Carotid artery–hypoglossal nerve relationships in the neck: an anatomical work

Abstract

Objective: To review the surgical anatomy of the hypoglossal nerve in the neck, analyse its relationship to surrounding structures and offer landmarks to identify the nerve during carotid endarterectomy.

Method: The carotid bifurcation, external carotid artery, internal carotid artery, extracranial part of the hypoglossal nerve, occipital artery, sternocleidomastoid artery and surrounding neurovascular structures were dissected and studied on 15 formalin-fixed adult cadaver heads (30 sides and 15 pairs) via a surgical microscope. Landmarks for the hypoglossal nerve and measurements of its distance from the carotid bifurcation are described. The relationship between the sternocleidomastoid artery and the occipital artery is also described.

Results: The distance from the carotid bifurcation to the point at which the hypoglossal nerve crosses over the internal carotid artery was variable, ranging from 3.89 to 37.03 mm (mean, 20.95 ± 7.78 mm). The distance from the bifurcation to the point at which the hypoglossal nerve crosses over the external carotid artery ranged from 2.63 to 29.43 mm (mean, 15.33 ± 7.86 mm; Table 1). The sternocleidomastoid artery had a very characteristic course and close relationship with the hypoglossal nerve. Ascending for a short distance in a cranial direction, it crossed over the hypoglossal nerve and then descended toward the sternocleidomastoid muscle. The sternocleidomastoid artery originated from the occipital artery (33.4%), the external carotid artery–internal carotid artery junction (30%), the external carotid artery itself (30%) or even the lingual artery (6.6%).

Conclusion: The relationship between the hypoglossal nerve and the carotid bifurcation is quite variable, and this explains the vulnerability of the nerve during carotid endarterectomy. The sternocleidomastoid artery is a good landmark for identifying the hypoglossal nerve. If there is exact anatomical knowledge about the relationship between the sternocleidomastoid artery and the hypoglossal nerve, the incidence of nerve injuries during carotid endarterectomy can be minimized.     

Acute effect of calcium citrate on serum calcium and cardiovascular function

Calcium supplements have been associated with an increased risk of cardiovascular events. However, the validity of these findings has been questioned. A major concern is that the mechanism underlying an increase in cardiovascular events has not been demonstrated. Calcium initiates cardiac and vascular contraction following influx of calcium into cardiac and smooth muscle from extracellular fluid. We have investigated whether the acute rise in serum calcium following calcium supplement administration is associated with adverse changes in cardiovascular function. In an open interventional study, we recruited 25 volunteers (16 female, age 60.3 ± 6.5 years, body mass index 25.7 ± 2.7 kg/m²) from the community who were not taking calcium supplements. Participants were studied before and 3 hours after a single oral dose of 1000 mg calcium citrate. We assessed well‐validated markers of arterial stiffness (pulse wave velocity [PWV]), arterial wave reflection (augmentation index [AIx]), and myocardial perfusion (subendocardial viability ratio [SEVR]) by pulse wave analysis and endothelial function (reactive hyperemia index [RHI]) by peripheral arterial tonometry. Total and ionized serum calcium were acutely increased by 0.10 ± 0.07 and 0.06 ± 0.03 mmol/L, respectively, 3 hours after calcium citrate administration (p < 0.0001 for both comparisons). Following administration of calcium citrate there was a fall in AIx from a median of 29.7% (23.8% to 34.0%) to 26.4% (22.7% to 34.0%, p = 0.03) and an increase in SEVR from 163% (148% to 174%) to 170% (149% to 185%, p = 0.007). PWV and RHI were not significantly altered. The change in total calcium was negatively correlated with the change in AIx (r = –0.48, p = 0.02). In summary, the acute increase in serum calcium following calcium supplement administration is associated with reduced arterial wave reflection and a marker of increased myocardial perfusion. If maintained long‐term, these changes would be expected to reduce cardiovascular risk. Acute serum calcium–mediated changes in these parameters of cardiovascular function are unlikely to underlie an association between calcium supplementation and cardiovascular events. © 2013 American Society for Bone and Mineral Research     

Direct percutaneous carotid artery stenting with distal protection: technical case report

