Spontaneous regression of direct carotid-cavernous fistulas (CCFs) is extremely rare. Most of the patients with direct CCFs are usually treated using endovascular techniques. Spontaneous obliteration of the direct fistulas probably results from thrombosis of the venous drainage and/or cavernous sinus. We report spontaneous closure of nine direct CCFs in nine patients. From literature review, we found another 37 patients with 43 fistulas due to spontaneous obliteration of bilateral lesions in six cases. There was no spontaneous closure in large-sized fistula. The factors associated with spontaneous thrombosis of the fistulas may be low-flow and small-sized fistula, hypotension, severe ocular manifestations, dissections or spasm of carotid artery, and increased intracranial pressure. Spontaneous healing of direct traumatic CCFs should be confirmed with cerebral angiography. Conservative treatment of direct CCFs should be carefully restricted in patients with normal vision or minimal visual impairment, and the patients must be monitored closely for any changes in visual function. Prompt endovascular treatment for complete obliteration of the fistula should be performed in patients with rapidly progressive visual loss. Venous thrombosis can still effect vision and rerouting towards cortical veins remains a concern. Because spontaneous resolution cannot be reliably predicted, the fistula then should be treated rather than waiting for spontaneous thrombosis.

We describe a patient with traumatic carotid-cavernous fistula (CCF), subsequently developing contralateral extensive hemorrhagic venous infarction from retrograde venous reflux into the opposite basal vein of Rosenthal. A 54-year-old woman was involved in a motor vehicle accident and sustained severe traumatic brain injury. Two months later, she developed bilateral proptosis and audible bruit. Magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) of the brain demonstrated the right direct CCF. Fluid-attenuated inversion recovery (FLAIR) images showed a small hyperintense area at the left basal ganglia. Ten days later, she developed right-sided grade 2/5 hemiparesis, facial upper motor neuron weakness, and cognitive impairment. Follow-up MRI showed significant progression of hyperintensities involving the left-sided centrum semiovale, basal ganglia, thalamus, midbrain, pons, cerebellum, basal frontal, temporal lobes, especially subcortical white matter on FLAIR images, and multiple hypointense foci of hemorrhagic component on T2*-weighted gradient-echo images, representing hemorrhagic venous infarction. While waiting for embolization, she rapidly developed right hemiplegia and aphasia, and became somnolent. Under general anesthesia, emergency endovascular treatment was performed successfully to obliterate the fistula without surgical intervention. Five months after endovascular treatment, MRI and MRA confirmed no residual fistula and revealed nearly complete resolution of abnormal increased signal intensity. In the present case, the factors related to the presence of this rare condition were absence of the ipsilateral basal vein of Rosenthal (BVR), occlusion of posterior segment of the contralateral superior petrosal sinus, and a developed uncal vein with hypoplastic second and third segments of the contralateral BVR.

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