes place through
capillaries, where the blood flows most slowly. The arteries and veins that make
up AVMs, however, lack this intervening capillary network. Instead, arteries
dump blood directly into veins through a passageway called a fistula. The flow
rate is uncontrolled and extremely rapid—too rapid to allow oxygen to be
dispersed to surrounding tissues. When starved of normal amounts of oxygen,
the cells that make up these tissues begin to deteriorate, sometimes dying off
completely.

199. • This abnormally rapid rate of blood flow frequently causes blood
pressure inside the vessels located in the central portion of an AVM
directly adjacent to the fistula—refer as nidus,—to rise to dangerously
high levels. The arteries feeding blood into the AVM often become
swollen and distorted; the veins that drain blood away from it often
become abnormally constricted (stenosis).
• the walls of the involved arteries and veins are often abnormally thin
and weak. Aneurysms—balloon-like bulges in blood vessel walls that are
susceptible to rupture—may develop

200. • large lesions may compress the spinal cord or distort the shape of an
entire hemisphere of the brain w/c can constrict the flow of CSF—a
clear liquid that normally nourishes and protects the brain and spinal
cord—by distorting or closing the passageways and open chambers
(ventricles) inside the brain that allow this fluid to circulate freely.
• As CSF accumulates, hydrocephalus results w/c buildup further
increases the amount of pressure on fragile neurological structures,
adding to the damage caused by the AVM itself.

201. Types of vascular lesions affect
the central nervous system
• Cavernous malformations - lesions formed from groups of tightly
packed, abnormally thin-walled, small blood vessels that displace
normal neurological tissue in the brain or spinal cord.
• The vessels are filled with slow-moving or stagnant blood that is usually
clotted or in a state of decomposition. Although usually do not hemorrhage
as severely as AVMs do, they sometimes leak blood into surrounding
neurological tissues because the walls of the involved blood vessels are
extremely fragile.
• Although they are often not as symptomatic as AVMs, cavernous
malformations can cause seizures in some.

202. • Capillary telangiectases- The lesions consist of groups of
abnormally swollen capillaries and usually measure less than
an inch in diameter.
• rarely cause extensive damage to surrounding brain or spinal cord
tissues. Any isolated hemorrhages that occur are microscopic in
size. Thus, the lesions are usually benign. However, in some
inherited disorders in which people develop large numbers of
these lesions it can contribute to the development headaches or
seizures.

203. • Venous malformations- lesions consist of abnormally
enlarged veins. These structural defect usually does not
interfere with the function of the blood vessels
• Venous malformations rarely hemorrhage.
• Most venous malformations do not produce symptoms, remain
undetected, and follow a benign course.

204. Cause
• scientists believe that they most often result from mistakes that
occur during embryonic or fetal development linked to genetic
mutations.
• A few types of vascular malformations are known to be hereditary
and thus are known to have a genetic basis.
• Some evidence also suggests that at least some of these lesions are
acquired later in life as a result of injury to the central nervous
system.

205. Diagnostic test
• Angiography provides the most accurate pictures of blood
vessel structure in AVMs.
• computed axial tomography (CT) and magnetic resonance
imaging (MRI) scans
• magnetic resonance angiography (MRA)

206. Treatment
• the definitive treatment for AVMs is either surgery or focused
irradiation therapy.
• Venous malformations and capillary telangiectases rarely require
surgery-their structures are diffuse and usually not suitable for
surgical correction and they usually do not require treatment
• Cavernous malformations - surgery on these lesions is less common
than for AVMs because they do not pose the same risk of
hemorrhage.

207. • Conventional surgery involves entering the brain or spinal cord
and removing the central portion of the AVM, including the
fistula, while causing as little damage as possible to
surrounding neurological structures.
• This surgery is most appropriate when an AVM is located in a
superficial portion of the brain or spinal cord and is relatively
small in size.

