Bilateral Internal Carotid Artery Occlusion Research Articles

Ruptured Posterior Circulation Aneurysms with Bilateral Internal Carotid Artery Occlusion: Surgical Nuance.

Background:Craniotomy and surgical clipping is the standard modality of treatment in patients of cerebral aneurysms. However, the surgical clipping of aneurysm may pose serious difficulties in the case of a bilateral carotid artery occlusion. The endovascular treatment has shown promising results in this disease.Methods:A retrospective study of all patients of posterior circulation aneurysms in the background of carotid occlusive disease at our department was performed. The aim of this study was to describe the clinical, radiological characteristics, and the treatment of this rare entity.Results:Four patients were treated from January 2009 to October 2015. The mean age of our patients was 34 years with ages that ranged from 17 to 45 without any gender predominance. The mean period between onset of symptoms and diagnosis was 6 weeks. Angiographic localization of the disease was observed in all patients. All patients were treated by endovascular techniques. The postoperative course has been satisfactory with a complete neurological recovery in all patients.Conclusions:Rupture of posterior circulation aneurysms in the setting of bilateral internal carotid artery occlusion is extremely rare. Treatment is exclusively endovascular intervention. The functional outcome of ruptured posterior circulation aneurysms in setting of bilateral carotid occlusive disease is particularly favorable with good neurological recovery.

A Case of Acute Simultaneous Bilateral Internal Carotid Artery Occlusion Treated by Thrombectomy

A Case of Acute Simultaneous Bilateral Internal Carotid Artery Occlusion Treated by Thrombectomy

Determination of Brain-Regional Blood Perfusion and Endogenous cPKCγ Impact on Ischemic Vulnerability of Mice with Global Ischemia

Conventional protein kinase C (cPKC)γ participated in cerebral hypoxic preconditioning-induced neuroprotection and affected the neurological outcome of ischemic stroked mice. As an independent predictor of ischemic stroke, the internal carotid artery occlusion (ICAO)-caused brain-regional ischemic injury may worsen the neurological outcome of patients. However, the brain-regional ischemic vulnerability and its underlying mechanism remain unclear. In this study, the bilateral ICAO (BICAO) model was applied in cPKCγ wild type (WT) and knockout (KO) mice to determine the cPKCγ impact on brain-regional ischemic vulnerability. The arterial spin labeling (ASL) imaging results showed that 7days BICAO-induced global ischemia could cause significant blood perfusion loss in prefrontal cortex (69.13%), striatum (61.69%), hypothalamus (67.36%), hippocampus (69.82%) and midbrain (40.53%) of WT mice, along with neurological deficits. Nissl staining and Western blot results indicated that hypothalamus and midbrain had more severe neural cell loss than prefrontal cortex, striatum and hippocampus, which negatively coincided with endogenous cPKCγ protein levels but not blood perfusion loss and cPKCγ membrane translocation levels. Furthermore, we found that cPKCγ KO significantly aggravated the neuron loss in prefrontal cortex, striatum and hippocampus and abolish the regional ischemic vulnerability by using immunofluorescent staining with neuron-specific marker NeuN. Similarly, cPKCγ KO also significantly increased Caspase-3, -8 and -9 cleavage levels in prefrontal cortex, striatum, hippocampus, hypothalamus and midbrain of mice with 24h BICAO. These results suggested that hypothalamus and midbrain are more vulnerable to ischemia, and endogenous cPKCγ affects the regional ischemic vulnerability through modulating Caspase-8 and -9 dependent cell apoptosis.

Moyamoya disease with occlusion of bilateral vertebral arteries and the basilar artery fed by the collateral vessels of vertebral arteries: A rare case report

The main change of moyamoya disease (MMD) is steno-occlusion at the terminal portion of the bilateral internal carotid arteries (ICAs). Occlusion of distal portions of the bilateral vertebral arteries (VAs) in MMD has never been reported. An 18-year old female was admitted with repeated headache for 13years. Cerebral digital subtraction angiography (DSA) demonstrated occlusion of bilateral ICAs at their terminal portions, moyamoya vessels at the skull base, occlusion of bilateral distal VAs and the basilar artery (BA) fed by the tortuous collateral vessels arising from the cervical segment of VAs. We report this unique case for its rarity and discuss its mechanism.

