J Neurol (2015) 262:1775–1776 DOI 10.1007/s00415-015-7804-6

LETTER TO THE EDITORS

Impulsive aggressive obsessions following cerebellar strokes: a case study Arnaud Tessier1,2 • Charlotte Cosin2 • Willy Mayo2 • Micha Pfeuty2 David Misdrahi1,2 • Igor Sibon2,3



Received: 7 May 2015 / Revised: 28 May 2015 / Accepted: 28 May 2015 / Published online: 6 June 2015 Ó Springer-Verlag Berlin Heidelberg 2015

Dear Sirs, Out of the total ischemic stroke events, about 4 % of them affect the cerebellum [1]. Traditionally, studies on cerebellar function have focused on the motor functions. It is clear now that the cerebellum underlies numerous nonmotor networks [2] and has a role not only in higher cognitive functions [3], but also in emotional and behavioral processing [4]. ‘‘Mr. M’’ is a 56-year-old left-handed man with 11 years of educational level and was professionally active (baker). His medical history reveals neither significant previous medical history nor any mental disorder. He was admitted for a sudden vertigo and dysarthria and left paresthesia. Brain MRI showed a right cerebellar punctiform infarction (lobule VI). A stroke recurrence occurred few days later, with similar minor symptoms. Brain MRI demonstrated a new ischemic lesion in the left superior cerebellar artery territory (lobule VI), and in a right perforating branch of the pons (pyramidal tract) (Fig. 1). In the acute phase of stroke, Mr. M presented a moderate level of anxiety, but he had no apathy, depression or cognitive disorders when assessed by reliable scales (data & Arnaud Tessier [email protected] 1

De´partement de Psychiatrie Adulte, Centre Hospitalier Charles Perrens, 121 rue de la Be´chade, CS81285, 33076 Bordeaux Cedex, France

2

Service de Neuroimagerie et Cognition Humaine, INCIA CNRS UMR 5287, EPHE Bordeaux, 146 rue Le´o Saignat, 33076 Bordeaux Cedex, France

3

Unite´ Neurovasculaire, CHU Pellegrin, 33076 Bordeaux Cedex, France

available on request). Five months after stroke, the patient started to experience invasive obsessive thoughts leading to an important distress. The content of these obsessions focus on an unacceptable theme: stabbing a relative. The intensity of these obsessions was associated with daily life alteration, avoidance behavior and anxiety. In the distress to an immediate hetero-aggressive gesture by cold steel on his daughter, he committed impulsive suicide attempts by drowning. In this context, he was hospitalized in a psychiatric hospital with the final diagnosis of obsessive– compulsive disorder (OCD) complicated by a major depressive disorder (MDD). Following the recent guidelines for pharmacotherapy in OCD [5], first-line selective serotonin reuptake inhibitor (SSRI) (escitalopram, sertraline, paroxetine) then second-line antidepressant (venlafaxine) until the dosage of 225 mg/day with antipsychotic as adjunctive therapy (risperidone 2 mg/day) were tried but they failed. At last, the combination of diazepam (20 mg/day), paroxetine (40 mg/day) and quetiapine (100 mg/day) was efficient for MDD but failed to significantly improve the impulsive aggressive obsessions leading to recurrent hospitalizations. Cognitive behavioral therapy (CBT) was tried but was unfortunately poorly efficient on obsessions. A meta-analysis in 2008 reported that lobule VI is involved in emotional processing by a cerebellar-limbic circuit [6]. Chronology and infarct localization suggest that the second cerebellar stroke, involving lobules VI and Crus I, was preferentially responsible of the onset of psychiatric disorder and fully supports our hypothesis. However, we cannot exclude the potential influence of the first stroke’s stress, or the influence of bilateral lesions. The cerebellum seems to be less activated in patients with OCD [7, 8], but there is a lack of studies exploring the clinical implications of this phenomenon. Several studies

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J Neurol (2015) 262:1775–1776

