Left Extracranial Internal Carotid Artery Research Articles

Transcranial Doppler for Eagle Syndrome: Rare Presentation of Unilateral Internal Carotid Artery Compression by the Stylohyoid Ligament With Provocative Maneuvers

Eagle syndrome is a rare condition caused by compression of the internal carotid artery (ICA) or cranial nerves by an elongated styloid process or calcified stylohyoid ligament. This patient is a 56 year-old woman who presented with episodes of positional syncope for 8 years. Transcranial Doppler (TCD) demonstrated abnormally decreased flow in the left middle cerebral artery (MCA) during the syncopal episodes. The patient was evaluated by TCD, transcranial imaging (TCI), and carotid duplex (CD). First, a baseline CD and TCI were performed with the patient in a neutral position. TCD was then used during symptomatic provocative maneuvers to monitor the bilateral MCAs. Intraoperative TCD monitoring was also done during bilateral stylohyoid ligament resection, and postoperatively during the same provocative maneuvers. The baseline CD examination revealed normal extracranial carotid anatomy; TCD and TCI showed normal mean velocities and a normal anatomic variant of fetal origin of the left posterior cerebral artery. During provocative maneuvers, TCD showed abnormally dampened to absent flow in the left MCA, consistent with compression of the left extracranial ICA. CT scan confirmed elongated stylohyoid ligaments bilaterally. The MCA mean velocities were monitored intraoperatively and postoperatively by TCD and showed no changes with head positioning immediately following resection of the stylohyoid ligaments. The patient reported no syncopal episodes at follow-up 6 days after surgery. Although rare, Eagle syndrome should be considered as a cause of positional syncope. TCD can serve as a diagnostic test, an intraoperative monitoring tool, and a method for documenting the surgical outcome.

Superficial Temporal Artery to Middle Cerebral Artery Bypass and External Carotid Reconstruction for Carotid Restenosis After Angioplasty and Stent Placement

The recent proliferation of endovascular treatment of carotid atherosclerotic disease will increase the number of patients who require treatment for recurrent carotid stenosis after angioplasty and stent placement. The optimal management of these patients has not yet been defined. We describe a 66-year-old woman who required 2 surgical procedures for recurrent in-stent carotid stenosis. She experienced numerous transient ischemic attacks 5 months after left extracranial internal carotid artery angioplasty and stenting for asymptomatic stenosis. Angiography showed high-grade in-stent restenosis, left intracranial carotid artery stenosis, and poor collateral flow to the left middle cerebral artery circulation. The patient underwent a superficial temporal artery to middle cerebral artery bypass, and the transient ischemic attacks resolved. Five months later, angiography showed progressive stenosis of the external carotid artery at the site of the stent. The patient underwent successful external carotid reconstruction with an on-lay patch. Extracranial-intracranial bypass grafting may be used successfully in the treatment of recurrent extracranial carotid artery stenosis after angioplasty and stent placement. Also, external carotid artery reconstruction at the site of an internal carotid artery stent can be performed safely.

Displasia fibromuscular con fenómeno Moyamoya en paciente con síndrome de Alport. Patología del colágeno tipo IV

Alport's syndrome is a hereditary progressive nephropathy associated with neurosensorial deafness, secondary to mutations of the genes which codify the a chains of collagen IV. In the literature we have found isolated reports of cases with nervous system involvement. A 37 year old woman was diagnosed as having Alport's syndrome with terminal secondary chronic renal failure and bilateral neurosensorial deafness. She was assessed following repeated transient ischemic attacks of the left hemisphere over the previous three years. Neurological examination was normal. Magnetic resonance showed an ischemic stroke of the left frontal white matter, and on arteriography there was tubular stenosis of the left extracranial internal carotid artery and proximal occlusion of the homolateral anterior and medial cerebral arteries with a compensatory deep vascular network, compatible with fibromuscular dysplasia and secondary moyamoya phenomenon. Although the association between fibromuscular dysplasia and Alport's syndrome may be casual, we suggest that there may be a common mechanism of pathogenesis in both syndromes, related to the expression of type IV collagen in the vascular basal membranes.