INCREASE PRESSURE

INTRACRANIAL

MONROE KELLIE HYPOTHESIS Normal ICP is 0-15mmHg Brain 84% CSF 12% Blood volume 4% POSSIBLE CAUSE: 1. Increase brain volume Neoplasm, Tumor Brain Abscess Edema 2. Increase blood volume Hematoma formation and hemorrhage Hypoxemia (^O2 in blood) Hypercapnia (^O2 in blood) Decrease venous return High Arterial blood flow Pulling of venous blood 3. Increase CSF Flow Deficient CSF absorption ^ production of CSF Obstruction to CSF pathway MANIFESTATIONS: 1. Decrease Level of Consciousness 2. Headache 3. Motor and sensory dysfunction 4. Respiratory dysfunction 5. Nausea and Vomiting (r/t deficiency in blood supply) 6. Pupillary dysfunction 7. Abnormal posturing a. Decorticate (excessive flexion) b. Decerebrate (excessive extension) DIAGNOSTIC EVALUATION: 1. CT SCAN 2. MRI 3. Cerebral Angiography 4. Skull Xray 1. MANAGEMENT: 2. Osmotic Diuretics (Mannitol) 3. Corticosteroids (anti inflammatory drugs) 4. SURGICAL MANAGEMENT: a. CRANIOTOMY to relive pressure 5. Intraventricular Catheter ICP Monitoring NURSING INTERVENTION 1. Maintain Airway patency and oxygen as ordered 2. Monitor ABG level 3. WOF: Deliberate hyperventilatireon

4. Elevate the head of the bed 30-40 degrees to reduce edema of cerebral tissues 5. Assess LOC 6. Control Auditory, visual and tactile stimulation 7. Maintain room temperature 8. Avoid clustering of nursing care

CEREBROVASCULAR ACCIDENT (CVA)

Commonly known as STROKE or BRAIN ATTACK Define as sudden interruption in normal cerebral circulation POSSIBLE CAUSE: 1. Obstructive Type Obstruction due to blood clot commonly embolism, and thrombosis 2. Hemorrhagic Type RISK FACTOR 1. Hypertension 2. Diabetes Mellitus 3. Atherosclerosis (fatty deposits) & Arteriosclerosis (hardening) 4. Patient on anticoagulant therapy (risk for bleeding) 5. Stress 6. Obesity 7. Aging 8. Cardiac Disorder Other causes of ischemia Causes Occlusion of major vessels (embolus & thrombus) Decrease cerebral blood flow Hypoxia Cerebral edema Vascular congestion Tissue compression Cerebral infarction Impaired function
Anterior Cerebral Artery Confusion Impaired thought process Contralateral paralysis Urinary incontinence Sensory deficit Middle Cerebral Artery arm paralysis hemianopsia aphasia agnosia apaxia Posterior Cerebral Artery hemiparesis ataxia visual problem

Further compression of cerebral tissue Cerebral death

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MANIFESTATION: EARLIEST 1. Decrease/altered level of consciousness 2. Headache 3. Fever 4. Nuchal rigidity LATE SIGNS 1. Agnosia

2. Apraxia Inability to carry out purposeful/normal activity 3. Hemianopsia Homonymous Hemianopsia 4. Aphasia o Expressive Aphasia damage of frontal lobe esp. Brocas Area o Receptive Aphasia damage in temporal lobe Wernickes area Client unable to understand spoken words o Mixed Aphasia DIAGNOSTIC: 1. CSF Analysis to determine the cause 2. CT SCAN/MRI to locate type of hematoma and infarction 3. CEREBRAL ANGIOGRAM to reveal site of occlusion 4. PET SCAN reveal into cerebral metabolism and characteristics of blood flow 5. EEG MANAGEMENT: 1. Oxygen Therapy 2. Respiration Therapy 3. Mechanical Ventilation 4. IV Fluids 5. Bed rest during acute stage 6. Fowlers to semi-fowlers 7. Active/passive ROM 8. Low Sodium Low Cholesterol ____ Diet 9. Physical and speech therapy 10. Treatment and pre-existing condition NURSING INTERVENTION: 1. Promote oxygenation 2. DBC 3. Monitor Pulse Oximetry and ABG level 4. CBR 5. Appropriate diet Low Na, Cholesterol and fat 6. Assess gag reflex 7. Institue bowel and bladder program 8. MIO 9. Perform ROM exercises to maintain joint mobility and prevent contractures 10. Administer Meds as ordered

