The principal treatment goals for people with MODY — keeping the blood sugars as close to normal as possible ("good glycemic control"), while minimizing other vascular risk factors — are the same for all known forms of diabetes. The tools for management are similar for all forms of diabetes: blood testing, changes in diet, physical exercise, oral hypoglycemic agents, and insulin injections. In many cases these goals can be achieved more easily with MODY than with ordinary types 1 and 2 diabetes. Some people with MODY may require insulin injections to achieve the same glycemic control that another person may attain with careful eating or an oral medication. When oral hypoglycemic agents are used in MODY, the sulfonylureas remain the oral medication of first resort. When compared to patients with type 2 diabetes, MODY patients are often more sensitive to sulphonylureas, such that a lower dose should be used to initiate treatment to avoid hypoglycaemia. Patients with MODY less often suffer from obesity and insulin resistance than those with ordinary type 2 diabetes (for whom insulin sensitizers like metformin or the thiazolidinediones are often preferred over the sulfonylureas). Epidemiology
According to data from Saxony, Germany, MODY was responsible for 2.4% of diabetes incidence in children younger than 15 years. History
The term MODY dates back to 1964, when diabetes mellitus was considered to have two main forms: juvenile-onset and maturity-onset, which roughly corresponded to what we now call type 1 and type 2.
Bladder sphincter dyssynergia (also known as detrusor sphincter dyssynergia (DSD) (the ICS standard terminology agreed 1998)  and neurogenic detrusor overactivity (NDO)) is a consequence of a neurological pathology such as spinal injury  or multiple sclerosis which disrupts central nervous system regulation of the micturition (urination) reflex resulting in dyscoordination of the detrusor muscles of the bladder and the male or female external urethral sphincter muscles. In normal lower urinary tract function, these two separate muscle structures act in synergistic coordination. But in this neurogenic disorder, the urethral sphincter muscle, instead of relaxing completely during voiding, dyssynergically contracts causing the flow to be interrupted and the bladder pressure to rise. Presentation
People with this condition generally experience daytime and night time wetting, urinary retention, and often have a history of urinary tract and bladder infections. Constipation and encopresis are often associated with this condition. Pseudodyssynergia has different causes but presents similarly. Pathology
The pathophysiology of the condition results from neuronal plasticity associated with bladder afferents and motor neurons innervating the external urethral sphincter. Treatment
Botulinum A toxin is a valuable alternative for patients who do not want surgical methods. References
Further reading


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