Neurological disorders

CARE OF CLIENTS
WITH
NEUROLOGICAL
DISORDERS
Prepared by: Jessica M.
Saldana RN., MAN

ANATOMY AND PHYSIOLOGY OF THE
NERVOUS SYSTEM:
 The neuron is the structural and functional unit of the
nervous system.

Anatomy and Physiology
 The nervous system has three major divisions, the
central nervous system (CNS), the peripheral nervous
system (PNS) and the autonomic nervous system
(ANS).
 The CNS is composed of the brain and the spinal cord.
It regulates the higher level processes.
 The PNS is composed of 12 pairs of cranial nerves
and 31 pairs of spinal nerves. It provides pathways to
the CNS.
 The ANS (sympathetic and parasympathetic nervous
system coordinates involuntary activities, eg., digestion,
breathing

 The Central Nervous System (CNS)
1. The Brain
a. Cerebrum. Is divided into 2 sections called
cerebral hemispheres.
The outermost layer of the cerebrum is called
the cerebral cortex.

 The falx cerebri divides the brain into right and left
cerebral hemispheres; the commissural tracts known as
corpus collosum connects the 2 cerebral hemispheres.
 Both the left cortex and the right cortex interpret sensory
data, stores memories, learn and form concepts.
 The left cortex has dominance for systematic analysis
language and speech, mathematics, abstraction and
reasoning.
 The right cortex has dominance for assimilation of
sensory experiences, such as visual- spatial information
and activities such as dancing gymnastics, music and art
appreciation.

 The cerebral cortex is composed of gray mater formed
into raised convolutions called gyri; the shalow grooves
between the gyri are called sulci.

 The sulci divide the cerebral cortex into five lobes:
 Frontal lobe
 Parietal lobe
 Temporal lobe
 Occipital lobe
 Central lobe (insula)

 The frontal lobe has
the following functions:
 Controls voluntary motor
activity precentral gyrus
or motor cortex)
 Expressive (motor)
speech- ability to speak
clearly (Broca’s area).
Damage to this area
leaves the client unable
to speak clearly.
(expressive aphasia).

 The prefrontal areas
control
1) Concentration(attention
over time)
2) Motivation
3) Ability to formulate or
select goals
4) Ability to plan (e.g. future
planning)
5) Ability to initiate, maintain,
or terminate actions.

6) Ability to self- monitor
7) Ability to use feedback (“executive feedbacks”)
8) Reasoning, problem-solving activities, emotional stability.
9) Development of personality
10) Sense of humor
 The parietal lobe has the following functions:
1) Sensory perception (tactile sensations like temperature,
touch, pain, pressure)- post central gyrus.
2) Concept formation and abstraction.
3) Spatial Orientation and awareness of size and shapes
(stereognosis)and body position (proprioception)-right pareital
lobe.

 4) Right –left orientation and mathematics-left parietal
lobe.
 The temporal lobe has the following functions:
1) Auditory receptive area-ability to hear.
2) Auditory association areas- ability to store spoken
language memories (left Temporal); sound memories
that are not language like music, various animal sounds,
other noises (right temporal). Damage to these areas
leaves client unable to understand spoken or written
language or to recognize music or others environmental
sounds.

3) Wernicke’s area facilitates understanding language.
Damage to this area results to receptive or auditory
aphasia.
 The occipital lobe has the following functions:
1) Visual receptive (interpretation) area.
2) Visual association areas- storage of visually
recognize and understand the environment.
3) Visual speech center enables a person to read.
Damage to this area leaves the client unable to read
(Alexia).

 The central (insula) lobe. Nerve fibers for taste pass through
the parietal lobe to the insular lobe. Many association fibers
leading to other parts of the cerebral cortex pass through this
lobe.
b. Hippocampus. Is a part of the medial section of the temporal
lobe. It plays a vital role in the process of the memory. Three
levels of memory have been identified:
 Short-term (recent) memory is lost after seconds or
minutes.
 Intermediate memory lasts days and weeks and
eventually lost. The outermost layer of the cerebrum is
called the cerebral cortex.

The hippocampus assists in the conversion of short
term memory into the intermediate and long-term
memory in the thalamus.
c. Basal ganglia. Is composed of layers of gray mater
buried deep in the cerebral hemispheres. These
structures include nucleus Putamen, globus pallidus,
substantia nigra, subthalmic nucleus.
The basal ganglia is important in controlling
complex motor activity.

d. Diencephalon. Is composed of the thalamus and the
hypothalamus.
 The thalamus channels all sensory information
except smell to the appropriate cortical cells.
 The hypothalamus regulates the autonomic nervous
system (ANS) functions such as heart rate, blood ,
pressure, water and electrolyte balance, stomach
and intestinal motility, glandular activity, body
temperature, hunger, body weight and sleep-wakefulness.
It also serves to be the master over
the pituitary gland by releasing factors that stimulate
or inhibit pituitary gland output.

e. Limbic system. Is composed of the medial portion of
the frontal lobe, temporal lobe (hippocampus),
thalamus, hypothalamus and the basal ganglia.
 It is the center for feelings and control of emotional
expression (fear, anger ,pleasure, sorrow).
 The temporal lobe component of the limbic system
plays essential role in the interpretation of smell.

f. Brain Stem. Is composed of the midbrain, pons and
medulla oblangata.
The midbrain integrates visual and auditory reflexes.
E.g. if a person sees a wasp towards him, he ducks
or twist away (visual reflex). Another example is
turning the hear ( ear ) to sound (auditory reflex). The
midbrian is also responsible for the righting reflexes,
those that keep the head upright and maintain
balance or equilibrium.
The pons contains 2 respiratory centers that promote
normal rhythm of breathing. The apneustic center
prolongs inhalation; the pneumotoxic center
contributes to exhalation.

The medulla oblangata contains cardiac centers that
regulate heart rate; vasomotor centers that regulate blood
pressure; respiratory centers that regulate breathing. It
also contains reflex centers for coughing, sneezing,
swallowing, and vomiting.
g. Reticular formation. Assists in the regulation of skeletal
motor movement and spinal reflexes. It also filters
incoming sensory information to the cerebral cortex.
One component of the reticular formation, the reticular
activating system controls the sleep-wake cycle and
consciousness.

h. Cerebellum. IS composed of gray mater and white
matter.
 It controls balance (equilibrium) and posture.
It controls voluntary (purposeful) motor activities
and position of body parts.
Most of the tracts in the cerebellum do not cross.
Therefore, the right cerebellum hemisphere
predominantly affects the right (ipsilateral) side of
the body and vice versa.

• Left and Right Brain Functions
 Dominant Hemisphere (Left)
 Language and logical operations
1)Number skills
2)Written language
3)Reasoning
4)Spoken language
5)Scientific skills
6)Right-hand control

 Right Hemisphere
 Emotions, artistic and spatial skills
1) Insight
e.g. How does a client recognize implication of
illness?
How would the client respond to a given situation
( e.,) house on fire)?
1) Forms (3 dimensions)
2) Art awareness
3) Imagination
4) Music awareness
5) Left-hand control

2. The Spinal Cord
a. The spinal cord is composed of ascending and
descending pathways.
b. The ascending pathways (affarent fibers) are
sensory fibers. They carry impulses TO THE
BRAIN.
c. The descending pathways (efferent fibers) are
motor fibers. They carry impulses to the brain.
d. The spinal cord is the center for reflex acts.
e. It is the origin of ANS.

f. The craniosacral segment is the origin of the
parasympathetic nervous system. The thoracolumbar
segment is the origin of the sympathetic nervous
system.
g. Damage to the spinal cord causes paralysis and loss of
reflexes below the area of lesion. E.g. Cervical spinal
cord injury results to qaudriplegia ( paralysis of the four
extremities)
h. Protective and Nutritional structures
 Cranium and the vertebrae column
 The cranium is composed of eight bones that fuse
in early childhood. The fused junctions are called
sutures.

 The vertebral column consist of 7 cervical
vertebrae, 12 thorasic vertebrae, 5 lumbar
vertebrae, 5 sacral vertebrae fused into a sacrum
and 4 coccygeal vertebrae fused into a coccyx.
 Meninges. Consists on 3 membranes that envelope
the brain and spinal cord. These are the pia mater,
arachnoid and dura mater.
 The pia mater is a the tissuvascular layer of
connective tissues. It supports blood vessels
passing through the tissues of the brain and
spinal cord.
 The arachnoid is a thin layer of connective tissue,

 The arachnoid is a thin layer of connective
tissue. The space between the arachnoid and
the pia mater is called subarachnoid space.
Cerebrospinal fluid (CSF) flows through this
space.
 The cranial dura mater is a tough, non-stretchable
vascular membranes. The
subdural space is the potential space between
the inner dura matter and the arachnoid. The
epidural space is between the dura matter
and the periosteum

 Reflex mechanisms. Reflex responses are conscious
automatic response to internal and external stimuli. The
reflex centers are the spinal cord (flexion and extension) and
the brain stem ( heart rate, breathing, blood pressure,
swallowing, sneezing, coughing and vomiting).
 Cerebrospinal fluid and ventricular system.
 CSF is a clear, colorless fluid. Approximately 100 to 160
ml. in amount.
 The CSF is primarily produced by the choroid plexus of the
lateral ventricles (2/3 of the CSF).
 Approximately, 500 ml. of CSF is produced per day. But
normally, it is absorbed in the blood at the same rate at
which it is formed.

