Neurological Sciences https://doi.org/10.1007/s10072-018-3298-1 LETTER TO THE EDITOR Levofloxacin-induced hemichorea-hemiballism in a patient with previous thalamic infarction Ruggero Bacchin 1 & Francesco Macchione 1 & Davide Cardellini 1 & Riccardo Orlandi 1 & Alberto Gajofatto 1 & Gianluigi Zanusso 1 & Gaetano Vattemi 1 Received: 11 January 2018 / Accepted: 21 February 2018 # Springer-Verlag Italia S.r.l., part of Springer Nature 2018 Dear Editor, Chorea is a non-patterned, involuntary, and continuous hyperkinetic movement disorder that may be accompanied by ballism [1]. Drug-induced chorea represents one of the most common types of chorea in adults [2, 3]. Several medications have been reported to cause choreiform movements and implicated agents include L-dopa, dopamine agonists, anticonvulsants, benzodiazepines, and antipsychotics amongst others [2, 3]. Here we report a male patient with a previous left thalamic infarction, who developed a right hemichoreahemiballism after starting levofloxacin treatment. In April 2017, an 80-year-old right-handed man presented to his general practitioner because of flu-like symptoms. He was affected by chronic obstructive pulmonary disease Electronic supplementary material The online version of this article (https://doi.org/10.1007/s10072-018-3298-1) contains supplementary material, which is available to authorized users. * Ruggero Bacchin bacchin.ruggeroangelo@gmail.com Francesco Macchione macchione.francesco@hotmail.it Davide Cardellini davide.cardel@gmail.com Riccardo Orlandi riccardo.orlandi@gmail.com Alberto Gajofatto alberto.gajofatto@univr.it Gianluigi Zanusso gianluigi.zanusso@univr.it Gaetano Vattemi gaetano.vattemi@univr.it 1 Department of Neurosciences, Biomedicine and Movement Sciences, Section of Clinical Neurology, University of Verona, P.le L.A. Scuro 10, 37134 Verona, Italy (COPD) associated to long-term active smoking, so levofloxacin (1500 mg/die) and inhaled corticosteroids (Beclometason 168 mcg/die) were started based on suspicion of a pulmonary disease exacerbation. On the second day of treatment, unilateral involuntary movements of the right hand and foot arose. On the third day, these movements became more evident, involving the upper and lower extremities and overlapping with proximal ballistic movements, so the patient was admitted to our neurology clinic. His medical history was unremarkable except for COPD. There was no family history of neurological diseases. On admission, a fasting plasma glucose level was at range. Clinical examination showed a rightsided hemichoreic syndrome with superimposed ballistic movements (Video Part 1). The remaining neurological and physical examination were intact. A non-enhanced brain CT scan showed diffuse cortical atrophy but excluded cerebral bleeding, while a contrast-enhanced 1.5-T MRI documented scattered areas of T2 hyperintensity in the subcortical white matter and a small T1 hypointense and T2 hyperintense lesion in the left thalamus (Fig. 1a, b). No areas of signal restriction on diffusion-weighted imaging (DWI) or gadolinium enhancement on post-contrast T1 sequences were observed (Fig. 1c). Extensive laboratory investigations were unrevealing. Symptoms related to the suspected COPD exacerbation resolved at the time of the hospitalization, but levofloxacin was continued until the fifth day of therapy. In the meantime, tetrabenazine and clonazepam were started and increased until a daily dosage of 72.5 and 1.5 mg/die, respectively, with almost complete control of involuntary movements within 10 days (Video Part 2). One month later, a follow-up brain MRI, comprehensive of T2*-weighted gradient-echo (GRE) and susceptibility-weighted imaging (SWI) sequences, confirmed unchanged DWI, T1- and T2-weighted images, while GRE and SWI showed a Bblack dot^ hypointensity corresponding to the T2-hyperintense left thalamic lesion (Fig. 1d). Tetrabenazine and clonazepam were gradually discontinued over the following 8 weeks with no substantial Neurol Sci Fig. 1 Brain MRI. a–c MRI April 2017 shows a small lesion (arrow) of non-enhancing T1 hypointensity (a) and T2 hyperintensity (b) in the left thalamus. DWI sequences do not document any area of signal restriction (c). d MRI May 2017 with a Bblack dot^ hypointensity in the left thalamic lesion on SWI sequences resurface of the choreo-ballistic movements (Video Part 3). At the last neurological follow-up, one month after medication washout, the clinical condition of patient remained unchanged and only few choreic movements could be observed during voluntary activation of the right hand and foot. Chorea is a hyperkinetic movement disorder that can be due to a wide spectrum of disorders of the basal ganglia ranging from inherited to acquired etiologies [1, 3]. We describe herein an elderly patient who developed a right-sided hemichorea-hemiballism while receiving levofloxacin for the treatment of a suspected COPD exacerbation. Symptoms resolved within a week after drug discontinuation and diagnostic workup disclosed only brain MRI findings compatible with a previous lacunar infarct in left thalamus. In view of the temporal association with drug assumption and of laboratory and imaging data, we suggest that chorea in our patient was most likely due to toxicity from levofloxacin in an underlying structural brain lesion. Although the pathophysiology of chorea and ballism has not been fully clarified, current findings suggest that defects in functional connectivity rather than a single basal ganglia lesion account for these disorders [4]. Indeed, a disruption of the connections between thalamus, sub-thalamic nucleus, and internal globus pallidus may lead to a derangement in the basal ganglia-cortical circuit that results in a reduced inhibition of thalamocortical excitatory neurons and ultimately in hyperkinetic movements [4]. Drug-induced chorea is the most common form of chorea encountered in neurological practice [3, 4]. A number of medications cause choreiform movements only when there is a preexisting basal ganglia damage, whereas others appear to be more universally choreogenic [3]. In the former cases, the distribution of the involuntary movements is usually contralateral to structural lesion while the time-toonset and time-to-resolution occur, respectively, after introduction and withdrawal of the offending drug [3, 4]. Fluoroquinolone antibiotics, particularly ciprofloxacin, have been associated with hyperkinetic movement disorders, including propriospinal myoclonus, Tourette-like syndrome, and orofacial dyskinesia; in 2005, Azar and colleagues reported a case of chorea with complete recovery after ciprofloxacin discontinuation, but the involuntary movements were generalized and occurred during a subacute confusional state due to metabolic encephalopathy [5]; hence, to our knowledge, hemichorea hemiballismus syndrome has not yet been documented in patients treated with levofloxacin. Despite vascular disease could potentially account for the clinical course and distribution pattern of choreiform movements in our patient, MRI findings would appear to make this an unlikely diagnosis. In conclusion, our case indicates chorea as a potential neurological side effect of levofloxacin treatment and highlights the need for clinicians to be aware of the existence of this drug adverse reaction. Authors’ contributions R. Bacchin: drafting/revising the manuscript, acquisition of data. F. Macchione: acquisition of data. D. Cardellini: acquisition of data. R. Orlandi: acquisition of data. A. Gajofatto: drafting/ revising the manuscript, acquisition of data. G. Zanusso: drafting/ revising the manuscript, acquisition of data. G. Vattemi: drafting/ revising the manuscript, acquisition of data. Compliance with ethical standards Consent The patient consented to be filmed for scientific publication. Conflict of interest The authors declare that they have no conflict of interest. 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