Nervous System LECTURE

7/29/2019 Nervous System LECTURE

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STRUCTURAL CLASSIFICATION OF THE

NERVOUS SYSTEM :

1. CENTRAL NERVOUS SYSTEM Brain Spinal Cord

2. PERIPHERAL NERVOUS SYSTEM

Spinal Nerves Cranial Nerves


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FUNCTIONAL CLASSIFICATION OF THE

NERVOUS SYSTEM :

1. SENSORY or AFFERENT DIVISION Conveys impulses to the CNS

Consists of : Somatic Sensory Fibers delivers

impulses from the skin, skeletal musclesand joints

Visceral Sensory Fibers or VisceralAfferents delivers impulses from thevisceral organs


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2. MOTOR or EFFERENT DIVISION

Carries impulses from the CNS to the effector

organs Consists of:

Somatic Nervous System or VoluntaryNervous System allows us to

consciously or voluntarily control ourskeletal muscles

Autonomic Nervous System or InvoluntaryNervous System regulates events that

are automatic or involuntary Sympathetic Nervous System Parasympathetic Nervous System


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NEUROTRANSMITTERS : Acetylcholine used by somatic motor neurons and its

action is inhibited by neurotransmitter reuptake and is

inactivated by acetylcholinesterase Catecholamine Neurotransmitters : DOPAMINE,

EPINEPHRINE, NOREPINEPHRINE & SEROTONIN

these are categorized as MONOAMINES

The stimulatory effect of catecholamines are inhibitedby: Neurotransmitter reuptake Presynaptic degradation Monoamine Oxidase

(MAO) Postsynaptic degradation Catecholamine O-Methyltransferase (COMT)

Drugs like MAO inhibitors & SSRIs enhance theeffect of these neurotransmitters and are thus often

used to treat people with depression


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NEUROTRANSMITTERS :

Glycine and Gamma-Aminobutyric Acid (GABA) An inhibitory neurotransmitter, and inhibits the

activity of spinal motor neurons thus helping in thecontrol of skeletal movements

Acts as a general inhibitory neurotransmitter in thebrain, and is often used as a tranquilizer (e.g. thedrug : Benzodiazepine Valium ), for mood andemotion disorders

Endorphines & Enkephalins Helps to block the transmission of pain and also

provide pleasant sensations endogenously produced morphine-like substances


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CRANIAL NERVES

Name / Number Composition & Function

I - Olfactory Sensory - Olfaction

II - Optic Sensory - Vision

III - Oculomotor Motor - innervation to the inferior

oblique, superior, inferior &medial rectus muscles of the eyeMotor eyelidMotor muscles that regulate the

lens shape and pupil size

IV - Trochlear Motor superior oblique muscleof the eyeball


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CRANIAL NERVES


V Trigeminal Opthalmic Nerve

Maxillary Nerve

Mandibular Nerve

Sensory impulses from cornea,skin of nose, forehead and scalpSensory impulses from nasal

mucosa, upper teeth and gums,palate, upper lip and skin of cheekSensory muscles of masticationMotor muscles of mastication

VI - Abducens Motor lateral rectus muscle ofthe eyeball


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CRANIAL NERVES


VII - FacialMotor muscles of facialexpression, lacrimal and salivaryglandsSensory taste buds of anteriortongue, nasal and palatal

sensation

VIII - Vestibulocochlear Sensory impulses associatedwith equilibrium and hearing

IX - Glossopharyngeal Motor muscles of the pharynxthat promote swallowing,salivation of parotid glandSensory taste buds of posteriortongue and carotid artery


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X - Vagus Motor muscles of pharynx (swallowing)and larynx (Phonation)

Motor visceral activity: digestive tractand regulates heart rateSensory taste buds of rear tongue,auricle of the ear and general visceralsensations

XI - Accessory Motor Laryngeal movement, softpalateMotor & sensory sternocleidomastoid& trapezius muscles

XII - Hypoglossal Motor tongue movementSensory muscles of the tongue


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CN DYSFUNCTION INTERVENTIONS

I Decreased sense of smell Is often accompanied by impaired taste and weight

loss

II Decreased visual acuity and

visual fields

Frequent reorientation to environment. Position

objects around client in deference to visual

impairment

III

IV,VI

Double vision (diplopia) Intermittent eye patching

Lubricate eyes to protect against corneal abrasions

V Decreased facial sensation

Inability to chew

Decreased corneal reflexes

Caution in shaving and mouth care. Choose easy to

chew foods with high caloric content. Protect

corneas from abrasion by using lubricant

VII Facial weakness and

decreased taste (anterior

tongue)

Oral hygiene. Account for decreased food intake.

Cosmetic approach to hiding facial weakness.


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XII Dysarthria, dysphagia Maintain airway.

Prevent aspiration. Swallow therapy

CN DYSFUNCTION INTERVENTIONS

VIII Hearing loss, imbalance,

vertigo, tinnitus

SAFETY!

Move slowly to prevent nausea and emesis. Assist

ambulation

IX

X

Dysarthria, Dysphagia,

cardiac and respiratory

instability

Maintain airway.

Prevent aspiration. Swallow therapy

XI Inability to turn shoulders orturn head from side to side

Mobility aids. Physical therapy


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SPINAL NERVE PLEXUSES

Plexus ImportantNerves

Body Areas ServedResult if

Damaged

Cervical Phrenic Diaphragm andmuscles of the

shoulder & neck

Respiratory

paralysis

Brachial Axillary Deltoid muscle Paralysis and

atrophy of thedeltoids

Radial Triceps & extensormuscles of the

forearm

Wristdropinability to extendhand at the wrist

Median Flexor muscles of theforearm

Inability to pick upsmall objects

Ulnar Wrist & hand muscles Clawhandinability to spread

fingers apart

Result if


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Damaged

Lumbar Femoral Lower abdomen,buttocks, anterior

thighs and skin of legand thigh

Inability to extendthe leg and flex

hip, loss ofcutaneoussensation

Obturator Adductor muscles ofthigh and small hipmuscles, skin of thighand the hip joint

Inability to adductthe thigh

Sacral Sciatic

Fibular

Tibial

Lower trunk andposterior surface ofthe thigh and leg

Inability to extendhip and flex knee

Lateral aspect of leg &foot

Footdrop inability todorsiflex the foot

Posterior aspect of leg& foot

Inability to plantarflex & invert the

foot, shuffling gait

Result if


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Damaged

Sacral Superior &Inferior

Gluteal

Gluteus muscles Inability to extendthe hip (maximus)or abduct and

medially rotate thethigh (medius)

AUTONOMIC NERVOUS SYSTEM


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AUTONOMIC NERVOUS SYSTEM Consists of the SYMPATHETIC NERVOUS SYSTEM and

the PARASYMPATHETIC NERVOUS SYSTEM

SYMPATHETIC NERVOUS SYSTEM Called the FIGHT or FLIGHT system Also called the ADRENERGIC SYSTEM Four Main Adrenergic receptors:

Alpha

located in vascular tissues (vessels) of smoothmuscles

Stimulated: increases force of heart contraction.Vasoconstriction increasing BP. Mydriasis

dilates the pupils. Glandular decreases salivarysecretion

Alpha Inhibits release of norepinephrine dilates blood

vessels thus decreasing BP, producingHypotension


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SYMPATHETIC NERVOUS SYSTEM Four Main Adrenergic receptors:

Beta located primarily in the heart Stimulated: increases heart rate and force of

contraction / myocardial contractility Beta

Mostly in the smooth muscles of the lungs,

arterioles of skeletal muscles and the uterinemuscles

Stimulation: bronchodilation, increased blood flowto skeletal muscles and uterine relaxation

Other Adrenergic receptors: Dopaminergic

Located in renal, mesenteric, coronary andcerebral arteries

Stimulated: vessels dilate & blood flow increases

O


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SYMPATHETIC NERVOUS SYSTEM Neurotransmitters used:

Epinephrine Norepinephrine Dopamine

collectively, these are called Catecholamines

PARASYMPATHETIC NERVOUS SYSTEM

Neurotransmitter used: Acetylcholine

Two Main Adrenergic receptors: Muscarinic Receptors

Stimulate smooth muscles and slows down theheart rate Nicotinic Receptors

Affects skeletal muscles


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EFFECTS OF THE ANS

Organ PSNS SNS

Eye (iris) Constricts pupils Dilates Pupils

Eye(Ciliary muscle)

Contraction for nearvision

Relaxation for farvision

Lacrimal Glands Production of tears Inhibits : dry eyes

Salivary Glands Production of saliva Decreased : dry mouth

Sweat Glands No effect Perspiration

DigestiveSystem

Increased peristalsisand amount ofsecretion, relaxation ofsphincters

Decreased activity andamount of secretion,constriction ofsphincters

Adrenals No effect Hormone secretion

Liver No effect Release of Glucose

Lungs Bronchoconstriction Bronchodilation

Heart Dereased HR, slows

and steadies

Increased HR & force

of contraction

O PSNS SNS


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Organ PSNS SNS

Urinary bladder Relaxes sphincters(allowing voiding)

Constricts sphincters(Prevents voiding)

Kidneys No effect Decreased urine

production

Blood vessels No effect on most,

dilation on a few (penis)Constricts in viscera

and skin / dilatesthose in skeletalmuscles and heart,

increased BP

Arrector PiliMuscles

No effect Hair erection -goosebumps

CellularMetabolism

No effect Increased metabolicrate, increased bloodsugar and stimulatesfat breakdown

Penis Erection Ejaculation

Uterus No effect Contraction in

pregnant women


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Technique of objectifying a clients level of responses;clients bestresponse in each area is given a numerical value,and the three valuesis totaled for a score ranging from 3 - 15.

EYE OPENING ABILITY:Spontaneous ---------- (4)

To voice / speech ---------- (3)To pain ---------- (2)None ---------- (1)

BEST MOTOR RESPONSE - UPPER LIMB:

Obeys commands ---------- (6)Localizes to pain ---------- (5)Flexor withdrawal(decorticate posturing) ---------- (4)Abnormal flexion(decerebrate posturing) ---------- (3)Extension ---------- (2)

Flaccid ---------- (1)


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BEST VERBAL RESPONSE:Oriented ---------- (5)Confused conversation ---------- (4)

Inappropriate words ---------- (3)Incomprehensible sounds ---------- (2)None ---------- (1)

A score of 15 indicates client is awake and oriented.

A score of 7 - 4 is considered coma.The lowest score is 3,client is considered in deep coma.


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SKULL AND SPINAL X-RAY

reveal the size and shape of the skull

bones, suture separation in infants,

fractures or bony defects, erosion, or

calcification identify fractures, dislocation, compression,

curvature, erosion, narrowed spinal cord,

and degenerative processes


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immobilization of the neck if a spinalfracture is suspected

Remove metal items from body parts

If the client has thick and heavy hair, this

should be documented, because it may

affect interpretation of the x-ray film


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COMPUTED TOMOGRAPHY (CT) SCAN

a type of brain scanning that may or may

not require an injection of a dye

used to detect intracranial bleeding, space-

occupying lesions, cerebral edema,

infarctions, hydrocephalus, cerebral

atrophy, and shifts of brain structures


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IMPLEMENTATION PREPROCEDURE

Obtain a consent if a dye is used

Assess for allergies to iodine, contrast dyes, or

shellfish if a dye is used

Instruct the client in the need to lie still and flatduring the test

Remove objects from the head, such as wigs,

barrettes, earrings, and hairpins

Assess for claustrophobia


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Inform the client if possible mechanicalnoises as the scanning occurs

Inform the client that there may be a hot,flushed sensation and a metallic taste in themouth when the dye is injected

Note that some clients may be given the dyeeven if they report an allergy, and are

treated with an antihistamine andcorticosteroids prior to the injection, toreduce the severity of a reaction


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Provide replacement fluids becausediuresis from the dye is expected

Monitor for an allergic reaction to dye

Assess dye injection site for bleeding or

hematoma, and monitor extremity for color,warmth, and the presence of distal pulses


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a noninvasive procedure that identifies

types of tissues, tumors, and vascular

abnormalities

Similar to the CT scan but provides more

detailed pictures and does not expose the

client to ionizing radiation


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1. Remove all metal objects from the client

2. Determine if the client has a pacemaker, implanted

defibrillator, or metal implants such as a hip prosthesis

or vascular clips because these clients cannot have this

test performed

3. Instruct the client that he or she will need to remain still

during the procedure


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1. client may resume normal activities

2. expect diuresis if a contrast agent was used


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Insertion of a spinal needle through L3-L4interspace into the lumbar subarachnoid space toobtain cerebrospinal fluid (CSF), measure CSFfluid or pressure, or instill air, dye or medications

Contraindicated in clients with increasedintracranial pressure, because the procedure willcause a rapid decrease in pressure within theCSF around the spinal cord, leading to brain

herniation


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AMERICAN DREAM REVIEW INSTITUTE


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obtain a consent

have the client empty the bladder


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IMPLEMENTATION DURING THE

PROCEDURE position the client in a lateral

recumbent position and have the

client draw knees up to theabdomen and chin onto the chest

Assist with the collection of

specimens (label the specimens insequence)

Maintain strict asepsis


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IMPLEMENTATION POSTPROCEDURE

Monitor vital signs and neurological signs

Position the client flat as prescribed

Force fluids

Monitor I & O


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Injection of dye or air into the subarachnoid

space to detect abnormalities of the spinal

cord and vertebrae


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Obtain a consent

Provide hydration for at least 12 hours

before the test

Assess for allergies to iodine

Premedicate for sedation as prescribed


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if a water-based dye is used, elevate the

head 15 to 30 degrees for 8 hours as

prescribed

If an oil-based dye is used, keep the clientflat 6 to 8 hours as prescribed

If air is used, keep the head lower than the

trunk as prescribed

Assess for bladder distention and voiding


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Injection of contrast through the femoral artery

into the carotid arteries to visualize the

cerebral arteries and assess for lesions


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obtain a consent Assess the client for allergies to iodine and

shellfish

Encourage hydration for 2 days before the test

NPO 4 to 6 hours prior to the test as prescribed

Mark the peripheral pulses

Remove metal items from the hair



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Monitor for swelling in the neck and for difficultyswallowing and notify the physician if these symptomsoccur

Elevate the head of the bed 15 to 30 degrees only if

prescribed Keep the bed flat if the femoral artery is used, as

prescribed

Assess peripheral pulses

Immobilize the puncture site for 12 hours as prescribed

Apply sandbags and a pressure dressing to theinjection site as prescribed

Force fluids


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A graphic recording of the electrical activity ofthe superficial layers of the cerebral cortex


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Wash the clients hair

Inform the client that electrodes are attached to

the head and that electricity does not enter the

head Withhold stimulants, antidepressants,

tranquilizers, and anticonvulsants for 24 to48

hours prior to the test as prescribed



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Wash the clients hair

Maintain side rails and safety precautions if

the client was sedated

CALORIC TESTING


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CALORIC TESTING

(OCULOVESTIBULAR TESTING)

Provides information about the function of

the vestibular portion of the eighth cranial

nerve and aids in the diagnosis ofcerebellum and brainstem lesions


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Patency of the external canal is confirmed

Cold or warm water is introduced into the external auditorycanal

Stimulation of the auditory canal with warm waterproduces a horizontal nystagmus toward the side of theirrigated ear when the vestibular eighth cranial nerve isnormal

Stimulation of the auditory canal with cold water producesa horizontal nystagmus away from the side of the irrigatedear if the brainstem is intact


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CRANIOTIOMY


NURSING INTERVENTIONS


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PREOPERATIVE

Routine pre-op care Shampoo the scalp and check for signs of infection

Shave hair

Evaluate and record baseline vital signs and neurochecks

Avoid enemas unless directed (straining increaseICP)

Give pre-op steroids as ordered to decrease brainswelling

Insert Foley catheter as ordered



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NURSING INTERVENTIONS:

POSTOPERATIVE

Supratentorial incision elevate head of bed 15-45degrees as ordered; position on back (if intubatedor conscious) or on unaffected side; turn every2hours to facilitate breathing and venous return

Infratentorial incision keep of head flat or elevate20-30 degrees as ordered; do not flex head onchest; turn side to side every 2 hours using aturning sheet; check respirations closely and reportany signs of respiratory distress


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watch for signs of diabetes insipidus (severethirst, polyuria, dehydration) and

inappropriate ADH secretion (decreased

urine output, hunger, thirst, irritability,decreased LOC, muscle weakness)

For infratentorial surgery may be NPO for

24 hours due to possible impairedswallowing and gag reflexes


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check dressings for excessive drainage, CSF, infection,displacement, and report to physician

if surgical drain is in place, note color, amount, and odor ofdrainage

Administer medications as ordered

a. Corticosteroids to decrease cerebral edemab. anticonvulsants to prevent seizures

c. stool softeners to prevent straining

d. mild analgesics

Apply ice to swollen eyelids; lubricate lids and areas aroundeyes with petrolatum jelly


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an increase in intracranial bulk due to an increase

in any of the major intracranial components: Brain tissue (1400 g) Blood (75ml) CSF (75ml)

CSF fluid pressure greater than 15 mmHg Common Causes:

Head injury Tumors

Abscesses Hemorrhage Edema Hydrocephalus inflammation Surgery

Monroe-Kellie hypothesis:


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Monroe Kellie hypothesis:

Because of limited space for expansion

in the skull, an increase in any one of the 3components (Brain, Blood & CSF) causesa change in the volume in the others by:

Displacing them or shifting CSF Increasing the absorption of CSF Or decreasing cerebral blood flow

Increased ICP significantly reduces blood flow resulting toischemia if complete ischemia lasts for 3-5 minutes (6 minutes max),irreversible brain damage occurs

Autoregulation


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refers to the brains ability to change the diameter ofthe blood vessels automatically to maintain a constantcerebral blood flow during alterations in systemic blood

flow.

Cushings Triad occurs once the brains protectivemechanism is no longer effective

Bradycardia Hypertension Bradypnea

ICPif untreated could lead to herniation / displacement of

brain tissue & occlusion of cerebral blood flowbrain death follows if ischemia and infarction are left

untreated

Intracranial pressure may be measured


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p y During a Spinal Tap / Lumbar Puncture By directly attaching a device referred to as a

bolt to a small hole in the skull

Increased intracranial pressure is almost alwaysindicative of severe medical problems.

The pressure itself can be responsible for furtherdamage to the CNS by

Decreasing blood flow to the brain Causing the brain to herniate (push through)the opening in the back of the skull where thespinal cord is attached (Foramen Magnum)

which is Fatal


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Signs and symptoms:Infants:


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Infants: Bulging fontanel High-pitched cry Poor feeding Separated sutures

Older children and adults: Change in LOC (earliest sign)

Progresses from Restlessness -----> to Confusion -----> toDisorientation -----> to Lethargy -----> to Stuporous -----> to Coma

Tachypnea (initial manifestation) Widening Pulse Pressure (initial manifestation)

Projectile vomiting Headache increasing in intensity, aggravated by movement andstraining Changes in behavior Seizures

Ipsilateral pupillary dilatation due to compression of C.Nerve III Pupils eventually become fixed and Dilated Setting-Sun Sign (sunset eyes) a late and ominous sign ofincreased ICP

Note: Slow increases are tolerated fairly well in young children before

they become symptomatic. Adults tolerate increased ICP less well.


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Management:


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Establish and maintain a patent airway and provide

adequate ventilation Monitor V/S Position: head of bed elevated 30 45% Prevent further increase in ICP

Maintain a quiet and comfortable environment

Avoid use of restraints Prevent straining stool softeners and laxatives asordered Prevent vomiting antiemetics

Prevent excessive coughing avoid clustering nursing care activities together

Prevent complications of immobility


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Management:


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Medications Osmotic Diuretics (Mannitol Osmitrol)

Furosemide (Lasix) Corticosteroids (Dexamethasone Decadron) Anticonvulsants (Phenytoin Dilantin) Analgesics : Small doses of Codeine stronger

analgesics are Contraindicated because they cause: Respiratory depression Altered LOC Pupillary changes

Treat fever aggressively increases cerebral blood flowand cerebral blood volume

HYDROCEPHALUS


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HYDROCEPHALUS

A condition of altered production, flow, or

absorption of cerebrospinal fluid (CSF)

Characterized by an abnormal increase inCSF volume within the intracranial cavity

and by enlargement of the head in infancy

Occurs in approximately 3 to 4 cases per

1,000 births


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HYDROCEPHALUS


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HYDROCEPHALUS

Two causes:

Decreased absorption of CSFOverproduction of CSF

Two types:

Non-communicating(obstructive/internal/intraventricular)

Obstruction in the system between theCSF production (ventricles) and the area of

its reabsorption (subarachnoid space)Causes: congenital malformations, tumors

encroaching on the ventricular system,inflammation or hemorrhage

HYDROCEPHALUS


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HYDROCEPHALUS

Two types:

1. Non-communicating(obstructive/internal/intraventricular)

Obstruction in the system between the CSF

production (ventricles) and the area of itsreabsorption (subarachnoid space)

Causes: congenital malformations, tumors

encroaching on the ventricular system,

inflammation or hemorrhage

May be partial, intermittent, or complete

Occurs in majority of cases

HYDROCEPHALUS


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HYDROCEPHALUS

Two types:

2. Communicating (extraventricular)

Results from impaired reabsorption of CSF

from the arachnoid villi into the venous

system or excessive production of CSFCauses: SAH, developmental malformation,

head injury, neoplasm

HYDROCEPHALUS


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HYDROCEPHALUS

Pathophysiology

Ventricular system becomes greatly

enlarged as well as the cerebral

hemispheres, gyri become less prominent,

white matter is reduced in volume

Increased ICP is determined by fluid

accumulation and type of hydrocephalus,

age at onset, rapidity and extent ofpressure rise

HYDROCEPHALUS


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HYDROCEPHALUS

Acute hydrocephalus usually seen in

head injury, related to increased ICP

Slowly developing hydrocephalus may not

cause IICP but produce progressive

dementia, and gait changes

HYDROCEPHALUS


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HYDROCEPHALUS

Clinical ManifestationsHydrocephalus in utero or infancy or

before cranial suture fusion Expansion of the ventricles, cranial sutures separate,

head expands, and bulging of fontanels

Increased ICP to a lesser as the head is able toexpand

Alteration in muscle tone including clonus andspasticity

Scalp with prominent scalp veins, sunset eyes as

infant cannot gaze upward Strabismus, nystagmus, optic atrophy

Infant has difficulty holdig head up

Child may experience physical or mental devt. lag

HYDROCEPHALUS


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HYDROCEPHALUS

Clinical Manifestations

Hydrocephalus in older children and adults

Head does not expand leading to signs of

increased ICP: headache, vomiting,

papilledema, mental deterioration

Declining memory , apathy,

inattentiveness, indifference to self and

others.