 The ventricular system is a series of activities within the brain.
 CSF Flow
Lateral ventricles
Foramen of Monro
Third ventricles
Aquduct of Sylvius
Foiurth ventricle
Foramina of Luschka
Foramen of Megendie
Subarachnoid space(Cisterna Magna) behind medulla, below the cerebellum
Brain spinal cord
CSF circulates upward into the superior sagittal sinus where it is absorbed across the
arachnoid villi

 Blood Supply of the Brain
a. The brain receives 750 to 900 ml. of blood flow per
minute.
b. The vertebral arteries and the internal carotid arteries
provide the arterial supply to the brain.
c. The vertebral arteries join to form the basillar artery.
The basilar artery bifurcates to form 2 posterior
cerebral arteries.
d. The vertebral artery system supplies the brain stem, the
cerebellum, the lower portion of the diencephalon and
the medial and inferior regions of the temporal and
occipital lobes (posterior lobes)

e. The internal carotid arteries bifurcate into the anterior
and middle cerebral arteries.
f. The circle of Willis is a ring of blood vessels at the base
of the brain. It is formed by the posterior cerebral
arteries posterior communicating arteries, internal carotid
arteries, and anterior communicating branches.
g. The internal carotid arteries supply the upper
diencephalon, basal ganglia, lateral temporal, occipital
lobes and parietal and frontal lobes ( anterior brain).

h. The middle cerebral arteries supply large portions of the
frontal, parietal, temporal, occipital and insular lobes
and basal ganglia and thalamus.
i. The anterior cerebral arteries supply the medial portions
of the frontal and parietal lobes and the upper basal
ganglia.
j. Most of the venous blood from the head returns to the
heart through internal jugular veins, the external jugular
veins, and the vertebral veins.

 The Peripheral Nervous system (PNS)
It consists of pathways of nerve fibers.
a.Sensory (affarent) neurons. Conduct impulses to the
brain and the spinal cord.
1.Spinal Nerves.
 There are 31 pairs of spinal nerves; 8 pairs of
cervical nerves; 12 pairs of thoracic nerves, 5
pairs of lumbar nerves, 1 pair of coccygeal
nerves. (8-12-5-5-1)

 The 3 major plexus formed from the peripheral nerves are as
follows:
1) Cervical plexus: supplies the muscles and skin of the neck
and branches to form the phrenic nerve, which innervates the
diaphragm.
2) Brachial plexus: supplies the muscles and skin of the
shoulder, axilla, arm, forearm and hand. It branches to form
the ulnar, median and radial nerves.
3) Lumbosacral plexus: supplies sensory and motor impulses
to the muscles and skin of the perineum gluteal region, thighs,
legs and feet. Its branches include pudendal, gluteal, femoral,
sciatic, tibial and common fibular nerves.

 The Autonomous Nervous System (ANS)
The autonomic nervous system is the part of the PNS
that coordinates involuntary activities, such as the
visceral functions, smooth and cardiac muscle
changes, and glandular responses.
The ANS has 2 divisions: the sympathetic and
parasympathetic nervous systems.
The sympathetic nervous release norephineprine.
The parasympathetic nerves release acetylcholine

CRANIAL NERVES
Cranial Nerves Functions Abdominal Findings
Olfactory Smell Anasomia(absence of
smell
Optic Vision Papilledema; blurred
vision; scotoma; blindess
Oculomotor Pupil constriction
elevation of the upper lid
Anisucuria;pinpoint
pupils; fixed dilated
pupils
Trochlear Eye movement; controls
superior oblique muscles
Nystagmus
Trigemenal Controls muscles of
mastication; sensations
for the entire face and
cornea
Trigeminal Neuralgia (Tic
douloureux)
Abducens Eye movement; control
the lateral rectus
muscles
Diplopia;ptosis of eyelid

Cranial Nerves
Cranial Nerve Functions Abnormal Findings
Facial Controls muscles for
facial expression;
anterior 2/3 of the tongue
Bell’s palsy ageusia (loss
of sense of taste) on the
anterior 2/3 of the
tongue.
Acoustic Cochlear branch permits
hearing; vestibular
branch helps maintain
equilibrium
Tinnitus: Vertigo
Glossopharyngeal Controls muscles of the
throat; taste of posterior
1/3 of the tongue
Loss of gag reflex,
drooling of saliva
dysphagia, dysphonia,
posterior third ageusia
Vagus Nerve Controls muscles of the
throat, Parasympathetic
Nervous System
stimulation of thoracic
and abdominal organs.
Loss of gag reflex,
drooling of saliva
dysphagia, dysarthria,
bradycardia, increase
HCL secretion

Cranial Nerves
Cranial Nerves Functions Abnormal Findings
Spinal Accessory Controls
sternocleidomastoid and
trapezius
Inability to rotate the
head and move the
shoulders.
Hypoglossal Movement of the tongue Protrusion of the tongue
or deviation of the
tongue to one side of the
mouth

EFFECTS OF THE SYMPATHETIC AND
PARASYMPATHETIC NERVOUS SYSTEM ON
ORGANS
Organ Effects of Sympathetic
Stimulation
Effects of
Parasympathetic
Stimulation
Eye
Pupil
Ciliary muscle
Dilation (alpha)*
Slight relaxation ( far
vision)
Constriction
Constriction (nrear
vision)
Glands
Nasal
Lacrimal
Parotid
Submandibular
Gastric
Pancreatic
Vasocontriction and
slight secretion
Stimulation of copius
secretions
(containing many
enzymes for enzyme
secreting glands

ORGANS
Stimulation
Effects of
Parasympathetic
Stimulation
Sweat Glands Copius sweating Sweating on palms of
hands
Heart
Muscle
Coronaries
Increased rate (beta1)
Increased force of
contraction (beta1)
Dilated (beta2);
Constricted (alpha)
Slowed heart rate
Decreased force of
contraction (especially
of atria
Dilatation
Lungs Dilated (beta2) Constriction

ORGANS
Stimulation
Effects of
Parasympathetic
Stimulation
Gut
Lumen
Sphincter
Decreased peristalsis
and tone (beta2)
Increased tone (alpha)
Increased peristalsis
and tone
Relaxation (most of the
time)
Liver Gluconeogenesis,
glycogenolysis (beta2)
Slight glycogen synthesis
Gallbladder and bile
ducts
Relaxation Contraction
Kidney Decreased output and
renin secretion
None

Stimulation
Effects of
Parasympathetic
Stimulation
Bladder
Detrusor
Trigone
Relaxation ( slight)
(beta2)
Contraction (alpha)
Contraction
Relaxation
Penis Ejaculation Erection
Systemic arterioles
Abdominal viscera
Constriction (alpha)
None
Muscle
Constriction
ORGANS

Normal functioning of the nervous
system requires the following:
1. Oxygen Supply. The brain requires 20 % of the oxygen in
the body.
2. Glucose supply. The brain requires 65 to 70 % of the
glucose in the body. The cardiac output.
3. Blood supply. The brain requires 1/3 of the cardiac output.
4. Acid-base balance.
 Acidosis causes cerebral vasodilatation and increases
intracranial pressure (ICP). It also a CNS depressant and
may lead to coma.
 Alkalosis causes cerebral vasoconstriction and
Increases intracranial pressure. It also a CNS depressant
and may lead to coma

Normal functioning of the nervous
system requires the following:
5. Blood-brain barrier. Intact blood-brain barrier protects
the brain from certain drugs, chemicals and
microorganisms.
6. Cerebro spinal fluid( CSF) Volume . CSF cushions the
brain and determines the ICP.CSF cushions and
nourishes

NEUROLOGIC ASSESSMENT
1. Mental Status
 Assess orientation and memory (consider educational
background)
 Orientation involves people, time and place.
 Memory includes short-term (immediate recall), recent and
remote memory.
2. Level of consciousness (LOC). It is the single most
sensitive indicator of changes in the neurlologic status
of a client.
 The levels of consciousness are as follows:
a. Level 1 Conscious, coherent, cognitive (3
C’s)
b. Level II. Confused, drowsy, lethargic,
somnolent, obtunded.

NEUROLOGIC ASSESSMENT
c. Level III Stuporous; responds only to noxious,
strong or intense stimuli, e.g. sternal pressure,
trapezius pinch, pressure at the base of the nail or
supraorbital area; very strong light or very loud
sound.
d. Level IV.
Light coma: response is only grimace or
withdrawing limb from pain, primitive and
disorganized response to painful stimuli.
Deep Coma: absence of response to even the
most painful stimuli.

Normal 14-15
Lethargy 11-13
Stupor: 8-10
Coma: 7
Deep
Coma: 3

Neurological Assessment
3. Sensory Function
 Test for sensory function assess the functioning of
the parietal lobe.
 The tests are done with the client’s eyes closed, e.g.,
placing cold and warm fluid in test tubes over the
skin; pricking skin with blunt objects; giving cinnamon
to taste ; coffee to smell.
 Agnosia is inability to perceive sensory stimuli.

4. Motor Function
 If the frontal lobe is affected, the client experiences
inability to perform motor activities.
 Apaxia is inability to perform fine motor
activities( done by fingers)
 Agraphia is inability to write.
 Romberg test is done to assess cerebellar function
(sense of equilibrium). The test is done by asking
the client to stand with the feet together and eyes
closed or the client is asked to walk in a imaginary
line.

