Spontaneous intracranial hypotension resulting in stupor caused by diencephalic compression.

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.

Neurovisual findings in the syndrome of spontaneous intracranial hypotension from dural cerebrospinal fluid leak.

BACKGROUND: Spontaneous intracranial hypotension has been considered a rare clinical entity, with less than 75 cases reported in the medical literature. With the advent of magnetic resonance imaging (MRI), spontaneous intracranial hypotension currently is being recognized more frequently. The authors report the neurovisual manifestations of this disorder in a consecutive series of three patients. METHODS: Each patient underwent clinical examination, computerized visual field testing, and MRI. After treatment, each patient was re-examined, and MRI was repeated. RESULTS: Two patients had transient visual obscurations and unusual binasal visual field defects on automated perimetry. A third patient had diplopia from an abducens nerve paresis. After treatment of spontaneous intracranial hypotension, these findings improved or resolved. CONCLUSIONS: This case series, and a review of previously reported cases, indicates that neurovisual problems are common in patients with spontaneous intracranial hypotension. Findings may include diplopia from sixth nerve paresis, transient visual obscurations, blurred vision, visual field defects, photophobia, and nystagmus.

Dural enhancement and cerebral displacement secondary to 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.

Spontaneous intracranial hypotension: report of two cases and review of the literature.

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.

Liposome-entrapped superoxide dismutase reduces cerebral infarction in cerebral ischemia in rats.

We studied the role of superoxide radicals in the pathogenesis of ischemic brain injury using a model of focal cerebral ischemia in 102 rats and liposome-entrapped CuZn-superoxide dismutase, which can penetrate the blood-brain barrier and cell membranes efficiently. The bolus intravenous administration of 25,000 units of liposome-entrapped CuZn-superoxide dismutase elevated superoxide dismutase activities in the blood and brain 1, 2, 8, and 24 hours later as well as in the ischemic hemisphere and contralateral cortex. Determined 24 hours after right middle cerebral and bilateral common carotid artery occlusion by the lack of staining for mitochondrial dehydrogenase activity with 2,3,5-triphenyltetrazolium chloride, infarct sizes were reduced by 33%, 25%, and 18% in the anterior, middle, and posterior brain slices, respectively, by treatment with liposome-entrapped CuZn-superoxide dismutase. Our data demonstrate that superoxide radicals are important determinants of infarct size following focal cerebral ischemia and that liposome-entrapped CuZn-superoxide dismutase may have pharmacologic value for the treatment of focal cerebral ischemic injury.

Pathogenesis of vasogenic edema in focal cerebral ischemia. Role of superoxide radicals.

Oxygen-derived free radicals have been postulated to be involved in brain edema and cell death secondary to ischemia and traumatic injury. Using a model of vasogenic brain edema produced by a permanent occlusion of the left MCA in rats, we have studied the role of superoxide radicals in pathogenesis of ischemic edema. The levels of NBF in ischemic brain were increased by 222%, 420%, and 614%, respectively, at 1, 4, and 24 hr after the MCAO. Topical application of superoxide dismutase to the injured cortex through a modified cranial window significantly reduced the NBF levels, indicating the involvement of superoxide radicals in ischemic brain. Liposome-entrapped SOD, when IV injected 5 min after the MCAO, significantly reduced the degree of edema at 24 hr. Our data indicate that superoxide radicals play an important role in the pathogenesis of vasogenic edema in cerebral ischemia.

Liposome-entrapped superoxide dismutase ameliorates infarct volume in focal cerebral ischaemia.

We studied the role of superoxide radicals in the pathogenesis of focal ischaemic brain injury using liposome-entrapped copper-zinc-superoxide dismutase which can penetrate the blood-brain barrier and cell membranes efficiently. Superoxide dismutase activities were significantly elevated in the blood and in the normal brain tissue 1, 2, 8, and 24 hours after a bolus intravenous administration of liposome-entrapped copper-zinc-superoxide dismutase. Copper-zinc-superoxide dismutase activities were also increased significantly in the ischaemic hemisphere and the contralateral cortex as well. The infarct sizes were reduced by 33%, 24% and 18%, respectively, for the anterior artery area, middle artery area, and posterior artery area by treatment at 24 hours following the injection of liposome-entrapped superoxide dismutase. These data demonstrate that superoxide radicals are important determinants of the size of an infarct following focal cerebral ischaemia, and that liposome-entrapped copper-zinc-superoxide dismutase may have pharmacological value for focal cerebral ischaemic injury.

Reduction of activities of superoxide dismutase but not of glutathione peroxidase in rat brain regions following decapitation ischemia.

Effects of complete ischemia on levels of antioxidative enzymes including copper-zinc (CuZn) superoxide dismutase (SOD), manganese (Mn)-SOD, and glutathione peroxidase (GSH-Px) were studied in rat brain regions at 30 and 60 min following decapitation. CuZn-SOD activities were significantly decreased in cerebral cortex and hippocampus at both time points whereas the enzyme activities were decreased at 60 min in cerebellum and caudate areas. The reduction of Mn-SOD activities followed the same pattern of CuZn-SOD in various brain regions. However, GSH-Px activities in these brain regions were not affected by decapitation ischemia. These data suggest that the reduction of CuZn-SOD and Mn-SOD activities during ischemia, in conjunction with the significant decrease in the contents of alpha-tocopherol and other endogenous antioxidants, may compromise the brain's ability to defend against the toxic effects of superoxide radicals formed by ischemia and by subsequent reoxygenation.