Foramen magnum (shown in red), the hole at the base of the skull. The most widely accepted pathophysiological mechanism by which<unk>  type I<unk> s occur is by a reduction or lack of development of the posterior fossa as a result of congenital or acquired disorders. Congenital causes include hydrocephalus, craniosynostosis (especially of the lambdoid suture), hyperostosis (such as craniometaphyseal dysplasia, osteopetrosis, erythroid hyperplasia), X-linked vitamin D-resistant rickets, and neurofibromatosis type I. Acquired disorders include space occupying lesions due to one of several potential causes ranging from brain tumors to hematomas. Traumatic brain injury may cause delayed acquired<unk> , but the pathophysiology of this is unknown. Additionally, ectopia may be present but asymptomatic until a whiplash injury causes it to become symptomatic. Some neurological experts believe that<unk>  type I is developed as a result of Filum Disease, an abnormal traction of the spinal cord caused by an excessively tense Filum terminale. This theory was first introduced by Dr. Miguel B. Royo Salvador in 1993.
Chiari malformation
Glial tumor
Central nervous system cyst
Dandy–Walker malformation
Arachnoid cyst
Subdural hygroma
Cavernous venous malformation
Meningism