Purkinje cell loss is a characteristic of essential tremor.

This paper began as a letter to the editor, commenting on several methodological and conceptual problems with the paper by Rajput et al. [1]. We were asked by the editors to expand the paper to include a more general discussion of the role of the cerebellum in essential tremor (ET). The study of the...

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Publicado en:Parkinsonism & Related Disorders Vol. 17; no. 6; pp. 406 - 410
Autores principales: Louis ED, Faust PL, Vonsattel JP, Louis, Elan D, Faust, Phyllis L, Vonsattel, John-Paul G
Formato: research review Journal Article
Publicado: Elsevier B.V. Jul2011
Acceso en línea:Ver este registro en EBSCOhost
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        atl: Purkinje cell loss is a characteristic of essential tremor.
      aug:
        au:
          Louis ED
          Faust PL
          Vonsattel JP
          Louis, Elan D
          Faust, Phyllis L
          Vonsattel, John-Paul G
        affil: Department of Neurology, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA
      sug:
        subj:
          Essential Tremor Pathology
          Nerve Degeneration Pathology
          Neurons Pathology
          Study Design
          Funding Source
      ab: This paper began as a letter to the editor, commenting on several methodological and conceptual problems with the paper by Rajput et al. [1]. We were asked by the editors to expand the paper to include a more general discussion of the role of the cerebellum in essential tremor (ET). The study of the neuropathological underpinnings of essential tremor (ET) is a relatively new undertaking. The purpose of this paper is three-fold. The first is to comment on methodological problems in a recently-published paper by Rajput et al., the major one being the small sample size of that study, which resulted in a Type II statistical error. Hence, one cannot conclude based on their data that there is no Purkinje cell (PC) loss in ET. Secondly, we comment on conceptual problems with that study, which suggested that PC loss might not be a featured characteristic of ET because it is also found in other disease states. We discuss why this is an erroneous conclusion. Our third purpose is to more broadly discuss the role of the cerebellum in ET, giving consideration to the wealth of clinical and postmortem data that have accumulated over recent years. In this discussion, we make the following points: (1) it is now generally recognized that ET is a disease of cerebellar systems dysfunction, (2) given the nature of the postmortem work, revealing the presence of several types of structural-anatomical changes within the cerebellum and absence of detectable changes in other brain regions, the most empirically-based explanation is that the primary problem in ET is in the cerebellum itself, (3) that the collection of cellular changes in the cerebellum in ET are also present in other cerebellar degenerations should add to rather than detract from the notion that ET is a disease of cerebellar degeneration.
      pubtype: Academic Journal
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        Journal Article
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    language: English
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