Cerebrovascular reactivity in multiple sclerosis patients

A close relationship between multiple sclerosis (MS) lesions and the cerebral vasculature has long been recognised. Some studies have suggested that vascular endothelial cell activation might be an early event in the evolution of MS, and demyelisation may have an ischemic basis in this condition. Hypoxia caused by breath holding (BH) results in autoregulatory vasodilatation, and an increase in CBF to the cortex. The increased CBF can be evaluated by transcranial Doppler (TCD), and can provide information about the vascular integrity. In this study, we aimed to examine the vascular integrity and assess the vasomotor reactivity of MS patients in response to BH in different activation phases of the disease by means of TCD. We studied 12 patients with clinically diagnosed relapsing remitting (RR) MS, according to the Poser criteria. The initial TCD examination was performed in the first two days of an acute exacerbation of disease and prior to any treatment. The second test was performed just after iv methylprednisolone (IVMP) treatment, and the third examination occurred one month later, when the patient was in the remission phase. A group of 11 healthy subjects was also examined by TCD as control. Blood flow velocities were recorded during 30 seconds of normal breathing and 15 seconds BH. Vasomotor reactivity was calculated as a ratio of difference of cerebral flow velocities during BH. There were no significant vasomotor reactivity differences between the controls (55.7%) and the patients during attacks (46.5%), as well as after treatment (48.3%) and during attack free periods (50.9%). There were also no significant changes amongst the patients groups throughout the study. In this study, in different disease activity stages, we observed non-significant cerebrovascular vasomotor reactivity difference between the RRMS patients and the healthy controls, although it was slightly lower in the MS patients. This observation suggests that cerebrovascular reactivity is normal in different disease activity levels.     

Pure homonymous hemianopia due to anterior choroidal artery territory infarction

The most consistently observed neurological deficits in the anterior choroidal artery (AChA) territory infarction are pure motor or sensorimotor syndromes. Visual field defects and higher cortical dysfunction are occasionally accompanied, but pure homonymous hemianopia without motor and sensory symptom has never been reported yet. We present 2 patients with pure homonymous hemianopia, whose MRI disclosed cerebral infarction in the well-known territory of the AChA. In most patients with ischemic stroke, pure homonymous hemianopia indicates infarction in the posterior circulation, particularly in the posterior cerebral artery territory. However, the present cases provide evidence that it can also be caused by infarction in the anterior circulation, i.e. the AChA.     

Systemic atherosclerosis in patients with perforating artery territorial infarction

Background: Perforating artery territorial infarction (PAI) is usually a small artery disease (SAD). However, it may also result from branch artery occlusion or arterial embolism from the proximal atherosclerotic lesions. We hypothesized that patients with PAI caused by a SAD may have a distinct pattern of systemic artery involvement from those with PAI caused by large artery diseases. Methods: We investigated retrospectively 329 consecutive patients with PAI who had angiographic studies. Patients were grouped according to the presence or absence of atherosclerosis in the parent artery or relevant artery: no arterial lesion (NAL), relevant artery atherosclerosis (RAA) and parent artery atherosclerosis (PAA). The relevant artery was defined as any artery which can cause index stroke. The parent artery was defined as an original artery that branches out and forms small artery which was responsible for index PAI. Systemic evidence of atherosclerosis and risk factors were compared. Results: Of the 329 patients with PAI, 109 had RAA, 45 had PAA and 175 had neither RAA nor PAA. There were no differences amongst the groups in the classic risk factors for atherosclerosis. Evidence of atherosclerosis in arterial beds other than the relevant artery to the infarction (other cerebral arteries, coronary arteries, descending aorta and peripheral arteries) was significantly lower in the NAL group (49.7%) than in either the PAA group (88.9%) or RAA group (93.6%). Conclusions: Perforating artery territorial infarction with RAA or PAA when compared to PAI without atherosclerosis showed different involvement patterns of systemic atherosclerosis, suggesting potentially different aetiological mechanisms.     