CHRONIC D/O OF NERVOUS SYSTEM

ALS: AMYOTHROPIC LATERAL SCLEROSIS

LOU GEHRIG DISEASE Progressive degenerative d/o that leads to a decrease in motor function of upper and lower motor neuron system It affects male 3x more commonly than female EXACT CAUSE: UNKNOWN POSSIBLE CAUSE: 1. Genetic Predisposition 2. Nutritional Deficiency 3. Slow Acting Virus UNKNOWN CAUSE Myelin Sheath Destruction (Serves as insulator) Degeneration of motor neuron (Brain, Spinal Cord) Replace with Scar Tissue Distortion or blockage of Nerve Impulse Death of Nerve Cells Progressive motor Dysfunction Weakness of Respiratory Muscle Respiratory Compromised/Failure DEATH MANIFESTATIONS: 1. Generalized muscle weakness 2. Dysphagia 3. Fatigue 4. Tongue Atrophy 5. Monotonous speech or nasal quality of voice 6. Spasticity DIAGNOSTIC: CK-MM MUSCLE ENZYME Normal 5-70IU/L MANAGEMENT: 1. SYMPTOMATIC/SUPPORTIVE NURSING INTERVENTIONS: 1. Assess neurologic and respiratory status 2. Assess swallowing and gag reflex to decrease the risk for aspiration 3. MIO and V/S particularly RR and BP 4. Administer medication as prescribed 5. Used alternate method of communication

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6. Encourage verbalization of feelings and maintain independence 7. Suction oral cavity as necessary to stimulate cough and clear the airway 8. Maintain the clients to improve nutritional status

GUILLAIN BARRE SYNDROME

INFECTIOUS POLYNEURITIS OR ACUTE IDIOPATHIC POLYNEURITIS This acute rapidly progressive potentially form of polyneuritis that lead to severe muscle weakness and distal sensory loss EXACT CAUSE: Unknown POSSIBLE CAUSE: 1. Autoimmunity 2. Demyelination of peripheral Nerves 3. Respiratory Infection 4. GI Infection 5. Hepatobiliary Infection
Triggering Event Immunologic Destruction of Peripheral Myelin Sheath Myelin Sheath (Damage of Myelin Sheath Axon) Slow Nerve Conduction (Axonal Pathway) Loss of Reflexes (SYMMETRIC AND ASCENDING)
Paralysis of Muscle Decrease respiratory & Difficulty of breathing Apnea Hypoxia DEATH -------------------Fxn Decrease/Loss of Automatic Reflexes Decrease capacity of lungs _______________________(+) Demyelination ceases Remyelination Return of Nerve Impulse Transmission Function restored from lost area involve upward (descending)

Eg. Beta blockers LIDOCAINE combat electro 3. ANTICHOLINERGIC DRUGS slow down PNS function resulting increase respiratory and cardiovascular function a. Eg. Atropine Sulfate NURSING INTERVENTION: 1. Assess and treat respiratory function 2. Monitor ABG and be alert for signs of increasing PCO2 3. Auscultate for breath sounds 4. Encourage DBCT 5. Begin Respiratory Support at first sign of dyspnea 6. Assess for signs of dysphagia to prevent aspiration 7. Place the client to semi to high fowlers position 8. NGT feeding if there is aspiration tendency 9. Give an eye and mouth care if there is facial paralysis 10. Encourage adequate fluid unless contraindicated a.

HUNTINGTONS DISEASE
HUNTINGTONS CHOREA Hereditary disease that involves degeneration of a neuron in cerebral cortex and basal ganglia (protective covering) EXACT CAUSE: UNKNOWN POSSIBLE CAUSE: 1. Chronic, irregular, involuntary movement 2. Cognitive deterioration 3. Dementia 4. Genetic Transmission MANIFESTATION: 1. Loss of musculoskeletal control 2. Dementia 3. Choreic Movement rapid and usually violent purposely movement accompanied by the following: a. Dysarthria b. Athetoid Movement c. Slow movement esp. of the hands d. Torticollis twisting of the neck MANAGEMENT: 1. Supportive and symptomatic 2. ANTI PSYCHOTIC DRUGS that will control CHOREIC MOVEMENT a. EG. HALOPEREDOL 3. ANTI DEPRESSANT a. EG. TCA NURSING INTERVENTION: 1. Provide physical support by attending the clients basic needs 2. Provide emotional support to the client and family 3. Stay alert suicide attempt, pad the side rails of the bed

MANIFESTATION: 1. Muscle weakness (legs to arms) up ascending 2. Dysphagia 3. Dysarthria (difficulty of articulation or poor speech) 4. Facial deplegia 5. Opthalmoplegia (ocular paralysis) 6. Hypertonia (excessive muscle tone) 7. Areflexia (Absences of reflexes) 8. Paresthesia ( numbness of peripheral parts) 9. Weakness of cranial nerve #11 Spinal Accessories DIAGNOSTIC TEST: CSF ANALYSIS reveals elevated total protein MANAGEMENT: 1. Intubation and tracheostomy 2. Possible mechanical ventilation 3. Parenteral Nutrition MEDICATION: 1. CORTICOSTEROIDS - decrease inflammatory process a. Eg. PREDNISONE 2. ANTI ARYTHMIC DRUGS

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MULTIPLE SCLEROSIS
Progressive degenerative disease that affects the myelin sheath surrounding the axon EXACT CAUSE: UNKNOWN Myelin sheath is loss Degeneration of neurons-Motor (CNS) Replace the scar tissue Resulting to distortion or blockage of nerve impulse Nerve cell death Muscle Atrophy Progressive motor dysfunction Weakness of respiratory muscle Respiratory compromise DEATH