 Normal result of Romberg test is that, the client
should be able to stand erect. Slight swaying is
normal. If the client falls, this is a positive Romberg
that indicates cerebellar function impairment.
 Ataxia is uncoordinated movement, characterized by
wide base stance and swaying manner of walking.
 Assessing motor function includes the following:
a. General appearance. Assess for
 Presence of involuntary, unpurposeful, and
uncoordinated movements, asymmetry of the face
muscle dystrophy.

b. Muscle Power. Assess for
 Weakness (“paresis)
 Paralysis (“plegia”)
c. Muscle Tone. Assess for
 Flaccidity (hypotonicity)
 Rigidity (hypertenocity)
c. Muscle volume. Assess for
 Atrophy (loss of muscle volume)
 Hyperthrophy ( increase in muscle volume

e. Movement. Assess for
 Bradykenesia ( slow muscle movement not associated
with weakness).
 Akinesia (absence of muscle movement not associated
with weakness).
f. Coordination. Assess by
 FTNT (finger-to nose-test)
 H-K-T ( heel-to-knee-to-toe-test)
f. Station and gait. Station is posture; gait is manner of
walking
 Parkinson’s disease is characterized by shuffling,
festinating gait (tiptoe walking, starting at slow
motion, the pace keeps on increasing until
client assumes running pace.

5. Reflex Testing.
 Superficial Reflexes
 Pupillary Reflexes
 Direct light reflex is elicited by applying light
stimulus movement side to side into the pupil;
this results to constriction of the pupils.
 Consensual light reflex results to stimulus
constriction of both pupils even if light is
applied to one pupil only.
 Accommodation reflex results to constriction
of pupils when gaze is shifted from a distant
object to a near object.

 The pupillary reflexes are represented by
PERRLA ( pupils, equal, round, reactive to light,
accommodation.)
 A fixed and dilated pupil in a client who has had
previously reactive pupils is a neurologic
emergency. Notify the physician immediately.
 Corneal reflex is elicited by touching the cornea with
a wisp of cotton, as the client looks toward opposite
direction; blinking of the eyes occurs.
 Abdominal reflex results to contraction of the side
of the abdomen stroked with blunt object.

 Cremasteric reflex is elicited by downward stroking of the
inner thigh of the male; elevation of the scrotum on the
same side occurs; this done only among unconscious
males.
 Babinski reflex is elicited by stroking the sole of the foot
from the heel upwards; plantar flexion (negative
Babinski) is the normal result among adults.
 Interpretation of Superficial Reflexes
 0 absent
 + slightly present
 + normally active

 Deep Tendon Reflexes (DTR’s)
 Ankle jerk is produced by tapping the tendon of Achilles;
plantar flexion of the foot occurs (also called Tendon of
Achilles reflex)
 Knee jerk (patellar reflex) is produced by tapping the
quadriceps femoris, just below the patella; it results to leg
extension
 Reflexes to assess meningeal irritation
 Kernig’s sign. The client in supine position. Flex the
knee, attempt to extend the leg. Pain is experienced.
 Brudzinski’s reflex. The client is placed in supine
position. Passively flex the neck, spontaneous flexion of
the hips occurs. This is more accurate indicator of
meningeal irritation than kernig’s sign.

 Oculocephalic Reflex or Doll’s eye phenomenon.
This is demonstrated by holding the person’s eyelids
open and rotating the head from side to side. Positive or
normal doll’s eye is demonstrated by conjugate
movement of the eyes towards the opposite side.

 Oculovestibular Reflex or Caloric Ice Water Test.
This is done by irrigating the semi-circular canals of the
ear with ice water. It causes conjugate eye
movements or nystagmus. This is an accurate method
of assessing brainstem functioning.

6. Language and Speech.
The speech centers are as follows:
 Broca’s area in the left frontal lobe. This is the motor speech
center. This enables a person to speak and make gestures.
Impairment of the Borca’s area results to expressive or
motor aphasia which is inability to speak and make gestures.
 Wernicke’s area in the temporal lobes. This is the auditory
speech center. This e sounds nables a person to interpret
sounds or language. Impairment of the Wernicke’s area
results to receptive or auditory aphasia, which is inability to
understand sounds or language.

 Global aphasia is inability to use and understand
language. This occurs from impairment to both the
Broca’s and Wernicke’s areas.
 Visual speech center in the occipital lobe. This enables
a person to read or interpret symbols. Impairment of the
visual speech center results to alexia, which is inability
to read.
7. Bowel and Bladder Function
 The sympathetic nervous system (SNS) which
originates from the thoracolumbar segment of the
spinal cord is the inhibitory impulse. Impairment of
the SNS leads to bowel and bladder retention.

 The parasympathetic nervous system, (PNS) which
originates from the craniosacral segment of the spinal
cord is the motor impulses. Impairment of the PNS
leads to bowel and bladder incontinence.

DISORDERS
AFFECTING NERVOUS
SYSTEM

The three common problems among clients
with neurologic disorders are as follows:
1. Increased intracranial pressure
2. Seizures
3. Altered level of consciousness

Care of the client with Increased
Intracranial Pressure (ICP)
• Increased ICP occurs whenever there is increase in the bulk
of the brain.
• The bulk of the brain consists of the brain tissues, blood
supply and CSF.
• The disorders that increase the bulk of the brain tissues are
called space-occupying lesions. E.g. cerebral tumor, abscess,
edema (due to infection or trauma).
• The factors that may increase the blood supply to the brain
are cerebral hemorrhage, trombosis, embolism, aneursym,
anteriovenous malformation (A-V mal)
• The factors that increase bulk of of CSF are obstruction to the
flow of CSF caused by brain tumor or ventricular system
defects (hydrocephalus); or over production of CSF caused by
tumor in the choroid plexus.
• Increased ICP causes cerebral hypoxia.

• The clinical manifestations of increased ICP are as
follows:
 Restlessness. Is the initial sign of increased ICP.
 Headache is due to traction on pain-sensitive brain
structures and on cranial nerves.
 Nausea and vomiting. Is due to pressure at the
medulla oblangata. Vomiting may be projectile.
 Diplopia (double vision). Is due to pressure on the
cranial nerve VI (abducens), which controls the lateral
rectus muscles of the eyes. Cranial nerve VI is the
longest intracranial nerve. Therefore, it is very
vulnerable to compression.

 Altered level of consciousness. Is due to affection of ascending reticular
activating system (ARAS)
 Vital signs changes. Are due to stimulation of the Cushing’s reflex in
response to cerebral hypoxia: The Cushing’s triad are as follows:
a. Blood Pressure
 Systolic pressure is elevated. This is due to increased force of
cardiac contractility, the body’s attempt to increase cerebral
tissue perfusion and oxygenation.
 Diastolic pressure remains normal or decreased. This is due
to longer time required for the heart to relax.
 Widening of pulse pressure. It is more than 40 mm. hg. (pulse
pressure is the difference between systolic pressure and the
diastolic pressure: S – D = pulse pressure).
a. Pulse rate. Bradycardia ( slow bounding pulse) occurs.
b. Respiratory rate, is slow due to involvement of the medulla
oblangata and pons.

 The other vital signs changes are as follows:
a. Body temperature. Hyperthermia or hypothermia may
occur due to the involvement of the hypothalamus
 Pupillary Changes
a. Anisucuria (unequal pupil). Is due to Cranial nerve III
(oculomotor) compression. There is ipsilateral (same
side) pupil dilatation; e.g. left brain affection, left pupil is
dilated.
b. Pinpoint pupils indicates pons involvement.
c. Fixed dilated pupils. Indicates uncal herniation. This
causes compression of the brainstem that may result to
cardiopulmonary arrest.

 Papilledema (Chocked disc). Is due to the compression
of the optic nerve.
 Laterilizing Sign. This is contralateral (opposite side)
loss of motor function due to decussation ( crossing) of
motor fibers at the level of medulla oblangata, eg., left
brain affection leads to right hemiplegia (paralysis of he
right lateral half of the body); right brain affection leads to
left hemiplgeia (paralysis of the left lateral half of the
body).
 Brainstem Function impairment
a. Negative Doll’s eye sign. Dysconjugate movement
of the eyes as the head is moved to pone side.

 b. Decortication( flexion , adduction and internal rotation
of upper extremities. Lower extremities are extended).
This indicates involvement above the mid brain.

c. Decerebration ( extension adduction, and internal
rotation of the arms and extension of the lower
extremities). This indicates involvement of the brain
stem. The signals poor prognosis. The client may have
cardiopulmonary arrest, anytime.

d. Oculovestibular Test (Caloric Ice water test).
Dysconjugate movement of the eyes occurs in response
to irrigation of the ear with cold water.

ICP
 Alterations in:
a. Sensory Function (anosia)
b. Motor Function (seizures)
c. Lnaguage and Speech (expressive aphasia, receptive
aphasia. A;exia).
d. Bowel and bladder function (retention or
incontinence).

Collaborative Management for ICP includes
the following:
NURSE ALERT: Increased ICP is an
emergency. The cerebral cortex can
tolerate hypoxia only for 4 to 6
minutes. The medulla oblangata can
tolerate hypoxia only for 10 to 15
minutes.

