J Neurosurg 74:985-990, 1991

Fatal rupture of the intracranial carotid artery during transluminal angioplasty for vasospasm induced by subarachnoid hemorrhage Case report MARK E. LINSKEV, M.D., JOSEPH A. HORXON, M.D., Gu'rTI R. RAO, M.D., AND HOWARD YONAS, M.D. Departments ~?fNeurological Surgery, Radiology, and Pathology, University of Pittsburgh School of Medicine, Presbuerian-University Hospital, and Department of Pathology, Veterans Administration Hospital, Pittsburgh, Pennsylvania t,- The authors report the clinical course, radiographic findings, and gross and microscopic pathology of a patient with fatal rupture of the supraclinoid segment of the left internal carotid artery during transluminal angioplasty for subarachnoid hemorrhage-induced vasospasm. The rupture most likely resulted from a small portion of aneurism neck which remained unclipped, thereby leaving an area of structural weakness in the arterial wall at the site of clipping. ]~he area of structural weakness predisposed the artery to rupture upon the addition of transmural pressure induced by balloon inflation during transluminal angioplasty. Caution is advised when performing transluminal angioplasty in the region of aneurism clipping since the vessel lumen "recreated" during the clipping procedure may contain some residual and structurally incomplete aneurysm neck in the vessel wall. KEy WORDS aneurysm subarachnoid hemorrhage

9 angioplasty vasospasm

YMPTOMATICintracranial artery vasospasm occurs in approximately 30% of patients following a subarachnoid hemorrhage (SAH) from ruptured aneurysmsJ ~'24 Vasospasm begins 4 to 12 days after SAH and is a significant cause of patient morbidity and mortality even if the aneurysm has been clipped.~-~2 Currently accepted therapies for the preventing and treatment of vasospasm include hypervolemic hypertensive therapy 5,~7 and the use of calcium channel blockers. 3"4'-5"26Frustration with the effectiveness of current methods has led to the development of more invasive and more effective methods of treatment. Zubkov, et al., 3: were the first to report transluminal angioplasty for SAH-induced vasospasm in 1984. The use of this technique was first reported in the United States by Barnwell, et al.,~ in 1989, and that case report was soon followed by reports of two series of patients successfully treated with this technique by Higashida, et HI., J4and Newell, et al., 2~in late 1989. Complications resulting from this procedure have been few and include

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hemorrhage from an unclipped aneurysm, 23 a middle cerebral artery (MCA) branch occlusion, 23 and a hemorrhagic infarction in the vasospastic vascular territory leading to death, thought to result from reperfusion hemorrhage. ~4 We report a case of rapidly fatal intracranial carotid artery rupture which occurred during transluminal angioplasty for SAH-induced vasospasm. Case Report This previously healthy 51-year-old right-handed woman "passed out" suddenly while walking outside her home. She was nasally intubated by paramedics, hyperventilated, and taken to an outlying hospital where a computerized tomography (CT) scan of the head, without contrast material, revealed diffuse SAH with no intraparenchymal or intraventricular hemorrhage. The patient was given a loading dose of phenobarbital intravenously and was started on a course of nimodipine, 60 rag/4 hrs via nasogastric tube. That 985

M. E. Linskey, J. A. Horton, G. R. Rao, and H. Yonas

Fit.;. i. Left internal carotid artery (ICA) angiogram, let1 anterior-oblique view, obtained on December 10, 1989. A large 16 x l l-mm aneurysm arises from the supraclinoid segment of the left ICA pointing superiorly and medially.

n~;. 2. Digital subtraction left common carotid anglograms, lateral (A) and anteroposterior (B) views, taken on December 16, 1989. Severe vasospasm of the M~ segment of the left middle cerebral artery with lesser spasm of the A~ segment of the left anterior cerebral artery and the supraclinoid segment of the left internal carotid artery is demonstrated. The aneurysm clip and a small dilatation proximal to the aneuusm clip which may represent residual aneurysm neck are also visualized.

Operation and Course. A C T scan of the head revealed Grade III SAH as described by Fisher, et al. ~2 A stable xenon/CT cerebral blood flow (CBF) study demonstrated normal CBF in all vascular territories. The next day a left pterional craniotomy was performed with uneventful clipping of the aneurysm using a long, straight bayoneted Ya~argil aneurysm clip* (closing pressure 180 gin). A stable xenon/CT CBF study performed immediately after surgery revealed normal flow in all vascular territories. The central venous pressure was maintained above 10 m m Hg, systolic blood pres-

sure above 170 m m Hg, and hematocrit between 28% and 32%. On the 3rd postoperative day (post-SAH Day 5), the patient's right hemiparesis worsened and she became less responsive. A repeat stable xenon/CT CBF study demonstrated decreased blood flow in the left MCA (10 to 15 cc/100 gm/min) and left anterior cerebral artery (ACA) territories (20 cc/100 gm/min). Cerebral angiography revealed severe vasospasm of the M~ segment of the left MCA with lesser spasm of the A~ segment of the left ACA and left supraclinoid ICA (Fig. 2). A small dilatation just proximal to the aneurysm clip suggested that some residual aneurysm neck might be present. After a 2500-U intravenous bolus of heparin, transluminal angioplasty was performed by passing a No. 7.3 French nontapered catheter from the right femoral artery into the left ICA. A coaxial No. 2/4 French polyethylene catheter with a nonvalved, nondetachable silicone microballoon? was navigated into the left supraclinoid ICA. The balloon measured 0.85 m m uninflated but expanded to 3 m m in diameter and 12 m m in length when inflated with 0.15 cc of iodinated contrast material. The catheter was advanced by repetitive inflation and deflation of the balloon at approximately 1-second intervals. The left supraclinoid ICA was readily dilated as was the proximal A~ segment of the left ACA. On attempting to enter and dilate the M~ segment of the left MCA, the balloon was observed by fluoroscopy to change configuration from cylindrical to a more spherical shape and to move superiorly and medially.

