Primary<unk>  is suspected when the<unk>  is the only sign and there is no identifiable cause or structural abnormality in the central nervous system. Researchers suspect it is caused by a pathology of the central nervous system, likely originating in those parts of the brain concerned with motor function—such as the basal ganglia and the GABA (gamma-aminobutyric acid) producing Purkinje neurons. The precise cause of primary<unk>  is unknown. In many cases it may involve some genetic predisposition towards the disorder combined with environmental conditions. Secondary<unk>  refers to<unk>  brought on by some identified cause, such as head injury, drug side effect (e.g. tardive<unk> , or neurological disease (e.g. Wilson's disease, stroke). Meningitis and encephalitis caused by viral, bacterial, and fungal infections of the brain have been associated with<unk> . The main mechanism is inflammation of the blood vessels, causing restriction of blood flow to the basal ganglia. Other mechanisms include direct nerve injury by the organism or a toxin, or autoimmune mechanisms. Environmental and task-related factors are suspected to trigger the development of focal<unk> s because they appear disproportionately in individuals who perform high precision hand movements such as musicians, engineers, architects, and artists. Chlorpromazine can also cause<unk> , which can be often misjudged as a seizure. Neuroleptic drugs often cause<unk> , including oculogyric crisis. Malfunction of the sodium-potassium pump may be a factor in some<unk> s. The - pump has been shown to control and set the intrinsic activity mode of cerebellar Purkinje neurons. This suggests that the pump might not simply be a homeostatic, "housekeeping" molecule for ionic gradients; but could be a computational element in the cerebellum and the brain. Indeed, an ouabain block of - pumps in the cerebellum of a live mouse results in it displaying ataxia and<unk> . Ataxia is observed for lower ouabain concentrations,<unk>  is observed at higher ouabain concentrations. A mutation in the - pump (ATP1A3 gene) can cause rapid onset<unk>  parkinsonism. The parkinsonism aspect of this disease may be attributable to malfunctioning - pumps in the basal ganglia; the<unk>  aspect may be attributable to malfunctioning - pumps in the cerebellum (that act to corrupt its input to the basal ganglia) possibly in Purkinje neurons. Cerebellum issues causing<unk>  is described by Filip et al. 2013: "Although<unk>  has traditionally been regarded as a basal ganglia dysfunction, recent provocative evidence has emerged of cerebellar involvement in the pathophysiology of this enigmatic disease. It has been suggested that the cerebellum plays an important role in<unk>  etiology, from neuroanatomical research of complex networks showing that the cerebellum is connected to a wide range of other central nervous system structures involved in movement control to animal models indicating that signs of<unk>  are due to cerebellum dysfunction and completely disappear after cerebellectomy, and finally to clinical observations in secondary<unk>  patients with various types of cerebellar lesions. It is proposed that<unk>  is a large-scale dysfunction, involving not only cortico-basal ganglia-thalamo-cortical pathways, but the cortico-ponto-cerebello-thalamo-cortical loop as well. Even in the absence of traditional "cerebellar signs" in most<unk>  patients, there are more subtle indications of cerebellar dysfunction. It is clear that as long as the cerebellum's role in<unk>  genesis remains unexamined, it will be difficult to significantly improve the current standards of<unk>  treatment or to provide curative treatment."
Dystonia
Akathisia
Paratonia
Lesch–Nyhan syndrome
Hypophonia
Essential tremor
Misophonia
Tardive dyskinesia  Tardive dyskinesia  1