Evidence map›Paper›PMID 34444449›Full record

ReviewInternational journal of environmental research and public health2021

Mechanisms of Ethanol-Induced Cerebellar Ataxia: Underpinnings of Neuronal Death in the Cerebellum.

Hiroshi Mitoma, Mario Manto, Aasef G Shaikh

Open access · goldAbstract readReview
In one paragraph

Review in International journal of environmental research and public health, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
10.3field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

  1. Pooled it
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  5. Article
  6. Article
  7. Tremor pathophysiology.Clinical parkinsonism & related disorders · 2026
    Review
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  18. Review
  19. Alcohol Toxicity in the Developing Cerebellum.Diagnostics (Basel, Switzerland) · 2024
    Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 3 institutions in 3 countries.

Hiroshi MitomaMedical Education Promotion Center, Tokyo Medical University, Tokyo 160-0023, Japan.ORCID 0000-0003-0513-1811
Mario MantoUnité des Ataxies Cérébelleuses, Service de Neurologie, CHU-Charleroi, 6000 Charleroi, Belgium.
Aasef G ShaikhLouis Stokes Cleveland VA Medical Center, University Hospitals Cleveland Medical Center, Cleveland, OH 44022, USA.
Louis Stokes Cleveland VA Medical Center · USTokyo Medical University · JPUniversity of Mons · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ethanol consumption remains a major concern at a world scale in terms of transient or irreversible neurological consequences, with motor, cognitive, or social consequences. Cerebellum is particularly vulnerable to ethanol, both during development and at the adult stage. In adults, chronic alcoholism elicits, in particular, cerebellar vermis atrophy, the anterior lobe of the cerebellum being highly vulnerable. Alcohol-dependent patients develop gait ataxia and lower limb postural tremor. Prenatal exposure to ethanol causes fetal alcohol spectrum disorder (FASD), characterized by permanent congenital disabilities in both motor and cognitive domains, including deficits in general intelligence, attention, executive function, language, memory, visual perception, and communication/social skills. Children with FASD show volume deficits in the anterior lobules related to sensorimotor functions (Lobules I, II, IV, V, and VI), and lobules related to cognitive functions (Crus II and Lobule VIIB). Various mechanisms underlie ethanol-induced cell death, with oxidative stress and endoplasmic reticulum (ER) stress being the main pro-apoptotic mechanisms in alcohol abuse and FASD. Oxidative and ER stresses are induced by thiamine deficiency, especially in alcohol abuse, and are exacerbated by neuroinflammation, particularly in fetal ethanol exposure. Furthermore, exposure to ethanol during the prenatal period interferes with neurotransmission, neurotrophic factors and retinoic acid-mediated signaling, and reduces the number of microglia, which diminishes expected cerebellar development. We highlight the spectrum of cerebellar damage induced by ethanol, emphasizing physiological-based clinical profiles and biological mechanisms leading to cell death and disorganized development.

Indexed as

Cerebellar AtaxiaFetal Alcohol Spectrum DisordersCell DeathCerebellumEthanolFemaleHumansPregnancyEthanolalcoholcerebellar ataxiascerebellumethanolfetal alcohol spectrum disorder

Identifiers

PMID34444449
PMCPMC8391842
OpenAlexW3194111452

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.