A cardioembolic stroke case involving both the posterior cerebral artery and anterior choroidal artery territories]

We reported a rare case of cardioembolic stroke involving the territories of both the posterior cerebral artery (PCA) and the anterior choroidal artery. An 86-year-old man with atrial fibrillation was admitted to our hospital with consciousness disturbance and left hemiparesis. Diffusion-weighted imaging revealed high intensity lesions in the territories of the PCA and the anterior choroidal artery, leading us to make a diagnosis of cardioembolic stroke. Magnetic resonance angiography disclosed occlusion of the right internal carotid artery (ICA) and the right PCA. The P1 segment of the right PCA was absent, indicating that the right PCA had branched from the right ICA. Therefore, we believed that ICA occlusion caused the infarcts in the territories of both the PCA and the anterior choroidal artery. This is a rare stroke case involving the territories of both the PCA and the anterior choroidal artery.     

Recurrent cerebral infarction in anterior and posterior circulation territories associated with persistent primitive hypoglossal artery and carotid artery dissection: a case report

The persistent primitive hypoglossal artery (PPHA) is the second most common persistent carotid-vertebrobasilar anastomosis. We present a rare case of an 82-year-old woman who diagnosed as acute cerebral infarction three times in both the anterior and posterior circulation territories with a right-sided PPHA and ipsilateral carotid artery dissection (CAD). Microembolus monitoring results suggested that microembolic caused by CAD associated with PPHA should be recognized as a possible cause of multiple infarctions in both the anterior and posterior circulation territories. For these patients, appropriate treatment measures should be taken for prevention of stroke recurrence.     

Confusional states following posterior cerebral artery infarction

Four patients with left-sided posterior cerebral artery infarction developed acute confusional states. Fifteen additional patients with confusion following unilateral posterior cerebral artery infarction were identified from a review of the literature; in 14 the lesion was left sided. Destruction or disconnection of dominant hemisphere neocortex from limbic structures, resulting in impairment of focal attention, loss of linguistically organized memory, and/or disruption of temporal sequencing may be responsible for this syndrome.     

Aphasia and infarction of the posterior cerebral artery territory

Spoken language disorders are rarely mentioned in superficial infarction of the posterior cerebral (PCA) territory. Two clinical types have been reported: transcortical sensory and amnesic aphasia. Between 1979 and 1990, we studied retrospectively 76 patients suffering from an occipitotemporal infarction located in the superficial territory of the posterior cerebral artery, all well documented by CT. Aphasia was one of the first and prominent signs in 18 cases. Middle cerebral artery concomitant infarction could have been the cause of language impairment in 10. In 8 patients aphasia was only explained by a PCA territory infarct. Three patients showed features of transcortical sensory aphasia. CT localization showed internal lobe and thalamic involvement of the dominant hemisphere. Five patients exhibited word finding impairment with various degrees of amnestic syndrome. The dominant internal temporal lobe was always afffected. Dominant thalamus involvement was found in one case only. Some correlations between clinical features and anatomical support (vascular supply and anatomical structure) might be suggested in our 8 cases of aphasic disorders due to PCA infarcts. They are discussed and compared with data in the literature.     

Visual neglect after right posterior cerebral artery infarction

Objectives

To investigate the characteristics and neuroanatomical correlates of visual neglect after right‐sided posterior cerebral artery (PCA) infarction.

Methods

15 patients with acute PCA strokes were screened for the presence of neglect on a comprehensive battery of cognitive tests. Extra tests of visual perception were also carried out on six patients. To establish which areas were critically associated with neglect, the lesions of patients with and without neglect were compared.

Results

Neglect of varying severity was documented in 8 patients. In addition, higher‐order visual perception was impaired in 5 of the 6 patients. Neglect was critically associated with damage to an area of white matter in the occipital lobe corresponding to a white matter tract connecting the parahippocampal gyrus with the angular gyrus of the parietal lobe. Lesions of the thalamus or splenium of the corpus callosum did not appear necessary or sufficient to cause neglect, but may mediate its severity in these patients.

