Parkinson's Disease Lecture Notes: Symptoms & Management PDF

PARKINSON’S DISEASE JENIFER G. DETORIO, MAN, RN, PT, PHDN© LEMAR A. DETORIO, MAN, RN, PT, PHDN© NSG. 116 LECTURE UPDATED 2ND SEMESTER AY 2024-2025  Parkinson’s Disease Parkinson’s disease (PD) is a slow, progressive, neurodegenerative disease of the extra...

PARKINSON’S DISEASE JENIFER G. DETORIO, MAN, RN, PT, PHDN© LEMAR A. DETORIO, MAN, RN, PT, PHDN© NSG. 116 LECTURE UPDATED 2ND SEMESTER AY 2024-2025  Parkinson’s Disease Parkinson’s disease (PD) is a slow, progressive, neurodegenerative disease of the extrapyramidal motor system. Dopamine neurons in the substantia nigra are primarily affected, and degeneration of these neurons causes a disruption in the ability to generate body movements.  Incidence of Parkinson’s Disease PD is the second most common neurodegenerative disease of mid-to-late life in developed countries In United States (US) and Western Europe: Age Incidence 60 – 69 year old ~1 in 200 70’s ~1 in 100 80’s ~1 in 35 An estimate of approximately 10 million people worldwide are living with Parkinson’s Disease.  RISK FACTORS 1. Age It ordinarily begins in middle or late life, and the risk increases with age. Symptoms usually first appear in the fifth decade of life, however, cases have been diagnosed as early as 30 years of age. 2. Heredity 3. Gender Affects men more often than women  RISK FACTORS 4. Exposure to toxins Ongoing exposure to herbicides and pesticides, metals( manganese, iron) and steel alloy industries. 5. Atherosclerosis 6. Excessive accumulation of oxygen free radicals 7. Viral infections 8. Head trauma 9. Chronic use of antipsychotic medications 10. Life experiences such as emotional stress  Parkinson’s Disease Primary or Idiopathic Parkinson’s Disease The cause of the disease is unknown. Over the years the dopaminergic neurons degenerate Parkinsonism or Secondary Parkinson’s There is no degeneration as seen in above case, but the decrease in dopamine is drug induced.  Parkinsonism or Secondary Parkinson’s a neurologic syndrome in which a patient exhibits some of the symptoms associated with Parkinson’s disease— tremor, rigidity, bradykinesia, and postural instability. But parkinsonism is not Parkinson’s disease. Parkinsonism often has an identifiable cause  Pathophysiology Destruction of Degeneration dopaminergic neuronal cells Depletion of of the dopamine dopaminergic in the substantia nigra in the basal stores nigrostriatal ganglia pathway Imbalance of excitatory (acetylcholine) and inhibiting Impairment of (dopamine) extrapyramidal tracts neurotransmitters in the corpus striatum controlling complex body movements  Pathophysiology Imbalance of excitatory (acetylcholine) and inhibiting (dopamine) neurotransmitters in the corpus striatum Postural Tremors Rigidity Bradykinesia Changes TRIAD MANIFESTATIONS  Pathophysiology Clinical symptoms do not appear until 60% of the pigmented neurons are lost and the striatal dopamine level is decreased by 80%. Cellular degeneration impairs the extrapyramidal tracts that control semiautomatic functions and coordinated movements; motor cells of the motor cortex and the pyramidal tracts are not affected.  The Role of Dopamine Dopamine transmits chemical messages from one nerve cell to another across the synapse A synapse is a space between the presynaptic cell and the postsynaptic receptor. Dopamine is secreted into the synapse from membrane storage vesicles in the presynaptic membrane. Dopamine crosses the synapse and binds to the postsynaptic membrane, where it activates dopamine receptors. The Role of Dopamine  The Role of Dopamine Within the synapse, as dopamine travels from one cell to another, it can be broken down and rendered inactive by two enzymes, MAO (monoamine oxidase) and COMT (catechol-O-methyl transferase). One therapeutic strategy introduces a MAO inhibitor into the synapse, which interrupts the action of the MAO enzyme and prevents the breakdown of dopamine. This allows more dopamine to remain in the synapse and increases the likelihood that it will bind to the postsynaptic membrane.  Clinical Manifestations Parkinson’s disease has a gradual onset, and symptoms progress slowly over a chronic, prolonged course. Cardinal signs: A. Tremor B. Rigidity C. Bradykinesia (abnormally slow movements) D. Postural instability  Clinical Manifestations A. Tremor Slow, unilateral resting tremor Manifested as rhythmic, slow turning motion (pronation–supination) of the forearm and the hand and a motion of the thumb against the fingers as if rolling a pill between the fingers. Tremor is present while the patient is at rest; it increases when the patient is walking, concentrating, or feeling anxious.  