Role of ATP-sensitive potassium channels and inflammatory response of basilar artery smooth muscle cells in subarachnoid hemorrhage of rabbit and immune-modulation by shikonin.

OBJECTIVE: To investigate the role of inflammatory response, oxidative damage and changes of ATP-sensitive potassium channels (sKATP) in basilar artery (BA) smooth muscle cells (SMCS) of rabbits in subarachnoid hemorrhage (SAH) model. METHODS: Time course studies on inflammatory response by real-time PCR, oxidative process and function of isolated basilar artery after SAH in New Zealand White rabbits were performed. Basilar artery smooth muscle cells (BASMCs) in each group were obtained and whole-cell patch-clamp technique was applied to record cell membrane capacitance and KATP currents. The morphologies of basal arteries were analyzed. Protective effect of shikonin were also determine by same parameters. RESULTS: Inflammatory cytokines levels were highest at 24h compare to 72h after SAH whereas the oxidative damage and cell death marker were at highest peak at 72h. Oxidative damage peak coincided with significant alterations in cell membrane capacitance, KATP currents and morphological changes in basilar arteries. Shikokin pretreatment attenuated early inflammatory response at 24h and associated oxidative damage at 72h. Finally, shikonin attenuated morphological changes in basilar arteries and dysfunction. CONCLUSION: Currents of ATP-sensitive potassium channels in basilar smooth muscle cells decreased after SAH by putative oxidative modification from immediate inflammatory response and can be protected by shikonin pretreatment.

Icariin ameliorates angiotensin II-induced cerebrovascular remodeling by inhibiting Nox2-containing NADPH oxidase activation.

Cerebrovascular smooth muscle cells (SMCs) hyperplasia is an important contributor to cerebrovascular remodeling during hypertension. The aim of present study was to investigate the effects of Icariin on cerebrovascular SMCs proliferation and remodeling and the underlying mechanisms. The results revealed that Icariin administration attenuated the enhanced basilar artery constriction in angiotensin II (AngII)-induced hypertension rat model, as well as the inhibition of basilar artery diameter reduction in response to AngII and phenylephrine. In addition, histological analyses showed that Icariin also significantly ameliorated basilar artery remodeling in AngII hypertensive rats. In human brain vascular SMCs (HBVSMCs), AngII-induced cell proliferation, migration and invasion were markedly inhibited by Icariin treatment. Moreover, Icariin treatment largely limited AngII-induced the increase of reactive oxygen species (ROS) production in HBVSMCs, which was closely associated with cell proliferation. Analysis of the mechanisms showed that Icariin decreased ROS production via inhibiting NADPH oxidase activity but not mitochondria-derived ROS production. Further, Icariin promoted Nox2 degradation and consequently reduced its protein expression. In conclusion, these findings demonstrate that Icariin attenuates cerebrovascular SMCs hyperplasia and subsequent remodeling through inhibiting Nox2-containing NADPH oxidase activation, suggesting Icariin may be a potential therapeutic agent to prevent the onset and progression of stroke.

Punica granatum L. Juice Attenuates Experimental Cerebral Vasospasm in the Rabbit Subarachnoid Hemorrhage Model: A Basilar Artery Morphometric Study and Apoptosis.

Background This study investigated the effect of Punica granatum L. (pomegranate) juice on the rabbit basilar artery in an experimental subarachnoid hemorrhage (SAH) model. Methods Eighteen adult male New Zealand white rabbits were randomly divided into three groups: a control group (n = 6), SAH group (n = 6), and SAH + treatment group (n = 6). Basilar artery diameter was measured with magnetic resonance angiography (MRA) in all groups at the beginning of the study. Experimental SAH was created by injecting autologous arterial blood into the cisterna magna. In the treatment group, the subjects were administered a daily dose of 30 ml/kg pomegranate juice via gastric gavage for 4 days after the SAH. The SAH group and SAH + treatment group underwent cerebral MRA after 72 hours. After a neurologic score assessment, all the animals were killed. The wall thickness and lumen area of the basilar artery were measured histometrically in all groups, and the apoptotic cell percentage in the artery was identified. The mean diameter of the basilar artery during MRA was measured. Results Pomegranate improved neurologic functions compared with the SAH group (p < 0.01). The mean basilar artery diameter on MRA in the SAH + treatment group was larger than in the SAH group and smaller than in the control group (p < 0.01 and p < 0.05, respectively). The mean vessel wall thickness value in the SAH + treatment group was lower than in the SAH group (p < 0.01), whereas there was no difference between the control and the SAH + treatment group (p > 0.05). The apoptotic cell rate in the SAH + treatment group was significantly lower than in the SAH group (p < 0.001). Evaluation of the basilar artery luminal area showed no difference between the three groups (p > 0.05). Discussion Pomegranate was shown to have a vasospasm- attenuating effect on the basilar artery in the rabbit SAH model for the first time in our study.