Bilateral Blunt Internal Carotid Artery Occlusions Associated with Multiple Trauma: A Case Report

In multiple trauma, blunt carotid artery injuries (BCAIs) have occasionally been reported. However, bilateral blunt carotid artery occlusions (Grade 4 BCAIs) associated with multiple trauma are rare, and delays in diagnosis and treatment result in a lethal outcome. Here, we report our experience with bilateral carotid artery occlusions. A 76-year-old female suffered multiple traumas in a motor vehicle accident. On arrival at our hospital, she presented in a coma, with left mydriasis and unreactive pupils. Computed tomography (CT) showed bifrontal intracranial epidural hematoma and fractures of the facial bone and anterior skull base, and osteoplastic craniotomy was urgently undertaken for the epidural hematoma. However, the comatose state and unreactive pupils persisted during the post-operative course. Serial head CT findings showed progressive bilateral ischemic changes, and radiological examinations revealed bilateral internal carotid artery occlusions. We speculated that bilateral Grade 4 BCAIs had induced progressive cerebral infarctions. The patient partially responded to anticoagulation therapy with heparin infusion, but died of multiple organ failure on day 15. When bilateral progressive ischemic changes are observed in a patient with severe traumatic brain injury, bilateral Grade 4 BCAIs should be considered in the differential diagnosis. CT angiography as part of whole-body CT at admission may be effective for preventing delays in diagnosis and treatment of bilateral Grade 4 BCAIs.

Moyamoya Disease, Still a Mysterious Disorder.

Moyamoya disease (MMD) is a chronic occlusive cerebrovascular disease characterized by progressive stenosis at the terminal portion of the internal carotid artery and an abnormal vascular network at the base of the brain. The etiology remains unknown, and the treatment is not satisfactory. In this issue of Journal of Stroke, important review papers on MMD are published. They showed that genetic variations of RNF213 in the 17q25-ter region make it an important susceptibility gene, and that MMD is most common in East Asian countries such as Korea and Japan. These epidemiological characteristics may be attributed to the high prevalence of the susceptibility gene in this region. Other issues including recent advances in surgical and interventional therapy are also summarized. However, MMD is still a mysterious disorder. MMD is diagnosed on the basis of imaging findings: bilateral (or unilateral) distal internal carotid artery occlusion and basal collaterals. However, simple middle cerebral artery stenosis may evolve into MMD over time, and intracranial atherosclerosis may angiographically mimic MMD. Although gene testing is useful in the differential diagnosis, questions remain. RNF gene polymorphism is found to be present in 1/4 of patients with non-MMD intracranial atherosclerosis in East Asia [1], suggesting that it is not specific for MMD. In practice, when we encounter a patient with RNF gene variation and intracranial arterial disease that is not angiographically consistent with MMD, we are not sure whether this case is of atypical MMD or of atherosclerosis. Given the fact that RNF gene polymorphism is not uncommon in the Japanese and Koreans and only a few develop MMD, RNF may simply be a susceptibility gene, and the final clinical presentation, that is, MMD, intracranial atherosclerosis, or no vascular lesion, may depend on the nature of a secondary insult or perhaps other genetic variations. This is a puzzling issue, and a recent case report of combined pathology (both MMD and atherosclerosis) [2] has provided further confusion. Reviews on this issue showed that MMD cases are also found in Western countries, and the prevalence is increasing worldwide. Are the characteristics of MMD in the East and West the same? Is the real incidence increasing or are we simply detecting more cases with advanced imaging tools? Other difficult questions are; why are there two peaks of age, around 10 years and at 30-45 years? Why are patients 20-30 years old relatively unaffected? Are antiplatelet agents useful for MMD patients? Is surgical revascularization therapy beneficial for patients presenting with hemorrhagic stroke? In patients with asymptomatic MMD, what is the risk of future stroke and what are the predictive factors? Is there any way to prevent the progression of the disease? The reviews provide more questions than solutions, and it seems that the answers remain far off. However, we have to realize that polymorphism in RNF 213 gene was completely unheard of until 10 years ago. Ten years from now, with continued research, we might be involved in clinical trials that examine ways to prevent the development of MMD in young individuals with a susceptible gene.