Fig. 1 MRI acquisition obtained on the day of infarction (hospitalization). a MRI1, first stroke event, right cerebellar stroke; b MRI2, second stroke event, left cerebellar stroke and right brainstem stroke

have investigated the potential role of cerebellar infarcts in the occurrence of post-stroke behavior changes [9, 10]. A case of late-onset OCD with impulsive aggressive obsessions has been reported in a patient with an arachnoid cyst in the posterior fossa of the cerebellum [4]. Indeed, authors have reported that impulsive behavior involves the cerebellar nuclei, possibly through a decreased selective attention caused by a disruption of the cerebello-thalamocortical pathways [11]. In the present case, the late-onset and treatment-refractory OCD after cerebellar infarctions would suggest the critical role of the stroke-related disruption in neural connections. A recent study has suggested that deep brain stimulation (DBS) might be a promising adjunctive therapy in patients with treatment-refractory OCD [12]. This case highlights the potential role of cerebellum in OCD pathophysiology. Conflicts of interest

None.

Ethical standards The manuscript submitted for publication has been performed in accordance with the ethical standards laid down in the 1964 Declaration of Helsinki and its later amendments.

References 1. Vuillier F, Decavel P, Medeiros de Bustos E et al (2011) Les infarctus cerebelleux. Rev Neurol (Paris) 167:418–430 2. Konarski JZ, McIntyre RS, Grupp LA, Kennedy SH (2005) Is the cerebellum relevant in the circuitry of neuropsychiatric disorders? J Psychiatry Neurosci 30:178–186

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3. Stoodley CJ (2012) The cerebellum and cognition: evidence from functional imaging studies. Cerebellum Lond Engl 11:352–365. doi:10.1007/s12311-011-0260-7 4. Tonna M, Ottoni R, Ossola P et al (2014) Late-onset obsessive– compulsive disorder associated with left cerebellar lesion. Cerebellum Lond Engl 13:531–535. doi:10.1007/s12311-014-0561-8 5. Katzman MA, Bleau P, Blier P et al (2014) Canadian clinical practice guidelines for the management of anxiety, posttraumatic stress and obsessive–compulsive disorders. BMC Psychiatry 14(Suppl 1):S1. doi:10.1186/1471-244X-14-S1-S1 6. Stoodley CJ, Schmahmann JD (2009) Functional topography in the human cerebellum: a meta-analysis of neuroimaging studies. NeuroImage 44:489–501. doi:10.1016/j.neuroimage.2008.08.039 7. Milad MR, Furtak SC, Greenberg JL et al (2013) Deficits in conditioned fear extinction in obsessive–compulsive disorder and neurobiological changes in the fear circuit. JAMA Psychiatry 70:608–618 (quiz 554). doi:10.1001/jamapsychiatry.2013.914 8. Ping L, Su-Fang L, Hai-Ying H et al (2013) Abnormal spontaneous neural activity in obsessive–compulsive disorder: a restingstate functional magnetic resonance imaging study. PLoS ONE 8:e67262. doi:10.1371/journal.pone.0067262 9. Hackett ML, Ko¨hler S, O’Brien JT, Mead GE (2014) Neuropsychiatric outcomes of stroke. Lancet Neurol 13:525–534. doi:10.1016/S1474-4422(14)70016-X 10. Lassalle-Lagadec S, Catheline G, Mayo W et al (2013) Cerebellum involvement in post-stroke mood: a combined ecological and MRI study. Psychiatry Res 212:158–160. doi:10.1016/j. pscychresns.2013.01.003 11. Moers-Hornikx VMP, Sesia T, Basar K et al (2009) Cerebellar nuclei are involved in impulsive behaviour. Behav Brain Res 203:256–263. doi:10.1016/j.bbr.2009.05.011 12. Figee M, de Koning P, Klaassen S et al (2014) Deep brain stimulation induces striatal dopamine release in obsessive–compulsive disorder. Biol Psychiatry 75:647–652. doi:10.1016/j. biopsych.2013.06.021

Impulsive aggressive obsessions following cerebellar strokes: a case study.

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