4.7 Article

Temporal Cognitive and Brain Changes in Korsakoff Syndrome

期刊

NEUROLOGY
卷 96, 期 15, 页码 E1987-E1998

出版社

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1212/WNL.0000000000011749

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资金

  1. Fondation pour la Recherche Medicale (FMR) [ING20140129160]
  2. ANR-Retour postdoctorant
  3. Conseil Regional Basse Normandie
  4. MILDECA
  5. Institut National de la Sante et de la Recherche Medicale (Inserm)
  6. Fondation Plan Alzheimer (Alzheimer Plan)
  7. Programme Hospitalier de Recherche Clinique (PHRCN) [A0149338, 12-006-0347]
  8. Agence Nationale de la Recherche
  9. Region Basse-Normandie
  10. Association France Alzheimer et maladies apparentees
  11. Fondation Vaincre Alzheimer

向作者/读者索取更多资源

The study found that cognitive, motor, and brain changes in patients with Korsakoff syndrome did not deteriorate over a period of 10 years, but there was also no significant improvement, with only modest recovery in the frontocerebellar circuit. Long-term retention of episodic memory and widespread structural and metabolic alterations in the brain demonstrated the irreversible negative effects of KS.
Objective To investigate cognitive and brain changes in patients with Korsakoff syndrome (KS) over months and up to 10 years after the diagnosis. Methods Two groups of 8 patients with KS underwent neuropsychological, motor, and neuroimaging investigations, including structural MRI and F-18-fluorodeoxyglucose-PET. The KSC group, recruited at Caen University Hospital, was examined early after the KS diagnosis (KSC-T1) and 1 year later (KSC-T2). The KSR group, recruited at nursing home at Roubaix, was evaluated 10 years after the diagnosis. Longitudinal comparisons in KSC explored short-term changes, while cross-sectional comparisons between KSC-T1 and KSR informed about long-term changes. Results No cognitive, motor, or brain deterioration occurred over time in patients with KS. There was no clear improvement either, with only modest recovery in the frontocerebellar circuit. Compared to the norms, KSC-T1 had severe episodic memory impairments, ataxia, and some executive dysfunctions. They also presented widespread atrophy and hypometabolism as well as cerebellar hypermetabolism compared to 44 healthy matched controls. Episodic memory remained significantly impaired in KSC-T2 and KSR. Contrary to KSC at T1 and T2, KSR had preserved inhibition abilities. Atrophy was similar but less extended in KSC-T2 and even more limited in KSR. At all times, the thalamus, hypothalamus, and fornix remained severely atrophied. Hypometabolism was still widespread in KSC-T2 and KSR, notably affecting the diencephalon. Cerebellar metabolism decreased over time and normalized in KSR, whereas motor dysfunction persisted. Conclusion In KS, structural and metabolic alterations of the Papez circuit persisted over time, in accordance with the irreversible nature of amnesia. There was neither significant recovery as observed in patients with alcohol use disorder nor progressive decline as in neurodegenerative diseases.

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