perception and coordination

Perception and Coordination

Structure & Functions of cells in the nervous system

• Neurons are the basic anatomical and functional units in the nervous system; each neuron has 3 parts:

• Neurons (nerve cells)- the most important cells in the brain.

-They transmit chemical and electric signals that

determine thought, memory, emotion, speech, muscle

movement, sensation,

-Neurons send these signals through their nerve fibers (axons).

Parts of Neuron

1. The cell body

2. Axon-carries the stimulus away from the cell body

- Axon in the PNS are covered w/ an insulating lipid layer

called myelin sheath for rapid conduction of nerve impulses

- Each axon terminates at a synapse where neurotransmitters and other chemical substances are released

3. Dendrites- direct impulses toward the cell body

• Nerve cells are separated by a synaptic cleft; neurotransmitters are secreted into the cleft by one neuron to stimulate the dendrites of another neuron

• Conduction of a nerve impulse is initiated when a stimulus is sufficient to create an action potential (a summation of impulses from the dendrites) it is then sent down the axon by depolarization; in myelinated nerves the action potential hops from one node of Ranvier to the next for rapid conduction

• 2. Glial cells- supportive structure of the nervous

system that nourish, support and protect the

brain neurons

4 Main Types of the Glial Cells

1. Astrocytes- star-like cells that provide nutrition to neurons, regulate synaptic connectivity, remove cellular debris, and control movement of molecules in the blood-brain barrier

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

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

4. Microglia- small phagocytic cells scattered in the CNS that disintegrate and remove cellular debris and waste products

5. Oligodendrocytes- produce the myelin sheath w/in the CNS that insulates the neuron allowing for fast transmission of impulses

The CNS

• Consists of the brain and the spinal cord

The Brain

• Divisions of Brain (Main areas):

Cerebrum, Cerebellum and brain stem.

- responsible for planned (voluntary) muscle movements (throwing a ball, walking, chewing, etc.) and for taking in and interpreting sensory information such as vision, hearing, smell, touch, and pain.

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

The Cerebrum

• Has 2 hemispheres, each of which is divided into frontal lobe, temporal, parietal, occipital

• Right hemisphere- generally controls the left side of the body; the left controls the right side

• Frontal lobe performs high level cognitive function, has memory storage, influences somatic motor control, controls

voluntary eye movements and controls motor aspect of speech (Broca’s area)

• Temporal lobe-located behind the frontal and under the parietal lobe and has a primary auditory reeptive areas and the auditory association area (Wernicke’s area), w/c is usually found on the dominant side and is responsible for interpreting speech

-Interpretative area that integrates somatic, auditory and visual data (perception, learning, memory, emotions and intellectual abilities)

• Parietal lobe holds the primary sensory cortex and sensory association areas; processes visual-spatial information and controls spatial orientation

• Occipital lobe- the visual center for the eyes; controls both eye reflexes and interpretation of sight

• Meninges: These are layers of tissue that line and protect the brain and spinal cord. CSF travels through spaces formed by the meninges

• Choroid plexus: The choroid plexus is the area of the brain within the ventricles that makes CSF, which nourishes and protects the brain.

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

The Diencephalons & Hypophysis

• Located at the bottom of the cerebrum near the midbrain

• Includes: thalamus, pituitary gland and other related structures

• Controls the temperature, water metabolism, pituitary secretion, visceral and somatic activities, visible physical expressions in response to emotions, sleep-wake cycle and food-getting reflex

The Cerebellum

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

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

The brainstem

• Is an integration system that controls basic functions

• 3 major divisions of the brainstem: Midbrain, Pons, medulla

• Reticular activating system (RAS)-responsible for alertness

• Brain stem: The brain stem is the lower part of the brain that connects to the spinal cord.

- It contains bundles of very long nerve fibers that carry signals controlling muscles and sensation or feeling between the cerebrum and the rest the body.

-Special centers in the brain stem also help control breathing and the beating of the heart.

The spinal cord

• Is an elongated mass of nerve tissue

that runs most of the length of the vertebral column

Divisions:

• Cervical area –C1 to C7

• Thoracic area - T1 to T12

• Lumbar- L1 to L5

• Sacral area- S1 to S4

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

• Sensory tracts (dorsal roots) carry afferent impulses from the periphery to the dorsal root ganglia where the cell bodies of the sensory components are located and messages send to the brain.2 Types of Sensory Fibers

1. General somatic afferent fibers carry pain, temp, touch and proprioception from the body wall, tendon and joints

2. General visceral fibers carry sensory input from the organs of the body

• Motor tracts (ventral roots) convey efferent impulses from the spinal cord to the body

2 Types of Fibers

1. General somatic fibers-innervates voluntary striated muscles

2. General somatic visceral afferent fiber- innervate smooth and cardiac muscle and regulate glandular secretions

The peripheral nervous system

• Has 31 pairs of spinal nerves, 12 pairs of cranial nerves and the autonomic system that is divided into the sympathetic and parasympathetic nervous system

• Each pair of spinal nerves has dorsal and ganglion roots that exit the spinal cord by way of an intervertebral foramina that corresponds with the spinal level; these nerves carry input between specific areas called dermatomes and the spine

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

• Autonomic Nervous System- a collection of motor nerves that regulate activities of the viscera, smooth muscles, and glands to maintain a stable internal environment;

• 2 parts of the ANS: sympathetic and parasympathetic w/c work antagonistically.

a. The sympathetic nervous system (SNS) is active during times of stress, such as the fright, flight or fight response;

- it increases heart rate and blood pressure and vasoconstricts the peripheral blood vessels

b. The parasympathetic system is a conservation, restoration, and maintenance system;

- it decreases heart rate and increases gastrointestinal (GI) activity

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

Blood Supply

• The brain is unique in that it can only use glucose for its energy supply; a lack of glucose for 5 minutes results in irreversible brain damage

• the brain receives 750mL/min of blood or 15 to 20% of the resting cardiac output;

• blood flow rates for specific sites correspond directly with the rate of metabolism

• The cerebral arteries are thinner, have more internal elasticity and less smooth muscle than the arteries in the rest of the body

• the brain is supplied with blood by two sets of arteries that divide it into anterior and posterior circulation

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

• The first affected if there is hypoperfusion

• The posterior circulation from the vertebral arteries, delivers blood to the posterior fossa; at the bottom of the posterior fossa, blood flows together into one basilar artery and delivers it to the cerebellum, midbrain, pons, and medulla

• The meninges are supplied with blood from branches of the external carotid arteries that ascend into the brain at the base of the skull

• The venous system of the brain is unique

a. Vessel walls are thinner than other veins of the body

b. They do not follow the path of arteries but follow their own course

c. There are no valves in the brain’s venous system and therefore drainage depends on venous pressure and gravity

d. Dural sinuses collect blood from the brain and empty it into the jugular veins

THE BLOOD-BRAIN BARRIER• It refers to a network of endothelial cells in the

wall of the capillaries and astrocyte projections in close proximity that do not have pores between them

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

• The movement of substances across this barrier depends on particle size, lipid solubility, chemical dissociation and protein-binding potential

• The barrier is very permeable to water, oxygen, carbon dioxide, other gases, glucose and lipid soluble compounds

Protective structures

• Meninges: cover the brain and spinal cord to protect and support; it is divided into 3 layers from outer to inner (duramater, arachnoid, and pia mater)

a. dura - a tough membranous tissue that surrounds and extends into the brain tissue that provides important landmarks, such as the falx cerebri and the tentorium cerebelli, which is an important structure to note because nursing care differs based whether an injury is supratentorial (above the tentorium) or infratentorial (below the tentorium)

b. arachnoid membrane- lies below the dura and is a network of delicate, elastic tissue that contains blood vessels of varying sizes

c. pia mater- a vascular membrane that covers the entire brain with tiny vesssels that extend into the gray matter of the brain

d. Within the meninges, there are important potential spaces (epidural, subdural, subarachnoid) where bleeding can occur

• Skull- includes 8 fused cranial bones and 14 facial bones; the cranium encloses the brain in a protective vault;

• Foramen magnum is the large hole at the base of the skull through which the spinal cord runs

• Spine- a flexible column that encloses the spinal cord, formed from the stacking of 33 vertebrae

Cerebrospinal fluid andventricular system

a. CSF is a clear colorless, odorless solution that surrounds the brain and spinal cord;

-it acts as a shock absorber to cushion the brain from injuries caused by movement;

• Cerebrospinal fluid is made by the choroid plexus, which is located in spaces within the brain called ventricles.

• The ventricles and the spaces around the

brain and spinal cord are filled with CSF.

• CSF has electrolytes, glucose protein, oxygen and carbon dioxide

• Ventricular system - is composed of 2 lateral ventricles (one in each hemisphere of the cerebrum), a third ventricular that lies midline in the thalamic area, and a fourth ventricle that lies below the third, anterior to the cerebellum and the subarachnoid space

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

• Meninges: These are layers of tissue that line and protect the brain and spinal cord. CSF travels through spaces formed by the meninges

• Choroid plexus: The choroid plexus is the area of the brain within the ventricles that makes CSF, which nourishes and protects the brain.

• Pituitary gland and hypothalamus

Pituitary gland is a small gland at the base of the brain connected to the hypothalamus.

• They help regulate the activity of glands in the body.

