Cerebral blood flow following induced subarachnoid hemorrhage in the monkey

1972 ◽  
Vol 37 (3) ◽  
pp. 316-324 ◽  
Author(s):  
K. C. Petruk ◽  
G. R. West ◽  
M. R. Marriott ◽  
J. W. McIntyre ◽  
T. R. Overtone ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Perfusion ◽  
Neurological Status ◽  
Neurological Deficits ◽  
Content Type ◽  
Arterial Vasospasm ◽  
Experimental Subarachnoid Hemorrhage ◽  
Angiographic Demonstration

✓ The acute effects of experimental subarachnoid hemorrhage on cerebral blood flow were investigated in 14 adult rhesus monkeys injected with fresh autogenous blood through a needle positioned within the subfrontal subarachnoid space. Cerebral blood flow was measured by the xenon133 tissue clearance method before hemorrhage, and afterward at 30-minute intervals for a 3-hour period. Post-anesthetic neurological status was graded according to Botterell's classification. Twelve monkeys showed a significant decrease in cerebral perfusion, eight displayed focal neurological deficits, and four were moribund. There was a correlation between the degree of impaired circulation and the severity of neurological deficit. Four additional monkeys subjected to subarachnoid acidic saline injection showed no reduction in cerebral blood flow. In three animals cerebral perfusion was increased during the first hour after injection. It is suggested that measurement of cerebral blood flow may be a more valuable prognostic indication of cerebral function and survival than the angiographic demonstration of arterial vasospasm.

Experimental cerebral vasospasm

1974 ◽  
Vol 41 (3) ◽  
pp. 285-292 ◽  
Author(s):  
Hajime Nagai ◽  
Yoshiaki Suzuki ◽  
Mitsuo Sugiura ◽  
Satoshi Noda ◽  
Hideo Mabe
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Posterior Communicating Artery ◽  
Content Type ◽  
Aneurysmal Rupture ◽  
Experimental Subarachnoid Hemorrhage ◽  
Fine Print

✓The authors describe a model for making an experimental subarachnoid hemorrhage that closely simulates human aneurysmal rupture. A needle previously inserted into the posterior communicating artery is subsequently withdrawn by traction on a thread. Using this model they demonstrate biphasic spasm by measurement of cerebral blood flow and angiography after rupture of the artery; the early spasm lasted 60 minutes and the late spasm began 3 or 4 hours after subarachnoid hemorrhage and continued for several days. The authors discuss the pathogenesis of early and late spasm.

Serial measurement of regional cerebral blood flow in patients with SAH using 133Xe inhalation and emission computerized tomography

1984 ◽  
Vol 60 (5) ◽  
pp. 916-922 ◽  
Author(s):  
Bruce Mickey ◽  
Sissel Vorstrup ◽  
Bo Voldby ◽  
Helle Lindewald ◽  
Aage Harmsen ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Computerized Tomography ◽  
Cerebral Arteries ◽  
Three Dimensional ◽  
Neurological Deficits ◽  
Content Type ◽  
Serial Measurement ◽  
Regional Flow ◽  
Delayed Neurological Deterioration

✓ A noninvasive three-dimensional method for measuring cerebral blood flow (CBF), xenon-133 inhalation and emission computerized tomography, was used to investigate the CBF changes accompanying delayed neurological deterioration following subarachnoid hemorrhage (SAH). A total of 67 measurements were performed on 20 patients in Hunt and Hess' clinical Grades I to III in the first 21 days post SAH. Five patients with normal CBF tomograms on admission developed delayed neurological deficits in the 2nd week after hemorrhage, at which time repeat CBF tomograms in four patients revealed large areas of well defined regional flow decrease in the vascular territories of the anterior or middle cerebral arteries. Severe vasospasm was noted in three of these patients in whom arteriography was performed in the 2nd week post SAH. Diffuse bihemispheric CBF decreases were noted later in the course of delayed neurological deficits; however, measurements obtained soon after the onset of focal symptoms suggest that the only CBF decreases directly produced by vasospasm in Grade III patients are regional changes.