208. • Endovascular embolization and radiosurgery are less invasive than conventional surgery
• In endovascular embolization the surgeon guides a catheter though the arterial network
until the tip reaches the site of the AVM. The surgeon then introduces a substance that will
plug the fistula, correcting the abnormal pattern of blood flow. This process is known as
embolization because it causes an embolus to travel through blood vessels, eventually
becoming lodged in a vessel and obstructing blood flow.
• The embolic materials used to create an artificial blood clot in the center of an AVM include
fast-drying biologically inert glues, fibered titanium coils, and tiny balloons. it is usually
used as an adjunct to surgery or to radiosurgery to reduce the blood flow through the AVM
and make the surgery safer.

209. • Radiosurgery is less invasive therapeutic approach w/c
involves aiming a beam of highly focused radiation directly on
the AVM. The high dose of radiation damages the walls of the
blood vessels making up the lesion. Over the course of the
next several months, the irradiated vessels gradually
degenerate and eventually close, leading to the resolution of
the AVM.

210. Headache
-warning signals of more serious disorders for headaches caused
by inflammation, including those related to meningitis as well as
those resulting from diseases of the sinuses, spine, neck, ears,
and teeth.
4 types of headache
1. Vascular headache

211. • most common type of vascular headache is migraine
• Migraine headaches are usually characterized by severe pain on
one or both sides of the head, an upset stomach, and, at times,
disturbed vision
• toxic headache produced by fever
• "cluster” headaches- cause repeated episodes of intense pain,
and headaches resulting from high blood pressure

212. 2. muscle contraction (tension)-Muscle contraction headaches
appear to involve the tightening or tensing of facial and neck
muscles
3. Traction-Traction and inflammatory headaches are symptoms
of other disorders, ranging from stroke to sinus infection
4. inflammatory

213. Treatment
• Drug therapy: sumatriptan, methysergide maleate, which
counteracts blood vessel constriction, propranolol hydrochloride,
ergotamine tartrate (a vasoconstrictor that helps counteract the
painful dilation stage of the headache); amitriptyline (an
antidepressant); valproic acid, (anticonvulsant); and verapamil, a
calcium channel blocker
• biofeedback training
• stress reduction, relaxation training
• elimination of certain foods from the diet are the most common
methods of preventing and controlling migraine and other vascular
headaches.
• Regular exercise such as swimming or vigorous walking, can also
reduce the frequency and severity of migraine headaches.

214. Disturbances in Peripheral Nerve/
Neurologic Function
• Cranial nerve disorders- involve dysfunction of the cranial
nerves, the most commonly affected are the trigeminal nerves
(CN V) and the facial nerve (CN VII);
• trigeminal neuralgia is a chronic disease of the trigeminal nerve
that causes severe facial pain;
• Bell’s palsy is a unilateral paralysis of the facial muscles.

215. Etiology & Pathophysiology
• Trigeminal neuralgia: cause is unknown
• It affects 1 or more of the 3 divisions of the trigeminal nerve; the
opthalmic, maxillary and mandibular
• Bell’s palsy: cause is unknown
• Inflammation of the nerve an a viral cause has been suggested

216. Assessment
• Clinical Manifestations
1. Trigeminal neuralgia
 Characteristic symptom: Brief intense skin surface pain (May
occur as frequently as 100 times a day or as little as a few times
each year; pain typically starts peripherally and advances
centrally; motor or sensory deficits do not occur; some clients
may have trigger zones that initiate the onset of pain; in others,
pain may be triggered by light touch, eating, swallowing, talking,
shaving, sneezing, brushing teeth or washing the face.

217. 2. Bell’s Palsy: one-sided paralysis of the facial muscles, paralysis
of the upper eyelid with loss of the corneal reflex on the affected
side, loss or impairment of taste over the anterior portion of the
tongue on affected side, and increased tearing from lacrimal
gland on the affected side.

