Perception and
White matter-less perfusion (bundles of fibers, terminal ends)
Coordination
Perception-conscious recognition and interpretation
(awareness) of the sensory stimuli that serve as a basis for
understanding, learning and knowing or for the motivation of
a particular action or reaction
Coordination-when action or reaction towards a
stimulus is occurring in a purposeful, orderly fashion,
appropriate response to a stimulus
Role of Nervous System:
1. Reciprocally interact with the environment
2. Maintain homeostasis (with the endocrine system)
Function:
1. Sensory-interpret incoming message
2. Integrative-analyze, store, make decisions regarding
appropriate behavior
3. Motor-initiating muscular or glandular activity;
ongoing and evolving interaction with environment
Ventricles and CSF
• Ventricles- four fluid-filled cavities within the brain
that connect one another and with the spinal canal
• CSF- form in the choroids plexus; about 135 cc
o Cushions
o Provide nutrients
o Allow fluid shifts
3 essential components of skull:
1. Brain tissue-78%
2. Blood -12 %
3. CSF-10%
Monro-Kellie Hypothesis
If volume added to the cranial vault equals the
volume displaced from it, the total intracranial volume
will not change
Normal ICP: 60-150 mmH20 or 0-15 mmHg
Normal Compensatory Adaptations:
Initial:
o Increases CSF absorption
o Displacement of CSF into the spinal subarachnoid
space—space between arachnoid and pia mater)
o Collapse of the cerebral veins and dural sinuses
Other mechanisms:
o Distensibility of the dura
o Increased venous outflow
o Decreased CSF production
o Constriction and vasodilation
o Slight compression of brain tissue
Cerebral Blood Flow
• Amount of blood in milliliters passing
through 100g of brain tissue in 1 minute
• Global CBF-approximately 50 ml/min
• Brain needs constant supply of oxygen and
glucose (20% of body’s oxygen, 25% of
body’s glucose)
More than 10 minutes of oxygen deprivation-brain death
Gray matter-more perfusion (body of neurons)
Sources of Blood supply:
1. Internal carotid arteries-anterior circulation,
ipsilateral hemispheres
2. Vertebral arteries-posterior circulation, posterior
fossa
• Circle of Willis
• act as a safety valve; arises from basilar
arteries and internal carotid arteries;
vascular network at the base of the brain
• is important to total brain circulation
because it provides equal circulation
bilaterally. If one side of the circle of
Willis is unable to supply adequate
blood, the other side provides blood to
the area normally supplied by the
damaged side (Phipps, 1998, p. 1892)
• Cerebral arteries (2 each):
Anterior, Middle, Posterior
• Jugular veins-drains the brain venous blood
through dural sinuses
Special characteristics of Cerebral Perfusion
1. Autoregulation
3 Physiologic mechanisms under normal circumstances:
o Changes in intracranial pressure
o Cerebral vasodilation
o Metabolic factors
Mean arterial pressure at which autoregulation is effective
(70-105 mmHg)
-Upper limit is 150 mmHg
SBP + 2 (DBP)
MAP=
3
SBP-Systolic blood pressure
DBP-Diastolic blood pressure
Cerebral perfusion pressure needed to ensure blood flow to
the brain
CPP= MAP-ICP
As CPP decreases, autoregulation fails and CBF diminishes
-30 mmHg is incompatible with life
2. Blood brain barrier
• physiologic barrier between blood
capillaries and brain tissue
NEUROPHYSIOLOGY
Neurotransmission-conduction of an impulse
throughout the nervous system
Neurons
Receive and transmit impulses; non-mitotic
Excitable, conductive and can influence other cells
Parts: cell body (soma), dendrites (short) and axon
Myelinated and unmyelinated
Note:
 When injured, centrally located neurons are unable to Vertebral column-protects the spinal cord, supports the head
reproduce themselves because most cell bodies are located and provides flexibility; strengthened by ligaments and
centrally and nerve cell bodies cannot reproduce. However, fibrocartilage disc
nerve endings can regenerate (Phipps, 1998, p. 1887).

I. Transmission within the Nerve fiber Cranial meninges

Action potential Dura mater
• Chemical gradient Arachnoid
• Electrical gradient Pia mater
Propagation of Action Potential
1. Resting stage (positive outside, negative inside) Falx cerebri-divides the left from right hemispheres
2. Depolarization phase (negative outside, positive Subdural-more bleeding
inside)

II. Transmission across Synapse

Synapses-small gaps between neurons Central Nervous system:
I. Cerebrum
• Chemical or electrical
Consists of 2 hemisphere
• One-way junction Corpus callosum-connects two hemisphere
1. Impulses reaches the presynaptic Cerebral cortex-outer surface of the cerebrum
terminal Basal ganglia-located deep within cerebral hemisphere
2. Vesicles release neurotransmitters Internal capsule-white matter consisting of bundle of nerve
3. Neurotransmitters inactivated to prevent fibers carrying motor and sensory impulses to and from
sustained response cerebral cortex

Neurotransmitters-can be excitatory or inhibitory)

Types: Lobes of the Cerebrum and their Functions
1. Acetylcholine-muscle movement
2. Biogenic amines (thinking process) Area Functions
-Dopamine -Serotonin Frontal Controls movements of
-Norepinephrine -Histamine voluntary muscle
3. Amino acids
Primary motor area Facilitates voluntary
-GABA
movement of skeletal
-Peptides
muscle
Speech area (Wernick’s ) Understanding of spoken
Neuroglia-protect and nourish neurons; mitotic
- Located in the and written words
- do not transmit impulses
posterior part of the
Neuroglia Function superior temporal
Astrocytes Supply nutrients to neurons convolution
Microglia Provide protection against Motor area (Broca’s) Promotes vocalization of
microorganisms - Located in the lateral, words
Oligodendrocytes Wrap tightly around nerve inferior portion of the
fibers to form myelin sheath frontal lobe
Ependymal cells Ciliated; line brain cavities; Temporal Receives and interpret
forms CSF olfactory and auditory
Schwann cells Phagocytic cells that form stimuli
myelin sheath around nerve Parietal Promotes recognition of
fibers pain, coldness, light touch
Satellite cells Found in the PNS; may (Contralateral reception)
maintain chemical balance of Occipital Receives and interprets
neurons visual stimuli

Cranium and Cerebral column

• Cranium-composed of 8 cranial and facial bones
• Foramen magnum-largest hole through which the brain stem
extends to the spinal cord
II. Diencephalon
Embedded in the brain superior to brain stem
Thalamus-process sensory impulses before it reaches cerebral
cortex
• Hypothalamus-regulates endocrine and
autonomic function, temperature, water
metabolism, appetite, emotion, sleep-wake cycle
and thirst
• Epithalamus-includes pineal gland (secretes
melatonin and inhibits LH), part of endocrine
system, affects growth and development.

III. Brain Stem

Midbrain-center for auditory and visual reflexes
Pons-contains the fiber tracts; contains nuclei that controls
respiration
-contains pneumotaxic center—controls
rhythmic quality of respirations
Medulla-control cardiac rate, BP, respirators and swallowing
 • Reticular activating system (RAS)-influence Autonomic Nervous System
excitatory and inhibitory control of motor
Controls involuntary or automatic body functions
neuron; regulatory system for consciousness
Has two subdivisions, serving same organ but have
counterbalancing effects; each system can inhibit the organ
IV. Cerebellum stimulated by the other
Has two hemispheres
Coordination of skeletal muscle activity, maintenance of • Sympathetic Nervous System
balance, posture and control of voluntary movements  originates from lateral horns of first
thoracic through the first lumbar of spinal
cord (thoracolumbar)
V. Spinal cord  helps the body cope with events in the
• Extends from medulla up to first lumbar external environment
vertebra  Functions mainly during stress, triggering
• Gives rise to 31 pairs of spiral nerves (C1- the fight or flight response
C8, T1-T12, L1-L5, S1-S5, coccygeal nerve)  Increases heart rate and respiratory rate,
• Center for conducting messages to and from pupil dilation, cold, and sweaty palms
the brain; a reflex center
• Parasympathetic Nervous System
Divisions:  Consist of the vagus nerves originating in
the medulla of the brain stem and spinal
Ascending (Spinocerebellar) nerves originating from the sacral region
• Carry a specific sensory information to of the spinal cord (craniosacral)
higher levels of CNS  Activates GI system
• Spinocerebellar tracts-muscle tension and  Supports restorative, resting body
body position function through such actions as
• Spinothalamic-pain and temperature replenishing fluids and electrolytes
sensation
Effect organ Sympathetic Parasympathetic
Descending (Corticospinal) Heart Increased rate Decreased rate
• Pyramidal tracts-from the cortex to cranial and contractility and contractility
and peripheral nerves; inhibits muscle tone Lungs Relaxation Contraction
• Extrapyramidal tracts-from brain stem, GIT
basal ganglia, and cerebellum; maintains • Motility Decreased Increased
muscle tone and gross body movements • Tone Contraction Relaxation
• Upper motor neurons-from cerebral cortex sphincters
to anterior gray column of SC; spasticity Urinary bladder
and hyperactive reflexes • Bladder muscle Relaxation Contraction
• Lower motor neurons-“final common • Sphincter
pathways” from anterior gray column up to Contraction Relaxation
muscles; flaccidity and loss of reflexes Liver Glycogenolysis None