EPCs-Collagen Sponge Complex Promotes Neovascularization of Chronic Cerebral Ischemia following Multiple Burr Hole (MBH) Surgery

Objective: The aim of this study was to explore the effect of endothelial progenitor cells (EPCs)-collagen sponge complex on the neovascularization of chronic cerebral ischemia following multiple burr hole (MBH) surgery. Methods: Bone marrow-derived EPCs from 5 Fisher 344 (F344) inbred rats were cultured and amplified in vitro, then co-cultured to become the EPCs-collagen sponge complex. Chronic cerebral hypo-perfusion was induced in 30 inbred male F344 rats by permanent bilateral internal carotid artery occlusion (BICAO). The MBH operation was performed three days after BICAO surgery. Rats were then randomly divided into 3 groups (n=10 each group); EPCs-collagen sponge complex + MBH; collagen sponge + MBH and MBH group. Either EPCs-collagen sponge complex or collagen sponge was implanted at the burr hole site in the EPCs-collagen sponge complex + MBH and the collagen sponge + MBH group, respectively. Regional cerebral blood flow (rCBF) was measured by Laser Doppler Flowmetry (LDF), EPCs were tracked by fluorescein, and immune-histochemical analysis for the neovascularization was performed 21 days after MBH surgery. Results: Before the MBH surgery, no differences of rCBF between the EPCs-collagen sponge complex + MBH group, the collagen sponge + MBH group and the MBH alone group (P>0.05) were found. The increase of rCBF in the EPCs-collagen sponge complex + MBH group (20.29 ± 10.21%) was significantly higher when compared with the other two groups 21 days after MBH surgery (7.39 ± 6.85% and 10.32 ± 6.27%, respectively; P<0.05). The amount of new blood vessels in the EPCs-collagen sponge complex + MBH group was also significantly greater than the other two groups (78.2 ± 4.7 vs. 48.7 ± 6.1 vs. 46.9 ± 7.3; P<0.05). The labeled EPCs were incorporated into the endothelial cells of vessels at the burr hole sites. Conclusion: The EPCs-collagen sponge complex enhances angiogenesis after MBH surgery under chronic cerebral hypo-perfusion condition, and increases the blood flow perfusion in ischemic cerebral tissue.

Двусторонняя окклюзия внутренних сонных артерий: клиническое наблюдение

Двусторонняя окклюзия внутренних сонных артерий: клиническое наблюдение

Improvements in Cerebral Blood Flow and Recanalization Rates With Transcranial Diagnostic Ultrasound and Intravenous Microbubbles After Acute Cerebral Emboli

Intravenous microbubbles (MBs) and transcutaneous ultrasound have been used to recanalize intra-arterial thrombi without the use of tissue plasminogen activator. In the setting of acute ischemic stroke, it was our objective to determine whether skull attenuation would limit the ability of ultrasound alone to induce the type and level of cavitation required to dissolve thrombi and improve cerebral blood flow (CBF) in acute ischemic stroke. In 40 pigs, bilateral internal carotid artery occlusions were created with 4-hour-old thrombi. Pigs were then randomized to high-mechanical index (MI = 2.4) short-pulse (5 microseconds) transcranial ultrasound (TUS) alone or a systemic MB infusion (3% Definity) with customized cavitation detection and imaging system transmitting either high-MI (2.4) short pulses (5 microseconds) or intermediate-MI (1.7) long pulses (20 microseconds). Angiographic recanalization rates of both internal carotids were compared in 24 of the pigs (8 per group), and quantitative analysis of CBF with perfusion magnetic resonance imaging was measured before, immediately after, and at 24 hours using T2* intensity versus time curves in 16 pigs. Complete angiographic recanalization was achieved in 100% (8/8) of pigs treated with image-guided high-MI TUS and MBs, but in only 4 of 8 treated with high-MI TUS alone or 3 of 8 pigs treated with image-guided intermediate-MI TUS and MBs (both P < 0.05). Ipsilateral and contralateral CBF improved at 24 hours only after 2.4-MI 5-microsecond pulse treatments in the presence of MB (P < 0.005). There was no evidence of microvascular or macrovascular hemorrhage with any treatment. Guided high-MI impulses from an ultrasound imaging system produce sustained improvements in ipsilateral and contralateral CBF after acute cerebral emboli.

