Research Paper On Dementia

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Given that some non-Alzheimer’s dementias are potentially treatable (i.e., further cognitive deterioration can be avoided or minimized) and/or reversible (i.e., cognitive functioning can be improved), a thorough consideration of all potential etiologies is imperative. This disease thus appears to reflect an overlap between Parkinson’s disease and Alzheimer’s disease.

This research paper will describe the non-Alzheimer’s dementias along a continuum of relatively untreatable, progressive disorders to treatable and potentially reversible causes. A progressive dementia, consisting of impaired attention, memory, language (e.g., verbal fluency, praxis, and naming), and visuospatial/visuoperceptual skills, typically appears first, followed by parkinsonian features, including akinesia, tremor, and rigidity.

Language deficits tend to involve motor components of speech (e.g., dysarthria, diminished phrase length, dysprosody, micrographia) more severely than linguistic aspects of speech, such as naming and comprehension.

Bradyphrenia (cognitive slowing) is typically one of the earliest features of PD dementia.

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.

Small handwriting, dysarthria, reduced vocal volume, and a tendency to speak in a monotone fashion may also be seen.

PD is most prominently associated with motor abnormalities involving a resting tremor, loss of postural reflexes, stooped posture, bradykinesia (slowed movement), cogwheel rigidity, and slow shuffling gait.

Regional cerebral blood flow studies have shown reductions in frontal cortical blood flow.

Although CT and MRI exhibit little predictive value for diagnosis of PD in an individual case, PET studies using fluorodeoxyglucose may show hypometabolism in the basal ganglia and frontal cerebral cortex.

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