Pseudotumor cerebri (PTC), or idiopathic intracranial hypertension, is a syndrome associated with multiple clinical conditions. We hypothesize that most if not all etiologies result in an increase in intracranial venous pressure as a final common pathway. We studied 10 patients with PTC. Five had dural venous outflow obstruction as demonstrated by venography, and the five remaining patients had normal venous anatomy. Pressure measurements, made during venography in eight patients, all showed elevated pressures. Pressure measurements in the superior sagittal sinus ranged from 13 to 24 mm Hg (mean, 16.6 mm HG). Patients with obstruction tended to have a high pressure gradient across the stenotic segment. Five patients with normal dural venous anatomy had elevated right atrial pressures (range, 6 to 22 mm Hg; mean, 11.8 mm Hg), which were transmitted up to the intracranial venous sinuses. Endovascular techniques, including angioplasty and infusion of thrombolytic agents in some cases, improved outlet obstruction from a hemodynamic perspective but were ineffective in consistently and reliably alleviating the clinical manifestations of PTC. Patients in both groups tended to respond well to conventional CSF diversion procedures. Our study suggests that elevated intracranial venous pressure may be a universal mechanism in PTC of different etiologies. This elevated venous pressure leads to elevation in CSF and intracranial pressure by resisting CSF absorption. Although the mechanism leading to venous hypertension in the presence of outflow obstruction is obvious, the etiology of increased intracranial and central systemic venous pressure in PTC remains obscure.
The clinical and angiographic features of 46 vertebral arteriovenous fistulas (AVFs) seen during a 12-year period (45 patients) were reviewed. Fourteen patients were asymptomatic, with vertebral AVF discovered at routine clinical examination. Specific symptoms at presentation in the other patients were tinnitus (n = 21), vertigo (n = 6), neurologic deficit (n = 3), and pain (n = 2). Of the 46 AVFs, 19 (41%) were caused by trauma and 27 (59%) were spontaneous. The fistula was found at C-1 to C-2 in 21 (46%) cases, at C-2 to C-5 in five (11%), and below C-5 in 20 (44%). Thirty-four patients (35 vertebral AVFs) were treated with the endovascular technique. Embolization was performed with latex balloons filled with contrast medium in most cases. Endovascular therapy resulted in complete occlusion in 32 cases (91%) and partial occlusion in three (9%). The vertebral artery could not be preserved in three patients. Endovascular balloon treatment of vertebral AVFs is effective in occluding the shunt, avoids general anesthesia and surgical intervention, and results in minimal morbidity. Endovascular therapy is the treatment of choice for vertebral AVF.
Electrical stimulation of the cerebellar fastigial nucleus (FN) globally and profoundly increases cerebral blood flow via a cholinergic mechanism. In cerebral cortex, the vasodilation is unassociated with alterations in cerebral glucose utilization, a condition favoring protection against cerebral ischemia. We sought to determine whether FN stimulation would modify the size of the focal ischemic infarction resulting from occlusion of the middle cerebral artery (MCA). The MCA was occluded in anesthetized rats of the spontaneously hypertensive (SHR) or Sprague-Dawley (SD) strains with or without 1 h of electrical stimulation of the FN. Twenty-four hours later, rats were killed and the volume of the infarction established in thionin-stained sections. in SHRs, FN stimulation reduced by 40% the well-established cortical and partially subcortical infarctions elicited by occlusion of the MCA (from 186 +/- 35.2 to 113 +/- 47.1 mm3, mean +/- SD, n = 15; p less than 0.001). The zone of retrieval was anatomically constant, consisting of a rim of cortex dorsal and ventral to the infarction and medially within the thalamus and striatum corresponding to the penumbral zone described by others. The effect was comparable in rats of the SD strain having smaller infarctions. The effect of FN stimulation appears to be selective for the FN system in that it is not evoked by stimulation of the dentate nucleus and is blocked by systemic administration of atropine (1.0 mg/kg). We conclude that excitation of an intrinsic system in brain represented in the rostral FN has the capacity to reduce substantially an ischemic infarction.(ABSTRACT TRUNCATED AT 250 WORDS)
Intracranial dural arteriovenous (AV) fistulas with spinal perimedullary venous drainage are rare lesions that have distinctive clinical, radiological, and therapeutic aspects. Five patients presented with an ascending myelopathy, which extended to involve the brain stem in three cases. Myelography and magnetic resonance imaging showed slightly dilated spinal perimedullary vessels. Spinal angiograms were normal in the arterial phase. Diagnosis was only possible after cerebral angiography, which demonstrated posterior fossa AV fistulas fed by meningeal arteries and draining into spinal perimedullary veins. Endovascular treatment alone resulted in angiographic obliteration of the lesion in three patients. Two patients required surgery in addition to endovascular therapy. One patient died postoperatively, and in one a transient complication of embolization was observed. Improvement after treatment was good in two cases and fair in two. Transverse sinus thrombosis was observed in three cases and was probably the cause of the aberrant venous drainage of the fistula into the spinal perimedullary veins. The pathophysiology is related to spinal cord venous hypertension. These lesions were classified as Type 5 in the Djindjian and Merland classification of dural intracranial AV fistulas. Endovascular therapy is a safe effective method in the treatment of these fistulas and should be tried first.
The aim of this study was to evaluate the role of endovascular treatment for intracranial mycotic aneurysms. The clinical and angiographic features of three patients with endocarditic vegetation (two with Streptococcus viridans and one with Staphylococcus) were reviewed retrospectively. Patients were selected for this treatment according to the clinical setting and aneurysm location. In two cases, selective catheterization of a distal middle cerebral and posterior cerebral artery branch with a microcatheter followed by superselective amobarbital testing of the parent vessel was preliminary to the occlusion of that vessel with autologous clot or glue. The third patient was treated by selective occlusion of the aneurysm by intra-aneurysmal placement of platinum minicoils. Two patients presented with intracranial hemorrhage and in one the lesion was found on computerized tomography. All three aneurysms had been excluded from the circulation at the 6-month follow-up review. The only complication from the procedure, despite the septic nature and distal localization, was balloon deflation in one patient, who was successfully retreated with coils. Endovascular embolization is indicated in patients who are at risk of hemorrhage and cannot undergo the standard procedure. The superselective amobarbital test allows selection of patients who will tolerate distal vessel occlusion. This endovascular procedure represents a safe and effective treatment for these lesions.
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