Cerebral Vasospasm After Subarachnoid Hemorrhage
1984; Elsevier BV; Volume: 59; Issue: 7 Linguagem: Inglês
10.1016/s0025-6196(12)60441-8
ISSN1942-5546
AutoresDouglas Chyatte, Thoralf M. Sundt,
Tópico(s)Vascular Malformations Diagnosis and Treatment
ResumoChronic cerebral vasospasm remains the most important cause of subsequent morbidity in patients who survive the first 48 to 72 hours after a subarachnoid hemorrhage. Prolonged arterial narrowing compromises cerebral hemodynamics and results in cerebral ischemia. Among patients in whom symptomatic chronic cerebral vasospasm develops, almost half die or have a serious residual neurologic deficit. Present evidence indicates that sustained vessel narrowing results from structural changes within the arterial wall rather than from active contraction of vascular smooth muscle. The mechanism (or mechanisms) responsible for these changes is unknown, but damage from prolonged active arterial contraction, depression of vessel wall respiration, and an inflammatory response have all been proposed as explanations. Despite more than 30 years of intensive study, an effective treatment program for chronic cerebral vasospasm remains elusive. Recent therapeutic trials, however, based on efforts to interrupt the mechanisms responsible for these structural changes hold some promise. Chronic cerebral vasospasm remains the most important cause of subsequent morbidity in patients who survive the first 48 to 72 hours after a subarachnoid hemorrhage. Prolonged arterial narrowing compromises cerebral hemodynamics and results in cerebral ischemia. Among patients in whom symptomatic chronic cerebral vasospasm develops, almost half die or have a serious residual neurologic deficit. Present evidence indicates that sustained vessel narrowing results from structural changes within the arterial wall rather than from active contraction of vascular smooth muscle. The mechanism (or mechanisms) responsible for these changes is unknown, but damage from prolonged active arterial contraction, depression of vessel wall respiration, and an inflammatory response have all been proposed as explanations. Despite more than 30 years of intensive study, an effective treatment program for chronic cerebral vasospasm remains elusive. Recent therapeutic trials, however, based on efforts to interrupt the mechanisms responsible for these structural changes hold some promise. Cerebral vasospasm after subarachnoid hemorrhage was originally described in 1951 by Ecker and Riemen-schneider.1Ecker A Riemenschneider PA Arteriographic demonstration of spasm of the intracranial arteries: with special reference to saccular arterial aneurisms.J Neurosurg. 1951; 8: 660-667Crossref PubMed Scopus (246) Google Scholar Initially, the very existence of this phenomenon was disputed, but today it is recognized as the most important cause of morbidity in survivors of an acute subarachnoid hemorrhage. After more than 30 years of clinical and experimental research, its pathophysiologic features, cause (or causes), and treatment remain controversial. In part, this controversy has been due to confusion about what cerebral vasospasm actually is, and in part, it has been due to simplistic and poorly constructed studies. The purposes of this review were to identify those observations about cerebral vasospasm which seem to be valid and to relate them in a meaningful way. Plausible pathophysiologic explanations and their therapeutic implications will be discussed. Depending on the criteria used to define it, cerebral vasospasm has been reported to occur in 21 to 78% of all patients after a subarachnoid hemorrhage,1Ecker A Riemenschneider PA Arteriographic demonstration of spasm of the intracranial arteries: with special reference to saccular arterial aneurisms.J Neurosurg. 1951; 8: 660-667Crossref PubMed Scopus (246) Google Scholar, 2Fletcher TM Taveras JM Pool JL Cerebral vasospasm in angiography for intracranial aneurysms: incidence and significance in one hundred consecutive angiograms.Arch Neurol. 1959; 1: 38-47Crossref PubMed Scopus (57) Google Scholar, 3DuBoulay G Distribution of spasm in the intracranial arteries after subarachnoid haemorrhage.Acta Radiol [Diagn] (Stockh). 