218. Diagnostic and laboratory test
findings
• There are no specific laboratory test specific to cranial nerve
disorders

219. Therapeutic Management
a. Trigeminal neuralgia treatment
• Is centered on controlling pain with anticonvulsant
medications such as carbamazepine (Tegretol); surgical
procedures include microvascular decompression (removal of
blood vessel from posterior trigeminal root) or rhizotomy,
(surgical severing of the nerve root)

220. b. Bell’s Palsy
• The only medical treatment that influences outcome is
administration of corticosteroids , but their use has been
questioned; antiviral medication is also currently very popular

221. Priority Nursing Diagnosis
• Risk for imbalanced nutrition: less than body requirements; Pain;
Risk for injury

222. Planning and Implementation
a. Encourage client to chew on unaffected side
b. Monitor dietary intake
c. Assist with physiotherapy, including moist heat, gentle
massage, and facial nerve stimulation with faradic current
d. Protect cornea with artificial tears, sunglasses, eye patch at
night, and gentle intermittent closure of eye

223. Medication Therapy
a. Trigeminal neuralgia
• The most useful drug for controlling pain is carbamazepine
(Tegretol); when this is not effective, phenytoin (Dilantin) is
tried
b. Bell’s Palsy
• A corticosteroid such as prednisone (Deltasone) influences
outcome by decreasing edema of nerve tissue; antivirals are
also used

224. Client Education
a. Wear an eye patch at night
b. Wear protective glasses when outside
c. Inspect the inside of mouth on affected side for food that
may collect between mouth and teeth

225. Evaluation
• The eye is protected; pain is controlled

226. Guillain Barre Syndrome
• An acute, rapidly-progressive inflammation of peripheral
motor and sensory nerves characterized by motor weakness
and paralysis that ascends from lower extremities in a
majority of cases

227. Etiology & Pathophysiology
• Etiology: unknown
• Autoimmune reaction is suspected because it often develops
after viral infection, immunizations, fever, injury and surgery
• Antibody (IgM) formation targets peripheral nerve myelin, w/c
damages myelin sheat and disrupts nerve conduction; the
nerve remyelinizes in the opposite direction of the
demyelination.

228. Assessment
• Clinical Manifestations
• Weakness/paresis or partial paralysis progressing upward
from lower extremities (ground to the brain) and then to total
paralysis requiring ventilatory support
• Paresthesias (numbness and tingling) and pain
• Muscle aches, cramping and nighttime pain

229. • Respiratory compromise and/or failure (dyspnea, diminished
vital capacity and breath sounds), decreasing oxygen
saturation, abnormal ABGs
• Difficulty w/ extraocular eye movements, dysphagia, diplopia,
difficulty speaking
• Autonomic dysfunction (orthostatic hypotension),
hypertension, change in HR, bowel and bladder dysfunction,
flushing , diaphoresis

230. Diagnostic and Lab Findings
• Diminished nerve conduction test result , CSF examination
shows elevated protein

231. Therapeutic Mgt
• Supportive care to maintain functionof all body system (resp,.
Cardiac, renal)
• Plasmapheresis: plasma is removed and separated from whole
blood; blood cells are then returned w/o the plasma to
remove antibodies that cause disorder; monitor for
complications of this therapy, w/c include bleeding from loss
of clotting factors and f/e imbalance.

232. Planning & Intervention
• Monitor resp status: breath sounds, rate, depth, gag, coughing,
swallowing
• Monitor cardiac status: HR, BP, dysrhythmias
• Administer chest physiotherapy and pulmonary hygiene measures
• Maintain adequate nutrition: administer enteral or parenteral
nutrition as needed; if can swallow assist w/ small frequent feedings
of soft foods; weigh client weekly; check electrolytes status; provide
mouth care every 2 hours.