Positron Emission Tomographic Cerebral Perfusion Disturbances and Transcranial Doppler Findings among Patients with Neurological Deterioration after Subarachnoid Hemorrhage

Neurosurgery ◽  
2003 ◽  
Vol 52 (5) ◽  
pp. 1017-1024 ◽  
Author(s):  
Pawan S. Minhas ◽  
David K. Menon ◽  
Piotr Smielewski ◽  
Marek Czosnyka ◽  
Peter J. Kirkpatrick ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Carotid Artery ◽  
Cerebral Perfusion ◽  
Internal Carotid ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Neurological Deficits ◽  
Positron Emission Tomographic ◽  
Positron Emission ◽  
Arterial Vasospasm ◽  
The Mean

Abstract OBJECTIVE After aneurysmal subarachnoid hemorrhage, approximately 30% of patients experience delayed neurological deficits, related in part to arterial vasospasm and dysautoregulation. Transcranial Doppler (TCD) ultrasonography is commonly used to noninvasively detect arterial vasospasm. We studied cerebral perfusion patterns and associated TCD indices for 25 patients who developed clinical signs of delayed neurological deficits. METHODS Patients were treated in a neurosurgical intensive care unit and were studied if they exhibited delayed focal or global neurological deterioration. Positron emission tomographic cerebral blood flow (CBF) studies and TCD studies measuring the mean flow velocity (FV) of the middle cerebral artery and the middle cerebral artery FV/internal carotid artery FV ratio (with the internal carotid artery FV being measured extracranially at the cranial base) were performed. Glasgow Outcome Scale scores were assessed at 6 months. RESULTS A markedly heterogeneous pattern of CBF distribution was observed, with hyperemia, normal CBF values, and reduced flow being observed among patients with delayed neurological deficits. TCD indices were not indicative of the cerebral perfusion findings. The mean CBF value was slightly lower for patients who did not survive (32.3 ml/100 g/min), compared with those who did survive (36.0 ml/100 g/min, P= 0.05). CONCLUSION Among patients who developed delayed neurological deficits after aneurysmal subarachnoid hemorrhage, a wide range of cerebral perfusion disturbances was observed, calling into question the traditional concept of large-vessel vasospasm. Commonly used TCD indices do not reflect cerebral perfusion values.

Acute cerebral blood flow response to dopamine-induced hypertension after subarachnoid hemorrhage

1994 ◽  
Vol 80 (5) ◽  
pp. 857-864 ◽  
Author(s):  
Joseph M. Darby ◽  
Howard Yonas ◽  
Elizabeth C. Marks ◽  
Susan Durham ◽  
Robert W. Snyder ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Systemic Blood Pressure ◽  
Content Type ◽  
Arterial Blood ◽  
Induced Hypertension ◽  
Fine Print

✓ The effects of dopamine-induced hypertension on local cerebral blood flow (CBF) were investigated in 13 patients suspected of suffering clinical vasospasm after aneurysmal subarachnoid hemorrhage (SAH). The CBF was measured in multiple vascular territories using xenon-enhanced computerized tomography (CT) with and without dopamine-induced hypertension. A territorial local CBF of 25 ml/100 gm/min or less was used to define ischemia and was identified in nine of the 13 patients. Raising mean arterial blood pressure from 90 ± 11 mm Hg to 111 ± 13 mm Hg (p < 0.05) via dopamine administration increased territorial local CBF above the ischemic range in more than 90% of the uninfarcted territories identified on CT while decreasing local CBF in one-third of the nonischemic territories. Overall, the change in local CBF after dopamine-induced hypertension was correlated with resting local CBF at normotension and was unrelated to the change in blood pressure. Of the 13 patients initially suspected of suffering clinical vasospasm, only 54% had identifiable reversible ischemia. The authors conclude that dopamine-induced hypertension is associated with an increase in flow in patients with ischemia after SAH. However, flow changes associated with dopamine-induced hypertension may not be entirely dependent on changes in systemic blood pressure. The direct cerebrovascular effects of dopamine may have important, yet unpredictable, effects on CBF under clinical pathological conditions. Because there is a potential risk of dopamine-induced ischemia, treatment may be best guided by local CBF measurements.