1963; 1: 257-266Google Scholar, 4Schneck SA Kricheff II Intracranial aneurysm rupture, vasospasm, and infarction.Arch Neurol. 1964; 11: 668-680Crossref PubMed Scopus (55) Google Scholar, 5Allcock JM Drake CG Ruptured intracranial aneurysms-the role of arterial spasm.J Neurosurg. 1965; 22: 21-29Crossref PubMed Scopus (143) Google Scholar, 6Wilkins RH Alexander JA Odom GL Intracranial arterial spasm: a clinical analysis.J Neurosurg. 1968; 29: 121-134Crossref PubMed Scopus (82) Google Scholar, 7Ohta T Kawamura J Osaka K Kajikawa H Handa H Angiographic classification of so-called cerebral vasospasm-correlation between existence of vasospasm and postoperative prognosis in subarachnoid hemorrhage.No To Shinkei. 1969; 21: 1019-1027PubMed Google Scholar, 8Heilbrun MP The relationship of neurological status and the angiographical evidence of spasm to prognosis in patients with ruptured intracranial saccular aneurysms.Stroke. 1973; 4: 973-979Crossref PubMed Google Scholar, 9Millikan CH Cerebral vasospasm and ruptured intracranial aneurysm.Arch Neurol. 1975; 32: 433-449Crossref PubMed Scopus (78) Google Scholar, 10Kwak R Niizuma H Ohi T Suzuki J Angiographic study of cerebral vasospasm following rupture of intracranial aneurysms. Part I. Time of the appearance.Surg Neurol. 1979; 11: 257-262PubMed Google Scholar, 11Saito I Sano K Vasospasm following rupture of cerebral aneurysms.Neurol Med Chir (Tokyo). 1979; 19: 103-107Crossref PubMed Scopus (21) Google Scholar, 12Saito I Sano K Vasospasm after aneurysm rupture: incidence, onset, and course.in: Wilkins RH Cerebral Arterial Spasm: Proceedings of the Second International Workshop. Williams & Wilkins Company, Baltimore1980: 294-301Google Scholar, 13Weir BKA The incidence and onset of vasospasm after subarachnoid hemorrhage from ruptured aneurysm.in: Wilkins RH Cerebral Arterial Spasm: Proceedings of the Second International Workshop. Williams & Wilkins Company, Baltimore1980: 302-305Google Scholar although most studies estimate its frequency of occurrence to be between 40 and 60%. Most often, angiographic vasospasm occurs in cerebral arteries near the source of the subarachnoid hemorrhage and tends to occur in the segments of cerebral arteries that are intimately related to the densest collections of subarachnoid blood.11Saito I Sano K Vasospasm following rupture of cerebral aneurysms.Neurol Med Chir (Tokyo). 1979; 19: 103-107Crossref PubMed Scopus (21) Google Scholar, 14Kim H Mizukami M Kawase T Takemae T Araki G Time course of vasospasm-its clinical significance.Neurol Med Chir (Tokyo). 1979; 19: 95-102Crossref PubMed Scopus (11) Google Scholar Distant focal or diffuse global vasospasm does occur but is considerably less common. The frequency and severity of cerebral vasospasm increase with increasing volumes of subarachnoid blood, as judged by cranial computed tomography.15Fisher CM Kistler JP Davis JM Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computerized tomographic scanning.Neurosurgery. 1980; 6: 1-8Crossref PubMed Scopus (2367) Google Scholar, 16Mizukami M Takemae T Tazawa T Kawase T Matsuzaki T Value of computed tomography in the prediction of cerebral vasospasm after aneurysm rupture.Neurosurgery. 1980; 7: 583-585Crossref PubMed Scopus (72) Google Scholar Fisher and associates15Fisher CM Kistler JP Davis JM Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computerized tomographic scanning.Neurosurgery. 1980; 6: 1-8Crossref PubMed Scopus (2367) Google Scholar found that 23 of 24 patients with subarachnoid clots judged to be 5 by 3 mm or larger on initial computed tomographic scan subsequently had symptomatic chronic cerebral vasospasm in the corresponding arterial territories, whereas only 1 of 18 patients with no or diffusely distributed subarachnoid blood on initial computed tomographic scan subsequently had symptomatic vasospasm. The presence of intraventricular or intraparenchymal blood did not correlate with the frequency of occurrence of vasospasm. Similarly, the frequency and severity of vasospasm increase with worsening initial clinical grade11Saito I Sano K Vasospasm following rupture of cerebral aneurysms.Neurol Med Chir (Tokyo). 