• they control the amount of thyroid hormone made by the thyroid gland

• the production and release of milk by the breasts

• and the amount of male or female hormones made by the testicles or ovaries.

• Secretes growth hormone, which stimulates body growth

• Secretes vasopressin, which regulates water balance by the kidneys.

• Pineal gland-is not really part of the brain, it is a small endocrine gland that sits between the cerebral hemispheres.

• It makes melatonin, a hormone that regulates sleep, in response to changes in light

Nursing Process

• Assessment of the Nervous System

• Assess chief complaint

A- any associated symptoms w/ chief complaint

P- what provokes (makes worse) or palliates makes better) symptoms

Q- quality of pain

R- region and radiation

S- severity of pain on a scale of 1-10

T- timing (when did it stop and start, intermittent or constant, duration

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

Physical Assessment of the Neurologic System

Mental status

• Includes orientation to person, place, time, appearance and behavior, mood, speech pattern and thought and perception including insight, thought, content and judgment

• Considerations in conducting assessment: The client must be awake, alert and able to understand and respond to questions

• Assign: Research on Level of consciousness

Description of LOC

• Full consciousness- alert oriented to person,place, time, comprehend written & spoken words

• Confusion- disoriented to person, place, time; misterpretenvironment, has poor judgement; unable to think clearly

• Lethargic- oriented but slow & sluggish in speech, mental processes & motor activity

• Obtundation- readily arousable to stimuli; responds w/ one or 2 words; follows simple commands, but quickly drifts back to sleep

• Stupor- lies quietly w/ minimal movement; responds w/ a groan or eye opening only to vigorous and repeated verbal w/ tactile stimuli

Coma- unarousable to stimuli; nonverbal; may exhibit nonpurposeful response to stimuli

• Light coma- unarousable; withdraws nonpurposefully to pain; may decerebrate or decorticate; brainstem reflexes intact

• Deep coma- unarousable; unresponsive to painful stimuli; brainstem reflexes usually absent; decerebrate posturing usually noted.

• Delirium- rapid in onset; brief impairment of cognition including a clouding of consciousness and difficulty sustaining and shifting attention

• Dementia- a generalized. Long term decline in cognitive abilities such as memory, language, and clear consciousness

Cranial Nerve Assessment

Nurses Cranial Nerves Assessment Cranial

Nerve

Function Method Normal Findings

I Olfact

ory

Smell reception

and

interpretation

Ask client to

close eyes and

identify different

mild aromas

such alcohol,

powder and

vinegar.

Client should be

able to distinguish

different smells

II Optic Visual acuity

and fields

Ask client to

read newsprint

and determine

objects about 20

ft. away

Client should be

able to read

newsprint and

determine far

objects

III Oculomot

or

Extraocular eye

movements, lid

elevation,

papillary

constrictions

lens shape

Assess ocular

movements and

pupil reaction

Client should be able

to exhibit normal

EOM and normal

reaction of pupils to

light and

accommodation

IV Trochlear Downward and

inward eye

movement

Ask client to move

eyeballs obliquely


to move eyeballs

obliquely

V Trigeminal Sensation of face,

scalp, cornea, and oral

and nasal mucous

membranes. Chewing

movements of the jaw

Elicit blink reflex by lightly

touching lateral sclera; to

test sensation, wipe a wisp

of cotton over client’s

forehead for light

sensation and use

alternating blunt and sharp

ends of safety pin to test

deep sensation

Assess skin sensation as of

ophthalmic branch above

Ask client to clench teeth

VI Abducens Lateral eye

movement

Ask client to move

eyeball laterally


to move eyeballs

laterally

VII Facial Taste on

anterior 2/3 of

the tongue

Facial

movement, eye

closure, labial

speech

Ask client to do

different facial

expressions such as

smiling, frowning

and raising of

eyebrows; ask

client to identify

various tastes

placed on the tip

and sides of the

mouth: sugar, salt

and coffee


to do different facial

expressions such as

smiling, frowning and

raising of eyebrows;

able to identify

different tastes such

as sweet, salty and

bitter taste

VIII Acoustic Hearing and

balance

Assess client’s

ability to hear

loud and soft

spoken words;

do the watch

tick test

Client should be

able to hear loud

and soft spoken

words; able to

hear ticking of

watch on both

ears

IX Glossoph

aryngeal

Taste on

posterior 1/3 of

tongue,

pharyngeal gag

reflex,

sensation from

the eardrum

and ear canal.

Swallowing and

phonation

muscles of the

pharynx

Apply taste on

posterior tongue

for identification

(sugar, salt and

coffee); ask client

to move tongue

from side to side

and up and down;

ask client to

swallow and elicit

gag reflex through

sticking a clean

tongue depressor

into client’s mouth


to identify different

tastes such as sweet,

salty and bitter

taste; able to move

tongue from side to

side and up and

down; able to

swallow without

difficulty, with (+)

gag reflex

X Vagus Sensation

from

pharynx,

viscera,

carotid body

and carotid

sinus

Ask client to

swallow; assess

client’s speech

for hoarseness

Client should be

able to swallow

without

difficulty; has

absence of

hoarseness in

speech

XI Spinal

accessor

y

Trapezius and

sternocledom

astoid muscle

movement

Ask client to

shrug shoulders

and turn head

from side to

side against

resistance from

nurse’s hands

Client should be

able to shrug

shoulders and

turn head from

side to side

against resistance

from nurse’s

hands

XII Hypog

lossal

Tongue

movemen

t for

speech,

sound

articulati

on and

swallowin

g

Ask client

to protrude

tongue at

midline,

then move

it side to

side

Client should

be able to

protrude

tongue at

midline and

move it side

to side

Cerebellar Function Assessment

• Balance & Coordination

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

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

Assessment of the Sensory Function• Have the client close the eyes while you touch the client on all

dermatomes w/ objects that are sharp, dull, light to touch. And that vibrate (over bony prominence); the client should be able to discriminate the location and type of touch

• To assess a client’s sense of position (kinesthesia) have the client close the eyes and move the client’s finger or toe up or down and ask the client to describe the movement

• To assess for stereognosis, have the client identify an object in his/her hand w/ the eyes closed.

• To assess for graphesthesia have the client identify a number or letter traced on the palm of the hand

• Test two-point discrimination by touching a client w/ 2 simultaneous pinpricks and asking how many pinpricks there were; use dull points on a caliper and begin on finger pads

Assessment of the Motor Function

• Inspect all muscles for size,tone, movement and strength

• Compare left and right side for symmetry and equality

• Assess for tremors (rhythmic movements) and fasciculations(twitching)

Terminologies Used to describe Motor Function

• Strong- normal strength

• Weak- moves against resistance

• Unable to lift

• Withdraws

• Decorticate- to painful stimuli, flexes arms, wrist, fingers w/ adduction of the upper extremities and extension, internal rotation and plantar flexion of lower extremities

• Decerebrate- to painful stimuli, extends, adducts, and hyperpronates arms and stiffly extends legs and plantar flexes feet

• Flaccid- No response to pain; no muscle tone

• Ataxia-Incoordination of voluntary muscle groups

Assessment of the Reflexes

• The deep tendon reflexes (patellar, biceps, brachioradialis, triceps and achilles)

Standard Criteria for Grading Reflexes

0- no response

1= hypoactive; weaker than normal (+)

2= normal (++)

3= stronger than normal (+++)

4= hyperactive (++++)

• The superficial abdominal reflex is assessed by lightly stroking the abdomen from the side to the midline; normally the side stroked will contract

• The cremasteric reflex is assessed by lightly stroking the inside of the thigh on a male client to raise the testicle on that side

• Babinski reflex- stroke the foot laterally from the heel to ball of foot

(+)- dorsiflexion of the big toe and fanning of other toes

(-)- normal response- curling of the toes

Assessment of Speech

• Normal: clear normal fluent speech

• Dysarthria-ineffective articulation of speech; maybe a motor deficit of the tongue and speech muscles

• Aphasia- a language disorder classified as:

• Expressive, motor or nonfluent aphasia ( also called Broca’saphasia)- inability to express one’s self using motor aspects of speech

• Receptive, fluent or sensory aphasia (Wernicke’s aphasia)- inability to comprehend spoken words

• Global aphasia- can neither express nor comprehend language ( mixed receptive and expressive)

Diagnostic Studies/Lab Examinations• Cerebrospinal fluid analysis via lumbar puncture-it is studied

for color, clarity, glucose, protein, blood or bacteria

Nrsg considerations:

• Assess for CSF leakage and sign of infection at the site after the procedure

• Position the head higher than the body for water based contrast

• Flat position with oil-based contrast

Radiological studies• Cerebral angiography- to view the vascular structure of the

brain; can be used to find arterio-venous malformations and/or aneurysms; use standard measures asso w/ use of contrast medium

Assess for allergy to iodine or shellfish; force fluids to aid in its excretion after the procedure

• CT scan-detects bleeding, hydocephalus & ischemic stroke

• MRI: detects soft tissue changes(necrosis,tumor, edema, disorders)

assess client for implanted sources of metal that would contradict use MRI use

Electrographic Studies

• Electroencephalography (EEG)- measures brain waves w/ multiple scalp elctrodes; its patterns may suggest epilepsy, herpes simplex, encephalitis and dementia, also determines brain death

