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Letter to the Editor
Opsoclonus-myoclonus syndrome secondary to duloxetine toxicity
Síndrome de opsoclono-mioclono secundario a intoxicación por duloxetina
J. Trigo Lópeza,
Corresponding author
javiertrigolopez@gmail.com

Corresponding author.
, E. Martínez Píasa, A. Carrancho Garcíab, M.I. Pedraza Huesoa
a Servicio de Neurología, Hospital Clínico Universitario de Valladolid, Valladolid, Spain
b Servicio de Oftalmología, Complejo Asistencial Universitario de León, León, Spain
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Opsoclonus-myoclonus syndrome &#40;OMS&#41; is extremely rare&#44; with incidence estimated at 0&#46;18 cases&#47;1 000 000 person-years&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> Clinically&#44; it is characterised by the presence of 3 symptoms&#58; opsoclonus&#44; myoclonus&#44; and ataxia&#46; Opsoclonus is defined as involuntary&#44; rapid&#44; multidirectional conjugate saccadic eye movements&#46; Myoclonus most frequently affects the trunk or limbs&#44; and is usually postural or induced by movement&#46; Ataxia may be caused by severe myoclonus or by cerebellar damage&#46; Other associated symptoms include cognitive dysfunction&#44; behavioural alterations&#44; encephalopathy&#44; cranial nerve alterations &#40;cranial nerves IV&#44; V&#44; and VI&#41;&#44; and seizures&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">OMS in children is well characterised&#59; the most frequent aetiology is paraneoplastic&#44; in the context of neuroblastoma&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> According to the literature&#44; the most frequent aetiologies in adults are paraneoplastic&#44; infectious&#44; or idiopathic&#44; with metabolic or toxic causes being exceptional&#46;<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">We present a case of OMS secondary to duloxetine toxicity&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">The patient was a 44-year-old woman with history of anxiety and depression&#44; for which she was being treated with lorazepam&#46; She was referred by the emergency department after presenting blurred vision&#44; involuntary movements&#44; and visions of &#8220;hooded people&#8221; in her home&#44; who the patient believed had poisoned her&#59; symptoms began upon awakening&#46; Upon arrival&#44; she was haemodynamically stable&#44; but presented tachycardia&#46; In the assessment of higher cognitive functions&#44; she was alert&#44; oriented to time and person but disoriented to place&#44; and inattentive&#59; she spoke little but showed no signs of dysphasia&#44; with preserved comprehension&#46; One reiterative utterance was noted &#40;&#8220;I&#8217;ve been poisoned&#8221;&#41;&#46; In the cranial nerve examination&#44; we observed mydriasis with impaired pupillary light reflex&#44; and rapid&#44; multidirectional&#44; conjugate eye movements compatible with opsoclonus&#46; Finally&#44; she presented action myoclonus in all 4 limbs and the trunk &#40;see Supplementary Material for video&#41;&#46; Emergency complementary tests included a complete blood count and biochemistry profile&#44; venous blood gas analysis&#44; urine analysis&#44; urine toxicology&#44; and brain MRI&#46; All results were normal or negative&#44; with the exception of neutrophilic leukocytosis and positive results for benzodiazepines in the urine&#46; We also performed an emergency lumbar puncture&#59; cerebrospinal fluid biochemistry showed no significant alterations&#44; and samples were taken for a microbiology study&#44; oligoclonal banding&#44; an anatomical pathology study&#44; and antineuronal and onconeuronal antibody testing&#46; The patient was admitted with a diagnosis of OMS associated with delusional ideation and visual hallucinations&#46; We started empirical treatment with high-dose corticosteroids &#40;intravenous methylprednisolone dosed at 1&#8239;g for 5 days&#41;&#46; We also screened for a primary tumour&#58; results for tumour markers were negative&#44; and a mammogram and a chest-abdomen-pelvis CT scan revealed no signs of malignancy&#46; The serology study&#44; anatomical pathology study&#44; and antineuronal and onconeuronal antibody tests of cerebrospinal fluid samples all returned negative results&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">Five days after admission&#44; symptoms progressively improved and eventually resolved&#59; the patient acknowledged having consumed 3 packages of duloxetine 30&#8239;mg the night prior to symptom onset&#44; with suicidal intent&#46; We tested for duloxetine in the plasma&#44; finding a concentration of 371&#8239;ng&#47;mL &#40;therapeutic range&#44; 20-80&#41;&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">Toxic aetiology of OMS is extremely rare&#46; The literature includes cases of OMS induced by amitriptyline&#44; cocaine&#44; lithium&#44; phenytoin&#44; phenelzine&#44; ciclosporin&#44; ipilimumab&#47;nivolumab&#44; cefepime&#44; and venlafaxine&#46;<a class="elsevierStyleCrossRefs" href="#bib0025"><span class="elsevierStyleSup">5&#8211;13</span></a> To our knowledge&#44; this is the first case of OMS associated with duloxetine toxicity&#44; and the second case associated with a serotonin-norepinephrine reuptake inhibitor &#40;the first case was reported in a patient receiving venlafaxine&#41;&#46; The pathophysiological mechanisms explaining OMS of toxic aetiology are unclear&#46; In general&#44; the syndrome is thought to originate from dysfunction of the omnipause neurons of the nucleus raphe interpositus<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> or disinhibition of the fastigial nucleus in the cerebellum<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">14</span></a>&#59; however&#44; these structures are neither serotonergic nor norepinephrinergic&#46; Necp&#225;l and Skorvanek<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a> suggest that the case they report of OMS associated with venlafaxine toxicity may have been explained by serotonin syndrome&#44; as the patient presented mental&#44; neuromuscular&#44; and autonomic alterations&#46; Our patient also presented alterations in all 3 of these domains&#58; mental &#40;psychosis&#41;&#44; neuromuscular &#40;opsoclonus&#47;myoclonus&#41;&#44; and autonomic &#40;tachycardia&#44; mydriasis&#41;&#59; this supports the hypothesis proposed by Necp&#225;l and Skorvanek&#46;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a> Additionally&#44; while increased production of catecholamines is observed in patients with neuroblastoma&#44;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">15</span></a> there is very little evidence that a norepinephrinergic effect is involved in the pathogenesis of OMS&#46; Therefore&#44; while we cannot completely rule it out&#44; norepinephrinergic origin seems less likely in these cases&#46;</p><p id="par0035" class="elsevierStylePara elsevierViewall">In conclusion&#44; while it is very infrequent&#44; toxic aetiology is highly relevant in the aetiological diagnosis of OMS&#46; This is the second case of OMS associated with serotonin-norepinephrine reuptake inhibitors&#59; serotonin syndrome may have played a role in pathogenesis&#46;</p></span>"
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