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Key to success!
 Confidence  Test taking strategies  Ample test preparation and study habits  Review of frequent board examination topics  Focus on your goals  Above all- PRAYERS

Assessing Clients with Neurologic Disorders

Anatomy and Physiology

 Nervous system divided into 2 regions:

1.Central nervous system (CNS): brain and spinal cord 2.Peripheral nervous system (PNS): cranial nerves, spinal nerves and autonomic nervous system
 Function of the nervous system are

sensory input, integration, motor output, homeostasis, mental activity.


 Central Nervous System:


Spinal Cord


Nervous System: spinal nerves, cranial nerves and their branches


Central Nervous System: BRAIN

Central Nervous System : BRAIN

 Major regions are:

Diencephalon Brainstem Cerebrum Cerebellum

BRAIN : Diencephalon

BRAIN: Diencephalon
 Thalamus largest part, influences mood

and registers an unlocalized, uncomfortable perception of pain.  Epithalamus small area superior and posterior to the thalamus, involved in the emotional and visceral response to odors, pineal body (onset of puberty)

 Hypothalamus most inferior part, important

in maintaining homeostasis, plays a central role in the control of body temperature, hunger and thirst, plays a major role in controlling the secretion of hormones from the pituitary gland.


BRAIN : Brainstem
 Connects the spinal cord to the remainder of

the brain  Consists of the medulla oblongata, pons, and midbrain  Involved in vital body functions such as the control of HR, BP, and breathing

BRAIN : Brainstem

Brainstem : Medulla Oblongata

 Most inferior portion of the brainstem  Continuous with the spinal cord  Extends from the level of the foramen

magnum to the pons  CN 9, 10, 11, 12  Specific functions: regulation of HR and BV diameter, breathing, swallowing, vomiting, coughing, sneezing, balance and coordination

Brainstem : Pons
 Immediately superior to the medulla

oblongata  Means bridge  CN 5, 6, 7, 8  Lower part of the pons: breathing, swallowing and balance  Other nuclei in the pons control functions such as chewing and salivation

Brainstem : Midbrain
 Superior to the pons  Smallest region of the brainstem  CN 3 and 4  Found superior and inferior colliculus  Superior colliculi involved in visual reflexes,

turning the head, a sudden loud noise, bright flash of light  Inferior colliculi major relay centers for the auditory nerve pathways in the CNS

 General functions : coordination of eye

movements and in the control of pupil diameter and lens shape  Contains a nuclear black mass called Substantia Nigra

BRAIN : Cerebrum

BRAIN : Cerebrum
 Largest part of the brain  Divided into left and right hemisphere by a

longitudinal fissures  The surface of each hemisphere is wrinkled by presence of eminences known as Gyri and furrows called Sulci or Fissures

 Each cerebral hemispheres is divided into


Frontal lobes Principal motor area (4) Important in the control of voluntary motor functions, motivation, aggression, mood, and olfactory (smell) reception Brocas area (44,45) Brocas aphasia (executive, motor, nonfluent, anterior)


Parietal lobe Principal center for the reception and conscious perception of most sensory information, such as touch, pain, temperature, balance and taste Principal sensory area (3,1,2)


Occipital lobe Functions in the reception and perception of visual input Principal visual cortex (17)



Temporal lobe Involved in olfactory (smell) and auditory (hearing) sensations and plays an important role in memory They associated in abstract thought and judgement Primary auditory cortex (41,42) Wernickes area (22) wernickes aphasia (receptive, sensory, fluent, posterior)

Brain: Cerebellum

BRAIN : cerebellum
 Composed of gray matters  Posterior and inferior to the cerebrum  Involved in balance, maintenance of muscle

tone and coordination of fine motor movements  Major function of the cerebellum is that of comparator  Also involves learning motor skills (riding a bicycle/playing a piano)

Cerebellar comparator

Central Nervous System: Spinal Cord

 Spinal cord extends from the foramen

magnum to the 2nd lumbar vertebra below which is the cauda equina  It has a central gray part organized into horns and a peripheral white part forming nerve tracts  Roots of spinal nerves extend out of the cord

Central nervous system: Spinal Cord

Central Nervous System: Spinal Cord

Central Nervous System: Spinal Cord

 VERTEBRAL COLUMN  surrounds and protects the spinal cord  7 cervical, 12 thoracic, 5 lumbar, 5 sacral,

coccyx (4 fused vertebra)

Peripheral Nervous System

Peripheral Nervous System

 Consists of the nerves and ganglia located

outside the brain and spinal cord  Divided into two groups:

12 pairs of CN 31 pairs of SN

PNS: Cranial Nerves

 12 cranial nerves  Designated by numerals from I to XII  General categories:

Sensory Motor

Cranial nerves  sensory I,II,VIII  motor III, IV, VI, XI, XII  mixed V, VII, IX, X

Mnemonic: Cranial Nerves

 Oh Oh Oh  To Touch  And

Feel A is

 Girls Vagina

Such Heaven

 Some Say  Marry Money  But My Brother Says  Big Boobs  Matter Most

Cranial Nerves origin

PNS: Spinal Nerves

 Arise along the spinal cord from the union of

the dorsal and ventral roots

PNS: Spinal Nerves

 They contain axons of both sensory and

somatic motor neurons  Also contain parasympathetic and sympathetic axons

PNS: Spinal Nerves

PNS: Spinal Nerves

 Categorized by the

region of vertebral column  31 pairs (c8, t12, l5, s5, c1)  Organized into 3 plexuses

PNS: Spinal Nerves

Autonomic Nervous System

 Composed of:

Sympathetic and parasympathetic

Autonomic Nervous System

ANS: Sympathetic Nervous System

 Originates from the T1-L2/L3 segments of the

spinal cord (thoracolumbar)  Utilized by the body for FLIGHT and FIGHT response  Neurotransmitter agents are Epinephrine and Norepinephrine (coming from the adrenal gland)  ADRENERGIC system

Sympathetic Responses:

HR  RR  BP  Visual Acuity (Pupillary Dilation)  Smooth Muscle tone sphincters are contracted  Vasoconstriction - peripheral  Metabolism glucose, fatty acids

Sympathetic Responses:
 Peristalsis  Salivary



ANS: Parasympathetic Nervous System

 CHOLINERGIC system  The vegetative system  Feed and Breed responses  Cranio-sacral location  Cranial nerves- 3, 7, 9, 10 and S2-S4  Neurotransmitter is Acetylcholine

Parasympathetic Responses

HR  RR  BP  Visual Acuity (Pupillary constriction)  Smooth Muscle tone sphincters are relaxed  Vasodilation = peripheral  Metabolism dec glucose, fatty acids

Parasympathetic Responses:
 Peristalsis  Salivary



Comparison of UMN and LMN

Upper motor neuron lesions
 Loss of voluntary control  Increased muscle tone  Muscle spasticity  No muscle atrophy  Hyperactive and

Lower motor neuron lesions

 Loss of voluntary control  Decreased muscle tone  Flaccid muscle paralysis  Muscle atrophy  Absent or decreased

abnormal reflexes


Structures supporting the brain


Frontal bone Parietal bone Temporal bone Occipital bone


Surround and protect the spinal cord 3 layers: DAP

 Dura mater  Dural venous sinuses  Epidural space (SC)

 Arachnoid  Subdural space (space between dura mater and arachnoid, contains small amount of serous fluid)

 Pia mater  Tightly bound to the surface of brain and SC  Subarachnoid space (bet. Arachnoid and pia mater, filled with CSF and BV)

Cerebrospinal Fluid
 Bathes the brain and spinal cord  Protective cushion aound the CNS  Produced by the Choroid plexus of the lateral,

third, and fourth ventricles  Clear, colorless, SG of 1.007  In normal adult, approximately 500 ml of CSF produced each day, all but 125 to 150 ml is absorbed by the villi

CSF Flow

Cerebral Circulation
 Receives approximately 15% of the cardiac

output or 750 ml per minute  Does not store nutrients and has a high metabololic demand that requires high blood flow  Unique BF bec. It flows against gravity  Poor collateral BF

 Two internal carotid arteries and two vertebral

arteries  Empty into the dural sinuses

 CNS is inaccessible to many substances  Many substances cannot reach the neurons

of the CNS  Formed by the endothelial cells of the brains capillaries, which form continuous tight junctions, creating BBB to macromolecules  Must filter through the capillary endothelial cells and astrocytes  Can be altered by trauma, cerebral edema and hypoxia

 Basic functional unit

of the brain  Composed of a cell body, dendrite and an axon

 Dendrite- branch

type structure with synapses for receiving electrochemical messages  Axon long projection that carries impulses away from the cell body

 Acetycholine  Dopamine  Epinephrine and Norepinephrine  GABA (inhibitory)  Serotonin ( depression,  Glutamine (excitatory




5 categories:

 1. Cerebral function- LOC, mental status  2. Cranial nerves  3. Motor function  4. Sensory function  5. Reflexes


Neuro Check  Level of consciousness  Pupillary size and response  Verbal responsiveness  Motor responsiveness  Vital signs


 HISTORY  A confused client becomes an unreliable

source of history

A. Health assessment interview to collect subjective data 1. If clients ability to communicate is challenged by altered level of consciousness, interviewer may discuss with family member or close friend 2. If client has a health problem involving neurologic function, determine  a. Onset  b. Characteristics and course  c. Severity  d. Precipitating and relieving factors  e. Associated symptoms noting timing and circumstances

