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Neurology 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 Peripheral Nervous System: spinal nerves, cranial nerves and their branches

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. Diencephalon 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

ORGANIZATION OF NERVOUS SYSTEM Central Nervous System: BRAIN Central Nervous System : BRAIN Major regions are:

Function of the nervous system are sensory input, integration, homeostasis, mental activity, control of muscles and glands

Diencephalon Brainstem Cerebrum

NERVOUS SYSTEM Central Nervous System: Brain Spinal Cord


BRAIN : Diencephalon BRAIN: Diencephalon

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 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 lobes: 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)

Also involves learning motor skills (riding a bicycle/playing a piano) 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 VERTEBRAL COLUMN

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

Wernickes area (22) wernickes aphasia (receptive, sensory, fluent, posterior) 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

surrounds and protects the spinal cord 7 cervical, 12 thoracic, 5 lumbar, 5 sacral, coccyx (4 fused vertebra)

Mnemonic: Cranial Nerves Oh Oh Oh

Cranial Nerves origin PNS: Spinal Nerves Arise along the spinal cord from the union of the dorsal and ventral roots They contain axons of both sensory and somatic motor neurons

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)

To Touch


Feel Vagina

Also contain parasympathetic and sympathetic axons is Such Categorized by the region of vertebral column 31 pairs Organized into 3 plexuses

Grabbing Vagina Heaven Some Say

ADRENERGIC system Sympathetic Responses: Increased: HR RR BP Visual Acuity (Pupillary Dilation)

Marry Money

Autonomic Nervous System Composed of:

But My Brother Says

Sympathetic and parasympathetic Enteric nervous system

Big Boobs Smooth Muscle tone are contracted Matter Most Vasoconstriction sphincters

Metabolism acids

glucose, fatty

Decreased: HR RR

Temporal bone Occipital bone Meninges Surround and protect the spinal cord 3 layers: DAP Meninges Dura mater Dural venous sinuses Epidural space (SC) Meninges Arachnoid Subdural space (space between dura mater and arachnoid, contains small amount of serous fluid) Meninges Pia mater Tightly bound to the surface of brain and SC

Sympathetic Responses: Decreased Peristalsis Salivary secretions Ejaculation

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

ANS: Parasympathetic Nervous System CHOLINERGIC system The vegetative system Feed and Breed responses Cranio-sacral location Cranial nerves- 3, 7, 9, 10 and S2S4 Neurotransmitter is Acetylcholine

Increased Peristalsis Salivary secretions Erection

Structures supporting the brain Skull Frontal bone Parietal bone

Subarachnoid space (bet. Arachnoid and pia mater, filled with CSF and BV)

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 NEURONS 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 Neurotransmitters

Serotonin ( depression, manic) Glutamine (excitatory

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

ASSESSMENT OF THE NEUROLOGIC SYSTEM PHYSICAL EXAMINATION 5 categories: 1. Cerebral function- LOC, mental status 2. Cranial nerves 3. Motor function 4. Sensory function 5. Reflexes ASSESSMENT OF THE NEUROLOGIC SYSTEM Neuro Check Level of consciousness Pupillary size and response Verbal responsiveness

BLOOD-BRAIN BARRIER CNS is inaccessible to many substances Many substances cannot reach the neurons of the CNS

Acetycholine Dopamine Epinephrine and Norepinephrine GABA (inhibitory)

Motor responsiveness Vital signs

d. Precipitating and relieving factors e. Associated symptoms noting timing and circumstances


Weight changes

k. Prescribed and over the counter medications, frequency of use and duration

ASSESSMENT OF THE NEUROLOGIC SYSTEM HISTORY A confused client becomes an unreliable source of history 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 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. 2. 3. 4. 5. 6. 7. 8. Cardiac disease Strokes Pernicious anemia Sinus infections Liver dysfunctions Diabetes mellitus HPT Mental health problems

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. b. c. Onset Characteristics and course Severity

f. Feeling state, e.g. anxious, depressed g. Changes in sleep patterns

h. Ability to perform self-care and ADL i. Sexual activity

B. Physical assessment to collect objective data 1. Mental status assessment with abnormal findings a. Unilateral neglect: strokes involving middle cerebral artery b. Poor hygiene and grooming: dementing disorders c. Abnormal gait and posture: transient ischemic attacks (TIAs), strokes, Parkinsons disease d. Emotional swings, personality changes: strokes of anterior cerebral artery e. Masklike appearance on face: Parkinsons disease f. Apathy: dementing disease