表现为孤立性眩晕的大脑中动脉穿支梗死

目的孤立性眩晕主要见于前庭周围性病变,罕见于大脑中动脉(MCA)穿支脑梗死,本文探讨MCA穿支梗死出现孤立性眩晕与头晕的临床特征。方法报道3例表现为孤立性眩晕和头晕的MCA穿支急性腔隙性脑梗死患者的临床表现、影像学资料,同时通过PubMed检索之前报道的病例,回顾总结其临床特征。结果包括文献共5例表现为眩晕和头晕的MCA穿支梗死病例。3例表现为孤立性眩晕和头晕,1例表现为持续性头晕伴随短暂性言语不清,1例有轻偏瘫,2例有眼球震颤。眩晕与头晕严重程度均为中度,经治疗后眩晕和头晕多在病程7 d内完全缓解。4例梗死灶位于左侧内囊或放射冠区,1例位于右侧放射冠。颈部及头部增强血管成像有2例显示右侧椎动脉纤细狭窄,4例完成了头部增强CTA检查均提示前循环血管正常。本文3例患者在核磁共振成像(MRI)检查证实为急性腔隙性脑梗死之前,均未有明确诊断。结论 MCA穿支脑梗死可以表现为孤立性眩晕和头晕,严重程度较轻,持续时间通常数日,自主神经症状不明显。为了避免漏诊或误诊,推荐神经影像学检查,特别是MRI弥散成像(DWI)可作为老年首次眩晕和头晕的常规检查项目。     

大脑中动脉狭窄与其深穿支供血区单发脑梗死的关系

目的 分析大脑中动脉(MCA)深穿支供血区单发脑梗死的形态学表现,进一步探讨其与MCA狭窄的关系.方法 连续入选2005年1月至2006年12月于北京协和医院神经科住院治疗急性脑梗死,并经头颅DWI检查明确急性梗死灶为单发,且位于MCA深穿支供血区域的55例患者;所有患者均行TCD和MRA检查,颅外颈内动脉狭窄>50%以及有可疑心源性栓子来源的患者从研究中排除.根据是否存在病灶同侧MCA狭窄将入选患者分为两组:MCA狭窄组(14例)与MCA正常组(41例).测量DWI上急性梗死灶的直径、面积和体积,并将直径≤2 cm归为经典腔隙性梗死,直径>2 cm归为纹状体内囊梗死.DWI上的梗死灶区分为基底节区、侧脑室体旁和同时累及上述2个部位,并判断MRI T2>像上皮质下多发陈旧性小梗死灶或白质疏松是否存在.结果 55例患者中,病灶侧MCA狭窄患者14例(25.5%),MCA正常患者41例(74.5%).MCA狭窄组中经典腔隙性梗死占71.4%,MCA正常组中经典腔隙性梗死占67.3%,差异无统计学意义(χ2=0.147,P=0.701).MCA狭窄组与正常组患者MCA深穿支梗死病灶的大小(包括直径、面积及体积)差异均无统计学意义.MCA正常组和MCA狭窄组病灶在基底节区、侧脑室体旁及基底节区+侧脑室体旁分布的比例依次为:正常组31.7%、17.1%和51.2%;狭窄组35.7%、28.6%和35.7%,两组间差异无统计学意义(χ2=1.272,P=0.529).同时存在皮质下多发陈旧性小梗死灶或白质疏松的患者在MCA正常组有23例(56.1%),在MCA狭窄组有3例(21.4%),二者差异有统计学意义(χ2=5.033,P=0.025).结论 MCA深穿支供血区梗死具有不同的发病机制,MCA狭窄和穿支动脉本身病变均可造成深穿支供血区单发脑梗死.梗死灶的大小、体积及梗死发生的部位与是否存在同侧大脑中动脉狭窄无明显相关性,而同时存在皮质下多发陈旧性小梗死灶或白质疏松对穿支动脉病变有提示作用.     

