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NEUROLOGIC DISORDERS

NEUROLOGIC DISORDERS. Myasthenia Gravis Parkinsons Disease Multiple Sclerosis Amyotrophic Lateral Schlerosis Spinal Cord Injury Intervertebral Disc Herniation Cranial Nerve Problems 2009. Myasthenia Gravis. DEFINITION. problem in neurotransmission

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NEUROLOGIC DISORDERS

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  1. NEUROLOGIC DISORDERS Myasthenia Gravis Parkinsons Disease Multiple Sclerosis Amyotrophic Lateral Schlerosis Spinal Cord Injury Intervertebral Disc Herniation Cranial Nerve Problems 2009

  2. Myasthenia Gravis

  3. DEFINITION • problem in neurotransmission • severe fatigue of voluntary muscles • defect of acetylcholine receptor sites • at the myoneuronal junction • theories indicate autoimmune problem • Remissions/exacerbations • Progressive proximal muscle weakness improving with rest

  4. CLINICAL MANIFESTATIONS • Patients indicate abnormal fatigue of the voluntary muscles of the eye, the respiratory tract and the limb muscles • Also have difficulty with speech and swallowing • End up choking with meals • Ptosis, diplopia, dysphagia • MOST ADVANCED: all muscles weakened: no respiratory function, no bladder and bowel function

  5. DIAGNOSTIC TESTS • Tensilon test: • give patient a short acting anticholinesterase (Tensilon or edrophonium chloride) that enhances neurotransmission and results in abrupt, but short term improvement of symptoms • Atropine : antidote for Tensilon • EMG: electromyography:

  6. LABORATORY ASSESSMENT • THYROID FUNCTION STUDIES DONE: thyrotoxicosis seen with MG • Serum protein electrophoresis: for immunologic disorders • Acetylcholine receptor antibodies (AChR): important diagnositic criterion 80-90% of clients with MG have elevated AChR • Often have thymoma or hyperplasia of thymus gland

  7. DRUG THERAPY Anticholinesterase medications: • Pyridostigmine bromide (Mestinon), neostigmine bromide (Prostigmin) Increases acetylcholine at the neuromuscular junction • Dosage regulated based on improved strength and less fatigue • MUST BE GIVEN ON TIME to keep stable blood levels • RESULT: pt weakness worse

  8. DRUGS TO AVOID: increase weakness • Magnesium • Morphine • Curare • Quinine • Quinidine • Procainamide • Hypnotics • sedatives • Antibiotics: • Neomycin • Kanamycin • Polymyxin B • tetracyclines

  9. DRUG THERAPY • Corticosteroids used to control and improve symtoms: • prednisone(Deltasone, Winpred) • As steroids increased anticholinesterase dosage decreased • Cytotoxic medications used: • why they work unknown

  10. TREATMENT • PLASMAPHERESIS: plasma exchange • Used to treat exacerbations • HOW IS THIS DONE: Blood cells and antibody containing plasma separated out then the cells and a plasma substitute reinfused • Improves symptoms in 75% of patients

  11. TREATMENT CONTINUED • IV immune globulin (IVIG) • Works as well as plasmapheresis during exacerbations

  12. Summary of therapies • Not a cure • Does not stop the production of acetylcholine receptor antibiodies

  13. SURGICAL TREATMENT • Thymectomy continues to be associated with improvement in 50-92%% of patients • RESULT: • produces antigen specific immunosuppression • Results in clinical improvement • Decreases need for medication • Takes a year for benefit to be seen because of the long life of circulating T cells

  14. MYASTHENIC CRISIS • SEEN WITH UNDERMEDICATION WITH CHOLINESTERASE INHIBITORS • Severe generalized weakness and respiratory failure • Seen after stress (URI, infection, medication change, surgery, obstetrical delivery, high environmental temperature) • Patient needs ventilatory support • Patient will need help with all ADL • Suctioning, chest PT

  15. CHOLINERGIC CRISIS • RESULT OF OVERMEDICATION WITH ANTICHOLINESTERASE DRUGS • Can mimic symptoms of myasthenic crisis • Differentiated via Tensilon test • Pt with Myasthenic Crisis will show immediate improvement following Tensilon administration • Pt with Anticholinergic Crisis will show no improvement and may get worse

