In this study, a large sample of patients with PD was assessed with an instrument that evaluates relevant aspects of cognitive impairment in PD without being sensitive to motor symptoms.6
The findings of this study, however, should be viewed against the following background. Firstly, this is a clinic based study with a selection procedure based on age at onset and disease duration. Therefore, the results in this study cannot be generalised to the PD population in general. The percentage of patients with impaired cognition in this study cannot be interpreted as a prevalence estimate, which limits the possibility to compare our findings with prevalence rates of other studies. Secondly, the cross sectional design makes it impossible to draw conclusions about the direction of the reported relations.
In many studies on cognitive functioning in PD, the MMSE is applied as a gross measure of cognitive impairment.21
The MMSE includes items from domains which generally are less severely affected in PD (temporal orientation and language),3,22
whereas the SCOPA‐COG focuses on domains which are frequently affected in PD (memory, attention and executive and visuospatial functioning).6
Therefore, the SCOPA‐COG is expected to be more sensitive to the cognitive deficits of PD. This is demonstrated by the fact that in our study 58% of the patients with abnormal SCOPA‐COG scores had normal MMSE scores. In this comparison, both scores were corrected for age and years of education, indicating that the MMSE may substantially underestimate the degree of cognitive impairment in PD.
In comparison with controls, all four cognitive subdomains were impaired in patients. In accordance with other studies, executive functioning was most prominently affected, followed by memory.3,23
Both controls and patients had relatively low scores on the memory subdomain, indicating that items of this subdomain are more difficult compared with items of the other subdomains. As with other measures of cognition, we found that age3,5,23,24,25,26,27
and (years of) education25,28
were related to the SCOPA‐COG scores in both controls and patients. In line with other studies, more advanced disease (higher H&Y stage, higher SPES‐SCOPA motor score) was associated with poorer cognitive performance,2,3,5,6,24,28,29,30
indicating an additional influence of the disease process on cognitive performance. Additionally, in agreement with others,3,24,26
we found that the psychotic domain score was weakly associated with the total SCOPA‐COG score.
In daily practice, differences in levels of cognitive impairment suggest that there are subgroups of particular PD phenotypes.31
Therefore, an attempt was made to identify patients with impaired cognition by taking into account the influence of age and education. Using this approach, 22% of the patients had impaired cognition. Because of the cross sectional design of this study, we cannot exclude the fact that some patients had a decline over time in cognitive performance but still remained within the 95% confidence interval. Longitudinal research is needed to elucidate whether subgroups of PD patients exist where cognition is spared, or whether inter‐patient variability is mainly explained through differences in the rate of progression of the disease.
In this study, 14% of patients with impaired cognition had a disease duration less than 5 years. Generally it is assumed that cognitive impairment may develop early in the disease process,32,33
but clinical symptoms of dementia, as detailed in the DSM‐IV criteria, appear only late in the disease course.4,28,30
However, in PD, the term “dementia” is problematic because there is no disease specific definition3,21
and the DSM‐IV‐criteria10
require experienced disability in daily life, which poses a problem for any disease where motor impairment per se may cause such disability.3
To determine if patients with impaired cognition truly suffer dementia, a PD specific definition of dementia is required. In view of the fact that no adequate definition of dementia in PD was available, we made no attempt to distinguish demented from non‐demented patients.
Our results show that poorer cognitive performance is associated with more severe impairments in other domains of PD. In line with the findings of others, we found that patients with a tremor dominant phenotype showed higher cognition scores compared with patients with the PIGD dominant phenotype.34,35
However, since the assignment of this particular phenotype is based on a ratio, we evaluated the differential influences of the nominator and denominator. We found that this ratio is only driven by the denominator (PIGD score), and hence reflects increasing disease progression. According to Braak and colleagues,36
the symptoms of PD parallel the formation of Lewy bodies and Lewy neurites, and advance in a topographically predictable sequence beginning in the medulla oblongata/pontine tegmentum and olfactory bulb/anterior olfactory nucleus with a subsequent spread to the substantia nigra and other midbrain nuclei, forebrain and neocortex. However, the clinical findings may also be explained by a differential individual vulnerability of neuronal circuits for the underlying disease process.37
As such, neuronal circuits underlying all impairment domains in PD may be affected simultaneously, but because of different cell type vulnerability, become clinically manifest at different stages.