Collaborative Management for Icreased ICP
include the following:
 Position: Semi- Fowler’s. Lateral position. The HOB
elevation is 15 to 30 degree, maximum of 45 degree. To
promote drainage of CSF from subarachnoid space of the
spinal cord. This position also promotes maximum lung
expansion. CAUTION: do not elevate HOB at 90 degrees.
This may cause brain herniation.
 Adequate oxygenation. Mechanical ventilation helps
promote acid-base. Acidosis and Alkalosis may increase ICP.
 Safety. Prevent falls that may result from altered level of
consciousness and seizures.
 Rest. Physical and emotional stress may further increase ICP.

 Avoid factors that increase ICP as follows:
 Nausea and vomiting
 Valsalva maneuver, e.g. straining at stool
 Over suctioning
 Restraints application
 Rectal examination
 Enema
 Bending or stooping
 If coughing and sneezing could not be avoided,
follow[through with an open mouth.
 Control hypertension. Hypertension reduces cerebral tissue
perfusion.

 Restrict fluid intake. Limit fluid intake to 1,200 to 1, 500
mls./day to reduce CSF production.
 Pharmacotherapy
 Mannitol, an osmotic diuretic. It reduces cerebral edema
by increasing urine output.
 Check hourly urine output.
 Check BP for potential hypotension.
 Lasix (Furosemide), a diuretic. It helps reduce cerebral
edema by increasing urine output.
 Decadron (Dexamethasone), a corticosteroid. It has anti
inflammatory effect and reduces cerebral edema. This is
the only corticosteroid that can pass through the blood-brain
barrier.

 Anticonvulsants to prevent seizures.
 Valium (Diazepam)
 Dilantin (Phenytoin Sodium)
 Phenobarbital ( Sodium Luminal)
 Tegretol (Carbamezapine)
 Antacids to prevent G.I. irritation that may be induced by
Decadron (dexamethasone).
 Histamine- H2 receptor antagonists. To prevent stress ulcer
(Cushing’s ulcer), e.g. Zantac (Ranitidine).
 Anticoagulant, to prevent thromboembolism. Platelets may
aggregate in the areas of cerebral tissue injury.

CRITICAL TO REMEMBER:
OPIATES (narcotics) and SEDATIVES are
contraindicated to the client with increased ICP.
These drugs may cause respiratory depression and
acidosis.

Care of the client with Seizure Disorder
• Seizure (convulsions) are sudden, excessive, disorderly
electrical discharges of the neurons.
• The most common type of generalized seizures are
grand mal seizures.
• Grand mal seizures are characterized by aura. Aura
may be flashings lights, unusual smells, spots before the
eyes, dizziness.
• Tonic-clonic phase of grand mal seizures is
characterized by exhaustion, headache, drowsiness,
deep sleep of 1 to 2 hours, disorientation.
• The other types of seizures are Petit Mal, Jacksonian
seizures, psychomotor seizure, febrile seizures.

• Petiti Mal (“ Absence Seizure or “little Sickness”) is not
preceded by an aura. There is little or no tonic-clonic
movements. There is sudden cessation of ongoing
physical activities. It is characterized by blank facial
expression and autmatism like lip-chewing, cheek-smacking.
Regain of consciousness is a rapid as it was last; lasts for 10
to 20 seconds. It usually occurs during childhood and
adolescence.
• Jacksonian seizures (facial seizures) is common among
clients with organic brain lesion like frontal lobe tumor. Aura
is present like numbness, tingling, crawling feeling. It is
characterized by tonic – clonic movements of group of
muscles e.g. hands, foot, or face, then it proceeds to grand
mal seizure.

• Psychomotor seizure. It has a psychiatric component.
Aura is present (hallucinations or illusions). It is
characterized by mental clouding (being out of touch with
the environment). The client appears intoxicated.
During time of loss of consciousness, there are ongoing
physical activities. It is manifested by confusion,
amnesia and need to sleep. The client may commit
violent or antisocial acts, e.g. Going naked in public,
running amok during the time of loss of consciousness.
• Febrile seizures. This is common among children under
5 years of age, when body temperature is rising.

• Status epilepticus. A type of seizure occurring in rapid
succession and full consciousness is not regained
between seizures. Brain damage may occur secondary
to prolonged hypoxia and exhaustion. The client is often
in coma for 12 to 24 hours longer, during which time
recurring seizures occur. The attack is usually related to
failure to take sudden withdrawal of prescribed
anticonvulsants.
• Epilepsy. Denotes a group of clinical disorders
characterized by the repeated occurrence of any of the
various forms of seizures.

Collaborative management for seizure
disorders include the following:
1. Stay with the client.
2. Protect the client from injury.
 Put up-padded side - rails.
 If the client is sitting or standing, ease him up onto the
floor. Protect head with small pillow or place the head
onto the lap.
 Do not apply restraints.
 Do not insert tongue blade. To prevent trauma to gums
and teeth.
1. Promote patent airway.
 Turn the client to the side.
 Loosen constricting clothing especially around the neck.

4. Make relevant observation and documentation.
5. Pharmacotherapy: anticonvulsants.
1) Anticonvulsants are classified as follows.
 Hydantoins
 Barbiturates
 Succinimides
 Oxazolidones/ oxazolidonediones
 Benzodiazepines
 Iminostibenes
 Valproates

2) Anticonvulsant drugs suppress the abnormal electric impulses from
the seizure focus to other cortical areas, thus preventing the seizures
but eliminating the cause of the seizure.
3) Anticonvulsants are classified as central nervous (CNS)
depressants.
1) HYDANTOINS
 Dilantin (Phenytoin)
 (Mesantoin) Mephenytoin
 Ethotoin
 These anticonvulsants have least toxic effects and have small
effect on general sedation and are nonaddicting.
 The therapeutic serum level of Phenytoin is 10 to 20 mcg./ml.
 Intravenous infusion of Phenytoin should be administered by
direct injection into a large vein. It should be diluted with
normal saline solution. Dextrose solution not be used
because of drug precipitate.

 Intramascular (IM) injection of phenytoin irritates
tissues and may cause damage, therefore this route is
discouraged.
 Continuous IV infusion of Phenytoin should not be
used, because hypotension or cardiac dysrhythmias
may occur.
 Mephenytoin is more toxic than Phenytoin. This drug
is used for severe grand mal or psychomotor seizures
that do npot respond to Phenytoin or other
anticonvulsant therapy.
 Ethotoin produces similar responses as Phenytoin,
has a shorter half-life of 3 to 6 hours; therefore, the
chance of cumulative drug effects decreases.

Nursing Intervention in Phenytoin
Therapy
o Monitor serum drug levels to prevent toxicity.
o Ensure adequate nutrition. Phenytoin causes anorexia,
nausea and vomitin.
o Initially, avoid driving and performing HAZARDOUS
ACTIVITIES UNTIL THE CLIENT ADAPTS TO DRUG
DOSAGE. Drowsiness is apt to occur.
o Avoid alcohol and CNS depressants. These lower seizure
threshold.
o To prevent grandmal hyperplasia (overgrowth of gum
tissue-reddened gums that bleed easily), advise client to:
• Good oral care.
• Massage the gums.
• Use soft-bristled tootthbrush.
• Have preventive dental checkup.

Nursing Intervention in Phenytoin
Therapy
o Monitor serum glucose levels of diabetic clients.
Phenytoin inhibits insulin release, causing
hyperglycemia.
o Monitor complete blood count (cbc). Phenytoin may
cause bone marrow depression. Client should report
symptoms of sore throat, bruising and nose bleeds.
o Instruct client to take the anticonvulsant at the same time
every day with food or milk, to prevent G.I. irritation.
o Phenytoin is contraindicated to pregnancy. It may
cause fetal anomalies such as cardiac defects, cleft lip
and cleft palate.

The side effects and adverse effects of of
HYDANTOINS are as follows:
o Gingival hyperplasia.
o Neurologic and psychiatric effects such as ataxia,
nystagmus, sedation, slurred speech, confusion and
depression.
o Bone marrow depression- anemia, leukopenia,
thrombocytopenia
o Hyperglycemia- the drug inhibits release of insulin.
o Gastrointestinal efects: anorexia, nausea, vomiting,
constipation
o Drowsiness, headaches, alopecia, hirsutism.
o Phenytoin causes pinkish red or reddish-brown
discoloration of urine. This is harmless side effect.

Critical to Remember:
WITHDRAW ANTICONVULSANT
DRUGS GRADUALLY TO
PREVENT STATUS
EPILEPTICUS.

