Nonbenzodiazepine anticonvulsants

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Flashcards

Nonbenzodiazepine anticonvulsants

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Questions

USMLE® Step 1 style questions USMLE

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USMLE® Step 2 style questions USMLE

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A 30-year-old woman comes to the physician with a fever and sore throat. The patient’s symptoms started two days ago. She was diagnosed with a partial seizure last month and was started on anti-epileptic medication. Temperature is 38°C (100.4 °F), blood pressure is 120/80 mmHg, and pulse is 89 beats per minute. Laboratory results are shown below. Which of the following medications is this patient most likely taking?

 Erythrocyte count   5 million (cells/mcL) 
 Hemoglobin   13 (g/dL) 
 Mean corpuscular volume   80 (fL) 
 Leukocyte count   1500 (cells/mm3) 
 Absolute Neutrophil count   80 (cells/mm3) 
 Platelets count   200,000/mm3

External References

First Aid

2024

2023

2022

2021

Carbamazepine

agranulocytosis p. 249

aplastic anemia p. 249

bipolar disorder p. 578, 724

cytochrome P-444 and p. 251

epilepsy p. 560

SIADH and p. 248

teratogenicity p. 632

tonic-clonic seizures p. 724

trigeminal neuralgia p. 724

Transcript

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Anticonvulsants are a type of medication used to treat the various types of seizure disorders.

These include benzodiazepines and barbiturates which increase the activity of inhibitory neurons, but there are also many other classes of anticonvulsants with different mechanisms that we’ll talk about in this video.

Okay, so the cells that make up our brain are called neurons.

Neurons communicate with each other through neurotransmitters.

When one neuron is stimulated, it releases excitatory neurotransmitters that bind to receptors on the next neuron. This causes the next neuron to depolarize and release its own excitatory neurotransmitters, propagating the signal throughout the brain.

The main excitatory neurotransmitter in our brain is glutamate which can bind to several types of receptors that are basically ligand-gated ion channels, which open up and allow Na+ and Ca2+ to flow in, and K+ to flow out.

In the end, when it’s all added up, there’s an influx of positive charge that makes the cell less negative,and the neuron becomes depolarized. This causes nearby voltage-gated Na+ channels to open on the surface of the membrane, causing more Na+ to enter. This in turn triggers other nearby voltage-gated Na+ channels to open.

So this series of depolarization travels down the neuron like a wave and it’s called an action potential.

When it reaches the end of the neuron, called the synaptic terminal, it triggers the opening of voltage-gated Ca2+ channels, causing an influx of calcium ions which stimulates the release of neurotransmitters that are stored in synaptic vesicles.

Okay, we also have inhibitory neurons that shut down this chain of events.

These neurons release the main inhibitory neurotransmitter called gamma-aminobutyric acid or GABA, which binds to GABA receptors on other neurons.

These GABA receptors are also ligand-gated ion channels, but they open up to let the negatively charged Cl-, into the cell.

The influx of negative ions causes hyperpolarization where the cell’s membrane potential becomes more negative, which means it’s much more difficult for it to depolarize and fire off an action potential.

Alright, now there are cases where neurons in the brain start sending out more excitatory signals than normal. This can occur due to either too much excitation or too little inhibition in the brain.

Summary

Nonbenzodiazepine anticonvulsants are a class of drugs used to treat seizures, headaches, and neuropathic pain. These drugs are also used as mood stabilizers for bipolar disorders. Nonbenzodiazepine anticonvulsants decrease excitatory signals in the brain, primarily by blocking sodium and calcium channels, or by enhancing the actions of GABA. This lead to a decrease in the abnormal electrical activity in the brain responsible for the associated symptoms.

Common examples of nonbenzodiazepine anticonvulsants include carbamazepine, lamotrigine, and valproic acid. Side effects include double vision, ataxia, and liver toxicity for carbamazepine; Stevens Johnson syndrome for lamotrigine; and teratogenic effects like neural tube defects for valproic acid.

Sources

  1. "Katzung & Trevor's Pharmacology Examination and Board Review,12th Edition" McGraw-Hill Education / Medical (2018)
  2. "Rang and Dale's Pharmacology" Elsevier (2019)
  3. "Goodman and Gilman's The Pharmacological Basis of Therapeutics, 13th Edition" McGraw-Hill Education / Medical (2017)
  4. "Ethosuximide, sodium valproate or lamotrigine for absence seizures in children and adolescents" Cochrane Database Syst Rev (2017)
  5. "Adverse effects of antiepileptic drugs: a brief overview of important issues" Expert Rev Neurother (2010)
  6. "Antiepileptic action induced by a combination of vigabatrin and tiagabine" Neuroscience (2005)
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