Cholinergic‐dependent cognitive deficits in Parkinson's disease

Dubois, Bruno; Danze, F.; Pillon, B.; Cusimano, G; Lhermitte, F; Agid, Yves

doi:10.1002/ana.410220108

Cited by 170 publications

(72 citation statements)

References 24 publications

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“…Clock Setting and Clock Recognition tests. Dubois et al [34] have also found that, in Parkinson's disease, sub threshold doses of an anticholinesterase drug, scopol amine, impaired performance on complex visual tasks that demand selective attention and sequential-program ming but not memory abilities.…”

Section: Resultsmentioning

confidence: 99%

Psychometric Discrimination of Tetrahydroaminoacridine Responders in Alzheimer Patients

Alhainen

Helkala²,

Riekkinen³

1993

Dement Geriatr Cogn Disord

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Fourteen patients with probable Alzheimer''s disease (AD) participated in an open tetrahydroaminoacridine (THA) treatment trial. Before initiation of THA treatment, a brief battery of neuropsychological tests was performed by an experienced neuropsychologist. The tests were repeated 120 min after a single dose of 50 mg THA had been administered perorally. Thereafter, the patients had a 4-week active treatment with THA 100 mg/day. After the treatment period, eight patients were defined as responders (increase of Mini-Mental State Examination score ≧ 3) and six patients as nonresponders to the treatment. The responders showed significant improvement on Digit Span, Trail Making B, and on both Clock Setting and Clock Recognition tests after 50 mg of THA. The results suggest that in this subgroup of AD patients augmentation of the brain cholinergic systems mainly led to improvement of attentional and frontal-lobe rather than mnemonic functions.

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Section: Resultsmentioning

confidence: 99%

Psychometric Discrimination of Tetrahydroaminoacridine Responders in Alzheimer Patients

Alhainen

Helkala²,

Riekkinen³

1993

Dement Geriatr Cogn Disord

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“…Evidence also implicates other neurotransmitters such as acetylcholine in the cognitive manifestations of PD. 88,[103][104][105] …”

Section: Pathophysiology Of Executive Dysfunctionmentioning

confidence: 99%

Initial clinical manifestations of Parkinson's disease: features and pathophysiological mechanisms

Rodriguez-Oroz

Jahanshahi

Krack

et al. 2009

The Lancet Neurology

738

500

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A dopaminergic defi ciency in patients with Parkinson's disease (PD) causes abnormalities of movement, behaviour, learning, and emotions. The main motor features (ie, tremor, rigidity, and akinesia) are associated with a defi ciency of dopamine in the posterior putamen and the motor circuit. Hypokinesia and bradykinesia might have a dual anatomo-functional basis: hypokinesia mediated by brainstem mechanisms and bradykinesia by cortical mechanisms. The classic pathophysiological model for PD (ie, hyperactivity in the globus pallidus pars interna and substantia nigra pars reticulata) does not explain rigidity and tremor, which might be caused by changes in primary motor cortex activity. Executive functions (ie, planning and problem solving) are also impaired in early PD, but are usually not clinically noticed. These impairments are associated with dopamine defi ciency in the caudate nucleus and with dysfunction of the associative and other non-motor circuits. Apathy, anxiety, and depression are the main psychiatric manifestations in untreated PD, which might be caused by ventral striatum dopaminergic defi cit and depletion of serotonin and norepinephrine. In this Review we discuss the motor, cognitive, and psychiatric manifestations associated with the dopaminergic defi ciency in the early phase of the parkinsonian state and the diff erent circuits implicated, and we propose distinct mechanisms to explain the wide clinical range of PD symptoms at the time of diagnosis.

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“…Although the long-term effects of levodopa on the prevalence of dementia remain controversial (Rajput et at., 1984;Portin and Rinne, 1986), short-term confusional effects are well-recognized and specific cognitive functions may be affected (Gotham et at., 1988). Anticholinergic drugs produce memory loss and confusional states in demented PD patients (de Smet et at., 1982) and sub-threshold doses of anticholinergics impair visual memory of non-demented PD patients but do not affect normal subjects (Dubois et at., 1987). Clearly, it is essential to take account of current drug therapy in evaluation of the prevalence of dementia in PD and in investigation of the specific effects of additional drugs on cognitive function.…”

Section: Drugsmentioning

confidence: 99%

Specificity of Cognitive Impairment in Neurological Disease: A Methodological Critique of Parkinson’s Disease

Sagar

1991

Behavioural Neurology

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Multiple cognitive deficits have been recognized in many neurological disorders but the specificity of the findings and the relationship to the underlying neuropathology remain obscure. Definitions of dementia have been proposed based on symptom profiles of the cognitive disorder and qualitative differences have been claimed between dementias of different aetiology. Some conditions have been claimed to show patterns of cognitive deficit that are distinguished from dementia and related to specific neuropathology or psychological processes, e.g. frontal lobe deficits in Parkinson's disease. Sometimes, a relationship has been established between certain cognitive deficits and particular neurochemical deficits which has led to the notion of specific drug treatment, e.g. cholinergic deficits and memory failure in Alzheimer's disease. However, these conclusions are often potentially flawed by methodological inadequacies. This critique presents some methodological issues relevant to the study of brainbehaviour and drug-behaviour relationships in syndromes of multiple cognitive deficit, using Parkinson's disease as the model. The following recommendations are made: rigid diagnostic criteria; representative patient groups; avoidance of arbitrary quantitative criteria to limit definitions of dementia; matching of groups for overall level of cognitive impairment in the search for qualitative cognitive differences related to neuropathology or effects of particular drugs; the use of suitable controls in patient groups, neuropsychological tests and treatment regimes; the use of specific quantitative tests of cognition, affect and motor disability; and longitudinal, compared with cross-sectional, study design.

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Cholinergic‐dependent cognitive deficits in Parkinson's disease

Cited by 170 publications

References 24 publications

Psychometric Discrimination of Tetrahydroaminoacridine Responders in Alzheimer Patients

Psychometric Discrimination of Tetrahydroaminoacridine Responders in Alzheimer Patients

Initial clinical manifestations of Parkinson's disease: features and pathophysiological mechanisms

Specificity of Cognitive Impairment in Neurological Disease: A Methodological Critique of Parkinson’s Disease

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