233. • Monitor bowel and bladder function: Assess
• bowel sounds and frequency
• Amount, color of bowel movements
• Check for distention and residuals in client who cannot void
spontaneously
• Perform intermittent catheterization as needed
• Encourage fluid intake to 3500 ml/day

234. • Prevent complications of immobility:
• Encourage use of weak extremities as able
• Provide assistance w/ ROM and exercises prescribed by PT;
protect immobile extremities w/ use of air mattress or special
bed, and elbow and heel protectors; turn and reposition every 2
hours; elevate extremities to prevent dependent edema; use
antiembolism compression devices/stockings

235. • Provide eye care for the client with inability to close eyelids
completely; instill artificial tears, cleanse eyes as needed, use
eye shields and tape eyes closed if needed.
• Provide comfort and analgesics as needed
• Promote communication w/ client and family, using
alternative means of communication if client is on ventilator
or is unable to speak because of weak speech muscles

236. • Initiate discharge planning at time of admission

237. Medication Therapy
• IV immunoglobulins (may result in low grade fever, muscle
aches, headache, acute renal failure and retinal necrosis
(rare); adrenocorticotropic hormone (ACTH) and
corticosteroids or anti-inflammatory drugs; supportive
medications that include stool softeners, antacids or H2
receptor antagonists and analgesics.

238. Peripheral Nerve Disorders
• Multiple Sclerosis- a chronic disorder of the CNS where the myelin
and nerve axons in the brain and spinal cord are destroyed
4 Forms based on the Rate of Progression
1. benign
2. relapsing-remitting
3. primary progressive
4. secondary progressive

239. Etiology & Pathophysiology
• Etiology: unknown, possibly autoimmune or genetic or caused by
childhood viral infections
• The destruction of myelin and nerve axons causes a temporary,
repetitive or sustained interruption in the conduction of nerve
impulses which causes its symptoms
• Plaque formation occurs throughout the white matter of the CNS,
w/c also affects the nerve impulses of optic nerves, cervical spinal
cord, thoracic and lumbar spine

240. • Inflammation occurs around the plaques as well as normal
tissues
• Astrocytes appear in the lesions and scar tissue forms,
replacing the axons and leading to permanent disability.

241. Assessment
• Clinical Manifestations: visual disturbances or blindness
(retrobulbar neuritis), sudden, progressive weakness of one or
more limbs, spasticity of muscles, nystagmus, tremors, gait
instability, fatigue, bladder dysfunction (UTIs, incontinence),
depression

242. Dx and Lab Findings
• Lumbar puncture for CSF (clonal IgG bands present); MRI, Ct
scans, muscle testing shows characteristic changes

243. Therapeutic Mgt
• No cure, supportive care is indicated

244. Priority Nrsg Dx
• Risk for disuse syndrome
• Disturbed body image
• Risk for infection

245. Planning and Implementation
• Overall goal of care is to maintain independent as mush as possible
• Rest periods to prevent fatigue w/c is an exacerbating factor
• Assist client w/ ADLs
• Maintain fluid intake of atleast 2000 ml/day to maintain bowel and
bladder function and prevent impaction and/or urinary infection
• Avoid infection, illness can act as stressor w/c can trigger
exacerbation

246. • Possible triggers are : fatigue, extreme temperature, illness

247. Medication Therapy
• Immunosuppressant therapy, antiviral drugs, corticosteroids,
antibiotics for urinary tract infections, interferon-alpha,
glatiramer (Copaxone), anticholinergic drugs and
antispasmodics

248. Parkinson’s Disease (PD)
• Is a progressive, degenerative neurological disease
characterized by bradykinesia, muscle rigidity and
nonintentional tremor;

249. Etiology & Pathophysiology
• Atrophy occurs in the substantia nigra that produces the
neurotransmitter dopamine; as dopamine decreases,
acetylcholine is no longer inhibited.
• There is imbalance of these neurotransmitters

250. Assessment
• Clinical manifestations: begin subtly; fatigue and a slight
resting tremor may be the only initial symptoms
• bradykinesia- slow movements caused by muscle rigidity; they
affect also the eyes, mouth, voice; staring gaze
• Uncoordinated movements

