Akinetic-rigid and tremor-dominant parkinson's disease: Two distinct cognitive and behavioral evolutions

There is no agreement in the definition of cognitive and behavioral alterations in Parkinson's Disease (PD), not presenting as Dementia-Parkinson Complex or evolving towards Lewy Bodies Disease (DLB). The aim of this study was to examine the frontal executive functions, speech, gait, apathy, behavior and caregiver's stress in a community based sample of PD patients divided in two groups: akinetic-rigid type and tremor-dominant type. The patients have been followed for three years. In summary, our data suggest that there are some important cognitive differences in the two groups: the akinetic-rigid patients do worse in interference sub-items in phonological and semantic tasks, and generally in the so-called frontal tasks. Their gait is worse, and their freezing rate is higher. Moreover, they do show more insight, albeit their behavior and apathy scores are worse as well as their caregiver's burden. It can be argued that akinetic -rigid presentation is different from the tremor-pattern of PD and needs specific dedicated care. As previously stated, the connections between basal ganglia and cortex justify their interferences in cognition, behavior, insight, and gait. The salient aspect of this study is that the basal ganglia interferences seem to be rather different in tremor-type pattern or in akinetic-rigid PD. In fact, frontal executive control, divided-attention, language production and apathy seem to be more involved in akinetic-rigid than in tremor-type PD. This is the first work dedicated to define the neuropsychological pattern of the two variants; evidence from literature is limited. A previous, well-conducted study in very few cases stated that in the tremor-dominant and in the akinetic PD patients all subdivisions of the GPe had significantly reduced DA levels. In the classic cases DA loss was very marked (-90%) in all GPe subdivisions. The same degree of DA loss was present in the caudal GPe subdivisions in the akinetic-rigid group. In contrast, the rostral GPe subdivisions in the akinetic-rigid cases and all GPe subdivisions in the tremordominant cases were distinctly less affected (DA losses 57-83%). These subregional DA losses may be clinically relevant in view of the recent studies in nonhuman primates, indicating that anatomically defined associative, limbic, and motor subdivisions of the GPe participate in several aspects of attentional, motivational, and motor behaviors. In GPi, the subregional DA loss in the two subgroups differed from the GPe DA patterns. The akinetic-rigid cases had marked DA loss in the dorsal and ventral portions of rostral GPi, as well as in the ventral portion of the caudal subdivision. The classic cases had marked reduction of DA in the ventral and dorsal portions of rostral GPi. The tremordominant cases had (moderate) loss of DA (-50%) in the dorsal portions of the rostral and caudal GPi. From a clinical standpoint, DA in the rostral GPi (dorsal and ventral) was significantly lower in the akinetic-rigid than the tremor-dominant cases. Our data seem to demonstrate, in vivo, that there is an independent pathological involvement of basal ganglia-subcortical loops, determining heavier frontal impairment in akinetic-rigid PD patients, confirming previous works.