1979; 19: 103-107Crossref PubMed Scopus (21) Google Scholar, 12Saito I Sano K Vasospasm after aneurysm rupture: incidence, onset, and course.in: Wilkins RH Cerebral Arterial Spasm: Proceedings of the Second International Workshop. Williams & Wilkins Company, Baltimore1980: 294-301Google Scholar, 17Sundt Jr, TM Kobayashi S Fode NC Whisnant JP Results and complications of surgical management of 809 intracranial aneurysms in 722 cases: related and unrelated to grade of patient, type of aneurysm, and timing of surgery.J Neurosurg. 1982; 56: 753-765Crossref PubMed Scopus (195) Google Scholar and plurality of bleeding episodes.18Graf CJ Nibbelink DW Cooperative study of intracranial aneurysms and subarachnoid hemorrhage: report on a randomized treatment study. III. Intracranial surgery.Stroke. 1974; 5: 559-601Crossref Google Scholar One author of this review (T.M.S.) has observed that vasospasm is more common in patients with severe meningeal signs than in those without such signs. Although several reports have suggested that the frequency of vasospasm may vary with the location of the aneurysm, those sites identified as being associated with a high frequency of vasospasm differ from study to study. Other reports suggest that the frequency of vasospasm does not vary with anatomic position.11Saito I Sano K Vasospasm following rupture of cerebral aneurysms.Neurol Med Chir (Tokyo). 1979; 19: 103-107Crossref PubMed Scopus (21) Google Scholar, 12Saito I Sano K Vasospasm after aneurysm rupture: incidence, onset, and course.in: Wilkins RH Cerebral Arterial Spasm: Proceedings of the Second International Workshop. Williams & Wilkins Company, Baltimore1980: 294-301Google Scholar, 14Kim H Mizukami M Kawase T Takemae T Araki G Time course of vasospasm-its clinical significance.Neurol Med Chir (Tokyo). 1979; 19: 95-102Crossref PubMed Scopus (11) Google Scholar, 17Sundt Jr, TM Kobayashi S Fode NC Whisnant JP Results and complications of surgical management of 809 intracranial aneurysms in 722 cases: related and unrelated to grade of patient, type of aneurysm, and timing of surgery.J Neurosurg. 1982; 56: 753-765Crossref PubMed Scopus (195) Google Scholar, 18Graf CJ Nibbelink DW Cooperative study of intracranial aneurysms and subarachnoid hemorrhage: report on a randomized treatment study. III. Intracranial surgery.Stroke. 1974; 5: 559-601Crossref Google Scholar, 19Niizuma H Kwak R Ohi T Katakura R Mizoi K Suzuki J Angiographical study of cerebral vasospasm following rupture of intracranial aneurysm (2nd report). Relation between the site of aneurysm and the occurrence of the vasospasm.No Shinkei Geka. 1978; 6: 863-869PubMed Google Scholar, 20Post KD Flamm ES Goodgold A Ransohoff J Ruptured intracranial aneurysms: case morbidity and mortality.J Neurosurg. 1977; 46: 290-295Crossref PubMed Scopus (68) Google Scholar The age and sex of the patient and the size of the aneurysm do not seem to be related to the frequency of vasospasm.11Saito I Sano K Vasospasm following rupture of cerebral aneurysms.Neurol Med Chir (Tokyo). 1979; 19: 103-107Crossref PubMed Scopus (21) Google Scholar, 12Saito I Sano K Vasospasm after aneurysm rupture: incidence, onset, and course.in: Wilkins RH Cerebral Arterial Spasm: Proceedings of the Second International Workshop. Williams & Wilkins Company, Baltimore1980: 294-301Google Scholar, 18Graf CJ Nibbelink DW Cooperative study of intracranial aneurysms and subarachnoid hemorrhage: report on a randomized treatment study. III. Intracranial surgery.Stroke. 1974; 5: 559-601Crossref Google Scholar Experimental cerebral vasospasm after subarachnoid hemorrhage seems to be a biphasic event.21Brawley BW Strandness Jr, DE Kelly WA The biphasic response of cerebral vasospasm in experimental subarachnoid hemorrhage.J Neurosurg. 1968; 28: 1-8Crossref PubMed Scopus (118) Google Scholar, 22Kuwayama A Zervas NT Belson R Shintani A Pickren K A model for experimental cerebral arterial spasm.Stroke. 