Evidence map›Paper›PMID 17197371›Full record

ReviewNeurotoxicity research2006

The family of sensorimotor gating disorders: comorbidities or diagnostic overlaps?

Mark A Geyer

Open access · greenAbstract readReview
In one paragraph

Review in Neurotoxicity research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed, 3 pooled it
2.8field-weighted citation impact, top 9% 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

85 citing papers in PubMed, 3 syntheses or guidelines pooled it, 162 citations in OpenAlex.

  1. Pooled it
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  8. Mice lacking two alleles of the schizophrenia risk geneFrontiers in cellular neuroscience · 2026
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  18. Sex Differences in Psychosis: Focus on Animal Models.Current topics in behavioral neurosciences · 2023
    Review
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  20. Article

25 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

Mark A GeyerDepartment of Psychiatry, University of California San Diego, La Jolla, CA 92093-0804, USA. mgeyer@ucsd.edu
University of California, San Diego · US

Funding

SENSORY GATING &HABITUATION IN SCHIZOPHRENIAR01MH042228 · NIMH · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BRAFF, DAVID L. · 1987 to 2015
$6.5M
Inhibitory Deficits in Mania and Hyperdopaminiergic MiceR01MH071916 · NIMH · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GEYER, MARK A, PERRY, WILLIAM · 2004 to 2014
$4.2M
STARTLE GATING AND LOCOMOTION IN D2-FAMILY KNOCKOUT MICER01MH061326 · NIMH · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI GEYER, MARK A · 2000 to 2004
$1.5M
SENSORY GATING AND HABITUATION IN SCHIZOPHRENIAR37MH042228 · NIMH · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI BRAFF, DAVID L. · 1993 to 2002
$1.3M
NIMH NIH HHS MH071916NIMH NIH HHS MH42228NIMH NIH HHS MH61326NIMH NIH HHS R01 MH042228NIMH NIH HHS R01 MH061326NIMH NIH HHS R01 MH071916NIMH NIH HHS R37 MH042228
6 · The paper itself

Abstract

Prepulse inhibition (PPI) of startle is an operational measure of the pre-attentive filtering process known as sensorimotor gating. Originally identified in patients with schizophrenia, PPI deficits have been observed in multiple but not all psychiatric disorders. Thus, as with most signs and symptoms of psychiatric disorders, deficits in PPI cut across diagnostic categories. It remains unclear whether the diversity of disorders exhibiting deficient PPI bespeaks diagnostic overlaps or comorbidities. Given the recent focus on treatments for cognitive deficits of schizophrenia independently of treating psychosis, the relationship of PPI deficits to cognitive deficits becomes of interest. Although PPI cannot be considered to be a cognitive process per se, abnormalities in pre-attentive information processing may be predictive of or lead to complex cognitive deficits. Animal models of PPI deficits produced by dopamine agonists reliably predict existing antipsychotics. Nevertheless, since neither PPI nor cognitive deficits in schizophrenia are ameliorated by standard antipsychotics, current research is exploring the predictive value of non-dopaminergic PPI models in identifying treatments for gating disturbances independently of their relevance to specific disorders. Both PPI and cognitive deficits in schizophrenia patients are not reversed by first generation antipsychotics but may be attenuated by clozapine. Similarly, effects of glutamate antagonists on symptoms in patients and PPI in animals appear to be reduced by clozapine. Hence, treatment-induced reversals of deficits in PPI produced by glutamate antagonists may provide animal, and human, models to aid in the discovery of treatments of cognitive deficits in patients already treated with existing antipsychotics.

Indexed as

AnimalsDopamineDrug DesignHumansMovement DisordersReceptors, N-Methyl-D-AspartateReflex, StartleSchizophreniaSchizophrenic PsychologySensation DisordersDopamineReceptors, N-Methyl-D-Aspartate

Identifiers

PMID17197371
PMCPMC2667105
OpenAlexW1988299084

What OpenQuestion holds

Textmetadata
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.