PubMed · 847627
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A L Day, J E Maniscalco, J D Geissinger, A L Rhoton. 1977. Communicating hydromyelia.. https://pubmed.ncbi.nlm.nih.gov/847627/
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From July 1, 1994 to July 1, 1997 a total of 17 children with Chiari I malformation diagnosed by MRI was seen in our hospital. Six of them underwent craniocervical decompression and tonsilar resection. The major complaints of all these children were gait ataxia and persisting (longer than 6 month) headache, and one child had acutely presenting vertigo and problem of swallowing. The MRI showed that in all cases the tonsils were displaced below the level of CI. Hydrocephalus or syrinx was not seen. At surgery the tonsils were resected. All the patients can be considered cured and symptom free at an average follow up of 13 month.
Ultrasonic imaging of the human fetal brain has allowed ventriculomegaly and hydrocephalus to be categorized. In this study 40 fetuses with ventriculomegaly and 21 with an Arnold-Chiari malformation and a myelomeningocele had ventriculomegaly that resolved, stabilised or progressed in utero. Within the progressive group were those with hydrocephalus, hydrocephalus being defined as expansion of the cerebral ventricular atria together with disproportionate increase in the head circumference. The prognosis for fetuses with resolving and stable ventriculomegaly was good, reflecting the fact that the ventricular dilatation in these cases was probably caused by delayed parenchymal and cerebrospinal fluid pathway development. Whereas the prognosis for progressive ventriculomegaly was generally poor, suggesting that the causes were likely to have been chromosomal, genetic, an infective agent or a catastrophic event which had an adverse effect on parenchymal development. The causes of hydrocephalus also adversely affected brain development but additional damage was caused by raised intracranial pressure.
The pathophysiology of syrinx development is controversial. The authors report on a patient with progressive cervical myelopathy and a Chiari I malformation in whom spinal cord swelling preceded, by a few months, the development of a syrinx in the same location. The patient underwent a craniocervical decompressive procedure and duraplasty, and complete resolution of cord swelling and syringomyelia was achieved. This report is consistent with the theory that patients with Chiari I malformation have increased transmural flow of cerebrospinal fluid, which causes spinal cord swelling that later coalesces into a syrinx. The pathophysiology of syrinx development from spinal cord edema and the success of surgical decompressive treatments that do not invade the central nervous system support the prompt treatment of patients with spinal cord edema who are at risk for the development of a syrinx.