1972; 3: 49-56Crossref PubMed Scopus (57) Google Scholar In dogs, arterial narrowing begins immediately after subarachnoid hemorrhage and reaches maximal intensity by 30 minutes. Within 2 days, this early phase of vasospasm reverses spontaneously. Early spasm, however, has been difficult to substantiate in humans.23Odom GL Cerebral vasospasm.Clin Neurosurg. 1974; 22: 29-58Google Scholar, 24Wilkins RH Aneurysm rupture during angiography: does acute vasospasm occur?.Surg Neurol. 1976; 5: 299-303PubMed Google Scholar Although this difficulty may reflect the transient nature of acute vasospasm, the fact that human cerebral arteries contract less strongly when challenged with blood than do vessels from other species suggests that acute vasospasm may be attenuated in humans.25Wellum GR Irvine Jr, TW Zervas NT Dose responses of cerebral arteries of the dog, rabbit, and man to human hemoglobin in vitro.J Neurosurg. 1980; 53: 486-490Crossref PubMed Scopus (49) Google Scholar Late or chronic vasospasm begins approximately 48 hours after experimental subarachnoid hemorrhage and lasts from days to weeks. Unlike early vasospasm, chronic spasm clearly has a counterpart in humans and is the major cause of delayed neurologic deterioration.26Peerless SJ Pre- and postoperative management of cerebral aneurysms.Clin Neurosurg. 1979; 26: 209-231PubMed Google Scholar The onset of chronic vasospasm in humans has been reported to occur anytime from the first day to several weeks after a subarachnoid hemorrhage;10Kwak R Niizuma H Ohi T Suzuki J Angiographic study of cerebral vasospasm following rupture of intracranial aneurysms. Part I. Time of the appearance.Surg Neurol. 1979; 11: 257-262PubMed Google Scholar, 11Saito I Sano K Vasospasm following rupture of cerebral aneurysms.Neurol Med Chir (Tokyo). 1979; 19: 103-107Crossref PubMed Scopus (21) Google Scholar, 14Kim H Mizukami M Kawase T Takemae T Araki G Time course of vasospasm-its clinical significance.Neurol Med Chir (Tokyo). 1979; 19: 95-102Crossref PubMed Scopus (11) Google Scholar, 27Weir B Grace M Hansen J Rothberg C Time course of vasospasm in man.J Neurosurg. 1978; 48: 173-178Crossref PubMed Scopus (422) Google Scholar however, it most commonly becomes apparent 5 to 7 days after a subarachnoid hemorrhage and rarely becomes symptomatic after 2 weeks. When symptoms occur, they usually develop insidiously over hours and are heralded by signs and symptoms of a generalized reduction in cerebral blood flow (such as drowsiness, stupor, and semicoma). Later, focal abnormalities (for example, speech dysfunction, monoparesis, monoplegia, and hemiplegia) may appear as a result of the localized reduction in blood flow in the distribution of affected arteries. Rarely, patients will have focal symptoms in the absence of generalized changes in consciousness. The relationship of early vasospasm to late vasospasm is uncertain. Whether they share common mechanisms or whether the events occurring during early vasospasm lead to chronic vasospasm is unknown. Differences in hemodynamic properties facilitate classification of cerebral arteries into at least two types: proximal large conducting vessels on the surface of the brain and distal small penetrating arterioles. In normal subjects, cerebral arterial resistance and, consequently, cerebral blood flow are primarily regulated at the level of the penetrating arterioles rather than by the conducting arteries. With modification of resistance in this arteriolar bed, cerebral blood flow is maintained at a relatively constant level over a wide range of systemic blood pressures through a process referred to as autoregulation. After a subarachnoid hemorrhage, as chronic cerebral vasospasm narrows the lumen of conducting arteries, the relative contribution that these vessels make to intracranial arterial resistance increases. When severely spastic, conducting vessels may be the major site of intracranial resistance that results in depressed cerebral blood flow. Because of this shift in the site of the major arterial resistance, the capacity for autoregulation is lost and cerebral blood flow varies greatly with systemic arterial pressure and intravascular volume.28Davis DH Sundt Jr, TM Relationship of cerebral blood flow to cardiac output, mean arterial pressure, blood volume, and alpha and beta blockade in cats.J Neurosurg. 