3. Questions about present health status include a. Numbness or tingling sensations b. Tremors, problems with coordination or balance c. Loss of movement of any part of the body d. Difficulty with speaking or senses e. Information about memory f. Feeling state, e.g. anxious, depressed g. Changes in sleep patterns h. Ability to perform self-care and ADL i. Sexual activity j. Weight changes k. Prescribed and over the counter medications, frequency of use and duration

4. Determine history of a. Seizures, fainting, dizziness, headaches b. Trauma, tumors, surgery involving brain, spinal cord, nerves c. Diseases that might affect neurologic function 1. Cardiac disease 2. Strokes 3. Pernicious anemia 4. Sinus infections 5. Liver dysfunctions 6. Diabetes mellitus 7. HPT 8. Mental health problems

B. Physical assessment to collect objective data a. Unilateral neglect b. Poor hygiene and grooming c. Abnormal gait and posture d. Emotional swings, personality changes e. Masklike appearance on face f. Apathy

g. Aphasia (defective or absent language function): TIAs, strokes; strokes involving posterior or anterior artery involve receptive aphasia h. Dysphonia (change in tone of voice): strokes of posterior inferior cerebral artery, paralysis of vocal cords, cranial nerve X

i. Dysarthria (difficulty in speaking): strokes involving anterior inferior and superior cerebral arteries, lesions involving UMN, LMN, cerebellum, extrapyramidal tract j. Decreased level of consciousness: brain trauma, infections, TIAs, stroke, brain tumors k. Confusion, coma: strokes affecting vertebralbasilar arteries

2. Cognitive function assessment with abnormal findings  a. Disorientation to time and place: stroke of right cerebral hemisphere  b. Memory deficits: anterior cerebral artery and vertebralbasilar artery  c. Perceptual deficits: strokes of middle cerebral artery, brain trauma, dementing conditions  d. Impaired cognition: strokes of middle cerebral artery, cerebral trauma, brain tumors

 Assess the degree of wakefulness/alertness  Note the intensity of stimulus to cause a

response  Apply a painful stimulus over the nailbeds with a blunt instrument  Ask questions to assess orientation to person, place and time

Cerebral function
 Utilize the Glasgow Coma Scale  An easy method of describing mental status

and abnormality detection  Tests 3 areas- eye opening, verbal response and motor response  Scores are evaluated- range from 3-15  No ZERO score

Glasgow Coma Scale

Glasgow Coma Score Eye Opening (E) Verbal Response (V) Motor Response (M)

Glasgow Coma Scale

Glasgow Coma Score 8 and Below= COMA!

Glasgow Coma Scale

Glasgow Coma Score  Eye Opening (E) 4=Spontaneous 3=To voice (when told to) 2=To pain 1=None (No response)

Glasgow Coma Scale

Glasgow Coma Score  Verbal Response (V) 5=Normal/oriented 4=Disoriented/CONFUSED 3=Words, but incoherent/ inappropriate 2=Incomprehensible/mumbled words 1=None

Glasgow Coma Scale

Glasgow Coma Score  Motor Response (M) 6=Normal- obeys command 5=Localizes pain 4=Withdraws to pain (Flexion) 3=Decorticate posture 2=Decerebrate posture 1=None (flaccid)

Cranial Nerve Function: Cranial Nerve 1- Olfactory

 Check first for the patency of the nose  Instruct to close the eyes  Occlude one nostrils at a time  Hold familiar substance and asks for the

identification  Repeat with the other nostrils  PROBLEM- ANOSMIA- loss of smell

Cranial Nerve Function: Cranial Nerve 2- Optic

 Check the visual acuity with the use of the

Snellen chart  Check for visual field by confrontation test  Check for pupillary reflex- direct and consensual  Fundoscopy to check for papilledema

Snellen chart

Cranial Nerve Function: Cranial Nerve 3, 4 and 6

 Assess simultaneously the movement of the

extra-ocular muscles Deviations:  Opthalmoplegia- inability to move the eye in a direction  Diplopia- complaint of double vision

Cranial Nerve Function: Cranial Nerve 5 -trigeminal

 Sensory portion- assess for sensation of the

facial skin  Motor portion- assess the muscles of mastication  Assess corneal reflex

Cranial Nerve Function: Cranial Nerve 7 -facial

 Sensory portion- prepare salt, sugar, vinegar.

Place each substance in the anterior two thirds of the tongue, rinsing the mouth with water  Motor portion- ask the client to make facial expressions, ask to forcefully close the eyelids

Cranial Nerve Function: Cranial Nerve 8- vestibulo-auditory

 Test patients hearing acuity  Observe for nystagmus and disturbed


Cranial Nerve Function: Cranial Nerve 9- glossopharyngeal

 Together with Cranial nerve 10 vagus  Assess for gag reflex  Watch the soft palate rising after instructing

the client to say AH  The posterior one-third of the tongue is supplied by the glossopharyngeal nerve

Cranial Nerve Function: Cranial Nerve 11- accessory

 Press down the patients shoulder while he

attempts to shrug against resistance

Cranial Nerve Function: Cranial Nerve 12- hypoglossal

 Ask patient to protrude the tongue and note

for symmetry

ASSESS Motor function

 Assess muscle tone and strength by asking

patient to flex or extend the extremities while the examiner places resistance  Grading of muscle strength

Muscle Motor Grading:

5/5 normal active movement, full range of motion against full resistance 4/5 active movement, full ROM against moderate resistance 3/5 active movement, full ROM against gravity 2/5 active movement, full ROM w/ gravity eliminated(horizotal/side to side) 1/5 palpable or visible contraction 0/5 no movement, total paralysis

Assessing the motor function of the cerebellum

 Test for balance- heel to toe  Test for coordination- rapid alternating

movements and finger to nose test

 ROMBERGs is actually a test for the

posterior spinothalamic tract

Assessing the motor function of the brainstem

Test for the Oculocephalic reflex- dolls eye  Normal response- eyes appear to move opposite to the movement of the head  Abnormal- eyes move in the same direction

Assessing the motor function of the brainstem

Test for the Oculovestibular reflex  Slowly irrigate the ear with cold water and warm water  Normal response- cOld- OppOsite, wArMsAMe

Assessing the sensory function

 Evaluate symmetric areas of the body  Ask the patient to close the eyes while testing  Use of test tubes with cold and warm water  Use blunt and sharp objects  Use wisp of cotton  Ask to identify objects placed on the hands  Test for sense of position

Assessing the reflexes

 Deep tendon reflexes

Biceps (C5-C6) Triceps (C6-C8) Brachioradialis (C5-C6) Patellar Assessing the sensory function Achilles

Assessing the reflexes

 Superficial reflexes  Abdominal (T9-T10)  Cremasteric (L1-L2)  Anal (S3-S5)  Pathologic reflex  Babinski- stroke the lateral aspect of the soles doing an inverted J  (+)- DORSIFLEXION of the Big toe with fanning

out of the little toes

Grading of reflexes
Deep tendon reflex  0- absent  + present but diminished  ++ normal average  +++ increased but not necessary abnormal  ++++ hyperactive or clonic Superficial reflex  0 absent  +present

. Reflex assessment with abnormal findings  a. Hyperactive reflexes: lesions affecting UMN  b. Decreased reflexes: LMN involvement  c. Clonus of foot (hyperactive, rhythmic dorsiflexion and plantar flexion of foot): UMN disease  d. Superficial reflexes (such as abdominal) and cremasteric reflex may be absent with LMN and UMN diseases  e. Positive Babinski reflex (dorsiflexion of big toe with fanning of other toes): UMN diseases of pyramidal tract

Special neurologic assessment with abnormal findings Positive Brudzinskis sign (pain, resistance, flexion of hips and knees when head flexed to chest with client supine) indicates meningeal irritation

Abnormal Reflex
Positive Brudzinskis sign (pain, resistance, flexion of hips and knees when head flexed to chest with client supine) indicates meningeal irritation

Positive Kernigs sign (excessive pain and/or resistance when examiner attempts to straighten knees with client supine and knees and hips flexed) indicates meningeal irritation

Positive Babinski reflex (dorsiflexion of big toe with fanning of other toes): UMN diseases of pyramidal tract

 Decorticate posturing (upper arms close to

sides, elbows, wrists and fingers flexes, legs extended with internal rotation, feet are flexed: body parts pulled into core of body): lesions of corticospinal tracts

Decerebrate posturing (neck extended with jaw clenched, arms pronated, extended, close to sides, legs are extended straight out and feet plantar flexed): lesions of midbrain, pons, diencephalon

b. Positive Kernigs sign (excessive pain and/or resistance when examiner attempts to straighten knees with client supine and knees and hips flexed) indicates meningeal irritation c. Decorticate posturing (upper arms close to sides, elbows, wrists and fingers flexes, legs extended with internal rotation, feet are flexed: body parts pulled into core of body): lesions of corticospinal tracts d. Decerebrate posturing (neck extended with jaw clenched, arms pronated, extended, close to sides, legs are extended straight out and feet plantar flexed): lesions of midbrain, pons, diencephalon

Diagnostic Test

Skull and spinal x-ray - identify fractures dislocation. Compression, spinal cord problem Nursing Care - provide nursing support for the confused or combative patient - maintain immobilization - remove metal items

b. CT Scan - detect intracranial bleeding, space occupying lesion, cerebral edema. Hydrocephalus, infarction Nursing Care a. Assess for allergies b. Instruct to lie still and flat c. Inform pt that there may be hot, flushed sensation and metallic taste in the mouth d. Treat allergic reaction

c. Magnetic Resonance Imaging - provides more detailed pictures -Patients with pacemakers, orthopedic metal prosthesis and implanted metal devices cannot undergo this procedure


Withhold medications that may interfere with the results- anticonvulsants, sedatives and stimulants Wash hair thoroughly before procedure

Lumbar tap Contraindications:


Unstable vital signs or cardiopulmonary compromise space occupying lesions infections on the site hematologic problems

CSF obtained from LUMBAR Space bet. L4 & L5

1. skin/superficial fascia 2. Ligaments 3. Epidural Space 4. Dura mater 5. Subdural space 6. Archnoid space 7. Subarachnoid space

Don't let people drive you crazy when you know it's in walking distance.

