and approximately 2% are severely affected.DCD is a lifelong neurological condition that is expected to be as common in males as it is in females. Currently however, the diagnosis criteria favours males which results in over 80% of males being diagnosed before the age of 16 compared to only 22% for females. Management
There is no cure for the condition. Instead, it is managed through therapy. Physical therapy or occupational therapy can help those living with the condition. Some people with the condition find it helpful to find alternative ways of carrying out tasks or organizing themselves, such as typing on a laptop instead of writing by hand, or using diaries and calendars to keep organized. A review completed in 2017 by Cochrane of task-oriented interventions for DCD resulted in inconsistent findings and a call for further research and randomized controlled trials. Co-occuring conditions
DCD is know to co-occur with other Neurodevelopmental Disorders. Most commonly, Attention Deficit Hyperactivity Disorder (ADHD) co-occurs in an estimated 50% of cases, but other co-occurring conditions are Autistic Spectrum Disorder (ASD), Developmental Speech and Language Disorder and Developmental Learning Disorder. History
Collier first described developmental coordination disorder as "congenital maladroitness". A. Jean Ayres referred to developmental coordination disorder as a disorder of sensory integration in 1972, while in 1975 Sasson Gubbay, MD, called it the "clumsy child syndrome". Developmental coordination disorder has also been called "minimal brain dysfunction", although the two latter names are no longer in use.
X-linked hypophosphatemia (XLH) is an X-linked dominant form of rickets (or osteomalacia) that differs from most cases of dietary deficiency rickets in that vitamin D supplementation does not cure it. It can cause bone deformity including short stature and genu varum (bow-leggedness). It is associated with a mutation in the PHEX gene sequence (Xp.22) and subsequent inactivity of the PHEX protein. PHEX mutations lead to an elevated circulating (systemic) level of the hormone FGF23 which results in renal phosphate wasting, and locally in the extracellular matrix of bones and teeth an elevated level of the mineralization/calcification-inhibiting protein osteopontin. An inactivating mutation in the PHEX gene results in an increase in systemic circulating FGF23, and a decrease in the enzymatic activity of the PHEX enzyme which normally removes (degrades) mineralization-inhibiting osteopontin protein; in XLH, the decreased PHEX enzyme activity leads to an accumulation of inhibitory osteopontin locally in bones and teeth to block mineralization which, along with renal phosphate wasting, both cause osteomalacia and odontomalacia. For both XLH and hypophosphatasia, inhibitor-enzyme pair relationships function to regulate mineralization in the extracellular matrix through a double-negative (inhibiting the inhibitors) activation effect in a manner described as the Stenciling Principle. Both these underlying mechanisms (renal phosphate wasting systemically, and mineralization inhibitor accumulation locally) contribute to the pathophysiology of XLH that leads to soft bones and teeth (hypomineralization, osteomalacia/odontomalacia). The prevalence of the disease is 1 in 20,000.X-linked hypophosphatemia may be lumped in with autosomal dominant hypophosphatemic rickets under general terms such as hypophosphatemic rickets.