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NEUROMUSCULAR DYSFUNCTIONS Joanna Shedd, MS, CNS, RN LAUGHTER IS THE BEST MEDICINE LAUGHTER IS THE BEST MEDICINE CENTRAL NERVOUS SYSTEM Central Nervous System – Multiple Sclerosis – Parkinson’s Disease – Amyotrophic Lateral Sclerosis PERIPHERAL NERVOUS SYTEM Peripheral Nervous System – Myasthenia Gravis – Guillain-Barre Syndrome FUNCTIONS Motor – Weakness – Paralysis – Tremors Sensory – Numbness – Tingling – Pain FUNCTIONS Mental processes – Confusion – Coma Autonomic function – Regulates smooth muscle MULTIPLE SCLEROSIS Destruction of myelin sheath of brain & spinal cord Lack of myelin causes slowing or blockage of conduction MULTIPLE SCLEROSIS Demyelinated areas are scattered throughout CNS Can be both motor or sensory PATHOPHYSIOLOGY Characterized by remissions and exacerbations Disease progression differs from person to person Benign: Limited disability, slow progression Exacerbating: Remitting Chronic relapsing: Most common Chronic progressive: No remission STAGES Acute – Demyelinated areas remyelinate – Heal over with sclerotic or fibrous tissue Chronic – Nerve fibers degenerate – Disabilities become permanent ETIOLOGY Basically unknown, multiple theories Autoimmune response triggered by virus Delayed hypersensitivity response Family history Affects women more than men SIGNS & SYMPTOMS E: eye, optic neuritis A: ataxia, muscular incoordination S: speech, slurred, slow T: tremors, intentional tremor E: emotional, mood swings, depression R: rectal, bowel and/or bladder problems EXACERBATION Stress Fatigue Overheating Weather DIAGNOSTICS Thorough history and physical exam Cerebrospinal Fluid – Increase Tlymphocytes – IgG (oligoclonal banding) DIAGNOSTICS Magnetic Resonance Imaging: – visualize plaques and lesions DIAGNOSTICS Evoked response tests – Electroencephalogram (EEG) – Visual Evoked Response (VER) – Brainstem Auditory Evoked Response (BAER) GOALS Avoid or shorten exacerbations Maintain independence Decrease complications of immobility MEDICATIONS Interferon beta: 1B Interferon beta: 1A Steroids: acute exacerbations Immunosuppressants Muscle relaxants INTERVENTIONS Plasmapheresis in combination with medications Physical Therapy Occupational Therapy Patient education – Prevention – Protection PARKINSON’S DISEASE Imbalance of acetylcholine and dopamine Acetylcholine: excitatory Dopamine: inhibitory PARKINSON’S DISEASE Degeneration in substantia nigra Causes: – Trauma – Viral disease – Aging Degeneration accelerated, cause not known Increase excitatory SIGNS & SYMPTOMS T: tremor, resting tremor R: rigidity, muscle stiffness A: akinesia, slowness of movement P: postural instability, stooped posture SIGNS & SYMPTOMS Mask-like facial expression Shuffling gait Turns like a statue Speech difficulties: soft, slurred, monotonous SIGNS & SYMPTOMS General weakness Autonomic problems “Pill rolling” Slowness of thought Memory impairment DIAGNOSTICS History Physical exam Response to antiParkinson medications MEDICATIONS Levodopa/Carbidopa (Sinemet) Levoadpa is converted into dopamine by DOPA decarboxylase Carbidopa prevents Levodopa from converting to dopamine outside the brain MEDICATIONS Allows more dopamine to pass blood brain barrier Helps decrease side effects in the periphery Increases concentration of dopamine in the brain SIDE EFFECTS Nausea/Vomiting Sedation Hallucinations, psychosis Dyskinesia: involuntary wiggly movements Unsustained or unpredictable response (motor fluctuations) SIDE EFFECTS Postural hypotension Anxiety Depression Mood swings Cardiac arrhythmias Athetoid movements CAUTIONS Relieves most signs & symptoms On/Off response – sudden involuntary inability to initiate movement CAUTIONS Less effective with prolonged use Drug holiday Hospitalize during drug holiday Adjunctive therapy with Amantadine MEDICATIONS Dopamine agonists – mimic dopamine effect MAO-B inhibitors – slow progression Antiviral agent – Amantadine Anticholinergics – decrease effects of acetylcholine SURGERY Pallidotomy – Cauterize global pallidus in the basal ganglia – Interrupts nerve pathways – Decreases abnormal brain over activity SURGERY Adrenal medullary tissue transplants – Poor results – Transplanted tissue was necrotic – Fetal brain cell tissue transplants REHABILITATION Physical therapy Occupational therapy Speech therapy Nutrition High fowlers while eating Consistency and temperature of food AMYOTROPHIC LATERAL SCLEROSIS Lou Gehrig’s disease Motor neuron dysfunction Progressive, degenerative demyelinating disorder of motor neurons in the brain and spinal cord Both upper and lower AMYOTROPHIC LATERAL SCLEROSIS Motor disease NO sensory loss Mind intact CAUSES DNA abnormality Viral or autoimmune Metabolic or endocrine abnormality Over stimulation of glutamate SIGNS & SYMPTOMS Disease of middle age Fatigue, muscle weakness Progresses to paralysis Fasciculation, twitching, spasticity Atrophy r/t nerve cell death Starts in hands and spreads to arms then legs SIGNS & SYMPTOMS Difficulty swallowing, speaking Drooling due to affected head and neck muscles SIGNS & SYMPTOMS Difficulty breathing – affects diaphragm and intercostal muscles Death is usually from pneumonia or respiratory failure DIAGNOSTICS History Physical exam Rule out other diseases EMG – shows specific changes – loss of nerve supply to the muscle INTERVENTIONS No cure Riluzole (Rilutek) – May help prevent injury to motor neuron – Monitor liver function tests Supportive care 50% die within 5 years SUPPORTIVE CARE Keep independent as long as possible Prevent complications of immobility Comfort care Conserve energy SUPPORTIVE CARE Psychological support for patient and family Education regarding home care: – Gastrostomy tube feeding – Ventilator – Communication devices MEDICATIONS Antispasmodics – Baclofen (Lioresal) – Zanaflex (Tizanadien) – Spasticity interferes with functional ability MYASTHENIA GRAVIS Peripheral nervous system Autoimmune disease that causes a decrease in acetylcholine receptors MYASTHENIA GRAVIS Muscle receives weak stimulation, so unable to fully contract Muscle fatigues quickly After repeated stimulation, acetylcholine steadily decreases Muscles do not contract at all SIGNS & SYMPTOMS Classic sign: fluctuating weakness Affects voluntary muscles Onset insidious, progresses slowly Remissions and exacerbations Aggravated by infections, trauma, surgery, stress, change in medication regime Death usually r/t respiratory complications SIGNS & SYMPTOMS Ocular – Ptosis – Diplopia Facial – Flat expression – Open mouth Speech – voice fades with talking SIGNS & SYMPTOMS Difficulty chewing or swallowing Risk for aspiration Affects upper extremities before lower Proximal extremities more than distal Usually no sensory loss DIAGNOSTICS Tensilon test – Short-acting anticholinesterase drug – Inactivates cholinesterase – Positive test: dramatic improvement after IV injection DIAGNOSTICS EMG – Measures degree of muscle response to stimulation Anti-ach receptor antibody – 80% accurate Pulmonary function test – Assess degree of pulmonary involvement MEDICATIONS Short-acting anticholinesterase drugs – Increase Ach at all cholinergic receptors – GI tract irritation – Improves signs & symptoms, but is not a cure – Take on time – If late, decrease in function MEDICATIONS Steroids & Immunosuppressants – Decrease auto-antibody production – Steroid precautions SURGERY Thymectomy – Removal of thymus gland – 80% with myasthenia gravis have enlarged thymus – Improves signs & symptoms – In 40%, complete remission occurred INTERVENTIONS Pace activities – Plan rest periods, assist as needed – Assess respiratory status COMPLICATIONS Myasthenic crisis: exacerbation or progression of disease Cholinergic crisis: Overmedication with anticholinesterase drugs (less common) Signs & symptoms: generalized weakness, respiratory failure, requiring ventilator support Diagnosis: Tensilon test – Will improve myasthenic crisis – Will worsen cholinergic crisis GUILLAIN-BARRE SYNDROME Inflammatory disease process Demyelination of peripheral nerves Autoimmune response stimulated by viral illness GUILLAIN-BARRE SYNDROME Primarily motor affected Only one of 5 diseases processes that is NOT chronic Acute demyelinating polyneuropathy DIAGNOSTIC No influenza vaccine if history of GB No definitive test CSF protein – initially decrease followed by rapid, large increase EMG – slowed conduction velocity SIGNS & SYMPTOMS Acute Stage Paresthesia Pain Stiff Weakness Rapidly progressive paralysis Ascending paralysis SIGNS & SYMPTOMS Acute Stage Can progress to total paralysis May need ventilator support Cranial nerves affected – Cannot chew, swallow, talk, close eyes SIGNS & SYMPTOMS Acute Stage Autonomic dysfunction – Tachycarida or bradycardia – Cardiac arrthymias – Fluctuating BP – Urinary retention No change in LOC or thought processes SIGNS & SYMPTOMS Plateau/Stabilizing stage – Several days to weeks Recovery stage – 6 months to 2 years – Often resolves completely – Residual weakness – Complications of immobility INTERVENTIONS Supportive care Careful monitoring during acute stage May need ventilator, temporary pacemaker, tube feedings Prevent infection and complications of immobility No medications specific for disease process INTERVENTIONS Exercise limited in acute stage Rehab stage – gentle, passive ROM Psychological support – Frightened, anxious – Paralyzed, but mentally alert Plasmapheresis A client with numbness and tingling is tentatively diagnosed with Guillain-Barre. An important assessment for this client will be? A. B. C. D. Discomfort and pain on movement Breathing and tidal volume Metabolic and nutritional state Urine output and fluid intake What scale is used to measure neurological function? A. B. C. D. Bathroom scale Braden scale Glascow coma scale Pain scale Which of the following would be included when providing discharge teaching to a client with multiple sclerosis? A. B. C. D. “Avoid taking daytime naps” “Avoid taking hot baths and showers.” “Limit your fruit and vegetable intake.” “Restrict fluids to 1 liter a day.” A client is undergoing testing to confirm a diagnosis of Myasthenia gravis. What drug will most likely be given to test this disorder? A. B. C. D. Atenolol (Tenormin) Dopamine Kefzol (Ancef) Tensilon (Edrophonium) A client has Parkinson’s disease is on a thickened liquid diet and needs assistance with feedings. What position should the client be to prevent complications? A. High Fowler’s B. HOB up 20 degrees C. Flat on back D. Trendelenberg What intervention would inappropriate when caring for client with ALS? A. Active ROM exercises B. Airway maintained, especially on a vent C. Give Interferon IM daily using Z-track method D. Talk with client as you are doing procedures