Thank You.

Nursing Care of Client with Intracranial Disorders


 It is a function and symptom of multiple

pathophysiologic phenomena  Not a disorder  Causes: head injury, toxicity and metabolic derangement  Disruption in the basic functional units or neurotransmitters results in faulty impulse transmission

LEVEL OF CONSCIOUSNESS - awake, alert and responsive? - Assess different LOCs: 1. ALERT - speak in a normal voice - patient opens eyes, looks at you and responds fully and appropriately to stimuli

2. LETHARGY - Speak in a loud voice - Appears drowsy but opens the eyes and looks at you, responds to questions, and then falls asleep

3. OBTUNDED - Shake patient gently as if awakening the sleeper - Opens the eyes and looks at you, but responds slowly and is somewhat confused - Alertness and interest in the environment are decreased


Apply a painful stimulus


Pinching a tendon Rubbing the sternum Roll a pencil across a nail bed

Arouses from sleep after a painful stimulus Verbal responses are slow or absent Minimal awareness of self or environment

5. COMA - Apply repeated painful stimuli - Remains unarousable with eyes closed - No evident response to inner need or external stimuli

Assessment  Orientation to time, place and person  Motor function


Decerebrate Decorticate

 Sensory function

 Patient is not oriented  Patient does not follow command  Patient needs persistent stimuli to be awake  COMA= clinical state of unconsciousness

where patient is NOT aware of self and environment


unresponsiveness to the environment in which the patient makes no movement or sound but sometimes opens the eyes  PERSISTENT VEGETATIVE condition in which the patient is described as wakeful but devoid of conscious content, w/o cognitive or affective mental function

 1. 2. 3. 4. 5. 6.

Etiologic Factors Head injury Stroke Drug overdose Alcoholic intoxication Diabetic ketoacidosis Hepatic failure

ASSESSMENT 1. Behavioral changes initially 2. Pupils are slowly reactive 3. Then , patient becomes unresponsive and pupils become fixed dilated

Glasgow Coma Scale is utilized


Respiratory failure Pneumonia Pressure ulcers Aspiration Deep vein thrombosis

First priority of treatment is to obtain and maintain a patent airway

Nursing intervention
Nursing Intervention 1. Maintain patent airway  Elevate the head of the bed to 30 degrees  Suctioning 2. Protect the patient  Pad side rails  Prevent injury from equipments, restraints and etc.

Nursing Intervention 3. Maintain fluid and nutritional balance  Input an output monitoring  IVF therapy  Feeding through NGT 4. Provide mouth care  Cleansing and rinsing of mouth  Petrolatum on the lips

Nursing Intervention 5. Maintain skin integrity  Regular turning every 2 hours  30 degrees bed elevation  Maintain correct body alignment by using trochanter rolls, foot board 6. Preserve corneal integrity  Use of artificial tears every 2 hours

Nursing Intervention 7. Achieve thermoregulation  Minimum amount of beddings  Rectal or tympanic temperature  Administer acetaminophen as prescribed 8. Prevent urinary retention  Use of intermittent catheterization

Nursing Intervention 9. Promote bowel function  High fiber diet  Stool softeners and suppository 10. Provide sensory stimulation  Touch and communication  Frequent reorientation

Nursing diagnosis
 Ineffective airway clearance related to altered

LOC  Risk of injury related to decreased LOC  Deficient fluid volume related to inability to take fluids by mouth  Risk for impaired skin integrity related to immobility

 One of the most common ailments  Generally classified into 3 categories:

a. migraine b. tension c. cluster

 Causes of headache are multiple

Acute SAH, hemorrhagic stroke, meningitis, seizure, acutely elevated ICP, hypertensive encephalopathy, post-LP, ocular dse., new migraine headache

Subacute temporal arteritis, intracranial tumor, subdural hematoma, pseudotumor cerebri, trigeminal/glossopharyngeal neuralgia, postherpetic neuralgia, HTN

chronic/episodic migraine, cluster headache, tension headache, sinusitis, dental dse., neck pain

 Is the headache new or old?  Characteristics? Intensity, quality, location,

duration  Associated symptoms?  Neurologic symptoms?  If an SAH is suspected with negative head CT, LP is mandatory  CT w/out contrast

Migraine headache
 Most commonly affects women  (+) family history  Unkonwn cause but likely related to vascular

and brain neurotransmitters (serotonin)  Triggers include: foods, fasting stress, menses, OCPs, bright-lights


a. gradual onset severe unilateral b. throbbing pain that may become bilateral c. lasts 4 to 72 hours d. maybe preceded by sensory, motor, or mood alterations (AURA) e. nausea, vomiting and photophobia

Cluster headache
 Men > women  Pathogenesis: increased HISTAMINE


a. pain is severe, unilateral, involving the face, occurs on the same side and on the same time of the day, sometimes at night b. attacks last 20 minutes to 2 hours c. occurs in clusters of 2 to 8 weeks d. associated with unilateral excessive tearing, redness of the eye, nasal congestion, facial swelling, flushing and sweating

Tension headache
 Most common type of headache diagnosed in

adults  Result from irritation of sensitive nerve endings in the head, jaw and neck caused by prolonged muscle contraction


a. dull, bandlike pain and pressure in the back of the head and neck, across forehead, bitemporal areas; dull persistent ache; tender spots of head and neck

Collaborative Management:
 Therapeutic interventions:

1. non-pharmacologic: relaxation techniques 2. avoidance of TYRAMINE containing foods (cheese or chocolates) 3. identification of other triggers such as skipping of meals, intake of certain spices and preservatives, withdrawal from caffeine 4. inhalation of 100% O2 to abort cluster headache

 Pharmacologic interventions:

1. aspirin, acetaminophen, NSAIDs 2. antihistamines and decongestant 3. methysergide, ergotamine, sumatriptan 4. beta-adrenergic blockers, Ca channel blockers or antidepressants 5. corticosteroids 6. opioid analgesics, muscle relaxants and antianxiety

Drug Alert: vasoconstrictors and 5HT agonists are contraindicated in patients with uncontrolled HTN, CAD, hemiplegic migraine and PVD

Nursing Diagnoses:
 Acute pain  Disturbed sensory perception  Ineffective coping  Nausea

Nursing Interventions:
 Supportive care:

1. reduce environmental stimuli 2. to relieve tension headaches: a. suggest light massage of tight muscles in neck, scalp, and back b. apply warm, moist heat to areas of muscle tension c. teach progressive muscle relaxation

3. administer abortive and preventive medications as directed 4. encourage pt. to lie down and attempt to sleep 5. encourage adequate nutrition, rest and relaxation 6. review coping mechanisms and strengthen positive ones

 Education and health maintenance

1. teach proper administration of medications: a. Sumatriptan SC with autoinjection for quick relief or given orally b. oral and nasal fomulations 5HT agonist c. Ergotamine metered dose inhaler

2. teach patient about the adverse effects of headache medications. a. Ergot derivatives - numbness, coldness, paresthesias and pain of extremities b. Sumatriptan chest pain, wheezing, swelling of lips and flushing c. Beta-adrenergic blocker & Ca channel light headeness and hypotension

Intracranial Pressure
A.Intracranial Pressure (ICP) 1. Pressure within cranial cavity measured within lateral ventricles 2. Transient increases occur with normal activities coughing, sneezing, straining, bending forward

3. a. b. c. d. e. f. g.

Sustained increases associated with Cerebral edema Head trauma Tumors Abscesses Stroke Inflammation Hemorrhage

B. Monro-Kellie hypothesis 1. Within skull there are 3 components that maintain state of dynamic equilibrium a. Brain (80%) b. Cerebrospinal fluid (10%) c. Blood (10%) 2. If volume of any one increases the volume of others must decrease to maintain normal pressure

C. Normal intracranial pressure 1. 5 15 mm Hg, with pressure transducer with head elevated 30 degrees 10-20mmHg (Brunner)

D. Background regarding regulation of ICP Pathophysiology  The cranium only contains the brain substance, the CSF and the blood/blood vessels  MONRO-KELLIE hypothesis- an increase in any one of the components causes a change in the volume of the other  Any increase or alteration in these structures will cause increased ICP

Pathophysiology Compensatory mechanisms:  1. Increased CSF absorption  2. Blood shunting  3. Decreased CSF production

Pathophysiology Decompensatory mechanisms:  1. Decreased cerebral perfusion  2. Decreased PO2 leading to brain hypoxia  3. Cerebral edema  4. Brain herniation

Decreased Blood Flow

 Vasomotor reflexes are stimulated initially

slow bounding pulses  Increased concentration of carbon dioxide will cause VASODILATION increased flow increased ICP

Abnormal accumulation of fluid in the intracellular space, extracellular space or both.