Sulforaphane activates the cerebral vascular Nrf2-ARE pathway and suppresses inflammation to attenuate cerebral vasospasm in rat with subarachnoid hemorrhage.

Nrf2-ARE pathway reportedly plays a protective role in several central nervous system diseases. No study has explored the role of the Nrf2-ARE pathway in cerebral vasospasm(CVS) after subarachnoid hemorrhage(SAH). The purpose of the present study was to investigate the activation of the cerebral vascular Nrf2-ARE pathway and to determine the potential role of this pathway in the development of CVS following SAH. We investigated whether the administration of sulforaphane (SFN, a specific Nrf2 activator) modulated vascular caliber, Nrf2-ARE pathway activity, proinflammatory cytokine expression, and clinical behavior in a rat model of SAH. A two-hemorrhage protocol was used to generate an animal model of SAH in male Sprague-Dawley rats. Administration of SFN to these rats following SAH enhanced the activity of the Nrf2-ARE pathway and suppressed the release of proinflammatory cytokines. Vasospasm was markedly attenuated in the basilar arteries after SFN therapy. Additionally, SFN administration significantly ameliorated two behavioral functions disrupted by SAH. These results suggest that SFN has a therapeutic benefit in post-SAH, and this may be due to elevated Nrf2-ARE pathway activity and inhibition of cerebral vascular proinflammatory cytokine expression.

Rhinacanthin-C, A Fat-Soluble Extract from Rhinacanthus nasutus, Modulates High-Mobility Group Box 1-Related Neuro-Inflammation and Subarachnoid Hemorrhage-Induced Brain Apoptosis in a Rat Model.

OBJECTIVE: High-mobility group box 1 (HMGB1) was shown to be a major extracellular mediator involved in relayed neuro-inflammation in animals after subarachnoid hemorrhage (SAH). It is of interest to examine the effect of rhinacanthin-C (RCT-C, C25H30O5) on pro-inflammatory cytokines/HMGB1 in an SAH-related early brain injury model. METHODS: A rodent double SAH model was used. RCT-C was administered orally at 100, 200, and 400 µmol/kg/day. Cerebral spinal fluid samples were obtained to assess interleukin (IL)-1ß, IL-6, IL-8, and tumor necrosis factor α using a real-time polymerase chain reaction. Basilar arteries were harvested and cerebral cortex was examined for HMGB1 mRNA and protein expression (western blot) and caspases (real-time polymerase chain reaction). An intrathecal injection of 1 ng of HMGB-1 recombinant protein was given in the 400 µmol/kg/day RCT-C plus SAH groups. RESULTS: The levels of IL-1ß, IL-6, and tumor necrosis factor α mRNA were significantly increased in animals subject to SAH, compared with the healthy controls, but were absent in the RCT-C groups. Cleaved caspase-9a as well as HMGB-1 mRNA and protein were significantly reduced in the 400 µmol/kg/day RCT-C treatment groups. Similarly, administration of RCT-C reduced HMGB-1 mRNA and protein expression (P <0.01). CONCLUSIONS: RCT-C exerts a neuroprotective effect by reducing cleaved caspase-3- and caspase-9a-related apoptosis. Decreased HMGB-1 mRNA and protein expression in the RCT-C groups corresponds to its anti-inflammatory effect. HMGB-1 recombinant protein administration impaired the neuroprotective and immunosuppressive effect of RCT-C. This finding lends credence that RCT-C modulates the HMGB-1-related pathway and attenuates brain apoptosis in the pathogenesis of SAH.

Double cisterna magna blood injection model of experimental subarachnoid hemorrhage in dogs.

