Abstract and Introduction
The presence of abnormal neural oscillations within the cortico-basal ganglia-thalamo-cortical (CBGTC) network has emerged as one of the current principal theories to explain the pathophysiology of movement disorders. In theory, these oscillations can be used as biomarkers and thereby serve as a feedback signal to control the delivery of deep brain stimulation (DBS). This new form of DBS, dependent on different characteristics of pathological oscillations, is called adaptive DBS (aDBS), and it has already been applied in patients with Parkinson's disease. In this review, the authors summarize the scientific research to date on pathological oscillations in dystonia and address potential biomarkers that might be used as a feedback signal for controlling aDBS in patients with dystonia.
According to the latest expert consensus, dystonia is clinically defined as "a movement disorder characterized by sustained or intermittent muscle contractions causing abnormal, often repetitive, movements, postures, or both." Dystonia can be caused by numerous etiologies, including acquired and different biochemical, cellular, or genetic substrates. The similarity of the clinical dystonia phenotype, however, suggests a unifying common pathophysiological pathway at a functional or network level. A currently leading hypothesis on its neurophysiological basis is that dystonia is the result of abnormal activity in cortico-basal ganglia-thalamo-cortical (CBGTC) and cerebellar networks. The treatment for the majority of dystonia subtypes only provides symptomatic relief, without addressing the underlying cause of the disease. Options currently available include oral medication (e.g., anticholinergic and antidopaminergic drugs, benzodiazepines, and baclofen), botulinum toxin (treatment of choice in focal dystonias), and deep brain stimulation (DBS).
Neurosurg Focus. 2018;45(2):e3 © 2018 American Association of Neurological Surgeons