VI. Reflex arc

• Reflexes-automatic action; spinal cord Sensory System (General and special)
mediates most reflexes
• Automatic or perceptible, inhibited or Type of receptors:
conditioned 1. Exteroreceptors
2. Interoreceptors
• Hyperreflexia-disease or injury of certain
3. Proprioceptors-specific receptors to detect balance,
descending motor tracts
sense of position
• Hyporeflexia-damage or degeneration of the 4. Mechanoceptors-detect pressure, touch (any
sensory or motor neurons stimulus that is physical in nature)
5. Thermoreceptors-any changes in temperature
Peripheral Nervous system 6. Photoreceptors-light stimulus
Cranial nerves-innervate head and neck region, except the 7. Chemoreceptors-taste, olfactory, pancreatic enzymes
vagus nerve 8. Nociceptors-severe stimulus
Spinal nerves 9. Cutaneous receptors-touch
• Plexuses-complex cluster of
nerve fibers (cervical, brachial, Special senses:
lumbar and sacral region) Sense of Sight
• Dermatomes-area of the • Collect light waves and transmit them
skin innervated by cutaneous as impulses to the brain, which translate
branches of a single spinal nerve them into images
• Normally form of a clear retinal image
Somatic Nervous system of an object at 20 ft. away
Consists of motor and sensory nerves • Binocular vision—ability to judge
Controls skeletal muscles relative, distances of objects
• Produces a motor response through
efficient nerve fibers from CNS Anatomical features of the Eyeball
which transmit impulses to the skin Outer:
and skeletal muscles 1. Cornea-thin, tough, transparent layer
supplied with sensory nerve (touch and pain),
 no blood supply, oxygen and glucose through • Upper range decreases slight with increasing
diffusion age
2. Sclera • Speech falls in the range of 85-1050 Hz

Middle: Physiology of Hearing

1. Choroid –highly vascular, dark brown membrane
2. Ciliary body-contract and dilate ciliary process
which contain capillaries that secrete fluid
3. Iris-visible colored part of the eye; controls pupil
size
1. Sound waves moving through the air enter the canal
and move down to it to strike against the tympanic
membrane causing it to vibrate
2. Vibrations of the tympanic membrane move the
malleus

Inner: 3. Movement of the malleus to the incus

1. Retina-neural tissue, phagocytic, stores Vit. A, 4. As the incus moves, it moves the stapes against the
contains rods and cones oval window, it starts a ripple on the perilymph
2. Fovea-responsible for highly colored vision 5. Movement of the perilymph is transmitted to the
endolymph muscle inside the cochlear duct and
Refraction stimulates the organ of Corti
• bending of light when it meets surfaces of 6. Cochlear nerve conduct impulses from the organ of
different medium Corti to the brain; hearing occurs when impulses
reaches auditory area in the temporal lobe of
Refractory media of the Eye cerebral cortex
1. Cornea-performs most of the refraction because of
its convex form
2. Aqueous humor-fluid at the anterior and posterior Mental Status Examination
chamber of the anterior cavity An indication of how patient is functioning as a whole and how
3. Crystalline lens-greatest refractive power the patient is adapting to the environment
4. Vitrous humor- thick, gelatinous fluid found at 1. General appearance
posterior chamber, give spherical shape to the eye 2. State of consciousness
• Arousal component
Physiology of Vision • Content component
Formation of an image on the retina accomplished by the 3. Mood and effect-changes in the nervous system
following: 4. Thought content
1. Refraction 5. Intellectual capacity
2. Accomodation
3. Constriction of pupils NEUROLOGIC ASSESSMENT
4. Convergence of eyeballs I. Comprehensive History Taking
• Demographic Data
Stimulation of retina • Current health
• Dim light causes breakdown of the chemical • Past health history
rhodopsin present in rods • Medication history
• Cones-responsible for daylight and color vision
• Perception of color is dependent on the cones • Growth and development
• Most cones concentrated on fovea centralis • Family health history
• Condition to central area in occipital lobe • Psychosocial history
II. V/S
Sense of Hearing III. Mental Status Assessment
Parts of the ear • LOC
1. Outer-collects sound • Orientation
2. Inner-conducts sound • Memory
• Eustachian tube • Mood/affect
joins the middle ear and nasopharynx • Intellectual performance
transmit sound waves and maintain equilibrium • Judgment/Insight
• Language/communication
Interpretation of sound
IV. Motor System assessment-muscle strength, tone,
• Loudness- Neurologic or psychologic
coordination, gait and station movement
interpretation of intensity; the greater
V. Sensory Function-superficial sensation, touch/pain,
intensity of the sound waves stimulating
temperature, proprioception, discrimination
the organ of Corti, the greater will be
VI. Reflex activity
the size of nerve impulses
VII. Cranial nerve testing
Decibels(dB)-unit of measure of intensity of sound
Normal conversation= 65 dB
Amplified rock music= 120 dB
MENTAL STATUS ASSESSMENT WITH ABNORMAL
Nearby jetplane= about 140 dB FINDINGS

Pitch
• Corresponds to frequency; the higher the
• Unilateral neglect (lack of caring of the other side of the
body); strokes involving middle cerebral artery.
frequency the higher the pitch of the sound
• Humans can potentially hear sounds whose
frequency range from 16 to 2000 Hz • Poor hygiene and grooming: dementing disorders

