Coronal sections of human brain labeling the basal ganglia. The pathophysiology of<unk>  is<unk> ill relatively unknown.<unk>  is considered neurochemical in nature, and does not result in<unk> ructural neurodegenerative changes. Although no lesions are present in the basal ganglia in primary<unk> , fMRI and PET<unk> udies have shown abnormalities of the basal ganglia and hyper activation of the cortical areas.<unk> udies have suggested that there is a functional imbalance in the<unk> riatal control of the globus pallidus, specifically the substantia nigra pars reticulata. The<unk> udies hypothesize the hyper activation of the cortical areas is due to reduced pallidal inhibition of the thalamus, leading to over activity of the medial and prefrontal cortical areas and under activity of the primary motor cortex during movement. It has also been suggested that the functional imbalance is due to an imbalance of neurotransmitters such as dopamine, acetylcholine, and gamma-aminobutyric acid. These neurotransmitters are secreted from the basal ganglia, traveling to muscle groups in the neck. An increase in neurotransmitters causes spasms to occur in the neck, resulting in<unk> .<unk> udies of local field potentials have also shown an increase of 4–10 Hz oscillatory activity in the globus pallidus internus during myoclonic episodes and an increase of 5–7 Hz activity in dystonic muscles when compared to other primary dystonias. This indicates that oscillatory activity in these frequency bands may be involved in the pathophysiology of<unk> .
Spasmodic torticollis
Torticollis
Dysbarism
Superior oblique myokymia
Pseudostrabismus
Benign paroxysmal torticollis
Hemifacial spasm
Misophonia