Sequential Changes of Regional Cerebral Circulation in Cerebral Infarction

Uemura, Kazunori; Goto, Ken; Ishii, Kazunari; Z, Ito; R, Hen; Kawakami, Hiroshi

doi:10.1007/978-3-642-66959-0_73

Cited by 10 publications

(4 citation statements)

References 8 publications

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“…However, the previous report demonstrated that angiography performed when SPECT showed hyperperfusion never revealed any occlusion of the relevant artery [33]. It was also shown that luxury per fusion was recognized in the recanalized patients with cerebral infarction [6], In the present study, we observed 3 patients whose SPECT images demonstrated both high and low distributions of the tracer in the territory of the occluded and recanalized artery confirmed by angiogra phy. These observations suggest that a high distribution of 99mTc-HMPAO was induced by hyperperfusion after re opening of the occluded artery.…”

Section: Discussionsupporting

confidence: 55%

“…However, few data are available on the time course of the cerebral blood flow (CBF) measured by single-pho ton emission computed tomography (SPECT) in cerebral infarction [6][7][8][9][10], After the development of infarction in the cerebrum, the blood flow to the contralateral cerebellum is reduced, and this phenomenon is known as crossed cerebellar diaschisis or crossed cerebellar hypoperfusion [5]. Recent ly, the latter has been shown to indicate the degree of uncoupling between CBF and metabolism [11,12], How ever, the serial change in the contralateral cerebellar blood flow still remains controversial [7,[13][14][15][16][17].…”

Section: Introductionmentioning

confidence: 99%

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Changes in the Cerebral and Cerebellar Blood Flow in Cerebral Embolism

Kamouchi

Saku²,

Ibayashi

et al. 1996

Cerebrovasc Dis

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The present study was performed to elucidate the time course of the cerebral and cerebellar blood flows and the significance of SPECT for predicting the outcome in cerebral embolism. ^99mTc-hexamethylpropyleneamine oxime (^99mTc-HMPAO) SPECT was repeatedly performed in 60 patients with unilateral cerebral embolism. The distribution of ^99mTc-HMPAO in the infarct area decreased in the acute phase, increased from 3 h to 22 days after the stroke and then gradually and eventually decreased in the chronic stage. This tendency was observed irrespective of the thrombolytic therapy. The asymmetry index (AI) in the cerebral hemisphere in the first 6 h and later than 30 days correlated significantly with activities of daily living in the chronic stage (p < 0.05). The cerebellar AI after, but not up to 14 days also correlated with the long-term outcome (p < 0.05). In conclusion, a high distribution of ^99mTc-HMPAO frequently and transiently occurs in the subacute stage of cerebral embolism. The cerebral and cerebellar asymmetry of the ^99mTc-HMPAO distribution is an important predictive value for the outcome; however, the timing of SPECT is critically important.

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Section: Discussionsupporting

confidence: 55%

Section: Introductionmentioning

confidence: 99%

Changes in the Cerebral and Cerebellar Blood Flow in Cerebral Embolism

Kamouchi

Saku²,

Ibayashi

et al. 1996

Cerebrovasc Dis

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“…In the study of Christensen et al" 33% of patients investigated within 24 hours had hyperemia and in the study of Paulson 1970,' 50% of patients investigated within 3 days after stroke had it. Focal cerebral hyperemia was found in only 10% of patients investigated within 2 and 16 months after onset of stroke by Uemura et al, 13 and by Cronquist.' Focal cerebral hyperemia must be considered as a common but transient phenomenon most frequently found in the acute phase of stroke.…”

Section: Discussionmentioning

confidence: 95%

Focal cerebral hyperemia in acute stroke. Incidence, pathophysiology and clinical significance.

Olsen¹,

Larsen²,

Skriver³

et al. 1981

Stroke

113

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SUMMARY In a consecutive study comprising 41 patients with completed stroke of less than 72 hours duration, cerebral angiograpby and measurements of the regional cerebral blood flow (rCBF) were performed within 24 hours after admission. The rCBF study was done using the 133-Xenon intracarotid injection method and a 254 multi-detector camera. CT scan was done 24 hours after the rCBF study.Focal cerebral hyperemia was found in 16 patients. The study revealed 3 different types of hyperemia: Border-zone hyperemia, surrounding iscbemic areas, was seen in patients with occluded arteries on angiograpby, presumably resulting from accumulation of acid metabolites in the border-zone of acute infarcts. Postischemic hyperemia was seen in patients without occlusion, presumably due to recanalization of a prior occluded artery. Remote hyperemia was found distant from the infarcted area, presumably due to local tissue pressure on brain tissue.Cortical infarcts (10 patients) all had extensive hypereraic areas. Because the 254 detector camera has an excellent resolution in the cortical surface, our findings strongly suggest that all acute cerebral infarcts are, in fact, associated with hyperemic areas. The hyperemic areas are often extensive and vascular reactivity is commonly impaired. It is suggested that treatment aimed at reducing blood flow in hyperemic areas might improve prognosis.Stroke, Vol 12, No 5, 1981ISCHEMIC LESIONS are responsible for the neurological deficits in most patients with stroke.

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“…Cerebral autoregulatory responses to CO 2 recover 3 -4 weeks after cerebral infarction yet disautoregulation following induced hypertension may continue for up to 2 months after a stroke. 63 Although initial reports suggested that the risk of ICH following CEA in patients with acute stroke was as high as 60% 64 later studies indicated that the risk in patients with nondisabling stroke was no different whether CEA is performed within 30 days of symptoms or delayed beyond this time. 65,66 Conversely, patients with evolving neurological signs 67 or associated comorbidity (ASA III or IV) 68 have an increased risk when CEA is performed within 3 weeks.…”

Section: Potential Interventions For Patients Believed To Be At High mentioning

confidence: 99%

Intracerebral Haemorrhage Following Carotid Endarterectomy

RUSSELL¹,

GOUGH²

2004

European Journal of Vascular and Endovascular Surgery

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Objectives. To determine risk factors for the development of hyperperfusion and intra-cerebral haemorrhage following carotid endarterectomy and formulate potential protocols for prevention. Methods. MEDLINE database search of the English language literature (1966-2002) was performed using the words 'cerebral haemorrhage', 'intracranial haemorrhage' and 'carotid endarterectomy'. Other articles were cross-referenced by hand. Results. There are no data from randomised trials confirming the significance of any single risk factor. The evidence suggests that the following may have a role: pre-operative hypertension, recent ipsilateral non-haemorrhagic stroke, previous ischaemic cerebral infarction, surgery for a. 90% ipsilateral internal carotid artery (ICA) stenosis, impaired cerebrovascular reserve, intra-operative haemodynamic or embolic ischaemia, post-operative hypertension, an ipsilateral increase of $175% in peak middle cerebral artery velocity (MCAV) and/or a $100% increase in pulsatility index. Conclusions. A critical ICA stenosis with impaired cerebrovascular reserve resulting in maximal intracerebral vasodilatation and post-operative hyperperfusion (impaired autoregulation) appear to be central to the development of ICH. Appropriate pre-operative screening and post-operative monitoring in high risk patients might identify those who would benefit from manipulation of the haemodynamic events that appear to promote ICH.

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Sequential Changes of Regional Cerebral Circulation in Cerebral Infarction

Cited by 10 publications

References 8 publications

Changes in the Cerebral and Cerebellar Blood Flow in Cerebral Embolism

Changes in the Cerebral and Cerebellar Blood Flow in Cerebral Embolism

Focal cerebral hyperemia in acute stroke. Incidence, pathophysiology and clinical significance.

Intracerebral Haemorrhage Following Carotid Endarterectomy

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