Evidence map›Paper›PMID 19552655›Full record

ReviewEpilepsia2009

Pursuing paradoxical proconvulsant prophylaxis for epileptogenesis.

Caren Armstrong, Robert J Morgan, Ivan Soltesz

Open access · bronzeAbstract readReview
In one paragraph

Review in Epilepsia, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
4.0field-weighted citation impact, top 7% 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

16 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Searching for the ideal antiepileptogenic agent in experimental models: single treatment versus combinatorial treatment strategies.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2014
    Review
  9. Review
  10. Article
  11. Basket cell dichotomy in microcircuit function.The Journal of physiology · 2012
    Review
  12. Article
  13. Review
  14. Article
  15. Selective reduction of cholecystokinin-positive basket cell innervation in a model of temporal lobe epilepsy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010
    Article
  16. Disease-modifying effects of phenobarbital and the NKCC1 inhibitor bumetanide in the pilocarpine model of temporal lobe epilepsy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010
    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

3 authors at 1 institution in 1 country.

Caren ArmstrongDepartment of Anatomy and Neurobiology, University of California, Irvine, California, USA. cmarmstr@uci.edu
Robert J Morgan
Ivan Soltesz
University of California, Irvine · US

Funding

LIMBIC EXCITABILITY AFTER FEBRILE SEIZURESR01NS038580 · NINDS · UNIVERSITY OF CALIFORNIA-IRVINE · PI SOLTESZ, IVAN · 1999 to 2010
$2.9M
Plasticity of GABAergic Inhibition Following Head InjuryR01NS035915 · NINDS · UNIVERSITY OF CALIFORNIA-IRVINE · PI SOLTESZ, IVAN · 2002 to 2017
$2.6M
Plasticity Of GABAergic Inhibition Following Head InjuryR37NS035915 · NINDS · UNIVERSITY OF CALIFORNIA-IRVINE · PI SOLTESZ, IVAN · 2005 to 2011
$2.5M
PLASTICITY OF GABAERGIC INHIBITION FOLLOWING HEAD INJURYR29NS035915 · NINDS · UNIVERSITY OF CALIFORNIA IRVINE · PI SOLTESZ, IVAN · 1997 to 2001
$273k
NINDS NIH HHS NS35915NINDS NIH HHS NS38580NINDS NIH HHS R01 NS035915NINDS NIH HHS R01 NS038580NINDS NIH HHS R29 NS035915NINDS NIH HHS R37 NS035915
6 · The paper itself

Abstract

There are essentially two potential treatment options for any acquired disorder: symptomatic or prophylactic. For acquired epilepsies that follow a variety of different brain insults, there remains a complete lack of prophylactic treatment options, whereas at the same time these epilepsies are notoriously resistant, once they have emerged, to symptomatic treatments with antiepileptic drugs. The development of prophylactic strategies is logistically challenging, both for basic researchers and clinicians. Nevertheless, cannabinoid-targeting drugs provide a very interesting example of a system within the central nervous system (CNS) that can have very different acute and long-term effects on hyperexcitability and seizures. In this review, we outline research on cannabinoids suggesting that although cannabinoid antagonists are acutely proconvulsant, they may have beneficial effects on long-term hyperexcitability following brain insults of multiple etiologies, making them promising candidates for further investigation as prophylactics against acquired epilepsy. We then discuss some of the implications of this finding on future attempts at prophylactic treatments, specifically, the very short window within which prevention may be possible, the possibility that traditional anticonvulsants may interfere with prophylactic strategies, and the importance of moving beyond anticonvulsants-even to proconvulsants-to find the ideal preventative strategy for acquired epilepsy.

Indexed as

AnimalsAnticonvulsantsBrainBrain DiseasesCannabinoidsConvulsantsDisease Models, AnimalDrug Delivery SystemsEpilepsyHumansNeuroprotective AgentsAnticonvulsantsCannabinoidsConvulsantsNeuroprotective Agents

Identifiers

PMID19552655
PMCPMC2894282
OpenAlexW2076420822

What OpenQuestion holds

Textmetadata
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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.