Nonbenzodiazepine anticonvulsants

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Nonbenzodiazepine anticonvulsants


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Nonbenzodiazepine anticonvulsants

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agranulocytosis p. 251

aplastic anemia p. 251

bipolar disorder p. 584, 726

cytochrome P-448 and p. 253

epilepsy p. 565

SIADH and p. 250

teratogenicity p. 638

tonic-clonic seizures p. 726

trigeminal neuralgia p. 726


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.

Excessive excitatory signals can cause a variety of disorders like seizures and epilepsy.

Seizures are categorized based on the region of the brain that’s affected.

When it’s limited to one hemisphere or a single lobe, we call it a focal or partial seizure, and these can cause the person to experience strange sensations, like hearing or tasting something that isn’t there, but can also involve jerking movements in specific muscle groups if the neurons controlling these muscles are affected.


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.


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  2. "Rang and Dale's Pharmacology" Elsevier (2019)
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  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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