Neurological Autoimmune Disorders PDF (University of Belize)

Summary

This document is a lecture on Neurological Autoimmune Disorders, focusing on Multiple Sclerosis, Myasthenia Gravis, Parkinson's, and Alzheimer's Disease. The lecture notes, prepared in 2020 by Ms. Michelle Cox Hoare, cover various aspects including pathophysiology, clinical manifestations, assessment and diagnostic findings, and medical management. It's a great resource for nursing and medical students.

Full Transcript

UNIVERSITY OF BELIZE NURS3101 – CARE OF THE ADULT NEUROLOGICAL AUTOIMMUNE DISORDERS POPULATION WEEK THIRTEEN BACHELORS OF SCIENCE IN NURSING FACULTY OF HEALTH SCIENCES...

UNIVERSITY OF BELIZE NURS3101 – CARE OF THE ADULT NEUROLOGICAL AUTOIMMUNE DISORDERS POPULATION WEEK THIRTEEN BACHELORS OF SCIENCE IN NURSING FACULTY OF HEALTH SCIENCES No. MS. MICHELLE COX HOARE ( 125 MINUTES) Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. LEARNING OBJECTIVES At the end of this session students will be able to: 1. define what is Multiple Sclerosis. 2. describe the pathophysiology of Multiple Sclerosis, and Myasthenia Gravis. 3. describe the clinical manifestations of Multiple Sclerosis and Myasthenia Gravis. 4. state what is Parkinson and Alzheimer’s disease. 5. describe the pathophysiology of Parkinson and Alzheimer's disease 6. describe the medical and nursing management of the named neurological disorders: Myasthenia Gravis, Guillain-Barre Syndrome, Parkinson and Alzheimer’s disease. 7. apply the nursing process in the nursing management of patients with Multiple Sclerosis, Guillain-Barre Syndrome, and Parkinson disease. Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. WHAT IS MULTIPLE SCLEROSIS (MS)? MS is an autoimmune condition, which means your immune system mistakes part of your body for a foreign substance and attacks. MS is an immune-mediated, progressive demyelinating disease of the CNS. Demyelination refers to the destruction of myelin—the fatty and protein material that surrounds certain nerve fibers in the brain and spinal cord; it results in impaired transmission of nerve impulses. The cause of MS is an area of ongoing research. Autoimmune activity results in demyelination, but the sensitized antigen has not been identified. Multiple factors play a role in the initiation of the immune process. Autoimmune activity results in demyelination, but the sensitized antigen has not been identified. Multiple factors play a role in the initiation of the immune process. MS is considered to have many risks, including genetic, immunological and environmental factors. However, it has not been found to be genetically transmitted. Environmental risks include smoking, lack of vitamin D exposure, and exposure to the Epstein-Barr virus. Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. DEMYELINATION Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. Clinical Manifestations Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. Assessment and Diagnostic Findings The diagnosis of MS is based on the presence of multiple plaques in the CNS observed with Magnetic resonance imaging (MRI). Spinal tap test (Lumbar puncture) high levels of antibodies in CSF is indicative of MS Visual evoked potential. Measures response to visual stimulus Neuropsychological testing may be indicated to assess cognitive impairment. Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. MEDICAL MANAGEMENT There is no cure for MS Management strategies target speeding recovery from attacks; slowing the progression of the disease and managing MS symptoms: the various motor and sensory symptoms and effects of immobility that can occur. Pharmaceuticals: Immunomodulators; Corticosteroids (dexamethasone, methylprednisolone); immunosuppressants (methotrexate) Disease modifying therapies Symptom Management Symptoms requiring intervention include spasticity, fatigue, bladder dysfunction, and ataxia. Physical therapy Muscle relaxanats Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. NURSING PROCESS Assessment Nursing Diagnoses Assessment of function is carried out both when the patient is Impaired bed and physical mobility related to weakness, well rested and when fatigued. muscle paresis, spasticity, increased weight The patient is assessed for weakness, spasticity, visual Risk for injury related to sensory and visual impairment impairment, incontinence, and disorders of swallowing and speech. Impaired urinary and bowel elimination (urgency, frequency, incontinence, constipation) related to nervous system Additional areas of assessment include how MS has affected dysfunction the patient’s lifestyle, Impaired verbal communication and risk for aspiration related to cranial nerve involvement Chronic confusion related to cerebral dysfunction Ineffective individual coping related to uncertainty