Evidence map›Paper›PMID 26896093›Full record

ArticleNeurocritical care2016

Long-Term Cognitive Deficits After Subarachnoid Hemorrhage in Rats.

Toshihiro Sasaki, Ulrike Hoffmann, Motomu Kobayashi, Huaxin Sheng, Abdelkader Ennaceur, Frederick W Lombard, David S Warner

Abstract read
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In one paragraph

Article in Neurocritical care, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 18% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Pooled it
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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

7 authors at 4 institutions in 2 countries.

Toshihiro SasakiMultidisciplinary Neuroprotection Laboratories, Department of Anesthesiology, Duke University Medical Center, Box 3094, Durham, NC, 27710, USA.
Ulrike HoffmannMultidisciplinary Neuroprotection Laboratories, Department of Anesthesiology, Duke University Medical Center, Box 3094, Durham, NC, 27710, USA.
Motomu KobayashiMultidisciplinary Neuroprotection Laboratories, Department of Anesthesiology, Duke University Medical Center, Box 3094, Durham, NC, 27710, USA.
Huaxin ShengMultidisciplinary Neuroprotection Laboratories, Department of Anesthesiology, Duke University Medical Center, Box 3094, Durham, NC, 27710, USA.
Abdelkader EnnaceurDepartment of Pharmacy, University of Sunderland, Wharncliffe Street, Sunderland, SR1 3SD, UK.
Frederick W LombardMultidisciplinary Neuroprotection Laboratories, Department of Anesthesiology, Duke University Medical Center, Box 3094, Durham, NC, 27710, USA.
David S WarnerMultidisciplinary Neuroprotection Laboratories, Department of Anesthesiology, Duke University Medical Center, Box 3094, Durham, NC, 27710, USA. warne002@mc.duke.edu.
Duke University · USDuke Medical Center · USDuke University Hospital · USUniversity of Sunderland · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCognitive dysfunction can be a long-term complication following subarachnoid hemorrhage (SAH). Preclinical models have been variously characterized to emulate this disorder. This study was designed to directly compare long-term cognitive deficits in the context of similar levels of insult severity in the cisterna magna double-blood (DB) injection versus prechiasmatic blood (PB) injection SAH models.

methodsPilot work identified blood injectate volumes necessary to provide similar mortality rates (20-25 %). Rats were then randomly assigned to DB or PB insults. Saline injection and naïve rats were used as controls. Functional and cognitive outcome was assessed over 35 days.

resultsDB and PB caused similar transient rotarod deficits. PB rats exhibited decreased anxiety behavior on the elevated plus maze, while anxiety was increased in DB. DB and PB caused differential deficits in the novel object recognition and novel object location tasks. Morris water maze performance was similarly altered in both models (decreased escape latency and increased swimming speed). SAH caused histologic damage in the medial prefrontal cortex, perirhinal cortex, and hippocampal CA1, although severity of injury in the respective regions differed between DB and PB.

conclusionBoth SAH models caused long-term cognitive deficits in the context of similar insult severity. Cognitive deficits differed between the two models, as did distribution of histologic injury. Each model offers unique properties and both models may be useful for study of SAH-induced cognitive deficits.

Indexed as

AnimalsBehavior, AnimalCognitive DysfunctionDisease Models, AnimalMaleMaze LearningRatsRats, WistarSubarachnoid HemorrhageCisterna magna double blood injection modelCognitive dysfunctionPrechiasmatic blood injection modelRatSubarachnoid hemorrhage

Identifiers

PMID26896093
OpenAlexW2286848419

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.