Structural changes of the intradural arteries following subarachnoid hemorrhage

1972 ◽  
Vol 37 (6) ◽  
pp. 715-723 ◽  
Author(s):  
Louis W. Conway ◽  
Larry W. McDonald
Keyword(s):  
Structural Change ◽  
Subarachnoid Hemorrhage ◽  
Structural Changes ◽  
Intimal Thickening ◽  
Muscular Layer ◽  
Content Type ◽  
Intracranial Arteries ◽  
Subarachnoid Blood ◽  
Spontaneous Subarachnoid Hemorrhage ◽  
Fine Print

✓ The histology of the intradural arteries was studied in 12 consecutive autopsy cases of patients dying 1 day to 15 months after their initial spontaneous subarachnoid hemorrhage. In all patients surviving 4 weeks or more and in one surviving 4 days, the lumina of the intracranial arteries were narrowed by subendothelial granulation tissue which thickened the intima. In all seven cases with structural changes in the intracranial arteries, vessels near the site of hemorrhage were involved; in four cases vessels remote from the site of hemorrhage were also involved. Changes were usually restricted to large arteries with a prominent muscular layer and confined to the subarachnoid space. The presence and degree of intimal thickening correlated with the distribution and amount of subarachnoid blood or its breakdown products. This process apparently does not represent an obliterative endarteritis involving vessels exclusively supplying infarcted brain, but is probably a reaction to mechanical or anoxic damage to the intima following vasoconstriction. It is suggested that this arterial structural change might be confused with delayed or prolonged “vasopasm.”

Spontaneous subarachnoid hemorrhage and negative cerebral panangiography

1986 ◽  
Vol 64 (4) ◽  
pp. 537-542 ◽  
Author(s):  
Mark S. M. Alexander ◽  
P. S. Dias ◽  
David Uttley
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Loss Of Consciousness ◽  
Clinical Grade ◽  
Content Type ◽  
Subarachnoid Blood ◽  
Spontaneous Subarachnoid Hemorrhage ◽  
Eventual Outcome ◽  
Basal Cisterns ◽  
Fine Print

✓ One hundred and forty consecutive patients who sustained proven spontaneous subarachnoid hemorrhage (SAH) with negative cerebral panangiography were studied retrospectively. Attention was directed to the presence, amount, and distribution of subarachnoid blood on computerized tomography (CT) scans. It was determined that the finding of blood on CT had a significant association with clinical grade, loss of consciousness, ventricular ratio, fixed ischemic deficit, and total of all complications, but not with epilepsy, hypertension (previously known or detected on admission), treated hydrocephalus, rebleeding, angiographic spasm, and eventual outcome (which was generally excellent on follow-up examination). The distribution of blood, predominantly around the basal cisterns, suggests leakage from ventriculostriate and thalamoperforating vessels as the cause of SAH, and closer study of these vessels is suggested.

Chronic subdural hematoma presenting as spontaneous subarachnoid hemorrhage

1985 ◽  
Vol 63 (5) ◽  
pp. 691-692 ◽  
Author(s):  
Zbigniew Kotwica ◽  
Jerzy Brzeziński
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Subdural Hematoma ◽  
Chronic Subdural Hematoma ◽  
Clinical Findings ◽  
Content Type ◽  
Acute Subarachnoid Hemorrhage ◽  
Spontaneous Subarachnoid Hemorrhage ◽  
Fine Print

✓ Six cases of chronic subdural hematoma presenting with the clinical findings of acute subarachnoid hemorrhage are reported. No systemic or focal cause for the bleeding was found, and possible mechanisms are discussed.