Results from an excessive increase in ICP when the pressure builds up and the brain tissue presses down on the brain stem

Cerebral response to increased ICP

Steady perfusion up to 40 mmHg 2. Cushings response

Vasomotor center triggers rise in BP to increase ICP Sympathetic response is increased BP but the heart rate is SLOW Respiration becomes SLOW

CLINICAL MANIFESTATIONS Early manifestations:  Changes in the LOC- usually the earliest  Pupillary changes- fixed, slowed response  Headache  vomiting

CLINICAL MANIFESTATIONS late manifestations:  Cushing reflex- systolic hypertension, bradycardia and wide pulse pressure  bradypnea  Hyperthermia  Abnormal posturing

Nursing interventions: Maintain patent airway  1. Elevate the head of the bed 15-30 degrees- to promote venous drainage  2. assists in administering 100% oxygen or controlled hyperventilation- to reduce the CO2 blood levels constricts blood vessels reduces edema

Nursing interventions  3. Administer prescribed medications- usually


Mannitol- to produce negative fluid balance corticosteroid- to reduce edema anticonvulsants-p to prevent seizures

Nursing interventions  4. Reduce environmental stimuli  5. Avoid activities that can increase ICP like valsalva, coughing, shivering, and vigorous suctioning

Nursing interventions  6. Keep head on a neutral position. AVOIDextreme flexion, valsalva  7. monitor for secondary complications

Diabetes insipidus- output of >200 mL/hr SIADH

Seizure Disorder
 also known as convulsions, epileptic

seizures, and if recurrent epilepsy

Sudden alterations in normal brain activity that cause distinct behavior and body function Pathophysio: poorly understood but may be related to metabolic and electrochemical factors at the cellular level(fever, rapid withdrawal from alcohol, electrolyte imbalance, brain pathology)

PREDISPOSING FACTORS: 1. head or brain trauma 2. tumors 3. cranial surgery 4. metabolic disorders 5. CNS infections 6. circulatory disorders 7. drug toxicity/drug withdrawal states 8. congenital neurodegenerative disorders

classified as: a. partial seizures INVOLVES 1 HEMISPHERE 1. simple partial motor, somatosensory an psychomotor symptoms w/o impairment of consciousness - can progress to complex partial

2. COMPLEX PARTIAL SEIZURES - manifest impairment of consciousness w/ or w/o simple partial symptoms - can secondarily become generalized

2. Generalized seizures: involves both brain hemispheres; consciousness always impaired a. Absence seizures (petit mal) - characterized by sudden brief cessation of all motor activity, blank stare and unresponsiveness often with eye fluttering - lost of contact w/ environment for 5 to 30 secs. - resumes activity and is not aware of seizure

b. Tonic-clonic seizures (GRAND MAL) 1. Most common type in adults 2. Preceded by aura, sudden loss of consciousness 3. Tonic phase: rigid muscles, incontinence (LAST 30 TO 60 SECS.) 4. Clonic phase: altered contraction, relaxation; eyes roll back, froths at mouth (LAST SEVERAL MINUTES) 5. Postictal phase: unconscious and unresponsive to stimuli (UP TO SEVERAL HOURS)

Status Epilepticus - acute, prolonged, repetitive seizure activity - series of generalized seizures w/o return to consciousness between attacks - continuous clinical or electrical seizures lasting at least 5 minutes, even w/o impairment of consciousness

CRITERIA: 1. Age: 9 mos. To 5 yrs. 2. Generalized tonic-clonic lasting not more than 15 mins 3. Onset of fever > 39C within hours of the seizure 4. Family history of BFC 5. No neurologic deficit that would explain the seizure

Diagnostic Tests 1. Neurologic exam 2. EEG to confirm diagnosis and locate lesion 3. Xray, MRI, CT scan identify any neurologic abnormalities 4. Lumbar puncture may be done if infection suspected 5. CBC, electrolytes, BUN, blood glucose 6. ECG to determine cardiac dysrhythmias

Therapeutic Interventions:
1. Maintain good nutrition/sleep hygiene/avoid stress 2. Ketogenic diet a. precisely calculated portions of CHON and fats w/o CHO b. IV fluids should be dextrose free, and all medications should be in sugarfree suspensions

a. Antiepileptic drugs Phenytoin (Dilantin) for partial and generalized seizures except absence seizures Nsg. Considerations: 1. Encourage good oral hygiene 2. therapeutic range is 10 to 20 mcg/ml, administer IV w/ normal saline 3. watchout SE: rash, nystagmus, ataxia, drug-induced lupus, anemia,

Phenobarbital(Luminal) - for partial and generalized seizures (tonic-clonic) Nsg. Considerations: 1. contraindicated in hepatic or renal dysfunction 2. avoid use w/ other CNS depressants 3. watchout SE: hyperactivity, sedation, nystagmus, ataxia

Valproic Acid (Depakene)/Divalproex Na (Depakote) sole therapy for absence seizures and adjunct therapy for partial and generalized seizures Nsg. Considerations: 1. liver function test and platelet count should be monitored monthly for at least 1st 6 months 2. take w/ food to minimize adverse effect 3. avoid use w/ other CNS depressants 4. watchout SE: hepatotoxicity, nausea and vomiting, abdominal pain, anemia, decreased WBC & platelet

Carbamazepine (Tegretol) refractory partial and generalized seizures Nsg. Considerations: 1. use cautiously in patients w/ existing cardiac, renal, or liver probs. 2. give w/ food 3. watchout SE: dizziness, nausea and vomiting, liver dysfunction, anemia, decreased WBC & platelet

Gabapentin (Neurontin) adjunct treatment of partial and secondarily generalized seizures Nsg. Considerations: 1. serum levels not necessary 2. watchout SE: somnolence, dizziness, ataxia, headache, tremor, vomiting, nystagmus, fatigue

NURSING INTERVENTIONS: 1. Monitor the entire seizure event, including prodromal signs, seizure behavior, and postictal state 2. Monitor serum levels for therapeutic range of medications 3. Monitor pt. for adverse reactions of medications 4. Monitor CBC, UA, and liver function

Surgery: if all attempts to control seizures are not successful 1. May attempt to excise tissue involved in seizure activity 2. EEG done during surgery to identify epileptogenic focus

Care of client during a seizure 1. Protect client from injury and maintain airway 2. Do not force anything into clients mouth 3. Loosen clothing around neck

Health Promotion: Stress the following to clients 1. Importance of medical follow-up, taking prescribed medications 2. Driving privileges are prohibited in clients with seizure disorders; drivers licenses are reinstated after seizure free period and statement from health care practitioner 3. Client needs proper identification 4. Family members need to be educated in preventing injury if seizure occurs

Nursing Diagnoses 1. Risk for Ineffective Airway Clearance 2. Anxiety Home Care 1. Education of client and family regarding seizure disorder; safety measures, avoidance of alcohol and caffeine 2. Referral to support group, national organizations

B. Mechanisms of trauma 1. Acceleration injury: head struck by moving object 2. Deceleration injury: head hits stationary object 3. Acceleration-deceleration (coup-contrecoup phenomenon): head hits object and brain rebounds within skull 4. Deformation: force deforms and disrupts body integrity: skull fracture

c. Basilar: 1. Involves base of skull and usually involve extension of adjacent fractures 2. If dura disrupted may have leakage of CSF occurring as a. Rhinorrhea: through nose b. Otorrhea: through ear

CNS infection
A. CNS infections 1. Most common is bacterial meningitis 2. Mortality rate 25% in adults 3. Meningococcal occurs in epidemics with people living in close contact 4. Pneumococcal effects very young and very old

B. Risk Factors 1. High risk for old and young 2. High risk for clients with debilitating diseases, or immunosuppressed

C. Pathophysiology 1. Pathogens enter CNS and meninges causing inflammatory process, which leads to inflammation and increased ICP 2. May result in brain damage and lifethreatening complications

D. Meningitis 1. Inflammation of pia mater, arachnoid, and subarachnoid space 2. Spreads rapidly through CNS because of circulation of CSF around brain and spinal cord 3. May be bacterial, viral, fungal, parasitic in origin 4. Infection enters CNS though invasive procedure or through bloodstream, secondary to another infection in body

E. Bacterial meningitis 1. Causative organisms: Neisseria meningitis, meningoccus, Streptococcus pneumoniae, Haemophilus influenzae, E. Coli 2. Risk factors: head trauma with basilar skull fracture, otitis media, sinusitis, immunocompromised, neurosurgery, systemic sepsis

3. Manifestations a. Fever chills b. Headache, back and abdominal pain c. Nausea and vomiting d. Meningeal irritation: nuchal rigidity, positive Brudzinskis sign, Kernigs sign, photophobia e. Meningococcal meningitis: rapidly spreading petechial rash of skin and mucous membranes f. Increased ICP: decreased LOC, papilledema

4. a. b. c.

