On the physiology of cognitive decline in type 1 diabetes.

Cognition Cognitive impairment Diabetes mellitus type 1 EEG Evoked potential Human Psychomotor speed

Journal

Neurophysiologie clinique = Clinical neurophysiology
ISSN: 1769-7131
Titre abrégé: Neurophysiol Clin
Pays: France
ID NLM: 8804532

Informations de publication

Date de publication:
Jun 2021
Historique:
received: 29 12 2020
revised: 25 02 2021
accepted: 25 02 2021
pubmed: 21 3 2021
medline: 11 9 2021
entrez: 20 3 2021
Statut: ppublish

Résumé

Type 1 diabetes mellitus (T1DM) may be associated with cognitive impairment and notably a decline in psychomotor speed, information processing speed and attention. The mechanism for this decline is uncertain. Previous studies by our group and others have demonstrated a decline in EEG-power and event-related potential amplitude in T1DM. The objectives of the present study were to explore whether 1) the association between event-related potential (N100) amplitude and psychomotor speed is different between T1DM and healthy subjects, and 2) the decline in N100 amplitude depends on duration of diabetes. Patients with T1DM (N = 204) and healthy control subjects (N = 358) were included in a cross-sectional study. Event-related brain potentials were recorded with auditory reaction tasks. Psychomotor speed was evaluated with the Grooved Pegboard test in a subset of the patients (N = 70) and the healthy control subjects (N = 89). Patients with T1DM had a decrease in the N100 amplitude that correlated with a decline in psychomotor speed, longer duration of diabetes and increasing age. In healthy controls, the N100 amplitude did not decrease with age and the association between psychomotor speed and N100 amplitude was absent. The association between psychomotor speed and N100 amplitude is likely to be a specific trait for T1DM since it was not found in healthy controls and was dependent on diabetes duration. Our findings indicate that the pathogenesis of cognitive decline in T1DM may involve a disease-related factor with a long-term influence on the N100 amplitude.

Identifiants

pubmed: 33741257
pii: S0987-7053(21)00027-7
doi: 10.1016/j.neucli.2021.02.005
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

259-265

Informations de copyright

Copyright © 2021 Elsevier Masson SAS. All rights reserved.

Auteurs

Tom Brismar (T)

Department of Clinical Neuroscience, Karolinska Institutet, Karolinska University Hospital, SE-17176 Stockholm, Sweden; Department of Clinical Neurophysiology, Karolinska University Hospital, SE-17176 Stockholm, Sweden. Electronic address: tom.brismar@ki.se.

Gerald Cooray (G)

Department of Clinical Neuroscience, Karolinska Institutet, Karolinska University Hospital, SE-17176 Stockholm, Sweden; Department of Clinical Neurophysiology, Karolinska University Hospital, SE-17176 Stockholm, Sweden.

Mathias Sundgren (M)

Department of Clinical Neuroscience, Karolinska Institutet, Karolinska University Hospital, SE-17176 Stockholm, Sweden; Department of Neurology, Karolinska University Hospital, SE-17176 Stockholm, Sweden.

Lars Hyllienmark (L)

Department of Clinical Neuroscience, Karolinska Institutet, Karolinska University Hospital, SE-17176 Stockholm, Sweden; Department of Clinical Neurophysiology, Karolinska University Hospital, SE-17176 Stockholm, Sweden.

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