Worsening abducens paresis and chronic orbital venous congestion after carotid–cavernous fistula embolization: long-term motility outcomes

PURPOSE: Carotid-cavernous fistulas (CCFs) produce abnormal arteriovenous communication between the carotid circulation and the cavernous sinus, leading to orbital venous hypertension and neuro-ophthalmic manifestations. Although endovascular embolization is the treatment of choice and usually results in rapid hemodynamic normalization, delayed ocular motor sequelae after successful closure remain incompletely characterized. We report a case of persistent and worsening abducens nerve paresis and chronic orbital venous congestion following embolization of a direct CCF. METHODS: This case report describes longitudinal neuro-ophthalmologic follow-up over more than four years. Clinical assessment included best-corrected visual acuity, slit-lamp examination, intraocular pressure measurement, dilated fundus examination, and structured ocular motility evaluation using serial Hess chart testing. Retinal morphology was assessed with spectral-domain optical coherence tomography, and orbital and intracranial vascular structures were evaluated with MRI and time-of-flight MR angiography. RESULTS: A 78-year-old woman presented with intermittent diplopia and mild right abduction deficit. Imaging confirmed a right-sided direct CCF, which was successfully treated with endovascular embolization. Shortly after treatment, she developed marked worsening of right abducens nerve paresis with constant diplopia and transient visual acuity reduction. Retinal venous complications developed after treatment, with central retinal vein occlusion and macular edema resolving after intravitreal aflibercept. Persistent VI nerve paresis gradually improved after botulinum toxin injection into the right medial rectus muscle, and serial Hess chart analysis documented progressive expansion of the binocular single vision field, indicating partial functional recovery of abducens nerve function. Long-term imaging showed persistent asymmetry of orbital venous drainage and later development of >50% stenosis of the intracavernous-ophthalmic segment of the internal carotid artery without recurrent fistulous flow. CONCLUSION: This case highlights that delayed neuro-ophthalmic complications and venous congestion may occur despite successful CCF embolization. Post-embolization worsening of the abducens nerve paresis may reflect hemodynamic alterations affecting the cavernous sinus and orbital venous circulation. Gradual functional improvement was observed during long-term follow-up, although interpretation of the natural recovery trajectory is limited by botulinum toxin treatment. These findings further support that angiographic cure does not necessarily indicate complete functional recovery and emphasize the importance of long-term neuro-ophthalmologic and motility follow-up after CCF embolization.