251. • Short stepped, shuffling and propulsive gait, w/c leads to
increased risk of falls
• Postural disturbance, trunk tilted forward
• Seborrhea
• Excessive sweating of face and neck w/ absence of sweating on
trunk and extremities
• Heat intolerance
• Constipation, anxiety, depression
• Sleep disturbances and dysphagia

252. Diagnostic & lab Tests
• CBC shows anemia
• Chemistry profile show albumin and protein
• Drug screens to rule out toxic causes
• EEG shows a slow pattern and disorganization
• An upper GI series show delayed emptying, distention and
megacolon
• Video fluoroscopy show slowed response of the cricopharyngeal
muscles when swallowing

253. Therapeutic Mgt
• Medications
• Surgery
• Rehabilitation to optimize functional level

254. Planning & Implementation
• Perform active ROM twice a day
• Ambulate at least 4 times a day
• Use assistive devices when recommended
• Assess communication skills, speech, hearing, and writing
• Consult with a speech pathologist if necessary
• Monitor diet for foods high in bulk and fluids

255. Medication Therapy
• Drugs used to treat: monoamine oxidase (MAO) inhibitors,
dopaminergics, dopamine agonists, and anticholinergics
• Antidepressant used to treat depression (amitriptyline)
• Propranolol to treat tremors

256. Client Education
• Teach preventive measures for malnutrition, falls and other
environmental hazards, constipation, skin breakdown from
incontinence and joint contractures
• Trait gait training and exercise for improving ambulation,
swallowing, speech, and self-care.

257. Myasthenia Gravis
• A chronic progressive disorder of the peripheral nervous
system affecting transmission of nerve impulses to voluntary
muscles; causes muscles weakness and fatigue that increases
with exertion and improves w/ rest; eventually leads to fatigue
w/o relief from rest

258. Etiology & Pathophysiology
• Etiology: unknown; family Hx of autoimmune disorders,
thyroid tumors
• An autoimmune process triggers the formation of
autoantibodies that decrease the number of acetylcholine
receptors and widen the gap between the axon ending and
the muscle fiber in the neuromuscular (myoneural) junction

259. • Is associated / continued production of autoantibodies by the
thymus gland in 75 % of cases
• The onset is usually slow but can be precipitated by emotional
stress, hormonal disturbance (pregnancy, menses, thyroid
disorders), infections/vaccinations, trauma and surgery, temperature
extremes, excessive exercise, and drugs that block or decrease
neuromuscular transmission (opioids, sedatives, barbiturates,
alcohol, quinidine, anesthetics), and thymus tumor

260. Assessment
Clinical Manifestations
• Mild diplopia (double vision) and unilateral ptosis (eyelid drooping)
caused by weakness in the extraocular muscles; weakness may also
involve the face, jaw, neck and hip.
• Complications arise when severe weakness affects the muscles of
swallowing, chewing and respiration; respiratory distress is
manifested by tachypnea, decreased depth, abnormal ABGs, oxygen
saturation<92% and decreased breath sounds.

261. • Bowel and bladder incontinence, paresthesias and pain in weak
muscles.
• Myasthenic crisis: sudden motor weakness; risk of respiratory failure
and aspiration; most often caused by insuficient dose of medication
or an infection.
• Cholinergic crisis-severe muscle weakness caused by
overmedication; also cramps, diarrhea, bradycardia, bronchial
spasm w/ increased pulmonary secretions and risk of respiratory
compromise

262. Diagnostic and Laboratory Tests
• ABG and pulmonary function tests may show repiratory
insufficiency
• EMG- electromyography shows decreased amplitude when motor
neurons are stimulated
-electromyogram is a test that is used to record the electrical
activity of muscles. When muscles are active, they produce an
electrical current. This current is usually proportional to the level of
the muscle activity. - also referred to as a myogram.