Anticonvulsants are classified as (CNS)
depressants.
2) BARBITURATES
 Amytal (Ambarbital)-status epilepticus
 Meberal (Mephobarbital)- grandmal, petit mal
 Luminal (Phenobarbital)- grandmal, petit mal, status
epilepticus
 )Mysoline) Primadone- grand mal, psychomotor
seizure
 Phenobarbital is used to treat grandmal seizures
and acute episodes of status epilepticus seizures.
It causes general sedation and drug tolerance.
 Discontinue Phenobarbital gradually to avoid
recurrence of seizure.

depressants.
3) SUCCINIMIDES
 Zarontin (Etosuximide)
 Celontin (Methsuximide)
 Milontin (Phensuximide)
 Used to treat absence or petit mal seizures.
 Ethosuximide is the drug of choice in this group
of anticonvulsants.
 Gastric irritation is common; these drugs
should be taken with food.

depressants.
4) OXAZOLIDONES /OXAZOLIDINEDIONES
 Paradione (paramethadione)
 Tridione (Trimetadione)
 Prescribed to treat petit masl seizures.
 Withdraw drugs gradually to prevent rebound
seizure.

depressants.
5) BENZODIAZEPINES
 The benzodiasepines that have anticonvulsant effects are
as follows:
o Klonopin (Clonazepam)
o Tranxene (Clorazepate dipotassium)
o Valium (Diazepam)
o Ativan ( Lorazepam)
 Clonazepam is effective in cotrolling petit mal (absence)
seizures, myoclonus and status epilepticus.
 Chlorazepate dipotassium is administered for treating
partial seizures.
 Diazepam is prescribed to treat acute status epilepticus. It
must be administered IV to achieve the desired response.
 Lorazepam is used to control status epilepticus. Infusion
rate not exceed 2 mg/min.

depressants.
6) IMINOSTILBENES
 Tegretol Carbamazepine)
 Trileptal (Oxcarbazepine)
 Carbamazepine is effective in treating
refractory seizure disorders that have not
responded to other anticonvulsant therapies. It
is used to control grandmal and partial
seizures.
 Carbamazepine is also used for psychiatric
disorders (e.g. bipolar disease), trigimenal
neuralgia ( as an analgesic), and alcohol
withdrawal.

depressants.
7) VALPROATE
 Depakene (Valproic Acid)
 Depakote (Divalproex Na)
 Valproic acid is indicated for grand mal, petit
mal and mixed type seizures.
 Valproic acid is hepatotoxic so liver enzymes
should be monotored.
 Divalproex Sodium is also used for treatment of
manic episodes associated with bipolar
disorder.

 Anticonvulsant and Pregnancy
 Phneytoin, carbamazepine, trimethadione, valproic acid
have tertogenic properties. Valproic acid may cause
neural tube deffects (spina bifida).
 Anticonvulsant drugs cause loss of folate (folic acid) in
pregnant women; thus folate supplements should be
taken.
 Anticonvulsants tend to act as inhibitors of vitamin k,
which contributes to hemorrhaging in infants shortly after
birth. Pregnant women taking anticonvulsants are given
an oral vitamin k supplement during the last week or 10
days of the pregnancy, or vitamin k is administered to the
infant as soon after birth.

Care of the Clients with Altered Level of
Consciousness
• Assessment of consciousness includes arousal and
content of thoughts.
• Decreased level of cpnsciousness may be due to
primary brain injury or disease or systemic conditions
like metabolic encephalopathies, hypoxic
encephalopathies, toxicity, deficiency conditions.

Collaborative management for altered level of
consciousness include the following:
1. Maintain stimulation. Speak to the patient before teaching.
2. Maintain nutrition. Administer enteral or parenteral feedings safely.
3. Maintain Elimination. Administer stool softeners as ordered.
4. Maintain Circulation. Change client’s position at regular basis.
5. Maintain normal body temperature.
6. Promote safety. Position bed in lowest position and put up padded
side rails.
7. Promote activity. Change client’s position, passive ROM exercises.
8. Maintain skin integrity. Render hygienic measures, apply lotion, use
protective devices like flotation mattress or air-loss mattress.
9. Maintain good hygiene. Render bed bath, hair shampoo, oral care,
nose, ear and eye care, perianal care.
10.Support family. Involve family members in the are of the client; help
them explore their concerns, thoughts and feelings.

Care of clients with Headache
(Cephalgia)
 The different types of headaches are as follows;
1. Migraine headache.
 Is caused by inflammation and dilatation of blood
vessels in the brain. One side of the head is more
affected than the other. It tends to occur with stress or
life crisis. It lasts for hours or days. The pain is
throbbing and pulsatile.
 Aura of acute attacks of migraine includes visual field
defects, confusion, paresthesia, paralysis in extreme
cases.
 Associated symptoms of migraine are as follows:
nausea and vomiting, chills, fatigue, irritability,
sweating, edema, photophobia (sound sensitivity)

Collaborative management for migraine
 Provide quiet, dark environment.
 Stress therapy and relaxation techniques.
 Diet: small, frequent meals. Avoid the following foods
chocolate, nuts, onions, food seasoning, cheese, citrus
fruits, coffee, pork, dairy products, red wine.
 Pharmacotherapy for migraine
1) Beta- adrenergic blockers
 Inderal (propranolol)
 Tenormin (Atenolol)
 Lopressor (Metroprolol)

 2) Calcium- channel blockers
 Calan (Verapamil)
3)Tricyclic antidepressants
Elavil (Amitriptyline)
Tofranil (Imipramine)
4)Ergotamine tartrate
5)NSAIDs
Motrin (Ibuprofen)
Naprosyn(Naproxen)

6) Opioid analgesics
 Demerol (Meperedine)
 Butorphanol nasal spray
7) Triptans ( Selective Serotonin Receptor Agonists)
 Imitrex (Sumatripton)
 Amerge (Naratriptan)
 Maxalt (Rizatriptan)
 Zamig (Zalmitriptan)
 Triptans cause vasoconstriction, reduce inflammation,
and relieve migraine.

 Side effects and adverse reactions to lmitrex
(Sumatriptan)
o Tingling, nasal discomfort
o Dizziness, vertigo, drowsiness
o Hypertension
o Skin rash, swelling of eyelids, lips face
o Nausea and vomiting
o Tremors
o Wheezing, heart throbbing
o Reduced respirations
o Seizures, paralysis
 Lamitrex is contraindicated in hypertension, renal and
hepatic impairment, it should be taken with full glass of
water.

2. Cluster headache. Is characterized buy episodes
clustered together in quick succession for few days
or weeks with remission that lasts for months. The
headache is intense, throbbing, deep and often
unilateral. It begins in infraorbital region and
spread to head and neck.
 It is precipitated by alcohol or nitrate.
 The associated symptoms are flushing, tearing of
eyes, nasal stuffiness, sweating and swelling
temporal vessels.
 Treatment includes narcotic analgesic during acute
phase.

3. Tension headache. Is related to tension and muscle
contraction. It is episodic and vary with stress. It is
usually bilateral, involves neck and shoulders.
 The associated symptoms are sustained contraction of
the head and neck muscles.
 Treatment includes the following:
1) Non narcotic analgesics
o Acetaminophen
o Propoxyphene
o Phenacetin
o ASA
2) Elavil (Amitriptyline)
3) Relaxation Techniques

CARE OF THE CLIENT WITH
CEREBROVASCULAR ACCIDENT(CVA)
• CVA is caused by disruption of the blood supply to the brain
causing neurologic deficit.
• The middle cerebral artery (MCA) is most commonly affected
in CVA.
• The second most frequently affected is the internal carotid
artery.
• The most common CVA is thrombosis, then followed by
embolism, then cerebral hemorrhage.
• CVA due to hemorrhage is associated with activities and
occurs during working hours. It is characterized by
extensive , permanent loss of function. There is rapid onset
of hemephlegia and rapid progression into coma. It is usually
fatal.

• Trancient Ischemic Attack (TIA) refer to transient
cerebral ichemia with temporary episodes of neurologic
dysfunction.
• COMPARISON OF LEFT AND RIGHT CVA
Left CVA Right CVA
• Right hemiplegia • Left Hemiplegia
• Right visual field defect • Left visual field defect
• Aphasia: expressive
receptive, global
• Spatial-perceptual field
defect
• Altered intellectual activity • Increased distractibility
• Slow, cautious behavior • Impulsive behavior, poor
judgment, lack of
awareness of deficit

• The clinical manifestations of CVA are as follows:
Signs and symptoms of ICP
Perceptual defects
Aphasia
Hemanopsia (Loss of half of the visual field)
• The collaborative management for CVA are as follows:
Emergency Care: Care of client with Increased ICP.
Care of he client with aphasia.
 Promote communication.
 Practice saying one word at a time.
 Associate words with objects.

 TPN, NGT feeding, gastrostomy feeding.
 Promote Activity
 Turn frequently
 Perform ROM exercises
 Prevent contractures.
 Promote Elimination
 Monitor I and O to check for urinary retention
 Start urinary bowel program

 Promote Communication
 Care of the client with APHASIA
oPractice i=one word at a time.
oIdentify one object at a time.
oGive simple commands.
oAnticipate needs
oAllow the client to verbalize, no matter how long it
takes him.
oReinforce success in speech.
oAssist the client in speech therapy.

 Care of the client with Hemianopsia
 Approach the client from the unaffected side of the visual field.
 Place frequently used articles on the unaffected side of the
visual field.
 Teach the client scanning technique. Turn the head from side to
side to be able to see the entire visual field.
 Supportive care:
 Promote nutrition (enteral feedings, TPN)
 Promote activity (Turn frequently, passive ROM exercises).
 Promote elimination (Monitor I and O, urinary and bowel
program).
 Provide Emotional Support.
 Assist in rehabilitation of the client.

Care of the client with Thalmic syndrome:
 The client experiences emotional lability-unprovoked
crying or crying and laughing at the
same time. This behavior is a part of the disease
process in CVA. This is due to affection of
thalamus that has a center for feelings and the
control of emotional expression. The appropriate
nursing intervention for the client is provide
activities and divert his/ her attention.

