Impulsive aggressive obsessions following cerebellar strokes: a case study

Abstract

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 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 obsessivecompulsive 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 ...

The Cerebellum on Cocaine

“…Moreover, they may explain why both cerebellar disfunction and prefrontal impairment enhance susceptibility to compulsive and impulsive disorders including drug addiction, eating disorders, attention deficit/hyperactivity (ADHD), and obsessivecompulsive disorder (OCD) (Miquel et al, 2019). Accordingly, it has been described that in humans, the impairment of the vermis results in impulsivity and disinhibition (Silveri et al, 1994;Schmahmann and Sherman, 1998;Kim et al, 2013;Tessier et al, 2015), inducing what has been called the Cerebellar Cognitive Affective Syndrome (CAS) (Schmahmann and Sherman, 1998). It would be of the utmost importance to test whether similar cerebellar disfunctions that lead to CAS increase the risk for drug addiction or are sufficient for inducing a compulsive addictive phenotype.…”

A Working Hypothesis for the Role of the Cerebellum in Impulsivity and Compulsivity

“…Clinical reports on cerebellar diseases give support to the fundamental role of the cerebellum in modulating diverse motor, affective and cognitive domains. Beyond motor dysfunction, patients with lesions or disease affecting the posterior cerebellum showed difficulties in controlling their behavior and emotions, language deficits, and lack of concentration (Silveri et al, 1994; Schmahmann and Sherman, 1998; Kim et al, 2013; Tessier et al, 2015). The syndrome, which has been called “the cerebellar cognitive-affective syndrome,” is characterized by impairments in executive functions with disinhibited and inappropriate behavior, social aberrant behavior, personality changes, and language deficits (Schmahmann and Sherman, 1998).…”

“…A comprehensive understanding of the cerebellar function in compulsivity and impulsivity will require further research involving causative manipulation of the cerebellar activity and its connectivity since the majority of the current information comes from correlational research and clinical reports. For instance, it is known that impulsivity and disinhibition result from impairment of the cerebellar cortex, especially in the middle line (vermis; Silveri et al, 1994; Schmahmann and Sherman, 1998; Kim et al, 2013; Tessier et al, 2015). Thus, it should be possible to interfere with or mimic these effects by using pharmacogenetics tools as DREADDs (designer receptor exclusively activated by designer drugs) or optogenetics in paradigms such as Go/No-Go tasks and reward devaluation tests.…”

From general factors to response generalisation: the importance of the cerebellum for mental health and social effectiveness

“…This work reinforces this and expands on this to include the cerebellum. Much work links the cerebellum with impulsivity (Jung et al, 2014;Miquel, Nicola, Gil-Miravet, Guarque-Chabrera, & Sanchez-Hernandez, 2019;Moers-Hornikx et al, 2009;Tessier et al, 2015). To integrate a cerebellar role with the HiToP model (Kotov et al, 2017), it could be reasoned that because of the inverse relation between the 'p-factor' and the GFP, then high scores on the general factor in the HiToP model represent social ineffectiveness.…”