Complications Arthritis Cranial nerve damage (deafness) Hydrocephalus

F. Viral meningitis 1. Less severe, benign course with short duration 2. Intense headache with malaise, nausea, vomiting, lethargy 3. Signs of meningeal irritation

G. Encephalitis 1. Acute inflammation of parenchyma of brain or spinal cord 2. Usually caused by virus 3. Inflammation occurs with manifestations similar to meningitis 4. LOC deteriorates and client may become comatose 5. Arboviruses are agents including West Nile virus

H. Brain abscess 1. Infection with a collection of purulent material within brain tissue usually in cerebrum 2. Causes include open trauma and neurosurgery; infections of ear, sinuses 3. Common pathogens are streptococci, staphylococci, bacteroids

4. Becomes space-occupying lesion 5. At risk for infection and increased ICP 6. Manifestations a. General symptoms associated with acute infectious process b. Client develops seizures, altered LOC, signs of increased ICP c. Specific neurologic symptoms are related to location 7. May be drained surgically, if considered feasible

I. Collaborative Care 1. Bacterial meningitis: requires immediate treatment and isolation of client 2. Viral meningitis: supportive treatment and management of client symptoms 3. Brain abscess treatment focuses on antibiotic therapy

J. Diagnostic Tests 1. Lumbar puncture: definitive test for bacterial meningitis demonstrating infection: turbid cloudy appearance, increased WBC, gram stain, culture 2. CT scan, MRI

K. Medications 1. Meningitis: immediate treatment with effective antibiotics for 7 21 days; according to culture results; dexamethasone to suppress inflammation 2. Encephalitis: viral treated with anti-viral medications 3. Brain abscess: antibiotic therapy, which may include intraventricular administration; anticonvulsant medications, antipyretics

L. Health Promotion 1. Vaccinations for meningococcal, pneumococcal, hemophilic meningitis 2. Prophytlactic rifampin for persons exposed to meningococcal meningitis 3. Mosquito control 4. Prompt diagnosis and treatment of clients with infections 5. Asepsis care for clients with open head injury or neurosurgery

M. Nursing Diagnoses 1. Ineffective Protection 2. Risk for Deficient Fluid Volume

N. Home Care 1. Client education for future prevention 2. Complete medications and treatment plan

Brain Tumor
A. Description 1. Growths within cranium including tumors of brain tissue, meninges, pituitary gland, blood vessels 2. May be benign or malignant, primary or metastatic 3. May be lethal, due to location (inaccessible to treatment) and capacity to impinge on CNS structures

4. In adults most common tumor is glioblastoma followed by meningioma and cytoma 5. Cause is unknown: factor associated include heredity, cranial irradiation, exposure to some chemicals

6. Tumors within brain a. Compress or destroy brain tissue b. Cause edema in adjacent tissues c. Cause hemorrhage d. Obstruct circulation of CSF, causing hydrocephalus 7. Estimated 25% persons with cancer develop brain metastasis, often multiple sites throughout the brain

B. Manifestations: Multiple depending on location of lesion and rate of growth 1. Changes in cognition and LOC 2. Headache usually worse in morning 3. Seizures 4. Vomiting 5. Manifestations associated with cerebral edema, increased ICP, cerebral ischemia leading to brain herniation syndromes

C. Collaborative Care 1. Effective treatment includes chemotherapy, radiation therapy, and/or surgery 2. Treatment depends on size and location of tumor, type of tumor, neurologic deficits, and clients over all condition

D. Diagnostic Tests 1. CT scan or MRI: determine tumor location and extent 2. Arteriography 3. EEG: information about cerebral function, seizure data 4. Endocrine studies if pituitary tumor suspected

E. Treatment 1. Medications: Chemotherapy, corticosteroids, anticonvulsants 2. Surgery a. Purposes include tumor excision, reduction, or for symptom relief b. Craniotomy: location according to approach to tumor 3. Radiation: Alone or as adjunctive therapy

F. Nursing Care 1. Support during diagnosis and management through selected treatment 2. Nursing care involves interventions to deal with altered LOC, increased ICP, and seizures

G. 1. 2. 3. 4. 5.

Nursing Diagnoses Anxiety Risk for Infection Ineffective Protection Acute Pain Disturbed Self-esteem

H. Home Care 1. Education, support to client and family 2. Instructions for treatment plan and followup care 3. Referral to home care agencies 4. Referrals to therapies, community resources, support groups as appropriate


Nursing Care of Clients with Cerebrovascular Accident

 An umbrella term that refers to any

functional abnormality of the CNS related to disrupted blood supply  Similaraties between The 2 broad types, overall the etiology, pathophysiology, medical & surgical management, and nursing care differs

 Can be divided into two major categories

1. Ischemic stroke- caused by thrombus and embolus 2. Hemorrhagic stroke- caused commonly by hypertensive bleeding

Stroke (CVA)

Ischemic (85%)

Hemorrhagic (15%)

Cerebral thrombosis

Cerebral embolus(20%)

Intracerebral Hge


Large artery thrombosis(20%)

Lacunar infarct(25%)

The stroke continuum  1. TIA- transient ischemic attack, temporary neurologic loss less than 24 hours duration  2. Reversible Neurologic deficits- s/sx last more the 24 hrs. resolve in days w/o permanent neurologic deficit  3. Stroke in evolution- worsening of neuro s/sx over several minutes or hours  4. Completed stroke- indicates no further progression of the hypoxic insult

General manifestations

Anterior cerebral artery:  Weakness  Numbness on the opposite side  Personality changes  Impaired motor and sensory function

Middle cerebral artery:  Aphasia  Dysphagia  HEMIPARESIS on the OPPOSITE side- more severe on the face and arm than on the legs

Posterior cerebral artery:  Visual field defects  Sensory impairment  Coma  Less likely paralysis


 There is disruption of the cerebral blood flow

due to obstruction by embolus or thrombus

Non-modifiable  Advanced age  Gender  race Modifiable  Hypertension  Cardio disease  Obesity  Smoking  Diabetes mellitus  hypercholesterolemia

Pathophysiology of ischemic stroke

 Disruption of blood supply  Ischemic cascade (PENUMBRA REGION)  Anaerobic metabolism ensues  Decreased ATP production leads to impaired

membrane function  Cellular injury and death can occur


DIAGNOSTIC test  1. CT scan infarct vs. hge  2. MRI- infarct, brainstem vs. cererebellum  3. Angiography


CLINICAL MANIFESTATIONS (table 62.2 , p. 1890, 10th ed.,p. 2208-2209, 11th ed., p. 1898 12th ed. BRUNNER)  1. Numbness or weakness  2. confusion or change of LOC  3. motor and speech difficulties  4. Visual disturbance  5. Severe headache


Motor Loss  Hemiplegia  Hemiparesis


Communication loss  Dysarthria= difficulty in speaking  Aphasia= Loss of speech  Apraxia= inability to perform a previously learned action


Perceptual disturbances  Hemianopsia Sensory loss  paresthesia

 Paralysis/weakness on    

 Paralysis/weakness on     

the right side Right visual field deficit Aphasia Altered intellectual ability Slow, cautious behavior

the left side Left visual field deficit Spatial-perceptual deficits Increased distractibility Impulsive behaviour and poor judgement Lack of awareness of deficits

Patient recovering from an Ischemic Stroke

NURSING INTERVENTIONS: ACUTE 1. Ensure patent airway 2. Keep patient on LATERAL position 3. Monitor VS and GCS, pupil size 4. IVF is ordered but given with caution as not to increase ICP 5. NGT inserted 6. Medications: Steroids, Mannitol (to decrease edema), Diazepam


NURSING INTERVENTIONS: Hospital 1. Improve Mobility and prevent joint deformities  Correctly position patient to prevent contractures

Place pillow under axilla Hand is placed in slight supination Change position every 2 hours


NURSING INTERVENTIONS 2. Enhance self-care  Carry out activities on the unaffected side  Prevent unilateral neglect- place some items on the affected side!!!  Keep environment organized  Use large mirror


NURSING INTERVENTIONS 3. Manage sensory-perceptual difficulties  Approach patient on the Unaffected side  Encourage to turn the head to the affected side to compensate for visual loss


NURSING INTERVENTIONS 4. Manage dysphagia  Place food on the UNAFFECTED side  Provide smaller bolus of food  Manage tube feedings if prescribed


NURSING INTERVENTIONS 5. Help patient attain bowel and bladder control  Intermittent catheterization is done in the acute stage  Offer bedpan on a regular schedule  High fiber diet and prescribed fluid intake


NURSING INTERVENTIONS 6. Improve thought processes  Support patient and capitalize on the remaining strengths


NURSING INTERVENTIONS 7. Improve communication  Anticipate the needs of the patient  Offer support  Provide time to complete the sentence  Provide a written copy of scheduled activities  Use of communication board  Give one instruction at a time


NURSING INTERVENTIONS 8. Maintain skin integrity  Use of specialty bed  Regular turning and positioning  Keep skin dry and massage NON-reddened areas  Provide adequate nutrition


NURSING INTERVENTIONS 9. Promote continuing care  Referral to other health care providers


NURSING INTERVENTIONS 10. Improve family coping 11. Help patient cope with sexual dysfunction


MEDICAL MANAGEMENT 1. Pharmacologic:

Aspirin Diazepam to prevent seizures Thrombolytics Stool softeners Antihypertensives Analgesics, Muscle relaxants, STEROIDS

MEDICAL MGNT: 1. TIA/Mild stroke non surgical approach -- platelet inhibiting medications 2. Thrombolytic therapy t-PA administration -- eligibility criteria for t-PA administration -- should be done w/in 3 hrs. -- VS impt -- bleeding- most common S.E.