Clinical Manifestations B. Rigidity Resistance to passive limb movement Passive movement of an extremity may cause the limb to move in jerky increments lead- pipe or cog-wheel movements Stiffness of the arms, legs, face, and posture are common. Early in the disease, the patient may complain of shoulder pain due to rigidity  Clinical Manifestations C. Bradykinesia overall slowing of active movement may take longer to complete activities difficulty initiating movement  Clinical Manifestations D. Postural Instability postural and gait problems loss of postural reflexes and the patient stands with the head bent forward and walks with a propulsive gait. The patient may walk faster and faster shuffling gait loss of balance increased risk for falls  Other Manifestations Aphonia Excessive secretion of salivary glands Absence of control over movements of eye. Loss of personal interest, loss of reasoning and orientation. Hypokinesia Psychiatric changes - depression, dementia delirium, and hallucinations.  Assessment and Diagnostic Findings PET Scan (Positron Emission Tomography) Single photon emission computed tomography (SPECT) Presence of two of the four cardinal manifestations: tremor, rigidity, bradykinesia, and postural changes. Early changes noticed: a. stooped posture b. Stiff arm c. slight limp d. Tremor e. slow, small handwriting  Medical Management 1. Pharmacologic Therapy Levodopa is the most effective agent and the mainstay of treatment. Levodopa is available in three forms: immediate-release, orally disintegrating, and sustained-release tablets Confusion, hallucinations, depression, and sleep alterations are associated with prolonged use  Medical Management Complications of dopaminergic medication long-term use: Within 5 to 10 years, most patients develop: 1. dyskinesia (abnormal involuntary movements) facial grimacing Rhythmic jerking movements of the hands head bobbing Chewing and smacking movements involuntary movements of the trunk and extremities. 2. Neuroleptic malignant syndrome characterized by severe rigidity, stupor, and hyperthermia  Medical Management 2. Surgical Management In patients with disabling tremor, rigidity, or severe levodopa-induced dyskinesia, surgery may be considered. Pallidotomy and Thalamotomy Neural Transplantation Deep Brain Stimulation  Nursing Management 1. Improving Mobility progressive program of daily exercise will increase muscle strength, improve coordination and dexterity, reduce muscular rigidity, and prevent contractures that occur when muscles are not used E.g walking, riding a stationary bicycle, swimming, gardening, stretching activities, postural exercises  Nursing Management 2. Enhancing Self-Care Activities Encouraging, teaching, and supporting the patient during ADLs promote self- care Environmental modifications Adaptive or assistive devices may be useful  Nursing Management 3. Improving Bowel Elimination Establish a regular bowel routine by encouraging the patient to follow a regular time pattern Increase fluid intake Eat foods with moderate-fiber content Laxatives should be avoided Raised toilet seat is useful  Nursing Management 4. Improving Nutrition 5. Enhancing Swallowing Sit upright during mealtime Semisolid diet with thick liquids Teach patient to place the food on the tongue, close the lips and teeth, lift the tongue up and then back, and swallow. Encouraged to chew first on one side of the mouth and then on the other. Remind patient to hold the head upright and make a conscious effort to swallow. Massaging the facial and neck muscles before meals  Nursing Management 6. Encouraging Use of Assistive Devices 6. Improving Communication 7. Supporting Coping Abilities A combination of physiotherapy, psychotherapy, medication therapy, and support group participation  Thank you! References & further Readings: ▪ Stromberg, H.K. (2023) Medical-Surgical Nursing Concepts and Practice 5th ed. Elservier ▪ Smeltzer, SC., Bare, BG., Brunner & Suddarth Textbook of Medical Surgical Nursing 15 ed. © 2022 Lippincott Williams & Wilkins Lemone.Burke.Bauldoff; Medical-Surgical Nursing Critical thinking in patient care 5th edition; Pearson 2011. ▪ Ignatavicius, Donna and Workman, Linda; Medical-Surgical Nursing: Patient- centered Collaborative Care 7th edition 2012.