263. • Confirmation of the clinical diagnosis can be made by IV
administration of edrophonium chloride (Tensilon), w/c allows
voluntary muscle contraction; Tenslon allows acetylcholine to
bind w/ its receptrs, w/c temporarily improves symptoms;
weakness returns after the effects of Tensilon are
discontinued; a positive Tensilon test confirms diagnosis of
myasthenia gravis

264. Therapeutic Mgt
• Focuses on medication management w/ cholinesterases:
neostigmine (Prostigmin), pyridostigmine (Mestinon);
immunosuppressants: corticosteroids, azathiopirine (Imuran),
and cyclosporine (Cytoxan); antiinflmmatory drugs;
thymectomy ; plasmapheresis- removes IgG antibodies,
atropine sulfate (Atropine) for cholinergic crisis

265. Priority Nrsg Dx
• Ineffective airway clearance
• Impaired swallowing
• Activity intolerance
• Risk for injury
• Disturbed body image

266. Planning & Implementation
• Maintain effective breathing pattern and airway clearance;
thoroughly assess for respiratory distress
• Monitor meals and teach client to bend head slightly forward
while eating/drinking to improve swallowing
• Avoid exposure to infections, esp. respiratory

267. • Teach re effective coughing, use physiotherapy and incentive
spirometry; have oral suction available, teach client how to
use it; prepare for intubation if needed
• Provide adequate nutrition: schedule meds 30 to 45 minutes
before eating for peak muscle strength while eating; offer
food frequently in small amounts that are easy to chew and
swallow-soft or semisolid as needed; administer IVF and NGT
feedings if unable to swallow

268. • Promote improved physical mobility w/ referrals to PT/OT
• Provide eye care: instill artificial tears; use a patch over one
eye for double vision; wear sunglasses to protect eyes from
bright lights
• Promote positive body image and coping skills: encourage
participation in treatment plan; plan time for active listening
and encourage client to express feelings; reinforce progress
and explain all care

269. Medication Therapy
• Anticholinesterases, neostigmine (Prostigmin), pyridostigmine
(Mestinon); immunosupressants such as corticosteroids,
azathioprine (Imuran), and cyclosporine (Cytoxan); anti-
inflammatory drugs

270. Client Education
Instruct to :
• Plan rest periods and to conserve energy; plan major activities
early in day; schedule activities during peak medication effect
• Avoid extremes of hot and cold, exposure to infections,
emotional stress amd meds that may worsen or precipitate an
exacerbation (alcohol, sedatives, local anesthetics)
• Signs of sress

271. • Encourage to wear a Med-alert bracelet
• Alternative methods of communication if needed: eye blink,
finger wiggle for yes/no; flash cards or communication board

272. Evaluation
• Maintain patenct airway and breathing w/o aspiration
• Maintains ADL w/ assistance
• Demonstrate adequate coping skills for managing chronic and
debilitating illness

273. Alzheimer’s Disease
• Is a progressive dementia w/ irreversible deterioration of
general intellectual function; it affects adults in middle to late
life; AD incidence increases w/ age

274. Etiology & Pathophysiology
• Cause: unknown
• Chemical changes in the brain are found in the hippocampus,
and frontal and temporal lobes of the cerebral cortex; the
clients lose nerve cells; perfusion to affected areas is
decreased; the brain atrophies; amyloid, a starch-like protein
accumulates in brain tissue; as AD progresses more areas of
the brain are affected

275. Assessment
Clinical Manifestations: AD is classified into 3 stages based on
manifestations and abilities
• Early stage: lasts 2 to 4 years: the client appears healthy and
alert but maybe restless or uncoordinated; cognitive
impairment is not apparent; memory impairment, subtle
changes in personality, and problems doing simple calculations
may be the first manifestations of AD

276. • Middle stage: Lasts 2 to 12 years; memory impairment is more
evident (recent memory is lost before remote memory); the client is
less able to behvae spontaneously; the client may wander or get
lost; increasing confusion and disorientation evethough there are
periods of lucidity; language deficits including paraphasia (using the
wrong word) and echolalia (repetition of words or phrases) are
common; judgment is impaired; self-care is compromised because
sequencing of tasks is lost; sensorimotor deficits of apraxia,
astereognosis, and agraphia

