Combinations of these treatments have been used to control spasmodic torticollis. In addition, selective surgical denervation of nerves triggering muscle contractions may offer relief from spasms and pain, and limit damage to the spine as a result of torqued posture. Spinal fibrosis (i.e., locking of spinal facets due to muscular contortion resulting in fused vertebrae) may occur rapidly. This suggests that the desynchronization of the frequency range is movement related. Obtaining relief via a "sensory trick", also known as a geste antagoniste, is a common characteristic present in focal dystonias, most prevalently in cervical dystonia; however, it has also been seen in patients with blepharospasm. Sensory tricks offer only temporary and often partial relief of spasmodic torticollis. 74% of patients report only partial relief of spasmodic torticollis compared to 26% reporting complete relief. The sensory trick must also be applied by the patient themselves. When the sensory trick is applied by an examiner, only 32% of patients report relief comparable to relief during self-application. Since the root of the problem is neurological, doctors have explored sensorimotor retraining activities to enable the brain to "rewire" itself and eliminate dystonic movements. Oral medications
In the past, dopamine blocking agents have been used in the treatment of spasmodic torticollis. Treatment was based on the theory that there is an imbalance of the neurotransmitter dopamine in the basal ganglia. These drugs have fallen out of fashion due to various serious side effects: sedation, parkinsonism, and tardive dyskinesia.
Urinary fractional excretion potassium is high or inappropriately normal in the context of hypokalaemia, and high levels of urinary sodium and chloride are observed. Other clinical indicators include elevated serum renin and aldosterone in the bloodstream, and metabolic alkalosis. The symptomatic features of this syndrome are highly variable ranging from asymptomatic to mild manifestations (weakness, cramps) to severe symptoms (tetany, paralysis, rhabdomyolysis). Symptom severity is multi-factorial, with phenotypic expression varying amongst individuals within the same family. Genetic testing is another measure of identifying the underlying mutations which cause the pathologic symptoms of the disease. This mode of testing is available at select laboratories.Work-up to exclude the differential diagnosis of the electrolyte abnormalities is key. In Gitelman syndrome hypocalciuria is present, and a urine calcium:creatinine ratio may help distinguish it from Bartter syndrome as the two disorders can be clinically indistinguishable. Additionally in Bartter syndrome maximal urine concentrating ability is lost. Laxative abuse can mimic the serum electrolyte abnormalities, but fractional excretion of potassium will be low
Diuretic abuse could be suspected if urinary chloride excretion varies by time of day but may require a diuretic assay to detect
Surreptitious vomiting can cause metabolic alkalosis and hypokalaemia, but urinary chloride levels will be low
Medication history; Proton-pump inhibitors can cause an isolated hypomagnesaemia phenotype, and aminoglycosides such as gentamicin can cause a transient metabolic alkalosis with hypokalaemia and hypomagnesaemia that resolves 2–6 weeks after drug termination.