Wednesday, 20 August 2003
This presentation is part of : Dementia in Parkinson's Disease

S068-002 Dementia is a Preventable Disease

Amos Korczyn, Sieratzki Chair of Neurology, Sieratzki Chair of Neurology, Tel Aviv University Medical School, Ramat Aviv, Israel

The assertion by James Parkinson that in paralysis agitans, “the senses are not affected”, is being challenged by observations that a substantial proportion of cases with advanced Parkinson disease (PD) develop cognitive deficits. These are heterogeneous in nature, either having Alzheimer phenomenology or with features reminiscent of “subcortical” dementia.

In PD, autopsy data suggest Alzheimer-like changes, comprising cortical amyloid deposits, temporal lobe atrophy and degenerative changes in the nucleus basalis of Meynert. Therefore it is logical to study the effect of cholinonergic enhancement on cognition in PD.

In recent years another entity has been defined, of dementia with Lewy bodies (DLB). In this disorder, cognition is impaired with only minimal extrapyramidal findings (rarely without any). Pathological examination reveals widespread cortical deposition of Lewy bodies, which may also occur in the substantic nigra but only to a light extent. The cortical changes are typically accompanied by Alzheimer changes. Such changes also occur in PD patients with dementia, however these have a more extensive depletion of nigral neurons.

Although typically dementia in PD occurs late into the course of the disease, the time difference is quite variable. DLB has been defined when dementia occurred prior to the appearance of parkinsonism, or within a year or two afterwards. However this division is arbitrary and lacks biological explanation or theoretical support.

Clinical manifestations of DLB, like fluctuating cognition, sensitivity to neuroleptics and cognitive improvement by treatment with cholinesterase inhibitors are common to both conditions.

Thus, DLB is a special case of Lewy body disease where widespread cortical deposition of Lewy bodies precedes severe loss of nigral neurons and is manifested by prominent cognitive changes.

Remaining questions include the factors responsible for early cortical deposition of Lewy bodies and the mechanism inducing amyloid deposition in DLB.

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