Conclusions

PCA stroke can result in visual neglect. Interruption of the white matter fibres connecting the parahippocampal gyrus to the angular gyrus may be important in determining whether a patient will manifest neglect.Visual neglect is a frequently observed syndrome after unilateral brain damage, characterised by a failure to respond to contralesional stimuli.^1,2 Neglect is particularly prevalent acutely after right‐hemisphere stroke. Most patients with the syndrome have damage in the territory of the middle cerebral artery, although the critical lesion areas responsible for causing neglect are controversial.^2,3,4,5 Neglect has also been reported after lesions of the thalamus,^2,6,7 but it is less well documented that the syndrome can follow strokes in the wider territory of the superficial posterior cerebral artery (PCA).The anatomy of neglect after PCA infarction was first directly addressed only recently by Mort et al.⁵ Visual neglect was associated with lesions that extended from the occipital lobe anteriorally to the parahippocampal region and centred on an area of white matter in the ventromedial temporal lobe. The authors raised the possibility that disruption of the parietotemporal white matter tracts may explain the presence of neglect in these patients. Interestingly, in this context, a recent study⁸ using diffusion‐weighted imaging and probabilistic tractography in healthy humans has documented robust projections between the parahippocampal gyrus and the angular gyrus of the parietal lobe, homologous to the tract that connects the same regions in non‐human primates.⁹ A second study by Park et al¹⁰ reported several areas as being associated with visual neglect, including the parahippocampal gyrus and the thalamus. However, multiple regression analyses showed that the only combination of lesions to contribute considerably to the frequency and severity of neglect was damage to both the occipital lobe and the splenium of the corpus callosum. The authors proposed that this pattern of damage results in deafferentation and disconnection of visual information to one hemisphere, which may be sufficient to cause neglect.In addition to neglect, PCA infarction may also lead to other visual perceptual deficits, as might be expected with damage to areas characterised as being in the ventral visual pathway.¹¹ However, visual perceptual deficits from damage to areas in the ventral visual stream in the right hemisphere are usually documented only in the context of category‐specific agnosias, such as prosopagnosia or landmark agnosia (or topographagnosia).^{12,13,14,15,16} It therefore remains an open question whether damage to the ventral medial temporal and occipital cortices results in more general perceptual impairments. We aimed (1) to examine the characteristics of neglect and perceptual deficits from PCA infarction, by assessing patients with right‐sided PCA infarction on a battery of neglect tests and a subgroup on tests of visual perception; (2) to investigate which anatomical areas are most commonly damaged in PCA neglect, paying particular attention to those areas implicated in previous studies (the thalamus, parahippocampal gyrus and splenium); and (3) to explore whether disconnection of cortical areas is a likely cause of neglect after PCA infarction.     

以三偏征为临床表现的大脑后动脉区梗死

目的 分析大脑后动脉区梗死所致三偏征的临床特点。方法 对11例表现三偏征的大脑后动脉区梗死患者的临床和影像资料进行总结并分析其特点。结果 PCAI的三偏征患者中，偏盲及偏身感觉障碍明显且恢复较差，多数偏身运动障碍恢复快，常伴有头痛。结论 对有上述三偏征的患者应考虑PCAI所致，影像学检查可帮助明确诊断。     

Topography of cerebral infarction associated with carotid artery dissection

Because the pathogenesis of cerebral ischaemia in internal carotid artery dissection (ICAD) is controversial we studied the topography of cerebral infarction that results from ICAD according to pathophysiology of embolic and haemodynamic stroke. Sixty-four patients with 67 ICADs diagnosed by angiography, Doppler duplex sonography and magnetic resonance imaging (MRI) were studied prospectively during the past decade. According to current pathophysiological concepts, cortical territorial infarcts and large subcortical lenticulostriate infarcts revealed by CT or MRI were classified as embolic, while smaller infarcts in the subcortical junctional zone and infarcts in the cortical borderzone between the middle (MCA) and anterior cerebral artery were interpreted as haemodynamic infarcts. Of the 67 dissections 37 (55%) were associated with brain infarcts, of which territorial MCA infarcts of variable size accounted for 60%. These were combined with infarcts of the anterior and posterior cerebral artery in 5%; 8% of the patients had complete MCA infarction. Large lenticulostriate infarcts were present in 11%. Haemodynamic infarcts involved the subcortical junctional zone in 16% but never the anterior cortical borderzone. Although different abnormal Doppler findings indicated haemodynamically significant carotid obstruction in all symptomatic ICADs, only the characteristic high-resistance Doppler signal was significantly associated with the occurrence of brain infarction (in 66%,P < 0.01). The angiographic features of ICAD did not correlate with the incidence or with the topography of cerebral infarction. Patterns of infarction in ICAD indicate a predominantly embolic causation probably due to thrombus formation in the dissected carotid artery in the presence of severe haemodynamic obstruction, as demonstrated by Dopppler sonography.Presented in part at the 3rd European Stroke Conference, Stockholm, May 1994     

小脑幕切开治疗脑疝后大脑后动脉梗塞

目的探讨小脑幕切开对小脑幕切迹疝后大脑后动脉梗塞的疗效。方法回顾分析72例颅脑损伤并小脑幕切迹疝患者的临床资料,其中39例患者仅行标准外伤大骨瓣减压,33例患者行标准外伤大骨瓣减压＋小脑幕切开术。结果术后动态CT显示小脑幕切开组发生大脑后动脉支配的枕叶及部分颞叶脑梗死明显低于小脑幕未切开组。结论颅脑损伤并小脑幕切迹疝患者行标准外伤大骨瓣减压＋小脑幕切开可以明显降低脑梗死的发生率、降低致残率、提高生存质量。     

Bilateral simultaneous cerebellar infarction in the medial branches of the posterior inferior cerebellar artery territories