POSSIBLE CAUSE: 1. 2. 3. 4. Autoimmune Genetic factor Environmental factor Infection by slow latent virus

Myelin sheath of: 1. Optic Nerve (Cranial Nerve #20 visual disturbances 2. Cerebrum 3. Brain Stem difficulty of respiratory and cardiovascular function 4. Cerebellum 5. Spinal Cord MANIFESTATION: CEREBELLUM o Ataxia loss of balance o Dysarthria difficulty of articulation o Incoordination o Tremors o Vertigo CEREBRUM o Decrease concentration o Short and long term memory loss o Depression o Difficulty finding words and learning new information o Euphoria (over excitement) o Short attention span

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CRANIAL NERVE o Blind spots o Blurred central vision o Diplopia (double vision) o Facial weakness o Numbness o pain SPINAL CORD o Motor function including abnormal gait o Paralysis o Muscle weakness o Spasticity o Sensory dysfunction o Paresthesia o Decrease perception of temperature o Bowel and bladder dysfunction including constipation, fecal incontinence, urgency, nocturia, urinary frequency, hesistancy, incontinence o Sexual dysfunction DIAGNOSTIC 1. CT SCAN 2. MRI to reveal demyelination of CNS 3. ELECTROMYOGRAM to reveal slowing of nerve conduction MANAGEMENT 1. High Fiber Diet 2. Active and Passive ROM 3. Physical and Speech Therapy 4. PLASMAPHERESIS usually done to autoimmune type, removing of antibody MEDICAL MANAGEMENT: 1. Cholinergic drugs It increases function of parasympathetic to prevent urinary stasis a. Eg. Betanechol (URECHOLINE) 2. GLUCOCORTICOIDS to reduce inflammatory and edema 3. IMMUNOSUPPRESSANT to stabilize the disease process a. Eg. Methorexane b. Cyclofospamide 4. SKELETAL MUSCLE RELAXANT to decrease muscle spasticity a. Eg. Ballofen (LLONESAL) b. DANTROZENE (DANTRIUM) NURSING MANAGEMENT: 1. Assess neurologic and V/S 2. Encourage to eat High Fiber Diet 3. Assess gag reflex and ability 4. Monitor weight to determine nutritional status 5. Encourage fluid intake 6. Institute bowel and bladder program

7. Provide uninterrupted period of sleeps to help conserve energy 8. Perform active and passive ROM to maintain joint mobility and prevent contractures 9. Encourage to express feelings

12. Shallow and slow respiratory 13. Soft and audible voice 14. strabismus DIAGNOSTIC TEST: 1. CT Scan/MRI 2. Tensilon Test - to determine if the patient is really suffering to MG a. Using Drug Prostigmine b. If complaint of relief of muscle weakness(+) c. If complaint of additional muscle weakness it means Myasthenia Crisis MANAGEMENT: 1. Oxygen Therapy 2. Mechanical Ventilation and Suctioning 3. Active and Passive ROM 4. Physical and Speech Therapy 5. Plasma Therapy PLASMAPHERESIS removal of antibody from blood plasma 6. THYMECTOMY removal of the thymus gland just beneath the thyroid gland MEDICATION: Thymus gland secretes acetylcholine receptor antibodies Increase level of Acetylcholine at Myoneural junction site o Neostigmine (Prostigmine) o Pyredostigmine (Mestinon) o Tensilon (Edrophonium) NURSING INTERVENTION: 1. Promote oxygenation 2. Have emergency equipment ready at bedside 3. Assess neurologic Status 4. Assess gag reflex 5. Administered prescribed medication (lifetime tensilon) 6. Plan activities early in the morning or during energy peak levels that follows administration of medication 7. Encourage to eat, small, frequent and high calorie meals and snacks 8. Give Tensilon before meals 9. Allow verbalization of feelings

MYASTHENIA GRAVIS
Chronic progressive neuromuscular d/o that affects normal condition that of nerve impulse across the neuromuscular conjunction A problem deficiency in Acetylcholine receptor sites in myoneural junction ACETYLCHOLINE NEUROTRANSMITTER NEURON Nerve impulse EFFECTORS muscle Glands

EXACT CAUSE: UNKNOWN POSSIBLE CAUSE: 1. Autoimmune and Genetic Transmission Unknown Cause Decrease level of Acetylcholine (Passage of nerve impulse from the nerve to effector organ) Disturbance on transmission of impulse Slower impulse transmission at the neuromuscular junction Extreme muscle weakness Weakness of respiratory muscle DEATH MANIFESTATIONS: 1. Extreme muscle weakness and fatigue Muscle strong in the morning, weaken through the day 2. Blurred Vision 3. Chewing Difficulty 4. Diminished vital capacity of the legs 5. Diplopia 6. Drooling 7. Dysarthria 8. Dyspnea 9. Flat facial affect 10. Nasal regurgitation/nasal monotone speech 11. PTOSIS (drooping eyelid)

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PARKINSONS DISEASE
CNS problems that results in widespread, progressive, degeneration of producing cell of substantia negra of the brain and consequently a decrease in the level of neurotransmitter dopamine PRIMARY ParkinsoniaSecondary Parkinsonian

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