• Abnormal gait and posture: transient ischemic
attacks(TIAs) , strokes, and Parkinson’s disease
• Emotional swings, personality changes: strokes
• Aphasia-defective or absent language function: TIA’s,
strokes involving anterior/posterior artery; general term
for impairment of language
• Dysphonia- change in tone of voice
• Dysarthria- (different in speaking); is indistinctness of
words in word articulation resulting from interference
with the peripheral speech mechanisms (e.g. muscles of
the tongue, palate, pharynx, or lips) [Phipps, 1998, p.
1901]
• Decreased level of consciousness
• Confusion, Coma
COGNITIVE FUNCTION ASSESSMENT WITH
ABNORMAL FINDINGS
• Disorientation to time and place: stroke of right cerebral
hemisphere
1. Memory deficits
2. Emotional defense
CRANIAL NERVE ASSESSMENTS
• Cranial I (Olfactory): Anosmia
1. lesions of frontal lobes
2. impaired blood flow to middle cerebral
artery.
• Cranial II (Optic)
1. blindness in eye: strokes of internal carotid
artery, TIA’s
2. Homonymous hemianopia - impaired vision
or blindness in one side of both eyes;
blockage of posterior cerebral artery.
3. Impaired vision: strokes of anterior cerebral
artery; brain tumors
Note:
• Visual acquity-mediated by the cones of the
retina
• Field of vision or peripheral vision-portion of
space in which objects are visible during the
fixation of vision in one direction. The
receptors for peripheral fields are the rod
neurons of the retina. (Phipps, 1998, p.
1906)
• Cranial nerve III, IV, VI (Oculomotor, Trochlear,
Abducens)-motor nerves that arise from the brainstem
1. Nystagmus –- involuntary eye movement;
strokes of anterior, inferior, superior,
cerebellar arteries
2. Constricted pupils: may signify impaired
blood flow to vertebralbasilar arteries.
3. Ptosis (eyelid falldown); dropping of the
upper eyelid over the globe—strokes of
posterior inferior cerebellar artery;
myasthenia gravis, palsy of CN III
Cranial nerve V (Trigeminal)—largest cranial nerve with motor
and sensory components: changes in facial sensations;
impaired blood flow to carotid artery
1. Decreased sensation of face and cornea on same
side of body; strokes of posterior inferior cerebral
artery
2. Lip and mouth numbness
3. Loss of facial sensation: contraction of masseter and
temporal muscles, lesions CN V
4. Severe facial pain: trigeminal neuralgia (tic
dorlourex)
Cranial VII (Facial nerve)—mixed nerve concerned with facial
movement and sensation of taste
1. Loss of ability to taste
2. Decreased movement of facial muscles
3. Inability to close eyes, flat nasolabial fold, paralysis
of lower face, inability to wrinkle the forehead
4. Eyelid weakness; paralysis of lower face; paralysis of
upper motor neuron
5. Pain, paralysis, sagging of facial muscles: affected
side in Bell’s palsy
Cranial VIII (Acoustic)—composed of a cochlear division
related to hearing and a vestibular division related to
equilibrium (Phipps, 1998, p. 1909)
• Decreased hearing or deafness: strokes of
vertebralbasilar arteries or tumors of CN VIII
Cranial IX(Glossopharyngeal) and cranial X (Vagus)—chief
function of cranial nerve IX is sensory to the pharynx and
taste to the posterior third of tongue; cranial nerve X is the
chief motor nerve to the soft palatal, pharyngeal and
laryngeal muscles (Phipps, 1998, p. 1909)
1. Dysphagia (difficulty swallowing)
2. Unilateral loss of gag reflex
Cranial XI (Spinal accessory)—motor nerve that supplies the
sternocleidomastoid muscle and upper part of trapezius
muscles
1. Muscle weakness
2. Cortralateral hemiparesis: strokes affecting middle
cerebral artery and internal artery
Cranial XII (Hypoglossal)
1. Atrophy, fasciculations (twitches): LMN disease
2. Tongue deviation toward involved side of the body
SENSORY FUNCTION ASSESSMENT WITH
ABNORMAL FINDINGS
Altered sensation occurs with variety of neurologic pathology
Altered sense of position: lesions of posterior column of spinal
cord
Inability to discriminate fine touch: injury to posterior
columns
MOTOR FUNCTION ASSESSMENT WITH
ABNORMAL FINDINGS
Muscle atrophy: LMNs disease
Tremors (groups, large of muscle fibers)-Parkinson’s disease
(tremors at rest), multiple sclerosis (tremors observed in
activity)
Fasciculations (single muscle fiber): disease or trauma to
LMN, side effects of medications, fever, sodium deficiency,
anemia
Flaccidity (decreased muscle tone): disease or trauma to LMN
and early stroke
Spasticity (increased muscle tone): disease of corticospinal
motor tract
Muscle rigidity: disease of EP motor tract
Cogwheel rigidity (muscular movement with small regular
jerky movement; parkinson’s disease
Muscle weakness-in arms, legs, hands: TIAs
Hemiplegia-paralysis of half of body vertically
Flaccid paralysis: strokes of anterior spinal artery, multiple
sclerosis or myasthenia gravis
Total loss of motor function: below level of injury
Spasticity of muscle: incomplete cord injuries

Decerebrate posturing (down)

CEREBELLAR FUNCTION ASSESSMENT WITH
ABNORMAL FINDINGS
Ataxia (lack of coordination and clumsiness of movement,
#Altered Level of consciousness
staggering, wide-based and unbalanced gait)
1. Consciousness
Steppage gait (client drags or lifts foot high, then slaps foot Requires:
onto floor; inability to walk on heels; disease of LMN 1. Arousal: alertness; dependent upon
Sensory ataxia (client walks on heels before bringing down reticular activating system (RAS); system of
toes and feet are held wide apart; gait worsens with eyes neurons in thalamus and upper brain stem
closed 2. Cognition: complex process, involving all
mental activities; controlled by cerebral
Parkinsonian gait (stooped over position while walking with
hemispheres
shuffling gait with arms held close to the side)
Romberg’s test (Positive)- With feet approximated, the Process that affect LOC:
patient stands with eyes open and then closed; if closing the a. Increased ICP
eyes increases the unsteadiness, a loss of proprioceptive b. Stroke, hematoma, intracranial hemorrhage
control is indicated c. Tumors
d. Infections
REFLEX e. Demyelinating disorders
Hyperactive: reflexes
Decreased reflexes Systemic Conditions affecting LOC
Clonus of foot (Hyperactive, rhythmic dorsiflexion and plantar  Hypoglycemia
flexion of foot)  F/E imbalance
Superficial reflexes (such as abdominal) and cremasteric  Accumulated waste products from liver or
reflex renal failure
Positive Babinski reflex (dorsiflexion of big toe)  Drugs affecting CNS: alcohol, analgesics,
anesthetics
 Seizure activity: exhausts energy
metabolites
Special Neurologic Assessment  Level of Consciousness
• Alert
Brudzinski’s sign (pain, resistance, flexion of hips and knees • Lethargic-very sleepy
when head flexed to chest with client supine) • Obtunded
• Stuporous
• Coma
• Death

Client Assessment with Decreased LOC

a. Increased stimulation required to elicit response
from client
b. More difficult to arouse; client agitated and confused
when awakened
c. Orientation changes: losses orientation to time first,
then place, person
d. Continuous stimulation required to maintain
wakefulness
e. Client has no response, even to painful stimulation
• Positive Kernig’s sign-excessive pain when examiner
attempts to straighten knees with client
Loss of Simultaneous Eye Movement
supine and knees and hips flexed
Loss of normal reflex functioning:
1. Doll’s eye movement: eye movement in opposite
direction of head rotation (normal function of brain
stem)
2. Oculocephalic reflex: eye move upward with passive
flexion of neck; downward with passive neck
extension (normal function)
3. Oculovestibular response (cold caloric testing):
instillation of cold water in ear canal cause
nystagmus (lateral tonic deviation of eyes) toward
stimulus (normal function)

Decorticate posturing (up) GLASGOW RESPONSE

Eye opening responses
4 Opens eyes spontaneously
3 Opens eyes in
response to voice 2 Opens eye in
response to painful stimuli 1 Does not
open eyes
 Best verbal response
5 Oriented NURSING DIAGNOSIS
4 Confused • Ineffective airway clearance: limit
3 Utters inappropriate words suctioning to <10-15 seconds,
2 Incomprehensible words hyperoxygenate
1 None • Risk for aspiration
• Risk for impaired skin integrity: preventive
measures, continual inspection
• Impaired physical mobility: maintain
functionality of joints, physical therapy
• Risk for Imbalanced Nutrition: Less than
body requirements
• Anxiety (of family)
Best motor response
6 Obeys command
ICP
5 Localizes pain Increased blood volume, increased brain volume, increased
4 Withdraws with painful stimuli CSF volume
3 Flexion (Decorticate posturing)
2 Extension (Decerebrate posturing Normal pressure: 5-15 mmHg, with pressure tranducer with
1 None head elevated 30˚; 60-180 cmH20, water manometer with
client lateral recumbent
Total 3-15 Sustained increases associated with:
14 – no impairment a. Cerebral edema
3 – compatible with brain death b. Head trauma
7 – state of coma c. Tumors
d. Abscesses
MOTOR FUNCTION ASSESSMENT e. Stroke
a. Client follows verbal commands f. Inflammation
b. Pushes away purposely from noxious stimuli g. Hemorrhage
c. Movements are more generalized and less purposeful
Factors that Increases ICP
(withdrawal, grimacing)
Hypercapnea, hypoxemia
d. Reflexive motor responses
Cerebral vasodilating agents
e. Flaccid with little or no motor response
Valsalva maneuver; coughing or sneezing
Body positioning (prone, neck flexion, extreme hip flexion)
COMA Isometric muscle contraction
Emotional upset; noxious stimuli
Irreversible coma - vegetative state Arousal from sleep
• Permanent condition of complete unawareness of self and Clustering of activities
environment, death of cerebral hemispheres with continued Pain and agitation
function of brain stem and cerebellum
• Client does not respond meaningfully to environment but has ICP
sleep-wake cycles and retains ability to chew, swallow and
cough Cranial insult Tissue edema Increased ICP
• Eyes may wander but cannot track objects
• Minimally conscious state: client aware of environment, can Compression of blood vessels
follow simple commands, indicates yes/no responses; make
meaningful movements (blink, smile)
• Often results from severe head injury or global anoxia Decreased cerebral blood flow