Shampoo the hair before for hygiene and after to remove residual electrode gel

Withold anticonvulsnat and other meds as ordered for 12-24 hrsprior

Have the client eat regular meals to avoid hypoglycemia that could affect results

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

Ultrasound

• Carotid doppler scan- a noninvasive ultrasound of the carotids that detects occlusions and stenosis; ultrasound procedures cause no discomfort

• Transcranial doppler ultrasonography (TCD)- a portable non-invasive technique used to assess intracranial circulation by measuring blood flow velocity; it is used to assess vasospasm, TIA, headache, subarachnoid hemorrhage (SAH), head injury and arteriovenousmalformations (AVM)

Planning for Health Promotion, Maintenance and Restoration

COMMON HEALTH PROBLEMS

A. Disturbances in Cerebral Function

Acute Disorders of the Nervous System• Altered level of Consciousness

Is a change in arousal or alertness and/or a change in cognition or solving complex problems (thought process , memory, perception, problem solving and emotion); it is often the first sign of a change in neurologic status

Etiology & Pathophysiology

• Causes for unconsciousness vary from primary CNS disorders (such as damage to the reticular activating system or the cerebrum) to dysfunction of other organ systems

• Metabolic disorders may alter the cellular environment enough to inhibit neuronal activity

• Is reserve for those who have long periods of unconsciousness, lasting from hours to months

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

Assessment

• Clinical Manifestations

• Except for case where there is damage to the brainstem, brain function deterioration and changes in LOC follow a predictable pattern

• Confusion, forgetfulness, disorientation to time, person, place, agitation, poor problem solving abilities.

• Any change in behavior may be an early change in cerebrum function.

• Lethargy, obtundation and stupor result from greater cerebral deterioration

• Decorticate posturing, small reactive pupils, positive doll’s eyes

• manifest midbrain deterioration

• Decerebrate posturing, fixed pupils and positive cold caloric tests show deterioration at the pons

• Fixed pupils, flaccidity and negative cold caloric tests indicate involvement at the medulla level

• Glasgow coma scale assessment includes components of eye opening (scored from 1 to 4), best verbal response (scored from 1 to 5), and best motor response ( scored from 1 to 6); total score ranges from 3 to 15; a score of 8 or lower usually indicates coma.

Diagnostic & Laboratory Test Findings• CT and MRI detects hemorrhage, tumor, cysts, edema or brain

atrophy

• ECG evaluate unrecognized seizures as a cause for an altered LOC

• Cerebral angiography evaluates cerebral circulation for aneurysm and arterial-venous malformations

• Transcranial doppler- study blood flow

• Lumbar puncture w/ CSF analysis for analysis of infection

• Lab Test to rule out metabolic, toxic or drug-induced disorders: glucose, serum elect., osmolarity, creatinine, liver funcion, CBC, ABG and toxicology

Therapeutic Management

• Treat the cause of the problem

• Airway maintenance

• Skin integrity

• Preventing contractures

• Maintaining nutrition

Priority Nrg Dx

• Ineffective airway clearance

• Risk for aspiration

• Risk for impaired skin integrity

• Impaired physical mobility

• Risk for imbalance nutrition: less than body requirements

Planning & Implementation

• Assess for ability to clear secretions, breath sounds

• Maintain potent airway for unconscious client

• Maintain in side-lying position

• For clients who have tracheostomy, provide tracheostomy care every 4 hours

• Asess swaloowing and gag reflex; prevent aspiration

• Monitor and report possible aspiration

• Assess skin integrity every shift, reposition every 2 hrs

• Prevent skin breakdown: keep linens clean, dry and wrinkle-free

• Prevent contractures and perform passive ROM regularly

Increased ICP

• A prolonged pressure greater than 15 mmHg or 180mmH2O measured in the lateral ventricles

• Can increased ICP but does not cause significant tissue ischemia: Coughing, sneezing, straining and bending

• Cushing’s triad/response: involves 3 classic signs or responses to increased ICP (increasd systolic BP while diastolic remains the same, widening pulse pressure and reflex bradycardia from stimulation of the carotid bodies

• A prolonged increase in ICP causes tissue ischemia because cerebral blood flow and perfusion are compromised

• Autoregulation, a compensatory mechanism to maintain cerebral blood flow, is disrupted and can lead to cellular hypoxia and ischemia

• Untreated ↑ ICP leads to herniation and ultimately death


• Because the brain is encased in a closed cavity, expansion of any of the contents of the cavity can cause increased ICP

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

• Hydrocephalus- is an 9ncrease in the volume of CSF w/in the ventricular system

• Noncommunicating hydrocephalus- the drainage from the ventricular system is impaired (as when a mass blocks the flow of CSF)

• Communicating hydrocephalus-when blood blocks the arachnoid villi from absorbing CSF in a subarachnoid hemorrhage

Assessment

• Clinical Manifestations:

• Earliest sign of ↑ICP: blurred vision, ↓ visual acuity, diplopia

because of pressure on the visual pathways; headache,

papilledema or swelling of the optic disk

• Vomiting

• Most significant sign: change in LOC,

Diagnostic and Lab Test

• To identify and treat underlying cause of ↑ ICP

• CT and MRI scanning

• Lab Test: serum osmolality monitors hydration status and

ABGs measure pH, oxygen, and carbon dioxide

(hydrogen ions)


• Increased ICP is a medical emergency with little time for lengthy diagnostic studies; it centers on restoring normal pressure and can be accomplished through medications, surgery, and drainage of CSF from the ventricular system

• A drainage catheter, inserted via ventriculostomy into the lateral ventricle, can be done o monitor ICP and to drain CSF to maintain normal pressure; if used, the system is calibrated with the trasducer is leveled 1 inch above the ear (height of foramen of Munro); sterile technique is of utmost importance)

Priority Nursing Diagnosis

Planning and Implementation

• Assess neurological status every 1 to 2 hours and report any deterioration; assessment areas include LOC, behavior, motor/sensory function, pupil size and response vital signs with temperature

• Maintain airway; elevate head of bed 30 degree or keep flat as prescribed; maintain head and neck in neutral position to promote venous drainage

• Assess bladder distention and bowel constipation; assist client when necessary to prevent valsalva maneuver

• Avoid prolonged activity, it may increased ICP; provide quiet environment (lights kept low) and limit noxious stimuli; limit stimulants such as radio, TV, and newspaper

• Avoid ingesting stimulants; coffee, tea, cola and cigarette smokes

• Maintain fluid restriction

• Keep dressings over catheter dry and change dressings asprescribed; monitor insertion site for CSF leakage or infection;monitor clients for signs and symptoms of infection; used aseptictechnique when in contact with ICP monitor

Medication Therapy

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

• Corticosteroids decreases ICP esp. with tumors

Client Education

• Teach the client at risk for increased ICP to avoid coughing, blowing the nose, straining for bowel movements, pushing against the bed side rails, or performing isometric exercises

• Advise the client to maintain neutral head and neck alignment

• Encourage the family to maintain a quiet environment and minimize stimuli

Head Trauma; Skull Fractures

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

Etiology and Pathophysiology

• Skull fractures occur from trauma

• 4 Classifications of Fracture;

1. Linear fractures; infection and CSF leakage is minimal because the dura remains intact; hematoma formation is possible

• Comminuted and depressed; skull fractures have a higher risk of brain tissue damage and infection especially if the overlying skin and dura is torn or damaged; the risk of secondary brain injury is reduced because, impact energy caused bone fracture instead of being transferred to brain tissue

• Basilar; skull fractures involve the base of the skull and are usually secondary injuries; most are uncomplicated, but those that disrupt the sinuses and middle ear bones can lead to infection and CSF leakage

Assessment

• Clinical manifestations of basilar skull fracture

1. Battle’s sign, ecchymosis over the mastoid process

2. Hemoytmpanum, blood visible behind the tympanic membrane

3. Raccoon eyes, bilateral periorbital ecchymosis

4. Rhinorrhea, CSF leakage through the nose

5. Otorrhea, CSF leakage through the ear

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


• Linear skull fractures generally require bed rest and observation for underlying brain injury; no specific treatment is necessary

• Commuted and depressed skull fractures require surgical intervention within 24 hours

• Basilar skull fractures do not require surgery unless there is persistent CSF leakage; regular neurological assessments and observations for meningitis are required

Priority Nrsg Dx

• Risk for infection

• Risk for injury


• Observe for otorrhea or rhinorrhea

• Test clear ear and sinus drainage for glucose; only CSF has glucose; mucous secretions do not

• Observe blood tinged drainage for halo sign: glucose-containing CSF dries in concentric rings on gauze or tissues

• Keep nasopharynx and external ear clean; use sterile technique and supplies when cleaning drainage from nose and/or ears

• Instruct client not to blow nose, cough or inhibit sneeze and to sneeze through an open mouth

• Use aseptic technique when changing head dressings

Medication Therapy

• Dexamethasone to decrease cerebral edema

• Antibiotics for risk of infection

Client Education

• Is an escape of blood into the cranium, most commonly associated with blunt trauma: hemorrhage may cause a very slow to very rapid neurological deterioration

• Etiology and pathophysiology: intracranial hemorrhage results directly from trauma or from the shearing forces on cerebral arteries and veins from acceleration-deceleration injuries; they are classified by location