大脑前动脉供血区梗死的临床特征

目的 探讨大脑前动脉(anterior cerebral artery,ACA)梗死的危险因素、病因、发病机制、临床表现和影像学特征.方法 回顾性分析急性ACA梗死患者的临床和影像学资料,总结其危险因素、病因、梗死灶分布和临床表现;比较栓塞组(心源性或颈动脉源性栓塞)和ACA粥样硬化组患者梗死灶分布和临床表现;分析ACA粥样硬化性梗死的发病机制.结果 58例ACA梗死,占同期住院急性脑梗死患者的6.9％,其中52例完整评估颅内外血管的患者纳入研究.最常见危险因素为高血压(80.8％);病因分型中大动脉粥样硬化最常见共45例,占86.5％:其次为心源性栓塞5例,占9.6％,2例病因不确定,占3.8％.栓塞组(16/52,30.8％)和ACA粥样硬化组(30/52,57.7％)相比,ACA粥样硬化组梗死累及胼胝体发生率更高(26/30 vs.6/16,x2=9.705,P=0.002),意志减退/淡漠更常见(19/30 vs.5/16,x2=4.305,P=0.038);而栓塞组梗死更易累及其他供血区(8/16 vs.2/30,x2=9.111,P=0.003).两组间其他临床表现差异无统计学意义(P＞0.05).30例ACA粥样硬化性梗死中A2段狭窄或闭塞有23例(76.7％);发病机制包括局部分支闭塞12例,原位血栓性闭塞5例,动脉-动脉栓塞5例,局部分支闭塞合并动脉-动脉栓塞8例.结论 ACA梗死发病率低,高血压是其最主要的危险因素,运动障碍是最常见的临床表现.ACA粥样硬化是主要病因,A2段病变最多见,存在多种梗死发病机制.心源性或颈动脉源性栓塞易累及其他供血区,ACA粥样硬化性梗死累及胼胝体和意志减退/淡漠多见.     

Cerebrovascular reactivity to L-arginine in patients with lacunar infarctions

BACKGROUND: It is well known that endothelial dysfunction plays an important role in the pathogenesis of many cardiovascular disorders. The aim of this study was to test the hypothesis that specific, marked endothelial dysfunction of cerebral arteries is present in patients with lacunar cerebral infarctions. METHODS: Cerebrovascular reactivity to L-arginine, which reveals the function of the cerebral endothelium, was investigated in patients with lacunar infarctions (20 patients, 11 male and 9 female, aged 60.9 +/- 7.3 years), 21 age- and gender-matched asymptomatic patients with similar cardiovascular risk factors (all patients had arterial hypertension) and 21 age- and gender-matched healthy controls. The mean arterial velocity (vm) in both middle cerebral arteries was measured by transcranial Doppler sonography during a 15-min baseline period, a 30-min intravenous infusion of L-arginine and a 15-min interval after L-arginine infusion. Arterial blood pressure, heart rate and CO2 were measured continuously. RESULTS: The measured vm increase during L-arginine infusion in the patients with lacunar infarctions (13.4 +/- 9.1%) was significantly lower compared to the healthy controls (20.5 +/- 9.9%) but similar to that obtained in the patients with cardiovascular risk factors (11.5 +/- 8.9%). CONCLUSIONS: Our results showed that cerebrovascular reactivity to L-arginine, which demonstrates cerebral endothelial function, is significantly impaired in patients with cardiovascular risk factors. Importantly, we found that patients with lacunar infarctions do not show any additional impairment of cerebral endothelial function.     

对比分析高分辨MRI与MRA对穿支动脉供血区脑梗死责任血管的诊断价值

目的对比分析高分辨率MRI(HRMRI)与MRA对穿支动脉供血区脑梗死患者责任血管的诊断评估价值。方法对24例穿支动脉供血区脑梗死患者进行常规MRI、MRA检查,根据梗死区解剖学的血管支配参照MRA行相应责任血管的HRMRI检查。Fisher精确概率法比较HRMRI与MRA对穿支动脉的载体血管(大脑中动脉、椎动脉、基底动脉)狭窄的识别情况;Wilcoxon配对秩和检验比较HRMRI与MRA评估的穿支动脉载体血管的狭窄程度。分析患者颅内动脉斑块的特征、斑块对穿支血管开口及本身的影响。结果24例患者,梗死灶位于基底节区17例、脑干7例(其中3例小脑受累)。共检查24支穿支动脉载体血管包括大脑中动脉17支、椎动脉1支、基底动脉6支。HRMRI判断责任载体血管狭窄的检出率(91.67%,22/24)明显高于MRA(62.5%,15/24)(P0.05)。对狭窄程度的判断HRMRI比MRA更准确(Z=91,P0.05)。HRMRI示23支载体血管有斑块形成,1支内膜增厚。8例HRMRI显示斑块覆盖或累及穿支血动脉开口;5例HRMRI示穿支动脉本身狭窄。而MRA不能显示穿支动脉及开口情况(P0.05)。结论 HRMRI对穿支动脉的载体血管有无狭窄及狭窄程度的判断优于MRA,还能显示穿支动脉本身管径和开口受累情况,为穿支动脉供血区脑梗死的发生机制提供更多的循证医学的依据。     