Eligibility criteria for t-PA administration

 Age 18years and above  Clinical diagnosis of Ischemic stroke  Time of onset of stroke known and is 3 hours or less  Systolic BP 185mmHg, diastolic mmHg  Not a minor stroke or rapidly resolving stroke  No seizure at onset of stroke  Not taking Warfatin (Coumadin)  PTT secs. Or INR 1.7  Not receiving heparin during the past 48 hrs. w/ elevated partial

thromboplastin time  Platelet ct. 100,000/mm  No prior intracranial Hge, neoplasms, AV malformation, or aneurysms

 No major surgical procedures w/in 14 days  No stroke, serious head injury or intracranial

surgery w/in 3 mos.  No gastrointestinal or urinary bleeding w/in 21 days

ISCHEMIC STROKE not receiving t-PA

1. Reduce ICP 2. Maintaining PaCO2 (30-35mmHg) 3. Proper positioning 4. Intubation 5. Continuous hemodynamic monitoring

(<180/100) 6. Neurologic assessment 7. anticoagulant

CVA: Hemorrhagic Stroke

 Normal brain metabolism is impaired by

interruption of blood supply, compression and increased ICP  More sever deficits and longer recovery time  Pathophysio depends on the cause

CVA: Hemorrhagic Stroke

 Sudden and severe headache  Same neurologic deficits as ischemic

stroke  Loss of consciousness  Meningeal irritation  Visual disturbances

Intracerebral Hemorrhage
 Most common in patients w/ HPN and

cerebral atherosclerosis ---causing rupture of the vessels involve usually ARTERIAL  Occurs most commonly in the cerebral lobes, basal ganglia, thalamus and brainstem  Arterial pathology, brain tumor and the use of meds (oral anticoagulant, amphetamines, crack and coccaines)

Intracranial (Cerebral) Aneurysm

 Dilatation of the walls of a cerebral artery that

develops as a result of weakness in the arterial wall  Unknown  Usually happens in the bifurcation of the large Artery at the circle of willis

Arteriovenous Malformation (AVM)

 Due to an abnormality in embryonal

development that leads to a tangle of arteries and veins in the brain w/o capillary bed  (-) capillary beds leads to dilation of the AV and eventual RUPTURES  Cause of He in young adult

Subarachnoid Hemorrhage
 May occur as a result of an AVM, intracranial

aneurysms, trauma, or HPN  Most common cause is a leaking aneurysm in the area of the circle of Willis or a congenital AVM

UNIQUE CLINICAL MANIFESTATIONS: 1. sudden, unusually severe headache and often LOC 2. (+) meningeal irritation 3. Visual disturbances adjacent of oculomotor nerve

CVA: Hemorrhagic Stroke

DIAGNOSTIC TESTS  1. CT scan  2. angiography confirms the dx of an AVM  3. MRI  4. Lumbar puncture (only if with no increased ICP) causes brain herniation and rebleeding

CVA: Hemorrhagic Stroke

NURSING INTERVENTIONS  1. Optimize cerebral tissue perfusion  2. relieve Sensory deprivation and anxiety  3. Monitor and manage potential complications

Medical management: 1. Complete bed rest w/ elastic compression stockings 2. Management of vasospams 3. Surgical and medical treatment to prevent rebleeding

Complications: 1. Rebleeding 2. Cerebral hypoxia 3. Vasospasms 4. Increased ICP 5. Systemic HPN

Acute Stroke

1. Anticoagulant therapy a. Ordered for thrombotic stroke during strokein-evolution b. Contraindicated in completed stroke c. Never used in hemorrhagic stroke d. Prevent further extension of clot ; Heparin, warfarin sodium (Coumadin)

Acute Stroke

2. Thrombolytic therapy: must be given within 3 hours of onset of manifestations and will dissolve clot; recombinant altephase (Activase rt-pa) 3. Antithrombotic: inhibit platelet phase of clot formation; contraindicated with hemorrhagic stroke (aspirin, dipyidamole) 4. Calcium channel blockers: reduce ischemic deficits, death (Nimodipine (Nimotop)) 5. Corticosteroids: used to treat cerebral edema 6. Diuretics: reduce increased intracranial pressure: mannitol, furosemide 7. Anticonvulsants: phenytoin (Dilantin)

1. Surgery  a. Carotid endarterectomy: in clients who have had TIAs  b. Extracranial-intracranial bypass 2. Physical therapy: prevents contractures, improves muscle strength and coordination 3. Occupational therapy: provides assistive devices and plans for regaining lost motor skills 4. Speech therapy: improves communication disorder

Nursing Diagnoses

1. Ineffective Tissue Perfusion: Cerebral; frequent monitoring of neurologic status, cardiac status 2. Impaired Physical Mobility 3. Self-care Deficit 4. Impaired Verbal Communication 5. Impaired Urinary Elimination and Risk for Constipation 6. Impaired Swallowing

1. Motor Deficits a. Affects connections involving motor areas of cerebral cortex, basal ganglia, cerebellum, peripheral nerves b. Produce effects in contralateral side ranging from mild weakness to severe limitation c. Hemiplegia: paralysis of half of body d. Hemiparesis: weakness of half of body e. Flaccidity: absence of muscle tone (hypotonia)

f. Spasticity: increased muscle tone usually with some degree of weakness g. Affected arm and leg are initially flaccid and become spastic in 6 8 weeks, causes characteristic body positioning: 1. Adduction of shoulder 2. Pronation of forearm 3. Flexion of fingers 4. Extension of hip and knee 5. Foot drop, outward rotation of leg, with dependent edema

Sensory-perceptual Deficits
 a. Hemianopsia: loss of half of visual field on

one or both eyes; homonymous hemianopia: same half missing in each eye  b. Agnosia: inability to recognize one or more subjects that were previously familiar: includes visual, tactile, auditory

Sensory-perceptual Deficits

Apraxia: inability to carry out some motor pattern even when strength and coordination is adequate (e.g. getting dressed)  d. Neglect syndrome (unilateral neglect): attention disorder in which client ignores affected part of body; client cannot integrate or use perceptions from affected side of body or from environment on affected side

Communication Disorders
a. Usually result of stroke affecting dominant hemisphere (left hemisphere dominant in 95% right-handed persons; 70% left-handed persons) b. Aphasia: inability to use or understand language

Communication Disorders

Expressive: motor speech problem; client understands what is said but can only respond verbally in short phases: Brocas aphasia  2. Receptive aphasia: sensory speech problem in which one cannot understand spoken or written word; speech may be fluent but with inappropriate content: Wenickes aphasia  3. Mixed or global aphasia: language dysfunction in both understand and expression

Traumatic brain injury

1. CONCUSSION  Involves jarring of head without tissue injury  Temporary loss of neurologic function lasting fore a few minutes to hours

Traumatic brain injury

2. CONTUSION  Involves structural damage  The patient becomes unconscious for hours

Traumatic brain injury

3. Diffuse Axonal injury  Involves widespread damage to the neurons  Patient has decerebrate and decorticate posture

Traumatic brain injury

4. Intracranial hemorrhage Epidural Hematoma- blood collects in the epidural space between skull and dura mater. Usually due to laceration of the middle meningeal artery Symptoms develop rapidly

Traumatic brain injury

4. Intracranial hemorrhage Subdural hematoma- a collection of blood between the dura and the arachnoid mater caused by trauma. This is usually due to tear of dural sinuses or dural venous vessels Symptoms usually develop slowly

Traumatic brain injury

4. Intracranial hemorrhage Intracerebral Hemorrhage and hematoma- bleeding into the substance of the brain resulting from trauma, hypertensive rupture of aneurysm, coagulopahties, vascular abnormalities Symptoms develop insidiously, beginning with severe headache and neurologic deficits

Traumatic brain injury

MANIFESTATIONS  1. Altered LOC  2. CSF otorrhea  3. CSF rhinorrhea  4. Racoon eyes and battle sign

HALO SIGN- blood stain surrounded by a yellowish stain

Traumatic brain injury

NURSING MANAGEMENT 1. Monitor for declining LOC- use of Glasgow 2. Maintain patent airway  Elevate bed, suction prn, monitor ABG

Traumatic brain injury

NURSING MANAGEMENT 3. Monitor F and E balance  Daily weights  IVF therapy  Monitor possible development of DI and SIADH

Traumatic brain injury

4. Provide adequate nutrition 5. Prevent injury  Use padded side rails  Minimize environmental stimuli  Assess bladder  Consider the use of intermittent catheter

Traumatic brain injury

6. Maintain skin integrity  Prolonged immobility will likely cause skin breakdown  Turn patient every 2 hours  Provide skin care every 4 hours  Avoid friction and shear forces

Traumatic brain injury

7. Monitor potential complications  Increased ICP  Post-traumatic seizures  Impaired ventilation

Spinal cord injury

 The most frequent vertebrae C5-C7, T12

and L1  Concussion  Contusion  Compression  Transection

Spinal cord injury

Clinical manifestations  1. Paraplegia  2. quadriplegia  3. spinal shock

Spinal cord injury

 DIAGNOSTIC TEST  Spinal x-ray  CT scan  MRI

Spinal cord injury

 EMERGENCY MANAGEMENT  A-B-C  Immobilization  Immediate transfer to tertiary facility

