Ann E. Taylor

Memory and learning in early Parkinson's disease: evidence for a "frontal lobe syndrome".

Fifteen untreated patients in the earliest stages of Parkinsons disease were compared to fifteen age- and intellectually matched control subjects on a number of memory tasks assessing short- and long-term recall of both meaningful and unrelated material, semantic relations in the organization of memory, priming, and source forgetting, and the ability to form new stimulus-response associations under conditions of maximal task interference. While patients demonstrated considerable evidence of preserved function, impaired performance on a subgroup of tasks was consistent with selective frontostriatal system involvement. These findings are discussed with reference to the underlying pathological processes in Parkinsons disease.

Cognitive processes in idiopathic dystonia treated with high-dose anticholinergic therapy : implications for treatment strategies

Studies utilizing single doses of scopolamine have suggested a role for the cholinergic system in memory. Results are consistent in identifying a selective effect on the early encoding stage of information processing. In terms of long-term administration of anticholinergics, patients with Parkinsons disease often display memory deficits. However, underlying pathology within the forebrain cholinergic system complicates the study of treatment effects in this disorder. We therefore assessed multiple memory routines in 20 cognitively intact patients with dystonia where no such pathology has been identified. Patients were tested before and after 2-4 months of 15-74 mg of trihexyphenidyl daily. Twelve tolerated this regime. Compared to control subjects, matched for age and I.Q., only tests with a single presentation of the material to be remembered were affected at follow-up. The speed of information processing was also significantly reduced. Age was strongly related to memory performance in the patient group alone and interacted with dose and duration of treatment. Results suggest that drug-induced slowing of mentation was responsible for impaired encoding, particularly in older patients. These findings affect treatment strategies, especially now that injections of botulinum toxin have proved to be highly effective for certain forms of focal dystonia.

Movement sequencing disorders in parkinson's disease

Ten PD patients and ten age-matched normal controls learned a sequence of 3 or 4 different hand movements to a criterion of 5 consecutive correct trials. They also performed a control sequence of 3 or 4 movements which involved the repetition of the same hand posture. Trials to reach criterion, errors, total response time and its components, response time for each movement and inter-response time were examined. There were no group differences in trials to criterion or errors. Total movement time as well as response and inter-response times were significantly longer for the PD patients, however, but only for sequences involving different hand movements not for the repetitive sequences. The relative timing of the responses was also different with the PD patients spending proportionately more time on each response and the controls spending more time between responses. The implications of these findings for understanding the movement sequencing impairments in PD are discussed.

Idiopathic Parkinson's disease: revised concepts of cognitive and affective status

Assumptions regarding increased risk of dementia in Parkinsons disease and of depression mimicking the endogenous form are reviewed and challenged from the perspectives of recent findings in both the neuropsychological and anatomical domains. Evidence suggests that depression, while frequent, behaviourally resembles the reactive variety and that selective impairment of cognitive functions considered to depend upon the integrity of the frontal lobes accompanies this disorder. In this regard, it is speculated that the cognitive alterations seen in non-demented parkinson patients are the consequences of dysfunction of the caudate nucleus which contributes significantly to the normal activities processed through the frontostriate complex loop.

Subcognitive processing in the frontocaudate "complex loop": the role of the striatum.

Anatomical connections between the frontal lobes and basal ganglia have long suggested joint participation in behavioural operations. Early experiments with nonhuman primates and patients are reviewed, followed by current research investigating the specific cognitive routines at risk in Parkinson disease. An hypothesis regarding the functional contribution of the basal ganglia to the frontostriate system is offered. The basal ganglia are considered to set limits on the context within which mental and motor events occur. It is argued that the nature of such processing is subcognitive.

Parkinson's disease and dementia

Wakayama concerning our study of a sensory level on the trunk in lower lateral brainstem lesions. Hayakawa’s report3 on the claseification of the sensory impairment dealt with the side of the face that was affected when there was involvement of the entire contralateral trunk and limbs. Hayakawa’s type 1 (with ipsilateral facial involvement) is the same sensory defect as in typical Wallenberg’s syndrome. ?Lpe 2 (with contralateral facial involvement) is the complete unilateral sensory defect such as that usually seen in supratentorial lesions, and type 3 (with bilateral facial involvement) corresponds to our case 9. His careful clinical observations and speculations on localization of the lesions according to the type of sensory defect were noteworthy. The main focus of our report, however, was the existence of a sensory level on the trunk that was not shown in any of Hayakawa’s cases. Hemisensory defects in our 3 canes and in the 1 case of Kase et al involved the face, arm, and trunk, with the lower border demarcated at a sensory level (termed “unilateral” pattern in our study). The sensory defect had an ususual distribution and is apparently distinct from Hayakawa’s type 2 or 4, which Dr. Wakayama referred to as the unilateral type. Furthermore, by use of MRI, we were able to precisely localize the lesions and confirm the clinicoanatomic correlation of the sensory defect. Hayakawa showed no anatomic verification by either autopsy or radiologic findinge. We were aware of Dr. Wakayama’s work‘ in this field as well as that of Hata et al,6 and chose not to comment on their work because, again, there were no descriptions of a sensory level on the trunk. We have provided the evidence that such a sensory level appeared as the result of the partial disruption of the lateral spinothalamic tract by MRI. To our knowledge, no similar studies have been reported heretofore.