Anatomy of sensory findings in patients with posterior cerebral artery territory infarction.

BACKGROUND: Posterior cerebral arteries (PCAs) supply the ventrolateral thalamic sensory nuclei and white matter sensory tracts to the somatosensory parietal cortex. Patients with PCA territory strokes often have visual, memory, cognitive, and sensory signs. Clinicoanatomic correlation of visual, cognitive, and memory functions are well defined but, to our knowledge, no systematic study has analyzed the anatomy of sensory abnormalities. OBJECTIVE: To assess the frequency and anatomic correlation of sensory symptoms and signs in patients with PCA territory infarction. PATIENTS AND METHODS: Sixty patients with hemispheral and hemispheral and deep PCA territory infarcts apparent on computed tomographic and magnetic resonance imaging scans were studied for the presence of sensory findings and location of infarcts. RESULTS: Sensory symptoms or signs were present in 15 (25%) of 60 patients. Among patients with sensory findings, 11 of 15 had infarcts in the ventrolateral thalamus in the territory of the thalamogeniculate or lateral posterior choroidal arteries. The other 4 patients had no ventrolateral thalamic or white matter infarction but had severe proximal vascular occlusive lesions that could have caused temporary thalamic ischemia. One of these 4 patients had a medial thalamic infarct and transient hemisensory symptoms. Twelve patients had thalamic infarcts and no recorded sensory findings. Seven patients with thalamic infarcts (6 medial and 1 ventrolateral) had no sensory findings, and sensory findings could not be accurately assessed in 4 patients with ventrolateral and 1 patient with medial thalamic infarcts. CONCLUSIONS: All patients with PCA territory infarcts and sensory findings either had thalamic infarcts in thalamogeniculate or lateral posterior choroidal artery territory or had thalamic ischemia. Sensory findings in PCA territory infarction indicate ventrolateral thalamic ischemia.     

A study on middle cerebral artery territory infarction with transcranial Doppler sonography]

The transcranial Doppler sonographic findings of 40 patients with middle cerebral artery (MCA) territory infarction were compared with those of 40 controls. The results showed that in the group of acute phase patients there was a large reduction of MCA mean flow velocity (Vm) of the infarcted side compared with the normal hemisphere (P < 0.01) and controls (P < 0.05). At the same time the anterior cerebral artery (ACA) Vm rose on both sides (esp. on the infarcted side) in comparison with controls (P < 0.05). The posterior cerebral artery (PCA) Vm did not change significantly (P > 0.05). In the group of chronic phase patients there were changes similar to the group of acute phase patients in MCA Vm and ACA Vm, but not statistically significant. Follow-up TCD examinations were carried out in 8 cases during the acute phase of stroke. We found that the decreased MCA Vm on the infarcted side returned to normal in 4 cases, remained lower in another 2 cases within 4 weeks after onset. The increased MCA Vm on the infarcted side in 2 cases returned to normal within 2 weeks after onset. Various types of TCD findings in patients with MCA occlusion were described and analysed.     