INTRACRANIAL TUMORS
• The most common type of brain tumor is glioma. Other types
of brain tumor are menigioma, neuroma, hamangioma.
• The clinical manifestations of brain tumor are as follows:
Frontal lobe
Personality distrubances
Inappropriate affect
Indifference of bodily functions
(Precental gyrus-Jacksonian seizures)
Temporal lobe
 Olfactory, visual or gustatory hallucinations
Psychomotor seizures with automatic behavior

INTRACRANIAL TUMORS
Parietal lobe
Inability to replicate pictures
Loss of right left discrimination
Occipital lobe
Visual disturbances preceding convulsions
• Collaborative management for brain tumor include the
following:
 Care of the client with increased ICP (Preop and post op)
 Surgery
 Supratentotial craniotomy
o Place the client in Semi-Fowler’s position.

CARE OF THE CaLIENT WITH
INTRACRANIAL TUMORS
 Intratentorial craniotomy
o Place the client in flat position; turn to sides, avoid
supine position for the first 48 hours. To avoid pressure
on the suture line. Avoid neck flexion.
o Report immediately to the physician, yellowish
drainage on the head dressing. This indicates CSF
leakage.
o Monitor intake and output. Excessive urine output
indicates diabetes insipidus. This is due to pressure
on the neurophypohysis (posterior pituitary gland).
o Test the urine glucose and acetone when steroids are
administered. Steroids stimulate breakdown of fats and
proteins. This results to elevation of blood and urine
glucose levels and production of ketones.

CARE OF THE CLIENT WITH HEAD
TRAUMA
• Head trauma involves injury to the scalp, skull, and or
brain tissues.
• Concussion. Is jarring of the brain and against the skull.
There is transient period of unconsciousness.
• Contusion. There is bruising or extravasations of blood
cells.
• Lacerations. Tearing of tissues caused by a sharp
object.
• Compression of the brain. This results from depressed
fracture of the skull that causes hemorrhage and edema.

TRAUMA
• The clinical manifestations of head trauma are as
follows:
1) Signs and symptoms of increased ICP.
2) Signs of basilar head injury
CSF leaf from ers (otorrhea) and
nose( rhinorrhea).
Battle’s sign (Hematoma at the mastoid process/
behind the ear)
NURSE ALERT: BASILAR HEAD INJURYCAUSES
COMPRESSION OF THE BRAINSTEM. THE
CLIENT MAY HAVE CARDIOPULMONARY
ARREST ANYTIME

TRAUMA
• Collaborative management for head trauma include the
following:
1) Care of the client with increased ICP.
2) Monitor the client for drainage from the ears and
nose. Test the fluid for glucose; CSF is positive for
glucose).
3) Monitor the client for signs and symptoms of
meningitis atelectasis, pneumonia, urinary tract
infection.

CARE OF CLIENTS WITH
NEUROMASCULAR DISORDERS.
1. Parkinson’s Disease (Paralysis of Agitans)
• A degenerative disease that affects the extrapyramidal system
(EPS). This causes decreased dopamine production.
• The causes of Parkinson’s diseases are as follows: unknown,
viral infections, drugs, disequilibrium between dopamine and
acetylcholine, encephalitis, arteriosclerosis and carbon
monoxide poisoning.
• The initial sign tremors –pillrolling tremors, to and fro tremors
of the head
• Resting tremors (non-intention tremors). Shaking are more
severe when the client is not performing physical activities.
• Rigidity occurs due to decreased dopamine production.
Dopamine is a neurotransmitter that promotes muscle
relaxation.

• Cogwheel rigidity and absence of arm swing when
walking.
• Bradykinesia is slow muscle movement, not
associated with muscle weakness.
• Akinesia is absence of muscle movement, not
associated with muscle weakness.
• The characteristic gait of the client is shuffling,
festinating gait. This is tiptoe walking, starting at a
slow pace which keeps on increasing until the client
assumes a running pace. The client is unable to
stop until obstruction is met.

• The other signs and symptoms of Parkinson’s disease are
as follows:
 Flattened effect (mask-like facial expression)
 Stooped posture
 Moist, oily skin (sticky skin)
 Emotional instability
 Fatigue
 Soft, monotonous voice (Microphonia)
 Shaky, small handwriting(micrographia)
• In Parkinson’s disease, there is no intellectual
impairment, no true paralysis, no loss of sensation.

• The collaborative management of Parkinson’s disease are as
follows:
 Thickened liquid diet to soft diet for dysphagia.
 Firm bed to prevent contractures.
 Aspiration precaution
 Increase fluid intake and fiber in the diet to prevent constipation
 Pharmacotherapy
 Antichollinergics. Reduce the rigidity and some of the
tremors in Parkinson’s disease.
 Artane (Trihexyphenidyl)
 Cogentin (Benstropine)
 Akineton (Biperiden)
 Kemadrin (Procyclidine)
 Parsidol Ethopropazine)
 Norflex (Orphenadrine)

• Nursing Interventions for Anticholinergics
1) Monitor VS, urine output, and towel sounds.
Increased pulse rate, urinary retention and
constipation are side effects of anticholinergics.
2) Observe the client for involuntary movements
3) Advice to avoid alcohol, cigarette,
caffeine and aspirin to decrease gastric motility.
4) Prevent and relieve side effects of anticholinergic decrease salivation.
o Relieve dry mouth with hard candy, ice chips or sugarless chewing
gum. Anticholinergics decrease salivation.
o Suggest that the client use sunglasses in direct sun because of
possible photophobia.
o Advise the client to void before taking the drug to minimize urinary
retention.
o Advise the client to have routine eye examinations to determine the
presence of increased intraocular pressure which indicates glaucoma.
Clients who have glaucoma should not take anticholinergics.

 Dopaminergics. These drugs improve muscle
flexibility.
 Levedopa
 Carbidopa with levodopa (Sinemet).
 Dopamine cannot cross blood-brain barrier.
 Levodopa, a precusror of dopamine can cross the
blood-brain barrier.

 The enzyme dopa decarboxylase converts levadopa
to dopamine in brain. However, this enzyme is also
found in the peripheral nervous system, thereby
allowing 99% of levodopa to be converted to
dopamine before it reaches the brain (1% reaches
the brain). Therefore, a higher dose is required to
achieve therapeutic effect of the drug. Because of
high doses, many , side effects occur including
nausea, vomiting, dyskenesia, orthostatic
hypotension, cardiac dysrhythmias nand psychosis.
 Carbidopa and levodopa (Sinemet). Carbidopa
reduces destruction of levedopa at the periphery. A
single dose per day is administered.

 Nursing Interventions in Carbidopa-Levodopa
therapy
1) Monitor the client’s vital signs and ECG. Orthostatic
hypotension may occur.
2) Check weakness, dizziness or syncope, which
indicate orthostatic hypotension.
3) Advise client to practice gradual change in position
to prevent orthostatic hypotension.
4) Inform the client that urine may discolor and will
darken (reddish brown) with exposure to air.
Perspiration may also be discolored. Both are
harmless but clothes may be stained .

5) Symptoms of dyskinesia (impaired voluntary
movement) may take weeks or months to be
controlled.
6) Advise client to avoid the following drugs:
a. Phenothiazines, pyridoxine (Vit. B6). Reserpine.
These Block the effect of Levedovapa.
b. Monoamine oxidase inhibitors (MOAI)
o Marplan (Isocarboxacid)
o Parnate (Tranyclypromine)
o Nardil (Phenelzine)

MAOIs enhance norepinephrine activity.
MAOis + Carbidopa w/ Levedo= Hypertensive crisis
c. Aldomet (Methyldopa). This potentiates effect
7) Avoid the following foods when on Carbidopa- Levodopa
therapy:
a. Vitamins B6- rich foods like tuna, pork, dried
beans, salmon, beef liver,. These foods block
effects of levodopa.
b. Tyramine- rich foods. These foods may cause
hypertensive crisis among clients on Levodopa
therapy.
o Cheeze
o Cream

o Yogurt
o Coffee
o Chocolate
o Bananas
o Raisins
o Italian green beans
o Liver
o Pickled herring
o Sausage
o Soy sauce
o Yeast
o Beer
o Redwine
(These foods are proteins, aged, smoked and fermented)

8) Prevent and relieve the following side effects of Levodopa.
 Nausea and vomiting
 Hypertension, Orthostatic hyppotension
 Insomnia, Agitation
 Mental confusion
 Renal damage
 Dopamine Agonists/ Antiviral Drugs. These
medications act on the dopamine recpetors and produce
improvement in symptoms of Parkinsonism.
 Symmetrel (Amantadine HCL)
 Parlodel ( Bromocriptine Mesylate)
 Requip (Ropinozole HCL)

Nursing Intervention in Dopamine agonists therapy
1) Advise the client to report signs of skin lesions,
seizures or depression (Amantadine).
2) Suggest to the client to report lightheadedness when
chaning positions (Bromocriptine)
3) Avoid alcohol.
4) Advise client not to abruptly stop the drug without
notifying the health care provider.