277. • Late stage: Lasts 2 to 4 years; characterized by increasing
dependence, aphasia, incontinence, loss of motor skills and
gross loss of cognitive abilities

278. Diagnostic and Lab Tests
• To diagnose other causes of symptoms are ruled out to dx an
AD
• CBC reflects anemia
• EEG shows slowing in the later stages of AD
• Ct and MRI shows atrophy
• Psychometric evaluations reflect memory and cognitive
impairment

279. Therapeutic Mgt
• No cure , the main objective is to match function w/
environment; safety and least restrictive environment

280. Priority Nrsg Dx
• Altered thought processes, anxiety, hopelessness

281. Planning & Implementation
• Label room, drawers or other items
• Orient client o person, place, time as needed
• Keep daily routine consistent as possible
• Remove client from activities that increase anxiety
• Avoid criticizing or judging expressed feelings
• Provide realistic information about disease process

282. • Use therapeutic communication and listening skills to reduce
agitartion; listening to client’s recollection of past events

283. Medication Therapy
• Reversible acetylcholinesterase inhibitors, such as tacrine
(cognex) donazepil (Aricept), and rivastigmine (Exelon)
improves memory;
• Avoid antihistamine and TCA beauces they have high
anticholinergic activity
• Tranquilizer to treat agitation

284. Client Education
• Avoid stopping reversible acetylcholinesterase inhibitors
suddenly because it can trigger behavior problems
• Teach caregivers about community resources
• Educate client and caregivers about expectations for client’s
disease process

285. Amyotrophic Lateral Sclerosis
• ALS-Amyotrophic lateral sclerosis is a rapidly progressive, fatal
neurodegenerative disease that attacks the nerve cells in the
brain and spinal cord responsible for controlling voluntary
muscles.
• There is gradual degeneration and death of motor neurons.
• Also called Lou Gehrig's disease.

286. • progressive degeneration of the motor neurons
motor neurons die,
lost of ability of the brain to initiate and control
muscle movement.
may become totally paralyzed.

287. • Motor neurons are nerve cells located in the brain, brainstem, and spinal cord
that serve as controlling units and vital communication links between the
nervous system and the voluntary muscles of the body. Messages from motor
neurons in the brain (called upper motor neurons) are transmitted to motor
neurons in the spinal cord (called lower motor neurons) and from them to
particular muscles. In ALS, both the upper motor neurons and the lower motor
neurons degenerate or die, ceasing to send messages to muscles.
• Unable to function, the muscles gradually weaken, waste away (atrophy), and
twitch (fasciculations) . Eventually, the ability of the brain to start and control
voluntary movement is lost.

288. • Cause: Unknown
• Scientists have discovered that mutations in the gene that
produces the SOD1 enzyme were associated with some cases
of familial ALS.

289. Clinical Manifestations
• Early symptoms: increasing muscle weakness, especially involving
the arms and legs, twitching, cramping, or stiffness of muscles
(spasticity) ; slurred (dysarthria) and nasal speech; or difficulty
chewing or swallowing (dysphagia) or breathing.
• exaggerated reflexes (hyperreflexia), muscle cramps
• Babinski's sign (the large toe extends upward as the sole of the foot
is stimulated in a certain way) indicates upper motor neuron
damage

290. • When muscles no longer receive the messages from the motor
neurons that they require to function, the muscles begin to atrophy
(become smaller). Limbs begin to look "thinner" as muscle tissue
atrophies.
• eventually patients will not be able to stand or walk, get in or out of
bed on their own, or use their hands and arms.
• Difficulty swallowing and chewing impair the patient's ability to eat
normally and increase the risk of choking

291. • usually the person's mind or intelligence is not impaired,
several recent studies suggest that some ALS patients may
have alterations in cognitive functions such as depression and
problems with decision-making and memory.
• The person's senses are not impaired

