Spectrum of superficial posterior cerebral artery territory infarcts

Posterior cerebral artery (PCA) territory infarction is not uncommon. Published series were concentrated either on isolated deep PCA territory infarcts or on incomplete calcarine artery territory infarcts. Although, correlations between clinical symptoms, causes of stroke and outcome at 6-months in patients with superficial PCA territory stroke are less well known. We sought prospectively stroke causes, infarct topography, and clinical findings of 137 patients with superficial PCA territory infarcts with or without mesencephalic/thalamic involvement, representing 11% of patients with posterior circulation ischemic stroke in our Stroke Registry. We analyzed patients by subdividing into three subgroups; (1). cortical infarct (CI) group; (2). cortical and deep infarcts (CDI) (thalamic and/or mesencephalic involvement) group; (3). bilateral infarcts (BI) group. We studied the outcomes of patients at 6-month regarding clinical findings, risk factors and vascular mechanisms by means of comprehensive vascular and cardiac studies. Seventy-one patients (52%) had cortical (CI) PCA infarct, 52 patients (38%) had CDI, and 14 patients (10%) had bilateral PCA infarct (BI). In the CDI group, unilateral thalamus was involved in 38 patients (73%) and unilateral mesencephalic involvement was present in 27% of patients. The presumed causes of infarction were intrinsic PCA disease in 33 patients (26%), proximal large-artery disease (PLAD) in 33 (24%), cardioembolism in 23 (17%), co-existence of PLAD and cardioembolism in 7 (5%), vertebral or basilar artery dissection in 8 (6%), and coagulopathy in 2. The death rate was 7% in our series and stroke recurrence was 16% during 6-month follow-up period. Features of the stroke that was associated with significant increased risk of poor outcome included, consciousness disturbances at stroke onset (RR, 66.6; 95% CI, 8.6-515.5), mesencephalic and/or thalamic involvement (RR, 3.79; 95% CI, 1.49-9.65), PLAD (RR, 2.71; 95% CI, 1.09-6.73), and basilar artery disease (RR, 5.94; 95% CI, 1.73-20.47). The infarct mechanisms in three different types of superficial PCA territory stroke were quite similar, but cardioembolism was found more frequent in those with cortical PCA territory infarction. Although, the cause of stroke could not reliably dictate the infarct topography and clinical features. Visual field defect was the main clinical symptom in all groups, but sensorial, motor and neuropsychological deficits occurred mostly in those with CDI. Outcome is good in general, although patients having PLAD and basilar artery disease had more risk of stroke recurrence and poor outcome rather than those with intrinsic PCA disease.     

Mechanisms of infarction in the superficial posterior cerebral artery territory

Numerous reports have described a variety of clinical syndromes resulting from posterior cerebral artery (PCA) infarction, whereas only a few pathoanatomical and retrospective clinical studies have investigated the underlying mechanisms. Therefore we attempted to determine the causes of infarction in the superficial posterior cerebral artery (PCA) territory by means of a more comprehensive, modern vascular and cardiac study. During a 4-year period 74 consecutive patients (49 men, 25 women) with acute PCA infarction documented on CT (n = 74) and MRI (n = 41) were included in the study. Patients had a neurological examination, vascular studies [extra- and transcranial Doppler (n = 74), magnetic resonance (n = 31) or intra-arterial (n = 22) angiography], cardiac evaluation [ECG (n = 74), transthoracic (n = 74) and transoesophageal echocardiography (n = 30)], and coagulation tests. A cardiac source of embolism was established in 31%, significant vertebrobasilar artery disease in 22%, and PCA stenosis or occlusion in 8% of the patients. Rare causes, such as hypercoagulopathy or paradoxical embolism via a patent foramen ovale, were present in 15%. However, in spite of the comprehensive diagnostic evaluation, the cause of the stroke remained undetermined in 24% of the cases. Apart from complete infarcts of the posterior branches of the PCA, which occurred more frequently in cardioembolic strokes (18%, P < 0.05), the topographical patterns of infarct extension and the coincidence of infarction in the deep territories of the PCA, the cerebellum and brainstem were not significantly different among the causal subgroups. The frequency of haemorrhagic transformation (18%) was highest among cardioembolic strokes (44%, P < 0.001). This prospective study of PCA infarction demonstrated embolism from cardiac and vascular sources as the predominant cause. In contrast to previous studies, we found no evidence of migraine as a cause of PCA infarction, whereas paradoxical embolism was the presumed cause in a considerable number of cases. Whereas the cause of stroke could not reliably be derived from infarct topography, haemorrhagic transformation indicated there had been cardioembolism in most cases. Received: 9 January 1997 Received in revised form: 24 June 1997 Accepted: 24 July 1997     