Rapid, sequential bilateral acute carotid blowout syndrome

This study aims to report the treatment and outcome of sequential bilateral acute carotid artery blowout syndrome. From 2004 to 2010, we treated seven male patients with sequential bilateral blowout syndrome long after irradiation treatment for head and neck cancer. After first common carotid artery (CCA)-internal carotid artery (ICA) rupture, six were treated with CCA-ICA occlusion and one with graft stenting. The contralateral ICAs were normal or stenotic on angiography in all patients. After the contralateral CCA-ICA rupture, five patients received CCA-ICA occlusion, one received graft stent treatment, and one received no treatment. Five of the seven patients died soon after the final treatment. Two patients developed cerebral infarctions (one treated with bilateral stenting, one treated with occlusion), one died from extensive local infection, one died soon after a third treatment, one died of progression of the disease, and one refused a second treatment and died soon after the diagnostic angiography. Two patients survived with follow-up periods of 1 and 5 years. In all seven patients, the contralateral CCA-ICA blowout occurred within 3 months after the first ICA occlusion. Bilateral ICA occlusion is an alternative management for sequential carotid artery blowout, but the mortality is high and outcome is poor. A normal angiogram cannot exclude the possibility of rapid development of a contralateral carotid artery blowout shortly after a first episode in patients who have received radiotherapy for head and neck cancer.

Looking at the Missing Brain: Hydranencephaly Case Series and Literature Review

Hydranencephaly is a severe congenital condition where most of the cerebral hemispheres are replaced by a membranous sac. Despite the growing amount of case reports, most pathogenic, phenotypic, and prognostic aspects of hydranencephaly remain controversial. By matching the recent literature data with the findings of our own series (four cases: two fetuses at the twelfth gestational week, a 32-year-old man, and a 14-year-old female), we attempted to date back the insult leading to hydranencephaly to understand its pathogenesis and to explain the basis of its protean phenotype. The variable detection of cerebral remnants seems to mirror the developmental pathway of cerebral arteries. Moreover, fetal and postnatal neuroimaging data and histopathologic findings point toward an early bilateral internal carotid artery occlusion, mostly occurring between the eighth and twelfth gestational weeks, as the main pathogenic mechanism of hydranencephaly.

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Case Reports: Sickle cell anemia, an autosomal recessive disease, results from a valine for glutamic acid substitution at position six of the β-globin gene. Vaso-occlusive, sequestration, hemolytic and aplastic crises are common critical manifestations of this disease. Sickle cell trait (SCT) is the heterozygous form of the disease, and people with this genotype rarely exhibit disease manifestations. Sickle cell anemia occurs in about 1/500 African American births’ while the trait occurs in 1 in 12 African Americans. Cocaine, a central nervous system stimulant, is known to cause vascular ischemia through a multifactorial mechanism. We present the rare case of a cocaine-induced sickle cell crisis in a patient with SCT leading to splenic and intestinal infarction. A 50-year-old female with SCT presented to the Emergency Department with a three day history of diffuse abdominal pain, emesis and diarrhea. On questioning she admitted to recent cocaine use, and blood tests showed a total bilirubin of 2.5 mg/dL. Physical examination revealed a distended and diffusely tender abdomen. A Computed Tomography scan was performed and showed a splenic infarct, mildly dilated small bowel loops and moderate ascites. On hospital day 3, the patient became hemodynamically unstable, requiring endotracheal intubation and initiation of vasopressor support. Laboratory investigations revealed a severe lactic acidosis and a total bilirubin of 9.5 mg/dL. The patient was brought to the operating room and an exploratory laparotomy was performed. Operative findings were a diffusely ischemic appearing colon, infarcted spleen, and necrotic omentum. A splenectomy, omentectomy, subtotal colectomy and small bowel resection was carried out. Post-operatively, she developed multisystem organ failure including acute renal failure requiring continuous veno-venous hemodialysis, shock liver, cardiopulmonary failure and bilateral anterior cerebral artery and middle cerebral artery territory acute, nonhemorrhagic infarcts with prominent mass effect from bilateral internal carotid artery occlusions of sickled cells. Supportive care was withdrawn. Final pathology showed vascular congestion with sickled red blood cells throughout the omentum, spleen, colon and terminal ileum consistent with sickle crisis.There is limited data and few reports describing the impact of cocaine use in sickle cell patients. To our knowledge, there are no reports of cocaine-associated sickle cell crisis and sequelae in patients with SCT. We propose that cocaine induced vasoconstriction contributed to a cyclical cascade of tissue hypoxia, red blood cell sickling and vaso-occlusion which led to splenic, intestinal, omental and cerebral infarctions and acute multisystem organ failure. Cocaine use in sickle cell patients may elicit a crisis leading to a deadly cascade of events. It is important that clinicians are aware that patients with SCT can suffer sickle cell crises and recognize the risk factors associated with its development. This case illustrates a unique cause of multisystem organ failure in a sickle cell trait patient. A comprehensive history, physical examination and consideration of a sickle crisis in the differential diagnosis of the SCT population is vital and can optimally direct early recognition and management including intensive supportive care prior to developing a potentially irreversible course.

