A Nurse-Led Clinic Model for the Treatment of Cervical Dystonia Using Botulinum Toxin

Dystonia is a movement disorder characterised by sustained or intermittent muscle contractions causing abnormal, often repetitive, movements, postures, or both. It is frequently initiated or worsened by voluntary action and associated with overflow muscle activation. The dystonic movements are typically patterned, twisting, and may be tremulous (Albanese et al, 2013). The severity of dystonia can change, depending on activity and posture (Blood, 2008; Beena, 2017). Although the pathophysiology of dystonia is currently not completely understood, recent research to identify dystonia genes and advances in functional neuroimaging have led to important insights into the mechanisms of the condition (Sharma, 2019; Gonzalez-Alegre, 2019). Conceptually, dystonia is a neurofunctional disorder with multiple causes for the alterations at various levels and multiple points along the sensorimotor circuit (see Figure 1) (Lubarr and Bressman, 2011). There is evidence that the pathophysiology of dystonia may involve a combination of dysfunction within neurons of the brainstem, cerebellum, putamen, and globus pallidus (Sharma, 2019). Furthermore, genetic research over the past two decades has identified that DYT1 is the most common early-onset inherited dystonia, caused by dominant disease-causing mutations in the TOR1A gene. TorsinA, a glycoprotein encoded by the TOR1A gene in the endoplasmic reticulum and nuclear envelope, influences various important cellular functions (Gonzalez-Alegre, 2019).