Temporal Ordering and Short-Term Memory Deficits in Parkinson's Disease

Sagar, H. J.; Sullivan, Edith V.; Gabrieli, John D. E.; Corkin, Suzanne; Growdon, John H.

doi:10.1093/brain/111.3.525

Cited by 177 publications

(84 citation statements)

References 34 publications

(36 reference statements)

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“…1 These deficits are similar to those seen in patients with frontal lobe damage and include problems with verbal learning, 2 problem solving, 3 self-ordered pointing, 4 temporal sequencing, 5 delayed response, 6 conditional associative learning, 2,7 implicit learning, 7 and forward planning. 8 Because most patients with PD do not suffer from primary frontal lobe pathology, these cognitive deficits must be a direct or indirect consequence of degeneration of ascending catecholaminergic projections from the brainstem.…”

mentioning

confidence: 77%

Dopaminergic modulation of cortical function in patients with Parkinson's disease

Mattay

Tessitore

Callicott

et al. 2002

Annals of Neurology

379

233

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Patients with idiopathic Parkinson's disease suffer not only from classic motor symptoms, but from deficits in cognitive function, primarily those subserved by the prefrontal cortex as well. The aim of the current study was to investigate the modulatory effects of dopaminergic therapy on neural systems subserving working memory and motor function in patients with Parkinson's disease. Ten patients with stage I and II Parkinson's disease were studied with functional magnetic resonance imaging, during a relatively hypodopaminergic state (ie, 12 hours after a last dose of dopamimetic treatment), and again during a dopamine-replete state. Functional magnetic resonance imaging was performed under three conditions: a working memory task, a cued sensorimotor task and rest. Consistent with prior data, the cortical motor regions activated during the motor task showed greater activation during the dopamine-replete state; however, the cortical regions subserving working memory displayed greater activation during the hypodopaminergic state. Interestingly, the increase in cortical activation during the working memory task in the hypodopaminergic state positively correlated with errors in task performance, and the increased activation in the cortical motor regions during the dopamine-replete state was positively correlated with improvement in motor function. These results support evidence from basic research that dopamine modulates cortical networks subserving working memory and motor function via two distinct mechanisms: nigrostriatal projections facilitate motor function indirectly via thalamic projections to motor cortices, whereas the mesocortical dopaminergic system facilitates working memory function via direct inputs to prefrontal cortex. The results are also consistent with evidence that the hypodopaminergic state is associated with decreased efficiency of prefrontal cortical information processing and that dopaminergic therapy improves the physiological efficiency of this region.

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mentioning

confidence: 77%

Dopaminergic modulation of cortical function in patients with Parkinson's disease

Mattay

Tessitore

Callicott

et al. 2002

Annals of Neurology

379

233

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“…Circumscribed cognitive deficits not severe enough to interfere social or occupational functioning of the patient, such as visuospatial and frontal lobe dysfunction, are frequent findings in PD (Gotham et al, 1988). Memory deficits are also common in PD; particularly, impairment of recency discrimination and procedural learning has been demonstrated (E1- Awar et al, 1987;Mohr et al, 1987;Sagar et al, 1988). On the other hand, cortical functions such as verbal and praxic abilities have been described to be relatively spared in PD (Mahler and Cummings, 1990;Pillon et al, 1991).…”

Section: Discussionmentioning

confidence: 99%

Cognitive profile of Alzheimer patients with extrapyramidal signs: A longitudinal study

Helkala¹,

Laulumaa²,

Soikkeli³

et al. 1992

J Neural Transm Gen Sect

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The cognitive profile of Alzheimer patients without (ADE-, n = 17) and with (AD, E+, n = 15) extrapyramidal signs (rigidity or bradykinesia), at the time of diagnosis, was examined in a 3-year follow-up study and compared to cognitive performance of demented (PD D+, n = 18) and nondemented (PD D-, n = 17) patients with Parkinson's disease and normal elderly controls (n = 19). Although the AD E+ and AD E- groups did not differ significantly at the initial testing, the AD E+ patients showed greater deterioration on visual, praxic and expressive speech functions as well as in category memory. The cognitive profile of the AD E+ patients was similar to that of the PD D+ patients except that the AD E+ patients recognized more false positive targets on list-learning task. The AD E- patients had better preserved praxic functions and WAIS Performance IQ but they, like AD E+ patients, recognized more false positive targets on list-learning than the PD D+ patients did. The results suggest that AD patients with extrapyramidal signs, even if mild, at the time of diagnosis may have greater progression of cognitive impairment, especially on cortical functions, which may explain earlier need for institutional care observed in previous studies as compared to patients without these signs.

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“…These results indicate that the storing and consolidating processes that are under the control of the temporal lobes tend to be preserved in the disease [65]. In contrast, the performance of PD patients in explicit memory tests is significantly decreased in those tasks which require organization of the to-be-remembered material [15,79,80], temporal ordering [70,83], or conditional associative learning [72]. Thus, internal control of attention, required to generate spontaneously efficient encoding and retrieval strategies, is impaired in PD.…”

Section: Introductionmentioning

confidence: 91%

Cognitive deficits in Parkinson’s disease

1996

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Neuropsychological investigations of patients with Parkinson's disease have shown specific impairments even in the early stages of the disease, which include deficit of behavioural regulation in sorting or planning tasks, defective use of memory stores, and impaired manipulation of internal representation of visuospatial stimuli. These deficits, reported in a disease which predominantly involves subcortical structures, have drawn attention to a potential role of the basal ganglia in cognitive processes. Given the modulatory role of the basal ganglia, these disorders might result from more fundamental deficits concerning the allocation of attentional resources, the temporal organization of behaviour, the maintenance of representations in working memory or the self-elaboration of internal strategies, all of which resemble dysfunctions of processes that are commonly considered to be controlled by the frontal lobes. This suggests a functional continuity or complementarity between the basal ganglia and association areas of the prefrontal cortex. The recent description in primates of segregated loops that interconnect discrete regions of the caudate nucleus to the dorsolateral and orbitofrontal regions of the prefrontal cortex via the thalamus may give some support to this hypothesis. Alternatively, degeneration of the ascending cholinergic and catecholaminergic neuronal systems may contribute, at least in part, to the occurrence of this frontal-lobe-like symptomatology associated with Parkinson's disease.

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Temporal Ordering and Short-Term Memory Deficits in Parkinson's Disease

Cited by 177 publications

References 34 publications

Dopaminergic modulation of cortical function in patients with Parkinson's disease

Dopaminergic modulation of cortical function in patients with Parkinson's disease

Cognitive profile of Alzheimer patients with extrapyramidal signs: A longitudinal study

Cognitive deficits in Parkinson’s disease

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