Several animal subarachnoid hemorrhage (SAH) models have been proposed to study the etiology and treatment for cerebral vasospasm. We describe the experimental procedures of a canine double-hemorrhage model of SAH and discuss the pathophysiological parameters and occurrence of angiographic delayed cerebral vasospasm using magnetic resonance (MR) imaging and digital subtraction angiography. Autologous blood was injected twice on days 1 and 3 into the cerebellomedullary cistern of 36 female beagles. All animals showed delayed angiographic vasospasm in the vertebrobasilar arteries on day 7. The degree of vasospasm was 29-42 % of the arterial diameter. However, this model showed no symptomatic vasospasm or ischemic changes detected by MR imaging. This animal model can produce reproducible delayed vasospasm without detectable cerebral infarction on MR imaging. This model allows evaluation of the effect of treatment on delayed vasospasm in the same animals. The canine double-hemorrhage model of SAH is suitable for the quantitative and chronological study of delayed angiographic vasospasm, but not for investigating early brain injury and delayed cerebral ischemia.

The ferric iron chelator 2,2'-dipyridyl attenuates basilar artery vasospasm and improves neurological function after subarachnoid hemorrhage in rabbits.

We investigated the efficacy of the ferrous iron (Fe(2+)) chelator 2,2'-dipyridyl (DP) to attenuate cerebral vasospasm after subarachnoid hemorrhage (SAH). Thirty-six New Zealand white rabbits were randomly assigned to four groups: untreated control, SAH, SAH + dimethyl sulfoxide (DMSO) vehicle, and SAH + DP. SAH was induced by injection of autologous blood into the cisterna magna and then DP or vehicle was infused into the cistern magna for 5 days (20 mg/kg/day or an equal volume of DMSO). Neurological deficit score (NDS) was used to assess neurological function and cerebral angiography to measure basilar artery (BA) diameter following SAH. TUNEL staining was used to detect BA endothelial cell apoptosis, and immunohistochemistry and Western blotting to assess changes in caspase-3 protein levels 5 days post-SAH. The SAH + DP group had a significantly larger mean BA diameter and lower mean NDS post-SAH compared to the SAH + DMSO and SAH groups (p < 0.05). TUNEL-positive cell numbers and caspase-3 levels were significantly reduced in BA endothelial cells of the SAH + DP group as compared to the SAH and SAH + DMSO groups (p < 0.05). The iron chelator DP reduced vasospasm and neurological sequelae in rabbits, likely by chelating the Fe(2+) in oxyhemoglobin and reducing oxidative stress-induced endothelial cell apoptosis.

Craniocervical arterial dissections as sequelae of chiropractic manipulation: patterns of injury and management.

OBJECT: Chiropractic manipulation of the cervical spine is a known cause of craniocervical arterial dissections. In this paper, the authors describe the patterns of arterial injury after chiropractic manipulation and their management in the modern endovascular era. METHODS: A prospectively maintained endovascular database was reviewed to identify patients presenting with craniocervical arterial dissections after chiropractic manipulation. Factors assessed included time to symptomatic presentation, location of the injured arterial segment, neurological symptoms, endovascular treatment, surgical treatment, clinical outcome, and radiographic follow-up. RESULTS: Thirteen patients (8 women and 5 men, mean age 44 years, range 30-73 years) presented with neurological deficits, head and neck pain, or both, typically within hours or days of chiropractic manipulation. Arterial dissections were identified along the entire course of the vertebral artery, including the origin through the V(4) segment. Three patients had vertebral artery dissections that continued rostrally to involve the basilar artery. Two patients had dissections of the internal carotid artery (ICA): 1 involved the cervical ICA and 1 involved the petrocavernous ICA. Stenting was performed in 5 cases, and thrombolysis of the basilar artery was performed in 1 case. Three patients underwent emergency cerebellar decompression because of impending herniation. Six patients were treated with medication alone, including either anticoagulation or antiplatelet therapy. Clinical follow-up was obtained in all patients (mean 19 months). Three patients had permanent neurological deficits, and 1 died of a massive cerebellar stroke. The remaining 9 patients recovered completely. Of the 12 patients who survived, radiographic follow-up was obtained in all but 1 of the most recently treated patients (mean 12 months). All stents were widely patent at follow-up. CONCLUSIONS: Chiropractic manipulation of the cervical spine can produce dissections involving the cervical and cranial segments of the vertebral and carotid arteries. These injuries can be severe, requiring endovascular stenting and cranial surgery. In this patient series, a significant percentage (31%, 4/13) of patients were left permanently disabled or died as a result of their arterial injuries.

Comparison of intrathecal cilostazol and nimodipine treatments in subarachnoid hemorrhage: an experimental study in rabbits.

