Parkinson s Disease Jean Van Kingsley MS, FNP-BC Objectives Describe the pathophysiolgy of PD. Review clinical charachteristics of PD. Identify management strategies, to maximize functional status. Recognize treatment goals. Review non-pharmacological treatment modalities Review terms associated with Parkinson s Disease. Identify newer developments and considerations in the field of PD. Patients will ask you. Can you determine the reason that I developed PD? What are my treatment options? What are the pros and cons of each? What short and long term side effects can I anticipate from the treatment? Is there anything that I can do to minimize the disease? 1
Prevelance More than 50,000 new cases each year Onset 40-70 Average age of onset is 62. Second most common neurodegenerative disorder in the elderly 3:2 ratio of men to women Diagnosing after age 70 Epidemiology of Parkinson s Disease Unknown cause Thought to be multifactorial Family history Exposure to pesticides Exposure to heavy metals Well water Old Age Motor Presentation Bradykinesia: slowness of initiation of voluntary movements with progressive reduction in speed and amplitude of repetitive actions AND Muscle rigidity 4-6 hertz resting tremor 2
Motor Presentation Tremor: 75% present with this at some point during their disease Rigidity: Cogwheeling often is unilateral Bradykinesia : may be described as feeling weak, slower speech Micrographia Non-Motor Symptoms Dysfunction of autonomic pathways: Dizziness Constipation Drooling Sweating Erectile dysfunction Swallowing problems Urinary problems 3
Parkinson s Disease Different from Parkinsonism Degenerative disorder of the basal ganglia in the CNS Loss of available dopamine in the brain 4
Diagnostic Evaluation Subjective history and physical exam!!!! DO cognitive testing Depression screening Assess cranial nerves: blinking is decreased, smell decreased, impairment in upward gaze Passive ROM of limbs Olfactory testing Stages of Parkinson s Disease Clinical Presentation (stage 1) Unilateral Resting Tremor (stops with activity) Slowing or freezing Decreased facial expression Bradykinesia Recurrent falls Masked face Micrographia Microphonia Reduced arm swing 5
Once Diagnosed Consult neurology Three different approaches. Neuroprotective Symptomatic Conservative Neuroprotective All newly diagnosed cases start on selegeline in concert with a neurologist When symptoms become disabling dopaminergic drugs are initiated Symptomatic At diagnosis treatment is immediately initiated with dopaminergic drugs Treatment is continuously modified to maintain maximum function for the maximum amount of time 6
Conservative Avoid drugs until symptoms are troublesome When symptoms are troublesome start amantadine and an anticholinergic drug When symptoms become distressing introduce L-dopa or agonists in small doses. Sinemet-Levadopa & Carbidopa Levadopa converts to dopamine. Carbidopa blocks an enzyme that breaks down levadopa, Also helps to control side effects of nausea associated with levadopa Adverse effects: Dizziness, drowsiness, insomnia, constipation, restlessness Dosing 3-6 times per day MAO-B s Selegeline: Blocks the breakdown of dopamine Initially felt to be neuroprotective Now, used in conjunction with Sinemet to aid in reducing motor symptoms. Side effects: Nausea, dry mouth, constipation, confusion Once daily (am dosing) 7
Dopamine Agonists Mirapex/Parlodel Stimulate dopamine receptors in the brain Given three times per day Amantadine Antidyskinetic Temporary benefit for management of movements COMT Inhibitors: catechol-o-methyl transferase (COMT) inhibitors tolcapone Always given with sinemet 8
Terms to remember Microphonia Sialorrhea Micrographia Wearing off Associated Illnesses Constipation Seborrhea Corneal abrasions Dementia Resources PT SLP OT 9
Current Research Treatments Fetal Cell transplantation Fetal cells transplanted into the brain Stem cell transplant Concerns: may create too much dopamine Deep Brain Stimulation Surgically implanted battery operated device called a neurostimulator, delivers electrical stimulation to the targeted areas of the brain Considerations Pre-operative discussions Hospitalization 10
Summary Test Olfactory function Unilateral bradykinesia Resting Tremor Assess ambulation Advocate for time sensitive medication management References: Aarons, S., Peisah, C., & Wijeratne, C. (2012). Neuropsychiatric effects of Parkinson's disease treatment. Australasian Journal On Ageing, 31(3), 198-202. Casjens, S., Eckert, A., Woitalla, D., Ellrichmann, G., Turewicz, M., Stephan, C., &... Pesch, B. (2013). Diagnostic value of the impairment of olfaction in Parkinson's disease. Plos One, 8(5), e64735. Kang, P., Kloke, J., & Jain, S. (2012). Olfactory dysfunction and parasympathetic dysautonomia in Parkinson's disease. Clinical AutonomicResearch: Official Journal Of The Clinical Autonomic Research Society, 22(4), 161-166. Lerche, S., Seppi, K., Behnke, S., Liepelt-Scarfone, I., Godau, J., Mahlknecht, P., &... Berg, D. (2014). Risk factors and prodromal markers and the development of Parkinson's disease. Journal Of Neurology, 261(1), 180-187. Lin, H., Lin, H., & Chen, Y. (2012). Increased risks of parkinsonism in the 3 years after chronic renal failure. International Journal Of Clinical Practice, 66(5), 499-503. Vance, R. C., Healy, D. G., Galvin, R., & French, H. P. (2015). Dual taskingwith thetimed "up & go" test improves detection of risk of falls in people with Parkinson disease. Physical Therapy, 95(1), 95-102. Yang, H., Kim, Y. E., Yun, J. Y., Kim, H., & Jeon, B. S. (2014). Identifying the clusters within nonmotor manifestations in early Parkinson's disease by using unsupervised cluster analysis. 11