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 CEREBRAL FUNCTION 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

g. Aphasia (defective or absent language function): TIAs, strokes; strokes involving posterior or anterior artery involve receptive aphasia

Scores are evaluated- range from 3-15 7 and Below= COMA! No ZERO score Eye Opening (E) Verbal Response (V) Motor Response (M) Eye Opening (E) 4=Spontaneous 3=To voice (when told to) 2=To pain 1=None (No response) Glasgow Coma Scale 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)

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 1- Olfactory Check first for the patency of the nose Instruct to close the eyes Occlude one nostrils at a time

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

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

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

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

Observe for nystagmus and disturbed balance 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 7 -facial Sensory portion- prepare salt, sugar, vinegar. Place each substance in the anterior two thirds of the tongue, rinsing the mouth with water

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

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, wArM- sAMe

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)

ROMBERGs is actually a test for the posterior spinothalamic tract

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 motor function of the brainstem Test for the Oculocephalic reflexdolls eye Normal response- eyes appear to move opposite to the movement of the head Abnormal- eyes move in the same direction

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 +++ increased ++++ hyperactive or clonic Superficial reflex 0 absent +present

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

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

Special neurologic assessment with abnormal findings a. 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

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

. 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

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

Nursing Care - provide nursing support for the confused or combative patient - maintain immobilization - remove metal items

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

-Patients with pacemakers, orthopedic metal prosthesis and implanted metal devices cannot undergo this procedure

EEG b. CT Scan - detect intracranial bleeding, space occupying lesion, cerebral edema. Hydrocephalus, infarction Nursing Care Assess for allergies Instruct to lie still and flat Lumbar tap Inform pt that there may be hot, flushed sensation and metallic taste in the mouth Treat allergic reaction Contraindications: Unstable vital signs or cardiopulmonary compromise space occupying lesions c. Magnetic Resonance Imaging - provides more detailed pictures infections on the site hematologic problems Withhold medications that may interfere with the resultsanticonvulsants, sedatives and stimulants Wash hair thoroughly before procedure

CSF obtained from LUMBAR Space bet. L4 & L5 skin/superficial fascia Ligaments Epidural Space Dura mater Subdural space Archnoid space Subarachnoid space Don't let people drive you crazy when you know it's in walking distance. Thank you!

II. Nursing Care of Client with Intracranial Disorders ALTERED LEVEL OF CONSCIOUNESS 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 4. STUPOROUS 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 AKINETIC MUTISM state of 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 Etiologic Factors

Diabetic ketoacidosis Hepatic failure

ASSESSMENT Behavioral changes initially Pupils are slowly reactive Then , patient becomes unresponsive and pupils become fixed dilated Glasgow Coma Scale is utilized Complications Respiratory failure Pneumonia Pressure ulcers

Head injury Aspiration Stroke Deep vein thrombosis Drug overdose Alcoholic intoxication

First priority of treatment is to obtain and maintain a patent airway 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 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 7. Achieve thermoregulation Minimum amount of beddings Rectal or tympanic temperature Administer acetaminophen as prescribed 8. Prevent urinary retention Use of intermittent catheterization 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

Headache 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 Evaluation:Headache 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 Assessment: 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

Assessment: 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

4. inhalation of 100% O2 to abort cluster headache

Disturbed sensory perception Ineffective coping Nausea

Pharmacologic interventions: Assessment: 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 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

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

c. Beta-adrenergic blocker & Ca channel light headedness and hypotension Intracranial Pressure


Monro-kellie hypothesis

1. Within skull there are 3 components that maintain state of dynamic equilibrium a. b. fluid (10%) c. Blood (10%) Brain (80%) Cerebrospinal

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


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. Sustained increases associated with a. b. c. d. e. f. g. Cerebral edema Head trauma Tumors Abscesses Stroke Inflammation Hemorrhage

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

Cerebral response to increased ICP Steady perfusion up to 40 mmHg

Decreased Blood Flow Vasomotor reflexes are stimulated initially slow bounding pulses Increased concentration of carbon dioxide will cause VASODILATION increased flow increased ICP

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

CEREBRAL EDEMA Abnormal accumulation of fluid in the intracellular space, extracellular space or both. CLINICAL MANIFESTATIONS Early manifestations: Changes in the LOC- usually the earliest Pupillary changes- fixed, slowed response Headache vomiting

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

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 1530 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 3. Administer prescribed medications- usually

Mannitol- to produce negative fluid balance corticosteroid- to reduce edema anticonvulsants-p to prevent seizures 4. Reduce environmental stimuli 5. Avoid activities that can increase ICP like valsalva, coughing, shivering, and vigorous suctioning 6. Keep head on a neutral position. AVOID- extreme flexion, valsalva 7. monitor for secondary complications Diabetes insipidus- output of >200 mL/hr SIADH