Spinal cord injury

NURSING INTERVENTION  1. Promote adequate breathing and airway clearance  2. Improve mobility and proper body alignment  3. Promote adaptation to sensory and perceptual alterations  4. Maintain skin integrity

Spinal cord injury


5. Maintain urinary elimination 6. Improve bowel function 7. Provide Comfort measures 8. Monitor and manage complications

Thromboplebhitis Orthostatic hypotension Spinal shock Autonomic dysreflexia

Spinal cord injury

 9. Assists with surgical reduction and

stabilization of cervical vertebral column

Laughing Out Loud

Nursing Care Clients with Degenerative disorder & Motor dysfunction

 Degenerative disorders- demyelinating


Multiple sclerosis Guillain-Barre syndrome

 Degenerative disorders-


Alzheimers disease Parkinsons disease

 Motor dysfunction- cranial nerve


Bells palsy Trigeminal neuralgia Myasthenia gravis

 Motor dysfunction- peripheral

ALZHEIMERS disease (non-demyelenating)

 A progressive, irreversible, degenerative

neurologic disorder that affects the brain resulting in cognitive impairments - Not exclusive in the elderly - 1 10% occurs in middle age  7th decade of life

CAUSES:  Unknown  Potential factors- Amyloid plaques in the brain, Oxidative stress, neurochemical deficiencies

3 stages:

Amnesia Forgetfulness and have diffulty retaining new information Word finding difficulty Poor abstract reasoning Perseveration Floating around


Apraxia Aphasia Agnosia Agraphia Wandering

 Latent/ Severe

Fragmented memory loss Increase irritability Urinary and fecal incontinence Unresponsiveness or coma

CLINICAL MANIFESTATIONS  1. Forgetfulness  2. Recent memory loss  3. Difficulty learning  4. Deterioration in personal hygiene  5. Inability to concentrate

LATE CLINICAL MANIFESTATIONS  6. Difficulty in abstract thinking  7. Difficulty communicating  8. Severe deterioration in memory, language and motor function  9. repetitive action  10. personality changes

DIAGNOSTIC TEST  Health history = Neurologic examination  PET scan  EEG, CT and MRI  Other tests to rule out Vit B deficiencies and hypothyroidism  Autopsy is the most definitive

Drug therapy  1. drugs to treat behavioral symptomsantipsychotics  2. anxiolytics  3. Tacrine HCL(cognex) first meds used, 1993  4. Donepezil (Aricept) 2nd meds, 1997  5. Rivastigmine (Exelon) - 2000

Nursing Interventions  1. Support cognitive function  2. Provide emotional support

3. Establish an effective communication system with the patient and family  Use short simple sentences, words and gestures  Maintain a calm and consistent approach  Attempt to analyze behavior for meaning

4. protect the patient from injury  Provide a safe and structured environment  Requests a family member to accompany client if he wanders around  Keep bed in low position  Provide adequate lightning  Assign consistent caregivers = nightlights are helpful

5. Encourage exercise to maintain mobility 6. Promoting independence in self-care activities - simplify daily activities by organizing them into short, achievable steps so that the patient experience a sense of accomplishment

MULTIPLE SCLEROSIS (demyelenating)

 An auto-immune mediated progressive

demyelinating disease of the CNS  The myelin sheath is destroyed and replaced by sclerotic tissue (sclerosis)

 CAUSE- unknown  Multiple factors- viral infection, environmental

factors, geographic location and genetic predisposition  Exacerbations and remissions  Common in WOMEN ages 20-40

PATHOPHYSIOLOGY  Sensitized T cells will enter the brain and promote antibody production that damages the myelin sheath  Plaques of sclerotic tissues appear on the demyelinated axons interrupting the neuronal transmission

 The most common areas affected are


Optic nerves and chiasm Cerebrum Cerebellum Spinal cord

- Eventually damage axons thus resulting to permanent and irreversible damage

CLINICAL MANIFESTATIONS 1. Primary symptomsa. fatigue- throughout the course b. depression as reaction to diagnosis c. weakness, numbness, difficulty in coordination, loss of balance d. pain occurs in 66% due to demyelination of pain fibers

2. Visual disturbances lesion in the optic nerve a. blurring of vision b. Diplopia initial sign c. patchy blindness (scotoma) d. total blindness CHARCOTS TRIAD Scanning speech Intentional tremors Nystagmus

3. Spasticity (muscle hypertonicity) of the extremities and loss of abdominal reflexes 4. Ataxia 5. Emotional lability and euphoria 6. bladder, bowel and sexual dysfunction

DIAGNOSTIC TESTS  1. MRI- primary diagnostic study  2. CSF Immunoglobulin G

NURSING INTERVENTIONS 1. Promote physical mobility  Exercise  Schedule activity and rest periods  Warm packs over the spastic area  Swimming and cycling are very useful

2. Protect client from injury by providing safety measures


Wide stance walking Use of walking aids Wheelchair

3. Enhance bladder and bowel control


Set a voiding schedule Intermittent bladder catheterization Adequate fluids, dietary fibers and bowel training program

4. Manage speech and swallowing difficulties


Careful feeding, proper positioning, suction machine availability Speech therapist

5. Improve Sensory and Cognitive function


Vision- use eye patch for diplopia Obtain large printed reading materials Offer emotional support Involve the family in the care

6. Strengthen coping mechanism


Alleviate the stress Referral to the appropriate agencies

7. improve self-care abilities


Modify activities according to physical strength Provide assistive devices

8. promote sexual functioning

Refer to sexual counselor


Interferons beta 1a (Avonex) and beta 1b (Betaseron), Glatiramer Acetate (Copaxone), Rebif

ABC and R drugs


Immunosuppresants to stabilize disease process Corticosteroids to reduce edema and inflammatory porcess BACLOFEN for muscle spasms NSAIDS for pain Antidepressants

PARKINSONs Disease (non-demyelenating)

 A slowly progressing neurologic

movement disorder  The degenerative idiopathic form is the most common form

CAUSATIVE FACTORS: unknown  Potential factors: genetics, atherosclerosis, free radical stress, viral infection, head trauma and environmental factors
 Parkinsonian symptoms occur in the 5th

decade of life

Pathophysiology  Decreased levels of dopamine due to destruction of pigmented neuronal cells in the substantia nigra in the basal ganglia  Clinical symptoms do not appear until 60% of the neurons have disappeared

CLINICAL MANIFESTATIONS 1. Tremor- resting, pill-rolling, unilateral (70%) 2. Rigidity- cog-wheel, lead-pipe 3. Bradykinesia- abnormally slow movement

Postural Changes

4. Dementia, depression, sleep disturbances and hallucinations 5. excessive sweating, paroxysmal flushing, orthostatic hypotension

Medications act by:

 Increasing striatal dopaminergic activity  Reducing excessive influence of excitatory

cholinegic neurons on the extrapyramidal tract to restore balance between cholinergic and dopaminergic activities.
 Acting on neurotransmitter pathways other

than the dopaminergic pathway

Medical management  1. Anti-parkinsonian drugs- Levodopa, Carbidopa  2. Anti-cholinergic therapy(Biperiden)  3. Antiviral therapy- Amantadine  4. Dopamine Agonists- bromocriptine and Pergolide, Ropirinole anmd Pramipexole

 5. MAOI  6. Anti-depressants  7. Antihistamine

 Cogentin tremor and rigidity  Artane tremor and rigidity  Parlodel/Permex useful in postponing L-Dopa  Akineton  Benadryl - tremors  Eldepryl (MAOI) inhibits dopamine

breakdown  L Dopa  S inemet/Symmetrel


1. Improve mobility 2. Enhance Self- care activities 3. Improve bowel elimination 4. Improve nutrition 5. Enhance swallowing 6. Encourage the use of assistive devices


7. improve communication 8. Support coping abilities 9. Proper Diet


low protein Excessive vitamin B6 intake (pyridoxine) intake effectiveness of L-dopa Sinemet can discolor urine and perspiration
 Can increase urine glucose intake

Myasthenia gravis (Motor Dysfunction-Peripheral)

 A sporadic, but progressive weakness and

abnormal fatigability of striated muscles which are exacerbated by exercise and repetitive movements  Autoimmune disorder affecting the myoneural junction  Characterized by varying degrees of weakness of the voluntary muscles

ETIOLOGY  Autoimmune disease  Thymoma Women suffer at an earlier age (20-40) compared to men (60-70) and are more affected

Pathophysiology:  1. Acetylcholine receptor antibodies interfere with impulse transmission  2. Follows an unpredictable course of periodic exacerbations and remissions

ASSESSMENT FINDINGS 1. Involves the ocular muscles a. diplopia double vision b. ptosis drooping of the eyelids 2. Bulbar symptoms weakness of the muscles of the face and throat 3. Generalized weakness a. bland facial expression b. dysphonia c. decrease vital capacity PURELY MOTOR WITH NO EFFECT ON SENSATION OR COORDINATION

DIAGNOSTIC TESTS  1. EMG  2. TENSILON TEST (Edrophonium)  3. CT scan  4. Serum anti-AchReceptor antibodies

MEDICAL THERAPY  Anticholinesterase drugs

Tension Pyridostigmine Neostigmine



 Corticosteroids  Immunosuppresants  Plasmapheresis  Thymectomy

NURSING INTERVENTIONS  1. Administer prescribed medication as scheduled  2. Prevent problems with chewing and swallowing  3. Promote respiratory function  4. Encourage adjustments in lifestyle to prevent fatigue  5.maximize functional abilities

 6. Prepare for complications like myasthenic

crisis and cholinergic crisis  7. prevent problems associated with impaired vision resulting from ptosis of eyelids  8. provide client teaching  9. promote client and family coping

Guillian-Barre Syndrome (Demyelinating)

 An auto-immune attack of the peripheral

nerve myelin  Acute, rapid segmental demyelination of peripheral nerves and some cranial nerves producing ascending weakness  POTENTIALLY FATAL!