"Malignant" middle cerebral artery territory infarction

The pathology, clinical course, outcome, diagnosis, treatment and prognosis of dramatic malignant middle cerebral artery territory infarction were presented. About 10% of stroke patients suffer from malignant middle cerebral artery territory infarction, mainly due to brain edema and herniation. This syndrome causes high mortality. The newest conservative and surgical treatment was presented.     

Thalamic atrophy following cerebral infarction in the territory of the middle cerebral artery

We investigated shrinkage of the ipsilateral thalamus following infarction in the territory of the middle cerebral artery in 33 patients who were admitted less than or equal to 2 days after the stroke and who were followed by computed tomography for greater than 1 year with no recurrences. The thalamic area was measured on the computed tomograms, and the ratio of the ipsilateral area to the contralateral area was calculated. All values were compared with values from the initial computed tomogram taken less than or equal to 2 days after the stroke. The values of the ratio on follow-up computed tomograms decreased gradually in 15 patients. In these cases, the area of the ipsilateral thalamus was significantly reduced after 1 year (p less than 0.01) and marked atrophy was observed. These results demonstrate the significance of remote changes over a long period of time after focal cerebral infarction.     

Pure superficial posterior cerebral artery territory infarction in The Lausanne Stroke Registry

Objective: To determine the patterns of clinical presentation, lesion topography, and etiology in patients with ischemic stroke limited to the superficial territory of the posterior cerebral artery (s-PCA). Methods: In the Lausanne Stroke Registry (LSR, 1983–1998), we determined the patterns of clinical presentation, lesion topography and mechanisms of stroke, among 117 patients with s-PCA infarction (s-PCAI) on brain imaging. Results: s-PCAIs accounted for 30.5 % of all PCA territory ischemic strokes. The presumed etiology was embolism in 64 (54.5 %) patients [cardiac in 51 (43.5 %) and arterial in 13 (11 %)], indeterminate in 38 (32 %), PCA atherothrombosis in 4 (3.4 %), migraine in 4 (3.4 %), other rare causes in 4 (3.4 %), and multiple potential sources of embolism in 3 (2.5 %). The clinical findings were hemianopsia in 78 (67 %), quadrantanopsia in 26 (22 %), and bilateral visual field defects in 8 (7 %). Motor, sensory, or sensorimotor deficits were detected in 14 (12 %), 8 (6.8 %), or 8 (6.8 %) patients, respectively. Neuropsychological dysfunction included memory impairment in 20 (17.5 %; with left [L], right [R], or bilateral [B] lesions in 15, 2, or 3 patients, respectively), dysphasia in 17 (14.5 %; L/B: 14/3), dyslexia with dysgraphia in 5 (4 %; L/B: 4/1), dyslexia without dysgraphia in 10 (8.5 %; L/B: 8/2), hallucinations in 12 (10 %; L/R/B: 5/5/2), visual neglect in 11 (9.5 %; L/R: 2/9), visual agnosia in 10 (8.5 %; L/B: 7/3), prosopagnosia in 7 (6 %; R/B: 4/3), and color dysnomia in 6 (5 %; L: 6). Conclusions: s-PCAIs are uncommon, representing less than a third of all PCA infarctions. Although embolism is the main cause in 60 % of patients, identification of the emboli source is often not possible. In 1/3 of cases, the stroke mechanism cannot be determined. Neuropsychological deficits are frequent if systematically searched for. Received: 31 July 2001, Received in revised form: 23 November 2001, Accepted: 4 December 2001     