1980; 52: 745-754Crossref PubMed Scopus (64) Google Scholar Efforts to demonstrate the hemodynamic importance of cerebral vasospasm have not always been successful. This result is not surprising when one considers that multiple mechanisms may alter cerebral perfusion after a subarachnoid hemorrhage. Vasospasm, increased intracranial pressure, decreased mean arterial blood pressure, altered responsiveness of small cerebral resistance vessels, abnormal cerebral metabolism, intravascular dehydration, and altered blood viscosity29Wood JH Simeone FA Kron RE Snyder LL Litt M Relationship of cortical blood flow and cardiovascular responses to alteration in fresh blood viscosity as determined by capillary step-response viscometry.J Cereb Blood Flow Metab 1 Suppl. 1981; 1: 233-234Crossref PubMed Scopus (11) Google Scholar, 30Wood JH Snyder LL Simeone FA Golden MA Fink EA Cerebrovascular and cardiac responses to intravascular volume expansion following focal cerebral ischemia (abstract).Stroke. 1981; 12: 130Google Scholar, 31Watanabe H Hasegawa T Ishii S Studies on intravascular factors of cerebral ischemia in vasospasm after rupture of cerebral aneurysm.in: Wilkins RH Cerebral Arterial Spasm: Proceedings of the Second International Workshop. Williams & Wilkins Company, Baltimore1980: 378-384Google Scholar can all impede cerebral perfusion, whereas recruitment of collateral vascular channels, hypervolemia, and arterial hypertension may augment it. Thus, the hemodynamic importance of vasospasm will be a function of its severity and the summated influence of these modifying factors. Fisher and associates,32Fisher CM Roberson GH Ojemann RG Cerebral vasospasm with ruptured saccular aneurysm-the clinical manifestations.Neurosurgery. 1977; 1: 245-248Crossref PubMed Scopus (290) Google Scholar in a study of 25 patients with subarachnoid hemorrhage, were able to correlate the site and temporal profile of vasospasm with the location and time of appearance of cerebral infarction. Other investigators have reported similar findings.33Kodama N Mizoi K Sakurai Y Suzuki J Incidence and onset of vasospasm.in: Wilkins RH Cerebral Arterial Spasm: Proceedings of the Second International Workshop. Williams & Wilkins Company, Baltimore1980: 361-365Google Scholar Kelly and associates34Kelly PJ Gorten RJ Rose JE Grossman RG Cerebral infarction and ruptured intracranial aneurysms.in: Wilkins RH Cerebral Arterial Spasm: Proceedings of the Second International Workshop. Williams & Wilkins Company, Baltimore1980: 366-371Google Scholar studied 90 patients and concluded that cerebral infarction after subarachnoid hemorrhage is related to angiographic vasospasm in some cases but can occur even in its absence. In a clinicopathologic study, Schneck and Kricheff4Schneck SA Kricheff II Intracranial aneurysm rupture, vasospasm, and infarction.Arch Neurol. 1964; 11: 668-680Crossref PubMed Scopus (55) Google Scholar found a poor correlation between vasospasm and cerebral infarction. Global cerebral blood flow in humans is decreased after subarachnoid hemorrhage.35Kågström E, Greitz T, Hanson J, Galera R: Changes in cerebral blood flow after subarachnoid haemorrhage. Excerpta Medica International Congress Series, No. 110, 1966, pp 629-633Google Scholar, 36James IM Changes in cerebral blood flow and in systemic arterial pressure following spontaneous subarachnoid haemorrhage.Clin Sci. 1968; 35: 11-22PubMed Google Scholar, 37Heilbrun MP Olesen J Lassen NA Regional cerebral blood flow studies in subarachnoid hemorrhage.J Neurosurg. 1972; 37: 36-44Crossref PubMed Scopus (128) Google Scholar In addition, the decrease in global cerebral blood flow worsens with worsening clinical grade.38Nilsson BW Cerebral blood flow measurements in subarachnoid hemorrhage with intravenous 99Tc technique.in: Wilkins RH Cerebral Arterial Spasm: Proceedings of the Second International Workshop. 