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

Seizure Disorder also known as convulsions, epileptic seizures, and if recurrent epilepsy

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. Generalized seizures: involves both brain hemispheres; consciousness always impaired a. (petit mal) Absence seizures

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) Complications: 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 FEBRILE SEIZURES CRITERIA: Age: 9 mos. To 5 yrs. Generalized tonic-clonic lasting not more than 15 mins

- 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

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

b. Tonic-clonic seizures (GRAND MAL) 1. adults 2. Preceded by aura, sudden loss of consciousness 3. Tonic phase: rigid muscles, incontinence (LAST 30 TO 60 SECS.) Most common type in

Onset of fever > 39 C within hours of the seizure Family history of BFC No neurologic deficit that would explain the seizure

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

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

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

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

Surgery: if all attempts to control seizures are not successful 1. excise tissue seizure activity May attempt to involved in

2. EEG done during surgery to identify epileptogenic focus

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

NURSING INTERVENTIONS: 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

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

avoidance of alcohol and caffeine 2. Referral to support group, national organizations

2. If dura disrupted may have leakage of CSF occurring as a. through nose b. through ear Otorrhea: Rhinorrhea:

B. trauma

Mechanisms of

CNS infection A. CNS infections

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

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

Nursing Diagnoses 1. Risk for Ineffective Airway Clearance 2. Home Care 1. Education of client and family regarding seizure disorder; safety measures, Anxiety

1. Involves base of skull and usually involve extension of adjacent fractures

B. 1. young

Risk Factors High risk for old and

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

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

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 life-threatening complications


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

4. a. b. (deafness) c.

Complications Arthritis Cranial nerve damage




1. Inflammation of pia mater, arachnoid, and subarachnoid space 2. Spreads rapidly through CNS because of circulation of CSF around brain and spinal cord

F. 3. a. Manifestations Fever chills

Viral meningitis

1. Less severe, benign course with short duration 2. Intense headache with malaise, nausea, vomiting, lethargy

b. Headache, back and abdominal pain c. Nausea and vomiting

3. irritation

Signs of meningeal

2. Causes include open trauma and neurosurgery; infections of ear, sinuses 3. Common pathogens are streptococci, staphylococci, bacteroids


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

1. Acute inflammation of parenchyma of brain or spinal cord 2. 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 Usually caused by

4. Becomes spaceoccupying lesion 5. At risk for infection and increased ICP 6. Manifestations


Diagnostic Tests

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

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


Brain abscess

1. Infection with a collection of purulent material within brain tissue usually in cerebrum



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

M. 1.

Nursing Diagnoses Ineffective Protection

and capacity to impinge on CNS structures

2. Risk for Deficient Fluid Volume


Home Care

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

1. Client education for future prevention L. Health Promotion 2. Complete medications and treatment plan Brain Tumor 1. Vaccinations for meningococcal, pneumococcal, hemophilic meningitis 2. Prophytlactic rifampin for persons exposed to meningococcal meningitis 3. Mosquito control

6. 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)

Tumors within brain

a. Compress or destroy brain tissue b. Cause edema in adjacent tissues c. Cause hemorrhage

4. Prompt diagnosis and treatment of clients with infections 5. Asepsis care for clients with open head injury or neurosurgery

d. Obstruct circulation of CSF, causing hydrocephalus

7. Estimated 25% persons with cancer develop brain metastasis, often multiple sites throughout the brain

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



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

B. Manifestations: Multiple depending on location of lesion and rate of growth 1. and LOC Changes in cognition


Diagnostic Tests

2. Headache usually worse in morning 3. 4. Seizures Vomiting

1. CT scan or MRI: determine tumor location and extent 2. Arteriography F. Nursing Care

5. Manifestations associated with cerebral edema, increased ICP, cerebral ischemia leading to brain herniation syndromes

3. EEG: information about cerebral function, seizure data 4. Endocrine studies if pituitary tumor suspected

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

E. C. Collaborative Care


G. 1. 2.

Nursing Diagnoses Anxiety Risk for Infection

1. Medications: Chemotherapy, corticosteroids, anticonvulsants

3. 4. 5.

