Current knowledge of cognitive dysfunction in Parkinson's disease (PD) has largely been obtained from studies of chronically treated patients in whom effects of disease chronicity, treatment, depression and dementia are confounding factors. Studies of untreated patients have examined few cognitive domains and relationships between cognition, depression and motor disability have been incompletely explored. Accordingly, we studied 60 consecutive patients with newly diagnosed, untreated, idiopathic PD and 37 matched, healthy control subjects; no subject had clinical dementia or depression. All subjects received tests of specific processes of memory and cognition, including working memory, verbal and non-verbal short- and long-term memory, language, visuospatial capacity, set-formation and shifting and sequencing. Patients also received quantitative global clinical measures of severity of dementia, depression and motor disability. The PD group as a whole showed deficits in immediate recall of verbal material, language production and semantic fluency, set-formation, cognitive sequencing and working memory and visuomotor construction. However, this group was unimpaired in immediate memory span, long-term forgetting, naming, comprehension and visual perception. Language deficits and more severe frontal lobe impairments were confined to those PD patients scoring abnormally on a Mini Mental State examination. Motor disability correlated strongly with severity of depression but weakly with cognitive impairment. Cognitive sequencing, set-formation and set-shifting deficits tended to associate with depression, but otherwise there was no association between cognition and depression. The results indicate dissociation of cognition and motor control in early PD which suggests that cognitive dysfunction is largely independent of frontostriatal dopamine deficiency underlying motor disability. Some, but not all, of the frontal lobe deficits of chronic disease are detectable in early, untreated PD. The pathogenesis of the cognitive deficits shown here appears to involve extrastriatal dopamine systems or non-dopaminergic pathology. Longitudinal study is necessary to determine whether increasing disease duration exacerbates the early cognitive deficits and affects new cognitive domains, in addition to producing increasing motor disability.

The cognitive performance of a group of 82 newly diagnosed patients with Parkinson's disease who had never been treated was reassessed approximately 4 mths after randomization to one of three monotherapies (levodopa, bromocriptine or anticholinergic drugs). Dopaminergic and anticholinergic treatments both led to improvement in motor control but their effects upon cognitive performance dissociated. Anticholinergic drugs produced impairment in processes underlying the immediate registration of information whilst dopaminergic therapy produced improvement on a task dependent on working memory and cognitive sequencing. Other cognitive measures showed no change on treatment. The deficits that were affected by cholinergic and dopaminergic modulation are those that were most compromised in the early, untreated state in Parkinson's disease. The data support the notion that cognitive impairment in Parkinson's disease is multifactorial in origin: short-term memory processes are served by both dopaminergic and cholinergic subcortico-frontal systems but much of the cognitive impairment of Parkinson's disease is independent of this subcortical neurochemical pathology and may be due to early neuronal dysfunction within the cerebral cortex.

Remote memory for public and personal events was evaluated in Alzheimer's disease (AD) and Parkinson's disease (PD), using a series of recall and recognition tests. Information related to content and date of past events was assessed separately. In recall of the content of personal and public events, both groups showed a gradient of deficit in which remote events were affected less than recent ones; the magnitude and temporal extent of the retrograde loss was related to severity of dementia. By contrast, gradient effects were not evident in the recall of date and were less marked in the recognition of content or date. In public and personal events tests, patients with PD showed a relative impairment in dating capacity, compared with their memory for the content of events, which was independent of dementia. These results suggest that dementia affects the recall of distant events less than recall of recent ones. Furthermore, the selective gradient effects in recall of content suggest that memory for date is served by cognitive processes independent of memory for event content. In PD, dating capacity is a sensitive measure of remote memory function that may be disrupted independently of dementia.