We present an unusual case of simultaneous bilateral cerebellar infarction in the territory of the medial and intermediate branches of the posterior inferior cerebellar arteries (mPICA). The patient, a 57-yr old woman, had no risk factors for cerebrovascular disease but a long-standing hypertension. Pathogenetic hypotheses of this unusual ischemic site of lesion may be referred to: A) two PICAs arising from an occluded basilar artery; B) both medial branches arising from the same PICA on one side; C) a haemodynamic mechanism with hypoperfusion in the most peripheral branches of the arteries; D) a double, simultaneous embolic stroke in mPICAs territory. Based on clinical course, supraortic duplex-scan, echocardiography, MRI, angioMRI and CT scans, and digital subtraction angiography, none of these hypotheses could be clearly associated with the pathogenesis of the lesion. Nevertheless, we propose that an anomalous common mPICA for both cerebellar territories should represent the necessary condition for the ischemic insult and, simultaneously, other factors should intervene as possible determining events.

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Sommario Descriviamo il caso di un infarto bilaterale nel territorio delle branche mediali della arteria cerebellare postero inferiore (mPICA). La paziente, una donna di 57 anni, non aveva fattori di rischio per cerebropatia vascolare, eccettuata una lunga storia di ipertensione arteriosa. Sono state formulate diverse ipotesi patogenetiche in grado di giustificare questo inusuale sito di lesione: A) due PICA che originino da una arteria basilare occlusa; B) entrambe le branche mediali che originino dalla stessa PICA in un lato; C) una genesi emodinamica con una ipoperfusione nelle branche più periferiche delle arterie; D) un doppio simultaneo stroke embolico nel territorio delle mPICA. Sulla base del decorso clinico e degli esami strumentali (Ecodoppler dei vv. epiaortici, ecocardiogramma, RM, angioRM, TC ed angiografia digitale intrarteriosa) nessuna di queste ipotesi può essere singolarmente considerata come responsabile della lesione. Proponiamo, quindi, che una anastomosi tra le PICA debba rappresentare la necessaria predisponente condizione sulla quale siano poi intervenuti ulteriori fattori determinanti l'evento ischemico acuto.

     

Dominant ipsilateral posterior cerebral artery on magnetic resonance angiography in acute ischemic stroke

BACKGROUND: In acute infarction involving the anterior circulation, the ipsilateral posterior cerebral artery (PCA) often appears to be longer than the contralateral PCA on magnetic resonance angiography. We described this finding as dominant ipsilateral PCA (DIPCA). We sought to find the frequency of DIPCA and its predictors. METHODS: We recruited 164 consecutive individuals with acute infarct involving the anterior circulation, and analyzed their radiological and clinical features. RESULTS: DIPCA was noted in 27 patients (16.5%). It was more frequent in patients with than in patients without steno-occlusive disease of the ipsilateral anterior circulation (30.5 vs. 2.4%, p < 0.001). Multivariate analysis revealed a significant relationship between the severity of arterial lesions in the ipsilateral anterior circulation and DIPCA (p = 0.039). CONCLUSIONS: DIPCA may reflect increased leptomeningeal collateral flow via the ipsilateral PCA, and its development may be dependent on the stenotic anterior circulation.     

后循环脑梗死的血管影像学检查

动脉粥样硬化性血管狭窄或闭塞是后循环脑梗死的主要病因之一。对后循环脑梗死患者进行血管检查,有助于明确病因及发病机制,对制定临床治疗策略有重要指导意义。本文综述了不同影像学检查方法在评估后循环血管状况方面的临床价值及研究进展。     

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     

颈内动脉球囊闭塞术后产生对侧新生动脉瘤

目的 在国内献中首次报道1例床突旁动脉瘤(AN)病人在行载瘤动脉球囊闭塞术后5年出现对侧后交通AN并破裂。方法 行急诊手术夹闭该新生动脉瘤。结果 病人仍死于严重的颅内高压。回顾献共发现29例35个因颈动脉闭塞术后出现的新生AN，主要位于前、后交通动脉。结论 颈动脉闭塞后对侧血流代偿性增加可能是导致AN的原因，对大型AN应尽量采用保留载瘤动脉的方法；如闭塞载瘤动脉，应进行长期的影像学随访。     

伴有一侧胚胎型大脑后动脉的Percheron动脉梗死二例临床与影像分析

目的 Percheron动脉属于丘脑穿动脉的一种少见的先天变异,伴有一侧胚胎型大脑后动脉的Perch eron动脉梗死报道罕见.我们报告2例,旨在提高认识以利于早期诊断和治疗.方法 回顾性分析2例Percheron动脉梗死的临床表现、影像特征、治疗及预后.结果 1例急性昏迷,1例发作性视物不清后意识不清合并眼球垂直运动障碍.2例磁共振弥散加权成像(DWI)示双侧丘脑旁正中高信号,其中1例合并中脑“V”字型高信号;2例右侧大脑后动脉(PCA) P1段均显示发育不良,即胚胎型PCA.结论 典型的临床症状、丘脑旁正中部对称DWI高信号及中脑“V”字征有助于Percheron动脉梗死的诊断及治疗.一侧胚胎型PCA可能是Percheron动脉梗死的潜在变异因素.