Ineffective Protection Acute Pain Disturbed Self-esteem

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 strokecaused commonly by hypertensive bleeding The stroke continuum 1. TIA- transient ischemic attack, temporary neurologic loss less than 24 hours duration 2. Reversible Neurologic deficitss/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 Localization Anterior cerebral artery: Weakness Numbness on the opposite side Personality changes Impaired motor and sensory function Localization Middle cerebral artery: Aphasia Dysphagia HEMIPARESIS on the OPPOSITE side- more severe on the face and arm than on the legs


Home Care

1. Education, support to client and family 2. Instructions for treatment plan and follow-up care 3. agencies Referral to home care

4. Referrals to therapies, community resources, support groups as appropriate CHILLAX!


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

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

2. confusion or change of LOC 3. motor and speech difficulties 4. Visual disturbance 5. Severe headache

Motor Loss Hemiplegia Hemiparesis

CEREBROVASCULAR ACCIDENTS: Ischemic Stroke There is disruption of the cerebral blood flow due to obstruction by embolus or thrombus DIAGNOSTIC test 1. CT scan infarct vs. hge 2. MRI- infarct, brainstem vs. cererebellum 3. Angiography CEREBROVASCULAR ACCIDENTS: Ischemic Stroke CLINICAL MANIFESTATIONS (table 62.2 , p. 1890, 10th ed.,p. 2208-2209, 11th ed. BRUNNER) 1. Numbness or weakness

Communication loss Dysarthria= difficulty in speaking Aphasia= Loss of speech Apraxia= inability to perform a previously learned action Perceptual disturbances Hemianopsia Sensory loss paresthesia

RISKS FACTORS Non-modifiable Advanced age Gender race

NURSING INTERVENTIONS: ACUTE Ensure patent airway Keep patient on LATERAL position Monitor VS and GCS, pupil size IVF is ordered but given with caution as not to increase ICP NGT inserted 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 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 6. Improve thought processes Support patient and capitalize on the remaining strengths 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 8. Maintain skin integrity

Use of specialty bed Regular turning and positioning Keep skin dry and massage NONreddened areas Provide adequate nutrition 9. Promote continuing care Referral to other health care providers 10. Improve family coping 11. Help patient cope with sexual dysfunction MEDICAL MANAGEMENT Pharmacologic: Aspirin Diazepam to prevent seizures Thrombolytics Stool softeners Antihypertensives Analgesics, Muscle relaxants, STEROIDS

MEDICAL MGMT: 1. TIA/Mild stroke non surgical approach -- platelet inhibiting medications 2. Thrombolytic therapy t-PA administration -- eligibility criteria for t-PA administration ( chart 62-3 p. 1893, 10th ed BRUNNER) -- 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

Reduce ICP Maintaining PaCO2 (30-35mmHg) Proper positioning Intubation Continuous hemodynamic monitoring (<180/100) Neurologic assessment 7. anticoagulant

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

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: sudden, unusually severe headache and often LOC (+) meningeal irritation Visual disturbances adjacent of oculomotor nerve

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 Sudden and severe headache Same neurologic deficits as ischemic stroke

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

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

Surgical and medical treatment to prevent rebleeding

d. Prevent further extension of clot ; Heparin, warfarin sodium (Coumadin) Acute Stroke

Complications: Rebleeding Cerebral hypoxia Vasospasms Increased ICP Systemic HPN

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)

Acute Stroke


Anticoagulant therapy

a. Ordered for thrombotic stroke during stroke-in-evolution Medical management: Complete bed rest w/ elastic compression stockings Management of vasospams b. Contraindicated in completed stroke c. Never used in hemorrhagic stroke

Ancillary: 1. Surgery

4. Impaired Verbal Communication 5. Impaired Urinary Elimination and Risk for Constipation 6. Impaired Swallowing

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 Pronation of forearm Flexion of fingers Extension of hip and knee

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



Motor Deficits

2. 3. 4.

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) Complications

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

1. Ineffective Tissue Perfusion: Cerebral; frequent monitoring of neurologic status, cardiac status 2. 3. Impaired Physical Mobility Self-care Deficit

Communication Disorders c. 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 1. Expressive aphasia: 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

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

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 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 NURSING MANAGEMENT 3. Monitor F and E balance Daily weights IVF therapy Monitor possible development of DI and SIADH 4. Provide adequate nutrition 5. Prevent injury Use padded side rails Minimize environmental stimuli Assess bladder Consider the use of intermittent catheter 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 7. Monitor potential complications Increased ICP Post-traumatic seizures Impaired ventilation Spinal cord injury The most frequent vertebrae C5C7, T12 and L1 Concussion Contusion Compression Transection

Spinal cord injury Clinical manifestations 1. Paraplegia 2. quadriplegia 3. spinal shock