292. Dx Tests
• No one test can provide a definitive diagnosis
• the diagnosis of ALS is primarily based on the symptoms and
signs and a series of tests to rule out other diseases.
• electromyography (EMG)- detects electrical activity in
muscles.
•

293. • nerve conduction velocity (NCV)- helps rule out other diseases,
abnormalities in the NCV suggest, for example, that the patient has a
form of peripheral neuropathy (damage to peripheral nerves) or
myopathy (muscle disease) rather than ALS.
• magnetic resonance imaging (MRI), to take detailed images of the brain
and spinal cord. Although these MRI scans are often normal in patients
with ALS
• they can reveal evidence of other problems that may be causing the
symptoms, such as a spinal cord tumor, aherniated disk in the neck,
syringomyelia, or cervical spondylosis.

294. Therapy
• No cure
• The first drug treatment for the disease -- riluzole (Rilutek) is
believed to reduce damage to motor neurons by decreasing
the release of glutamate, but it does not reverse the damage
already done to motor neurons
• Symptomatic treatment to improve the quality of life for
patients.

295. • ventilatory support- most people with ALS die from
respiratory failure

296. Huntington’s Chorea
• Huntington's Disease (HD) is a progressive brain disorder
caused by a defective gene.
• caused by a single defective gene (mutation) on chromosome
4
• The huntingtin gene defect involves extra repeats of one
specific chemical code in one small section of chromosome 4.
The normal huntingtin gene includes 17 to 20 repetitions of
this code. The defect that causes Huntington's disease
includes 40 or more repeats.

297. • The defective gene codes the blueprint for a protein called
huntingtin.
• Defective huntingtin protein leads to brain changes that cause
abnormal involuntary movements, a severe decline in thinking
and reasoning skills, and irritability, depression and other
mood changes.

298. • The disease destroys cells in the
basal ganglia, the part of the brain
that controls movement,
emotion, and cognitive ability.
• The job of its protein product,
huntingtin, is to direct the
delivery of small packages
(vesicles containing important
molecules) to the outside of the
cell.

299. • have an abnormally high number of these CAG triplets,
approximately 40 or more. That disrupts the function of the
gene's protein product.
• The brain cells accumulate clumps of protein that become
toxic, resulting in cell death.

300. • Huntington's disease is inherited in an autosomal dominant
pattern

301. Signs & Symptoms
• The hallmark symptom: uncontrolled /abnormal movement of
the arms, legs, head, face and upper body (difficulty walking,
speaking, and/or swallowing) , lack of coordination, twitching
or other uncontrolled movements
• decline in thinking and reasoning skills, poor memory,
concentration, judgment and ability to plan and organize and
talk

302. • Irregular, random movements of the arms, legs and face;
restlessness, fidgeting
• mental deterioration, premature senility, and rigid muscles
• brain changes lead to mood swing: depression, anxiety, and
uncharacteristic anger and irritability.
• common symptom: obsessive-compulsive behavior, leading a
person to repeat the same question or activity over and over.

303. Dx Test
• Genetic tests for Huntington's disease measure the number of
repeats present in an individual's huntingtin protein gene.

304. Therapy
• currently no cure
• Treatments focus on managing symptoms, such as anxiety,
depression and insomnia
• Experts recommended the following treatments as first-line
strategies for 3 of the disease's most troubling symptoms:
1. Chorea (involuntary movements): atypical antipsychotic drug.

305. 2. Irritability: For severe anger and threatening behavior, an
atypical antipsychotic drug is the first-line approach; For less
severe, nonthreatening irritability, selective serotonin reuptake
inhibitor (SSRI), which is a type of antidepressant.
3. Obsessive-compulsive thoughts and actions: SSRIs as the
front-line treatment for obsessive-compulsive behaviors.

306. Trauma of the Spinal Cord
• Are injuries usually due to trauma
• The injury affects motor and sensory function at the level of
injury and below
• Perception, sexual function and elimination are affected