OBJECTIVE: intrathecal administration of calcium channel antagonists has been proposed to reduce cerebral vasospasm (CVS) in animal subarachnoid hemorrhage (SAH) models. Also, delayed CVS treatment model with oral administration of cilostazol can be seen in the literature. METHODS: in this study, 25 male New Zealand white rabbits were randomly assigned to five groups: control, SAH only, SAH/nimodipine, SAH/cilostazol, SAH/vehicle. The animals' basilar arteries were sectioned from four separate zones and four sections were obtained from each rabbit. Basilar artery luminal section areas were measured by using SPOT for windows Version 4.1 computer program. RESULTS: basilar artery luminal section areas in SAH/ nimodipine and SAH/ cilostazol groups were significantly higher than SAH only group (P < 0.05). CONCLUSION: phosphodiesterase 3 inhibitor cilostazol has vasodilatory effects without affecting cerebral blood flow. Nimodipine is a calcium channel blocker and is still used in vasospasm therapy either oral or intravenously. This study demonstrates that prophylactic bolus intrathecal administration of either cilostazol or nimodipine equally prevents SAH-associated CVS in an animal model. We therefore propose that cilostazol is a candidate for clinical trials in the treatment of delayed vasospasm.

Comparison of intrathecal dotarizine and nimodipine treatments in cerebral vasospasm after subarachnoid hemorrhage: an experimental study in rabbits.

BACKGROUND: cerebral vasospasm (CVS) is one of the most considerable complications of subarachnoid hemorrhage (SAH). The aim of this study was to assess and to compare the ability of intrathecal dotarizine and nimodipine to prevent and treat vasospasm in a rabbit model of subarachnoid hemorrhage. METHOD: thirty male New Zealand white rabbits weighing 2,500-3,000 g were allocated into five groups randomly. The treatment groups were as follows: Control, only SAH, SAH/Dotarizine, SAH/Nimodipine, SAH/Vehicle. Forty-eight hours after SAH injection, all animals underwent femoral artery catheterization procedure by open surgery under anesthesia and angiography performed for each animal in the fifth day just before sacrifice. FINDINGS: basilar artery vessel diameters are measured by angiography. Basilar artery vessel diameters and luminal sectional areas are measured in pathology slides. There was a statistically significant difference between the mean basilar artery cross-sectional areas and the mean arterial wall thickness measurements of the control and SAH-only groups (p < 0.05). CONCLUSIONS: these findings demonstrate that calcium channel blocker dotarizine has marked vasodilatory effect in an experimental model of SAH in rabbits. Nimodipine is an effect-proven agent in CVS, but dotarizine may take place of it.

Comparison of intrathecal flunarizine and nimodipine treatments in cerebral vasospasm after experimental subarachnoid hemorrhage in rabbits.

BACKGROUND: the aim of this study was to assess and to compare the ability of intrathecal flunarizine and nimodipine to prevent vasospasm in a rabbit model of subarachnoid hemorrhage (SAH). METHOD: forty male New Zealand white rabbits were allocated into 5 groups randomly. The treatment groups were as follows: (1) control (no SAH [n = 8]), (2) SAH only (n = 8), (3) SAH plus vehicle (n = 8), (4) SAH plus nimodipine (n = 8), and (5) SAH plus flunarizine (n = 8). Before sacrifice, all animals underwent femoral artery catheterization procedure by open surgery under anesthesia and angiography performed for each animal. FINDINGS: there was a statistically significant difference between the mean basilar artery cross-sectional areas and the mean arterial wall thickness measurements of the control and SAH-only groups (p < 0.05). Basilar artery vessel diameter and luminal section areas in group 4 were significantly higher than in group 2 (p < 0.05). Basilar artery vessel diameter and basilar artery luminal section areas in group 5 were significantly higher than in group 2 (p < 0.05).Basilar artery vessel diameter and basilar artery luminal section areas in group 5 were significantly higher than in group 4 (p < 0.05). CONCLUSIONS: these findings demonstrate that flunarizine has marked vasodilatatory effect in an experimental model of SAH in rabbits.

Treatment with ginsenoside rb1, a component of panax ginseng, provides neuroprotection in rats subjected to subarachnoid hemorrhage-induced brain injury.

