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Parkinson Disease

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Question
Answer
Parkinson Disease is caused by ____________________   a loss of dopamine  
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How many dopamine producing neurons must a person loose before Parkinson symptoms begin to show?   70-80%  
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Primary Parkinson is ____________.   idiopathic  
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Etiology of Parkinson   -idiopathic (primary parkinson) -Post-infectious -Toxic -more likely to be multifactorial & the trigger can be different for every person  
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Infections that have been reported to lead to Parkinson:   -measles -CMV -rubella -herpes  
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Toxic triggers of Parkinson:   manganese, carbon monoxide, synthetic heroine, cyanide  
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Parkinson-Plus Syndrome (PPS)   -distinguishing factor: if you give someone with Parkinson extra dopamine (L-dopa) their symptoms do not improve -worse that Primary Parkinson because there is no treatment or comfort)  
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Parkinson Disease   -chronic progressive disease of motor function of CNS  
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Incidence of Parkinson Disease   -1% of those over 55 years of age -incidence increases with age -mean age of onset is between 58-62 -10% of cases have an early onset (before 40)  
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Three Cardinal Features of Parkinson Disease   -Rigidity -Bradykinesia -Tremor  
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Rigidity   -increased tone of agonist & antagonist (equal resistance to flexion & extension) -patient becomes progressively more rigid in the later stages  
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Bradykinesia   -slow movement -loose trunk rotation and coordination, leading to akinesia or freezing movement  
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Tremor   -appears first -in Parkinson Disease there's a resting tremor -postural instability and festinating gait  
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Festinating gait   -a shuffle or gallop -arm swing may be first to go -putting music on may change motor program to get them walking again (freezing movement)  
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Cogwheel tremor   -cogwheel has teeth (stops, lets go, stops, etc) -as PT is moving a patient, the it goes, then stops, releases and moves further then stops, etc -due to tremors modifying rigidity (shaking it loose)  
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Pathogenesis of Parkinson   -dysfunction within the subcortical grey matter in basal ganglia -pathologic hallmark is the degeneration of substantia nigra in association with production of Lewy bodies -substantia nigra loses its ability to produce dopamine  
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where is dopamine produced?   substantia nigra pars compacta  
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Pathophysiology of Parkinson   -Basal gangli disorder -involves underactive direct pathway & overactive indirect pathway -decline in the ability to initiate movement -depletion of dopamine -80% loss before symptoms show -writing probs may be 1st thing noticed  
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How are Tremors caused?   lesion of the connection between the basal ganglia and the cerebellar-red-nucleus pathway  
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Basal Ganglia   -presets the motor system based on sensory movements -may need to see movement in periphery sometimes to be able to walk -excitatory direct pathwway activates thalamocortical pathway -inhibitory indirect pathway inhibits thalamocortical pathway  
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lesion of the basal ganglia   causes changes in the character of movement (slowing of movement, poor coordination & loss of adaptive control)  
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Clinical Manifestations   -hallmark= movement disorder -problem with movement activation tremor is the most common initial manifestation (pill rolling at rest) -tremor disappears during sleep -loss of ext against gravity -loss of up & out movement  
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systemic manifestations   -poverty of movement (move less & less) -fatigue -masked faces -flexion dystonia -festinating gait -dysphagia -visual/sensorimotor probs -depression -dementia (late phases) -bradyphrenia -dysautonomia -CV abnormality -airway obstruction -free  
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flexed dystonia   -proximal stiffness -face gets stiff  
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Masked Faces   -loss of facial expression muscles -person may think they are smiling but aren't  
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dysphagia   trouble swallowing  
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bradyphrenia   slowness of thought  
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dysautonomia   -autonomic NS involvement is gone: -excessive sweat -increased salivation/drooling -bladder dysfunction -GI motility  
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air trapping   -associated with airway obstruction -bronchioles collapse & trap air behind collapse & kills alveolar sacs  
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freezing   when periphery stops moving  
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Diagnosis of Parkinson   -look for the classic triad (tremor, rigidity and bradykinesia) -Asymmetry of signs and symptoms, resting tremor -a good response to Levodopa (diagnosis of IDP) -CT or MRI to assess dopamine levels  
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Stages of Disease Progression   Hoehn & Yahr Stages: Stage I=Min or absent signs Stage II=Min bilateral w/o balance impairment Stage III=Impaired postural responses, capable of living ind Stage IV=Severe disability, able to stand & walk w/ assistance Stage V=Wheelchair or bed depen  
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Clinical Course of Parkinson   -Benign= if in stage I or II and its been 4 years after diagnosis -Progressive -Malignant= progresses to stage II within a year of diagnosis  
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Treatment of Parkinson   -symptomatic= increase mobility -drug therapy -deep brain stimulation -implant electrodes in brain & stimulate to decr tremors -pallidotomy= make a lesion in brain (globis pallidis of basal ganglis) to decr rigidity  
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Pharmacological Management of Parkinson   -Selegiline or deprenyl (Eldepryl)= neuroprotective drug that buys times before L-dopa -Levodopa -Artane, Parsidol -Amantadine= acts like dopamine & anticholinergic -Bromocriptine & Pergolide  
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L-dopa   -Levodopa -allows more dopamine to basal ganglia -only affective for 5-7 yr then a neg response occurs -worsening of sympt when coming off meds -dyskinesia; facial grimacing; twitch of tongue & lips -On-Off phenom (sudden periods of immobility -dys  
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Artane, Parsidol   -anticholinergics -body begins to make more acetylcholine which adds to tremors so this is ANTI  
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dystonia from long term use of L-dopa   twisting; axial & prox extremities  
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Medical/Surgical management   -nutrition is crucial (high cal- low protein diet) -Stereotaxic surgery (pallidotomy, thalamotomy, deep brain stim) -transplantation (fetal/stem cells into basal ganglia- not perfected yet)  
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high cal - low protein diet   -high protein will block effectiveness of L-dopa  
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