Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2016 Mar;81(3):412-9.
doi: 10.1111/bcp.12720. Epub 2015 Sep 17.

Treatment of drug-induced seizures

Hsien-Yi Chen  1   2   3 , Timothy E Albertson  1   4 , Kent R Olson  1   3
Affiliations
Review

Treatment of drug-induced seizures

Hsien-Yi Chen et al. Br J Clin Pharmacol. 2016 Mar.

Abstract

Seizures are a common complication of drug intoxication, and up to 9% of status epilepticus cases are caused by a drug or poison. While the specific drugs associated with drug-induced seizures may vary by geography and change over time, common reported causes include antidepressants, stimulants and antihistamines. Seizures occur generally as a result of inadequate inhibitory influences (e.g., gamma aminobutyric acid, GABA) or excessive excitatory stimulation (e.g. glutamate) although many other neurotransmitters play a role. Most drug-induced seizures are self-limited. However, status epilepticus occurs in up to 10% of cases. Prolonged or recurrent seizures can lead to serious complications and require vigorous supportive care and anticonvulsant drugs. Benzodiazepines are generally accepted as the first line anticonvulsant therapy for drug-induced seizures. If benzodiazepines fail to halt seizures promptly, second line drugs include barbiturates and propofol. If isoniazid poisoning is a possibility, pyridoxine is given. Continuous infusion of one or more anticonvulsants may be required in refractory status epilepticus. There is no role for phenytoin in the treatment of drug-induced seizures. The potential role of ketamine and levetiracetam is promising but not established.

Keywords: anticonvulsants; poisoning; seizures.

PubMed Disclaimer

Figures

Figure 1
Figure 1
A model of drug‐ or chemical‐induced effects on neural activity. (A) The normal balance between excitatory and inhibitory neuronal activity, receptor function, transmitters and pathways. (B) Decreasing excitatory or increasing inhibitory neuronal activity can result in sedation, and is likely involved in terminating seizure activity. (C) When increased excitatory or decreased inhibitory neuronal activity results from drug or chemical exposure, seizures may occur. Although greatly simplified in this model, in actuality feedback loops, transmitter depletion and up‐and down‐regulation of receptor numbers and sensitivities are but a few of the complexities of this physiological process
Figure 2
Figure 2
Recommended treatment approach for drug‐induced seizures
See this image and copyright information in PMC

References

    1. Lowenstein DH, Alldredge BK. Status epilepticus at an urban public hospital in the 1980s. Neurology 1993; 43: 483–8. - PubMed
    1. Pesola GR, Avasarala J. Bupropion seizure proportion among new‐onset generalized seizures and drug related seizures presenting to an emergency department. J Emerg Med 2002; 22: 235–9. - PubMed
    1. Alldredge BK, Lowenstein DH, Simon RP. Seizures associated with recreational drug abuse. Neurology 1989; 39: 1037–9. - PubMed
    1. Delanty N, Vaughan CJ, French JA. Medical causes of seizures. Lancet 1998; 352: 383–90. - PubMed
    1. Finkelstein Y, Hutson JR, Freedman SB, Wax P, Brent J, Toxicology Investigators Consortium Case Registry . Drug‐induced seizures in children and adolescents presenting for emergency care: current and emerging trends. Clin Toxicol 2013; 51: 761–6. - PubMed

MeSH terms

Substances