title: Evaluation of multiple-session delay eyeblink conditioning comparing patients with focal cerebellar lesions and cerebellar degeneration.
abstract: The acquisition and timing of delay-conditioned eyeblink responses (CRs) have been shown to be significantly impaired in patients with disorders restricted to the cortex of the superior cerebellum. We were interested if patients improve incidences and timing of CRs across three sessions on three consecutive days. A standard delay paradigm was used in 9 patients with diffuse cerebellar degeneration, 13 patients with ischemic cortical cerebellar lesions and in 13 controls. High-resolution magnetic resonance imaging (MR imaging) was used to ensure that hemispheral lobules VI and/ or Crus I were lesioned in all stroke patients with the interposed nuclei being preserved. On day 1 patients with stroke but not with degenerative disorders showed significant CR acquisition, although total CR incidences remained significantly lower than in controls. No further improvement was visible on days 2 and 3 neither in patients with focal lesions nor in patients with cerebellar degeneration. CRs occurred earlier in cerebellar patients, most pronounced in patients with degenerative disorders. In patients with stroke but not in the degenerative group timing had improved on the third day close to values of the control subjects. Findings show that lesions of the cerebellar cortex produce permanent deficits in the acquisition of delay-conditioned eyeblink responses. Overall, mean CR incidence was higher in focal compared to degenerative disorders, most likely because the critical lobules (VI and Crus I) were lesioned only in part. Intact anterior lobe, which it thought to contribute to CR timing, may explain recovery of disordered timing in focal cerebellar patients.
authors.affiliation: Department of Neurology, University of Duisburg-Essen, Hufelandstrasse 55, D-45147 Essen, Germany. marcus.gerwig@uk-essen.de
authors.forename: Marcus
authors.initials: M
authors.lastname: Gerwig
authors.forename: Hana
authors.initials: H
authors.lastname: Guberina
authors.forename: Anna Catharina
authors.initials: AC
authors.lastname: Esser
authors.forename: Mario
authors.initials: M
authors.lastname: Siebler
authors.forename: Beate
authors.initials: B
authors.lastname: Schoch
authors.forename: Markus
authors.initials: M
authors.lastname: Frings
authors.forename: Florian P
authors.initials: FP
authors.lastname: Kolb
authors.forename: Volker
authors.initials: V
authors.lastname: Aurich
authors.forename: Andreas
authors.initials: A
authors.lastname: Beck
authors.forename: Michael
authors.initials: M
authors.lastname: Forsting
authors.forename: Dagmar
authors.initials: D
authors.lastname: Timmann
mesh_terms: D000328:Adult; D000368:Aged; D001767:Blinking / Q000502:physiology; D002545:Brain Ischemia / Q000473:pathology / Q000503:physiopathology*; D002524:Cerebellar Ataxia / Q000473:pathology / Q000503:physiopathology*; D002525:Cerebellar Cortex / Q000473:pathology / Q000503:physiopathology*; D002526:Cerebellar Diseases / Q000473:pathology / Q000503:physiopathology*; D003215:Conditioning, Eyelid / Q000502:physiology*; D005108:Extinction, Psychological / Q000502:physiology; D005260:Female; D006801:Humans; D008297:Male; D008568:Memory / Q000502:physiology; D008875:Middle Aged; D009483:Neuropsychological Tests; D012018:Reflex / Q000502:physiology; D013132:Spinocerebellar Degenerations / Q000473:pathology / Q000503:physiopathology*; D020521:Stroke / Q000473:pathology / Q000503:physiopathology; D013997:Time Factors; D055815:Young Adult