NEUROMASCULAR DISORDERS
 Other drugs for Parkinson’s disease
 Monoamine oxydase- B inhibotor. It inhibits
breakdown of Dopamine, thus prolonging action
of Levodopa.
o Tasmar (Tolcapone)
o Comtan (Entacapone)

2. MYASTHENIA GRAVIS (MG)
• Is a neuromascular disorder characterized by failure of
transmission of nerve impulses at the myoneural
junction.
• MG may be caused by decreased number of functioning
acetylcholine receptors sites. It is also associated with
autoimmune disorders.
• DECENDING MUSCLE WEAKNESS
• INCIDENCE RATE: Women aged 20-40 years old
• The clinical manifestations of MG are as follows:
 Muscle weakness associated with activity relieved by
rest, e.g. dyspnea, dysphagia, decreased physical activity.
Fatigue

Ptosis, diplopia, strabismus
Impaired speech
Snarl smile, masklike facial expression
Dysphagia, drooling
Respiratory difficulty
PTOSIS DIPLOPIA STRABISMUS

• The diagnostic test for MG is Tensilon Test (Edrophonium) test
• Tensilon test a short-acting cholinergicas
• Tensilon is administered IV (2mg. First, then 8 mg.). Positive
Tensilon Test is observed as improvement in mascular
strength. Muscles weakness returns in 3 to 5 minutes.
• The antidote for cholinergic is Atrophne sulfate
(anticholinergic).
• Tensilon is not used as a treatment for MG since it is short
acting, and has no sustained therapeutic effect.
• The client should not be informed that the medication is given
to obtain true results.

• Collaborative management for MG are as follows:
Assess swallowing and gag reflex before feeding the
and client. To prevent aspiration.
Administer medications 20- 30 minutes before
meals. To improve ability to swallow and to prevent
choking.
Administer medication at exact time. To prevent
myesthenia crisis that results to respiratory distress.
Protect the client from falls due to muscle weakness.
Implement aspiration precaution.
Start meal with cold beverage. To contract muscles
of the throat and improve ability to swallow.

Promote adequate ventilation. To relive respiratory
difficulty.
Avoid infections. Infections may trigger
excacerbations of MG.
Provide adequate rest with alternating activity.
Plasmapheresis. This involves separation of
antibodies from the plasma to inhibit autoimmune
response.

Pharmocotherapy for MG
1. Acetylcholinesterase
inhibitors/Cholinesterase inhibitors
 Prostigmin (Neostigmine)
 Mestinon (Pyridostigmine)
 Mytelase (Ambenomium)
 These medications transmits neuromuscular
impulses by prevening the destruction of
acetycholine. Therefore, there is increased
muscle strength.

Nursing interventions for Acetycholinesterase
Inhibitors
a) Monitor improvement of muscle strength and
respirations.
b) Observe the cliet for signs and symptoms of
cholinergic crisis caused by overdosing of the
drugs, eg., ,uscle weakness, increased salivation,
sweating, tearing and miosis.
c) Have a readily available antidote for cholinergic
crsisis(Atrophine sulfate).
d) Encourage the client to take medications before
meals for best drug absorption.

f) Observe and report possible side effects and adverse
reactions (cholinergic reaction):
 Nausea, vomiting, diarrhea, abdominal cramps
 Increased salivation
 Tearing
 Miosis (constriction of pupils)
 Possible hypertension
2.Glucocorticoids. For anti-inflammatroy effects.
3.Antacids. To prevent gastrointestinal upset due to
glucocorticoids.

• Surgery: Thymectomy (surgical removal of the thymus
gland). Twenty Five percent( 25%) of people with MG
have been found to have thymoma (tumor of the thymus
glands). This surgery achieves remission (symptom-free)
for 5 to 10 years.
• The 2major complications of MG are myesthenia crisis
and cholinergic crisis.
• Myastheni crisis is caused by undermedication.

• The clinical manifestations of myesthenia crisis are as
follows.
o Sudden marked rise in BP due to hypoxia.
o Increased heart rate.
o Severe respiratory distress and cyanosis.
o Absent cough and swallow reflex.
o Increased secretions, increases diaphoresis and
increased lacrimation.
o Restlessness, dysarthria
o Bowel and bladder incontinence.

Interventions for myasthenic crisis are as follows:
Increase doses of cholinergics as long as the client
responds positively to Endrophonium treatment.
Possible mechanical ventilation if respiratory
muscle paralysis is acute.
Cholinergic crisis is causd by excexssive medications.
The clinical manifestations of cholinergic crisis are as
follows:
oWeakness with difficulty swallowing, chewing,
speaking and breathing.
oApprehension, nausea and vomiting.

oAbdominal cramps and diarrhea
oIncreased salivation and secretions.
oSweating, lacrimation, fasciculation (muscle
twitch), and blurred vision.
Interventions for cholinergic crisis are as follows:
oDiscontinue all cholinergic drugs until cholinergic
effects decreases.
oProvide adequate ventilators support.
o1 mg. IV atropine may be necessary to counteract
severe cholinergic reactions.

 The following drugs should be avoided by the client with
MG:
Muscle relaxants
Barbiturates
Morphine sulfate
Tranquilizers
Neomycin
These drugs potentiate muscle weakness because
of effect on myoneural junction.

• Survival Guide for clients with MG
Reschedule daily tasks. To prevent weakness.
Secure “handicapped” parking sticker.
Frequent rest periods.
Have alarm clock available- to take medications on time.
This prevents myasthenic crisis.
Patch each eye alternately for diplopia (double vision).
Start the meal with cold beverage. To conduct constriction
of muscles of the throat and prevent aspiration.
Avoid factors that affect respiratory infections:
Very hot or very cold weather.
Aerosol, pesticides , cleaners.
Alcohol, tonic water, cigarette smoke.

• Multiple Sclerosis (MS)
Is an autoimmune disorder that causes destruction of
myelin sheath of nerve fibers in the brain and spinal
cord (CNS).
It is characterized by remissions and exacerbations.
There is elevated 1g /G in the CSF.
Evoked potentials show slowed nerve conduction.
MRI of the brain and spinal cord shows presence of
MS plaques.
Shawann’s cells of the myelin sheath are destroyed.
This results to interruption and distortion of impulse
(slowed or blocked).

The clinical manifestations of MS are as follows:
Eye manifestations (optic nerve involvement)- vision
loss
Weakness or tingling sensation (paresthesia due to
involvement of the cerebrum and soinal cord).
Incoordination due to cerebellar involvement (ataxic
gait).
Bowel and bladder dysfunction as a result of spinal
cord invovlement.
Muscle fatigue due to muscle spasticity.
Charcoat’s Triad:
 S – canning speech
 I – ntention tremors
 N – ystagmus

Exacerbations may be aggravated by fatigue, chilling and
emotional stress.
The collaborative management for MS are as follows:
Patch the eye alternately for diplopia.
Provide well-balanced diet, high in fiber to prevent
constipation.
Physical therapy to improve muscle strength and to
avoid contracture.
Avoid hot baths. Heat Increases weakness.
Force fluids to prevent constipation and infection.
Speech therapy to relieve scanning speech.
Plasmapheresis. To inhibit autoimmune response.

 Pharmacotherapy in MS
1. Glucocorticoids
 Prednisone
 Decadron (Dexamethasone)
 Corticotropin
2. Muscle Relaxants. To relieve muscle spasm.
 Lioresal (Baclofen)
 Betaseron (an interferon that reduces spacticity)
3. Immunosuppressants. To reduce relapse of MS.
 Imuran (Azathiorpine)
 Cytoxan (Cyoclophosphamide)

• ALZHEIMER’S DISEASE
Is a degenerative disorder of the cerebral cortex
resulting to microscopic plaques.
It is characterized by impaired intellectual function
and progressive loss of ability to carry out activities of
daily living.
Loss of recent memory occurs first. Remote memory
may remain intact for long period of time.
The cause of Alzheimer’s disease is unknown but it
may be associated with autoimmune disorders and
heredity.

 The stages and phases are as follows:
Stage 1. Mild (Early confusion).
Early cognitive decline in one or more areas,
memoryloss, decreased ability to function in work
situation, name- finding deficit, same decrease in
social functioning, recall difficulties, anxiety.
Stage 2. Moderate
Unable to perform complex tasks such as managing
personal finances or planning a dinner party, unable
to concentrate; no knowledge of current events.

Stage 3. Moderately severe (Early dementia)
 Usually needs assistance for survival; needs reminders to
bathe, help in selecting clothes and other daily functions,
maybe disoriented as to time and recent events although
this can fluctuate, may become tearful.
Stage 4. Severe (Demetia)
 Needs assistance with dressing, bathing and toilet
functions (flushing); may forget spouse, family and
caregiver’s names, details of their personal life; generally
unaware of their surroundings, incontinence of urine and
feces; increase in central nervous system disturbances
such as agitation, delusions, paranoia, obsessive anxiety,
increased potential for violent behavior and tendency to
wander.

Stage 5. Very severe (Late Dementia)
 Unable to speak (speech limited to five words or less), person
may scream or make other sounds, unable to ambulate, sit up,
smile , or feed self; unable to hold head erect; will ultimately slip
into stupor or coma.
• The collaborative management for Alzheimer’s disease:
 Protect the client form injury. The client has tendency to wander
around.
 Provide close supervision.
 Close and secure doors.
 Use ID bracelets and electronic surveillance.
 Remove throw rugs, toxic substances and dangerous electrical
appliances from the environment.
 Reduce hot water heater temperature.
 Orient client to the environment.

