Term
| what is parkinson's disease? |
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Definition
| a slowly progressive disease of late adult life characterized by akinesia, rigidity, and tremor. 2 of these is required for dx in addition of a neuropathologic exam. |
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Term
| what characterizes the incidence of parkinson's disease? |
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Definition
| parkinson's is the second most common neurodegenerative disease (2nd to alzheimer's). currently there are ~1,000,000 sufferers in the USA (half of which are in the early stages and are undiagnosed/untreated). parkinson's is exceeded only by CV disease and arthritis as a cause of chronic incapacity. usually parkinson's occurs in pts over 50 and has a slight predilection for males. |
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Term
| what is the etiology of parkinson's disease? |
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Definition
| the cause is mostly unknown and it is not thought of as familial or hereditary (even though more than one case may affect a family). |
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Term
| what are the types of parkinson's? |
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Definition
| idiopathic, pharmacologically induced (by tranquilizers), and post-encephalitic. |
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Term
| what is the pathophysiology of parkinson's? |
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Definition
| in parkinson's disease, there is a breakdown in the connection between the neurons in the substantia nigra and the putamen portion of the striatum. symptoms of parkinson's disease appear after 60% - 80% of these cells become impaired or die. it is not specifically the loss of the cells that causes the disease, but rather the decrease in dopamine, which occurs with the decreased number of substantia nigra neurons. this results in abnormal activity in the putamen, causing the primary features of the disease. typically, symptoms appear after striatal dopamine levels have decreased by 20% - 50% of normal levels. when substantia nigra projections to the putamen have been impaired, the globus pallidus interna and subthalamic nucleus begin to function abnormally (the subthalamic nucleus overexcites the globus pallidus interna, which in turn overinhibits the thalamus, which causes less excitation of the motor cortex). the result is that the brain is no longer able to sufficiently control motor function. |
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Term
| what are the primary symptoms of parkinson's disease? |
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Definition
| muscular rigidity, coarse resting tremors, bradykinesia, mask-like facies and impaired postural reflexes. these symptoms are not necessarily uniform or bilateral, but are progressive and may lead to complete disability. |
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Term
| which symptoms can be helped w/OMM in parkinson's pts? |
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Definition
| the motion loss and stiffness (not the resting tremor) |
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Term
| what characterizes the gait of parkinson's disease? |
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Definition
| shortened length, shuffling (pts widen their stance b/c of stiffness to increase balance), loss of arm movements, and a forward bent trunk (may cause the pt to lose balance - will take rapid steps to keep from falling forward = festination). associated falling injuries have prompted many quantitative studies - b/c most of the cost in tx of parkinson's pts is due to fall injury (OMM can help w/this by increasing range of motion). |
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Term
| what characterizes the rigidity in parkinson's disease? |
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Definition
| the rigidity in parkinson's disease is primarily of central origin and may be exaggerated by reflex cycles of pain, muscle spasm, and muscle contraction. |
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Term
| what does the rigidity in parkinson's disease eventually produce? |
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Definition
| increased muscle tension and muscle/fascial/tendon shortening with resultant decreased joint motion, instability, and limited general movement (including respiration). |
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Term
| how does the presence of pain affect parkinson's pts? |
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Definition
| pain causes further spasms, tension, and altered nutrition (gross+cellular), waste removal (gross+cellular), and lymphatic and circulatory function. |
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Term
| what does progression of parkinson's lead to? |
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Definition
| strength loss and decreased flexibility (resulting in balance and postural problems) |
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Term
| what is the rationale for OMT tx in parkinson's pts? |
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Definition
| as the peripheral expression of the disease exceeds the level of actual (central) neurologic deficit, OMT may be able to break the cycle of change (break reflex cycles). |
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Term
| can standard osteopathic manipulative tx acutely improve gait performance in pts w/parkinson's disease? |
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Definition
| yes, according to a 1999 JAOA article |
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Term
| what OMT techniques were used in the 1999 JAOA published study investigating tx of parkinson's? |
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Definition
| 14 osteopathic techniques were performed in specific order for ~30 min bilaterally including: range of motion, *muscle energy, *spencer techniques on the shoulder, OA release, and translational stretching. |
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Term
| what were the results of the 1999 JAOA published study investigating OMT tx of parkinson's? |
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Definition
| there was a significant increase in gait parameters related to stride and velocity for the upper/lower limbs compared w/their pretreatment values (particularly in terms of stride length/cadence and velocity of movement in the lower limbs - esp at the hip). |
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Term
| what does the AT101 bed anecdotally improve in parkinson's pts? |
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Definition
| range of motion, edema, and balance - via what is essentially the lymph pump mechanism. this may also have applications in MS. |
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Term
| what is the general benefit of OMT in parkinson's pts? |
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Definition
| even though the neuropathology of parkinson's may be centrally mediated, and thus out of the tx range of OMT - the pathologic and disabling sequelae may be positively affected by OMT (this may lead to less disability, injury, and progression). |
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