Which anticonvulsant has ocular side effects of nystagmus, diplopia, and EOM palsies?

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Multiple Choice

Which anticonvulsant has ocular side effects of nystagmus, diplopia, and EOM palsies?

Explanation:
Ocular toxicity is a classic sign of phenytoin excess. Nystagmus, diplopia, and extraocular muscle palsies occur when phenytoin levels are high enough to disrupt the brainstem and cerebellar circuits that coordinate eye movements. The first clue is often nystagmus, with diplopia and difficulties with eye movements appearing as toxicity progresses. This reflects phenytoin’s CNS effects, and it’s why monitoring levels is important: phenytoin has nonlinear, saturable metabolism and high protein binding, so small dose increases can lead to disproportionately higher serum concentrations and toxicity. If these signs appear, reducing the dose and rechecking levels typically resolve the symptoms. Other anticonvulsants have different ocular effects; for example, topiramate is more associated with angle-closure glaucoma and myopia, not the classic nystagmus/diplopia/EOM palsy pattern.

Ocular toxicity is a classic sign of phenytoin excess. Nystagmus, diplopia, and extraocular muscle palsies occur when phenytoin levels are high enough to disrupt the brainstem and cerebellar circuits that coordinate eye movements. The first clue is often nystagmus, with diplopia and difficulties with eye movements appearing as toxicity progresses. This reflects phenytoin’s CNS effects, and it’s why monitoring levels is important: phenytoin has nonlinear, saturable metabolism and high protein binding, so small dose increases can lead to disproportionately higher serum concentrations and toxicity. If these signs appear, reducing the dose and rechecking levels typically resolve the symptoms. Other anticonvulsants have different ocular effects; for example, topiramate is more associated with angle-closure glaucoma and myopia, not the classic nystagmus/diplopia/EOM palsy pattern.

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