Epidural Hematoma

• Develops between the dura and the skull

• As the hematoma forms, it strips the dura away from the skull

• Epidural hematoma usually develop from a tear in the meningeal artery

• Because this is an arterial blood, it rapidly expands, leading to a rapid deterioration in neurological status

Subdural hematoma

• Forms between the dura mater and the arachnoid-pia mater layers of the meninges

• Usually involves veins but may involve small arteries as well

• As blood collects, pressure is applied to the underlying brain tissue

• Subdural hematoma may be acute (developing within 48 hours after an acute injury), subacute (developing 2 days to 3 weeks after lesser injury), or they may develop spontaneously

Intracerebral hemorrhage

• Is bleeding into the brain tissue

• It can occur anywhere in the brain but is most common in the frontal or temporal lobes

• It may be the result of closed head trauma, where shearing forces are applied deep in the brain;

Assessment

• Clinical manifestation

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

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

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


• CT scan, MRI scan

Therapeutic Mgt

• Small hematomas will reabsorb spontaneously

• Surgery- needed for epidural hematomas and larger subdural hematomas

Planning & Intervention

• Assess neurological signs on a regular schedule: clear the client’s nose and mouth of secretions; suction airway as needed

• Monitor respiratory for rate, depth and rhythm, prep for oxygen admin and endotracheal intubation for resp. distress

• Prep for surgery for deteriorating neurological condition

• Preop and postop care

• Manage increased in ICP

Medication Therapy

• Anticonvulsants and steroids to treat seizures and increased ICP

Inflammatory Conditions: Meningitis• An inflammation of the meninges of the brain and spinal cord

due to exposure to infectious disease, skull fructure (basilar), otitis media, sinusitis, mastoiditis, neurosurgery or other invasive procedures, systemic sepsis and impaired immune function


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

Assessment

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

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


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

Therapeutic Mgt

• Bacterial meningitis (a medical emergency if not treated it is fatal): antibiotics

• Intrathecal (into the subarachnoid space) Ommaya reservoir to allow administration of antibiotics


• Assess neuro status and VS regularly• Assess and report changes in neuro status or presence of cranial

nerve dysfunction• Assess, prepare and report any seizure activity• Assess for signs of increased ICP• Maintain fluidrestrictions• Assess for fluid volume deficits, MIO, weight, skin turgor, lab values

and urine concentration.

Medication Therapy

• High-dose broad-spectrum antibiotics initially (bacterial meningitis) to cross the blood-brain barrier; anticonvulsants

(usually phenytoin [Dilantin]) are prescribed to prevent or

control seizures; antipyretic, antiemetic and analgesic medications are used for symptom relief; IV fluid replacement is continued until client can resume oral intake

Client Education

• Teach the client the name and purpose of prescribed antibiotics and to take them until they are gone; teach client about other ordered medications as well

• Teach the client and family to recognize and report signs and symptoms of ear, throat, and upper respiratory infections so they can be assessed for meningitis

Cerebrovascular Accident (CVA, brain attack, stroke)• Description: a CVA is a condition where neurological deficits

occur as a result of decreased blood flow to a localized area of the brain; hypertension, diabetes mellitus, sickle cell disease, substance abuse, and atherosclerosis are risk factors for stroke;

Etiology & pathophysiology

• Ischemia followed by cell death is the result of severe and prolonged cerebral blood flow obstruction

4 Types of Brain Attacks

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

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

-the thrombosis occurs quickly but deficits progress slowly

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

4. Hemorrhagic CVA or intracranial hemorrhage occurs when a blood vessel ruptures, this often occurs in long term poorly controlled HPN, a ruptured intracranial aneurysm, embolic CVA, tumors, arteriovenous malformations, anticoagulant therapy, liver disease and blood disorders

- Fatal because of rapidly increasijg ICP

- Onset is rapid

Assessment

A. Clinical Manifestations: vary according to cerebral vessel involved

1. Internal carotid: contralateral motor and sensory deficits of the arm, leg and face

In dominant hemispheric CVA: aphasia (loss of ability to use language)

In nondominant hemispheric CVA:

• apraxia (inability to perform known tasks)

• agnosia (inability to recognize)

• hemianopsia ( loss of one half of the visual field in each eye)

2. Middle cerebral artery: drowsiness, stupor, coma, contralateral hemiplegia and sensory deficits of arm and face, aphasia and homonymous hemianopsia

3. Anterior cerebral artery: contralateral weakness or paralyisisand sensory loss of the foot and leg, loss of decision making and voluntary action abilities and urinary incontinence

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


• CT and MRI

• Cerebral angiography to detect abnormal vessel structure, vasospasm, stenosis of the carotid artery and loss of vessel wall integrity; ultrasound evaluates blood flow


• Drug therapy is the most common treatment for CVAs; if it is a thrombotic stroke, medications could include thrombolyticsand/or heparin

• It is imperative not to disrupt a clot that has formed following hemorrhagic CVA

• Surgery is not usually indicated as a treatment modality

• Rehabilitation is crucial to improve deficits



• Encourage active range of motion on unaffected side and passive range of motion on affected side

• Turn client every 2 hours

• Monitor lower extremities for thrombophlebitis

• Encourage use of unaffected arm for ADLs

• Teach client to put clothing on affected side first

• Resume diet orally only after successfully completing a swallowing evaluation; clients may need thicken liquids, foods w/ the consistency of oatmeal, and to chew on unaffected side of mouth (dysphagia diet)

• Collaborate w/ PT for rehab

• Use alternate methods of communication w/ aphasia clients

• Teach client w/ homonymous hemianopsia to overcome the deficit by turning the head side to side to be able to fully scan the visual field.

Medication Therapy

• Antiplatelet to treat TIA and previous CVA clients (except hemorrhagic CVAs)

• Acute phase of thrombotic and embolic stroke, thrombolytic therapy –tissue plasminogen activator is admin w/in 3 hrs to dissolve the clot

• Anticoagulant therapy: heparin or oral anticoagulant

• In clients w/ cerebral edema, hyperosmolar solutions (mannitol) or diuretics (furosemide or lasix)

• In clients w/ seizures: anticonvulsants-phenytoin (Dilantin), barbiturates, diazepam (Valium) lorazepam (Ativan)

Seizures

• A seizure is an episode of excessive and abnormal electrical activity of all part of the brain

• It is manifested by disturbances in skeletal motor activity, sensation, autonomic dysfunction of the viscera, behavior or consciousness

• Seizures can be due to head injury, infection, acute febrile state, metabolic and endocrine disorders or exposure to toxins


• Can occur due to metabolic needs, oxygen requirements, metabolic by-products and compromised cerebral blood flow

• Maybe idiopathic (without identifiable cause) or may occur secondary to birth traumaa, infection, vascular abnormalities, trauma or tumors.

Seizure Classification

• Partial seizures- begin in one area of the cortex

• Generalized- involved both hemispheres and deeper brain structures

Assessment


• Simple partial seizures are limited to one hemisphere; alteration in motor functions, sensory signs or autonomic or psychic symptoms

• Complex partial seizures originate in the temporal lobe and maybe preceded by an aura: an impaired level of consciousness and repetitive nonpurposeful movements such as lip-smacking, picking, aimless walking, amnesia

• Generalized partial seizures- has spread to both hemispheres and deeper structures of the brain

• Advance seizure- is a generalized seizure that lasts 5 to 30 seconds; there is a sudden brief cessation of motor activity and a blank stare; they may occur occasionally or up to a 100 per day; accompanied by eyelid fluttering or automatisms such as lip-smacking

• Tonic-clonic seizures (grand mal)-most common type of seizures

• Maybe precede by an aura but often w/o warning

• Starts w/ a loss of consciouness and sharp muscle contractions

• May have urinary and/ or bowel incontinence

• Breathing ceases and cyanosis develops during the tonic phase (about 15 sec to 1 min)

• Clonic phase (60 to 90 sec) follows w/ alternating muscle contraction and relaxation in all extremities, hyperventilation, and eyes rolled back in the head.

• In the next phase (postictal period) the client is relaxed w/ quiet breathing, unconscious and unresponsive; the client gradually regains consciousness and may have transient confusion and disorientation; clients often complain of head and muscle aches, fatigue and may sleep several hours

• Clients may have amnesia of the seizures and events just prior to the seizures

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

Diagnostic and lab Test

• Complete neurological exam, EEG, skull x-ray series, CT scan, lumbar puncture w/ CSF analysis, blood studies, electrocardiogram

Therapeutic Mgt


• Maintain airway patency, turn client to side (maintain airway and promote drainage of secretions w/o aspiration), prep oxygen at the bedside, do not force an object into the mouth of a client

• Do not restrain client

• Protect him from injury

Medication Therapy

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

Health Education

• Avoid stress, lack of sleep, emotional upset and alcohol use

• Avoid alcohol and limit caffeine

• Avoid tub baths to avoid drowning

Intracranial Aneurysm

• is a weak or thin spot on a blood vessel in the brain that balloons out and fills with blood.

• The bulging aneurysm can put pressure on a nerve or surrounding brain tissue.

