Spontaneous intracerebral hematoma in carotid-cavernous fistula

Turner, Donn M.; VanGilder, John C.; Mojtahedi, Saeid; Pierson, Eric W.

doi:10.3171/jns.1983.59.4.0680

Cited by 56 publications

(22 citation statements)

References 34 publications

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“…3-5 For direct CCFs, venous cerebral congestion has been reported in 6 cases, 4,6,9,14,15 all of which showed brainstem congestion, including one case associated with congestion of the cervical spinal cord.…”

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confidence: 99%

Extensive basal ganglia edema caused by a traumatic carotid-cavernous fistula: a rare presentation related to a basal vein of Rosenthal anatomical variation

Ract

Drier²,

Leclercq³

et al. 2014

JNS

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A direct carotid-cavernous fistula (CCF) is an abnormal communication between the internal carotid artery (ICA) and the cavernous sinus leading to a high-flow shunt.11 The mechanisms that may be responsible for a direct CCF are traumatic conditions and spontaneous rupture of an aneurysm located on the cavernous segment of the ICA. Clinically, patients with a direct CCF usually present with pulsating proptosis, corneal edema, and chemosis that are related to engorgement of the superior ophthalmic vein draining into the cavernous sinus.12 Rarely, CCFs are responsible for brainstem edema due to reflux into a superior petrosal sinus (SPS) draining the lateral mesencephalic vein. 7We describe a rare presentation of traumatic CCF with edema of the basal ganglia (BG) due to an anatomical variation of the basal vein of Rosenthal (BVR). Case ReportHistory and Examination. A 45-year-old woman was emergently admitted to our hospital for dysarthria, left hemiparesis, and headache rapidly evolving to a comatose state. Right ocular trauma from a thin metal rod had recently occurred. Brain MRI (3 T) was emergently performed (Fig. 1). Three-dimensional time of flight (TOF) acquisition showed hyperintense signal within the right cavernous sinus; these findings were suggestive of a direct CCF. Both FLAIR and T2-weighted images showed a hyperintense signal in the right side of the pons, the mesencephalon extending to the right middle cerebellar peduncle, the right BG, and the medial aspect of the right temporal lobe. Since apparent diffusion coefficient values were not decreased in these areas, the T2-weighted hyperintense signals were suggestive of vasogenic edema. The authors report a very rare presentation of traumatic carotid-cavernous fistula (CCF) with extensive edema of the basal ganglia and brainstem because of an anatomical variation of the basal vein of Rosenthal (BVR). A 45-yearold woman was admitted to the authors' institution for left hemiparesis, dysarthria, and a comatose state caused by right orbital trauma from a thin metal rod. Brain MRI showed a right CCF and vasogenic edema of the right side of the brainstem, right temporal lobe, and basal ganglia. Digital subtraction angiography confirmed a high-flow direct CCF and revealed a hypoplastic second segment of the BVR responsible for the hypertension in inferior striate veins and venous congestion. Endovascular treatment was performed on an emergency basis. One month after treatment, the patient's symptoms and MRI signal abnormalities almost totally disappeared.Basal ganglia and brainstem venous congestion may occur in traumatic CCF in cases of a hypoplastic or agenetic second segment of the BVR and may provoke emergency treatment.

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confidence: 99%

Extensive basal ganglia edema caused by a traumatic carotid-cavernous fistula: a rare presentation related to a basal vein of Rosenthal anatomical variation

Ract

Drier²,

Leclercq³

et al. 2014

JNS

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“…This may occur as a result of the accumulation of contrasts in the cavernous sinus, since contrasts do not induce thrombus formation in normal blood vessels (22,23). In all six cases available with brainstem edema caused by TCCF, brainstem edema and its associated symptoms occurred following the use of contrast materials (2)(3)(4)(5)(6). In the present case, there was mild brainstem edema on MRI during the use of contrast materials, but the brainstem edema was aggravated following the use of contrast materials.…”

Section: Discussionmentioning

confidence: 54%

“…It is characterized by the following cardinal symptoms: Exophthalmos, ocular pulsation, intracranial bruit, cranial nerve palsy, epistaxis, brain ischemia and intracranial hemorrhage (1); however, the clinical presentation of brainstem edema in TCCF is rare, and only six cases to date have been reported (2)(3)(4)(5)(6). Clinical symptoms are primarily determined by the direction of the venous drainage.…”

Section: Introductionmentioning

confidence: 99%

Brainstem edema caused by traumatic carotid-cavernous fistula: A case report and review of the literature

Guo

Zhao

et al. 2015

Experimental and Therapeutic Medicine

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Abstract. Brainstem edema caused by traumatic carotid-cavernous fistula (TCCF) is rare, and there is little information available regarding its clinical characteristics. The present report describes the case of a 51-year-old man with TCCF, who presented with right exophthalmos and intracranial bruit for 1 week. One month prior to admission at hospital, he fractured the frontal and ethmoid sinuses. Digital subtraction angiography confirmed the diagnosis of TCCF, and magnetic resonance imaging (MRI) suggested edema on the right side of the pons. Five days after admission, the patient exhibited left hemiparesis, and MRI revealed aggravation of the brainstem edema. Following treatment with transarterial balloon embolization, the clinical symptoms, including hemiparesis, were relieved; at the 1-month follow-up, the brain edema had disappeared. The patient was normal at the 6-month follow-up. Following the report of the present case, we reviewed six additional cases previously reported in the literature and discussed the potential mechanisms of TCCF-associated brainstem edema. We conclude that occlusion of the superior petrosal sinus may contribute to brainstem edema caused by TCCF. Relief of the brainstem edema and brainstem edema-associated clinical symptoms can be achieved with transarterial coil or balloon embolization of the TCCF to reduce the drainage pressure in the brainstem veins.

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“…However, in deciding on treatment options, two important points need to be borne in mind. These lesions tend not to be life-threatening, although there are reports o f intracere bral haemorrhage in high flow CCSF [8], The main reason for intervention is protection of vision. Whilst high flow CCSF have a high risk of visual loss, the dural slow flow CCSF are much less frequently associated with visual loss and have a spontaneous remission rate of 10-60% [9][10][11][12][13].…”

Section: Discussionmentioning

confidence: 99%