Decreased oxygen with brain cell death

Locked-in syndrome
Edema around necrotic tissue
1. Client is alert and fully aware of environment; intact
cognitive abilities but unable to communicate
Increased ICP with brainstem and respiratory center
through speech or movement because of blocked
compression
efferent pathways from brain
2. Motor paralysis but cranial nerves may be intact
Carbon dioxide accumulation
allowing client to communicate through eye
movement and blinking
3. Occurs with hemorrhage or infarction of pons, Vasodilation Increased ICP DEATH
disorders of lower motor neurons or muscles
Pathophysiology: pressure results to lack of oxygen and
Brain Death blood supply
1. Cessation and irreversibility of all brain functions
2. General criteria: Manifestations:
a. Absent motor and reflex movements • Decreasing level of sensorium-most sensitive,
b. Apnea reliable and earliest indicator: due to
c. Fixed and dilated pupils cerebral hypoxia, interference with RAS
d. No ocular responses to head turning and caloric function
stimulation • Increasing BP, decreasing pulse
e. Flat EEG • Pupillary changes (a reflection of tissue shifts
 • Cushing’s triad-increasing systolic pressure,
widening pulse pressure and bradycardia
(final compensatory mechanism to maintain
CSF)
• Papilledema-due to the compression of optic disc
• Respiratory changes-dependent on site of
pressure
• Motor changes-dependent on site of pressure;
usually starts contralaterally; then
hemiplegia, decortication or decerebation
depending on pressure on brain stem
Late signs: coma, apnea, unilateral pupil changes
Medications for Increased ICP
• Osmotic diuretics increases osmolarity of blood and
draw fluid from edematous brain and tissue into
vascular bed
• Loop diuretics such as furosemide
• Antipyretics or hypothermia blanket: used to control
increases in cerebral metabolic rate
• Anticonvulsants to manage seizure activity
• Histamine H2 receptors to decrease risk of stress
ulcers
a. Establish and maintain airway
• Barbiturates: may be given as continuous infusion to
b. Diazepam (Valium) and Lorazepam (Ativan) intravenously at
induce coma and decrease metabolic demands of
c. 50% Dextrose IV
injured brain
d. Phenytoin (Dilantin) IV-increase seizure threshold
• Vasoactive medicine may be given to maintain blood
e. Pentobarbital-lessen nervous irritation
pressure to cerebral perfusion
Surgery-include removal of brain tumors, burr holes, insertion
of drainage catheter or shunt to drain excessive CSF
ICP monitoring
• Continuous intracranial pressure monitor is used for
continual assessment of ICP and to monitor effects
of medical therapy and nursing interventions
• Risk of infection exists with invasive procedure
Nursing Diagnosis
1. Ineffective Tissue perfusion
2. Risk for infection: open head wounds and intracranial
monitor device requires meticulous aseptic technique
3. Anxiety (family)
Client with Seizure Disorder
Seizures-alteration in consciousness, sensory and motor
• Paroxysmal motor, sensory, or cognitive
manifestations of spontaneous abnormal discharges
from neurons in cerebral cortex
• May involve all or part of brain consciousness,
autonomic function, motor function and sensation
Epilepsy: any disorder characterized by recurrent seizures
Categorization of seizures:
Partial seizures: activation of part of one cerebral
hemisphere
a. Simple partial seizure: no altered consciousness,
recurrent muscle contraction; motor portion of
cortex affected
b. Complex partial seizure: impaired consciousness;
may engage in automatisms (repetitive
nonpurposeful activity such as lip smacking,
preceded by aura, originates in the temporal lobe)
Generalized seizures:
 Involves both brain hemispheres;
consciousness always impaired
 Absence seizures (petit mal): characterized
by sudden brief cessation of all motor
activity, blank stare and unresponsiveness
often with eyes fluttering
Tonic-clonic seizures
 Preceded by aura, sudden loss of
consciousness
 Tonic phase: rigid muscles, incontinence (as
muscle contracts, bladder relax)
 Clonic phase: altered contraction,
relaxation, eyes roll back, froths at mouth
 Post-ictal phase: unconscious and
unresponsive to stimuli
State Epilepticus
1. Continuous seizure activity, generally tonic-clonic type
2. Client at risk to develop hypoxia, acidosis,
hypoglycemia, hyperthermia, exhaustion
3. Life threatening medical emergency requiring
immediate treatment:
Medications:
a. Manage but do not cure seizures
b. Raise seizure threshold
c. Carbamezepine
d. Phentoin
e. Valproic acid
Key Interventions:
1. Proper client from injury and maintaining airway
2. Do not force anything into the client’s mouth
3. Loosen clothing around neck
Nursing Diagnosis:
1. Risk for Ineffective airway clearance
2. Anxiety
Interventions:
1. Assess for signs and symptoms of seizure activity such
as report of aura or twitching of muscle groups
2. Have an oral airway oxygen and suction readily
available
3. Stay with client to protect him from injury and observe
seizure activity. If he is in bed, remove pillows, raise
side rails, put bed on flat position. Loosen any
restrictive clothing
4. After seizure, assess respiration and pulse. If they
present and he is unresponsive turn him onto his
side to keep his airway patent
5. Cover him with a blanket for warmth and privacy
6. Observe and document characteristics of the seizure
Client with Headache
1. May be due to benign or pathological condition
Pathophysiology: multiple pain sensitive structures within
cranial vault, face, and scalp are stimulated and cause
pain perception
Types:
Tension-characterized by sensation of tightness around
head and may have specific localized painful areas; areas
 caused by sustained contraction of muscles and head and
neck; precipitated by stress and anxiety
Migraine (more common in women)
- recurring vascular headache often initiated
by triggering event and accompanied by
neurologic dysfunction; or increase release
of sensory substances (e.g. serotonin);
triggers include stress, fluctuating glucose
levels, fatigue, hormones, bright lights
Cluster (common in men)
- typically awakens client with unilateral pain
around eye accompanied by rhinorrhea,
lacrimation, flushing; attacks occur in
clusters of 1-8 days for weeks
HEADACHE
2. Acetaminophen-tension headache; works in CNS to
reduce pain without effect on prostaglandin (safe for
gastritis)
3. Triptans-anti-migraine; activates serotonin receptors
decreasing inflammation of blood vessels
4. Botox (purified botulinum bacteria)
- small dosages allow it to be localized;
paralyses muscles locally and is not
absorbed into the blood stream (may cause
nerve paralysis if given in large doses)
5. Indomethacin-for cluster headaches; with pain killers
Nonpharmacological:
1. Biofeedback
2. Acupuncture
3. Massage
4. Yoga
5. Herbal remedies

1. Tension headache-90% ; noise, stress—sustained

contraction of muscles HEAD INJURY
2. Sinus Headache  Laceration
Virus, allergen, bacteria, temp  Hematoma
 Contussion
Nerves in sinuses swell  Bleeding

