The fibrous sutures specifically allow the deformation of the skull during birth and absorb mechanical forces during childhood They also allow the necessary expansion during brain growth.In the very first years of life the sutures serve as the most important centers of growth in the skull. The growth of the brain and the patency of the sutures depend on each other. Brain growth pushes the two sides of the patent sutures away from each other, thereby enabling growth of the neurocranium. This means that the neurocranium can only grow if the sutures remain open. The neurocranium will not grow when the forces induced by brain growth are not there. This will occur for example when the intracranial pressure drops; the sutures do not experience stretching anymore causing them to fuse. Diagnosis
The evaluation of a child suspected to have craniosynostosis is preferentially performed in a craniofacial center. The three main elements of analysis include medical history, physical examination and radiographic analysis.Medical history should in any case include questions about risk factors during pregnancy, the familial rate and the presence of symptoms of elevated intracranial pressure (ICP). Elevated ICP
Symptoms of increased intracranial pressure – such as headache and vomiting – should be questioned after. An elevation of ICP can be present in 4 to 20% of the children where only a single suture is affected. The incidence of ICP in children with more than one suture involved can be as high as 62%. However, even though the children are affected, symptoms are not always present.
Medications that extend or prolong the QT interval (macrolides, antihistamines, beta-2 agonists) should be avoided in these patients to prevent cardiac death. Epidemiology
Gitelman syndrome is estimated to have a prevalence of 1 in 40,000 homozygous people . The ratio of men to women affected is 1:1. This disease is encountered typically past the 1st decade of life, during adolescence or adulthood but can occur in the neonatal period. Heterozygous carriers of the SLC12A3 gene mutations are 1% of the population. Parents with Gitelman syndrome have a low probability of passing the disorder to their offspring roughly 1 in 400 unless they are both carriers of the disease. History
The condition is named for Hillel Jonathan Gitelman (1932– January 12, 2015), an American nephrologist working at University of North Carolina School of Medicine. He first described the condition in 1966, after observing a pair of sisters with the disorder. Gitelman and his colleagues later identified and isolated the gene responsible (SLC12A3) by molecular cloning. References
External links

"Gitelman syndrome". MedlinePlus. U.S. National Library of Medicine.