Promote activity.
Provide exercise such as walking with an escort.
Provide activity that distract and and occupy time
such as listening to music, coloring, and watching
television.
Provide mental stimulation with simple games and
activities.
Promote activities of daily living.

Promote sleep
 Allow client to wander in a safe place until he or she
becomes tired.
Prevent shadows in the room.
Avoid the use of hypnotics because they cause
confusion and aggravate the sundown effect.
Avoid Agitation and Violence
Assess and remove the cause of agitation.
Avoid scolding, embarrassing, arguing or reasoning
with the client.
Approach the client slowly and calmly.
Remove the client from stressful environment.

Minimize confusion and disorientation
Call the client by name.
Orient the client frequently
Ask only one question at a time and give one direction
at a time.
Use familiar objects in the room.
Place a calendar and clock in a visible place.
Provide structured activities (routine schedule).
Allow the client to reminisce (remote memory may
remain intact for a long time).
Provide simple environment that requires less decision
making.
Allow time for the client to complete task.

Prevent fatigue by avoiding the following:
Change of routine
Excessive demands
Physical stressors
Overwhelming situation.
These factors escalate behavioral dysfunction.
Prevent sundown syndrome.
Turn lights on before it becomes dark.
Refer Family to support groups: The Alzheimer’s
Disease and related disorders.

Tacrine
 May improve cognitive functions for mild to
moderate Alzheimer’s disease.
Check VS periodically, for tachycardia and
hypotension.
Exelon
G.I. upset common adverse effect. Weight loss
may be a problem.

Amyotrophic Lateral Sclerosis (ALS)
• Is a progressive degenerative disease involving the
motor system.
• It is also called Lou Gehrig’s Disease.
• The cause of the disease may be related to an excess of
glutamate, a chemical responsible for relaying messages
between motor neurons.
• The clinical manifestations of ALS are as follows:
Fatigue and weakness while talking.
Awkwardness of fine finger movements.
Dysphagia (1st sign)
Muscle weakness and atrophy

Muscle wasting
Unilateral disability of arm and leg.
Dysarthia
Fasciculation of the face.
Jaw clonus
Respiratory difficulty
• Collaborative management for ALS care as follows:
Supportive and symptomatic
Monitor and promote respiratory function.
Gastrostomy feeding
Avoid aspiration
Assist with ADL
Provide emotional support to the client and family.

Guillan –Barre Syndrome (GBS)
• Is an acute infections neuronitis of the cranial and
peripheral nerves.
• It involves destruction of the myelin sheath due to
autoimmune disorder.
• It may follow swine flu vaccine.
• It is usually preceded by mild upper respiratory
infection or gastroenteritis.
• The recovery is slow process.
• The main problem is difficulty of breathing.

The clinical manifestations of GBS are as follows:
Ascending or descending paralysis which may progress to
respiratory muscle paralysis.
Tingling and numbness.
Cardiac dysrhythmias.
Elevated protein levelin CSF.
Abnormal EEG (electro encephalography)
Collaborative management for GBS are as follows:
Symptomatic and supportive.
Monitor and promote respiratory function.
Prevent complications of immobility.
Monitor cardiac status.

Trigeminal Neuralgia (Tic Douloreux)
• A sensory disorder of the fifth cranial nerve.
• It is a manifested by excruciating, recurrent paroxysms of
sharp, stabbing facial pain along the trigeminal nerve (lips,
gums, nose, cheeks)
• Pain aggravated by cold, washing the face, chewing, hot or
cold foods and fluids, touch of wind on the face.
Collaborative management for Trigeminal Neuralgia are
as follows:
Instruct the client to avoid hot or cold foods and
beverages.
Provide liquid and soft foods.
Instruct client to chew food on the unaffected side.

Pharmacotherapy
Elavil (Amitriptyline)
Lioresal (Baclofen)
Tegretol (Carbamazepine)
Valium (Diazepam)
Dilantin (Phenetoin)

Bell’s Palsy (Facial paralysis)
• Is caused by lower motor neuron lesion of the seventh cranial
nerve.
• It may be caused by infection, trauma, hemorrhage,
meningitis or tumor.
• It is manifested by paralysis of one side of the face with
drooping of the eyelids, or puff out the cheeks.
Collaborative Management for Bell’s palsy are as follows:
 Encourage facial exercises.
 Protect the eyes from dryness and prevent injury.
 Promote frequent oral care.
 Instruct the client to chew on the unaffected side.

Pharmacotherapy
Steroids
Analgesic

Care of the Client’s with Spinal Cord injury (SCI)
 Spinal cord injury occurs in the following situations:
Falls, Diving, Vehicular accident.
 SCI results to the following effects below level of the
lesion:
Paralysis
Loss of reflexes
Loss of sensory function
Loss of motor function
Autonomic dysfunction

Clinical manifestations of spinal cord injury
1) Cervical SCI
 Injuries at C2 and C3 are usually fatal.
 Quadriplegia (paralysis of our four extremities)
 Respiratory muscle paralysis.
 Bowel and bladder retention.
2) Thoracic SCI
 Paraplegia (paralysis involving the lower extremities).
 Poor control of upper trunk.
 Bowel/ bladder retention.
 Autonomic dysreflexia with lesion or injury above T6

3) Lumbar SCI
 Paraplegia (Flaccid paralysis)
 Bowel and bladder retention.
4) Sacral SCI
 Injury above S2 in males allow erection but there
is no ejaculation.
 Injury between S2 to S4 prevents erection and
ejaculation.
 Paraplegia
 Bowel and bladder incontinence.

 The higher the level of lesion, the greater is the
probability to perform sexually.
 The lower the level of lesion, the lesser is the
probability to perform sexually.
 The paraplegic male may experience impotence.
 The paraplegic female is capable of pregnancy, but
is unable to experience orgasm.
Collaborative management for SCI are as follows:
 First priority: promotion of respiratory function
especially in cervical SCI.
 Immobilize in a flat, firm surface. To prevent further
injury.

 Apply cervical collar especially if cervical injury is
suspected.
 Transport client as a unit.
 Do not attempt to realign body parts.
 Definitive management.
1) Traction
2) Cast
3) Surgery
 Monitor and manage potential complications of SCI
1) Spinal Shock (neural sock, areflexia). It is a period of
flaccid paralysis and a complete loss of all reflexes
occurs.

 The clinical manifestations of spinal shock are as
follows:
o Absence of sweating below the level of the
lesion.
o Bowel and bladder retention.

o Hypotension, Bradycardia
 If the lumbosacral segment are undamaged, spinal
shock wears off in 2 to 3 weeks
 The first sign of resolution of spinal shock is
contraction of the quadriceps (Hamstring) muscles and
flexion or extension of toes on plantar stimulation.
 The other signs of resolution of spinal shock are
reflexive emptying of the bladder, reflex defecation and
return of sweating.
2) Autonomic Hyperreflexia (dysreflexia). It occurs in
clients with SCI above T6; most often cervical injuries.
 It causes hyperstimulation of symathethic nervous
system (SNS).

 It is caused by visceral distention like bladder distention,
fecal impaction and skin stimulation like pressure sore
below the level of lesion.
 The clinical manifestations of autonomic hyperflexia are as
follows:
o Severe headache
o Blurring of vision
o Nasal congestion
o Nausea and vomiting
o Hypertension, bradycardia
o Sweating above the lesion; pilomotor spasm (goose
flesh) below the lesion.
 The most dangerous effect of autonomic dysreflexia is severe
hypertension. This may lead to blindness and CVA.

 Collaborative management for autonomic
dysreflexia include the following:
o Place the client in sitting position. To lower BP
by gravity.
o Check bladder distention. Catheterize client as
indicated.
o Check fecal impaction. Perform manual extraction
as indicated.
o Turn the client to sides at regular intervals. To
prevent pressure sores.
o Pahrmacotherapy:
• Hexamethonium Chloride (a ganglonic
b;ocking agent)
• Nitroprusside ( a vasodilator)

Whiplash injury
 Is caused by violent hyoerextension and flexion of the
neck. It usually result from vehicular accident.
 There is damaged to muscles, disks, ligaments and
nervous tissues of the cervical spine.
 The clinical manifestations of whiplash injury are as
follows:
 Pallor
 Weakness
 Gait disturbance
 Dizziness
 Nausea and vomiting
 Occipital headache
 Nuchal rigidity

Collaborative management for whiplash injury include
the following:
 Promote bed rest.
 Apply cervical collar as needed.
 Apply hot packs to the neck as indicated.
 Administer analgesic and muscle relaxant as
prescribed.

MENINGITIS
- inflammation of the meninges of the brain and spinal
cord.

ETIOLOGIC AGENTS
• MENINGOCOCCUS – MOST DANGEROUS
• Pneumococcus
• Streptococcus – adult
• Hemophilus influenzae – pedia

MODE OF TRANSMISSION – airborne transmission via
droplet infection

meningitis
CSF analysis will reveal
• Increased CHON and WBC
• Decreased Glucose
• Increased CSF opening pressure
• N = 50-160 mmHg
• (+) cultured microorganisms
• These confirm presence of meningitis

NURSING MANAGEMENT
1. Complete bed rest
2. Administer medications as ordered
- Broad Spectrum Antibiotics
- Penicillin
- Analgesics
- Antipyretics
3. Institute strict respiratory isolation after initiation of
antibiotic therapy
4. Institute ICP monitoring
5. Dim environment  d/t photophobia

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