Cerebrovascular CO2 reactivity in migraine: assessment by transcranial Doppler ultrasound

Summary Cerebrovascular reactivity to CO₂ inhalation was studied by transcranial Doppler sonography in 30 patients with classic or common migraine and 39 healthy controls without clinical or ultrasonic signs of arteriosclerosis. Systolic and diastolic Doppler frequencies of the middle cerebral artery were plotted against end-tidal CO₂ partial pressure; the reactivity index (I×R) was defined as relative frequency change during a PCO₂ increase of 5 mm Hg. In the normal subjects, I×R was 20.0±6.3 for systolic velocities, and 26.0±8.2 for diastolic values. Migraineurs during their headache-free interval had significantly higher I×R values on the affected side (mean: 41.6 systolic, 61.2 diastolic), compared with either controls (P<0.01) or the contralateral side (mean: 28.3 systolic, 30.8 diastolic; P<0.01). During the headache attack, CO₂ reactivity was significantly lower than normal only for systolic velocities (mean: 8.3; P<0.05). Increased CO₂ reactivity is thought to be one phenomenon of migraine. Transcranial Doppler CO₂ testing of cerebrovascular reactivity is a reliable method that may be of interest for the diagnostic evaluation and management of migraine patients.     

Aphasia with infarction in the territory of the anterior cerebral artery.

Two right-handed patients with clinical evidence of major infarction in the territory of the left anterior cerebral artery developed a profound but transient aphasia characterized by (1) a striking dissociation between intact repetition and grossly disturbed spontaneous conversational speech, (2) an absence of phonemic paraphasia, (3) a lack of speech inhibition and (4) relative preservation of conformation naming and comprehension. Despite the initially profound motor aphasia, servicable spontaneous conversational speech returned in two to three months. However, more subtle changes in the form of lack of speech initiative and difficulties in narrating stories and describing complex pictures, remained many months after the onset. In these patients the major features of the disturbance could not be explained only on the basis of an interruption of the downgoing pathway from the dominant motor speech area, and in fact, may have been due to damage to the superior and mesial pre-motor area (particularly the supplementary motor region), an area that has been shown to play a role in processes which govern the initiation, continuation and inhibition of speech.     

Cerebral blood flow and CO2 reactivity in patients with transient ischemic attack]

To elucidate the changes in cerebral blood flow (CBF) and CO2 reactivity in patients with transient ischemic attack (TIA), 10 patients with TIA and 5 healthy adults (controls) underwent two consecutive CBF measurements (i.e. the first measurement during room air inhalation and the second measurement during 5%CO2 inhalation). Hemispheric mean CBF was determined by each CBF measurement using 133Xenon inhalation method. CO2 reactivity was evaluated by analysing delta CBF (= mean CBF during hypercapnea-mean CBF at rest) and delta CBF/delta PaCO2. The resting mean CBF values in the bilateral hemispheres (i.e. both of the affected and unaffected hemispheres) were significantly lower in TIA patients than controls (p less than 0.05). Inhalation of 5%CO2 significantly increased mean CBF in TIA patients bilaterally, however the mean CBF value during hypercapnea was again significantly lower in TIA patients than controls (p less than 0.05). CO2 reactivity in TIA patients was not significantly different from controls (p greater than 0.05). The result demonstrated that TIA patients have a chronic and global cerebral oligemia with normal CO2 reactivity. The chronic and global cerebral oligemia may develop a transient ischemic neurological symptom by being superimposed with local decrease of CBF.     

Cerebrovascular reactivity in patients with mild head injury

Transcranial Doppler sonography (TCD) is a non-invasive method that can be repeated to measure blood flow velocity in intracranial arteries and to assess cerebrovascular reactivity in patients with a variety of neurological diseases. The aim of this study was Doppler sonography evaluation of blood flow and reactivity in the middle cerebral artery in patients at different stages after mild head injuries. The dynamic assessment of blood flow velocity and pulsatility index both at rest and after hyperventilation in 73 patients with mild head injuries was carried out on the day of injury, the third day, sixth day and after 6 months to 5 years. The control group consisted of 61 healthy volunteers. Obtained results indicate an increase in blood flow velocity in the middle cerebral artery on the day of injury and a decrease within the following days in younger patients (aged xleq 30 yrs). Also their cerebrovascular reactivity was significantly lower. In older persons (age > 30 yrs) and in patients with remotely suffered injuries, neither blood flow velocity in the middle cerebral arteries nor cerebrovascular reactivity differed significantly from the results of the respective age control groups. The findings justify a conclusion that mild head injury is followed by changes both in the blood flow and cerebrovascular reactivity. In younger patients with mild head injuries these haemodynamic disturbances seem to be connected with altered activity of the autonomic system.