• It may also leak or rupture, spilling blood into the surrounding tissue (hemorrhage).• Possible risk factors for rupture include hypertension, alcohol

abuse, drug abuse (particularly cocaine), and smoking

Rupture of the Aneurysm can cause:

serious complications: hemorrhagic stroke, permanent nerve damage, or death

subarachnoid hemorrhage— bleeding into the space between the skull bone and the brain.

subarachnoid hemorrhage can cause hydrocephalus, in which the excessive buildup of CSF in the skull dilates fluid pathways (ventricles) that can swell and press on the brain tissue.

Vasospasm- other blood vessels in the brain contract and limit blood flow to vital areas of the brain w/c can cause stroke or tissue damage.

Causes

• Congenital- inborn abnormality in an artery wall.

• common in people with genetic diseases, such as connective tissue disorders and polycystic kidney disease, and certain circulatory disorders, such as arteriovenous malformations (snarled tangles of arteries and veins in the brain that disrupt blood flow).

• trauma or injury to the head

• high blood pressure

• infection

• tumors

• atherosclerosis and other diseases of the vascular system,

• cigarette smoking, and drug abuse.

3 Types of Cerebral Aneurysm

• saccular aneurysm- is a rounded or pouch-like sac of blood that is attached by a neck or stem to an artery or a branch of a blood vessel. • Also known as a berry aneurysm (because it resembles a berry, it

is typically found on arteries at the base of the brain.

• lateral aneurysm- appears as a bulge on one wall of the blood vessel

• fusiform aneurysm is formed by the widening along all walls of the vessel.

Assessment

Signs and Symptoms

• Small aneurysms are usually asymptomatic

• larger aneurysm that is steadily growing may press on tissues and nerves

• pain above and behind the eye; numbness, weakness, or paralysis on one side of the face; dilated pupils; and vision changes.

• When an aneurysm hemorrhages, an individual may experience : a sudden and extremely severe headache, double vision, nausea, vomiting, stiff neck, and/or loss of consciousness

• Other signs that a cerebral aneurysm has burst: nausea and vomiting associated with a severe headache, a drooping eyelid, sensitivity to light, and change in mental status or level of awareness, may have seizures, lose consciousness or go into prolonged coma.

Diagnostic Tests

• Angiography is a dye test used to analyze the arteries or veins. intracerebralangiogram-detects the degree of narrowing or obstruction of an artery or blood vessel in the brain, head, or neck, identifies changes in an artery or vein such as a weak spot like an aneurysm.

• Used to diagnose stroke and determine the location, size, and shape of a brain tumor, aneurysm, or blood vessel that has bled.

• Following the injection of a local anesthetic, a flexible catheter is inserted into an artery and threaded through the body to the affected artery. A small amount of contrast dye is released into the bloodstream and a series of x-rays is taken.

• Computed tomography (CT) see aneurysms that have burst and if blood has leaked into the brain. When a contrast dye is injected into the bloodstream prior to scanning CT angiography is done

• Magnetic resonance imaging (MRI) and Magnetic resonance angiography (MRA)

• Cerebrospinal fluid analysis - to detect any bleeding or brain hemorrhage.

ArteriovenousMalformations• are defects of the circulatory system that are generally believed to arise during

embryonic or fetal development or soon after birth. • They are comprised of snarled tangles of arteries and veins. • The absence of capillaries—small blood vessels that connect arteries to veins—

creates a short-cut for blood to pass directly from arteries to veins. The presence of an AVM disrupts this vital cyclical process. Although AVMs can develop in many different sites, those located in the brain or spinal cord—the two parts of the central nervous system—can have widespread effects on the body

• can form anywhere in the brain or spinal cord wherever arteries and veins exist

• Some are formed from blood vessels located in the duramater (outermost) or in the pia mater (innermost) of the three membranes surrounding the brain and spinal cord.

AVMs affecting the spinal cord are of two types

• AVMs of the dura mater- affect the function of the spinal cord by transmitting excess pressure to the venous system of the spinal cord, and AVMs of the spinal cord itself, which affect the function of the spinal cord by hemorrhage, by reducing blood flow to the spinal cord, or by causing excess venous pressure.

• Spinal AVMs frequently cause attacks of sudden, severe back pain, often concentrated at the roots of nerve fibers where they exit the vertebrae; the pain is similar to that caused by a slipped disk. These lesions also can cause sensory disturbances, muscle weakness, or paralysis in the parts of the body served by the spinal cord or the damaged nerve fibers. Spinal cord injury by the AVM by either of the mechanisms described above can lead to degeneration of the nerve fibers within the spinal cord below the level of the lesion, causing widespread paralysis in parts of the body controlled by those nerve fibers.

• Those located on the surface of the cerebral hemispheres—the uppermost portions of the brain—exert pressure on the cerebral cortex, the brain’s “gray matter.” Depending on their location, these AVMs may damage portions of the cerebral cortex involved with thinking, speaking, understanding language, hearing, taste, touch, or initiating and controlling voluntary movements.

• AVMs located on the frontal lobe close to the optic nerve or on the occipital lobe, the rear portion of the cerebrum where images are processed, may cause a variety of visual disturbances.

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

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

Assessment

Symptoms

• Seizures and headaches

• Seizures can be partial or total, involving a loss of control over movement, convulsions, or a change in a person’s level of consciousness.

• muscle weakness or paralysis in one part of the body

• loss of coordination (ataxia) that can lead to such problems as gait disturbances;

• apraxia, or difficulties carrying out tasks that require planning;

• dizziness;

• visual disturbances such as a loss of part of the visual field;

• an inability to control eye movement;

• papilledema (swelling of a part of the optic nerve known as the optic disk)

• various problems using or understanding language (aphasia); • abnormal sensations such as numbness, tingling, or spontaneous

pain (paresthesia or dysesthesia);• memory deficits; and mental confusion, • hallucinations, or dementia. • Researchers have recently uncovered evidence that AVMs may also

cause subtle learning or behavioral disorders in some people during their childhood or adolescence, long before more obvious symptoms become evident.

• Bruit- the rhythmic, whooshing sound caused by excessively rapid blood flow through the arteries and veins of an AVM.

• vein of Galen defect – a lesion located deep inside the brain. It is frequently associated with hydrocephalus, swollen veins visible on the scalp, seizures, failure to thrive, and congestive heart failure. Children born with this condition who survive past infancy often remain developmentally impaired.

• AVMs become symptomatic only when the damage they cause to the brain or spinal cord reaches a critical level

• AVMs damage the brain or spinal cord through three basic mechanisms: by reducing the amount of oxygen reaching neurological tissues; by causing bleeding (hemorrhage) into surrounding tissues; and by compressing or displacing parts of the brain or spinal cord.

Pathophysiology

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

• This abnormally rapid rate of blood flow frequently causes blood pressure inside the vessels located in the central portion of an AVM directly adjacent to the fistula—refer as nidus,—to rise to dangerously high levels. The arteries feeding blood into the AVM often become swollen and distorted; the veins that drain blood away from it often become abnormally constricted (stenosis).

• the walls of the involved arteries and veins are often abnormally thin and weak. Aneurysms—balloon-like bulges in blood vessel walls that are susceptible to rupture—may develop

• large lesions may compress the spinal cord or distort the shape of an entire hemisphere of the brain w/c can constrict the flow of CSF—a clear liquid that normally nourishes and protects the brain and spinal cord—by distorting or closing the passageways and open chambers (ventricles) inside the brain that allow this fluid to circulate freely.

• As CSF accumulates, hydrocephalus results w/c buildup further increases the amount of pressure on fragile neurological structures, adding to the damage caused by the AVM itself.

Types of vascular lesions affect the central nervous system

• Cavernous malformations - lesions formed from groups of tightly packed, abnormally thin-walled, small blood vessels that displace normal neurological tissue in the brain or spinal cord. • The vessels are filled with slow-moving or stagnant blood that is usually

clotted or in a state of decomposition. Although usually do not hemorrhage as severely as AVMs do, they sometimes leak blood into surrounding neurological tissues because the walls of the involved blood vessels are extremely fragile.

• Although they are often not as symptomatic as AVMs, cavernous malformations can cause seizures in some.

• Capillary telangiectases- The lesions consist of groups of abnormally swollen capillaries and usually measure less than an inch in diameter.• rarely cause extensive damage to surrounding brain or spinal cord

tissues. Any isolated hemorrhages that occur are microscopic in size. Thus, the lesions are usually benign. However, in some inherited disorders in which people develop large numbers of these lesions it can contribute to the development headaches or seizures.

• Venous malformations- lesions consist of abnormally enlarged veins. These structural defect usually does not interfere with the function of the blood vessels

• Venous malformations rarely hemorrhage.

• Most venous malformations do not produce symptoms, remain undetected, and follow a benign course.

Cause

• scientists believe that they most often result from mistakes that occur during embryonic or fetal development linked to genetic mutations.

• A few types of vascular malformations are known to be hereditary and thus are known to have a genetic basis.

• Some evidence also suggests that at least some of these lesions are acquired later in life as a result of injury to the central nervous system.

Diagnostic test

• Angiography provides the most accurate pictures of blood vessel structure in AVMs.

• computed axial tomography (CT) and magnetic resonance imaging (MRI) scans

• magnetic resonance angiography (MRA)

Treatment

• the definitive treatment for AVMs is either surgery or focused irradiation therapy.

• Venous malformations and capillary telangiectases rarely require surgery-their structures are diffuse and usually not suitable for surgical correction and they usually do not require treatment

• Cavernous malformations - surgery on these lesions is less common than for AVMs because they do not pose the same risk of hemorrhage.