Headache Sources:
Scalp injury
e.g. brain freeze due to swallowing of cold substances Skull fracture
rapidly Brain injury
Risk factors:
3. Hang-over headache a. Motor vehicle accidents
Alcohol blocks hormonal mechanisms b. Elevated blood alcohol levels
c. Greatest risk: male aged 15-30 and those over 75
Dehydration
Mechanism of trauma:
4. Wine headache 1. Acceleration injury: head struck by moving
Increases histamine/tyramine object
2. Deceleration injury: head hits stationary
Dilate blood vessels object
3. Acceleration-deceleration (coup-
Pressure on nerves countercoup phenomena) head hits objects
and brain rebounds within skull
5. Migraine headache: 1:4 household
 Women 3x more than men: 3days a week Diffuse axonal injury-most severe form of brain injury also
 May be caused by: called shearing injury
Light
Noise Types of brain Injury:
Irregular eating and sleep a. Open head injuries (dura)
Chocolate b. Closed head injuries –blunt trauma
Strong smell c. Concussions –caused by sudden blow to the head or
Peanut butter rapid acceleration-deceleration
 results in retrograde amnesia and loss of
Electrical impulse altered and triggers trigeminal consciousness for 5 minutes
nerve  No break in skull or dura
 May have headache, nausea or vomiting
Trigeminal nerve=vasodilation and nerve d. Contusions-cause more damage, damage to brain itself
irritation involve cortical bruising and laceration of vessels and
brain tissues
6. Cluster Headache
 Excruciating pain Complications of Brain Injury
 6 x more in men, 30 min to 2 hours A. Post concussion syndrome:
Manifestations:
Nerves irritated  Headache, dizziness
 Nervousness, irritability
Pain signals  Changes in intelligence, poor concentrating,
poor memory
Tension Headache
 Fatigability
 Insomia
Management:
Pharmacological
1. Aspirin, Ibuprofen-suppress prostaglandin that dilates
Traumatic Brain Injury
and sensitize nerve fibers
 Epidural
Subdural
Intracerebral
B. Hematoma Formation:
1. Subdural hematoma (slower progression)-veins,
poor prognosis due to late diagnosis; occurs within
24-48 hours of injury in acute, 2-14 days in
subacute; can occur up to several months in chronic
Manifestations:
Acute
• Progressive and marked depression of
consciousness
• Headache, drowsiness, agitation and
confusion
• Pupillary and motor changes
Chronic
• Increasing severe headache
• Slow cerebration and drowsiness
• Papilledema and ipsilateral pupil dilatation
Systemic-Bilateral
2. Epidural (extradural) Hematoma
• Immediate loss of consciousness, lucid
interval lasting for few minutes or hours;
lapse into unconsciousness
• Severe, headache, seizures, vomiting,
hemiparesis, fixed, dilated ipsilateral
pupils
3. Intracerebral Hematoma
• Contained well-defined blood clot; usually at
frontal and temporal lobes
Management: Craniotomy
a. Keep nasopharynx and external ear clean
b. No blowing nose, coughing or hard sneezing
c. Prophylactic antibiotic
Nursing Management for head injuries:
Immediately following surgery:
• Immobilize head and neck until cervical injury is ruled
out
• Avoid flexion: hyperextension and rotation of the neck
• Jaw thrust maneuver
- Patent airway and support ventilatory function
- Document baseline neurological assessment
After initial stabilization:
• Monitor neurological status every hour until stable
- LOC, responsiveness
- Pupillary size, position, direct and consensual
response
- Assess extraocular movements
- Note verbal and motor changes
• Monitor for complications
- Hematoma formation
- Infection
- Acute hydrocephalus
- ARDS
• Monitor temperature and maintain normothermia
(decrease metabolism)
• Report high urine output (over 200 ml/hr for 2
consecutive hours)
• Monitor osmolality and serum electrolytes
• CBC
• ROM exercises
• Eye/ear care
• Nutrition-NGT (high glucose-brain functioning; protein-
tissue repair)
• Elimination-laxatives, increase fiber

Craniotomy-surgical opening of the skull

C. Cerebral edema and Increasesd ICP Craniectomy –permanent removal of the cranium to relieve
pressure on the brain by providing space for expansion
Skull fracture Nursing management
• break in continuity of skull usually resulting in Preoperative
brain trauma • Parenteral corticosteroids
a. Linear: dura remains intact; subdural or epidural • Scalp preparation
hematoma may occur underneath • Antiembolism stockings
b. Comminuted and depressed skull fractures:
increase risk for direct injury to brain tissue Postoperative
from contusion (bruise) and bone fragment: risk 1. Neurological assessment
for infection 2. Head dressings:monitor for CSF leaks
c. Basilar: involves base of skull (softer) and 3. Control ICP
usually involves extension of adjacent fractures • Assess for signs of increasing ICP
• Positioning to prevent increase in ICP
 Supratentorial surgery-elevate
Assessment:
head of bed 30 degrees
• Rhinorrhea: through nose
 Infratentorial-keep flat, turn
• Otorrhea: through every 2 hours, but never onto
• May appear on x-ray the back (to prevent brain
• Hemotympanum: blood behind hernation)
tympanic membrane (purple or dark  Posterior fossa surgery-either
color) side but never on the back
Normal: pearly gray
 Bone flap-on the unoperated side
• Battle’s sign: blood over mastoid
process
• Raccoon eyes: bilateral periorbital STROKE
ecchymosis Stroke is a brain attack
• Glucose reagent strip: If positive • …needing emergency management, including
indicates CSF specific treatment and secondary and
tertiary prevention
Interventions: Stroke is an emergency
…where virtually no allowances for worsening are tolerated
 Stroke is treatable • Aphasia
• …optimally, through proven, affordable, - sensory/receptive-Wernick’s aphasia
culturally-acceptable and ethical means - motor/expressive-Broca’s aphasia (able to
Stroke is preventable understand the stimuli but cannot express
…in implementable ways across all levels of society • Global aphasia
- Agnosia
- Dysarthria
Basic Location of Cerebral Aneurysm - Incontinence
- Horner’s syndrome-decrease lacrimation
Cerebral embolus-moving - Unilateral neglect
Cerebral thrombus
Cerebral hemorrhage Emotional or Behavioral Reactions:
• Severe mood swings
Types of strokes • Social withdrawal
• Inappropriate sexual behavior
Ischemic stroke-little blood flow • Outbursts of frustration and/or anger
1. Thrombotic formation of a blood clot with
• Regression to an earlier behavior
coagulation the results in the narrowing of the
lumen of a blood vessel with eventual occlusion
Right brain damage Left brain damage
2. Embolic –occlusion of a cerebral artery by an
embolus, resulting in necrosis and edema of • Paralyzed left side • Paralyzed right side
the area supplied by the involved vessel • Spatial-perceptual • Impaired
deficits speech/language
Hemorrhagic stroke-disrupted blood flow • Tend to deny or • Impaired right and left
1. Intracerebral hemorrhage stroke-bleeding within the minimize problems discrimination
brain caused by a rupture of vessels • Impaired judgment • Aware of deficits,
2. Subarachnoid hemorrhagic stroke-cause by aneurysm or AV • Impaired time depression, anxiety
malformation concepts • Impaired
• Short term span comprehension
Development of CVA • Slow performance,
1. Transient Ischemic attack-brief episodes of neurologic cautious
manifestations which clear completely in less than 24
hours
2. Reversible ischemic neurologic deficit-neurologic
Middle cerebral artery Involvement
deficits remain after 24 hours but leaves no residual
signs and symptoms after days to weeks • Contralateral paralysis
• Contralateral anesthesia, loss of proprioception,
3. Stroke in-evolution-progressing stroke which
fine touch, localization
develops over a period of hours or days;
• Aphasia
manifestations don’t resolve and leave residual
neurologic effects • Neglect of opposite side
4. Completed stroke- when neurologic deficits remain • Homonymous hemianopia-loss of vision for one
unchanged over 2-3 day period half of the visual field

Risk Factors Diagnostic procedures

• Prior ischemic episodes CT scan-determine if vascular or nonvascular lesions
• Cardiac disease Angiography
• DM MRI
• Atherosclerotic diseasae Laboratory (CBC, PT, PTT)-not definitive to conform diagnosis
• Hypertension, hypercholesterolemia
• Polycythemia Medical management
• Smoking
Decreased ICP
• Oral contraceptives
• Emotional stress BP management
• Obesity Fluid volume management
• Family history of stroke Tissue plasminogen activator-must be given within 3 hours of
• Age onset of manifestations and will dissolve clot; recombinant
altephase (Activase rt-pa)
Warning signs that may precede CVA Antithrombotic (aspirin, clipyridamole)-prevent platelet
• Paresthesia aggregation
• Transient loss of speech Anticoagulant (heparin, clexane)
• Hemiplegia Steroids or osmotic, diuretics
• Severe occipital or nuchal headaches Antihypertensive and diuretics
• Vertigo or syncope
• Motor or sensory disturbances (tingling transient Nursing management
paralysis) Hourly neurological assessment
• Epistaxis Monitor and prevent intracranial hypertension

