Which medications in the drug class Anticonvulsants are used in the treatment of CNS Lupus?

Updated: May 04, 2021
  • Author: Pradeep C Bollu, MD; Chief Editor: Niranjan N Singh, MBBS, MD, DM, FAHS, FAANEM  more...
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Many anticonvulsants are used to alleviate painful dysesthesias, which frequently accompany peripheral neuropathies. Although they have many different mechanisms of action, their use for alleviating neuropathic pain probably depends on their general tendency to reduce neuronal excitability.

Gabapentin (Neurontin, Gralise)

Gabapentin is a membrane stabilizer, a structural analog of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA); paradoxically, it is thought not to exert an effect on GABA receptors. It appears to act via the alpha(2)delta-1 and alpha(2)delta-2 auxiliary subunits of voltage-gated calcium channels. Gabapentin is used to manage pain and provide sedation in neuropathic pain.

Pregabalin (Lyrica)

Pregabalin is a structural derivative of GABA. Its mechanism of action is unknown; it is known to binds with high affinity to alpha2-delta subunits of calcium channels. In vitro, pregabalin reduces the calcium-dependent release of several neurotransmitters, possibly by modulating calcium-channel function. It is approved by the US Food and Drug Administration (FDA) for neuropathic pain associated with diabetic peripheral neuropathy or postherpetic neuralgia and as adjunctive therapy in partial-onset seizures.

Lamotrigine (Lamictal)

Lamotrigine is a triazine derivative useful in the treatment of neuralgia. It inhibits the release of glutamate and inhibits voltage-sensitive sodium channels, which stabilizes the neuronal membrane. 

Topiramate (Topamax, Qudexy XR, Topiragen, Trokendi XR)

The precise mechanism by which topiramate acts is unknown, but the following properties may contribute to efficacy: (1) electrophysiologic and biochemical evidence showing blockage of voltage-dependent sodium channels, (2) augmentation of GABA activity at some GABA-A receptor subtypes, (3) antagonism of the AMPA/kainate subtype of the glutamate receptor, and (4) inhibition of carbonic anhydrase, particularly isozymes II and IV.

Levetiracetam (Keppra, Keppra XR)

Levetiracetam is another new anticonvulsant being used to combat the pain of peripheral neuropathies. The mechanism by which it alleviates pain is unknown but is probably related to the fact that anticonvulsants generally reduce nerve irritability. Levetiracetam is not FDA-approved for this indication.

Phenytoin (Dilantin, Phenytek)

Phenytoin blocks sodium channels nonspecifically and therefore reduces neuronal excitability in sensitized C-nociceptors. It is effective in neuropathic pain but suppresses insulin secretion and may precipitate hyperosmolar coma in patients with diabetes. Its antineuralgic effects may derive from the blocking of post-tetanic potentiation by reducing summation of temporal stimulation.

Carbamazepine (Tegretol, Carbatrol, Epitol, Equetro)

Carbamazepine is a sodium-channel blocker that typically provides substantial or complete relief of pain in 80% of individuals with both idiopathic and multiple sclerosis−associated trigeminal neuralgia within 24-48 hours. It reduces sustained high-frequency repetitive neural firing and is a potent enzyme inducer that can induce own metabolism. Because of the risk of potentially serious blood dyscrasias, a benefit-to-risk evaluation should be undertaken before administration of the drug is initiated.

Therapeutic plasma levels are between 4 and 12 µg/mL for analgesic and antiseizure response. Peak serum levels are reached in 4-5 hours. The serum half-life is 12-17 hours with repeated doses. Carbamazepine is metabolized in the liver to its active metabolite (i.e., epoxide derivative) with a half-life of 5-8 hours. Metabolites are excreted via feces and urine.

Oxcarbazepine (Trileptal, Oxtellar XR)

The pharmacologic activity of oxcarbazepine is primarily exerted by the 10-monohydroxy metabolite (MHD). Studies indicate that this drug may block voltage-sensitive sodium channels, inhibiting repetitive neuronal firing, and impair synaptic impulse propagation. The anticonvulsant effect also may occur by affecting potassium conductance and high-voltage activated calcium channels.

Pharmacokinetics are similar in older children (> 8 years) and adults; young children (< 8 years) have 30–40% greater clearance than older children and adults. Children younger than two years have not been studied in controlled clinical trials. Oxcarbazepine is not FDA-approved for this indication.

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