Effect of early operation for ruptured aneurysms on prevention of delayed ischemic symptoms

1982 ◽  
Vol 57 (5) ◽  
pp. 622-628 ◽  
Author(s):  
Mamoru Taneda
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Reliable Method ◽  
Early Operation ◽  
Permanent Disability ◽  
Content Type ◽  
Giant Aneurysms ◽  
Ruptured Aneurysms ◽  
Blood Clots ◽  
Subarachnoid Blood ◽  
Fine Print

✓ The effect of removal of subarachnoid blood clots on the prevention of delayed ischemic deficit was evaluated in 239 consecutive patients with ruptured supratentorial non-giant aneurysms. All patients were hospitalized within 24 hours after subarachnoid hemorrhage (SAH) and were classified in Grades 1 to 4 according to the system of Hunt and Hess; classification was made immediately preoperatively in patients operated on within 48 hours after SAH, or 48 hours after SAH in patients for whom delayed operation was planned. Delayed ischemic deficit causing permanent disability or death occurred in 11 (25%) of 44 patients in whom surgery was planned to be delayed for 10 days or more, in 26 (27.7%) of 94 patients in whom the aneurysms were obliterated and blood clots adjacent to them were removed within 48 hours of SAH, and in 11 (10.9%) of 101 patients in whom the aneurysms were obliterated and extensive and aggressive removal of thick subarachnoid clots lying along the arteries (identified on computerized tomographic scan) was performed within 48 hours of SAH. Accordingly, early operation is an effective and reliable method to reduce the occurrence of severe delayed ischemic deficit only when subarachnoid blood clots are removed extensively and aggressively along the arteries within 48 hours of SAH.

Ultra-early rebleeding in spontaneous subarachnoid hemorrhage

1996 ◽  
Vol 84 (1) ◽  
pp. 35-42 ◽  
Author(s):  
Yukihiko Fujii ◽  
Shigekazu Takeuchi ◽  
Osamu Sasaki ◽  
Takashi Minakawa ◽  
Tetsuo Koike ◽  
...  
Keyword(s):  
Risk Factors ◽  
Blood Pressure ◽  
Multivariate Analysis ◽  
Subarachnoid Hemorrhage ◽  
Early Operation ◽  
Time Interval ◽  
High Systolic Blood Pressure ◽  
Content Type ◽  
Spontaneous Subarachnoid Hemorrhage ◽  
Fine Print

✓ To determine the incidence of, and risk factors for, the occurrence of rebleeding between admission and early operation (ultra-early rebleeding) in patients with spontaneous subarachnoid hemorrhage (SAH), the authors reviewed the cases of 179 patients admitted within 24 hours after their last attack of SAH. Thirty-one (17.3%) of these patients had ultra-early rebleeding despite scheduling of early operation (within 24 hours after admission). The incidence of rebleeding significantly decreased as the time interval between the last attack and admission increased. Patients with rebleeding before admission, high systolic blood pressure, intracerebral or intraventricular hematoma, those in poor neurological condition on admission, and those who underwent angiography within 6 hours of the last SAH were significantly more likely to have ultra-early rebleeding than those without these factors. The incidence of rebleeding also significantly increased as levels of enhancement of platelet sensitivity and thrombin—antithrombin complex increased. Multivariate analysis revealed that the following three factors were independently associated with ultra-early rebleeding: the level of enhancement of platelet sensitivity; the time interval between the last attack and admission; and the level of thrombin—antithrombin complex. On the basis of these findings, the authors suggest that many of the risk factors for ultra-early rebleeding are interrelated. A particularly high risk of ultra-early rebleeding was observed in those patients 1) who had platelet hypoaggregability; 2) who were admitted shortly after their last SAH; and 3) whose thrombin—antithrombin complex levels were extremely high and were thus in severe clinical condition.

Responses to experimental subarachnoid hemorrhage in the spontaneously breathing primate

1980 ◽  
Vol 52 (3) ◽  
pp. 302-308 ◽  
Author(s):  
Charles Rothberg ◽  
Bryce Weir ◽  
Thomas Overton ◽  
Michael Grace
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Respiratory Pattern ◽  
Content Type ◽  
Cynomolgus Monkeys ◽  
Experimental Subarachnoid Hemorrhage ◽  
Subarachnoid Blood ◽  
Spontaneously Breathing ◽  
Fine Print

✓ The pathophysiological responses to experimental subarachnoid hemorrhage (SAH) were investigated in 20 spontaneously breathing cynomolgus monkeys. Four different volumes of fresh autogenous blood were used: 1.0, 1.33, 1.67, and 2.0 cc/kg. Five other animals had injection of 1.67 cc/kg of mock cerebrospinal fluid. Cerebral blood flow (CBF) was measured using the xenon-133 clearance technique. Respiratory rate and tidal volume were monitored by way of a Vertek pneumotach. The reduction of CBF after the SAH became more pronounced with increasing volumes of subarachnoid blood. The CBF remained reduced despite a return to normal of the cerebral perfusion pressure. Increasing SAH volumes were associated with greater abnormalities in the respiratory pattern, consisting of apnea and hyperventilation. These larger volumes were also associated with hypoxemia. Morbidity and mortality increased with increasing volumes of SAH, and are believed to be the result of a combination of decreased CBF, respiratory center disturbances, and pulmonary diffusion defects.