SPECIFIC DEFICITS • Positioning

- bed rest: keep mainly on unaffected side
Dependent upon area damaged - use of pillows to support to prevent flexion
• Hemiplegia deformity, thrombus formation
 - external hip rotation • Muscle atrophy
- assist in progressive activity (mobility) • Poikilothermia-abnormality in sensing change in
- Progressive self-care (ADL) temperature

• Prevention of injury
- eyes-normal saline, artificial tears, eye
patch
- side rails up
MUSCLE FUNCTION AFTER SPINAL CORD
- decubitus ulcer prevention/management INJURY (((log-rolling)
- Oral mucosa care Spinal Cord Injury Muscle Functioning Muscle Function
• Nutrition/prevention of aspiration remaining Loss
- Communication Cervical, above C4 None All including
- Others: respiration
 Reorientation C5 Neck, scapular Arm, chest, all
 Minimize environmental stimuli elevation below chest
 Emotional support C6-C7 Neck, some chest Some arm,
 Rehabilitative movement, some fingers, some
• Discharge care arm movement chest movement
- Ways to prevent recurrence all below chest
 dietary modification Thoracic Neck, arms (full), Trunk, all below
 Stress reduction some chest chest
 Smoking cessation Lumbo-sacral Neck, arms, chest, Legs
 Exercise program turnk
 Drug compliance
- Residual deficits and balancing realistic
expectation Laminectomy
- Special methods of feeding Autonomic dysreflexia (after spinal shock resolves)
- Ensure continuity of care and emotional  Exaggerated autonomic response to stimuli:
support such as distended bladder or bowel (e.g. pain)

• Severe hypertension
SPINAL CORD INJURY • Headache

Manifestations: • Flushed skin

Subjective
• Loss of sensation below level of injury • Diaphoresis
• Inability to move
Objectivity • Nasal Congestion

A. Early symptoms of spinal shock Management

• Absence of reflexes below level of lesion 1. Place in high-Fowler’s position
• Flaccid paralysis below level of injury
2. Ensure patency of urinary drainage and assess
• Hypotonia results in bowel and bladder distention for infection.
• Inability to perspire in affected parts
• Hypotension 3. Eliminate other potential stimuli

B. Later symptoms of spinal cord injury 4. Notify physician: administer prescribed

• Reflex hyperexcitability antihypertensive
• State of diminished reflex hyperexcitability
below site in all instances of cord damage following
hyperreflexia Nursing Diagnosis
• In total cord damage-loss of motor and sensory 1. Impaired gas exchange related to muscle fatigue
function is permanent and retained secretions.
• Sacral region-atonic bladder and bowel with
impairment of sphincter control 2. Decreased cardiac output r/t venous pooling and
• Lumbar region- spastic bladder and loss of immobility
bladder and anal sphincter control
• Thoracic-trunk below the diaphragm 3. Impaired skin integrity r/t immobility and poor
tissue perfusion
• Cervical-from neck down, if above C4
respirations and depressed
4. Constipation r/t the injury, inadequate fluid
• In partial cord damage, depends on the type of intake, diet low in roughage and immobility
neurons affected (spastic vs. flaccid)
5. Urinary retention
Clinical manifestations:
• Paralysis of muscles of respiration 6. Impaired physical mobility
• Bradycardia
• Hypotension 7. Risk for autonomic dysreflexia r/t reflex
• Urinary retention stimulation of SNS
• Hypomotility
 8. Altered nutrition less than body requirements r/t
increased metabolic demand
9. Sexual dysfunction r/t inability to achieve
erection or perceive pelvic sensations
Medical Management
 Immoblization—Gardner –well tongs, halo
external fixation
 Maintenance of heart rate (Atropine) and BP
(dopamine) vasopressors
 Methylprednisolone therapy
 Insertion of NGT
 Intubation, if needed
 Indwelling urinary catheter
 Stress ulcer prophylaxis (Proton-pump
inhibitos, H2 blockers)
 Physical therapy
Parkinson’s Disease
(fourth common
neurodegenerative disease)
• Degeneration of dopamine-providing cells in the
substantia nigra, which leads to degeneration of
neurons in the basal ganglia; usually develops after
60 age
• Associated with decreased levels of dopamine due to
destruction of pigmented neuronal cells in the
substantia nigra in the basal ganglia of the brain
(Smelzer & Bare, 2004, p. 1979)
• Imbalance between dopamine and acetylcholine
Three cardinal features:
1. Tremors at rest
• e.g. rhythmic, slow turning motion
(pronation-supination) of the forearm and
the hand and a motion of the thumb against
the fingers as if rolling a pill
• tremor is present while at rest, increases
when the patient is walking, concentrating,
feeling anxious (Smeltzer & Bare, 2004, p.
1980).
2. Rigidity-resistance to passive limb movement
3. Bradykinesia-most common features; patients
take longer to complete most activities and
have difficulty initiating movement
Clinical Manifestations:
• Generalized feelings of stiffness
• Mild, diffuse muscular pain
• Hand tremor at rest (pill rolling)
• Akinesia
• Gait changes –shuffling gait
• Characteristic stance-stooped posture
• Masklike-facial expression
• Speech pattern-slow, low volume monotonous in
tone with poor articulation
• Involuntary drooling
• Decreased lacrimation; constipation,
incontinence
• Heat intolerance; excessive perspiration
• Lack of spontaneous swallowing
Medical Management
• Levodopa-Carbidopa T-synthetic precursor of
dopamine for basal ganglia (Sinemet)
• Anticholinergic-to control symptoms (Cogentin,
Artane, Symmetrel); anticholinergics drugs act
at central sites to inhibit cerebral motor
impulses that cause rigidity of themusculature
• MAOI-Bomcriptine; inhibit breakdown of
dopamine
• Physiotherapy-reduces rigidity of muscles and
prevents contractures
• Surgical intervention-to destroy globus pallidus
(to relieve rigidity) and/or thalamus (relieve
tremors)
Nursing Management
• Provide safe environment
• Nutrition
 Small bite pieces of food to prevent
choking
 Small frequent meals for easy
mastication
 Adequate intake of roughage to prevent
constipation
 Encourage diet rich in nutrient-dense
foods such as fruits, vegetables, whole
grains
• Positioning and activity
 Limit postural activities
 Maintain gait as normal as possible:
may utilize cane or wheel chair
  Encourage daily physical therapy to
limit rigidity and prevent contractions
 Medication compliance; report side
effects
• Avoid rushing client as he is unable to work
under pressure
• Assist client in setting achievable goals to
improve self-esteem
• Total body function support in advanced stages
(respiratory elimination)
Myasthenia Gravis
• Disturbance in the transmission of impulses at the
myoneural junction resulting in profound weakness
(muscle of the eyes, eyelid, chewing, swallowing,
speaking and breathing)
• Believed to be due to reduced acetylcholine
receptors due to destruction and blockage attributed
to autoimmune process
• An autoimmune disorder, characterized by varying
degrees of weakness of the voluntary muscles
(Smeltzer & Bare, 2004, p. 1956)
• Highest in young adult females.
Manifestations
Subjective:
 Extreme muscle weakness, worsens as the
muscle is used but disappears with rest
 Dysphagia
 Diplopia (double vision)
 Dysarthria
Objective:
 Ptosis of the eyelid (both eyes)
 Myasthenia smile (nasal smile)
 Strabismus
Note:
Myasthenia gravis is purely a motor disorder with NO
effect on sensation or coordination (Smeltzer & Bare, 2004, p.
1956)
Diagnostic Test
 Neostigmine (Prostigmine)—subcutaneous or IV
administration of tensilon (prevents enzymatic
breakdown of Ach) to provided relief of symptoms
 The thymus gland, which is a site of acetylcholine
receptor antibody production is enlarged in
myasthenia gravis (Smeltzer & Bare, 2004)
Medical Management
 Pharmacologic
- Acetylcholinesterase blockers
- Corticosteroids to suppress immunity
 Plasmapheresis -
 X-ray or surgical removal of thymus (thymectomy)
Myasthenic Crisis
• Sudden inability to swallow or maintain respirations
due to weakness of the muscles of respiration;
undermedication
• Exacerbation of the disease process characterized by
severe generalized muscle weakness and respiratory
and bulbar weakness that may result in respiratory
failure (Smeltzer & Bare, 2004, p.1957)
Cholinergic Crisis
• Overdose of anticholinergic drugs
• May mimic the symptoms of exacerbation
Note:
Differentiation of myasthenic crisis and cholinergic
crisis can be achieved with the edrophonium chloride
(Tensilon) Test. The patient with myasthenic crisis
improves immediately following administration, while
patient with cholinergic crisis may experience no
improvement or deteriorate (Smeltzer & Bare, 2004)
Guillain-Barre Syndrome
• Immunologic status often follows respiratory or GIT
infection, viral immunization, trauma or surgery
• An autoimmune attack of the peripheral nerve
myelin (Smeltzer & Bare, 2004).
• Areas of demyelination in the motor cells of the
spinal cord and medulla (ascending loss) vs. ALS
(descending)
• Seen in adults 20-50 years
• After initial and plateau periods recovery in 1 year
sometimes with residual deficits, other dies of
complications
ALS- common in males
Manifestations
- begins with muscle weakness and
diminished reflexes of the lower
extremities
Subjective:
 Generalized weakness
 Paresthesia
  Diplopia • Inflammation of pia matter, arachnoid and
subarachnoid space
Objective
 Ascending paralysis within the • Spreads rapidly through CNS because of circulation
body usually 24-72 hours of CSF around brain and spinal cord