  16. TREATMENT OF CHOLINERGIC CRISIS • STOP ALL ANTICHOLINESTRASE MEDICATIONS • Give Atropine sulfate given IV • SE: secretions thickened

  17. NURSING DIAGNOSIS

  18. THYMECTOMY: • REMOVAL OF THYMUS GLAND DONE EARLY IN DISEASE • May take several years for remission to occur if it occurs at all • Review p 1017 Iggy

  19. NURSING CARE • Most pts seen on outpatient basis • Teaching: • use of medications • S&S of myasthenic crisis and choinergic crisis • How to conserve energy • Ways to avoid aspiration • Have suction at home • Gastrostomy feeding instruction • Avoid factors that increase crisis • Eye care

  20. PARKINSONS DISEASE

  21. DEFINED Presence of motor dysfunction with 4 cardinal symptoms • resting tremor • akinesia (slowness of body movement) • rigidity • Postural instability NO PREVENTION, NO CURE AGE RANGE: 40-70, PEAK 60 Michael J. Fox dx at age 30

  22. PATHOPHYSIOLOGY Reduced amount of dopamine • Result: inhibition effect lost • Excitatory effect predominant Reduced norepinephrine in sympathetic NS of the heart: • Orthostatic hypotension

  23. ASSESSMENT: • Initially: one limb involved with mild weakness and arm and hand trembling • Progresses to both limbs involved, slow shuffling gait • Continues to worsen: gait disturbances(slow shuffling, short hesitant steps, propulsive gait • Severe involvement: akinesia, rigidity, CANNOT GET OOD

  24. FURTHER ASSESSMENT: • Rigidity of facial muscles: • masklike facies • Drooling • Dysphagia • Dysarthria: Rapid slurred speech • Echolalia: repetition

  25. ASSESSMENT CONTINUED • PSYCHOSOCIAL • Emotionally labile • Delayed reaction time

  26. DRUGS • ANTIPARKINSON AGENT: monoamine oxidase type b inhibitor: selegiline (Eldepryl, Carbex, Novo-Selegiline): used to protect the neurons, successful in reducing the use of Levodopa until later • Catechol O-methyltransferase (COMT) inhibitors: • Tolcapone (Tasmar) • Entacapone (Comtan) Block breakdown of levodopa in body so more can go to brain and convert to dopamine

  27. DRUGS • DOPAMINE AGONISTS: providing dopamine that is missing • Levodopa (Dopar, L-dopa) and • carbidopa (Sinemet): ANTIPARKINSON AGENT/ANTIVIRAL: • amantadine (Symmetrel): potentiates action of dopamine in CNS, treats tremor; also treats symptoms of “wearing off”

  28. TREATMENT • Meds may need drug holiday - effectiveness after used for long time; admit to hospital to try other drugs • p693 FOR SURGICAL tx • Stereotactic Pallidotomy/Thalamotomy Deep brain stimulation fetal Tissue transplant

  29. NURSING DIAGNOSIS • Self-care deficit related to slowness of movement and muscle rigidity • Risk for injury related to postural instability and muscular rigidity • Impaired verbal communication related to slowness of movement • Altered nutrition related to poor muscle control

  30. NURSING DIAGNOSIS CONTINUED • Knowledge deficit related to complexity of and fluctuations in treatment regimen • Ineffective coping relate to progressive nature of illness

  31. IMPLEMENTATION • Establish routine for personal care • Safety in bathing, transferring, walking • AROM, PROM • Encourage pt to take a deep breath before initiating a conversation, using gestures • Rigidity of facial expression hides pts true feelings

  32. IMPLEMENTATION • Meals thickened liquids, semisolids • Eat sitting up • Suction • Daily wgts • Increase fluids/day for constipation • Drug flowsheet to document response to medications • Keep patient active as long as possible

  33. MULTIPLE SCLEROSIS AUTOIMMUNE DISORDER

  34. DEFINED • Demyelinating disease affecting nerve fibers of the brain and spinal cord • CAUSE unknown. Thought to be an autoimmune problem with a viral trigger • Lesions scattered through the white matter of the brain around the ventricles; some in grey matter • Inflammatory response triggers phagocytosis with myelin as the target