Spontaneous subarachnoid hemorrhage associated with spinal cord tumor

1974 ◽  
Vol 40 (2) ◽  
pp. 252-254 ◽  
Author(s):  
John B. Runnels ◽  
John W. Hanbery
Keyword(s):  
Spinal Cord ◽  
Differential Diagnosis ◽  
Subarachnoid Hemorrhage ◽  
Rare Case ◽  
Spinal Cord Tumor ◽  
Content Type ◽  
Upper Thoracic ◽  
Spontaneous Subarachnoid Hemorrhage ◽  
Fine Print

✓ A rare case of spontaneous subarachnoid hemorrhage from an extramedullary upper thoracic astrocytoma is described. The differential diagnosis between cranial and spinal spontaneous subarachnoid hemorrhage is discussed.

Hydrocephalus following spontaneous subarachnoid hemorrhage

1973 ◽  
Vol 39 (4) ◽  
pp. 474-479 ◽  
Author(s):  
M. Gazi Yasargil ◽  
Yasuhiro Yonekawa ◽  
Bruno Zumstein ◽  
Hans-Jürgen Stahl
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Clinical Features ◽  
Intracranial Aneurysms ◽  
Communicating Hydrocephalus ◽  
Content Type ◽  
Spontaneous Subarachnoid Hemorrhage ◽  
The Relationship ◽  
Ruptured Intracranial Aneurysms ◽  
Fine Print

✓ Twenty-eight cases of communicating hydrocephalus after subarachnoid hemorrhage (SAH) due to ruptured intracranial aneurysms are reported. The relationship between the incidence of this complication and the various clinical features of SAH is discussed. The findings of RISA cisternography have little relationship to the findings of pneumoencephalography or the results of shunting procedures. The availability and value of echoencephalography in treating such patients is emphasized.

Traumatic subarachnoid hemorrhage as a predictable indicator of delayed ischemic symptoms

1996 ◽  
Vol 84 (5) ◽  
pp. 762-768 ◽  
Author(s):  
Mamoru Taneda ◽  
Kazuo Kataoka ◽  
Fumiharu Akai ◽  
Toshiharu Asai ◽  
Ikuhiro Sakata
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Delayed Cerebral Ischemia ◽  
Close Correlation ◽  
Ct Scans ◽  
Content Type ◽  
Main Site ◽  
Traumatic Subarachnoid Hemorrhage ◽  
Closed Head Trauma ◽  
Subarachnoid Blood ◽  
Fine Print

✓ This report provides findings of an investigation of the influence of traumatic subarachnoid hemorrhage on the development of delayed cerebral ischemia caused by vasospasm. The authors prospectively studied 130 patients with closed-head trauma, who exhibited subarachnoid blood on admission computerized tomography (CT) scans. Ten (7.7%) of these patients developed delayed ischemic symptoms between Days 4 and 16 after the head injury. They consisted of three (3.0%) of 101 patients with small amounts of subarachnoid blood and seven (24.1%) of 29 patients with massive quantities of subarachnoid blood on admission CT scans. In each of the 10 patients, severe vasospasm was demonstrated by angiography performed soon after development of ischemic symptoms. There was a close correlation between the main site of the subarachnoid blood and the location of severe vasospasm. In seven of the patients, follow-up CT scans showed development of focal ischemic areas in the cerebral territories corresponding to the vasospastic arteries. These results demonstrate that traumatic subarachnoid hemorrhage, especially if massive, is a predictable indicator of delayed ischemic symptoms.

