Other symptoms can be difficulty in breathing, snoring, day-time sleepiness and perspiration. The main causative agent of OSA is the [midface hypoplasia], which also poses a risk to the eyes that can be seen bulging out of the eye sockets. Other factors, such as a micrognathism and adenoid hypertrophy, are likely to contribute in causing OSA. The most common syndromic forms of craniosynostosis; i.e. Apert, Crouzon and Pfeiffer, have an increased risk of developing OSA. The children have nearly 50% chance of developing this condition.A theory regarding the involvement of OSA as a causative agent for elevated intracranial pressure suggests an association with the auto-regulation of blood flow in the brain. Certain cells in the brain respond specifically to an increase of CO2 in the blood. The response involves vasodilatation of the cranial vault blood vessels, increasing the volume of one of the elements in the Monro-Kellie doctrine. The increase of CO2 concentration in the blood is a consequence of impaired breathing, especially seen when the child with OSA is sleeping. It is well documented that the highest spikes in intracranial pressure often occur during sleep. Abnormalities in the skull base
Impaired venous outflow is often caused by a hypoplastic jugular foramen. This causes an increase in the intracranial blood volume, thereby causing an increase in intracranial pressure.This can be further complicated with a possible Arnold–Chiari malformation, which can partially obstruct the flow of cerebro-spinal fluid from the neurocranium to the spinal cord.
Craniosynostosis where no extracranial deformations are present, is called non-syndromic or isolated  craniosynostosis. When there are extracranial deformations present, for instance involving the limbs,  heart, central nervous system or the respiratory tract, you may speak of a syndromic form of craniosynostosis. More than 180 identified syndromes show deformations due to craniosynostosis. The following syndromes are associated with fibroblast growth factor receptors:In addition, the following syndromes have been identified:

Differential diagnosis
Deformational plagiocephaly
The main difference between plagiocephaly based on craniosynostosis and deformational plagiocephaly is that there is no suture fusion in the latter one. The malleability of the neonatal skull allows the skull to change shape due to extrinsic forces.With the tests a pediatrician should perform, as explained above, the difference is quite easy to make. In deformational plagiocephaly the skull does not show a bulging of the mastoid and in these patients the skull base and position of the ears is level, all in contrary with plagiocephaly due to craniosynostosis. Displacement of one ear to the front is characteristic for deformational plagiocephaly. Primary microcephaly
Primary microcephaly shows a clinical image of craniosynostosis, but due to a different cause. The primary failure is the absence of growth of the brain, rendering the sutures of the cranial vault useless. As a consequence, the sutures close, presenting a pansynostosis like image. A differentiation between these two conditions can be made with a computed tomography (CT) scan. The subarachnoid spaces are typically enlarged with primary microcephaly, whereas they are reduced or absent in true pansynostosis.