Abstract

We describe the technique of percutaneous carotid artery stent placement with distal protection in a patient in whom marked innominate artery ectasia prevented transfemoral access to the right common carotid artery. After induction of general anesthesia, ultrasound was used to guide direct puncture of the common carotid artery followed by the introduction of a 5 French sheath. A GuardWire distal protection balloon (Medtronic, Santa Rosa, CA) was placed distal to the lesion and deployed at nominal diameter. A balloon-expandable stent was deployed without difficulty. Following stent placement, angiography demonstrated improved flow in the entire right carotid artery territory. There were no complications related to cervical soft tissue damage or clinical embolism. The patient tolerated the procedure well and was discharged in 24 hours. Direct carotid access is acceptable in select patients in whom a transfemoral, brachial, or transradial approach is technically difficult. The use of distal cerebral protection devices may reduce cerebral embolism associated with these procedures.     

High plasma concentration of brain natriuretic peptide in patients with ruptured anterior communicating artery aneurysm

Abstract

The purpose of this study is to investigate the mechanism of increased atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in patients with subarachnoid hemorrhage due to ruptured aneurysms. ANP and BNP plasma concentrations were measured by immunoradiometoric assay in 53 patients at the day of onset of ruptured aneurysm, the correlation between values of increased ANP or BNP, and sex, age, location of ruptured aneurysm, degree of SAH, and severity of WFNS were statistically studied. The concentration of BNP in ruptured anterior communicating artery aneurysm (A-com) shows a significant elevation compared with other site aneurysms (p = 0.0007). The patients classified as WFNS Grade V, show a significantly higher concentration of BNP, compared with the patients classified as Grade I–IV (p=0.01). It is concluded that the hypersecretion of BNP, but not ANP, is caused by direct mechanical damage at the anterior hypothalamus by ruptured A-com aneurysm and a higher increase of BNP is also observed in cases suffering from severe neurological deficit.     

Endovascular management of symptomatic vertebral artery dissection achieved using stent angioplasty and emboli protection device

Abstract

Extracranial vertebral artery (VA) dissection may lead to significant arterial stenosis, occlusion, or pseudoaneurysm formation with subsequent hemodynamic and embolic infarcts. To prevent thromboembolic complications, anticoagulation with intravenous heparin followed by oral warfarin has been recommended for all patients with acute dissections, regardless of the type of symptoms, unless there are contra-indications. Nevertheless, anticoagulation is not innocuous, may be contra-indicated or may be ineffective to prevent symptoms or dissection progression. Because it is effective and less invasive than other surgical procedures, endovascular treatment of VA dissection has recently attracted interest. We present a case of a traumatic VA dissection, presenting with multiple embolic infarctions that was managed with protected stent-assisted angioplasty. Protected stent-assisted VA angioplasty has not been previously reported and appears to be a safe, effective and immediate method of restoring vessel lumen integrity and should be considered in the therapy of selected cases of VA dissection.     

Obliteration of bilateral dissecting aneurysms of the vertebral arteries following repeated subarachnoid hemorrhage: A case report

Abstract

A 51-year-old man presented with loss of consciousness when he underwent urological examination at another hospital. CT scans showed subarachnoid hemorrhage, and cerebral angiography showed bilateral dissecting aneurysms of the vertebral arteries. Following ventricular drainage, the lesion was managed conservatively with blood pressure control but again ruptured on day 8. Cerebral angiography revealed narrowing of both the dissecting aneurysms. On day 11, the right vertebral artery had been spontaneously obliterated and the right dissecting aneurysm was filled in a retrograde fashion via the left vertebral artery. Proximal occlusion of the right vertebral artery was performed to prevent recanalization. Two months later, cerebral angiography revealed that both vertebral arteries were obliterated and the basilar artery and right posterior inferior cerebellar artery were filled via the right posterior communicating artery. The present case demonstrated that the hemodynamic status of bilateral dissecting aneurysms of the vertebral artery changed variably indicating the necessity of careful angiographic observation.     