OBJECTIVE: recent trials have shown Ginsenoside Rb1 (GRb1), an active component of a well known Chinese medicine Panax Ginseng, plays a significant role in improving the complications seen after an ischemic brain event. In the present study, we investigated the use of GRb1 as a treatment modality to reduce brain edema, reduce arterial vasospasm, and improve neurobehavioral function after subarachnoid hemorrhage-induced brain injury (SAH) in rats. METHOD: male Sprague-Dawley rats weighing between 250 and 300 g were randomly assigned to three groups: (1) Sham group (n = 10), (2) Vehicle group (SAH + no treatment; n = 12); (3) Treatment group (SAH + GRb1 treatment at 20 mg/kg; n = 11). Subarachnoid hemorrhage was induced using the modified double hemorrhage model followed by treatment administration intravenously. Post-operative assessment included neurobehavioral testing using the spontaneous activity scoring system, brain water content, and histological examination of the basilar artery. RESULTS: post-operative findings indicated treatment with GRb1 had significantly reduced brain edema and improved neurobehavioral functioning. In addition, histological examination revealed a significant reduction in basilar artery vasospasm and lumen thickness with treatment. CONCLUSION: the results of the study suggest that GRb1 treatment reduces brain edema, improves neurobehavioral function, and blocks vasculature thickening and spasm after SAH in rats. Given the novelty of the study, further research will be needed to confirm the benefits of treatment and mechanisms behind neuroprotection.

The effects of intrathecal nicergoline and nimodipine in cerebral vasospasm: an experimental study in rabbits.

BACKGROUND: the aim of this study was to assess and to compare the ability of intrathecal nicergoline and nimodipine in prevention of cerebral vasospasm in a rabbit model of subarachnoid hemorrhage (SAH). METHOD: twenty male New Zealand white rabbits were allocated into four groups randomly. Subarachnoid hemorrhage was induced by injecting autologous blood into the cisterna magna. The treatment groups were as follows: (1) control [no SAH (n = 5)], (2) SAH only (n = 5), (3) SAH plus nimodipine (n = 5), and (4) SAH plus nicergoline (n = 5). FINDINGS: there was a statistically significant difference between the mean basilar artery cross-sectional areas and the mean arterial wall thickness measurements of the control and SAH-only groups (p < 0.05). Basilar artery vessel diameter and luminal section areas in group 3 were significantly higher than in group 2 (p < 0.05). Basilar artery vessel diameter and basilar artery luminal section areas in group 4 were significantly higher than in group 2 (p < 0.05). There was no significant difference between basilar artery vessel diameter and basilar artery luminal section areas in group 3 and group 4. CONCLUSIONS: these findings demonstrate that intrathecal nicergoline has a vasodilatatory effect in an experimental model of SAH in rabbits but not more than that of nimodipine.

Ginsenoside Rbeta1 reduces neurologic damage, is anti-apoptotic, and down-regulates p53 and BAX in subarachnoid hemorrhage.

Stroke is the second leading cause of death worldwide and the number one cause of adult disability in the United States and Europe. A subtype of stroke, subarachnoid hemorrhage (SAH), accounts for 7% of all strokes each year and claims one of the highest mortalities and morbidities. Many therapeutic interventions have been used to treat brain injury following SAH but none have reached the level of effectiveness needed to clinically reduce mortality. Ginsenoside Rb1 (GRb1), a major component of the Chinese traditional medicine Panax Ginseng, has been shown to reduce ischemic brain injury and myocardial injury via anti-apoptotic pathways. In the present study, we investigated the use of GRb1 on SAH induced brain injury in rats. Four groups were used: sham, vehicle (SAH), low dose treatment (SAH+ 5mg/kg GRb1), and high dose treatment (SAH+ 20mg/kg GRb1). Post assessment included wall thickness and mean cross-section area of basilar artery were measured for evaluating cerebral vasospasm, Evans blue extravasations to assess blood brain barrier (BBB) permeability, immunohistochemistry and Western Blot analysis looking for specific pro-apoptotic markers, and tunnel staining for cell death assessment. In addition, mortality, neurological function and brain edema were investigated. The results showed that high dose GRb1 treatment significantly enlarged mean cross-sectional area and decreased wall thickness of basilar artery, reduced neurological deficits, brain edema, BBB disruption, and TUNEL positive cell expression. Same time, we found that the proteins expression of P53, Bax and Caspase-3 were significantly reduced, whereas the expression of bcl-2 was up-regulated in Rb1 treatment. The results of this study suggest that GRb1 could relieve cerebral vasospasm and potentially provide neuroprotection in SAH victims. The underlying mechanisms may be partly related to inhibition of P53 and Bax dependent proapoptosis pathway. More studies will be needed to confirm these results and determine its potential as a long term agent.

Experimental model of brainstem stroke in rabbits via endovascular occlusion of the basilar artery.