Bilateral atherosclerotic internal carotid artery occlusion causing acute bihemispheric infarctions

Multiple acute brain infarctions in both cerebral hemispheres involving the anterior circulation are uncommon (affecting less 1.0–6.0 % of acute stroke patients) and usually suggest an embolic mechanism, particularly one of aortic or cardiac origin [1–4]. Unilateral internal carotid artery (ICA) atherosclerotic lesions may rarely cause acute bihemispheric infarctions through crossflow in the anterior communicating artery with the contralateral anterior cerebral artery (ACA) territory being invariably involved in all described cases [4]. To the best of our knowledge there has been no report of bilateral extracranial atherothrombotic ICA occlusion causing acute bihemispheric infarctions involving both middle cerebral artery territories. A 73-year-old man with a history of hypertension, hypercholesterolemia and smoking presented with an acute right upper arm weakness that he noticed on awakening. Admission brain CT and electrocardiogram were normal. Neurological examination disclosed a mild left hemipareris and left-side visual neglect with an NIH Stroke Scale score (NIHSS-score) of 5 points. The patient underwent emergent carotid duplex evaluation showing multiple hyperechoic plaques in both common carotid arteries (CCA) and acute bilateral ICA occlusion (Fig. 1a, b). Transcranial Doppler examination showed (1) acute bilateral middle cerebral artery (MCA) occlusion with minimal flow (thrombolysis in brain ischemia grade I) in right and blunted flow (thrombolysis in brain ischemia grade II) in left MCA, (2) present collateral flow through reversed ophthalmic artery (OA) bilaterally and (3) absent collateral flow through posterior communicating arteries. The patient also underwent 30-min bilateral transcranial doppler monitoring that documented the presence of microembolic signals in both MCAs (Fig. 2). Acute reperfusion therapies including intravenous or intra-arterial thrombolysis as well as mechanical thrombectomy were withheld because of unknown time of stroke onset. Emergent echocardiography excluded the presence of cardiac thrombus and other source of cardiogenic embolism (including aortic arch dissection). He was treated with aspirin (325 mg) and enoxeparin (40 mg). Fourteen hours later, he became quadriplegic and lethargic (NIHSS-score 26 points). Repeat brain CT (performed after 12 h from the baseline CT) showed bilateral cortical infarctions (Fig. 1c, d) in both MCA territories (arrowheads). The patient expired the following day. Simultaneous occurrence of multiple infarcts in different arterial territories is a characteristic feature of cardioembolic stroke according to the findings of recent studies G. Tsivgoulis (&) I. Heliopoulos K. Vadikolias M. Flamouridou S. Tsakaldimi C. Piperidou Department of Neurology, University Hospital of Alexandroupolis, Democritus University of Thrace, Kapodistriou 3, Nea Xili, Alexandroupolis 68100, Greece e-mail: tsivgoulisgiorg@yahoo.gr

Bilateral Intracavernous Carotid Artery Occlusion Caused by Invasive Lymphocytic Hypophysitis

Lymphocytic hypophysitis is a rarely recognized disease that is characterized by inflammatory infiltration and destruction of the pituitary gland. The etiology of lymphocytic hypophysitis is still unclear, but an autoimmune pathogenesis has been advocated. In fact, histopathologic specimens reveal a diffuse infiltration of the hypophysis by CD3(+)CD4(+) T cells and CD20(+) plasma cells, and antipituitary antibodies are usually found in sera of affected patients. Although previous cases were found to be correlated only to pregnancy and the postpartum period, recent reports in men and women (without association with pregnancy) suggest a possibly higher prevalence of disease. We present the case of a 55-year-old woman affected by an unusually aggressive form of lymphocytic hypophysitis that infiltrated both cavernous sinuses causing bilateral internal carotid artery occlusion and acute ischemic stroke. Diagnosis was achieved with both a biopsy specimen of the pituitary gland and the detection of antipituitary antibodies. The prompt administration of steroid therapy was effective to obtain regression and stabilization of the disease, but both carotid arteries remained permanently occluded. The natural history of lymphocytic hypophysitis is unpredictable. It usually has a benign evolution, but in exceptional cases the inflammatory process may extend beyond the pituitary gland and infiltrate the surrounding structures. These extremely serious consequences highlight the importance of early diagnosis and treatment of this otherwise curable disease.