• Conventional surgery involves entering the brain or spinal cord and removing the central portion of the AVM, including the fistula, while causing as little damage as possible to surrounding neurological structures.

• This surgery is most appropriate when an AVM is located in a superficial portion of the brain or spinal cord and is relatively small in size.

• Endovascular embolization and radiosurgery are less invasive than conventional surgery • In endovascular embolization the surgeon guides a catheter though the arterial network

until the tip reaches the site of the AVM. The surgeon then introduces a substance that will plug the fistula, correcting the abnormal pattern of blood flow. This process is known as embolization because it causes an embolus to travel through blood vessels, eventually becoming lodged in a vessel and obstructing blood flow.

• The embolic materials used to create an artificial blood clot in the center of an AVM include fast-drying biologically inert glues, fibered titanium coils, and tiny balloons. it is usually used as an adjunct to surgery or to radiosurgery to reduce the blood flow through the AVM and make the surgery safer.

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

Headache

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

4 types of headache

1. Vascular headache

• most common type of vascular headache is migraine

• Migraine headaches are usually characterized by severe pain on one or both sides of the head, an upset stomach, and, at times, disturbed vision

• toxic headache produced by fever

• "cluster” headaches- cause repeated episodes of intense pain, and headaches resulting from high blood pressure

2. muscle contraction (tension)-Muscle contraction headaches appear to involve the tightening or tensing of facial and neck muscles

3. Traction-Traction and inflammatory headaches are symptoms of other disorders, ranging from stroke to sinus infection

4. inflammatory

Treatment

• Drug therapy: sumatriptan, methysergide maleate, which counteracts blood vessel constriction, propranolol hydrochloride, ergotamine tartrate (a vasoconstrictor that helps counteract the painful dilation stage of the headache); amitriptyline (an antidepressant); valproic acid, (anticonvulsant); and verapamil, a calcium channel blocker

• biofeedback training

• stress reduction, relaxation training

• elimination of certain foods from the diet are the most common methods of preventing and controlling migraine and other vascular headaches.

• Regular exercise such as swimming or vigorous walking, can also reduce the frequency and severity of migraine headaches.

Disturbances in Peripheral Nerve/ Neurologic Function• Cranial nerve disorders- involve dysfunction of the cranial

nerves, the most commonly affected are the trigeminal nerves (CN V) and the facial nerve (CN VII);

• trigeminal neuralgia is a chronic disease of the trigeminal nerve that causes severe facial pain;

• Bell’s palsy is a unilateral paralysis of the facial muscles.


• Trigeminal neuralgia: cause is unknown

• It affects 1 or more of the 3 divisions of the trigeminal nerve; the opthalmic, maxillary and mandibular

• Bell’s palsy: cause is unknown

• Inflammation of the nerve an a viral cause has been suggested

Assessment


1. Trigeminal neuralgia

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

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

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

disorders


a. Trigeminal neuralgia treatment

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

b. Bell’s Palsy

• The only medical treatment that influences outcome is administration of corticosteroids , but their use has been questioned; antiviral medication is also currently very popular


• Risk for imbalanced nutrition: less than body requirements; Pain; Risk for injury


a. Encourage client to chew on unaffected side

b. Monitor dietary intake

c. Assist with physiotherapy, including moist heat, gentle massage, and facial nerve stimulation with faradic current

d. Protect cornea with artificial tears, sunglasses, eye patch at night, and gentle intermittent closure of eye

Medication Therapy

a. Trigeminal neuralgia

• The most useful drug for controlling pain is carbamazepine (Tegretol); when this is not effective, phenytoin (Dilantin) is tried

b. Bell’s Palsy

• A corticosteroid such as prednisone (Deltasone) influences outcome by decreasing edema of nerve tissue; antivirals are also used

Client Education

a. Wear an eye patch at night

b. Wear protective glasses when outside

c. Inspect the inside of mouth on affected side for food that may collect between mouth and teeth

Evaluation

• The eye is protected; pain is controlled

Guillain Barre Syndrome

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


• Etiology: unknown

• Autoimmune reaction is suspected because it often develops after viral infection, immunizations, fever, injury and surgery

• Antibody (IgM) formation targets peripheral nerve myelin, w/c damages myelin sheat and disrupts nerve conduction; the nerve remyelinizes in the opposite direction of the demyelination.

Assessment


• Weakness/paresis or partial paralysis progressing upward from lower extremities (ground to the brain) and then to total paralysis requiring ventilatory support

• Paresthesias (numbness and tingling) and pain

• Muscle aches, cramping and nighttime pain

• Respiratory compromise and/or failure (dyspnea, diminished vital capacity and breath sounds), decreasing oxygen saturation, abnormal ABGs

• Difficulty w/ extraocular eye movements, dysphagia, diplopia, difficulty speaking

• Autonomic dysfunction (orthostatic hypotension), hypertension, change in HR, bowel and bladder dysfunction, flushing , diaphoresis

Diagnostic and Lab Findings

• Diminished nerve conduction test result , CSF examination shows elevated protein

Therapeutic Mgt

• Supportive care to maintain functionof all body system (resp,. Cardiac, renal)

• Plasmapheresis: plasma is removed and separated from whole blood; blood cells are then returned w/o the plasma to remove antibodies that cause disorder; monitor for complications of this therapy, w/c include bleeding from loss of clotting factors and f/e imbalance.


• Monitor resp status: breath sounds, rate, depth, gag, coughing, swallowing

• Monitor cardiac status: HR, BP, dysrhythmias• Administer chest physiotherapy and pulmonary hygiene measures• Maintain adequate nutrition: administer enteral or parenteral

nutrition as needed; if can swallow assist w/ small frequent feedings of soft foods; weigh client weekly; check electrolytes status; provide mouth care every 2 hours.

• Monitor bowel and bladder function: Assess

• bowel sounds and frequency

• Amount, color of bowel movements

• Check for distention and residuals in client who cannot void spontaneously

• Perform intermittent catheterization as needed

• Encourage fluid intake to 3500 ml/day

• Prevent complications of immobility:

• Encourage use of weak extremities as able

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

• Provide eye care for the client with inability to close eyelids completely; instill artificial tears, cleanse eyes as needed, use eye shields and tape eyes closed if needed.

• Provide comfort and analgesics as needed

• Promote communication w/ client and family, using alternative means of communication if client is on ventilator or is unable to speak because of weak speech muscles

• Initiate discharge planning at time of admission

Medication Therapy

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

Peripheral Nerve Disorders

• Multiple Sclerosis- a chronic disorder of the CNS where the myelin and nerve axons in the brain and spinal cord are destroyed

4 Forms based on the Rate of Progression

1. benign

2. relapsing-remitting

3. primary progressive

4. secondary progressive


• Etiology: unknown, possibly autoimmune or genetic or caused by childhood viral infections

• The destruction of myelin and nerve axons causes a temporary, repetitive or sustained interruption in the conduction of nerve impulses which causes its symptoms

• Plaque formation occurs throughout the white matter of the CNS, w/c also affects the nerve impulses of optic nerves, cervical spinal cord, thoracic and lumbar spine

• Inflammation occurs around the plaques as well as normal tissues

• Astrocytes appear in the lesions and scar tissue forms, replacing the axons and leading to permanent disability.

Assessment

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

Dx and Lab Findings

• Lumbar puncture for CSF (clonal IgG bands present); MRI, Ct scans, muscle testing shows characteristic changes

Therapeutic Mgt

• No cure, supportive care is indicated

Priority Nrsg Dx

• Risk for disuse syndrome

• Disturbed body image

• Risk for infection


• Overall goal of care is to maintain independent as mush as possible

• Rest periods to prevent fatigue w/c is an exacerbating factor

• Assist client w/ ADLs

• Maintain fluid intake of atleast 2000 ml/day to maintain bowel and bladder function and prevent impaction and/or urinary infection

• Avoid infection, illness can act as stressor w/c can trigger exacerbation

• Possible triggers are : fatigue, extreme temperature, illness

Medication Therapy

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

Parkinson’s Disease (PD)

• Is a progressive, degenerative neurological disease characterized by bradykinesia, muscle rigidity and nonintentional tremor;


• Atrophy occurs in the substantia nigra that produces the neurotransmitter dopamine; as dopamine decreases, acetylcholine is no longer inhibited.

• There is imbalance of these neurotransmitters

Assessment

• Clinical manifestations: begin subtly; fatigue and a slight resting tremor may be the only initial symptoms

• bradykinesia- slow movements caused by muscle rigidity; they affect also the eyes, mouth, voice; staring gaze

• Uncoordinated movements

• Short stepped, shuffling and propulsive gait, w/c leads to increased risk of falls

• Postural disturbance, trunk tilted forward

• Seborrhea

• Excessive sweating of face and neck w/ absence of sweating on trunk and extremities

• Heat intolerance

• Constipation, anxiety, depression

• Sleep disturbances and dysphagia

Diagnostic & lab Tests

• CBC shows anemia

• Chemistry profile show albumin and protein

• Drug screens to rule out toxic causes

• EEG shows a slow pattern and disorganization

• An upper GI series show delayed emptying, distention and megacolon

• Video fluoroscopy show slowed response of the cricopharyngealmuscles when swallowing

Therapeutic Mgt

• Medications

• Surgery

• Rehabilitation to optimize functional level


• Perform active ROM twice a day

• Ambulate at least 4 times a day

• Use assistive devices when recommended

• Assess communication skills, speech, hearing, and writing

• Consult with a speech pathologist if necessary

• Monitor diet for foods high in bulk and fluids

Medication Therapy

• Drugs used to treat: monoamine oxidase (MAO) inhibitors, dopaminergics, dopamine agonists, and anticholinergics

• Antidepressant used to treat depression (amitriptyline)

• Propranolol to treat tremors

Client Education

• Teach preventive measures for malnutrition, falls and other environmental hazards, constipation, skin breakdown from incontinence and joint contractures

• Trait gait training and exercise for improving ambulation, swallowing, speech, and self-care.

