Dural arteriovenous malformations and papilledema.

We examined and managed two patients with posterior fossa dural arteriovenous malformations (DAVMs) and papilledema. Both DAVMs had venous drainage into the transverse, straight, and sigmoid dural venous sinuses. The mechanism of papilledema in the first case was presumed venous hypertension resulting in impaired cerebrospinal fluid absorption, as the malformation drained into the single transverse sinus. This was cured by selective arterial embolization of the causative DAVM. The second patient had venous sinus thrombosis that impaired venous drainage despite embolization. A lumboperitoneal shunt was necessary to treat the elevated intracranial pressure.

High-flow angiopathy: cerebral blood vessel changes in experimental chronic arteriovenous fistula.

Profound vascular damage secondary to high-flow extracranial states has been well characterized. However, changes in cerebral vasculature secondary to high-flow states have not been studied. To determine changes related to high-flow states in cerebral vessels, a rabbit model was developed in which torrential flow was created in the vertebrals, carotids, basilar, and vessels of the circle of Willis by means of a carotid-jugular shunt after ligation of the proximal carotid. The clinical, angiographic, and histologic changes noted in the animal model include: abrupt clinical deterioration after a variable interval with some animals developing ptosis, afferent vessel dilatation and the development of prominent anastomotic channels, variable cerebral vessel histopathology--related to duration and relative proximity to the shunt--affecting all three vessel layers, plump, irregular, and clumped endothelium, denuded with adherent platelets, irregular, duplicated, and thinned internal elastic membrane, frayed with invasion of the intima by mesenchymal cells, vacuolization and necrosis of the media muscle, and invasion of adventitia by foreign cells and small blood vessels. The high-flow angiopathy seen in this model may help explain vascular changes associated with high-flow cerebral vascular lesions, as well as other types of vascular damage.

Experimental in vivo imaging of the cranial perineural lymphatic pathway.

After intraventricular injection of 99mTc antimony sulfide in rabbits (n = 12) and cats (n = 14), radiolabeled colloid was imaged passing into the nasal mucosa and subsequently into the cervical lymph nodes. The cervical lymph nodes accounted for about 12% of the injected dose in rabbits sacrificed at 22-24 hr after injection and about 5% of the injected dose in cats sacrificed at 5-6 hr after injection. In both animals this represented at least one-third of the cerebrospinal fluid colloid clearance. This technique is applicable to in vivo imaging studies of the perineural lymphatic pathway for cerebrospinal fluid absorption in primates and, with modifications, in human subjects.