Treatment using botulinum toxin type B is comparable to type A, with an increased frequency of the side effect dry mouth.Common side effects include pain at the injection site (up to 28%), dysphagia due to the spread to adjacent muscles (11% to 40%), dry mouth (up to 33%), fatigue (up to 17%), and weakness of the injected or adjacent muscle (up to 56%). A Cochrane review published in 2016 reported moderate-quality evidence that a single Botulinum toxin-B treatment session could improve cervical dystonia symptoms by 10% to 20%, although with an increased risk of dry mouth and swallowing difficulties. Another Cochrane review published in 2020 for Botulinum toxin-A found similar results. Deep brain stimulation
Deep brain stimulation to the basal ganglia and thalamus has recently been used as a successful treatment for tremors of patients with Parkinsons disease. This technique is currently, as of 2007, being trialed in patients with spasmodic torticollis. Patients are subjected to stimulation of the globus pallidus internus, or the subthalamic nucleus. The device is analogous to a pacemaker: an external battery is placed subcutaneously, with wires under the skin which enter the skull and a region of the brain. To stimulate the globus pallidus internus, microelectrodes are placed into the globus pallidus internus bilaterally. After the surgery is performed, multiple visits are required to program the settings for the stimulator. The stimulation of the globus pallidus internus disrupts the abnormal discharge pattern in the globus pallidus internus, resulting in inhibition of hyperactive cortical activity.
Outcomes
People with KATP channel variations are at increased risk of developing attention deficit hyperactivity disorder, sleep disruptions, seizures, and experiencing developmental delay – all due to the presence of KATP channels in the brain. These can range from unnoticably mild to severe, and can sometimes improve with sulfonylurea treatment.Those with 6q24 overexpression tend to have transient diabetes, with hyperglycemia tending to disappear within the first year of life. Despite the return of euglycemia, people with 6q24 overexpression are at high risk of developing diabetes later in life, as teenagers or adults.Many of the genetic variations that cause neonatal diabetes are inherited in an autosomal dominant manner, i.e. receiving a single copy of the disease-associated variant results in disease. This is the case for the KATP genes KCNJ11 and ABCC8, and paternally inherited 6q24 amplifications, any of which have a 50% chance of being transmitted to each offspring of an affected individual. Epidemiology
About 1 in 90,000 to 160,000 children born develops neonatal diabetes, with approximately half developing permanent and half transient neonatal diabetes. Recent research
Clinical Trials of NDM

The research article is entitled, "A Successful Transition to sulfonamides treatment in male infant with novel neonatal diabetes mellitus (NDM) caused by the ABBC8 gene mutation and 3 years follow up". It is a case study on the transitioning of treatments from insulin therapy to sulfonamides therapy. NDM is not initiated by an autoimmune mechanism but mutations in KATP-sensitive channel, KCNJ11, ABCC8 and INS genes are successful targets for changing treatments from insulin to sulfonamides therapy.