Evidence map›Paper›PMID 10069406›Full record

ReviewDrugs & aging1999

Limiting neurological damage after stroke: a review of pharmacological treatment options.

S J Read, T Hirano, S M Davis, G A Donnan

Abstract readReview
PubMed Publisher
In one paragraph

Review in Drugs & aging, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. The protective effect of fish n-3 fatty acids on cerebral ischemia in rat prefrontal cortex.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2008
    Article
  6. Article
  7. Article
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

4 authors.

S J ReadDepartment of Neurology, Austin and Repatriation Medical Centre, Heidelberg, Victoria, Australia.
T Hirano
S M Davis
G A Donnan

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute ischaemic stroke is a leading cause of death and a major cause of long term disability worldwide. Effective treatments for limiting the neurological damage after stroke have proven elusive. An improved understanding of the complicated cascade of cellular events following the onset of cerebral ischaemia has led to exploration of a number of avenues for early intervention. Reperfusion of the ischaemic territory using thrombolytic drugs has shown promise in clinical trials as a method for achieving tissue salvage. Antithrombotic and antiplatelet agents have not demonstrated efficacy as acute therapies, although the early use of aspirin (acetylsalicylic acid) appears to produce a reduction in early stroke recurrence. A wide variety of drugs which interfere at various points in the ischaemic cascade, so-called 'neuroprotective agents', have also been studied, but with mixed success. Of these, antagonists of voltage-gated calcium channels, antagonists at the N-methyl-D-aspartate (NMDA) receptor and scavengers of free radicals have been most extensively studied. Despite proving effective in animal models of cerebral ischaemia, these drugs have largely failed to fulfil their promise in clinical trials. While individual compounds have proven ineffective, combinations of drugs with different mechanisms of action may yet provide the best treatment for acute ischaemic stroke.

Indexed as

Cerebrovascular DisordersFibrinolytic AgentsHumansNervous System DiseasesNeuroprotective AgentsFibrinolytic AgentsNeuroprotective Agents

Identifiers

What OpenQuestion holds

Texttitle and abstract
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.