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Although many authors have reported that the regional cerebral blood flow is depressed in the distribution of spastic arteries,36James IM Changes in cerebral blood flow and in systemic arterial pressure following spontaneous subarachnoid haemorrhage.Clin Sci. 1968; 35: 11-22PubMed Google Scholar, 41Symon L Ackerman R Bull JWD du Boulay EPGH Marshall J Rees JE Russell RWR The use of the xenon clearance method in subarachnoid haemorrhage: post-operative studies with clinical and angiographic correlation.Eur Neurol. 1972; 8: 8-14Crossref PubMed Scopus (22) Google Scholar, 42Heilbrun MP Olesen J Lassen NA Regional cerebral blood flow studies in subarachnoid hemorrhage.in: Wilkins RH Cerebral Arterial Spasm: Proceedings of the Second International Workshop. Williams & Wilkins Company, Baltimore1980: 314-319Google Scholar others have found no correlation.43Zingesser LH Schechter MM Dexter J Katzman R Scheinberg LC On the significance of spasm associated with rupture of a cerebral aneurysm: the relationship between spasm as noted angiographically and regional blood flow determinations.Arch Neurol. 1968; 18: 520-528Crossref PubMed Scopus (28) Google Scholar Interestingly, cerebral blood volume is elevated in regions supplied by severely spastic vessels, a finding that suggests that distal small penetrating arterioles may dilate and lose their capacity for autoregulation in an effort to decrease intracranial arterial resistance.39Pitts LH Macpherson P Wyper DJ Jennett B Blair I Cooke MBD Effects of vasospasm on cerebral blood flow after subarachnoid hemorrhage.in: Wilkins RH Cerebral Arterial Spasm: Proceedings of the Second International Workshop. Williams & Wilkins Company, Baltimore1980: 333-337Google Scholar Measurement of regional cerebral blood flows in experimentally induced early as well as late vasospasm has also produced divergent results.44Simeone FA Trepper PJ Brown DJ Cerebral blood flow evaluation of prolonged experimental vasospasm.J Neurosurg. 1972; 37: 302-311Crossref PubMed Scopus (49) Google Scholar, 45Petruk KC Weir BKA Marriott MR Overton TR Clinical grade, regional cerebral blood flow and angiographical spasm in the monkey after subarachnoid and subdural hemorrhage.Stroke. 1973; 4: 431-445Crossref PubMed Scopus (21) Google Scholar, 46Hashi K Meyer JS Shinmaru S Welch KMA Teraura T Hemodynamic and metabolic changes in experimental subarachnoid hemorrhage in monkeys.Eur Neurol. 1972; 8: 32-37Crossref PubMed Scopus (14) Google Scholar, 47Yamaguchi T Waltz AG Effects of subarachnoid hemorrhage from puncture of the middle cerebral artery on blood flow and vasculature of the cerebral cortex in the cat.J Neurosurg. 1971; 35: 664-671Crossref PubMed Scopus (15) Google Scholar Electroencephalographic abnormalities suggestive of focal cortical dysfunction routinely appear in the distribution of vasospastic arteries in humans after the occurrence of a subarachnoid hemorrhage.48Parkes JD James IM Electroencephalographic and cerebral blood flow changes following spontaneous subarachnoid haemorrhage.Brain. 1971; 94: 69-76Crossref PubMed Scopus (22) Google Scholar, 49Rumpl E Bauer G Gerstenbrand F Stampfel G Focal electroencephalographic changes associated with vasospasm after subarachnoid hemorrhage.in: Wilkins RH Cerebral Arterial Spasm: Proceedings of the Second International Workshop. Williams & Wilkins Company, Baltimore1980: 356-360Google Scholar Similarly, the findings on radionuclide cerebral perfusion scintigraphy suggest that at least severe spasm is associated with perfusion abnormalities in humans who have had a subarachnoid hemorrhage.50Kelly PJ Gorten RJ Grossman RG Eisenberg HM Cerebral perfusion, vascular spasm, and outcome in patients with ruptured intracranial aneurysms.J Neurosurg. 1977; 47: 44-49Crossref PubMed Scopus (34) Google Scholar Transmission electron microscopic examination of vasospastic cerebral arteries after experimentally induced subarachnoid hemorrhage in dogs and monkeys shows structural differences between arteries in the early phase of vasospasm and those in the chronic phase. Arteries examined within 48 hours after experimentally induced subarachnoid hemorrhage have few pathologic changes. The internal elastic lamina may appear corrugated as a result of arterial contraction. Subtle changes in the configuration of endothelial cells and degenerative changes in occasional smooth muscle cells are also noted.51Tanabe Y Sakata K Yamada H Ito T Takada M Cerebral vasospasm and ultrastructural changes in cerebral arterial wall: an experimental study.J Neurosurg. 