 Respiratory paralysis • May be bacterial, viral, fungal, parasitic in origin

 Hypertension, tachycardia and low • Infection enters CNS though invasive procedure or
grade fever through bloodstream, secondary to another infection
in body
 Incontinence

Bacterial Meningitis
Medical Management
1. Steroids • Causative organism: Neisseria meningitides,
Streptococcus pneumonia, Haemophilus influenza,
2. Plasmapheresis Escherichia coli

3. Support of vital function • Manifestations

a. Fever, chills
Nursing Management: Supportive care
1. Respiratory management b. Headache, back and abdominal pain

2. Nutritional management c. Nausea and vomiting

3. Prevent complications d. Meningeal irritation:

4. Emotional support  Nuchal rigidity (stiff neck)-early sign

 Positive Kernig’s sign

Client with Multiple  Positive Brudzinski’s sign-when the patient’s

neck is flexed, flexion of the knees and hips
Sclerosis is produced
1. Believed to be autoimmune response to prior viral
 Photophobia –extreme sensitivity to light
infection
e. Meningococcal meningitis: rapidly spreading
2. Inflammation destroys myelin leading to axon petechial rash of skin and mucous membrane
dysfunction; neurons in spinal cord, brain stem,
cerebrum, cerebellum and optic nerve affected f. Increased ICP: decreased LOC, papilledema –
edema of optic disc due to increased ICP
3. Stressors trigger multiple sclerosis—febrile states,
pregnancy, physical exertion and fatigue and these
can trigger relapses
Viral Meningitis
• Less severe, benign course with short duration,
4. Incidence is highest in young adults (20-40); onset
intense headache with malaise, nausea, vomiting,
between 20-50; females more than males
lethargy, signs of meningeal irritation

Manifestations Encephalitis
1. Fatigue 1. Acute inflammation of parenchyma of brain or spinal
cord
2. Optic nerve involvement: blurred vision, haziness
2. Usually caused by virus

3. Brain stem involvement: nystagmus, dysarthria

(scanning speech); cognitive dysfunction, vertigo, Medications
deafness 1. Meningitis: immediate treatment of effective
antibodies for 7-21 days according to culture
4. Weakness, numbness in legs, spastic paresis, results; dexamethasone to suppress inflammation
bladder and bowel dysfunction
Dilantin—Increase seizure threshold
5. Cerebellar involvement: nystagmus , ataxia,
hypotonia Health Promotion
1. Vaccinations for meningococcal, pneumococcal,
6. Blindness haemophilus meningitis

2. Prophylactic rifampins for persons exposed to

Meningitis meningococcal meningitis

 3. Mosquito control

4. Prompt diagnosis Fractures

- Break in the continuity of bone
5. Asepsis care for clients with open head injury or
neurosurgery Classification:
 Closed-no break in the skin

Hydrocephalus  Open-

• Increase in volume of CSF within ventricular system,  Complete-involves break across

which becomes dilated the entire cross-section of the bone and is
frequently displaced
Common Cause:
1. Noncommunicating obstruction in CSF drainage from  Incomplete e.g. greenstick, the
ventricular system break occurs through only part of the cross-
section of the bone
2. Communicating: CSF is not effectively reabsorbed
through arachnoid villi  Displaced

3. Normal pressure hydrocephalus: occurs in  Comminuted-several bone

persons>60 in which ventricles enlarge causing fragments
cerebral tissue compression
 Impacted or compression
4. Manifestations depend on rate of onset: progressive
cognitive dysfunction, gait disruptions, urinary  Complicated-accompanied by
incontinence infection

• Visual changes  Pathologic-systemic, loss of bone

density
• Increase in head size

• Increase ICP Clinical Manifestations

• Deformity

Treatment/Management • Swelling
1. Diuretics
• Bruising
2. Surgery
• Muscle spasm
3. Protect from injury from altered LOC and immobility
• Tenderness

• Pain
Skeletal muscle • Impaired sensation
• Attach to the skeleton
• Loss of normal function
• Permits voluntary movements
• Crepitus- grating sensation resulting from
rubbing of bone fragments against each other
• Maintain posture

• Generates heat • Abnormal mobility of affected part

• Innervated by the somatic nervous system • Hypovolemic shock

• Produce movement by contraction

Vasogenic shock-due to severe pain
• Sarcomeres-functional unit of striated muscle

Basic Principles of skeletal muscle action Surgical/Medical Management

1. Motor unit should be stimulated to contract, absence
of impulse conduction leads to paralysis
2. Muscles are attached to at least 2 bones; with each
contraction, muscle’s insertion bone moves and the
muscle origin bone remains stationary
 Open-reduction-alignment during surgery
 Internal fixation device placement: use of
screws, wires, nails or rods
 Closed reduction

3. Bone serve as levers; joint as fulcrums  Traction application

  Management of shock - Watch for: wet-spots-drainage: hot
spots-tissue infection or necrosis under
casts

Nursing Management for Fractures - Elevated injured extremity

especially for the first 24-48 hours
1. Assess neurovascular status (6 P’s)
- Prevents disuse syndrome

ulselessness • Exercise joints before and after

allor injured site
ain
aresthesia • Isometric exercises, gluteal setting,
oikilothermia abdominal tightening and deep
aresia/paralysis breathing exercises

2. Assess skin • Skin care

3. Assess for fat embolism-long bone fracture, may • Elimination

occur 24-48 hours after injury
• Nutrition- Vit C (absorption of
4. Analgesics-Opioid analgesics calcium)

5. Rehabilitation

Cast Application Cast care

 Keep cast dry; use plastic when bathing
Purposes:
 Do not use powder or insert objects inside cast
1. Immobilization
 Use of slings/crutches to enhance comfort safety and
2. Prevention or correction of deformity
ambulation
3. Maintenance support and protection to realign bone
 Reportable conditions:
4. Promotion of healing which allows early weight
- Increased swelling
bearing
- Tingling or burning sensation
Nursing Management: CAST
- Inability to move muscle around cast
Precast application
- Care- factual and sensory - Foul odor inside or around the edge
information

- Contraindications Therapeutic Traction

- Pulling force
Intracasting
Postcasting
- Drying 24-48 hours
Types:
1. Skin
- Proper handling
2. Skeletal
- Watch for neurovascular
complications
3. Cervical
- Watch for infection
4. Pelvic
- Watch for cast syndrome (occurs
5. Buck’s traction (unilateral or bilateral) is
with body casts)
skin traction to the lower leg
 Prolonged nausea and vomiting
6. Russel’s – one leg is higher than the other
 Abdominal distention and pain
Techniques:
1. Running (Straight) applies the pulling force
Cast syndrome-psychological (claustrophobic in a straight line with body part resting on bed
reaction) and physiologic (superior mesenteric artery
syndrome) responses to confinement in body cast
2. Suspension (Balanced)-supports the
(Smeltzer & Bare, 2004)
affected extremity off the bed and allows for some
patient movement without disruption of the line of
pull
 3. Continuous intermittent 2. Ensure strength of upper extremity opposite lower