BACKGROUND: Basilar artery thrombosis remains a significant clinical problem, and no reproducible animal model has been established to study the stroke within the vertebrobasilar distribution. We report a study designed to pilot test a novel model of brainstem stroke in rabbits, created by selective endovascular occlusion of the basilar artery. METHODS: Basilar artery occlusion was induced in 8 New Zealand white rabbits by injection of the autologous clot through the microcatheter positioned within the distal vertebral artery. Animals were divided into subgroups (I and II) based on the length of produced ischemia (3 and 6 hours, respectively). Magnetic resonance (MR) imaging of the brain and MR angiography of the intracranial vessels were performed before the procedure, and at 3 hours after induced ischemia for groups I and II, with continued imaging up to 6 hours for group II, with diffusion-weighted images acquired approximately every 30 minutes. Animals were killed at the end of the 3-hour (group I) or 6-hour (group II) ischemia time. RESULTS: Brainstem stroke was successfully induced in all animals, with pathological changes documented in all cases. The earliest changes of ischemia on MR diffusion-weighted images were identified at only 4.5 hours of basilar artery occlusion. CONCLUSION: These results suggest that a reproducible model of brainstem stroke can be induced in rabbits using selective endovascular occlusion of the basilar artery. The availability of such a model, integrated with state-of-the-art imaging techniques, holds promise for preclinical investigations of emergent therapeutic approaches in stroke.

Mechanism of tuberothalamic infarction.

BACKGROUND AND PURPOSE: The tuberothalamic artery (TTA), one of the arteries supplying the paramedian thalamic area, is peculiar because it originates from the posterior communicating artery (p-comA), which connects the vertebrobasilar and carotid systems. METHODS: From Stroke Registry, 23 consecutive patients with an acute infarction involving the TTA were selected. We investigated the mechanism of TTA infarction. RESULTS: Fourteen of 23 patients (61%) had coexisting infarctions outside the TTA territory (carotid in three, vertebrobasilar in seven, and both carotid and vertebrobasilar arteries in four patients). Coexisting lesions were most common in the posterior thalamoperforating arterial territory (seven patients). Eleven out of 14 patients (79%) with coexisting lesions had embolic sources from the heart or proximal atherosclerotic arteries, and cardioembolism was the most common mechanism. However, eight of the nine patients with isolated tuberothalamic lesions were classified as small vessel occlusions. More patients with embolic sources had visible p-comA or fetal-type posterior cerebral arteries. The vertebrobasilar arterial system played a more dominant role in developing tuberothalamic infarction than the carotid arterial system. CONCLUSIONS: Isolated TTA infarctions are rare and mostly because of small vessel occlusion. Patients with coexisting infarctions outside TTA territory usually have an embolic source, predominantly vertebral artery atherosclerosis.

The effect of traditional herbal medicines; Uyakujunkisan on trigeminal neuralgia in an elderly patient--a case report and literature review.

This report describes the successful treatment of a 72-year-old female with refractory trigeminal neuralgia using a traditional herbal medicine, Uyakujunkisan (UJS). The case report is of a 65-year-old female who developed right-sided trigeminal neuralgia that was partially responsive to carbamazepine (CZ). The pain gradually increased in intensity and at 72 years of age she presented for herbal medicine therapy. Cranial MRI demonstrated vascular compression of the right trigeminal nerve at the cerebellopontine angle by the anterior inferior cerebellar artery. Although microvascular decompression was considered, UJS was prescribed after informed consent. After 3 weeks of treatment with UJS, dramatic improvement of symptoms permitted a decrease in CZ dose.

Bilateral occipital infarcts associated with carotid atherosclerosis and a persistent hypoglossal artery.

The persistent hypoglossal artery (PHA) is the second most common persistent embryological carotid-basilar connection and usually represents an incidental finding in cerebral arteriograms. The hypoglossal artery connects the primordial carotid artery with the longitudinal neural arteries, which later form the basilar artery. The PHA leaves the internal carotid artery as an extracranial branch, enters the skull through the anterior condyloid foramen, the hypoglossal canal and joins the caudal portion of the basilar artery. We report magnetic resonance and digital subtraction angiography findings in the first case of bilateral occipital infarctions associated with PHA and carotid atherosclerosis. The probable mechanism underlying bilateral occipital infarcts was embolism from the carotid territory to the posterior cerebral arteries. PHA may present a challenge in diagnosis and management of patients with carotid atherosclerosis and vertebrobasilar ischemia.