Joanne M. Hamilton, PhD
Lewy Bodies, abnormal aggregates of several proteins including alpha-synuclein, develop in neurons of people with Parkinson’s disease (PD) and Dementia with Lewy bodies (DLB). Considerable confusion exists regarding the distinction between PD and DLB especially in light of estimates that upwards of 35% of people diagnosed with PD will develop cognitive problems of sufficient severity to meet criteria for dementia. Many scientists question the distinction between DLB and PD with dementia (PDD) because the disorders share so many clinical and neuropathological features. Both are associated with movement problems caused by damage to the extrapyramidal motor system and progressive cognitive decline. Currently, the Consortium on DLB (McKeith et al., 2005) recommends that a diagnosis of PDD be given if motor symptoms precede cognitive decline by more than a year and DLB be given if cognitive decline precedes or emerges in concert with motor symptoms. Clearly, these criteria contribute to the confusion since it is often difficult to judge which symptom came first.
In practice, both DLB and PDD are associated with prominent difficulties with attention and concentration, cognitive flexibility, problem-solving, and visuospatial processing. Visuospatial deficits can be particularly obvious even before changes in memory and language occur. Functionally, people whose visuospatial processing is impaired may tend to sit down on the edges of their chairs, bump into walls, trip on stairs, or misjudge distances while driving. Visual misperceptions and hallucinations are also associated with changes in visuospatial processing in patients with DLB and PD. These visual phenomena can be disturbing to people with the disorders and their caregivers and can be difficult to manage clinically because of drug sensitivities associated with the Lewy body disorders. A recent study has suggested a possible mechanism for the association between visuospatial problems and visual hallucinations in PD. Stebbins and colleagues (NEUROLOGY 2004;63:1409-1416) reported that visual information is abnormally processed in the frontal region rather than the posterior region of the brain in PD patients who have hallucinations. This transfer of functioning may occur because of damage to posterior regions where visual processing typically takes place. Thus, deficits in visuospatial functioning may serve as a proxy for the amount of posterior brain damage and signal an increased risk of developing hallucinations.
This hypothesis is being examined at the Dementia with Lewy Bodies Program at the
