Neuropsychological Characteristics of Dementia in PD

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Cognitive disturbances may range from relative circumscribed deficits to global dementia. Mild cognitive deficits are common in idiopathic Parkinson's disease (IPD) and are characterized by impaired cognitive flexibility, psychomotor slowing, reduced ability to learn and retrieve new information, and impaired visuospatial skills. The concept of subdividing dementias on clinical grounds into cortical and subcortical dementias has been adapted by many in the field as a clinically useful concept, but others remain critical of this notion. The concept of subcortical dementia was originally based on an analysis of the pattern of personality and cognitive deficits in PSP (Albert, Fledman, & Willis, 1974) and Huntington's disease (HD; Folstein et al., 1975; see Table 3.2). The majority of studies addressing the concept of subcortical dementia have used PD as the prototypic subcortical dementia and AD as the prototypic cortical dementia. The term subcortical dementia originally applied to the constellation of cognitive deficits attributed to subcortical brain damage in humans and was initially characterized as including:

• Impaired manipulation of acquired knowledge (i.e., calculation and abstracting abilities).

• Personality changes marked by apathy and inertia.

• General slowness of thought processes (Albert et al., 1974).


Aphasic disturbances are generally not part of PD dementia. Dysarthic disturbances are common, and there may be greater abnormalities in phrase-length speech melody, information content of spontaneous speech comprehension of written and spoken commands compared to PD without dementia.

Table 3.2 Common Medications Used in Treatment of LBD


Typical Starting Dose (mg/day)

Typical Maintenance Dose (mg/day)
































200 each ( l dopa dose)



Explicit verbal memory (word lists, paired associate learning, brief prose passages) is disturbed in PD patients with dementia; however, the quality of this memory impairment is different from that seen in AD. Most often, the deficit is in memory retrieval (where patients are able to develop a normal learning curve but exhibit increased rates of forgetting on delayed recall and are much better at recognition). This differential recall/recognition is seen for PD patients over a broad range of mental status changes.

Explicit nonverbal memory (reproducing complex drawings, learning locations of places on maps) also is found to be impaired in Parkinson's disease with dementia (PDD). Remote memory is generally intact in the nonde-mented PD patient but impaired in PDD as is implicit memory ( lexical priming and pursuit rotor learning) and procedural memory (perceptual or motor skills not readily accessible to conscious recollection but, when intact, can be executed with ease).


The term bradyphrenia was coined by a French neurologist to describe a new psychiatric syndrome that was produced by encephalitis lethargica. The notion is one of lengthening of normal information processing time or "slowing of the thinking process," a concept that has been the subject of long standing. One way to address this is to compare performance on simple and choice reaction-timed tasks. The precise relationship between bradyphrenia and dementia remains unclear.

Visuospatial Skills

Deficits in this arena are among the most frequently reported cognitive changes accompanying PD, but the precise nature of these deficits and their relation to PD dementia remains incompletely understood. One of the confounds is the potential motor demands of certain tasks. Visual sensory function is normal in PD. Visual acuity, color perception, and depth perception are all unaffected, but visuoperceptual abilities are abnormal.

Higher Executive Function

The term higher executive function is generally used to refer to the concept of abstract thinking—planning ability to profit from feedback, judgment, and initiative. The frontal lobes are directly implicated because of the close linkage of the striatum and the frontal lobes by way of cortico-striato-thalamo-cortical circuits. The concept that the basal ganglia are involved in a form of higher motor control, as well as cognitive function per se, is gaining increasing acceptance. The pathophysiology of the intellectual impairment in PD is controversial and the subject of ongoing research. Whether extent and severity of executive deficits are predictive of dementia remains to be determined. PD nondemented differed significantly from control subjects on Raven's progressive matrices, Boston naming, Stroop color naming, picture arrangement, story recall after 10-minute delay, and Benton visual retention. While cognitive disturbances may range from relatively circumscribed deficits to global dementia, no clear evidence exists that these represent a continuum.


Major depression in PD and dementia is 30% as opposed to 6% in AD matched for dementia severity. Dysthymia was found in 27% PDD and 27% AD (Starkstein et al., 1996). A further complication is that the presence of dementing symptoms is often difficult to separate from affective changes seen in many patients with PD (20% to 60% of patients experience affective changes some time during the course of their illness; Cummings, 1986).

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