1978; 49: 229-238Crossref PubMed Scopus (103) Google Scholar, 52Fein JM Flor WJ Cohan SL Parkhurst J Sequential changes of vascular ultrastructure in experimental cerebral vasospasm: myonecrosis of subarachnoid arteries.J Neurosurg. 1974; 41: 49-58Crossref PubMed Scopus (121) Google Scholar Later, during the phase of chronic vasospasm in this experimental situation, severe degeneration and necrosis of smooth muscle cells predominate and may persist for more than 1 year. Extracellular debris is abundant in all layers of the affected cerebral artery. In places, endothelial cells are elevated from the underlying internal elastic lamina or are frankly denuded (Fig. 1, Fig. 2). Leukocytes, mast cells, and erythrocytes are present in the arterial wall during the first few days of chronic vasospasm, and macrophages appear several weeks later.51Tanabe Y Sakata K Yamada H Ito T Takada M Cerebral vasospasm and ultrastructural changes in cerebral arterial wall: an experimental study.J Neurosurg. 1978; 49: 229-238Crossref PubMed Scopus (103) Google Scholar, 52Fein JM Flor WJ Cohan SL Parkhurst J Sequential changes of vascular ultrastructure in experimental cerebral vasospasm: myonecrosis of subarachnoid arteries.J Neurosurg. 1974; 41: 49-58Crossref PubMed Scopus (121) Google Scholar, 53Liszczak TM Varsos VG Black PM Kistler JP Zervas NT Cerebral arterial constriction after experimental subarachnoid hemorrhage is associated with blood components within the arterial wall.J Neurosurg. 1983; 58: 18-26Crossref PubMed Scopus (110) Google Scholar, 54Alksne JF Branson PJ Prevention of experimental subarachnoid hemorrhage-induced intracranial arterial vasonecrosis with phosphodiesterase inhibitor phthalazinol (EG-626).Stroke. 1979; 10: 638-644Crossref PubMed Scopus (15) Google Scholar, 55Tani E Yamagata S Ito Y Intercellular granules and vesicles in prolonged cerebral vasospasm.J Neurosurg. 1978; 48: 179-189Crossref PubMed Scopus (37) Google Scholar Vasospastic arteries of human victims of subarachnoid hemorrhage show similar pathologic changes.56Conway LW McDonald LW Structural changes of the intradural arteries following subarachnoid hemorrhage.J Neurosurg. 1972; 37: 715-723Crossref PubMed Scopus (86) Google Scholar, 57Crompton MR Cerebral infarction following the rupture of cerebral berry aneurysms.Brain. 1964; 87: 263-280Crossref Scopus (52) Google Scholar, 58Faleiro LCM Machado CRS Gripp Jr, A Resende RA Rodrigues PA Cerebral vasospasm: presence of mast cells in human cerebral arteries after aneurysm rupture; preliminary note.J Neurosurg. 1981; 54: 733-735Crossref PubMed Scopus (28) Google Scholar, 59Peerless SJ Kassell NF Komatsu K Hunter IG Cerebral vasospasm: acute proliferative vasculopathy? II. Morphology.in: Wilkins RH Cerebral Arterial Spasm: Proceedings of the Second International Workshop. Williams & Wilkins Company, Baltimore1980: 88-96Google Scholar, 60Mizukami M Kawase T Tazawa T Nagata K Yunoki K Yoshida Y Hypothesis and clinical evidence for the mechanism of chronic cerebral vasospasm after subarachnoid hemorrhage.in: Wilkins RH Cerebral Arterial Spasm: Proceedings of the Second International Workshop. Williams & Wilkins Company, Baltimore1980: 97-106Google ScholarFig. 2Electron micrograph of a chronically vasospastic canine basilar artery, showing striking necrosis of smooth muscle cells (S). Ultrastructural abnormalities involving endothelium (E) and elastic lamina (EL) are also apparent, (× 1,950.)View Large Image Figure ViewerDownload (PPT) Despite the fact that numerous investigators have successfully prevented or treated experimental vasospasm with a wide variety of vasodilating drugs, clinically the final result has been disappointing.61Wilkins RH Attempted prevention or treatment of intracranial arterial spasm: a survey.in: Wilkins RH Cerebral Arterial Spasm: Proceedings of the Second International Workshop. Williams & Wilkins Company, Baltimore1980: 542-555Go
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