Care of Client
1. Know the purpose and contraindicated movements

2. Pin site care-goal is avoid infection and development

of osteomyelitis; site is covered with a sterile
dressing (Smeltzer & Bare, 2004, p. 2028)

3. Ropes and pulley should hang free

4. Monitor color, warmth, movement and sensation of

extremity distal to the traction every 4-8 hours
( neurovascular check)

5. Devices such as trapeze, fracture pins

6. Immobility problems (thrombophlebitis, diversional extremity

therapies , among others)
3. Ensure proper length of cane

After traction:  Highest point approximately at

 Gradually assume sitting position level of greater trochanter

 Lack of proprioception response initially  30 degrees flexion of elbow

 Joints may be unstable; may feel faint or weak for  Tip of the cane 15 cm (6 inches)
a while lateral to the base of the fifth toe (Smeltzer
& Bare, 2004, p. 174)

Principles of Effective Traction 4. Ensure proper techniques

 Traction must be continuous to be effective in
reducing and immobilizing fractures  Opposite affected extremity

 Affected extremity cane simultaneously

 Skeletal traction is never interrupted
 Should be close to the body
 Weights are not removed unless intermittent traction
is prescribed
5. Observe for incorrect use
 Any factor that might reduce the effective pull or
 Leaning the body over the cane
alter its resultant line of pull must be eliminated:
 Shortening the stride of the unaffected side
- Patient must be in good body alignment in
the center of the bed when traction is applied
 Persistence of abnormal gait
- Ropes must be unobstructed

- Weights must hang free and not rest on the Crutch

bed or floor Nursing care
1. Ensure readiness of client
- Knots in the rope or the footplate must not
touch the pulley or the foot of the bed
 Strength of upper torso
- (Smeltzer & Bare, 2004, p. 2026)
 Psychological fitness

2. Ensure proper fit

Nursing Care of Clients with Braces or
Splints  Axillary bars 5 cm (2 inches below axilla),
1. Check body and equipment alignment 15 cm (6 inches infront and lateral) tripod
position
2. Keep equipment in good condition
3. Assist in use of proper technique
3. Examine integumentary integrity
 Four point- R crutch, L foot, LC, RF

 Two-point-R crutch with L foot, then LC with

RF

Use of Cane  Three point-advance both crutches and

1. Ascertain client capability to bear weight weak extremity, then follow good foot
  Swing to gait-advance crutches then swing
feet to the level of the crutches
Manifestations:
 Swing through gait-advance crutches then  Joint stiffness
swing through the crutches
 Pain after exercise; pain with movement
4. Incorrect position
 Heberden’s (distal) and Bouchard’s (proximal)
 Walking on ball of foot nodes

 Hunching shoulders  Decreased ROM

 Looking downward  Crepitus

 Hiking hips (common in amputees) Medical Management

 Steroids
 Bearing weight under arms may cause
brachial plexus damage  Antiinflammatory

 Lifting crutches while still bearing down on  Analgesics-salicylates and NSAIDs

them
 Physiotherapy/Exercise
5. Evaluate client’s response
 Surgery-replacement of mobility (knee and hips
common)

Arthritis Rheumatoid Arthritis

 Disease involving degeneration and or
inflammation of joints and surrounding
structures
 Out of 100 types of with unknown cause
 Systemic with synovial membrane inflammation
with blood, fibrin, and coagulation deposits
 Unknown cause: hereditary, autoimmune
psychophysiologic factors, 25-55 years old

 Common types:  Exacerbations linked to physical and emotional

stress
1. Inflammatory –RA and SLE
 Inflammatory changes in the connective tissue
2. Non-inflammatory –degenerative joint
disease
Pathophysiology:
3. Gout-crystal-produce disease from high Symmetrical joints
protein ingestion
Synovial lining of joints become inflamed

Synovitis
Osteoarthritis
 Autosomal recessive trait causing cartilages to Increased fluid with pannus
wear out or repair less effective; localized; NO
synovial membrane swelling Pannus destroys cartilage and invade joint capsule

o Wear and tear of joints Replaced by fibrous connective tissues

Affects tendons and ligaments

o Obesity; joint trauma
Cause joint subluxation, bony ankylosis and
o Aging: 55 years old and above
consolidation of joints
o Degeneration and atrophy of the Swelling, deformities
cartilage and calcification of ligaments
Pain
o Primarily affects weight-bearing joints, Manifestations:
spine and hands Subjective
 Fatigue, malaise, anorexia
 Degeneration of cartilages into the bony spur
 Joint pain, stiffness after periods of
 Formation of subchondral osteophyte inactivity especially a.m

 Secondary synovitis (late manifestation)-pain  Paresthesia (destruction of nerve

and swelling with joint movement involved)

Objective
  Joint inflammation and deformity
 Swan neck and Boutinniere
deformities; ulnar drift, joint
subluxation
 Increased ESR, low grade fever ,
positive rheumatoid factor
 Anemia, weight loss
urate crystals, called tophi, are deposited in peripheral
areas of the body, such as great toe, the hands, and the
ear (Smeltzer & Bare, 2004, p. 1630).
Manifestations:
- Tight/reddened skin around inflamed joint,
edema
- Pain
- Increase temperature

Medical Management - Hyperuricemia> 7.5 mg/dl

 Coticosteroids, anti-inflammatory,
analgesics, immune suppressive drugs Management of Gout
1. Decrease protein in diet
 Plasmapheresis
2. Weight control and decrease alcohol ingestion
 Antimalarial drugs—destroys
autoimmune antibodies 3. Increase fluids to 3000 ml/day (the more
dehydration, more crystallization)
 Cytotoxic drugs
4. Joint rest
Note:
Deformities of the hands and feet are common in RA. 5. Allupurinol/Probenecid, Colechicine
The deformity may be caused by misalignment resulting
from swelling, progressive joint destruction, or the
subluxation (partial dislocation) that occurs when bone High Purine foods
slips over another and eliminates the joint space 1. Poultry
(Smeltzer & Bare, 2004, p. 1621)
2. Organ meats
Gouty Arthritis 3. Meat extracts
 Mono-articular (one joint)
4. Seafoods, sardines, anchovies, shrimp herring
 Hyperuricemia; 40-50 years old
5. Asparagus, spinach, mushroom
1. Genetic increase in purine
metabolism and production
Surgical intervention
2. Ingestion of excessive alcohol or high
1. Arthrodesis-surgical fusion of a joint to render a joint
purine diet
immobile but decreases pain and increases strength

2. Osteotomy-transection of a bone to correct a

deformity or misalignment
Pathophysiology:
3. Resection-for partial removal of a degenerated bone
Uric acid-major by product of protein and nucleic acid
(wrist and foot)
metabolism
4. Replacement arthroplasty-joint replacement
Tendency to crystallize especially with dehydration, diuretics
use and increased
Assistive devices:
Tubular resorption to the systemic circulation
1. Eating utensils
Deposited in connective tissues and joints (esp. great toe)
2. Braces
Release of lysosomal enzymes
3. Walkers
Inflammation
4. Cane-single, quad
Joint degeneration and disability and tophaceous (white in
color) deposits in the joints
Therapies
May cause renal tubular damage leading to renal stones and 1. Diversion
failure
2. Exercise, ROM, quadriceps exercise

Note: 3. TENS
Attacks of gout appear to be related to sudden
increases or decreases of serum uric acid levels. When 4. Cold and warm pack 30 minutes before activities
the urate crystals precipitate within a joint, an
inflammatory response occurs and an attack of gout 5. Whirl pool bath
begins. With repeated attacks, accumulation of sodium
 6. Balance rest and activity

7. Assistive devices, elevated chair or toilet to 3-4

inches

Nursing Diagnosis
• Chronic pain related to joint degeneration

• Impaired physical activity r/t restricted

mobilization

• Activity intolerance

• Self-care deficit

• Body image disturbance r/t visible body

changes/deformities/misalignment

• Knowledge deficit

• Sleep pattern disturbance