Introduction to Parkinson's Science/Q Page 2
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The cause of the symptoms of Parkinson's relating to movement difficulties.
What causes the motor symptoms?Edit
This simple answer is that too little dopamine is being produced in a particular part of the brain.
What is dopamine and what does it do?Edit
Dopamine is a Neurotransmitter. A neurotransmitter is a chemical which is used to pass a signal from one nerve cell (or neuron) to the next. Dopamine is one of many neurotransmitters. It is used in several parts of the brain. In some parts it is associated with pleasure and feeling good.
In the case of Parkinson's, insufficient dopamine is delivered from one small region in the base of the brain to another nearby region.
Why is there a lack of dopamine?Editsubstantia nigra have died off. This means that the nerve cells in another part of the brain, the striatum, do not receive all the dopamine signalling that is required for proper movement.
Most movements that we make are complex, involving many muscles. These movements have to be coordinated so that, at the right time, some muscles contract and others relax. This complexity is controlled by bundles of cells at the base of the brain called the basal ganglia. The coordination of movement breaks down if dopamine is not produced in sufficient quantity or at the right time to convey messages and Parkinsonian symptoms arise.
Why and how does lack of dopamine affect movement?Edit
(A more detailed account of disruption of the basal ganglia circuitry is given on the next page.)
The cerebral cortex issues the instruction to make a movement but, before this is passed to the muscles, it is passed to the basal ganglia. These are a set of small, interconnected bunches of nerve cells which together coordinate movement. The signals are passed between the ganglia by different neurotransmitters. Some of these neurotransmitters are excitatory - they cause the target nerve cell to fire - or they are inhibitory - they stop the target nerve cell firing. This overall effect is a complex pattern of output signals that instruct some muscles to contract and others to relax and by differing extents in order to execute the appropriate movement. The basal ganglia hold, as it were, the 'programs' that orchestrate frequently-executed patterns of movement.
When dopamine is not produced by the substantia nigra at the time it is needed or in insufficient quantity, these instructions are disrupted which usually results in certain muscles not being given the signal to relax and they remain stiff and unresponsive. Tremor is another symptom associated with lack of dopamine but the exact mechanism for how it arises is the subject of considerable debate. The abnormal firing patterns of the neurons and aberrant oscillations in the neural circuitry in Parkinson's become very complex and are presently the subject of active study. 
The conventional treatment of Parkinson's is largely aimed at making up for the dopamine that is not being produced because of the death of the neurons in the substantia nigra. See the Current therapies subpage.
- Helmich, Rick C., Mark Hallett, Günther Deuschl, Ivan Toni, and Bastiaan R. Bloem. “Cerebral Causes and Consequences of Parkinsonian Resting Tremor: a Tale of Two Circuits?” Brain (March 1, 2012). http://brain.oxfordjournals.org/content/early/2012/03/01/brain.aws023.
- Weinberger, Moran, and Jonathan O Dostrovsky. “A Basis for the Pathological Oscillations in Basal Ganglia: The Crucial Role of Dopamine.” Neuroreport 22, no. 4 (March 9, 2011): 151–156, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3076312/.
- For recent research see papers by Peter Magill, http://www.ncbi.nlm.nih.gov/pubmed?cmd=Search&term=Magill,+Peter+J
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