We report two patients with spontaneous intracranial hypotension. In addition to the cardinal features of a postural headache and a low CSF pressure, the patients also had subdural fluid collections demonstrated by head MRI. In both patients, radionuclide cisternography revealed a CSF leak along the spinal axis and rapid accumulation of radioisotope in the bladder. CSF leakage from spinal meningeal defects may be the most common cause of this syndrome. The headache is a consequence of the low CSF pressure producing displacement of pain-sensitive structures. Associated symptoms, including tinnitus and vertigo, and subdural fluid collections are presumably from hydrostatic changes among intracranial fluid compartments that occur at low CSF pressures. Methods of treatment are identical to those for post-dural puncture headaches. Epidural blood patches and epidural saline infusions have rapidly ameliorated the symptoms of spontaneous intracranial hypotension.

We studied a patient with spontaneous intracranial hypotension whose gadolinium-enhanced MRI revealed an extraordinary degree of dural enhancement and striking displacement of the optic chiasm, flattening of the pons, and downward displacement of the cerebellar tonsils. These changes were reversed when a CSF leak at the site of a T12-L1 arachnoid cyst was closed following an epidural blood patch. Such diffuse meningeal enhancement results from the dural venous dilatation that accompanies a reduced CSF volume, a consequence of the Monro-Kellie rule.

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We studied the cerebral effects of oxygen-derived free radicals generated from the xanthine oxidase/hypoxanthine/ADP-Fe3+ system. Xanthine oxidase/hypoxanthine/ADP-Fe3+ solution (0.1 ml) was infused into caudate putamen, and brain was frozen rapidly in situ. Brain water and sodium content increased concomitant with decreased potassium content at 24 hours and 48 hours after the infusion. The degree of brain edema and injury depended on the dose of xanthine oxidase. Spongy neuropil and neuronal cytoplasmic vacuoles were seen at 2 hours, with an infiltration by polymorphonuclear leukocytes at 24 hours, followed by lipid-laden macrophages and reactive astrocytes. Leakage of fluorescent dye into neuropil was seen at 2 hours, but not later. These data suggest that oxygen-derived free radicals damage endothelial cells of the blood-brain barrier; the brain injury is characterized by edema and by structural damage of neurons and glia.

A 51-year-old man had a 4-month history of progressive headache and gradual onset of somnolence. MRI suggested spontaneous intracranial hypotension (SIH) with diencephalic compression, but he did not improve after three epidural blood patches. He became alert following intrathecal saline infusion that normalized his CSF pressure. A CSF leak was noted on spinal MRI and confirmed with CT contrast myelography. Surgical ligation of a torn dural root sleeve isolating a ruptured Tarlov's cyst resulted in permanent cure.