Abstract 2786: Moyamoya Syndrome Associated With Graves' Disease: Report Of 16 Cases

Background and purpose Moyamoya disease is a cerebrovascular disorder characterized by bilateral progressive stenosis and occlusion of terminal portions of internal carotid artery (ICA) accompanying by typical net-like collateral vessels. Patients with both the characteristic moyamoya vasculopathy and the associated conditions are categorized as moyamoya syndrome. These conditions include sickle cell disease, neurofibromatosis type 1, Down’s disease, cranial therapeutic irradiation and other rare diseases. Moyamoya syndrome associated with Graves’ disease has been rarely reported and the underlying coexisting mechanism remains unclear. The aim of this study is to identify the clinical and radiological findings of the patients with simultaneous diagnosis of moyamoya syndrome and Graves’ disease. Possible mechanisms predisposing these individuals to ischemic accidents are discussed. Methods We retrospectively identified 12 patients in Peking Union Medical College Hospital and 4 patients in 307 hospital of PLA between May 2000 and December 2010. All patients were female and mean age (range) was 35.13±12.34 years (11-57 years). The patients were diagnosed with Graves’ disease in endocrinology clinic which meet the full diagnostic criteria and no atherosclerotic factor was found in them. Moyamoya vasculopathy was definitely or probably diagnosed by digital subtract angiography or magnetic resonance angiography. The clinical characteristics and prognosis, laboratory data, vascular radiological characteristics were all collected. Results Stenosis or occlusion of bilateral distal ICA and/or proximal anterior /middle cerebral arteries was found in 13 patients. Three patients had unilateral distal ICA stenosis and abnormal collateral vessels. PCA stenosis was found in 2 patients. Fifteen patients presented with infarction or transient ischemic attack and one with dizziness. Interestingly, thyroid function tests demonstrated predominantly elevated thyroxine and suppressed thyroid stimulating hormone level in 15 patients when cerebrovascular accidents occurred. All patients received antithyroid therapy and two had recurrent ischemic attack after several months of drug withdrawal. Four patients underwent revascularization procedures after normalization of their hormonal conditions in 307 Hospital of PLA and their neurologic status has remained stable during follow-up. Conclusions: Compared with classical moyamoya disease, moyamoya syndrome associated Graves’ disease more commonly presented asymmetric stenosis or occlusion and PCA lesions. Cerebrovascular hemodynamic changes attributable to thyrotoxicosis might be responsible for ischemic attack and further studies are required to verify this hypothesis.

Bilateral hypoplasia of the internal carotid artery, presenting as a subarachnoid hemorrhage secondary to intracranial aneurysmal formation: a case report

IntroductionHypoplasia of the internal carotid artery is a rare congenital anomaly, with only 24 cases of bilateral internal carotid artery hypoplasia reported to date. Here, we present the case of a 48-year-old woman with bilateral internal carotid artery hypoplasia. She had a collateral circulation through the vertebrobasilar system; however given the high pressure flow she developed aneurysmal formations in the posterior communicating artery. To the best of our knowledge, only seven reported cases of internal carotid artery hypoplasia have been associated with intracranial aneurysmal formations.Case presentationA 48-year-old Sindhi woman from Karachi, Pakistan, presented to our emergency room with a sudden onset headache and was diagnosed as having a subarachnoid hemorrhage. Digital subtraction angiography revealed hypoplasia of her internal carotid artery bilaterally with an associated fusiform aneurysm of the posterior communicating artery. Our patient declined any operative intervention in view of the associated risks. She died of a rebleed six weeks after her initial presentation.ConclusionBilateral internal carotid artery occlusions can present with subarachnoid hemorrhages due to associated intracranial aneurysm formation. Prior knowledge about the possible existence of such angioarchitectural arrangement is mandatory for an early diagnosis. However, even with prompt diagnosis, management options with acceptable risk-benefit equations are still unavailable.