Infarcts in the middle cerebral artery territory

Correlates of the size of infarcts, the time from stroke to death, and the mechanisms of death were studied in 77 consecutive patients who died from infarction in the middle cerebral artery territory. The area of infarcts was assessed by planimetry on schemas of representative brain levels and the results were expressed as a ratio of infarcted area on the whole MCA territory. No clear relationship was found between the size of infarcts in the MCA territory, and any of the characteristics of the patients, but extensive infarcts were more frequent when the internal carotid artery was occluded. No evidence was found of an adverse effect of age, diabetes or initial hyperglycemia on the size of infarcts. The mechanisms of death were not linked to sex, age, high blood pressure, diabetes, blood glucose level at admission, presence and location of an arterial occlusion, or etiology of the infarct. On the contrary, they varied as a function of interval from stroke to death. Transtentorial herniation, the main cerebral cause of death, occured mainly in the first week and was related to the large size of infarcts. Rare recurrences of stroke and frequent extracerebral mechanisms of death (mainly pneumonia, pulmonary embolism and cardiopathy) occurred later on.     

Hemicraniectomy for large middle cerebral artery territory infarction: outcome in 19 patients

BACKGROUND: Large space-occupying middle cerebral artery infarction accounts for 10-15% of all supratentorial infarctions and carries a mortality of 50% to 80%. Hemicraniectomy may be useful when optimal medical management has failed. METHODS: Between June 1997 and June 2000, 19 patients who fulfilled the clinical and imaging criteria for large middle cerebral artery infarction underwent hemicraniectomy because of impending herniation despite best medical therapy. The National Institute of Health Stroke Scale (NIHSS) assessed neurological status on admission and at one week after surgery. At 3 month follow up, The Barthel Index (BI) and Rankin Scale (RS) were used to assess the functional outcome among survivors. RESULTS: There were 15 males and 4 females with a mean age of 46.5 years (range 27-76 years). Ten patients (53%) had dominant hemisphere stroke. The mean interval between stroke onset and surgery was 60.3 hours (range 20-103 hours). The mean NIHSS score before surgery was 20.5 (range 17-26) and 10.5 (range 6-22) after surgery. One patient (5.2%) died due to post-operative meningitis. At follow up, mean BI was 56.4 (range 25-90) and RS revealed severe handicap in 4 patients (21%). Patients under 50 years of age had a significantly better outcome with mean BI of 60.7 as compared to only 41.3 (p=<0.048) in older patients. Speech function, especially comprehension improved in all patients with dominant hemisphere infarction. CONCLUSION: These findings add to previous studies suggesting hemicraniectomy may be a useful procedure in patients with large middle cerebral artery territory infarction. The functional outcome is good in younger patients. A randomised controlled trial is required to substantiate these findings.     

Late thalamic atrophy in infarction of the middle cerebral artery territory in neonates

We report four cases of progressive thalamic atrophy following ipsilateral cerebral infarction in the territory of the middle cerebral artery in neonates, with prospective radiological and clinical follow-up. This type of atrophy appears within 6 months after the onset of cerebral infarction. In the short term, this atrophy has no action on sensory and memory function and/or on sensory evoked potentials. This atrophy is not the result of secondary ischemic neuronal damage. Judging from several other experimental studies, thalamic atrophy may primarily result from retrograde degeneration. It would be interesting to observe the consequences of this atrophy on sensory and memory function over a long period.     

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。     

Contralateral diaphragmatic palsy after subcortical middle cerebral artery infarction without capsular involvement

Diaphragmatic palsy after acute stroke is a novel clinical entity and may result in a high incidence of respiratory dysfunction and pneumonia, which especially cause greater morbidity and mortality. Generally, internal capsule and complete middle cerebral artery (MCA) infarctions are major risk-factors for developing diaphragmatic palsy. Herein, we present a case with contralateral diaphragmatic palsy after a subcortical MCA infarction without capsular involvement. Dyspnea occurred after stroke, while a chest X-ray and CT study disclosed an elevated right hemidiaphragm without significant infiltration or patch of pneumonia. A phrenic nerve conduction study showed bilateral mild prolonged onset-latency without any significant right–left difference. This suggested a lesion causing diaphragmatic palsy was not in the phrenic nerve itself, but could possibly originate from an above central location (subcortical MCA infarction). We also discussed the role of transcranial magnetic stimulation study in the survey of central pathway and demonstrated diaphragmatic palsy-related orthopnea.     

