Osteopontin in post-subarachnoid hemorrhage pathologies.

Rupture of intracranial aneurysms causes subarachnoid hemorrhage (SAH), of which the treatment remains the most difficult among cerebrovascular disorders even in this modern medical era. Following successful surgical ablation of ruptured intracranial aneurysms, other conditions may be encountered including delayed cerebral ischemia and chronic hydrocephalus, in addition to early brain injury. Osteopontin (OPN) is one of matricellular proteins that have cytokine-like effect on various cells and act as secretory extracellular matrix proteins between cells. The complexity of OPN functions is attributed to its several isoforms, cleavage sites and functional changes determined by its differing isoforms following various cleavages or other post-translational modifications. Notably, OPN functions beneficially or harmfully in accordance with the context of OPN upregulation. In the field of aneurysmal SAH, OPN has exerted neuroprotective effects against early brain injury and delayed cerebral ischemia by suppressing apoptosis of neurons, disruption of blood-brain barrier, and/or cerebrovascular constriction, while excessive and prolonged secretion of OPN can be harmful through the occurrence of chronic hydrocephalus requiring shunt surgery. This is a review article that is focused on OPN's potential roles in post-SAH pathologies.

A Case of Miyazaki Syndrome Caused by Arachnoid Cyst-Peritoneal Shunt.

BACKGROUND: Miyazaki syndrome is overshunting-associated myelopathy, which is a rare complication of ventriculoperitoneal shunt. We present the first case of Miyazaki syndrome caused by cystoperitoneal (CP) shunt for an arachnoid cyst (AC) in this report. CASE DESCRIPTION: We report a case of a 42-year-old man with 12-year progressive spastic paraplegia, who underwent CP shunt for an AC at the age of 15 years. Although few findings suggested overshunting on symptoms and head computed tomography, contrast-enhanced magnetic resonance imaging revealed the engorgement of the cervical spinal epidural venous plexus compressing the spinal cord. Shunt valve replacement with a pressure-adjustable valve was performed. Postoperatively, the cervical cord compression by the enlarged spinal epidural venous plexus was completely improved, but, possibly due to delayed diagnosis and treatment, the patient's symptoms only partially improved. CONCLUSIONS: When patients with a history of any kind of shunt surgery develop myelopathy, Miyazaki syndrome should be suspected and, for early diagnosis, cervical and/or contrast-enhanced magnetic resonance imaging should be performed.