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

9. Assists with surgical reduction and stabilization of cervical vertebral column Laughing Out Loud

IV. Nursing Care Clients with Degenerative disorder & Motor dysfunction Degenerative disordersdemyelinating Multiple sclerosis Guillain-Barre syndrome Degenerative disordersNON-demyelinating Alzheimers disease Parkinsons disease

DIAGNOSTIC TEST Spinal x-ray CT scan MRI

5. Maintain urinary elimination 6. Improve bowel function 7. Provide Comfort measures


8. Monitor and manage complications Thromboplebhitis

Immobilization Orthostatic hypotension Immediate transfer to tertiary facility Spinal shock Autonomic dysreflexia

Motor dysfunction- cranial nerve

Bells palsy Trigeminal neuralgia Motor dysfunction- peripheral Myasthenia gravis

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

Other tests to rule out Vit B deficiencies and hypothyroidism Autopsy is the most definitive Drug therapy 1. drugs to treat behavioral symptoms- antipsychotics 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

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

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

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 selfcare 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 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

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

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

2. Visual disturbances lesion in the optic nerve a. blurring of vision b. Diplopia c. patchy blindness (scotoma) d. total blindness

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. Prevent injuries

Obtain large printed reading materials Offer emotional support

3. Spasticity (muscle hypertonicity) of the extremities and loss of abdominal reflexes 4. Ataxia

Wide stance walking Involve the family in the care Use of walking aids 6. Strengthen coping mechanism Wheelchair Alleviate the stress 3. Enhance bladder and bowel control Set a voiding schedule Intermittent bladder catheterization Use of condom catheter Referral to the appropriate agencies 7. improve self-care abilities Modify activities according to physical strength

5. Emotional lability and euphoria 6. bladder, bowel and sexual dysfunction

Provide assistive devices 8. promote sexual functioning Refer to sexual counselor MEDICAL MANAGEMENT Pharmacotherapy Interferons beta 1a (Avonex) and beta 1b (Betaseron), Glatiramer Acetate (Copaxone), Rebif

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

CLINICAL MANIFESTATIONS 1. Tremor- resting, pill-rolling, unilateral (70%) 2. Rigidity- cog-wheel, lead-pipe 3. Bradykinesia- abnormally slow movement 4. Dementia, depression, sleep disturbances and hallucinations 5. excessive sweating, paroxysmal flushing, orthostatic hypotension Medical management 1. Anti-parkinsonian drugsLevodopa, Carbidopa 2. Anti-cholinergic therapy(Biperiden) 3. Antiviral therapy- Amantadine 4. Dopamine Agonistsbromocriptine and Pergolide, Ropirinole anmd Pramipexole

ABC and R drugs

Immunomodulators Corticosteroids BACLOFEN for muscle spasms NSAIDS for pain Antidepressants 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

5. MAOI 6. Anti-depressants 7. Antihistamine NURSING INTERVENTIONS 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

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 (2040) 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 drugspyridostigmine and 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

CAUSE: post-infectious polyneuritis of unknown origin commonly follows viral infection (66%) Assoc. with Gastrointestinal infection (Campylobacter Jejuni) and respiratory infection PATHOPHYSIOLOGY 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!

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!

CLINICAL MANIFESTATIONS: occurs 2 weeks before symptoms begins 1. Ascending weakness and paralysis: Leg affected first (1 month) 2. diminished reflexes 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

NURSING INTERVENTIONS 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

5. Decrease fear and anxiety Provide Referrals Answer questions Provide diversional activities 6. Monitor and manage complications DVT, Urinary retention, pulmonary embolism, respiratory failure MEDICAL MANAGEMENT ICU admission Mechanical Ventilation TPN and IVF PLASMAPHERESIS IV IMMUNOGLOBULIN

6. bulbar muscle weakness IVF 7. autonomic dysfunction Parenteral nutrition LABORATORY EXAMINATION CSF protein level is INCREASED but the WBC remains normal in the CSF EMG and nerve conduction velocity studies Assess frequently return of gag reflex 4. Improve communication Use other means of communication

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: Microvascular decompression of the trigeminal nerve 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. 2. Cause unknown No cure

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

3. Usually asymptomatic until age of 30 40

Collaborative Care: almost always requires long-term care

Nursing Diagnoses 1. Risk for Aspiration

Diagnostic Tests: genetic testing of blood

2. Imbalanced Nutrition: Less than body requirements 3. Impaired Skin Integrity

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 Manifestations 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

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

4. Impaired Verbal Communication Home Care: Referral to agencies to assist client and family, support group and organization Amyotrophic Lateral Sclerosis (ALS) 1. 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

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

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

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

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

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

Nursing Care

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