Background-Hallucinosis is a complication of the treatment of idiopathic Parkinson's disease commonly thought to aZict older, chronically medicated, cognitively impaired patients. However, patients with idiopathic Parkinson's disease of short durationexperiencinghallucinosisonrelatively low doses of dopaminergic medication have been found. The aim, therefore, was to investigate the homogeneity of a population of patients with idiopathic Parkinson's disease and hallucinosis. Methods-The clinical, demographic, and cognitive correlates of hallucinosis were investigated in a sample of 129 patients with idiopathic Parkinson's disease. Results-There were two subgroups of patients with idiopathic Parkinson's disease experiencing hallucinosis. In patients with a disease duration of five years or less, hallucinosis was associated with rapid progression of the motor component of the disease but not cognitive impairment. In patients with idiopathic Parkinson's disease of longer than five years duration, hallucinosis was associated with postural instability, global cognitive impairment, and lack of depressive aVect. In all patients with idiopathic Parkinson's disease, hallucinosis was more prevalent when they were treated with a direct acting dopamine receptor agonist. Hallucinosis was not associated with age at onset of idiopathic Parkinson's disease or dosage of dopaminergic medication. Conclusion-Hallucinosis in idiopathicParkinson's disease is heterogeneous, falling into two groups. The diVerence in the pathophysiological basis of hallucinosis in these two groups of patients is discussed.

As muscle spindles are involved in the sensation of position and movement of the body, we tested their involvement in the pathophysiology of idiopathic focal dystonia. Twenty patients with torticollis, nine with writer's cramp, two with blepharospasm and 16 healthy control subjects participated. In the first task, the blindfolded subject matched the position of the passively moved forearm with the opposite forearm when the elbow joint was slowly flexed. In a second matching task, passive movement was replaced by stimulation of one biceps tendon with a 50-Hz vibratory stimulus (a selective stimulus for muscle spindle Ia afferents). In normal individuals, this stimulus produces flexion of the vibrated arm around the elbow joint. Movement in both arms was recorded electronically. In experiments without vibratory stimuli, dystonic subjects showed normal movement of the tracking arm during attempts to match the position of the passively moved arm and no difference between the arms in the initial and final steady state positions. In experiments using vibratory stimuli, vibration of biceps tendons in normal subjects elicited flexion of the stimulated arm at the elbow and a matching movement of the opposite arm. In patients with dystonia, there was a similar flexion response to the vibratory stimulus in the stimulated arm but movement of the tracking arm was reduced. Taken together, these experiments suggest that there is abnormal perception of motion, but not position, in dystonic subjects. Dystonic subjects showed bilateral abnormalities of perception of the tonic vibration reflex which were remote from the clinically affected site. These findings are discussed in relationship to the role of muscle spindle Ia afferents in focal dystonia.

Idiopathic Parkinson's disease (IPD) has been subclassified on the basis of predominant motor symptomatology, age at disease onset, depressive affect, and cognitive performance. However, subgroups are usually arbitrarily defined and not reliably based on qualitatively distinct neuropathology. We explored heterogeneity in IPD in a data‐driven manner using comprehensive demographic, motor, mood, and cognitive information collected from 176 patients with IPD. Cluster analysis revealed three subgroups of patients at a disease duration of 5.6 years and two subgroups at 13.4 years. The subgroups may represent the clinical progression of three distinct subtypes of IPD. The “motor only” subtype was characterized by motor symptom progression in the absence of intellectual impairment. Equivalent motor symptom progression was shown by the “motor and cognitive” subtype which was accompanied by executive function deficits progressing to global cognitive impairment. The “rapid progression” subtype was characterized by an older age at disease onset and rapidly progressive motor and cognitive disability. There was no relationship between the motor and cognitive symptoms in any subtype of IPD. We conclude that the clinical heterogeneity of IPD is governed by distinct neuropathologic processes with independent etiologic influences.

Endovascular treatment may cause less structural brain damage than surgery and have a more favorable cognitive outcome. However, cognitive outcome appears to be dictated primarily by the complications of SAH.

Previous studies of remote memory function have indicated a dissociability between memory for the content and date of past events and suggested selective deficits of dating capacity in Parkinson's disease (PD). The present study examined the hypothesis that poor dating in PD is linked to a specific deficit in temporal contextual memory which also affects new learning. Patients with PD and patients with Alzheimer's disease (AD) were compared in their ability to perform tasks of content recognition and recency discrimination of words presented sequentially. Compared with AD patients, PD patients were disproportionately impaired in recency discrimination relative to content recognition. When performance was analysed as a function of retention interval, AD patients showed impairment in both tasks at all intervals. PD patients, by contrast, showed deficits in content recognition at the short stimulus-test intervals only, possibly reflecting the clinical phenomenon of bradyphrenia. These results suggest that recency discrimination deficits and impaired short-term memory processing are specific cognitive deficits in PD that may be linked to subcortical deafferentation of the frontal lobes.