Endovascular treatment of ruptured wide-necked basilar tip aneurysm with Y stenting and coiling in a case of bilateral internal carotid artery occlusion with moyamoya disease

Endovascular treatment of ruptured wide-necked basilar tip aneurysm with Y stenting and coiling in a case of bilateral internal carotid artery occlusion with moyamoya disease

Coil Embolization of a Ruptured Basilar Tip Aneurysm Associated with Bilateral Cervical Internal Carotid Artery Occlusion: A Case Report and Literature Review

We report here on a rare case of a ruptured basilar tip aneurysm that was successfully treated with coil embolization in the bilateral cervical internal carotid artery (ICA) occlusions with abnormal vascular networks from the posterior circulation. A 43-year old man with a familial history of moyamoya disease presented with subarachnoid hemorrhage. Digital subtraction angiography demonstrated complete occlusion of the bilateral ICAs at the proximal portion and a ruptured aneurysm at the basilar artery bifurcation. Each meningeal artery supplied the anterior cranial base, but most of both hemispheres were supplied with blood from the basilar artery and the posterior cerebral arteries through a large number of collateral vessels to the ICA bifurcation as well as the anterior cerebral and middle cerebral arteries. The perfusion computed tomography (CT) scans with acetazolamide (ACZ) injection revealed no reduction of cerebral blood flow and normal cerebrovascular reactivity to ACZ. An abdominal CT aortogram showed no other extracranial vessel abnormalities. A ruptured basilar tip aneurysm was successfully treated with coil embolization without complications. Endovascular embolization may be a good treatment option with excellent safety for a ruptured basilar tip aneurysm that accompanies proximal ICA occlusion with vulnerable collateral flow.

Persistent trigeminal artery and its variants on MR angiography

A persistent trigeminal artery (PTA) is the most common carotid-vertebrobasilar anastomosis. A cerebellar artery that arises from the precavernous segment of the internal carotid artery (ICA) without connecting to the basilar artery is regarded as a PTA variant. Our study aimed to determine the incidence of PTA and its variants and classify them based on magnetic resonance (MR) angiography. We retrospectively reviewed cranial images of 3,626 patients who underwent MR angiography in our institution from April 1, 2007 through December 31, 2009. We ultimately reviewed and analyzed images of 3,491 patients (2,066 men, 1,425 women) after excluding 135 with unilateral or bilateral ICA occlusion or suboptimal image quality. We found 12 cases of PTA (7 men, 5 women; right 4, left 8; incidence; 0.34%) and 6 of PTA variants (3 men, 3 women; right 3, left 3; incidence; 0.17%). 11 of the 12 PTAs were lateral type; 1 was medial. In two of the lateral-type cases, the superior cerebellar artery (SCA) arose from the PTA. Among the six variants, the anterior inferior cerebellar artery (AICA) arose in five and the posterior inferior cerebellar artery (PICA), in one. On MR angiography, the incidence of PTA was 0.34% and of PTA variants, 0.17%. Left PTA was twice as frequent as right PTA, but with no statistical significance. Medial-type PTA was extremely rare. AICA arose in most PTA variants. Rarely, a lateral-type PTA gave rise to the cerebellar artery.

The macaroni sign

A 41-year-old woman was referred to radiology department for the evaluation of sudden paresis in the left side. Brain magnetic resonance imaging (MRI) showed multiple bilateral ischemic regions in the watershed areas. Also, the brain magnetic resonance angiography (MRA) showed bilateral internal carotid artery (ICA) occlusions at the level of the cervical ICA region. Both vertebral arteries were found to be enlarged (arrow) and the retrograde filling of the anterior circulation was observed (Fig. A). For the investigation and the differentiation of the bilateral carotid lesions, the color Doppler ultrasonography was obtained. This study showed homogenous, hypoechoic, circumferential wall thickening of both distal common carotid artery arteries (CCA). The thickening of the arteries wall were like ‘Macaroni’. The wall thickness was 0.17 cm (Fig. B). The tapering of both CCA and total oclusion of both ICA were seen. The carotid MRA revealed collateral circulation from the subclavian arteries to the ECA and 50% stenosis of the left CCA (arrow) and 70% stenosis of the right CCA at its origin. Vertebral arteries were also prominant and there were 50% narrowing in the mid portion of the left subclavian artery (Fig. C). The radiological diagnosis of the Takayasu’s arteritis (TA) was made and the patient was referred to the rheumatology clinic for further diagnosis and work-up.