Cytoskeletal and extracellular matrix proteins in cerebral arteries following subarachnoid hemorrhage in monkeys

1992 ◽  
Vol 76 (1) ◽  
pp. 81-90 ◽  
Author(s):  
R. Loch Macdonald ◽  
Bryce K. A. Weir ◽  
James D. Young ◽  
Michael G. A. Grace
Keyword(s):  
Smooth Muscle ◽  
Subarachnoid Hemorrhage ◽  
Arterial Wall ◽  
Cerebral Arteries ◽  
Smooth Muscle Contraction ◽  
Intimal Thickening ◽  
Content Type ◽  
Tunica Media ◽  
Middle Cerebral Arteries ◽  
Fine Print

✓ It is unclear if vasospasm after subarachnoid hemorrhage (SAH) is predominantly due to smooth-muscle contraction, proliferative vasculopathy, or other changes within the arterial wall such as fibrosis or change in smooth-muscle phenotype. In this study, immunohistochemistry was used to examine changes in extracellular and cytoskeletal proteins in cerebral arteries after SAH that might support one of these mechanisms. Following baseline cerebral angiography, bilateral SAH was created in nine monkeys. Three animals each were killed 7, 14, or 28 days after SAH. Cerebral angiography was repeated on Day 7 in all animals and immediately prior to sacrifice in animals killed on Days 14 and 28. Both middle cerebral arteries and four control basilar arteries were examined using fluorescent antibody techniques with antisera to α-actin, myosin, fibronectin, fibrinogen, vimentin, desmin, laminin, and collagens (types I, III, IV, and V). Angiography showed that vasospasm was most severe on Day 7, present but resolving on Day 14, and completely resolved by Day 28. Microscopic study of arterial sections and blinded review of microphotographs of arterial sections by five independent observers did not reveal changes in intensity of density of staining for collagens, desmin, myosin, laminin, or α-actin in the tunica media of tunica adventitia. Fibronectin immunoreactivity increased 14 days after SAH. Seven days after SAH, occasional areas of tunica media showed immunoreactivity to fibrinogen. On Day 28, intimal thickening was observed in four of six middle cerebral arteries and this tissue demonstrated immunoreactivity to α-actin, myosin, vimentin, desmin, fibronectin, laminin, and each type of collagen. No significant increases in the number of intimal cells showing immunoreactivity to α-actin were seen and no significant changes in the hydroxyproline content of cerebral arteries developed at any time after SAH. These results suggest that rigidity and lumen narrowing of vasospasm are not due to increased arterial collagen, although other proteins in the arterial wall or an alteration in cross-linking of existing proteins could produce these changes. There is no indication that smooth-muscle contractile proteins change during vasospasm or that increases in the number of α-actin-containing myointimal cells contribute to vasospasm. The occurrence of intimal thickening and increased tunica media fibronectin after vasospasm suggests that vasospasm damages smooth muscle, possibly as a result of intense prolonged smooth-muscle contraction.

Cerebral artery spasm

1978 ◽  
Vol 48 (4) ◽  
pp. 515-525 ◽  
Author(s):  
J. Trevor Hughes ◽  
Pietro M. Schianchi
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Histological Examination ◽  
Cerebral Vasospasm ◽  
Arterial Wall ◽  
Arterial Occlusion ◽  
Intimal Thickening ◽  
Content Type ◽  
Small Arteries ◽  
Acute Changes ◽  
Fine Print

✓ From a larger series of autopsies with subarachnoid hemorrhage (SAH), 20 cases were selected for the known complication of cerebral vasospasm. Evidence for vasospasm was radiological and pathological in 17 cases and pathological alone in three. A systematic histological examination of the large arteries in places known formerly to have been in spasm showed that, in the 12 early cases (death before 3 weeks), there were relevant changes in all the layers of the arterial wall, the most significant being evidence of necrosis in the tunica media. In the eight late cases (death after 3 weeks), in addition to the sequelae of the earlier acute changes, there was marked concentric intimal thickening by subendothelial fibrosis, again located in the segments of arteries formerly in spasm. Changes were also found in the small arteries, capillaries, and veins, both in the early and late cases but these changes, although striking, were thought to be caused by the ischemia due to the vasospasm; similar changes were also seen in the control cases with ischemia from arterial occlusion.

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