  35. OLDER DRUG THERAPY • The most widely accepted drug treatment is corticosteroids : • Methylprednisolone(Solumedrol) • Given IV followed by oral prednisone • Steroids decrease the inflammatory response, decrease the edema, improvement of symptoms • Cyclophosphamide (Cytoxan) used for chronic progressive disease to produce temporary remission from 1-3 years

  36. DEFINITION CONTINUED • Edema around lesions • Eventually a hard plaque forms • Characterized by exacerbations and remissions • Progressive from benign with few symptoms to chronic with complete paralysis. • 70% of pts lead active productive lives with long periods of remission

  37. DIAGNOSIS • lumbar puncture: CSF shows increase protein, lymphocytes, IgG, presence of oligoclonal bands and increased myelin basic protein • EMG: prolonged impulse conduction • MRI: demonstrates white matter lesions (plaques) of brain, brainstem and spinal cord

  38. NEW DRUG THERAPY BIOLOGICAL RESPONSE MODIFIERS: recommended to use one of these three: • Interferon beta -1a (Avonex) - weekly IM • Interferon beta-1b recombinant (Betaseron) - every other day SQ • PURPOSE AND SIDE EFFECTS OF BOTH • Slows physical disability, decreases physical worsening of disease • Major SE: suicidal tendency, depression • Glatiramer acetate (formerly Copolymer I) (Copaxone) - every other day SQ

  39. SYMPTOMS • Blurred vision • Double vision • Dysphagia • Facial weakness • Numbness • Pain • Weakness

  40. Symptoms Continued • paralysis • abnormal gait • tremor • vertigo • fecal and urinary incontinence • decreased short term memory • word finding trouble

  41. Symptoms Continued • decreased concentration • mood alteration • decreased libido for women • ejaculatory dysfunction for men • overwhelming weakness

  42. DRUGS • Baclofen (Lioresal), Diazepam (Valium), Dantrolene sodium(Dantrium) - for spasticity • Carbamazepine (Tegretol), tricyclic antidepressants (amitriptyline),: paresthesia • propranolol (Inderal), clonazepam (Klonopin) – used for cerebral ataxia • Amantadine hydrochloride (Symmetrel): fatigue • oxybutynin chloride (Ditropan), propantheline bromide (ProBanthine) - decreased urinary urgency, incontinence • Bulk additives (Metamucil) - constipation • Colace - improved bowel control • Dulcolax – stimulant • Tizanidine (Sanaflex) antispasmodic for pain

  43. NURSING INTERVENTIONS • Self-care deficit: balance assistance with independence; promote own routine • Urinary retention/incontinence: intermittent catherization, Texas catheter for men • Bowel incontinence: regular routine, high fiber diet, and fluids • Impaired skin integrity related to immobility: skin assessment

  44. NURSING INTERVENTION • Fatigue related to disease process: pace self

  45. AMYOTROPHIC LATERAL SCLEROSIS Lou Gerhig’s Disease

  46. Amyotrophic Lateral Sclerosis or Lou Gehrig’s disease • Progresive degenerative disease involving the motor system (motor neurons) • Sensory and autonomic systems not involved • No mental status changes

  47. Cause • Excess of glutamate: chemical responsible for relaying messages between the motor neurons • As the motor neurons die the muscle cells they supply undergo atrophic changes leading to paralysis

  48. PROGRESSION OF DISEASE • Muscle weakness and atrophy develop leading to flaccid quadriplegia • Eventually respiratory muscles become affected leading to respiratory compromise, pneumonia and death • No known cure, treatment symptomatic

  49. FATIGUE Fatigue while talking Muscle weakness/atrophy Tongue atrophy Dysphagia (difficulty swallowing) Weakness hands and arms Fasciculations (twitching) of face Nasal quality of speech Dysarthria (difficulty speaking) WHAT DO YOU SEE?

  50. CARE • Focus on symptoms • Monitor respiratory status • Prepare to initiate respiratory support • Assess complications of immobility

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