Urinary incontinence

HYDROCEPHALUS


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HYDROCEPHALUS

Diagnostic Evaluation

Clinical presentations

Transillumination of infants head indicates

abnormal fluid collection

Percussion of infants skull produce a typicalcracked pot sound (Macewens sign)

Papilledema

CT San diagnostic tool of choice Skull x-ray shows widening of fontanelle,

sutures, and erosion of intracranial bone

HYDROCEPHALUS


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OC US

Management

Surgical procedures

Direct operation of lesion causing

obstruction such as tumors

Intracranial shunts for non-communicating

hydrocephalus diverts fluid from

obstructed segment of ventricular system

to the SAS

Extracanial shunts most common

HYDROCEPHALUS


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Extracranial Shunt procedures

Ventriculoperitoneal shunt (V-P shunt)Diverts CSF from a lateral venrticle or

spinal SAS to peritoneal cavity

Ventriculo-atrial shunt (V-A shunt) divertsCSF to right atrium or superior vena cava

Ventriculopleural shunt diverts CSF topleural cavity

Ventriculo-gallbladder shunt diverts CFin common bile duct


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HYDROCEPHALUS


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Shunt complications

Need for shunt revision from occlusion,

infection or malfunction

Shunt revision from grwoth of child

V-A shunt endocardial contusion and

clotting bacterial endocarditis,

bacteremia, ventriculitis, thromboembolism

HYDROCEPHALUS


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HYDROCEPHALUS

Complications Seizures

Herniation of brain

Spontaneous arrest from neuralcompensatory mechanism, IICP, and brain

herniation

Development delays

Mental deterioration in adult

HYDROCEPHALUS


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Nursing Assessment

Infants: head circumference, fontanelles fortense and bulging, pupilary response,

LOC, breathing patterns, emesis, motor,

devtal milestonesOlder child and adult: v/s, sings of IICP,

headache, emesis, LOC, motor function,

milestones, declining memory , apathy,inattentiveness, indifference to self and

others, Urinary incontinence

HYDROCEPHALUS


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Nursing Diagnoses

Altered cerebral tissue perfusion related to

IICP prior to surgery

Altered nutrition: LBR related to reduced

oral intake and vomiting

Risk for injury related to malfunctioning

shunt

Risk for infection related bacterial infiltration

of the shunt

HYDROCEPHALUS


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Nursing Interventions

Maintain cerebral tissue perfusion Provide adequate nutrition

Maintain skin integrity

Reduce anxiety

Maintain fluid balance

Prevent infection

Strengthen family coping

HYDROCEPHALUS


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Special consideration

Stress importance of resocgnizing s/s ofIICP

Report shunt malfunction or infection

immediately to prevent IICP

Regular follow up check ups esp for shunt

monitoring

HYDROCEPHALUS


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Evaluation

No changes in v/s, LOC, head size, no vomiting,

pupils equal and responsive

No significant weight loss, stable level of

consciousness No skin breakdown

Urine intake less than intake, skin turgor normal

Afebrile Parents seeking resources


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Acute peripheral facial paralysis involving

7th

cranial nerve (Facial Nerve) on one sideproducing weakness of facial muscle

Common between age 20 50

Lasts only for 2 8 weeks Etiology :

Unknown

Viral infectionVascular ischemia

Autoimmune disease


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Majority have upper respiratory infection 1-3 weeks before the onset of symptoms

Distortion of the face

Lagopthalmos unable to close the eyesDecrease taste sensation of anterior 2/3 of

the tongue

Decreased tear productionSpeech alteration

Difficulty Swallowing


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Prednisone

Protection of the involved eye

Artificial tear drops

Manually Close eyes if necessary

Physical therapy :

application of moist heat facial massage

facial exercise


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Condition of the 5th cranial nerve

Characterized by sudden paroxysms ofsharp, stabbing, excruciating pain in

the distribution of one or morebranches of the trigeminal nerve

Unknown etiology


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Sudden, severe pain on one side Without warning Ends abruptly With pain free interval Precipitated by :

Face movement TalkingChewingYawning

SwallowingShavingExposure to cold wind


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Carbamazepine (Tegretol)

Injection of alcohol & ethanol Percutaneous radiofrequency trigeminal

gangliolysis low voltage stimulation of thetrigeminal nerve by elctrodes which destroyssensory function

Microvascular decompression of trigeminalnerve treatment of choice for younger

generation willing to accept craniotomy & is themost effective form of treatment

Open surgery Rhizotomy (transsection ofnerve root)


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Any functional abnormality of the CNS when thenormal blood supply to the brain is disrupted Impairment could be due to a partial or complete

occlusion of a blood vessel or hemorrhageresulting from a tear in the vessel wall


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Transient or temporary episode of neurologicdysfunction due to an interruption of blood flow to afocal area in the brain

Lasts minutes hours (not longer than 24 hours) Risk Factors:

HPN Family History of Stroke

DM Atherosclerosis

Heart Disease Smoking

Obstruction of cerebral microcirculation (Emboli)


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Assessment:

Amaurosis Fugax (sudden painless loss of


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Amaurosis Fugax (sudden, painless loss ofvision in one eye)

Weakness

Aphasia

Vertigo, diplopia

Numbness, paresthesias or ataxia Dysphagia

Homonymous Hemianopsia

Carotid bruit History of headaches with a duration of days

before the attack

Management: Anti-coagulant therapy


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Platelet aggregation inhibitors - to reduce the incidenceof stroke:

Aspirin

Ticlopidine (Ticlid)

Surgical management:

carotid endarterectomy

Intracranial anastomosis

angioplasty

Reduce risk factors :

Control BP, DM, Hyperlipidemia and Smokingcessation

Thrombolytic therapy 3 to 5 hours after onset

Streptokinase

Recombinant Tissue Plasminogen Activator (rt-PA)


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Onset and persistence of neurologic dysfunctionlasting longer than 24 hours

Results from a disruption of blood supply to the brain

Two Major Categories:

1. Ischemic / Non - hemorrhagic Stroke

Thrombosis

Cerebral embolism

Ischemia

2. Hemorrhagic Stroke

Cerebral hemorrhage (rupture of a blood vessel)


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Hypertension

TIA

Heart disease

Elevated cholesterol

Diabetes Mellitus

Obesity

Atherosclerosis

Carotid bruit

Cigarette smoking

Sickle cell disease Emboli

Sedentary Lifestyle / immobility

Stress

Stroke.exe


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CT ScanCerebral angiography

PET Scan

CBC with platelet count

Lipid profile

ECG

Chest PA

FBS, Serum creatinine, sodium


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Sudden, severe headache and nuchal rigidity


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Sudden, severe headache and nuchal rigidity

Sudden numbness or muscle weakness

Difficulty of speaking Difficulty of swallowing

Impairment of sensation

Confusion / change in mental status

Parietal Cortex: Hemiparesis occurs on opposite side of thebody

Temporal Cortex: Difficulty speaking or understandinglanguage or both

Occipital Cortex: visual defects (homonymous hemianopsia) Cerebellum: Vertigo, Ataxia

Numbness (paresthesia), Weakness (paresis) or loss of motorparalysis (plegia) on one side of the body


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Management:

Acute Phase


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Maintain patent airway & adequate ventilation

V/S observe for signs of increased ICP, shock, hyperthermia and

seizures Complete bed rest

Maintain F&E imbalance and ensure adequate nutrition

IV therapy for the first few days

NGT if unable to swallow

Fluid restriction as ordered to decrease cerebral edema

Maintain proper positioning, body alignment & skin integrity:

Elevate head of bed 30 45 degrees to decrease ICP

Turn and reposition every 2 hours (only 20 minutes on affected side)

Passive ROM every 4 hours Turn client and apply lotion on skin

Maintain adequate elimination:

Offer bedpan and urinal every 2 hours, catheterize only if necessary

Stool softeners & laxatives as ordered

Management:

Acute Phase

Provide a quiet and restful environment


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Provide a quiet and restful environment

Medications

Osmotic diuretics (Mannitol) & corticosteroids (dexamethasone)to decrease cerebral edema

Anticonvulsants (phenytoin Dilantin)

Thrombolytics (hemorrhage must be ruled out first)

Streptokinase / Urokinase

Recombinant Tissue Plasminogen Activator (rt-PA)

Anticoagulants (hemorrhage must be ruled out first)

Heparin (Antidote: Protamine SO4)

Warfarin (Coumadin) : antidote - Vitamin K

Aspirin, Ticlopidine (Ticlid) & dipyridamole (Persantine) Antihypertensives for Hypertension

Neuroprotectants:

Citicholine

Piracetam

Management:

Rehabilitation


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Safety measures

Dysphagia Check gag reflex before feeding / upright position

Place food on unaffected side of the mouth

Offer soft foods

Homonymous Hemianopsia can lead to visual neglect

Approach client on unaffected side

Place personal belongings, food, etc on unaffected side

Gradually teach the client to compensate by SCANNING

turning head to see things on the unaffected side

Emotional lability mood swings / frustration Create a quiet, restful environment

Maintain calm, non-threatening manner

Explain to family that behavior is not purposeful

Management:

Rehabilitation


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Aphasia

Receptive Aphasia Give simple, slow directions

Give one command at a time, gradually shift topics

Use non-verbal techniques of communication

Speak at normal tone and volumeclients hearing is intact

Expressive Aphasia

Listen and watch carefully when the client speaks

Anticipate needs to decrease frustration

Allow sufficient time for client to answer, do not press for

answers Apraxia loss of ability to perform purposeful skilled acts

Guide client thru intended movement

Keep repeating the movement


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APHASIA


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Acquired disorder of communication

A general term that encompasses varyingdegrees of inability to comprehend, integrate,

and express language

May involve impairment of the ability:

To speak

To understand the speech of others

To read

To write

To calculate

To understand gestures

APHASIA


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Causes Vascular lesion of the cerebral artery

especially the dominant hemispheres (left:dominant in 95% of right handed and 70% inleft handed individuals)

Stroke

Head injury

Bran tumors

Brain cysts

3 Categories of Fluent Aphasia

Wernickes receptive aphasia


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Wernicke s, receptive aphasia

characterized by the inability to comprehend the speech

of others and of oneself and includes deficits of reading

Patient speaks readily but speech lacks clear content,

information, and direction, jargon frequently used

Anomic aphasia (amnesiac aphasia) speech is

nearly normal except for difficulty in finding singular

words

Marred by word-finding difficulty

Conductive (Conduction) aphasia characterizedby good comprehension of language but difficulty

repeating spoken material

APHASIA


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Expressive or non-fluent aphasia

Characterized by an inability to spontaneouslycommunicate or translate thoughts or ideas

into meaningful speech or writing

Speech production is limited, effortful, and

halting and poorly articulated

Comprehension is normal

Associated with lesions in Brocas area of the

frontal lobe

Brocas aphasia

APHASIA


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Global aphasia characterized by severedisruption of all aspects of communication

including verbal speech, written, reading,

understanding.

APHASIA Nursing Diagnosis


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Nursing Diagnosis

Impaired verbal communication related to brain injury

Nursing InterventionsAssess comprehension

Stand on patients unaffected side (stay within patientsvisual field)

Keep environment simple and relaxed; minimizedistractions

Speak at normal rate and volume since patient is nothard of hearing ,and there is no intellectual impairment

Allow plenty of time to answer

Dont ask questions requiring complex answers Provide pad and pens if patient prefers and is able to

write

Avoid forcing speech

Watch for clues and gestures if speech is jargon

ANEURYSMAL SUBARACHNOID

HEMORRHAGE


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HEMORRHAGE

Aneurysm is an abnormal localized dilatationof a blood vessel from congenital defect or

absence of the muscle layer of the vessel

Most are asymptomatic until rupture and producesymptoms of hemorrhagic stroke

Aneurysmal subarachnoid hemorrhage

represents bleeding into the subarachnoidspace caused by a ruptured cerebral aneurysm

A dreaded complication of cerebral aneurysm

ARTERIOVENOUS MALFORMATION


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Complex tangle of abnormal arteries and

veins linked by one or more fistulas

A system of dilated rteies and veins in

which the normal capillary bed is absent

A tangle mass of discolored vessels that

have the appearance of a cluster of

grapes

Approximately 50% of patients with AVMpresents with hemorrhage


Hemodynamic effects


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Hemodynamic effects

Blood passes from the high pressure arteries to the

low pressure veins without passing through the

capillaries due to their absence

The draining venous channels are exposed to highlevels of pressure predisposing them to rupture and

hemorrhage

Impaired perfusion affects cerebral tissues adjacent

to the AVM leading to slowly progressive neurologic

deficits referred to as Vascular Steal Phenomenon



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AVM is typically present before 40 years of age

Affects men and women equallyAccounts for approximately 2% of strokes

Manifestations

include hemorrhage, seizures, headaches,progressive neurologic deficits

50% present with intracerebral hemorrhage

SAH and intraventricular hemorrhage also occur

Headache: severe, throbbing and synchronouswith their heartbeat

Diplopia, hemianopia, hemiparesis, mentaldeterioration and speech deficits

ANEURYSMAL SUBARACHNOID

HEMORRHAGE


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HEMORRHAGE

ManifestationsSudden, severe headache, described as the

worst headache of my life accompanied bynausea, vomiting and dizziness

Signs of meningeal irritation such as nuchalrigidiy (neck stiffness), photophobia (lightintolerance), cranial nerve deficits esp. CNs II, III,and IV (diplopia and blurred vision), storke

syndrome, loss of consciousness, increased ICP,pituitary dysfunction

ANEURYSMAL SUBARACHNOIDHEMORRHAGE AND ARTERIOVENOUS


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MALFORMATIONS


Clinical presentations

CT scan- most commonly used method todetect SAH

Lumbar puncture- to detect blood in CSF

Cerebral Angiographydefinitive diagnostictool to detect aneurysm and AVM; also detect

vasospasm

ANEURYSMAL SUBARACHNOIDHEMORRHAGE


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ComplicationsRebleeding,

vasospasm, with cerebral ischemia,

hydrocephalus, hypothalamic dysfunction, and

seizure activity


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DEMENTIAS


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Syndrome of intellectual impairment or deterioration

severe enough to interfere with occupational or socialperformance

May involve disturbances in memory, language use ,

perception, and motor skills

May interrupt ability to learn necessary skill, solve

problems, think abstractly and make judgment

Sometimes called Senility is not a normal aging

process

A major cause of disability in the older population

DEMENTIAS


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2.5% to 24.6% of those older than 65 years of

age In long-term care facilities, up to 70% of

residents have cognitive impairments

Causes: disorders such as: Degenerative Vascular

Neoplastic

Demyelinating

Infectious

Inflammatory

Toxic

Metabolic

psychiatric

DEMENTIAS

T pes of Dementia


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Types of Dementia

Alzheimers disease most common

Vascular/multi-infarct dementia 2nd most

common

Picks disease

Creutzfeldt-Jakob disease

Wernick-Korsakoff Syndrome

Huntingtons disease

OTHER TYPES OF DEMENTIA


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Vascular Dementia/multi-infarct dementia associated with cerebrovascular disease from

multiple infarctions through out the brain

2nd most common, 20% to 25% of dementias

Incidence closely associated with hypertension Other contributing factors: arrhythmias, MI,

peripheral vascular disease, DM, and smoking

Gradual or abrupt onset

Focal neurologic symptoms related to local areas ofinfarction


Pi k di


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Picks disease Rare form of dementia characterized y atrophy

of frontal and temporal areas of brain

Neurons contain cytoplasmic inclusions knownas Pick bodies

Average onset: 38 years More common in women and men

Behavioral manifestation such absence ofconcern and care, loss of initiative, repetition,

hypotonia, incontinence, noticed earlier thanmemory loss

Short course, death within 2 to 10 years frominfection


C t f ldt J k b di


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Creutzfeldt-Jakob disease

Rare transmisible form of dementia

Caused by an infective protein called prion : lack agenome, a mutated protein, that when accumulates inhigh concentration in neurons lead to a toxic conditionand cell death

Transmitted through corneal transplant and humangrowth hormone taken from cadavers

Causes degeneration of pyramidal and extrapyramidalsystems

Has a rapid course; demented at 6 month of onset

Fatal, death within months; few may survive for severalyears

Symptoms include personality changes, dementia,

insomnia and ataxia as disease progresses


W i k K k ff d


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Wernicke-Korsakoff syndrome

Result from chronic alcoholism

Wernickes disease is characterized by acute

weakness and paralysis of extraocular muscles,

nystagmus, ataxia, and confusion as well asperipheral neuropathy

Signs from alcohol withdrawal: delirium,

confusion, hallucination

Cause: deficiency of thiamine (vit. B 1)