of course of MS Impaired home maintenance management related to physical, psychological, and social limits imposed by MS Potential for sexual dysfunction related to lesions or psychological reaction Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. Planning and Goals Nursing Interventions The major goals for the patient may include: - promoting physical activity promotion of physical mobility - exercise avoidance of injury - minimizing spasticity and contractures achievement of bladder and bowel continence - rest and nutrition promotion of speech and swallowing mechanisms improvement of cognitive function development of coping strengths improved home maintenance management adaptation to sexual dysfunction Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. MYASTHENIA GRAVIS Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. Myasthenia Gravis Myasthenia gravis, an autoimmune disorder affecting the myoneural junction, is characterized by varying degrees of weakness of the voluntary muscles. It is also a neuromuscular disorder It occurs when communication between nerve cells and muscles become impaired. This impairment prevents crucial muscle contractions from occurring, resulting in muscle weakness. The most commonly affected muscles are those of the eyes, face, and mouth. Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. Pathophysiology Normally, a chemical impulse precipitates the release of acetylcholine from vesicles on the nerve terminal at the myoneural junction. The acetylcholine attaches to receptor sites on the motor endplate and stimulates muscle contraction. Continuous binding of acetylcholine to the receptor site is required for muscular contraction to be sustained. In myasthenia gravis, antibodies directed at the acetylcholine receptor sites impair transmission of impulses across the myoneural junction. Therefore, fewer receptors are available for stimulation, resulting in voluntary muscle weakness that escalates with continued activity. Of people with myasthenia gravis, 75% have either thymic hyperplasia or a thymic tumor, and the thymus gland is believed to be the site of antibody production. Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. Clinical Manifestations The initial manifestation of myasthenia gravis in 80% of patients involves the ocular muscles. Diplopia and ptosis (drooping of the eyelids) are common Weakness of the muscles of the face and throat (bulbar symptoms) and generalized weakness. Weakness of the facial muscles results in a bland facial expression. Laryngeal involvement produces dysphonia (voice impairment) and dysphagia, which increases the risk of choking and aspiration. Generalized weakness affects all extremities and the intercostal muscles, resulting in decreasing vital capacity and respiratory failure. Myasthenia gravis is purely a motor disorder with no effect on sensation or coordination. Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. Assessment and Diagnostic Findings Physical examination Tensilon test - acetylcholinerase inhibitor test Edrophonium chloride (Tensilon), a fast-acting acetylcholinesterase inhibitor, is administered IV to diagnose myasthenia gravis. The ice test is a diagnostic test with comparable sensitivity to the Tensilon test. With the ice test, an ice pack is held over the eyes of the patient for 1 minute; the ptosis should temporarily resolve in a patient with myasthenia gravis MRI Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. Medical Management Management of myasthenia gravis is directed at improving function and reducing and removing circulating antibodies. Therapeutic modalities include administration of anticholinesterase medications and immunosuppressive therapy, plasmapheresis, and thymectomy. Examples of Pharmacologic Therapy: - Pyridostigmine bromide (Mestinon), an anticholinesterase medication, is the first line of therapy. - Corticosteroids (Prednisone) - Cytotoxic medications are used to treat myasthenia gravis if there is inadequate response to steroids - Intravenous immune globulin (IVIG) is also used to treat exacerbations - Plasmapheresis (plasma exchange) is a technique used to treat exacerbations. Plasma exchange produces a temporary reduction in the level of circulating antibodies. Surgical Management: Thymectomy (surgical removal of the thymus gland) can produce antigen-specific immunosuppression and result in clinical improvement. Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. Complications A myasthenic crisis is an exacerbation of the disease process characterized by: severe generalized muscle weakness, jaw and tongue weakness, inability to swallow,nasal tone respiratory and bulbar weakness that may result in respiratory failure. Crisis may result from disease exacerbation or a specific precipitating event. The most common precipitator is respiratory infection; stress, medication change, surgery, pregnancy, and adverse reactions to medications that can exacerbate myasthenia. Intubation and mechanical ventilation usually required Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. Nursing Management Myasthenia gravis is a chronic disease and most patients are seen on an outpatient basis, much of the nursing care focuses on patient and family education. Educational topics for outpatient self-care: medication management, energy conservation, strategies to help with ocular manifestations, and prevention and management of complications. Medication management emphasize consequences of delaying medication and the signs and symptoms of myasthenic and cholinergic crisis. To minimize the risk of aspiration, mealtimes should coincide with the peak effects of anticholinesterase medication. Impaired vision results from ptosis of one or both eyelids, decreased eye movement, or double vision. The patient is instructed to tape the eyes closed for short intervals and to regularly instill artificial tears. Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. Myasthenic Crisis Respiratory distress and varying degrees of dysphagia, dysarthria (difficulty speaking), eyelid ptosis, diplopia, and prominent muscle weakness are symptoms of myasthenic crisis. The patient is placed in an intensive care unit for constant monitoring Providing ventilatory assistance takes precedence in the immediate management of the patient with myasthenic crisis. Ongoing assessment for respiratory failure is essential. The nurse assesses the respiratory rate, depth, and breath sounds and monitors pulmonary function parameters (vital capacity and negative inspiratory force) to detect pulmonary problems before respiratory dysfunction progresses. Blood is drawn for arterial blood gas analysis. Endotracheal intubation and mechanical ventilation may be needed. If the abdominal, intercostal, and pharyngeal muscles are severely weak, the patient cannot cough, take deep breaths, or clear secretions. Chest physiotherapy, including postural drainage to mobilize secretions and suctioning to remove secretions, may have to be performed frequently. Note Postural drainage should not be performed for 30 minutes after feeding. Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. GUILLAIN-BARRE SYNDROME Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. Guillain-Barré syndrome is an autoimmune attack on the peripheral nerve myelin. The result is acute, rapid segmental demyelination of peripheral nerves and some cranial nerves, producing ascending weakness with dyskinesia (inability to execute voluntary movements), hyporeflexia, and paresthesias (a sensation of numbness, tingling, or a “pins and needles” sensation). An antecedent event (most often a viral infection) precipitates clinical presentation in approximately 60% to 70% of cases. The annual incidence of Guillain-Barré syndrome is 1 to 2 cases per 100,000 people, and it is more frequent in males between 16 and 25 years of age and those older than 55 years. Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. Pathophysiology Myelin is a complex substance that covers nerves, providing insulation and speeding the conduction of impulses from the cell body to the dendrites. The cell that produces myelin in the peripheral nervous system is the Schwann cell. In Guillain-Barré syndrome, the Schwann cell can be spared, allowing for remyelination in the recovery phase of the disease. When damage has occurred to the axons, then regrowth is required and takes months or years and is often incomplete. Guillain-Barré syndrome is the result of a cell-mediated and humoral immune attack on peripheral nerve myelin proteins that causes inflammatory demyelination. An infectious organism that contains an amino acid, mimics the peripheral nerve myelin protein. The immune system cannot distinguish between the two proteins and attacks and destroys peripheral nerve myelin. With the autoimmune attack, there is an influx of macrophages and other immune-mediated agents that attack myelin and cause inflammation and destruction, interruption of nerve conduction, and axonal loss. Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. Clinical Manifestations Guillain-Barré syndrome typically begins with muscle weakness and diminished reflexes of the lower extremities. Areflexia is a hallmark of GBS Hyporeflexia Ascending motor weakness may progress to tetraplegia. Ataxia Demyelination of the nerves that innervate the diaphragm and intercostal muscles results in neuromuscular respiratory failure. Sensory symptoms include dysesthesias of the hands and feet and pain related to the demyelination of sensory fibers. Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. Cranial nerve demyelination can result in a variety of clinical manifestations. Optic nerve demyelination may result in blindness. Bulbar muscle weakness related to demyelination of the glossopharyngeal and vagus nerves results in the inability to swallow or clear secretions Vagus nerve demyelination results in autonomic dysfunction, manifested by instability of the cardiovascular system. The presentation is variable and may include tachycardia, bradycardia, hypertension, or orthostatic hypotension. Guillain-Barré syndrome does not affect cognitive function or LOC. Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. Assessment and Diagnostic Findings The patient presents with symmetric weakness, diminished reflexes, and upward progression of motor weakness A history of a viral illness in the previous few weeks suggests the diagnosis. Changes in vital capacity and negative inspiratory force are assessed to identify impending neuromuscular respiratory failure. Serum laboratory tests are not useful in the diagnosis. However, elevated protein levels are detected in CSF evaluation, without an increase in other cells. Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. Medical Management Guillain-Barré syndrome is a medical emergency management in an intensive care unit. Assessment of changes in muscle strength and respiratory function alert the clinician to the physical and respiratory needs of the patient. Respiratory therapy or mechanical ventilation may be necessary to support pulmonary function and adequate oxygenation. Plasmapheresis and IVIG are used to directly affect the peripheral nerve myelin antibody level Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. NURSING MANAGEMENT Assessment Nursing Diagnoses Ongoing assessment for disease progression is Ineffective breathing pattern and impaired critical. gas exchange related to rapidly progressive weakness and impending respiratory failure The patient is monitored for life-threatening complications: Impaired bed and physical mobility related to paralysis - respiratory failure Imbalanced nutrition: less than body - cardiac dysrhythmias requirements related to inability to swallow - venous thromboembolism (VTE) including Impaired verbal communication related to deep vein thrombosis (DVT) or (PE) cranial nerve dysfunction Fear and anxiety related to loss of control and paralysis Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. Nursing Interventions Evaluation Maintaining Respiratory Function - Maintains effective respirations and airway Enhancing Physical Mobility clearance Providing Adequate Nutrition - Shows increasing mobility Improving Communication - Receives adequate nutrition and hydration Decreasing Fear and Anxiety - Demonstrates recovery of speech Monitoring and Managing Potential - Shows lessening fear and anxiety Complications - Has absence of complication Promoting Home and Community- Based Care Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. NEUROlOGICAL DEGENERATIVE DISORDER PARKINSON’S DISEASE Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. Parkinson’s Disease Parkinson’s disease is a progressive neurologic disorder that affects movement and eventually leads to disability. It is the fourth most common neurodegenerative disease, and 60,000 new cases are reported each year in the United States The disease affects men more often than women. Symptoms usually first appear in the fifth decade of life; however, cases have been diagnosed as early as 30 years of age. The degenerative or idiopathic form of Parkinson’s disease is the most common; Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. Pathophysiology Parkinson’s disease is associated with decreased levels of dopamine resulting from degeneration of dopamine storage cells in the substantia nigra in the basal ganglia region of the brain. Fibers or neuronal pathways project from the substantia nigra to the corpus striatum, where neurotransmitters are key to the control of complex body movements. Through the neurotransmitters acetylcholine (excitatory) and dopamine (inhibitory), striatal neurons relay messages to the higher motor centers that control and refine motor movements. The loss of dopamine stores in this area of the brain results in more excitatory neurotransmitters than inhibitory neurotransmitters, leading to an imbalance that affects voluntary movement. Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. Clinical Manifestations Parkinson’s disease has a gradual onset, and symptoms progress slowly over a chronic, prolonged course. The cardinal signs are tremor, rigidity, bradykinesia (abnormally slow movements), and postural instability. Tremor: a slow, unilateral resting tremor is present in the majority of patients at the time of diagnosis Rigidity: Resistance to passive limb movement characterizes muscle rigidity. Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. CLINICAL MANIFESTATIONS Bradykinesia: most common feature is the overall slowing of active movement. Postural instability: The patient commonly develops postural and gait problems. A loss of postural reflexes occurs, and the patient stands with the head bent forward and walks with a propulsive gait. The posture is caused by the forward flexion of the neck, hips, knees, and elbows. The patient may walk faster and faster, trying to move the feet forward under the body’s center of gravity. Difficulty in pivoting causes loss of balance (either forward or backward). Gait impairment and postural instability place the patient at increased risk for falls Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. Assessment and Diagnostic Findings The disease is diagnosed clinically from the patient’s history and the presence of two of the four cardinal manifestations: tremor, rigidity, bradykinesia, and postural changes. Early diagnosis can be challenging because patients rarely are able to pinpoint when the symptoms started. Medical Management Treatment is directed toward controlling symptoms and maintaining functional independence, because no medical or surgical approaches in current use prevent disease progression. Care is individualized for each patient based on presenting symptoms and social, occupational, and emotional needs. Pharmacologic management is the mainstay of treatment: Antiparkinsonian medications (1) increasing striatal dopaminergic activity; (2) reducing the excessive influence of excitatory cholinergic neurons on the extrapyramidal tract, thereby restoring a balance between dopaminergic and cholinergic activities; or (3) acting on neurotransmitter pathways other than the dopaminergic pathway. Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. NURSING MANAGEMENT Assessment Nursing Diagnoses Focuses on how the disease has affected the patient’s ADLs and functional abilities: mobility, feeding, communication, and Impaired physical mobility related to muscle rigidity and self-care difficulties. postural impairment Self-care deficits (feeding, dressing, hygiene, and Assess cranial nerves, cerebellar function (coordination) and toileting) related to tremor and muscle rigidity motor function. Constipation related to medication and reduced activity Observe gait and performance of activities Imbalanced nutrition: less than body requirements related to tremor, slowness in eating, difficulty in chewing and swallowing Assess for speech clarity and space Impaired verbal communication related to decreased speech volume, slowness of speech, inability to move facial muscles Assess for signs of depression Ineffective coping related to depression and dysfunction due to disease progression Assess family supports and access to social service Risk for fall-related injury Neurologic; musculoskeletal Impaired sleep pattern Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. ALZHEIMER’S DISEASE Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. Alzheimer’s Disease Chronic irreversible brain disease that is a type of dementia. Is a degenerative brain disorder of unknown etiology which is most common form of dementia, that usually starts in late middle age or in old age, results in progressive memory loss, impaired thinking , disorientation and changes in personality and mood. Begins gradually There is degeneration of brain neurons especially in the cerebral cortex and presence of neurofibrillary tangles and plagues containing beta-amyloid cess. Average length of the disease varies per person - can last up to 20+ years - not a normal part of the aging process Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. Incidence Over 5 million Americans have Alzheimer’s Disease. 20 million affected, including nearly 15.4 million unpaid caregivers Every 66 seconds someone in the US develops the disease CDC: 5th leading cause of death among adults > 65 years Risk Factors: Family History ( Hereditary) Age Gender Metabolic Syndrome: Diabetes; High Blood Pressure; High Cholesterol and Obesity Smoking Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. Pathophysiology To understand dementia and Alzheimer’s disease, it is important to understand the brain: - controls everything we do - Billions of cells that communicate with each other, repair themselves (in healthy brains) Neurons cannot communicate: - Development of plaques that form outside the neurons - Neurofibrillary tangles which form outside the neuron itself. - Severe stage: Brain atrophy When these healthy neurons dies: - memory loss - judgement impairs - learning problems - communication and behavior problems - mood swings - Inability to perform self-care Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. Alzheimer’s Disease Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. Warning Signs Misplacing objects and inability to retrace steps Memory loss that disrupts daily life Trouble with spatial relationships Difficulty planning or solving problems New problems with words in speaking or writing Forgetting how to do familiar tasks Mood swings and changes in personality Confusion with dates, time or place Altered decision making Withdrawal from work or social situations Poor judgement or relying on someone else, such Difficulty initiating activities in social as a spouse to make decisions or answer interactions questions. Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. Stages of Alzheimer’s Disease Mild Cognitive Impairment (MCI) - Memory difficulties greater than would be expected for an individual’s age and education. - Most MCI progresses to Alzheimer’s disease Early Stage - Forgets material just read, loses misplaces objects, has trouble coming up with the right word. Middle Stage - Asks the same question over and over, fine motor impairment, becomes confused about where they are, begins to wander Late Stage - Unable to communicate with words, becomes incontinent, unable to walk, requires 24 hour care Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. Medical Management Medications Non-Pharmacological symptom management - Communication and interaction - Therapeutic activities - Home environment modification - Maintaining overall health Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. Nursing Management Keeping client healthy Research suggest that a host of factors beyond genetics may play a role in reducing the risk of developing Alzheimer's disease Promote mental activity Promote social activity Physical Activity Nutrition Support No Smoking Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. Summary We have reviewed the neurologic autoimmune disorders namely: MS is an immune-mediated, progressive demyelinating disease of the CNS. Demyelination refers to the destruction of myelin—the fatty and protein material that surrounds certain nerve fibers in the brain and spinal cord; it results in impaired transmission of nerve impulses. Management strategies target speeding recovery from attacks; slowing the progression of the disease and managing MS symptoms: the various motor and sensory symptoms and effects of immobility that can occur. Pharmaceuticals: Immunomodulators; Corticosteroids (dexamethasone, methylprednisolone); immunosuppressants (methotrexate) Disease modifying therapies Symptom Management Guillain-Barré syndrome is an autoimmune attack on the peripheral nerve myelin. The result is acute, rapid segmental demyelination of peripheral nerves and some cranial nerves, producing ascending weakness with dyskinesia (inability to execute voluntary movements), hyporeflexia, and paresthesia (a sensation of numbness, tingling, or a “pins and needles” sensation). Parkinson’s disease is a chronic, progressive neurologic disorder that results from the loss of the neurotransmitter dopamine in a group of brain structures that controls movement. The cardinal symptoms are resting tremors, rigidity, akinesia and postural instability. Nursing care is focused on the health assessment, medication instruction and monitoring, client and family education. Alzheimer’s disease is a progressive degenerative disorder of the brain that is irreversible. The initial stages include recent memory loss and impaired judgement, inability to learn and retain new information, and difficulty finding words. Later stages include decreased ability to care for self, wandering, agitation and hostility, and possibly inability to walk, incontinence and no intelligible speech. Medications may help memory in early stages but there is no cure. Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. REFERENCES Hinkle. J. and Cheever, K.H. (2014). Brunner and Suddarth’s Textbook of Medical-Surgical Nursing. 13th. Ed. Wolters Kluwer. Lippincott Williams and Wilkins Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize. The End Recorded Lecture Policy: Students who are unable to attend virtual classes or consultation sessions have the right to download and view recorded lectures and consultation sessions for their personal study only. Lectures recorded for this purpose may not be shared with other people without the consent of the instructor. The recorded lectures may not be published without the express consent of the instructor and without giving proper identity and credit to the instructor. Students who use screen-recording softwares are required to adhere to the recording guidelines stated above. Copyright© 2020 University of Belize. All rights reserved Not to be reproduced or disseminated without permission from the University of Belize.

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