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106 - Phenobarbital

Published online by Cambridge University Press:  06 October 2020

Stephen D. Silberstein
Affiliation:
Thomas Jefferson University, Philadelphia
Michael J. Marmura
Affiliation:
Thomas Jefferson University, Philadelphia
Hsiangkuo Yuan
Affiliation:
Thomas Jefferson University, Philadelphia
Stephen M. Stahl
Affiliation:
University of California, San Diego
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Summary

THERAPEUTICS

Brands

• Luminal, Alkabel, Solfoton

Generic?

• Yes

Class

• Antiepileptic drug (AED)

Commonly Prescribed for

(FDA approved in bold)

Generalized tonic-clonic, psychomotor, and partial seizures (monotherapy and adjunctive, children and adults)

Sedation

• Status epilepticus

• Seizures resulting from cerebral malaria

• Anxiety

• Alcohol or barbiturate withdrawal

How the Drug Works

• Phenobarbital raises seizure thresholds or alters seizure patterns in animal models

• The exact mechanism of action is unknown but likely enhances GABAA receptor activity

• Depresses glutamate excitability, alters sodium, calcium, and potassium channel conductance

• It affects polysynaptic midbrain reticular formation

How Long Until It Works

• Seizure prevention: should decrease by 2 weeks

• Status epilepticus: onset of action is 5 minutes following IV injection. Maximal CNS depression after at least 15 minutes

If It Works

• Seizures: goal is the remission of seizures. Continue as long as effective and well-tolerated. Consider tapering and slowly stopping after 2 years without seizures, depending on the type of epilepsy

If It Doesn't Work

• Increase to highest tolerated dose

• Epilepsy: consider changing to another agent, adding a second agent, or referral for epilepsy surgery evaluation. When adding a second agent, keep in mind drug interactions

Best Augmenting Combos for Partial Response or Treatment-Resistance

• Epilepsy: drug interactions complicate multi-drug therapy. Phenobarbital is a second-line agent in developed countries due to its AE profile

Tests

• CBC, hepatic and kidney function panels at baseline and every 6 months

ADVERSE EFFECTS (AEs)

How the Drug Causes AEs

• CNS AEs are probably caused by effects of increased GABA activity and alteration of ion channel function

• Vitamin D deficiency is caused by induction of metabolism

Notable AEs

• Sedation, ataxia, vertigo, cognitive dulling, depression, nystagmus, irritability, emotional disturbances

• Nausea, vomiting, hypotension

• Rash, uncommonly Stevens-Johnson syndrome

Type
Chapter
Information
Essential Neuropharmacology
The Prescriber's Guide
, pp. 388 - 391
Publisher: Cambridge University Press
Print publication year: 2015

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