Symptoms are reversed when nutrition is

improved with supplemental thiamine




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Korsakoff syndromeChronic phase with severe impairment of recent

memory

Characterized by difficulty in dealing withabstractions and defective capacity to learn

Confabulations (recitation of imaginaryexperiences to fill gaps in memory) mostdistinctive feature of the disease

Polyneuritis is common

Does not improve significantly with treatment


Huntingtons Disease


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Huntington s Disease

Also known as Huntingtons chorea

Rare hereditary degenerative d/o characterized

by chronic progressive chore, psychological

changes, and dementiaAn autosomal dominant disorder: gene in

chromosome 4

Age of onset: 4th and 5th decades

By the time diagnosis is made, gene has already

been passed on to the children

Occurs in 5 per 100,000 persons

HUNTINGTONS DISEASE


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Pathophysiology Principal pathologic feature:

Severe degeneration of the basal ganglia particularly

the caudate and putamine nuclei and frontal cortex

causing a decrease in GABA synthesis and secretion

resulting decrease inhibitory activity on the

dopaminergic pathway and decrease in acetylcholine

level leading to increase dopaminergic activity in the

basal ganglia with the cerebral cortex leading tohypotonia and hyperkinesia (involuntary, fragmentary

movement such as chorea)

HUNTINGTONS DISEASE



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Abnormal movement and progressivedysfunction of intellectual processes (dementia)and thought processes

Chorea (to dance) or choreiform movement

(sudden jerky and irregular but coordinated, andgraceful movement beginning in face, and arms,and eventually affecting the entire body

Impaired memory and judgment, impulsive

behaviors Delusions and depressions

HUNTINGTONS DISEASE


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Based on family history and clinical

presentations

Genetic testing: disease marker G8 on

chromosome 4

HUNTINGTONS DISEASE

Management


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Management

No cure for the disease

Treatment: symptomatic

Drugs used to treat dyskinesias and

behavioral disturbances

Progressive degenerative d/o of the cerebral cortex


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SenileDementia

Dementia impairment of intellectual function, usually accompaniedby memory loss and personality changes

Profound loss of memory, cognition and ability for self-care

Poor prognosis

2 15 years (death) ; average of 8 years

unknown etiology

Contributing factors:

Neurotransmitter deficiency (acetylcholine & norepinephrine)

Viral factors

Trauma Genetic factors : 70% - chromosome abnormality at C21

Positive protein: Amyloid plaques damages brain tissue (deathof neurons)

Commonly affects frontal, pareital and occipital lobes


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Clinical manifestations1. Stage 1

Lasts 2 - 4 years

Memory loss (recent memory)


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Memory loss (recent memory)

Difficulty with abstract thinking & mathematical tasks Lack of spontaneity

Loss of sense of humor

Disorientation to the time and date

Lack of energy

2. Stage 2

Lasts several years

Impaired cognition and abstract thinking

Restlessness and agitation

Wandering ---> Sundowning (wandering in the late afternoonand evening)

Inability to carry out ADL

Impaired judgment & impulse control

Inappropriate social behavior

Clinical manifestations


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3. Stage 3 Usually lasts only for 1-2 years but can last

as long as 10 years

Emanciation

Indifference to food

Inability to concentrate

Urinary and fecal incontinence

Seizures

Interventions : Institute safety measures

Side rails up & bed in low position

Check patient frequently especially at night


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Check patient frequently, especially at night

Use restraints only when absolutely necessary and with adoctors order

Never leave anything at the bedside that could harm thepatient

Approach the client with a friendly, relaxed manner patients

mirror the affect of those around them Orient client to person, time and place frequently

Label items, use visual cues like pictures

For hyperactive clients: finger-foods

Schedule activities & tests in the morning & early afternoon to

avoid overstimulation at bedtime Cholinesterase inhibitors : for cognitive impairment

donepezil (Aricept)

taccrine (Cognex)

rivostigmine (Exxelon)

The Five (5) Cs of Alzheimers

Management:


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Management:

1. Use of Calendar

2. Use of Clock

3. Use of Colors4. Consistency of Caregiver

5. Administration of Cognex (tacrine)

to increase mental ability


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Assessment : Cardinal Signs:

Resting tremorspill-rolling tremors (initial manifestation) Increases when stressed, anxious or concentrating


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, g Decreases with purposeful activity and sleep

Muscle rigidity (Cogwheel rigidity) - movements are jerky and stiff Bradykinesia abnormally slow movements

Difficulty initiating movement Freezing phenomenon (extreme form)

Propulsive, shuffling gait and decrease in arm swing

Stooped posture, microphonia Difficulty rising from sitting position Mask-like face with decreased blinking of the eyes Fatigue, emotional lability Muscle weakness

- affected eating- chewing- swallowing- speaking

Autonomic disorder- salivation, sweating, orthostatic hypotension


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Management:

MedicationsL d (L d / L d / D )


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Levodopa (L- dopa / Larodopa / Dopar)

Converted to dopamine in the body Increases dopamine levels Relieves tremors, rigidity & bradykinesia Give with meals to decrease GI distress

Avoid coffee can increase Nausea Postural hypotension

Carbidopa Levodopa (Sinemet) Prevents breakdown of dopamine

Fewer side effects Amantadine (Symmetrel)

For mild cases Decreases rigidity, tremor & bradykinesia

Management: Anticholinergics - Trihexyphenidyl (Artane),

Benztropine (Cogentin) Biperiden (Akineton)


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Benztropine (Cogentin), Biperiden (Akineton)

Inhibit action of acetylcholine For mild cases / relieves tremors and

rigidity Antihistamines decreases tremors and

rigidity Antispasmodics improves rigidity Deprenyl prolong the action of levodopa Bromocriptine (Parlodel) / Pergolide

stimulates dopamine release Used when levodopa loses its

effectiveness

Management: Provide safe environment

side rails on bed, handlebars on toilet, bathtub


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and hallways, remove hazards that might cause

falls, use rubber soled shoes & low heels Maintain adequate nutrition, allow sufficient time for

meals Remember in teaching the client: intellect is usually

not impaired High fiber and fluids to prevent constipation from the

anti-cholinergic drugs Low-protein diet at daytime because it decreases

absorption of Levodopa which is usually given atdaytime

High-protein diet at night

Chronic, progressive, non-contagious degenerative diseaseof the CNS characterized by demyelination of the neurons


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of the CNS characterized by demyelination of the neurons

Demyelination destruction of myelin sheath of the nervefiber in the brain & spinal cord

Most disabling neurologic disease in young adults duringtheir productive years, characterized by remissions &exacerbations

Frequently involves the optic, oculomotor & spinal nervetracts

Affects women more than men, 20 40 years old

Etiology: unknown

Theories:

infection, autoimmune response, allergic reaction, trauma,anoxia, toxins, stress, fatigue & vascular lesions destroy

axons and myelin sheath


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Damaged myelin sheath impairs the normal conduction ofthe nerves


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the nerves

Usually affects : Optic nerves & Oculomotor nerves: visual problems

Cerebellum : timing, coordination of skeletal muscleactivity and balance

Brainstem

Midbrain Vision & hearing (corpora quadrigemina)

Pons control of breathing

Medulla Oblongata HR, BP, vomiting, swallowing &breathing


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Assessment:

Charcots Triad : nystagmus, intention tremor & speechdeficits

Ataxia, loss of coordination


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Diplopia initial manifestation

Fatigue, weakness, numbness, tingling, loss of positionsense & paralysis

Bladder & bowel incontinence

Dysphagia

Emotional instability, mood swings & impaired judgment Pain due to muscular spasm

Blurred vision, scotomas (blind spots)

Sexual impotence in males

Impaired sensation: touch, pain, cold & warmth CSF contains abnormal amounts of IgG antibodies

MRI shows areas of demyelination


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Management:

Avoid precipitation of exacerbations

Avoid fatigue, stress, infection, extremes in temperature

Establish regular program of exercise & rest


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Balanced diet

Medications

Acute Exacerbations:

Corticosteroids to decrease edema at sites ofdemylination

For spasticity lioresal (Baclofen), dantrolene (Dantrium)or diazepam (Valium)

To alter immune response Interferon (still experimental)

Mood swings chlordiazepoxide (Librium)

Encourage self-care activities

Prevent complications of immobility DVT, bed sores &contractures

Promote safety & prevent injury

Disorder affecting the NM transmission of voluntary muscles

Produces sporadic progressive weakness & abnormal fatigue of


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Produces sporadic, progressive weakness & abnormal fatigue of

voluntary muscles exacerbated by exercise & repeated movementsand is relieved by rest

Patient gets tired on exertion even by just combing hair, chewingor talking

Common in women: 15-35, men: above 40

Pathology: Autoimmune: antibodies attach to Ach receptor sites blocking,

destroying & weakening them, leaving them insensitive to acetylcholine

Deficiency in Acetylcholine

Excess Acetylcholinesterase

usually affects muscles innervated by the cranial nerves : face, lips,tongue, neck, throat, eyes, head control, chewing, swallowing,speech, etc.

