The Cerebellum

, Volume 18, Issue 1, pp 67–75 | Cite as

Long Trace Eyeblink Conditioning Is Largely Preserved in Essential Tremor

  • Kasja Solbach
  • Simba-Joshua Oostdam
  • Martin Kronenbuerger
  • Dagmar Timmann
  • Marcus GerwigEmail author
Original Paper


The cerebellum and the prefrontal cortex are assumed to play a role in the pathophysiology of essential tremor (ET). Trace eyeblink conditioning with a long interstimulus interval relies on an intact function of the hippocampus, prefrontal cortex (PFC), and, although marginally, of the cerebellum. The aim of the present study was to evaluate whether long trace eyeblink conditioning is impaired in patients with ET. In 18 patients with ET and 18 controls, a long trace conditioning paradigm was applied. Following 100 paired conditioned response-unconditioned response trials, 30 conditioned response alone trials were given as extinction trials. The degree of tremor and the presence of accompanying cerebellar signs were determined based on clinical scales. The acquisition of conditioned eyeblink responses was not impaired in the group of all patients compared to controls (mean total incidences of conditioned responses in patients 23.3 ± 14.5%, in controls 24.1 ± 13.9%; P = 0.88). In the subgroup of six patients with cerebellar signs, incidences of conditioned responses were numerically but not significantly lower (16.4 ± 9.9%) compared to patients without cerebellar signs (26.8 ± 15.5%; P = 0.16). Trace eyeblink conditioning with a long interstimulus interval was not impaired in subjects with ET. Patients with clinical cerebellar signs presented slightly reduced conditioning. Areas of the PFC contributing to trace eyeblink conditioning appear less affected in ET. Future studies also using a shorter trace interval should include a larger group of subjects in all stages of ET.


Essential tremor Trace eyeblink conditioning Cerebellum Associative learning 



The authors like to thank Beate Brol for her help in conducting the experiments, in data analysis, and preparing the figures.

Author Contributions

KS: Research project; Statistical Analysis; Manuscript Preparation.

SJO: Research project; Statistical Analysis; Manuscript Preparation.

MK: Research project; Manuscript Preparation.

DT: Research project; Statistical Analysis; Manuscript Preparation.

MG: Research project; Statistical Analysis; Manuscript Preparation.

Funding Information

KS received speaker honoraria from Allergan.

SJO has received no funding sources.

MK has received no funding sources, regardless of relationship to the current research in the article.

DT received grants from the German Research Foundation, the German Heredoataxia Foundation and Mercur Research Center Ruhr and a honorium from Bayer AG.

MG received speaker honoraria and/or travel reimbursement from Novartis, Pfizer and Ipsen Pharma and research support from MSD.

Compliance with Ethical Standards

Conflict of Interest

The authors declare that they have no conflict of interest.


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Copyright information

© Springer Science+Business Media, LLC, part of Springer Nature 2018

Authors and Affiliations

  1. 1.Department of NeurologyUniversity of Duisburg-EssenEssenGermany
  2. 2.Department of NeurologyJohns Hopkins UniversityBaltimoreUSA
  3. 3.Department of NeurologyUniversity of GreifswaldGreifswaldGermany

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