Myasthenia Gravis

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


• Etiology: unknown; family Hx of autoimmune disorders, thyroid tumors

• An autoimmune process triggers the formation of autoantibodies that decrease the number of acetylcholine receptors and widen the gap between the axon ending and the muscle fiber in the neuromuscular (myoneural) junction

• Is associated / continued production of autoantibodies by the thymus gland in 75 % of cases

• The onset is usually slow but can be precipitated by emotional stress, hormonal disturbance (pregnancy, menses, thyroid disorders), infections/vaccinations, trauma and surgery, temperature extremes, excessive exercise, and drugs that block or decrease neuromuscular transmission (opioids, sedatives, barbiturates, alcohol, quinidine, anesthetics), and thymus tumor

Assessment

Clinical Manifestations• Mild diplopia (double vision) and unilateral ptosis (eyelid drooping)

caused by weakness in the extraocular muscles; weakness may also involve the face, jaw, neck and hip.

• Complications arise when severe weakness affects the muscles of swallowing, chewing and respiration; respiratory distress is manifested by tachypnea, decreased depth, abnormal ABGs, oxygen saturation<92% and decreased breath sounds.

• Bowel and bladder incontinence, paresthesias and pain in weak muscles.

• Myasthenic crisis: sudden motor weakness; risk of respiratory failure and aspiration; most often caused by insuficient dose of medication or an infection.

• Cholinergic crisis-severe muscle weakness caused by overmedication; also cramps, diarrhea, bradycardia, bronchial spasm w/ increased pulmonary secretions and risk of respiratory compromise

Diagnostic and Laboratory Tests

• ABG and pulmonary function tests may show repiratoryinsufficiency

• EMG- electromyography shows decreased amplitude when motor neurons are stimulated

-electromyogram is a test that is used to record the electrical activity of muscles. When muscles are active, they produce an electrical current. This current is usually proportional to the level of the muscle activity. - also referred to as a myogram.

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

Therapeutic Mgt

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

Priority Nrsg Dx

• Ineffective airway clearance

• Impaired swallowing

• Activity intolerance

• Risk for injury

• Disturbed body image


• Maintain effective breathing pattern and airway clearance; thoroughly assess for respiratory distress

• Monitor meals and teach client to bend head slightly forward while eating/drinking to improve swallowing

• Avoid exposure to infections, esp. respiratory

• Teach re effective coughing, use physiotherapy and incentive spirometry; have oral suction available, teach client how to use it; prepare for intubation if needed

• Provide adequate nutrition: schedule meds 30 to 45 minutes before eating for peak muscle strength while eating; offer food frequently in small amounts that are easy to chew and swallow-soft or semisolid as needed; administer IVF and NGT feedings if unable to swallow

• Promote improved physical mobility w/ referrals to PT/OT

• Provide eye care: instill artificial tears; use a patch over one eye for double vision; wear sunglasses to protect eyes from bright lights

• Promote positive body image and coping skills: encourage participation in treatment plan; plan time for active listening and encourage client to express feelings; reinforce progress and explain all care

Medication Therapy

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

Client Education

Instruct to :

• Plan rest periods and to conserve energy; plan major activities early in day; schedule activities during peak medication effect

• Avoid extremes of hot and cold, exposure to infections, emotional stress amd meds that may worsen or precipitate an exacerbation (alcohol, sedatives, local anesthetics)

• Signs of sress

• Encourage to wear a Med-alert bracelet

• Alternative methods of communication if needed: eye blink, finger wiggle for yes/no; flash cards or communication board

Evaluation

• Maintain patenct airway and breathing w/o aspiration

• Maintains ADL w/ assistance

• Demonstrate adequate coping skills for managing chronic and debilitating illness

Alzheimer’s Disease

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


• Cause: unknown

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

Assessment

Clinical Manifestations: AD is classified into 3 stages based on manifestations and abilities

• Early stage: lasts 2 to 4 years: the client appears healthy and alert but maybe restless or uncoordinated; cognitive impairment is not apparent; memory impairment, subtle changes in personality, and problems doing simple calculations may be the first manifestations of AD

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

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

Diagnostic and Lab Tests

• To diagnose other causes of symptoms are ruled out to dx an AD

• CBC reflects anemia

• EEG shows slowing in the later stages of AD

• Ct and MRI shows atrophy

• Psychometric evaluations reflect memory and cognitive impairment

Therapeutic Mgt

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

Priority Nrsg Dx

• Altered thought processes, anxiety, hopelessness


• Label room, drawers or other items

• Orient client o person, place, time as needed

• Keep daily routine consistent as possible

• Remove client from activities that increase anxiety

• Avoid criticizing or judging expressed feelings

• Provide realistic information about disease process

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

Medication Therapy

• Reversible acetylcholinesterase inhibitors, such as tacrine(cognex) donazepil (Aricept), and rivastigmine (Exelon) improves memory;

• Avoid antihistamine and TCA beauces they have high anticholinergic activity

• Tranquilizer to treat agitation

Client Education

• Avoid stopping reversible acetylcholinesterase inhibitors suddenly because it can trigger behavior problems

• Teach caregivers about community resources

• Educate client and caregivers about expectations for client’s disease process

Amyotrophic Lateral Sclerosis

• ALS-Amyotrophic lateral sclerosis is a rapidly progressive, fatal neurodegenerative disease that attacks the nerve cells in the brain and spinal cord responsible for controlling voluntary muscles.

• There is gradual degeneration and death of motor neurons.

• Also called Lou Gehrig's disease.

• progressive degeneration of the motor neurons

motor neurons die,

lost of ability of the brain to initiate and control

muscle movement.

may become totally paralyzed.

• Motor neurons are nerve cells located in the brain, brainstem, and spinal cord that serve as controlling units and vital communication links between the nervous system and the voluntary muscles of the body. Messages from motor neurons in the brain (called upper motor neurons) are transmitted to motor neurons in the spinal cord (called lower motor neurons) and from them to particular muscles. In ALS, both the upper motor neurons and the lower motor neurons degenerate or die, ceasing to send messages to muscles.

• Unable to function, the muscles gradually weaken, waste away (atrophy), and twitch (fasciculations) . Eventually, the ability of the brain to start and control voluntary movement is lost.

• Cause: Unknown

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

Clinical Manifestations

• Early symptoms: increasing muscle weakness, especially involving the arms and legs, twitching, cramping, or stiffness of muscles (spasticity) ; slurred (dysarthria) and nasal speech; or difficulty chewing or swallowing (dysphagia) or breathing.

• exaggerated reflexes (hyperreflexia), muscle cramps

• Babinski's sign (the large toe extends upward as the sole of the foot is stimulated in a certain way) indicates upper motor neuron damage

• When muscles no longer receive the messages from the motor neurons that they require to function, the muscles begin to atrophy (become smaller). Limbs begin to look "thinner" as muscle tissue atrophies.

• eventually patients will not be able to stand or walk, get in or out of bed on their own, or use their hands and arms.

• Difficulty swallowing and chewing impair the patient's ability to eat normally and increase the risk of choking

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

• The person's senses are not impaired

http://www.medicinenet.com/depression/article.htm

Dx Tests

• No one test can provide a definitive diagnosis

• the diagnosis of ALS is primarily based on the symptoms and signs and a series of tests to rule out other diseases.

• electromyography (EMG)- detects electrical activity in muscles.

•

• nerve conduction velocity (NCV)- helps rule out other diseases, abnormalities in the NCV suggest, for example, that the patient has a form of peripheral neuropathy (damage to peripheral nerves) or myopathy (muscle disease) rather than ALS.

• magnetic resonance imaging (MRI), to take detailed images of the brain and spinal cord. Although these MRI scans are often normal in patients with ALS

• they can reveal evidence of other problems that may be causing the symptoms, such as a spinal cord tumor, aherniated disk in the neck, syringomyelia, or cervical spondylosis.

http://www.medicinenet.com/peripheral_neuropathy/article.htm

http://www.medicinenet.com/mri_scan/article.htm

http://www.medicinenet.com/tumor_grade/article.htm

http://www.medicinenet.com/herniated_disc/article.htm

Therapy

• No cure

• The first drug treatment for the disease -- riluzole (Rilutek) is believed to reduce damage to motor neurons by decreasing the release of glutamate, but it does not reverse the damage already done to motor neurons

• Symptomatic treatment to improve the quality of life for patients.

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

Huntington’s Chorea

• Huntington's Disease (HD) is a progressive brain disorder caused by a defective gene.

