I see a number of cases of cervical dystonia (spasmodic torticollis) that features awkward posturing and movement of the head and neck. This can be painful and have consequences for normal activities. We rely upon being able to orientate ourselves to our environment by controlling our head and gaze direction and then responding appropriately.
Primary dystonia has no neurological or metabolic cause whereas secondary dystonia is attributable to outside factors such as physical trauma, exposure to certain medications and other neurological or metabolic diseases.
Common treatment of cervical dystonia includes botulinum toxin injections and physiotherapy.
Modern physiotherapy for cervical dystonia at the Specialist Pain Physio Clinics
In addition to the manual techniques that are used to help ease tension and the soreness associated with spasm and tightness in the muscles, we use strategies that target the motor centres in the brain where the signals are coming from. In other words, as well as treating the symptoms, we are focusing upon the mechanisms and causes of the muscles going into spasm. The Graded Motor Imagery programme provides a way of aiming to retrain movement by targeting the adaptations that have occured in the motor system. Initially this programme was devised for complex regional pain syndrome, but since then the training has been found to help those with a range of painful problems with associated movement issues.
Typically a treatment programme includes themes that aim to develop a deep understanding of the problem(s), nourish and mobilise the body tissues, improve motor control, body sense and awareness, manage posture, increase exercise an activity tolerance and ultimately improve quality of life. We call the approach biobehavioural because it is a comprehensive way of tackling the issues and influencing factors that are unique to the individual, addressing the physical signs and symptoms as much as the underpinning beliefs and lifestyle factors that impact.
Call for appointments: 07518 445493
Dr Marie-Helene Marion, a consultant neurologist specialising in the treatment of dystonia and movement disorders has a comprehensive blog here
Recent research papers
Behav Neurol. 2012 May 24.
Cervical dystonia: From pathophysiology to pharmacotherapy.
Patel S, Martino D.
Background: Dystonia is a chronic disorder characterised by an aberration in the control of movement. Sustained co-contraction of opposing agonist and antagonist muscles can cause repetitive and twisting movements, or abnormal postures. Cervical dystonia (CD), often referred to as spasmodic torticollis, is a type of focal dystonia involving the muscles of the neck and sometimes the shoulders. Methods: This systematic review collates the available evidence regarding the safety and efficacy of a range of treatments for CD, focusing on their effectiveness as shown by double-blinded, randomised controlled trials. Results: Our review suggests that botulinum toxin type A (BTA), botulinum toxin type B (BTB) and trihexyphenidyl are safe and efficacious treatments for CD. Evidence shows that botulinum toxin therapies are more reliable for symptomatic relief and have fewer adverse effects than trihexyphenidyl. When comparing BTA to BTB, both are found to have similar clinical benefits, with BTA possibly having a longer duration of action and a marginally better side effect profile. BTB is also safe and probably just as efficacious a treatment in those patients who are unresponsive or have become resistant to BTA.
Discussion: The current evidence shows that the pharmacological management of CD relies on BTA and BTB, two agents with established efficacy and tolerability profiles.
Lancet Neurol. 2002 Sep;1(5):316-25.
Classification and genetics of dystonia.
de Carvalho Aguiar PM, Ozelius LJ.
Dystonia is a syndrome characterised by sustained muscle contractions, producing twisting, repetitive, and patterned movements, or abnormal postures. The dystonic syndromes include a large group of diseases that have been classified into various aetiological categories, such as primary, dystonia-plus, heredodegenerative, and secondary. The diverse clinical features of these disorders are reflected in the traditional clinical classification based on age at onset, distribution of symptoms, and site of onset. However, with an increased awareness of the molecular and environmental causes, the classification schemes have changed to reflect different genetic forms of dystonia. To date, at least 13 dystonic syndromes have been distinguished on a genetic basis and their loci are referred to as DYT1 to DYT13. This review focuses on the molecular and phenotypic features of the hereditary dystonias, with emphasis on recent advances.
Mov Disord. 2002;17 Suppl 3:S49-62.
Pathophysiology of dystonia: a neuronal model.
Dystonia has commonly been thought to represent a disorder of basal ganglia function. Although long considered a hyperkinetic movement disorder, the evidence to support such a classification was based on the presence of excessive involuntary movement, not on physiological data. Only recently, with the return of surgical procedures using microelectrode guidance for the treatment of dystonia, has electrophysiological data demonstrated an alteration in mean discharge rate, somatosensory responsiveness and the pattern of neuronal activity in the basal ganglia thalamocortical motor circuit. Previous models of dystonia suggested that reduced mean discharge rates in the globus pallidus internus (GPi) led to unopposed increases in activity in the thalamocortical circuit that precipitated the development of involuntary movement associated with dystonia. This model has subsequently been modified given the clear improvement in dystonic symptoms following lesions in the GPi, a procedure that is associated with a further reduction in pallidal output. The improvement in dystonia following pallidal lesions is difficult to reconcile with the “rate” hypothesis for hypokinetic and hyperkinetic movement disorders and has led to the development of alternative models that, in addition to rate, incorporate changes in pattern, somatosensory responsiveness and degree of synchronization of neuronal activity. Present models of dystonia, however, must not only take these changes into account but must reconcile these changes with the reported changes in cortical excitability reported with transcranial magnetic stimulation, the changes in metabolic activity in cortical and subcortical structures documented by positron emission tomography (PET), and the alterations in spinal and brainstem reflexes. A model incorporating these changes together with the reported changes in neuronal activity in the basal ganglia and thalamus is presented.