An anatomical-angiographic classification for carotid-cavernous sinus fistulas is introduced and a series of 14 patients with spontaneous carotid-cavernous sinus fistulas is reviewed to illustrate the usefulness of such a classification for patient evaluation and treatment. Fistulas are divided into four types: Type A are direct high-flow shunts between the internal carotid artery and the cavernous sinus; Type B are dural shunts between meningeal branches of the internal carotid artery and the cavernous sinus; Type C are dural shunts between meningeal branches of the external carotid artery and the cavernous sinus; and Type D are dural shunts between meningeal branches of both the internal and external carotid arteries and the cavernous sinus. The anatomy, clinical manifestations, angiographic evaluation, indications for therapy, and therapeutic options for spontaneous carotid-cavernous sinus fistulas are discussed.

Three cases of an entirely suprasellar symptomatic Rathke's cleft cyst, two of which were associated with normal sella turcicas, are reported. In all cases, the cysts caused compression of the optic chiasm, and two produced hypothalamic dysfunction. The diagnosis of these entirely suprasellar masses was enhanced by metrizamide cisternography. Two cases were treated by frontal craniotomy and one was treated transsphenoidally, with good results in all cases. The radiology, pathology, and surgical treatment of these unusual cases is presented. An embryological pathogenesis for the occurrence of an entirely suprasellar Rathke's cleft cyst is discussed.

Four patients with presumed Tolosa-Hunt syndrome ultimately proved to have a parasellar tumor. All four had manifestations of a cavernous sinus syndrome, normal radiologic and medical investigations, and response to steroid therapy. The Tolosa-Hunt syndrome is a diagnosis of exclusion; many other lesions can simulate the clinical manifestations, including steroid responsiveness.

Pseudotumor cerebri developed in a 14-year-old girl with nodulocystic acne, who was taking excessive amounts of a synthetic vitamin A derivative. Although hypervitaminosis A has reportedly caused pseudotumor, Accutane has not previously been implicated.

Total external ophthalmoplegia was observed in five patients consequent to the oral or intravenous administration of phenytoin. Coincident with the ophthalmoplegia, the state of consciousness varied from drowsiness to coma and the blood levels of phenytoin ranged from 36 to 55 mug per milliliter. Initially, the eyes were fixed in midposition, and oculocephalic and oculovestibular stimulation failed to evoke either horizontal or vertical eye movements. The return of vestibulo-ocular responsiveness lagged behind the return of consciousness and other reflex activity. The mechanism underlying this ophthalmoplegia may be related to the ability of phenytoin to potentiate inhibitory synapses in the vestibulo-oculomotor pathway which utilize gamma aminobutyric acid, and to increase the discharge rate of Purkinge cells which exert an inhibitory influence on the same structures.