 CAUSE: post-infectious polyneuritis of

unknown origin commonly follows viral infection (66%)  Assoc. with Gastrointestinal infection (Campylobacter Jejuni) and respiratory infection


Cell-mediated immune attack to the myelin sheath of the peripheral nerves Infectious agent may elicit antibody production that can also destroy the myelin sheath of the PERIPHERAL NERVES!!

 Because this syndrome causes inflammation

and degenerative changes in the posterior and anterior nerve roots, MOTOR and SENSORY losses occur SIMULTANEOUSLY!

CLINICAL MANIFESTATIONS: occurs 2 weeks before symptoms begins  1. Ascending weakness and paralysis: Leg affected first (1 month)  2. AREFLEXIA of the lower extremities  3. paresthesia  4. potential respiratory failure Duration of symptoms are variable:complete functional recovery may take up to 2 yrs.

 5. blindness  6. bulbar muscle weakness  7. autonomic dysfunction

LABORATORY EXAMINATION 1. CSF protein level is INCREASED but the WBC remains normal in the CSF 2. EMG and nerve conduction velocity studies

NURSING INTERVENTIONS 1. Maintain respiratory function  Chest physiotherapy and incentive spirometry  Mechanical ventilator

 2. Enhance physical mobility


Support paralyzed extremities Provide passive range of motion exercise Prevent DVT and pulmonary embolism Padding over bony prominences

 3. Provide adequate nutrition


IVF Parenteral nutrition Assess frequently return of gag reflex

 4. Improve communication

Use other means of communication

 5. Decrease fear and anxiety


Provide Referrals Answer questions Provide diversional activities DVT, Urinary retention, pulmonary embolism, respiratory failure

 6. Monitor and manage complications


Trigeminal neuralgia (Motor Dysfunction-CN)

 Also called Tic Douloureux  Condition of the 5th CN characterized by

paroxysms of pain  Most commonly occurs in the 2nd and 3rd branch  CAUSES:NOT CERTAIN, chronic compression or irritation of 5th CN  400x more common in MS

 Pain is more often cyclic  Most often in the 5th decade of life  Paroxsyms can occur with any stimulation of

the affected nerves, such as washing of face, shaving, brushing the teeth, eating and drinking

ASSESSMENT  1. Pain history (UNILATERAL)  2. Searing or burning jabs of pain lasting from 1-15 minutes in an area innervated by the trigeminal nerve (shooting/stabbing) DIAGNOSTIC TESTS Skull x-ray or CT scan

Medical management: 1. Carbamazepine (Tegretol) - taken w/ meals - serum levels must be monitored - S.E. nausea, dizziness, drowsiness and aplastic anemia 2. Gabapentin (Neurontin)

Surgical Management: 1. Microvascular decompression of the trigeminal nerve 2. Percutaneous radiofrequency trigeminal gangliolysis TRIGEMINAL RHIZOTOMY - surgical treatment of choice

NURSING INTERVENTIONS  1. provide emotional support  2. encourage to express feelings  3. provide adequate nutrition in small frequent meals at room temperature

BELLS PALSY (Motor Dysfunction-CN)

PRESSURE PARALYSIS Causes:  1. infection  2. hemorrhage  3. tumor  4. local traumatic injury

MANIFESTATIONS  1. Unilateral facial weakness  2. Mouth drooping  3. Distorted taste perception  4. Smooth forehead  5. Inability to close eyelid on the affected side  6. Incomplete eye closure  7. excessive tearing when attempting to close the eyes  8. Inability to raise eyebrows, puff out the cheek

Diagnostic tests  EMG Medical management  1. Prednisone  2. Artificial tears

Nursing Interventions  1. Apply moist heat to reduce pain  2. Massage the face to maintain muscle tone  3. Give frequent mouth care  4. protect the eye with an eye patch. Eyelid can be taped at night  5. instruct to chew on unaffected side Reassure that no stroke has occurred and recovery occurs w/in 3-5 weeks

Huntingtons Disease (chorea)

 Progressive, degenerative inherited

neurologic disease characterized by increasing dementia and chorea (rapid, jerky involuntary movements)  1. Cause unknown  2. No cure  3. Usually asymptomatic until age of 30 40

Pathophysiology: involves destruction of cells in basal ganglia and other brain areas, decrease in acetylcholine

Manifestations  1. Abnormal movement and progressive dementia  2. Early signs are personality change with severe depression, memory loss; mood swings, signs of dementia

 3. Increasing restlessness, worsened by

environmental stimuli and emotional stress; arms and face and entire body develops choreiform movements, lurching gait; difficulty swallowing, chewing, speaking

 4. Slow progressive debilitation and total

dependence  5. Death usually results from aspiration pneumonia or another infectious process

 Collaborative Care: almost always requires

long-term care

 Diagnostic Tests: genetic testing of blood

Medications  1. Antipsychotic (phenothiazines and butyrophenones) to restore neurotransmitters  2. Antidepressants

Nursing Care  1. Very challenging: physiological, psychosocial and ethical problems  2. Genetic counseling

Nursing Diagnoses  1. Risk for Aspiration  2. Imbalanced Nutrition: Less than body requirements  3. Impaired Skin Integrity  4. Impaired Verbal Communication

 Home Care: Referral to agencies to assist

client and family, support group and organization

Amyotrophic Lateral Sclerosis (ALS)


Progressive, degenerative neurologic disease characterized by weakness and wasting of muscles without sensory or cognitive changes  2. Several types of disease including a familial type; onset is usually between age of 40 60; higher incidence in males at earlier ages but equally post menopause  3. Physiologic problems involve swallowing, managing secretions, communication, respiratory muscle dysfunction  4. Death usually occurs in 2 5 years due to respiratory failure

Pathophysiology  1. Degeneration and demyelination of motor neurons in anterior horn of spinal cord, brain stem and cerebral cortex  2. Involves upper and lower motor neurons  3. Reinnervation occurs in the early course of disease, but fails as disease progresses


 1. Initial: spastic, weak muscles with

increased DTRs (UMN involvement); muscle flaccidity, paresis, paralysis, atrophy (LMN involvement); clients note muscle weakness and fasciculations (twitching of involved muscles); muscles weaken, atrophy; client complains of progressive fatigue; usually involves hands, shoulders, upper arms, and then legs

 2. Atrophy of tongue and facial muscles

result in dysphagia and dysarthria; emotional lability and loss of control occur  3. 50% of clients die within 2 5 years of diagnosis, often from respiratory failure or aspiration pneumonia

Collaborative Care  1. Evaluation to make the diagnosis  2. Referrals for home health support;  3. Client needs to make decisions regarding gastrostomy tube, ventilator support

Diagnostic Test  1. Testing rules out other conditions that may mimic early ALS such as hyperthyroidism, compression of spinal cord, infections, neoplasms  2. EMG to differentiate neuropathy from myopathy  3. Muscle biopsy shows atrophy and loss of muscle fiber  4. Serum creatine kinase if elevated (non-specific)  5. Pulmonary function tests: to determine degree of respiratory involvement

Medications: Rilutek (Riluzole) antiglutamate  1. Prescribed to slow muscle degeneration  2. Requires monitoring of liver function, blood count, chemistries, alkaline phosphatase

Nursing Care  1. Help client and family deal with current health problems  2. Plan for future needs including inability to communicate

Nursing Diagnoses  1. Risk for Disuse Syndrome  2. Ineffective Breathing Pattern: may require mechanical ventilation and tracheostomy

 Home Care: Education regarding disease,

community resources for health care assistance and dealing with disabilities

Creutzfeldt-Jakob disease (CJD, spongiform encephalopathy)

Description  1. Rapid progressive degenerative neurologic disease causing brain degeneration without inflammation  2. Transmissible and progressively fatal  3. Caused by prion protein: transmission of prion is through direct contamination with infected neural tissue

 4. Rare in USA affecting persons 55 - 74  5. Variant form of CJD is mad cow disease:

believed transmitted by consumption of beef contaminated with bovine form of disease; none identified in USA as of yet  6. Pathophysiology: spongiform degeneration of gray matter of brain

Manifestations  1. Onset: memory changes, exaggerated startle reflex, sleep disturbances  2. Rapid deterioration in motor, sensory, language function  3. Confusion progresses to dementia  4. Terminal states: clients are comatose with decorticate and decerebrate posturing

Diagnostic Tests  1. Clinical pictures, suggestive changes on EEG and CT scan  2. Similar to Alzheimers in early stages  3. Final diagnosis made on postmortem exam

Nursing Care  1. Use of standard precautions with blood and body fluids  2. Support and assistance to client and family

The end.