A high percentage of Parkinson’s disease (PD) patients show cognitive impairments in addition to the cardinal motor symptoms. These deficits primarily concern executive functions most probably linked to dysfunctions in prefrontal regions due to decreased dopaminergic transmission in fronto-striatal loops. To investigate possible associations between decision-making and executive functions in PD, we examined 20 non-demented PD patients and 20 healthy control subjects with a neuropsychological test battery and the Game of Dice Task. In this computerised decision-making task, the rules for gains and losses and the winning probabilities are obvious and stable. Thus, strategic components besides feedback processing might influence decision-making in this task. We found that PD patients were impaired in the Game of Dice task performance and that the frequency of disadvantageous choices correlated with both executive functions and feedback processing. We suggest that decision-making deficits of PD patients in explicit gambling situations might be associated with dysfunctions in two different fronto-striatal loops: the limbic-orbitofrontal-striatal loop, involved in feedback processing, and the dorsolateral prefrontal-striatal loop, involved in executive functions.

The afferent connections of the primate's temporopolar cortex were investigated with the retrograde horseradish peroxidase technique. Old World and New World monkeys received small unilateral injections of horseradish peroxidase. These labeled cells in a number of cortical, thalamic, and brainstem regions and in a few further telencephalic and diencephalic regions. Cortically, the neighboring areas of the inferior and superior temporal gyrus and the insula contained a considerable number of labeled cells. Furthermore, a substantial projection arose from the orbitofrontal and the frontopolar cortex. The cingulate gyrus contained only very few labeled cells. Interhemispherically, corticocortical connections arose mainly from temporal lobe areas. Labeled cells were seen in various regions of the basal forebrain and cells labeled only faintly in the lateral and basal accessory nuclei of the amygdala. The claustrum contained labeled neurons only in one rhesus monkey. On the diencephalic level, the caudal medial portion of the medial pulvinar was the principal thalamic source of afferents to the temporopolar cortex. Furthermore, labeled cells were found in the neighboring, caudal part of the mediodorsal nucleus, within and along the nucleus limitans, in the medial geniculate nucleus, and in several nuclei of the nonspecific system. The fields of Forel, the zona incerta, and lateral and dorsomedial hypothalamic areas contained a few labeled cells. Within the brainstem of the rhesus monkeys those regions projecting diffusely to the cortex contained a few labeled neurons. Furthermore, these brains had some labeled cells in the regions of the nuclei medialis annuli aqueductus, tractus mesencephalicus nervi trigemini, and trochlearis. Although among the three species differences in the cortical and thalamic projection patterns were observed, the regions projecting most densely to the temporal pole were similar in principle. This statement holds in particular for cortical and thalamic sites. However, the greatest number of labeled cells was found in the rhesus monkey, a fact that cannot be attributed solely to the size of the horseradish peroxidase injections and the size of the brain, but that appears rather to represent a true species difference. From our results we conclude that the temporopolar cortex constitutes a cortical area necessary for effective affectional-sensory integration.

This study describes a new method, based on accelerometry, which quantifies tremor activity and posture continuously. A total of 25 right-handed patients with Parkinson's disease were recorded in a rest condition and in a postural tremor test, and during 24-h ambulatory monitoring. The tremor parameters, such as amplitude, frequency, and occurrence (percent of time), were derived by joint amplitude-frequency analysis. The DC components of multi-channel accelerometry allowed the detection of posture. A repeated measurement MANOVA was used to test the effects of posture and night-day differences in tremor activity. Further issues included consistencies of amplitude measurements across hands, between tasks, and between segments of recordings. Findings indicated an increase between resting tremor and postural tremor in the three tremor parameters, an increase under distraction, and enhanced activity in sitting compared to standing/walking. The best predictions of daytime monitoring measures, based on resting measures, were made for left hand tremor. This methodology is suitable for the detection of diurnal changes in tremor activity, especially amplitude changes, and for the psychophysiological investigation of enhanced tremor caused by task demands and emotional reactions.

Dementia in idiopathicParkinson's syndrome JON 1607 Jean Marie Charcot first described cognitive deficits in Parkinson patients in 1875: ". . . psychic faculties are definitely impaired . . . at a given point the mind becomes clouded and memory is lost." Modern research has shown some degree of loss in the level of cognitive functioning to be an integral part of basal ganglia disturbances in the idiopathic Parkinson's syndrome. Disturbances in both frontal lobe functions (with effects on level of arousal and executive abilities such as planning) and memory (in particular free recall) are already demonstrable in the early stage of the disease in over 90 % of patients.There is however a high degree of variability in the literature published to date on the frequency of idiopathic Parkinson patients who subsequently develop clinically relevant dementia, ranging between 10 and 80 %. Very carefully detailed data were given for a community-based prevalence study [1] which found a prevalence of 27.7 % among Parkinson patients, who thus have a two-to three-fold higher risk for dementia than the general population.Particular risk factors for the development of dementia after the onset of idiopathic Parkinson's disease (IPD) have been identified: above-average age at the initial diagnosis of IPD, increased occurrence of dementia among other family members, higher level of severity in the extrapyramidal symptoms, early appearance of bilateral motor involvement, lower educational level, and the early development of confusional states or psychotic symptoms under L-dopa substitution.A considerable number of authors relate dementia developing after the onset of Parkinson's to the so-called subcortical dementias which are characterized by psychomotor bradyphrenia, forgetfulness, depression and alterations in personality, whereby primary cognitive disturbances such as amnesia, apraxia or aphasia are lacking. This intimate association of Parkinson's dementia with subcortical dementia is based on common neuropathological findings such as the presence of (1) Lewy bodies only in subcortical areas, and not in cortical areas, as well as (2) neuritic plaques. However, E. and H. Braak demonstrated extra-cellular amyloid deposits in all areas of the cortex, while neurofibrillary tangles were missing in the isocortex. Other elements which they considered essential for the development of dementia are (1) the decline of cholinergic neurons in the Nucleus basalis of Meynert and (2) distinct changes in the entorhinal region, whereas only minor damage should be found in the hippocampal areas. In addition, serotonergic neurons will be lost in the Nu-■ Abstract Approximately 25 % of patients with idiopathic Parkinson's disease (IPD) later develop

The afferent connections of the squirrel monkey's lateral premotor cortex were investigated with the horseradish peroxidase (HRP) technique. Seven monkeys received small, unilateral injections of HRP spaced between the most dorsal and the most lateral region of the premotor cortex. Results are based on six brains, all of which showed a considerable number of labeled neurons both cortically and subcortically. At the cortical level, labeled cells were found both ipsi- and contralateral to the injection site. Heavy labeling occurred in the fields surrounding the prefrontal, central, and precentral cortex, while the temporal regions usually innervated the premotor cortex with a moderate number of cells, and the parietal fields with only a minor number. Surprisingly, in all brains, but especially in those with the more lateral injections, we also found a considerable number of afferents originating from occipital fields, including a few neurons from the striate cortex. Subcortically, a few labeled cells were seen in basal forebrain regions, the amygdala, and the claustrum; a considerable number of thalamic nuclei and also some hypothalamic nuclei contained labeled cells; and within the brainstem, labeling was found most consistently in the locus ceruleus and in the tegmental fields. It is concluded that the (lateral) premotor cortex is involved in sensorimotor integration to a higher degree than has been recognized up to now.