ELENITA H.

TINIO,RN,MD,USRN

NEURO CONTINUATION

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

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

 The thymus is a specialized organ of

the immune system The only known function of the thymus is the production and "education" of T-lymphocytes(T cells), which are critical cells of the adaptive immune system The thymus is composed of two identical lobes and is located anatomically in the anterior superior mediastinum in front of the heart and behind the sternum

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)

IV injection- provides spontaneous relief of symptoms ( last 5-10 mintutes)- positive

3. CT scan 4. Serum anti-AchReceptor antibodies

MEDICAL THERAPY Anticholinesterase drugs

PYridostigmine ( mestinon) Neostigmine ( Prostigmin)

SHOULD BE GIVEN ON TIME 30 MINS. BEFORE MEALS W/ MILK AND CRACKERS TO PREVENT CRISIS

Corticosteroids- suppress autoimmune response Immunosuppresants

Plasmapheresis- remove circulating acetylcholine receptor antibodies

Thymectomy- removal of thymus gland

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

Cholinergic Crisis

caused by overmedication Worsen with tensilon test Antidote : atropine sulfate Myasthenic crisis Abrupt generalized muscle weakness Caused by undermedication, physical, emotional stress, infection Symptoms improved temporarily with tensilon test

 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

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!
AKA.. Acute febrile neuritis, acute ascending paralysis, Infectious neuritis Acute polyradiculopathy

 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!

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

Dizziness -Lightheadedness -Vertigo (room spinning or the sensation of spinning) -Feeling faint (pre-syncope) -Fainting (syncope) -Chest pain or pressure -Excessive fatigue -Rapid heart rate (tachycardia) -Stomach pain , Intestinal cramping, Nausea Vomiting, Retching

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

MEDICAL MANAGEMENT ICU admission Mechanical Ventilation TPN and IVF PLASMAPHERESIS IV IMMUNOGLOBULIN

TN

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

BELLS PALSY (Motor Dysfunction-CN)

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

 Bells palsy is considered by some

to represent a type of pressure paralysis. The inflamed, edematous nerve becomes compressed to the point of damage, or its nutrient vessel is occluded, producing ischemic necrosis of the nerve

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

SUMMARY

Disorder

Parkinsons

MS

MG

AD

Onset
Gender Cause

50-60
Males Unknown

20-40
Females

20-50
Females

50-60
females

Unknown Unknown unknown Autoimmun but its e or viral autoimmun e Myoneural junction of voluntary muscles Cerebral cortex

Area affected

Substantia White nigra in basal matter of ganglia brain & spinal cord

Disorder Patho-physio

Parkinsons Deficiency in dopamine which impairs coordination and autonomic function Muscle stiffness, nonintentional tremor, and autonomic dysfunction

MS Impair nerve impulse conduction, which is related the loss of myelin sheath Loss of bowel and bladder control, blurry of vision, paralysis, intentional tremor, and labile emotions

MG Impair transmission of impulses due to lack of acetylcholine

AD Loss of brain cells from cerebral cortex and creation of neurofibrillary tangles Memory loss, overactivity, emotional distress, Agitation, and feeling of disaster

s/sx

Profound muscle weakness, fatigue, and respiratory failure

Treatment

Disorder

Parkinsons

MS

MG

AD

Treatment

Supportive care and medications such as Ldopa, Artane, and cogentin

Supportive care and medications such as steroids, immuran, interferons,gla tiramers, rebif, baclofen

Supportive care and medications such as mestinon, prostigmin and steroids

Supportive care and medication such as tacrine hydrochloride ( cognex), folic acid, Aricept and Exelon

" It is better to aim high and miss the mark than aim low and hit it. You're better off getting close to your dream than not getting there at all.
Author Unknown