Vasospasm following subarachnoid hemorrhage: Evidence against functional upregulation of Rho kinase constrictor pathway

Abstract

This study tested the hypothesis that vasospasm due to subarachnoid hemorrhage involves the functional upregulation of Rho kinase. Spasm of the rabbit basilar artery was achieved using a double hemorrhage model, which we previously demonstrated was endothelin-1 dependent. In situ effects of agents were determined by direct measurement of vessel diameter following their suffusion in a cranial window. Y-27632, a Rho kinase inhibitor, relaxed the spasm. However, relaxations to Y-27632 were not significantly greater in endothelin-1 constricted spastic vessels initially relaxed with the endothelin converting enzyme inhibitor, phosphoramidon, as compared to endothelin-1 constricted control vessels. These results suggest that, at least in the rabbit double subarachnoid hemorrhage model, vasospasm does not involve the functional upregulation of Rho kinase. [Neurol Res 2002; 24: 392-394]     

清开灵注射液治疗原发性肝癌介入后综合征

[目的]观察清开灵注射液治疗原发性肝癌行经肝动脉化疗栓塞（TACE）介入后综合征的疗效。[方法]将46例行经肝动脉灌注化疗栓塞的原发性肝癌患者,随机分库药组和对照组。于ATXE治疗后当天,中药组予清开灵注射液40mL静脉滴注,1次/d。连续7d;对照组予抗生素静脉滴注。[结果]中药组在减轻发热、腹痛、恶心呕吐、便秘等副作用的程度以及在缩短TACE后毒副反应持续时间方面,均优于对照组,中药组在TACE后有显著的护肝降酶作用,能提高原发性肝癌患者对TACE所致肝功损害的耐受性。[结论]清开灵注射液对原发性肝癌行TACE治疗后的栓塞综合征有较好的疗效。     

肾动脉平面以上主动脉瘤的治疗

目的　探讨肾动脉平面以上主动脉瘤 (AAARA)的治疗经验。方法　回顾性分析12 0例AAARA的临床资料。结果　夹层动脉瘤 84例 ,真性动脉瘤 2 7例 ,假性动脉瘤 9例。病变累及全程主动脉者 12例 ,主动脉弓 9例 ,胸降主动脉 2 0例 ,降胸至腹主动脉分叉部或以下 43例 ,胸腹主动脉 2 5例 ,涉及内脏动脉 11例。施行手术或支架型人工血管微创治疗74例。术中至术后 30d内死亡 11例 (14 9% )。术后并发症 9例 ,无截瘫、偏瘫或卒中发生。 16例腔内治疗病人中无严重并发症或死亡者。随访 48例 ,随访时间 1个月～ 15年 ,5例死亡 (10 4% )。保守治疗 46例中 ,44 1%死于瘤体破裂或其它严重并发症。结论　AAARA开胸手术仍存在着很大风险 ,而多种多样的支架型人工血管腔内置放和腔内开窗治疗有着良好前景 ,腔内血管外科技术将成为治疗AAARA的主流。     

Physiological levels of β-amyloid induce cerebral vessel dysfunction and reduce endothelial nitric oxide production

Abstract

β-amyloid (Aβ), the major component of senile plaques in Alzheimer's disease (AD), normally circulates in the blood at nanomolar levels but is elevated in AD. Previous studies have found that high concentrations (10^-5 -10^-4 M) of Aβ result in neuronal cell death. Here we show that physiological levels of soluble Aβ can induce dysfunction in perfused rat cerebral vessels and in cultured endothelial cells. At concentrations of 10^-9 -10^-6 M, Aβ induced a significant concentration-dependent reduction of NO production in endothelial cells. At 10^-8 M, Aβ significantly decreased the sensitivity of cerebral vessels to acetylcholine (ACh), an endothelium dependent vasodilator. At 10^-7 M and higher concentrations, Aβ significantly reduced the maximum response of vessels to ACh, and induced significant endothelial cell death. Aβ (10^-9 -10^-5 M) did not cause any detectable change in nitric oxide synthase levels. The results suggest that a modest increase in the concentration of Aβ above its normal physiological level in the circulation, as found in the early stages of AD, results in decreased NO production and vessel sensitivity to endothelium-dependent vasodilation that could lead to constricted blood vessels and ischemia in the surrounding tissue. Further increases in Aβ concentration, which may occur in the later stages of AD, result in cell death and decreased maximum vasodilator response of cerebral vessels. [Neurol Res 2001; 23: 506-512]