It’s key that you acquire a mastery of the basics. Master the basic causes and mechanisms of Parkinson’s disease and you’ll better understand your therapy. you will also have the ability to better know what questions to ask, and I daresay, become better at debunking the quacks. Do that and you’re on your own track to guiding your own care. Become more a part of you own care team a bit more as a colleague with your neurologist and your other caregivers.Thus, it’s key to your treatment that you begin to understand the basic mechanisms and alleged causes of Parkinson’s disease.
Although the specific causes might vary quite a bit from person to person, the mechanism by which Parkinson’s manifests itself follows a fairly straightforward pathway. I will invoke some of the previous diagrams I have used in other articles, which explain the mechanisms by which cell death in the substantia nigra causes a dopamine deficiency resulting in Parkinson’s symptoms.
The Substantia Nigra
The root of the cause can be found in this rather small region of the deep brain sitting atop the brainstem. This is where dopamine-producing neurons die in Parkinson’s although the mechanisms by which cells die here are less clear.beyond genetics, there are many environmental toxins that increase the risk including herbicides, pesticides, organic solvents, heavy metals and manganese. Head trauma may also be another mechanism: anyone who has lost consciousness more than once is at least at double the risk for Parkinson’s. Whatever the cause, brain-cell bodies within this substantia nigra region start dying off. These cells of which there are about 10,000 on each side of the brain normally get stimulated by various mechanisms (intense emotion, sexual arousal, novel stimuli). That stimulation causes the activation of dopamine production in those cell bodies. Normally their very long extensions that reach to other brain areas, called “axons,” deliver dopamine to the nearby basal ganglia regions (controls movement and part of the mechanism of drive and motivation) and hypothalamus (controls bodily cycles like sleep and autonomic functions like cardiovascular tone and body temperature) and other further–away areas like the frontal lobe of the cortex. Dopamine-producing cell death causes a deficiency of dopamine in these regions. In one way or another, the normal mechanisms of function of each of these regions relies on a steady supply of dopamine.
Local deficiencies of dopamine cause the neural circuits in these regions to misfire. these disrupted mechanisms of neural regulation cause the various symptoms of Parkinson’s disease seen. Disruption in the basal ganglia for instance, causes an abnormal pattern of movement control and feedback to the higher brain, a very delicate mechanism upon which crisp initiation of movement and smooth control of that movement in becomes disrupted.
This causes the classic triad of symptoms originally described by Dr. Parkinson 150 years ago. Although he did not understand the mechanism, Dr. Parkinson noted that patients would present with three primary movement abnormalities that caused a great deal of distress and disability for them in normal everyday function. the classic three findings were coarse tremor, rigidity, and slowness of movement, which we now know are caused by dopamine deficiency and the resulting abnormal regulation of those movements via a disrupted pattern of function in the basal ganglia.
In fact the mechanism by which adequate dopamine fails to reach these regions where it’s needed causes every one of the described symptoms in Parkinson’s, even those that have nothing to do with movement. One mechanism by which at least some of these “other” “non-–motor symptoms” arise, originates via this malfunction of the basal ganglia region, which besides controlling movement, also regulates motivation and drive behaviors. Thus, malfunction here might also be the cause of diminished motivation seen in Parkinson’s, and at least in-part, the cause of daytime sleepiness.
Other non-motor abnormalities involve dopamine deficiency causing malfunction in the other regions supplied with dopamine. These dying neurons from the substantia nigra also supply dopamine to the hypothalamus, as mentioned above, whose malfunction causes disrupted sleep cycles and the loss of vascula stability which causes postularal dizziness.
Dopamine deficiency in other areas to be specified in later articles causes depression, memory impairment, and may even lead to dementia, common in late Parkinson’s.
The exact mechanism by which these substantia nigra dopamine neurons die has not been fully elucidated however somehow all roads seem to lead to the lethal accumulation of an abnormal protein called “alpha-synuclein” which causes early cell death. by the time movement symptoms start appearing, as many as 70-80 percent of these neurons have already died.
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