Parity with limb clonus. To our understanding, isolated pendular nystagmus as a sign of serotonin toxicity has in no way been described, nor has pendular nystagmus as a consequence of venlafaxine overdose. We suspect that our case represents an incomplete form (`forme fruste’) with the serotonin syndrome. The absence of other clinical features of serotonin toxicity plus the typical investigations preluded a diagnosis from the total serotonin syndrome, along with the case would not have met either the Sternbach or Hunter criteria.1 2 Recognition of such incomplete types is significant, as theCASE PRESENTATIONA 54-year-old woman ingested 3 g of venlafaxine in a modified-release preparation (40 tablets of 75 mg). She presented for the emergency department four h just after ingestion, reporting blurred vision, dry mouth, nausea and vomiting. She denied co-ingestion of alcohol or any other substances, and was not on any typical medication. On examination, temperature was 36.4 , pulse 101 bpm, blood pressure 142/89 mm Hg and oxygen saturation 98 on room air. She was calm, alert and oriented. She was not sweaty, shivery or tremulous. Muscle tone was normal. All reflexes have been markedly brisk but there was no limb clonus, and plantars were downgoing. Examination of eye movements demonstrated binocular horizontal pendular nystagmus using the eyes in the principal position (see video 1). Amplitude of nystagmus decreased with lateral gaze and was improved by central visual fixation. There was no ophthalmoplegia, and smooth pursuit and saccadic eye movements were SSTR2 list preserved.To cite: Varatharaj A, Moran J. BMJ Case Rep Published on the internet: [please involve Day Month Year] doi:ten.1136/bcr-INVESTIGATIONSAn ECG showed sinus rhythm with suitable axis deviation and ideal bundle branch block, with a corrected QT interval of 415 ms. Routine blood tests had been inside typical limits, using a creatine kinase degree of 132 units/L (range 0?45). ParacetamolVaratharaj A, et al. BMJ Case Rep 2014. doi:ten.1136/bcr-2013-Findings that shed new light around the achievable pathogenesis of a illness or an adverse effectLearning points The serotonin JAK1 Formulation syndrome happens as a result of drugs which raise synaptic serotonin, frequently selective serotonin reuptake inhibitors and serotonin orepinephrine reuptake inhibitor. In its full kind, the syndrome presents using a triad of neuromuscular, autonomic and mental hyperexcitability. Incomplete types might happen and must be treated seriously, to avoid deterioration towards the total syndrome. Ocular manifestations may possibly be the predominant sign of serotonin toxicitypeting interests None. Patient consent Obtained. Provenance and peer overview Not commissioned; externally peer reviewed.Video 1 Binocular horizontal pendular nystagmus, lowered in amplitude by lateral gaze, and improved by central visual fixation.serotonin syndrome is not a side effect per se; it’s aspect on the clinical spectrum that final results from agonism of central serotonin receptors, which is exploited for therapeutic impact by psychotropic medicines. Adverse consequences of enhanced serotonin levels may perhaps happen at therapeutic doses, and if overlooked, one particular may inadvertently precipitate the full-blown serotonin syndrome with an elevated dose with the causative agent or addition of a further provocative drug. Also, with the use of modified-release preparations, the improvement of the full syndrome might take longer than anticipated, as well as the presence of incomplete toxicity may herald clinical deterioration.
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