The view that the cerebellum is involved in the experience and regulation of emotions was already posited more than half a century ago [
1,
2]. One of the first papers reporting on cerebellar involvement in the experience of emotions involved a patient who underwent electrical stimulation of the dentate nucleus and superior peduncle and reported unpleasant feelings [
3]. Furthermore, electrophysiological responses in several limbic structures, including the hippocampus, amygdala, and septum were recorded following electrical stimulation of the fastigial part of the deep cerebellar nuclei in mammals [
4,
5]. Additional support in humans was provided by an emotionally disturbed patient who received electrical stimulation of the fastigial nucleus [
6]. It was found that the electrical discharges induced by electric stimulation correlated with the experience of anger and tension. Changing the focus from the deep cerebellar nuclei to the more superficial layers of the cerebellum Heath demonstrated that chronic stimulation of the vermis using implanted subdural electrodes normalizes behavior in severe emotionally dysregulated patients [
7]. Schmahmann and Sherman were the first to describe a clinical condition, the cerebellar cognitive–affective syndrome characterized by executive dysfunctions, behavioral disinhibition and emotion dysregulation that resulted from posterior and vermal lesions of the cerebellum [
8]. Similar behavioral problems have been observed in children with extensive lesions to the vermis [
9]. Even though cerebellar lesions certainly do not always lead abnormal or pathological behavior, Parvizi and colleagues, for example, have provided evidence for cerebellar damage and deficits in the regulation of pathological crying and laughter [
10]. Additional evidence for emotion dysregulation has been provided by findings showing cerebellar abnormalities in disorders that are characterized by emotion dysregulation such as attention deficit/hyperactivity disorder, bipolar disorder, schizophrenia, and depression [
11‐
13]. The fact that the cerebellum is reciprocally connected to a broad range of limbic structures including the amygdala, hippocampus, and septum, as well as the cerebral cortex including the prefrontal areas [
4,
14], provides a strong neuroanatomical argument in favor of cerebellar involvement in emotion regulation. Particularly, the connections between the cerebellum and limbic system and the cerebello-thalamo-cortical projections provide a neuro-anatomical foundation for cognition and emotion interactions [
15,
16]. Taken together, there seems to be sufficient empirical ground to assume that the cerebellum plays a role in the regulation of emotions.
The critical insights for the function of the cerebellum still come from early invasive electric stimulation studies. A new noninvasive way of obtaining direct insights into the cerebellar function is transcranial magnetic stimulation (TMS). TMS utilizes magnetic fields to get electrical currents in the brain and influence neuronal activity. In a previous study, we applied high-frequency repetitive TMS (rTMS) over the medial cerebellum to facilitate cerebellar function and found elevations in mood and changes in frontal electric activity [
17]. Interestingly, electrophysiological studies that addressed the functional relationships between the different frequency bandwidths of the human electroencephalogram (EEG) suggest that elevated ratios of slow and fast brain wave oscillations recorded over the frontal midline indicate impaired emotion regulation [
18].
The aim of the present sham and occiput controlled within-subjects study was to obtain electrophysiological and phenomenological evidence for cerebellar involvement in emotion regulation by applying slow frequency inhibitory rTMS. It was hypothesized that 1 Hz rTMS over the medial cerebellum in healthy volunteers would (1) lead to elevations in frontal EEG ratios during emotion regulation, and (2) increases in negative mood as a result of impaired emotion regulation.