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Binswanger’s Disease (Subcortical Arteriosclerotic Encephalopathy) E. Surgical intervention using placement of a lesion in the globus pallidus (pallidotomy) had also been attempted, although wide variability in the accuracy of lesion placement produced inconsistent and often devastating results. Although this procedure improved tremor and reduced rigidity, this procedure had little effect on the akinesia associated with PD.
When present, PD dementia typically occurs during the later stages of the disorder.
Between 25 and 40% of PD patients may develop dementia.
Pallidotomy produces relatively rapid and substantial improvement in the motor symptoms, although there tends to be little effect on neuropsychological and psychiatric status postsurgically.
Using new microelectrode-guided lesion placement techniques, pallidotomy has reemerged as a potential treatment for PD with much fewer complications.
Cerebellar and Olivopontocerebellar Degeneration II. The occurrence of diffuse Lewy body disease appears to be linked to a genetic mutation in the betaamyloid precursor protein gene on chromosome 21.
This disorder has received considerable attention within recent years as an important cause of dementia with parkinsonian features, although it has also been considered by some to be a variant of Alzheirner’s disease.
The cause of PD is not known, although toxic agents such as manganese poisoning in industrial workers and injection of 1-methyl-4-phenyl 1,2,3,6 tetrahydropyridine (MPTP) in drug abusers, are known to produce PD symptoms and pathology, suggesting the possibility that an environmental factor could play a role in the etiology.
Dopamine depletion in the frontal cortex and striatum (particularly in the anterodorsal portion of the head of the caudate nucleus), is the major neurochemical deficit associated with PD, although reduced levels of norepinephrine, acetylcholine, and somatostatin, and diminished serotonin receptors have also been reported.
Levodopa, a dopamine precursor that readily crosses the blood-brain barrier and is metabolized to dopamine, is the most common pharmacologic agent used to treat PD.
Executive functioning deficits involving establishing, maintaining, and shifting cognitive set also are common in PD dementia and are similar to deficits in patients with discrete lesions of the frontal lobes. PD is most commonly treated with medication designed to ameliorate the central dopamine deficiency.