Endovascular occlusion of intracranial vessels for curative treatment of unclippable aneurysms: report of 16 cases

1991 ◽  
Vol 75 (5) ◽  
pp. 694-701 ◽  
Author(s):  
Jonathan E. Hodes ◽  
Armand Aymard ◽  
Y. Pierre Gobin ◽  
Daniel Rüfenacht ◽  
Siegfried Bien ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Artery ◽  
Basilar Artery ◽  
Posterior Inferior Cerebellar Artery ◽  
Artery Aneurysm ◽  
Neurological Deficits ◽  
Parent Vessel ◽  
Content Type ◽  
Fine Print

✓ Among 121 intracerebral aneurysms presenting at one institution between 1984 and 1989, 16 were treated by endovascular means. All 16 lesions were intradural and intracranial, and had failed either surgical or endovascular attempts at selective exclusion with parent vessel preservation. The lesions included four giant middle cerebral artery (MCA) aneurysms, one giant anterior communicating artery aneurysm, six giant posterior cerebral artery aneurysms, one posterior inferior cerebellar artery aneurysm, one giant mid-basilar artery aneurysm, two giant fusiform basilar artery aneurysms, and one dissecting vertebral artery aneurysm. One of the 16 patients failed an MCA test occlusion and was approached surgically after attempted endovascular selective occlusion. Treatment involved pretreatment evaluation of cerebral blood flow followed by a preliminary parent vessel test occlusion under neuroleptic analgesia with vigilant neurological monitoring. If the test occlusion was tolerated, it was immediately followed by permanent occlusion of the parent vessel with either detachable or nondetachable balloon or coils. The follow-up period ranged from 1 to 8 years. Excellent outcomes were obtained in 12 cases with complete angiographic obliteration of the aneurysm and no new neurological deficits and/or improvement of the pre-embolization symptoms. Four patients died: two related to the procedure, one secondary to rupture of another untreated aneurysm, and the fourth from a postoperative MCA thrombosis after having failed endovascular test occlusion. The angiographic, clinical, and cerebral blood flow criteria for occlusion tolerance are discussed.

Effects of profound hypotension on cerebral blood flow during surgery for intracranial aneurysms

1981 ◽  
Vol 55 (6) ◽  
pp. 857-864 ◽  
Author(s):  
J. Keith Farrar ◽  
Francis W. Gamache ◽  
Gary G. Ferguson ◽  
John Barker ◽  
George P. Varkey ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Neurological Status ◽  
Neurological Deficits ◽  
Arterial Spasm ◽  
Arterial Blood ◽  
Flow Disturbances ◽  
Group I ◽  
Increased Risk ◽  
Profound Hypotension

✓ The progression of changes in cerebral blood flow (CBF) and neurological status were measured in 12 patients in whom profound hypotension (mean arterial blood pressure (MABP): 30 to 40 mm Hg) was used during intracranial aneurysm surgery. Nine patients (Group I) showed autoregulation of CBF to an MABP of 40 to 50 mm Hg during surgery. None of these patients had arterial spasm preoperatively. Postoperatively, mild flow disturbances were noted at the site of retraction. Three Group I patients developed arterial spasm postoperatively, but there was no associated neurological deterioration. The remaining three patients (Group II) had impaired autoregulation during surgery, and CBF decreased by 35% to 65% at an MABP of 50 mm Hg. Two of these patients had angiography immediately before surgery, and both showed moderate to severe arterial spasm. Relatively severe flow disturbances were noted postoperatively at the site of retraction, and two patients developed ischemic deficits of late onset. Brain retractor pressure and the degree and duration of hypotension were equivalent in the two patient groups. There was no correlation between intraoperative reductions in CBF (to as low as 20 ml/100 gm/min in the unretracted hemisphere) and immediate postoperative neurological deficits. The use of halothane and mannitol and the relatively short duration of the flow reductions were suggested as factors contributing to the protection from ischemia that was observed. Arterial spasm was found to produce hemodynamic instability and reduced CBF, although neurological status was unaffected in the majority of patients. Patients with impaired autoregulation during surgery were at increased risk of delayed ischemic complications postoperatively, and showed characteristic flow disturbances at all three stages of their clinical course.

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