When it involves the muscles for breathing life-threatening!


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Assessment: Diplopia (double vision) Ptosis Sleepy, mask-like expression

D j


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Droopy jaw Extreme muscle weakness (initial manifestation) Fatigue Weak voice Difficulty in chewing, swallowing, closing of mouth or smiling Weakness of arm, hand & leg muscles Progressive weakness of diaphragm & intercostal muscles

difficult breathing Bobbing head


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Serum test for Ach receptor antibodies

Edrophonium (Tensilon) test


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Edrophonium (Tensilon) test

IV Provides spontaneous relief of symptoms (lasts 5-10

minutes)

CT Scan of the neck area thymoma & thymus

hyperplasia Electrophysiologic testing decremental response to

repetitive nerve stimulation

Management:

Medications Steroids

Anticholinesterase Drugs Increases acetylcholine levels at the NM junction Pyridostigmine bromide (Mestinon)


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Neostigmine bromide (Prostigmine)

Nsg resp: Give meds exactly on time Give 30 minutes before meals Give with milk and crackers to avoid GI upset Monitor effectiveness : assess muscle strength

Avoid drugs that block NM transmission

Morphine SO4 Strong sedatives ether, novocaine, curare

Streptomycin, kanamycin, neomycin & gentamycin

Management: Plasmapheresis (plasma exchange)

Thymectomy


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Promote optimal activity Short periods of activity, long periods of rest

Time activity with max muscle strength

Encourage normal ADL

Promote optimal nutrition Mealtime coincide with peak effect of drug

Check gag reflex & swallowing ability before feeding

Promote mechanical soft diet

Myasthenic Crisis: Abrupt onset of severe, generalized muscle weakness Sudden respiratory distress failure Cause:

U d di i


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Undermedication Stress Infection or trauma

Symptoms improve with Tensilon Test Care:

Maintain tracheostomy or E-tube to assist with ventilation ABGs Bedrest Increase Anticholinesterase drugs

Cholinergic Crisis:

Abrupt onset of severe, generalized muscle weakness Sudden respiratory distress failure S/E of Anticholinesterse drugs

Abdominal cramps, diarrhea, N&V, excessive salivation, excessive sweating

Cause:


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Cause:

Overmedication of Anticholinesterase drugs Symptoms worsen with Tensilon Test Care:

Maintain tracheostomy or E-tube to assist with ventilation ABGs Bedrest Discontinue Anticholinesterase drugs Give Atrophine SO4

Polyradiculoneuritis


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y

Rapidly progressing syndrome of unknown causeinvolving the peripheral sensory and motor nerves andnerve roots

Segmented demyelination of the peripheral nerves

Age: 30 50 years old Characterized by ascending paralysis

Theories: Autoimmune disorder

Predisposing factors:

Recent viral infection

Recent immunization

30 40% follows a Campylobacter infection(infectious diarrhea)

Assessment: Clumsiness usually the first sign

Paresthesia (tingling/numbness) often startingat the legs ascending to the upper extremities


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at the legs, ascending to the upper extremities,trunk and face

Paralysis of facial, ocular and oropharyngealmuscles

Difficulty in swallowing, chewing and talking Progressive, ascending motor paralysis

Ventilatory insufficiency if paralysis ascends to

the respiratory musclesConsidered a medical emergency

May require mechanical ventilation


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Management: Maintain adequate ventilation

Monitor RR, maintain open airway, suction secretions

Assist with Endotracheal intubation and mechanical ventilation as


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Assist with Endotracheal intubation and mechanical ventilation as

indicated

V/S

Corticosteroids to suppress immune response

Prevent complications of immobility

Promote comfort

Optimum nutrition

Gag reflex

Pureed foods

Assess need for NGT

Rehab training to regain strength refer to PT

Plasmapheresis

AMYOTROPHIC LATERAL SCLEROSIS

Also known as Lou Gehrigs disease after thefamous New York Yankee baseball player


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famous New York Yankee baseball player

Incapacitating/devastating neurologic diseaseresulting in progressive weakness accompaniedby other lower motor neuron signs such as atrophyor fasciculation

Affects upper and lower motor neuronsAmyotrophic means without muscle nutrition or

progressive muscle wasting refers to the LMNcomponent of the syndrome

Lateral sclerosis scarring of the corticospinaltract in lateral column of spinal cord refers to theUMN component of the syndrome


A disorder of middle to late adulthood


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May begin anytime in the 4th decade of life

Peak of occurrence is in the early 50s

Male to female ratio: 3 or 3 is to 1

Follows a progressive course with mean

survival period of 2 to 5 years from onset of

symptoms


Cause is unknown


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5% to 10% of cases are familial

Mutation of gene encoding superoxide desmutase

1 (SOD1) was mapped to chromosome 21. SOD1

functions in the prevention of free radical formation Mutation accounts for 20% of familial ALS

Remaining 80% caused by mutations in other

genes

Exotoxic injury from glutamate excitotoxicity =

increased glutamine in CSF of patients with ALS


Other possible cause under investigation:


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Viral-immune factors

Metabolic

Nutritional

Systemic stimuli such infection or

trauma

Serum immune complexes are elevated

in ALS but nature of complexes isunknown


Pathophysiology


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y gy

Degeneration ofupper motor neurons (nerveleading from the brain to the medulla orspinal cord) and lower motor neurons(nerves leading from spinal cord to the

muscles of the body) progressive loss ofvoluntary, muscle contraction and functionalcapacity

Death of neurons result in axonal

degeneration and secondary demyelinationwith glial proliferation and sclerosing(scarring)




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UMN lesionWeakness, and spasticity or stiffness

Impaired fine motor control

Dysphagia (difficulty swallowing)

Dysarthria (impaired articulation of speech0Dysphonia (difficulty making the sounds of speech)

LMN lesionprogressive with wasting of muscles of arms, trunk and

legs, fasciculation, hyporeflexia, loss of body hair,decreased sweating

Muscle cramp involving the distal legs is an earlysymptom


Progressive weakness and atrophy of distal


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muscles of one upper extremity followed byregional spread of clinical weakness (reflectsinvolvement of neighboring areas of spinal cordleading to involvement of UMN and LMN in limbsand head affecting muscles of palate, pharynx,tongue, neck, and shoulders causing impairmentof swallowing, chewing, and speech.

