Introduction

In the early stages of Parkinson’s disease (PD) already executive function impairments arise. Unfortunately many of these patients develop Parkinson’s disease dementia (PDD), which brings more severe cognition deficits along. Between these two diseases comes Mild Cognitive Impairment (MCI). The diagnose of PDD is difficult, because to be diagnosed with PDD there must be severe enough impairment to create problems in social and occupational functions, but it’s hard to distinguish if these problems result from cognitive or motor impairments (for example bradykinesia). Also PD medications and comorbid mood disturbances have an impact on diagnosing. Differentiating between PDD and dementia with Lewie bodies is another difficult problem. When the Parkinsonian symptoms arise a year before the onset of the dementia PDD is diagnosed, when they arise simultaneously dementia with Lewie bodies is diagnosed.

Prevalence of Dementia in Parkinson’s Disease

10-40% of the population develops PDD. Risk factors include: advanced age, severity of motor disease (especially bradykinesia), early levodopa associated confusion, depression and atypical neurological features at presentation. Especially after the age 70/80 risk increases till 70 percent.

Clinical, Neuropsychological, and Imaging Characteristic of Parkinson’s Disease Dementia

In Parkinson’s disease subcortical disruptions cause problems. Fronto-subcortical circuits are responsible for the behavioural and cognitive consequences. Disrupted dorso-lateral prefrontal circuits cause the executive function problems already in an early stage. The disruption of the anterior cingulate circuit leads to apathy and decreased motivation. This pattern differs from Alzheimer’s disease, because Alzheimer’s disease is caused by cortical disruptions and leads to cortical deficits (apraxia, aphasia, amnesia).

Single photon emission CT studies have shown frontal hypo perfusion or bilateral temporoparietal deficits in PDD. Recent PET studies have shown hypometabolism in the occipital lobes, which differentiates PDD from Alzheimer’s disease (also hypometabolism in temporoparietal lobes)

Dementia with Lewie Bodies (DLB)

A very typical characteristic of DLB is change in alertness/arousal. Patients with dementia with Lewie Bodies’ attention and concentration span fluctuates a lot, which leads to excessive sleepiness. A precursor of DLB is rapid eye movement sleeping disorder (RBD), and 50% of DLB patients suffers from RBD. Attentional deficits, executive abnormalities, and frequent concomitant neuropsychiatric disturbances, including visual hallucinations and delusions are clinical features in both DLB and PDD. DLB patients are more affected by apathy than Alzheimer’s disease patients. Executive functions of Alzheimer’s disease patients are also better than those from patients with DLB, but the latter perform better on memory tasks.

Treatment

Non-pharmalogical treatment

It is important that caregivers are educated about the disease and progression. Locally available community resources like support groups can help both patient and caregiver. Non-essential medication should be eliminated as soon as possible, because some of them can have severe side effects. Perry et al. found for example that people chronically use anticholinergic medications have a 2,5 higher density of amyloid plagues and higher neurofibrillary tangle densities. These two are the pathological hallmark of Alzheimer’s disease.

Pharmalogical treatment

Levodopa improves attention, mood and arousal. But in further stages of dementia levodopa may induce hallucinations, delusions and confusion. Because of damaged cholinergic pathways, choline acetyltransferase (ChAT) activity is decreased to 40 to 60% of control values in frontal, temporal, and hippocampal cortex. This process and cell loss in the nucleus basalis of Meynert correlate with the level of cognitive impairment. Based on this, acetylcholinesterase inhibitors seems reasonable. There has only been one dubbelblind study on this, but the results show that cognitive functions indeed improve in the acetylhcolinesterare inhibitor- condition (rivastigmine).