Embryologic phenomenons that lead to dysraphisms are known, but pathophysiology remains questioned. It is supposed not to be a simple mechanistic dysfunction, and other biological phenomenons are implied in spinal cord damaging. Two main hypothesis are that manual deformation of the cells and mitochondrial membranes lead to energy deficiency and blood flow changes. On the other hand, considering traumatic spinal cord injuries (SCI), inflammation has been shown to have dramatic effects on spinal cord function and physiology. Indeed, all essays about SCI have demonstrated that the initial trauma leads to mechanical injury to cells, accompanied by damages of microvasculature, initiation of pro-apoptotic signaling and ischemia. Therefore, we could imagine that similar inflammatory processes can be implied in stretched spinal cord. In our review of literature, we found few papers highlighting the question of inflammation and CSF sampling.

Inclusion Criteria:

• Infants and children under 18 years of age
• Carriers of an attached marrow: lipomatous fiilum, meningocele, myelomeningocele, myelolipoma,
• Consent of the child's parents,
• Socially insured patient,
• Patient willing to comply with all study procedures and duration,

Exclusion Criteria:

• Patients over 18 years of age,
• Chronic inflammatory disease,
• Ongoing anti-inflammatory treatments,
• No parental consent,