Abstract

Dystonia is a movement disorder characterized by sustained or intermittent muscle contractions causing abnormal, and often repetitive, movements, postures, or both [1]. It has been attributed to basal ganglia abnormalities and to dysfunctional cortico-striato-thalamo-cortical circuitry [2–4]. Dystonia has a number of possible etiological causes. Focal dystonia is more common than generalized dystonia. In cranial and cervical focal dystonia, neurophysiological investigations have revealed abnormally excitable interneuronal pathways in the brainstem. For instance, several studies reported changes in the length of the recovery cycle of the eye blink reflex and the masseter inhibitory reflex [5–7]. Cortical dysfunctions have also been explored using transcranial magnetic stimulation [8, 9]. Acquired forms of dystonia have been associated with a wide variety of vascular, traumatic, infectious, toxic, and degenerative processes, which can affect either the central or peripheral nervous system [10–14]. The underlying mechanisms of acquired dystonia are not yet completely understood, although several different studies have implicated a neural network linking the cerebral cortex, basal ganglia, and cerebellum [2–4]. In such a network, dysfunctional activity at any level could lead to the onset of dystonia. While the role of the basal ganglia is well known and had been widely demonstrated with respect to the pathogenesis of acquired dystonia, the role of the cerebellum has not been well defined. Both animal studies [15–17] and clinical reports [3, 18–34] have explored the role of the cerebellum in the pathogenesis of dystonia. Overall, there is consensus regarding the idea that acquired dystonia is caused by lesions, leading to abnormal cerebellar output (Table 1). In this case report, we describe our diagnostic and therapeutic processes for a patient with masticatory dystonia resulting from cerebellar haemorrhage.

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