Dysphagia with recurrent aspiration and weaknessof respiratory muscles

Death results from involvement of cranial andrespiratory muscles


Course of the Disease


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Average duration of life is approximately 2 to3 years from appearance of symptoms

May run from a few months to 15 years

20% survive 5 to 20 years




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g Electromyography evaluates denervation and

muscle atrophy

Nerve conduction study evaluates nervepathways

Barium swallow - evaluates ability to achievevarious phases of swallow

MRI, CT rule out other disorders

Lab tests rule out other causes of muscleweakness


Management

Currently there is no cure/ no specific treatment to


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Currently, there is no cure/ no specific treatment to

arrest or alter disease progression. Treatment is

palliative and symptomatic

Rehabilitation measures assist persons to manage

disability together respiratory and nutritionalsupport to survive longer

Riluzole antiglutamate drug, to decrease

accumulation of glutamate and slow the

progression of the disease. Drug prolonged

survival by 3 to 6 months


Symptomatic treatment:


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Baclofen to control spasticity

Diazepam to control fasciculations

Antidepressants, sleep medications Feeding gastrostomy

Mechanical ventilation, eventually becomes

necessary


Complications


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p

Respiratory failure

Aspiration pneumonia

Respiratory arrest


Nursing Assessment


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Based on History and PE

Respiratory status and function

Cranial nerve functions; gag reflex and

wallowing

Voluntary motor function and strength


Nursing Diagnoses


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Ineffective breathing pattern related to respiratorymuscle weakness

Impaired physical mobility related to disease

process

Altered nutrition: LBR related to inability to swallow

Fatigue related to denervation of muscles

Social isolation related to fatigability and

decreased communication skills

Risk for infection related to inability to clear airway


Nursing Interventions


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GoalsMaintain respiration

Optimize mobility

Meet nutritional requirements: highcalorie, small frequent feedings, semi-solid

Minimize fatigueMaintain social interaction

Prevent aspiration and infection


Outcome-based Evaluation


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Respirations unlabored

Feeding self with assistive utensils, w/o

aspiration

Napping twice a day,

Communicating needs effectively to staff

and family

No signs of respiratory or urinary infections

CNS INFECTIONS

Meningitis - inflammation of the meninges of the brain and spinalcord, caused by bacteria, viruses, or other microorganisms.

Encephalitis - inflammation of the brain, caused by a virus; may


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p , y ; y

occur as a sequela of measles, mumps, chickenpox.

Signs and symptoms:headache (initial manifestation), photophobia, irritability, chills, fever,vomiting possible seizures,decreasing LOC

signs of meningeal irritation- nuchal rigidity: stiff neck- opisthotonos: head and heels bent backward and body arched

forward- Kernigs sign

- Brudzinkis sign

Tests:Lumbar puncture- measurement and analysis of CSF shows

increased pressure, elevated WBC and protein, decrease

glucose and culture positive for specific microorganism.


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KERNIGS SIGN

Present if lower leg cannot extend due to pain and spasmwhen client is lying supine with one leg bent over his


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when client is lying supine with one leg bent over hisabdomen.

BRUDZINSKIS SIGN

Present if the clients hips and knees flex when he is


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p

lying supine with his head lifted towards his chest.

Management: give large doses of antibiotics as ordered dexamethasone digoxin to help control arrythmias mannitol to decrease cerebral edema


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mannitol to decrease cerebral edema enforce respiratory isolation after initiation antibiotic therapy forsome types of meningitis give nsg. care for increased ICP, seizures, and hyperthermia provide nsg. Care for delirious or unconscious client as needed bed rest

keep room quiet & dark if photophobia or headache occurs maintain fluid and electrolyte balance prevent complications of immobility monitor vital signs and neuro checks frequently teach client concerning discharge plans:

- maintain a good diet high in protein, high calories, with smallfrequent feedings- rehabilitation program for residual deficits

refer patient to Audiologist, hearing impairment is a commoncomplication of meningitis

episodes of abnormal motor, sensory or autonomic due to


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p , y

abnormal discharge from brain cells.

Epilepsy - chronic recurrent seizures. may be caused by :

infantile fever head injury

hypertension CNS infection brain tumor or metastasis drug withdrawal (alcohol / barbiturates) stroke trauma

subdural hematomas circulatory disorders drug toxicity: lidocaine, penicillin, theophylline unknown


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TYPES:Generalized seizures Major motor seizure (grand mal)

aura, usually starts with tonic or stiffening phase,


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followed by clonic or jerking phase; may have bowel/bladder incontinence; then in postictal phase, sleeps /loss of consciousness, lasts 2-5 minutes

Absence seizure(petit mal)sudden onset, with twitching or rolling of eyes; lasts afew seconds, appears daydreaming

Febrile seizures- common under 5yrs. of age; seizure occurs only when

fever is rising; EEG is normal 2 weeks after a seizure

Atonic or akinetic seizuredropseizure sudden, momentary loss of muscle tone, usually fallsto the ground


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During seizure activity protect from injury:

prevent falls support head decrease external stimuli do not restrain


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dont use tongue blades or insert anything in the mouth keep airway open:

side lying position, suction excess mucous, loosen clothing observe and record seizure- note any preictal aura:

fear, anxiety, hallucinations, djvu symptoms- note nature of the ictal phase:

symmetry of movement, response to stimuli, LOC, respiratorypattern- note postictal response:

amount of time it takes to orient to time and place; sleepinessProvide client teaching and discharge planning need to drug therapy wear a Medic-Alert identification bracelet or carry ID availability of support groups and community agencies


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Drug therapy : (Anticonvulsants) Phenytoin (Dilantin)

most commonly used can only be administered with in normal saline and levels aremonitored to titrate dosage


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therapeutic level is 10-20 mg/dl side effects include gum hyperplasia, hirsutism, ataxia, gastricdistress, nystagmus, anemia, sedation

Diazepam (Valium) drug of choice for status epilepticus monitor RR

Valproic Acid (Depakene) used to treat absence seizures

Phenobarbital Na used for general and absence seizures

Tegretol (Carbamazepine) used when seizure have not responded to other anticonvulsants

give with meals

Surgeryto remove the tumor, hematoma or epileptic focus


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GINGIVAL HYPERPLASIA


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Localized intracranial neoplasm that

occupies space & cause a rise inintracranial pressure

Benign or malignant

2nd most common cancer in children

Supratentorial location adults

Infratentorial location children


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Tumor from the meningesMeningioma

Tumors in the cranial nerves


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Acoustic neuromaOptic nerve spongioblastoma

Metastatic cancers

lung carcinoma

breast cancer

Blood vessel tumorhemangioblastoma

angioma


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Symptom due to increaseICP

Localized neurologicimpairement


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Changes in behavior Restless, drowsiness

Pupillodilation

Headache in the

morning Projectile vomiting

VS : increase BP,bradycardia andirregular respiration

p

Motor weakness,paralysis, lack ofcoordination, ataxia,dysphagia

Sensory visiondisturbances, problemsof hearing, no touch,pressure, position sense

Management :Dexamethasone

Anticonvulsants


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Antacids & H2antagonist

Radiation therapy

Surgery

Chemotherapy


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HEAD INJURY

usually caused by car accidents, falls,


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y y

assaults

Types:Concussion

Contusion

Hemorrhage


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severe blow to the head jostles brain causing it


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to strike the skull; results in temporary

neural dysfunction


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CONTUSION

results from more severe blow that bruises the


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brain and disrupts neural function

epidural hematoma

l ti f bl d b t th d t d


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accumulation of blood between the dura mater and

skull; commonly results from laceration of middle

meningeal artery during skull fracture; blood

accumulates rapidly

subdural hematoma

accumulation of blood between the dura and

arachnoid; venous bleeding that forms slowly; may be

acute, subacute, or chronic

HEMORRHAGE

subarachnoid hematoma


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bleeding in the subarachnoid space

intracerebral hematoma

accumulation of blood within the cerebrum

ASSESSMENT FINDINGS

Concussion headache, transient loss of


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consciousness, retrograde or posttraumatic

amnesia, nausea, dizziness, irritability

Contusion neurologic deficits depend on

the site and extent of damage; include

decreased LOC, aphasia, hemiplagia,

sensory deficits

ASSESSMENT FINDINGS

Hemorrhages


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a. epidural hematoma

- brief loss of consciousness followed by lucid

interval; progresses to severe headache,vomiting, rapidly deteriorating LOC, possible

seizure, ipsilateral papillary dilation

ASSESSMENT FINDINGS

b. subdural hematoma


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- alterations in LOC, headache, focalneurologic deficits, personality changes,ipsilateral papillary dilation

c. intracerbral hematoma

- headache, decreased LOC, hemiplegia,

ipsilateral papillary dilation


Maintain a patent airway an adequate ventilation

7/29/2019 Nervous System

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Nervous System LECTURE