Parkinsons Dementia Disease

Parkinson's Dementia Disease

Parkinson's disease (PD) is one of the most common neurodegenerative movement disorder, which affects about 1% of the population over age 60. Although PD is often recognized as a motor disorder, there are several non-motor signs and symptoms that may cause a considerable burden to the patient.

Dementia is common and affects approximately 40% of PD patients during the course of the disease. The risk for the development of dementia in PD patients is approximately 6 times higher than compared to non-PD age matched controls.

The dementia associated with PD is characterized by

• dysexecutive syndrome affecting mainly executive and
• visuospatial functions while memory is relatively preserved.

In patients with Dementia with Lewy bodies (DLB), dementia is the central feature of the disease. The overlap of clinical symptoms between PDD and DLB suggest that they probably represent different points on a spectrum of lewy body diseases sharing similar underlying processes. Currently, only symptomatic treatment of cognitive impairment is available. Recently, several clinical trials using cholinesterase inhibitors have shown its efficacy in PDD and DLB patients.

How is Parkinson's disease diagnosed?

There are not lab tests to definitively diagnose Parkinson's disease. A systematic neurological exam will include testing your reflexes and observing things like muscle strength throughout your body, coordination, balance, and other details of movement. You may be given tests to exclude the possibility of other disorders. These tests include blood tests, urine tests, CT scans, or MRI scans. Although none of these tests actually diagnose Parkinson's disease, they may reveal the presence of some other conditions that could be responsible for the symptoms.

Food Causing Dementia, Parkinson's Disease

Acetylcholine is also needed for muscle-contractions. Normally, secretion of acetylcholine is regulated by dopamine. In Parkinson's however, dopamine-receptors have been damaged, or occupied by dietary protein-oxidation products. Therefore, in Parkinson's muscle-contractions can not be controlled as well.

Whether you will get Parkinson's, depends on how sensitive your receptors are.

Medications and Treatment for Parkinson's

There are several symptomatic treatments for people with Parkinson's including medication, surgery, and physical therapy. The degree of success of each treatment varies among individuals, as does the length of time the treatment option remains effective.

• Levodopa - a dopamine precursor

• Combining Levodopa with Carbidopa

• Stalevo (carbidopa, levodopa and entacapone)

• Symmetrel (amantadine hydrochloride)

• Anticholinergics (trihexyphenidyl, benztropine mesylate, procyclidine, etc.)

• Selegiline or deprenyl (Eldepryl)

• Dopamine agonists

• COMT inhibitors such as tolcapone (Tasmar) and entacapone (Comtan)

Neuropathological distinction between Parkinson's dementia and Parkinson's plus Alzheimer's disease

The distinctive clinical features of dementia in Parkinson's disease (PDD) and Parkinson's plus Alzheimer's disease (PD + AD) suggest different patterns of cerebral atrophy in these conditions. To determine the pathoanatomical substrates of dementia in PDD and PD + AD, morphometric analysis of 5 standardized coronal slices was used to identify volumetric changes in cerebral tissue. In PDD (n = 4) there were 9 to 23% reductions in cross-sectional area of cerebral cortex, a 38% loss of tissue in the globus pallidus + putamen, and an 18% reduction in area of the amygdala, whereas in PD + AD (n = 6) there was severe global atrophy of the cerebral cortex (27-29% reductions), moderate atrophy of white matter (10-19% reductions), and 40% reductions in areas of globus pallidus + putamen and the amygdala relative to neuropathologically intact controls (n = 14). Immunostaining with anti-glial fibrillary acidic protein disclosed significant gliosis of all four major subdivisions of neocortex in PD + AD and gray matter of the caudate, putamen, globus pallidus, and thalamus in both PDD and PD + AD relative to controls. The findings suggest that dementia in PDD is mainly subcortical in origin and due to neuronal degeneration in basal ganglia, the amygdala, and thalamus. In PD + AD the same pattern and degree of subcortical degeneration is evident, but there are clearly superimposed lesions involving cortical neurons and long projection fibers coursing through cerebral white matter that most likely account for the distinctive manifestations of dementia in this condition compared with PDD.

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Site last updated: March 4, 2008

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