Posterior cerebral artery infarction from middle cerebral artery infarction

BACKGROUND: While it is known that posterior cerebral artery (PCA) infarction may simulate middle cerebral artery (MCA) infarction, the frequency and localization of this occurrence are unknown. OBJECTIVE: To determine the frequency of PCA infarction mimicking MCA infarction and the territory of the PCA most commonly involved in this simulation. DESIGN: We studied 202 patients with isolated infarction in the PCA admitted to our stroke center to determine the frequency of PCA infarction simulating MCA infarction, the involved PCA territory, and the patterns of clinical presentation. RESULTS: We found 36 patients (17.8%) with PCA ischemic stroke who had clinical features suggesting MCA stroke. The PCA territory most commonly involved was the superficial PCA territory (66.7%), followed by the proximal PCA territory (16.7%) and both the proximal and the superficial PCA territories (16.7%). The principal stroke mechanism was cardioembolic (54.1%) in the superficial PCA territory, lacunar (46.2%) in the proximal PCA territory, and undetermined (40.2%) in both the proximal and the superficial territories. Among the 36 patients, the most common clinical associations were aphasia (13 patients), visuospatial neglect (13 patients), and severe hemiparesis (7 patients). CONCLUSIONS: Posterior cerebral artery infarction simulating MCA infarction is more common than previously thought. Early recognition of the different stroke subtypes in these 2 arteries may allow specific management.     

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.     

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.     

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.     

Middle cerebral artery pial territory infarcts: a study of the Lausanne Stroke Registry

Using a standard protocol (Doppler ultrasonography, electrocardiography, brain computed tomography, and in selected cases angiography, echocardiography, and Holter monitoring) we studied the clinical characteristics and etiological factors in 380 patients with first stroke who had a corresponding infarct limited to the territory of the pial branches of the middle cerebral artery (MCA) on computed tomography. The presumed cause of infarction was large-artery disease (greater than or equal to 50% carotid artery or MCA stenosis or occlusion) in one-third of the patients and cardioembolism in one-fourth of the patients. Half of 230 patients undergoing angiography showed evidence for distal occlusions suggesting artery-to-artery or cardiac emboli. Severe heart disease and potential cardiac sources of embolism were more common in patients with infarcts in the territory of the posterior (inferior) division of MCA than in patients with infarcts in the territory of the anterior (superior) division of MCA. Persisting functional disability on discharge was also more severe in patients with the former than in patients with the latter. The neurological picture was polymorphous and it could sometimes even be misleading, as in some patients with a classical lacunar syndrome or with aphasia and unexpected sparing of speech areas. However, a few clinical syndromes apparently specific for involvement of a single MCA branch could be delineated, and in some instances they were highly predictive of embolism from heart or proximal artery.     

Acute confusional state and acute agitated delirium. Occurrence after infarction in the right middle cerebral artery territory

Acute confusional state (ACS) and acute agitated delirium (AAD) after infarction in the right middle cerebral artery territory were investigated in 41 consecutive patients. Acute confusional state was diagnosed on the basis of the results of the Mini-Mental State Examination, and AAD was distinguished from ACS by the characteristic behavioral abnormality. Of these patients, 25 presented with ACS, and six with AAD. Acute confusional state and AAD are common syndromes after infarction of the right middle cerebral artery, and infarction in this territory, therefore, has an important clinical implication as a cause of these syndromes. Acute confusional state is a disorder in which cognitive and integrative functions become defective, reflecting disturbance of global attention, and is closely correlated with other right hemispheric global and directed attentional disorders. It is linked to damage to the right frontostriatal region and is associated with lesion volume. In comparison, AAD is a disorder in which emotional and affective components are predominantly altered. None of the right hemispheric behavioral syndromes correlated with AAD. It may be related to damage to the right middle temporal gyrus.