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

22 October 2020
Volume 29 · Issue 19


Dystonia is a neurological movement disorder characterised by sustained or intermittent muscle contractions, producing abnormal and often repetitive movements, abnormal posture or both. It is often accompanied by chronic pain, depression and anxiety. The treatment of dystonia is primarily symptomatic, designed to improve posture and function and to relieve associated pain. This can include oral medications, botulinum toxin (BoNT) injection, and deep brain stimulation (DBS). This article will focus on BoNT treatment, which is just one facet in the treatment of cervical dystonia. The involvement of clinical nurse specialists and the use of a nurse-led clinic can increase efficiency and effectiveness (namely, increased clinic efficiency and capacity, reduced appointment waiting times, and improved continuity of care for the patients), as well as patient access, education, psychosocial support, monitoring and, ultimately, empowerment. This article will discuss the key elements, considerations and benefits of setting up a nurse-led clinic for patients with dystonia.

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).

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