• caused by a single defective gene (mutation) on chromosome 4

• The huntingtin gene defect involves extra repeats of one specific chemical code in one small section of chromosome 4. The normal huntingtin gene includes 17 to 20 repetitions of this code. The defect that causes Huntington's disease includes 40 or more repeats.

• The defective gene codes the blueprint for a protein called huntingtin.

• Defective huntingtin protein leads to brain changes that cause abnormal involuntary movements, a severe decline in thinking and reasoning skills, and irritability, depression and other mood changes.

• The disease destroys cells in the basal ganglia, the part of the brain that controls movement, emotion, and cognitive ability.

• The job of its protein product, huntingtin, is to direct the delivery of small packages (vesicles containing important molecules) to the outside of the cell.

• have an abnormally high number of these CAG triplets, approximately 40 or more. That disrupts the function of the gene's protein product.

• The brain cells accumulate clumps of protein that become toxic, resulting in cell death.

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

Signs & Symptoms

• The hallmark symptom: uncontrolled /abnormal movement of the arms, legs, head, face and upper body (difficulty walking, speaking, and/or swallowing) , lack of coordination, twitching or other uncontrolled movements

• decline in thinking and reasoning skills, poor memory, concentration, judgment and ability to plan and organize and talk

• Irregular, random movements of the arms, legs and face; restlessness, fidgeting

• mental deterioration, premature senility, and rigid muscles

• brain changes lead to mood swing: depression, anxiety, and uncharacteristic anger and irritability.

• common symptom: obsessive-compulsive behavior, leading a person to repeat the same question or activity over and over.

Dx Test

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

Therapy

• currently no cure

• Treatments focus on managing symptoms, such as anxiety, depression and insomnia

• Experts recommended the following treatments as first-line strategies for 3 of the disease's most troubling symptoms:

1. Chorea (involuntary movements): atypical antipsychotic drug.

2. Irritability: For severe anger and threatening behavior, an atypical antipsychotic drug is the first-line approach; For less severe, nonthreatening irritability, selective serotonin reuptake inhibitor (SSRI), which is a type of antidepressant.

3. Obsessive-compulsive thoughts and actions: SSRIs as the front-line treatment for obsessive-compulsive behaviors.

Trauma of the Spinal Cord

• Are injuries usually due to trauma

• The injury affects motor and sensory function at the level of injury and below

• Perception, sexual function and elimination are affected


• Are usually the result of excessive force applied to the spinal cord and vertebral column

4 Types of Injuries

• Hyperflexion-compresses the vertebral bodies and disrupts ligaments and disc

• Hyperextension disrupts ligaments and causes vertebral fructures

• Axial loading- the application of excessive vertical force and may cause compression fractures

• Excessive rotation tears ligaments and fractures articular surfaces and causes compression fractures

Assessment

Clinical Manifestations

• Spinal shock (temporary loss of reflex function may occur following a spinal cord injury)• s/s:

• Bradycardia

• Hypotension

• Flaccid paralysis of skeletal muscles

• Loss of pain, touch, temperature, pressure, visceral and somatic sensations

• Bowel and bladder dysfunction

• Loss of ability to perspire

Spinals shock has resolve once spinal reflexes return

• Paraplegia- paralysis of the lower portion of the body; it occurs when the injury is in the thoracic spine or lower.

• Tetraplegia (quadriplegia)- is paralysis of the arms, trunk, legs and pelvic portion; it occurs when the level of injury is in the cervical spine.

• Autonomic dysreflexia- an exaggerated sympathetic response that occurs in clients w/ T6 injuries or higher, the response is seen after spinal shock occurs when a stimuli cannot ascend the cord; a stimulus such as the urge to void or abdominal discomfort triggers massive vasoconstriction below the injury, vasodilation above the injury and bradycardia

Diagnostic Tests

• X-ray

• CT scan

• MRI

• EMG to locate the level of injury

Therapeutic Mgt

• Immobilize injury and treat complications of respiratory distress, atonic bladder, paralytic ileus, cardiovascular alterations

• Steroids to prevent secondary cord injury from edema and ischemia

• Stabilize the injury w/ halo traction and Gardner-Wells tongs or surgery

Priority Nrsg Dx

• Impaired gas exchange, dysreflexia, disturbed self-esteem


• Monitor vital capacity and respiratory effectiveness, high cervical cord injuries may inhibit respiratory function

• Monitor for signs of ascending edema; may cause respiratory compromise

• Treat autonomic dysreflexia immediately

• Elevate head of the bed and remove TEDS

• Assess BP every 2-3 minutes while assessing for stimuli that initiated response; remove the stimulus immediately

• Institute bowel and bladder programs to restore a regular schedule for elimination

• Encourage self-care and independent decision making

• Clients w/ spinal cord injury because of fracture/dislocation of cervical vertebrae may use Halo brace (an external fixation device that allows earlier mobility)

Medication Therapy

• Corticosteroids (methylprednisolone, solumedrol)- to control edema of the cord

• Vasopressors- to treat hypertension due to spinal shock or autonomic dysreflexia

• Antispasmodics (Baclofen or lioresal and diazepam or valium) treat spasticity in clients

• Analgesics and TCA to treat pain

Client Education

• Teach to promote independence in self-care

• Educate re resources that are needed

• If client has a halo vest teach that it raises the center of gravity; avoid bending over to reduce risk of falls; neck is immobilized in midline so client needs to turn entire body to scan environment; driving is prohibited; food is cut into small pieces and use straw for liquids

Evaluation

• Maintains adequate respiratory status

• Autonomic dysreflexia resolves

• Feelings about loss of function are verbalized

• Client makes satisfactory adjustments in lifestyle

Herniated Intervertebral disk

• Also called: Bulging disk, Compressed disk, Herniated intervertebral disk, Herniated nucleus pulposus, Prolapsed disk, Ruptured disk, Slipped disk

• A herniated disk is a disk that ruptures. This allows the jelly-like center of the disk to leak, irritating the nearby nerves. This can cause sciatica or back pain.

The spine is made of bones (vertebrae) separated by soft cushions (intervertebral discs).

Normal Disc Herniated Disc

Symptoms

• pain that radiates along the path of the nerve through the buttock and down the leg (sciatica or aradiculopathy

• Numbness and tingling of the feet and legs

Pathophysiology

weak disc (attributed to aging)

the outer part of the disc may tear

inside part of the disk pushes through the tear

presses on the nerves PAIN

Diagnosis

• Computed Tomography (CT) - Spine

• Discography (Discogram)

• Radiographic: x-ray

• Treatment• Artificial Disc Replacement• Epidural Injections for Spinal Pain• Laparoscopic Spine Surgery• Lumbar (Open) Microscopic Discectomy• Spinal Fusion• Rest• Pain and anti-inflammatory medicines• Physical therapy (exercise)• Surgery• chiropractor to relieve pain

Spinal Cord Tumors

• are masses of abnormal cells in the spinal cord that have grown out of control.

• as they grow, press on and destroy normal tissue, causing damage that is disabling and sometimes fatal.

• Tumors in any part of the brain may cause the pressure inside the skull (known as intracranial pressure) to rise.

• This can be caused by growth of the tumor itself, swelling in the brain, or blockage of the flow of cerebrospinal fluid (CSF).

ICP can lead to general symptoms such

as:

• Headache

• Nausea

• Vomiting

• Blurred vision

• Balance problems

• Personality or behavior changes

• Seizures

• Drowsiness or even coma

• tumors in the part of cerebrum that control movement or sensation can cause weakness or numbness of part of the body, often on just one side.

• Tumors in or near the parts of the cerebrum responsible for language can cause problems with speech or even understanding words.

• Tumors in the front part of the cerebrum can sometimes affect thinking, personality, and language.

• Tumors in an area of the brain called the basal ganglia cause abnormal movements and an abnormal positioning of the body.

• Tumor in the cerebellum, which controls coordination, have trouble with walking or other everyday functions, even eating.

• Tumors in the back part of the cerebrum, or around the pituitary gland, the optic nerve, or certain other cranial nerves can cause vision problems.

• Tumors in or near other cranial nerves might lead to loss of hearing, balance problems, weakness of some facial muscles, or trouble swallowing.

• Spinal cord tumors can cause numbness, weakness, or lack of coordination in the arms and/or legs (usually on both sides of the body), as well as bladder or bowel problems.

Diagnostic Tests

• Magnetic resonance angiography (MRA)- special form of MRI that looks at the blood vessels in the brain.

• Magnetic resonance spectroscopy (MRS): it measures radio wave interactions with different chemicals in the brain, it highlights some features of brain tumors that are not clearly seen by MRI.

• Magnetic resonance perfusion- also known as perfusion MRI

• a contrast dye is injected into a vein. It is a special type of MR image is obtained to look at the amount of blood going through different parts of the brain and tumor.

(Tumors often have a bigger blood supply than normal areas of the brain since a faster growing tumor may need more blood.)

• Computed tomography (CT) scan

• Positron emission tomography (PET) scan

• Biopsy

• Lumbar puncture (spinal tap)- to look for cancer cells in the CSF (This fluid is sent to a lab to be looked at under a microscope for cancer cells)

perception and coordination

Health & Medicine

neurons nerve cells

schwann cells pns cells

important cells

cell body nerve cells

ependymal cells lines

brain stem

bloodbrain barrier

parietal lobe