Patient with abnormal eye movement.

CASE PRESENTATION

A 27‐year‐old woman attempted suicide by ingesting 17.5 g of carisoprodol and presented to the emergency department approximately 12 hours later. She was comatose, tachycardic, and febrile. She developed a generalized tonic–clonic seizure and was intubated and treated with intravenous diazepam. Ocular examination revealed isocoric pupils (3 mm); spontaneous, slow, vertical, and discordant eye movements (Figure 1; see Video S1); and no vestibulo‐ocular reflex.

FIGURE 1

Spontaneous, slow, vertical, and discordant eye movements observed in the patient

DIAGNOSIS

2.1 Ocular skew deviation associated with carisoprodol overdose

Brain computed tomography angiography did not reveal any abnormality. Quantitative analysis (liquid chromatography–tandem mass spectrometry) of a serum specimen obtained 14 hours after ingestion revealed a carisoprodol level of 23 μg/mL (therapeutic range, 2.5–10 μg/mL) and a meprobamate level of 31 μg/mL (range, 10–30 μg/mL). She recovered consciousness 48 hours after ingestion, and the abnormal eye movement subsided.

Skew deviation is a non‐paralytic, prenuclear vertical ocular misalignment attributable to unbalanced utricular inputs to the ocular motor system. Skew deviation is usually caused by acute injury to the posterior fossa of the brain (eg, brainstem stroke, organic lesion) and has been rarely reported in cases of metabolic encephalopathy and acute poisoning. , Carisoprodol, a centrally acting muscle relaxant, and its active metabolite meprobamate modulate the function of the γ‐aminobutyric acid type A (GABAA) receptor in a manner similar to central nervous system depressants. , Although the exact mechanism remains unclear, the inhibitory effects of carisoprodol and meprobamate on the brainstem, thalamus, and cerebellum may cause temporary dysfunction of the otolithic pathway, which leads to ocular skew deviation.

Supporting Information.

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