* Aneurysm clip manufactured by Aesculap, Burlingame, California.

$ Silicone microballoon manufactured by Intraventional Therapeutics Corp., South San Francisco, California.

evening she "woke up" and extubated herself. A cerebral angiogram the next morning revealed a 16 • 1 l-mm aneurysm arising from the left supraclinoid internal carotid artery (ICA) pointing medially and superiorly (Fig. 1). The patient was transferred to PresbyterianUniversity Hospital. Examination. The patient was admitted with a Grade III SAH according to the classification of Hunt and Hess? 6 She was sleepy but easily aroused by voice. She was oriented only to person and would follow simple one-step motor commands bilaterally. Her pupils were reactive bilaterally at 3 m m in the fight eye and 5 m m in the left. All cranial nerve functions were intact; motor and sensory function was intact and symmetrical. A right pronator drift was present. Reflexes were symmetrical and plantar responses were flexor bilaterally.

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Aneurysm rupture during angioplasty

FIG. 3. Left: Photograph of the arterial system at the base of the brain after postmortem removal from the brain with a dissecting microscope. Right. Line drawing of the same specimen depicting both optic nerves (stars), which are included within the specimen. The aneurysm dome lies beneath the left optic nerve. A tear at the artery-ancurysm neck junction is visualized (thin arrow), as is a small portion of residual aneu~sm neck (large arrow).

An immediate test injection of iodinated contrast material revealed massive extravasation of material into the subarachnoid space. Within several minutes of rupture, contrast injection of the left ICA, the right ICA, and the left vertebral artery showed no significant dye entering the intradural cerebral circulation. Clinical examination immediately alter the procedure revealed fixed dilated pupils in each eye, no corneal reflexes, an absent gag reflex, and no motor response to deep trigeminal pain; but there were cGntinued spontaneous agonal respirations. A C T scan of the head showed massive SAH, and repeat stable xenon/CT CBF studies revealed absent cortical CBF. At the family's request ventilatory support was withdrawn and the patient died 7 hours after the attempted transluminal angioplasty. Postmortem Examination. At autopsy, the brain was removed with the carotid arteries sectioned where they entered the subarachnoid space and was fixed in 10% buffered formalin for 3 weeks. The brain was edematous with flattened and widened gyri. Subarachnoid blood was present in all sulci and both sylvian fissures. The subarachnoid cisterns at the base of the brain were filled with thick blood clot. There was softening of the brain parenchyma in the left MCA territory. The left optic nerve just anterior to the optic chiasm was swollen and compressed superiorly by a J. Neurosurg. / Volume 74~June, 1991

ventrally located cerebral aneurysm. A long, straight bayoneted aneurysm clip was in place across the neck of the aneurysm but there appeared to be a small (approximately 3 mm) portion of aneurysm neck remaining unclipped proximal to it. A tear in the left ICA measuring 2 x 3 mm was found at the junction of the ICA and the aneurysm neck. The circle of Willis, aneu~'sm, and optic nerves were carefully dissected free from the brain specimen using a dissecting microscope after the specimen was washed free of blood clot (Fig. 3). The aneurysm clip was carefully removed and the specimen cut so that microscopic sections would include the left ICA, the arterial tear, the aneurysm neck, the aneurysm, and the optic nerve. The cut specimen was serially sectioned in toto and stained with Masson trichrome and Verhoeff-Van Gieson elastic stains for microscopy. Microscopic examination of the cut sections revealed a large muscular artery (Fig. 4). There was no evidence of intimal thickening, subendothelial granulation tissue, or fibrosis. The media demonstrated small scattered foci of smooth-muscle cells with eosinophilic cytoplasm consistent with myonecrosis, as well as small scattered foci of myofibers with intracytoplasmic vacuolation. The adventitia was unremarkable except for evidence of recent SAH. The elastic lamina of the artery was intact circumferentially up to the point of the aneurys987

M. E. Linskey, J. A. Horton, G. R. Rao, and H. Yonas

FI(;. 4. Microscopic sections of the brain specimen. Le/l: Overview demonstrating the left internal carotid after, (arrowhead), the point of rupture (open arro~9, the region of clip-crush artifact (opposing arrows), the optic nerve (on), and the previous site of aneurysm sac rupture with a fibrin cap (long arrow). Verhoeff-Van Gieson elastic stain, x 1.2. Ri,r View of the site of rupture (open arrow). The internal elastic lamina ends proximal to the point of rupture (arrot~'hcad V, and no media is present at the point of rupture or in the aneurysm wall. The region of clip-crush artifact can be seen distal to the site of rupture (r)pposing arrows), Verhoeff-Van Gieson elastic stain, x 6.

real defect, where it was absent. The aneurysm sac contained no elastic lamina or smooth-muscle cells. A discrete focus of crush artifact without evidence of necrosis (the width of the aneurysm clip blade) was present. The aneurysm sac was ventral to the optic nerve and a defect in the aneurysm fundus, corresponding to the original site of rupture and covered by a fibrin plug, was present distal to the clip site. A tear was present proximal to the clip site in a small portion of arterial wall that contained no smooth-muscle cells or internal elastic lamina.

Discussion Transluminal angioplasty for SAH-induced arterial vasospasm has generated a great deal of excitement in the neurosurgical and neuroradiological community due to the dramatic and immediate radiographic and clinical results that have been achieved in the small series of patients reported. 14-2332 The complications described as a result of this procedure have been few and include hemorrhage from an unclipped aneurysm 1 week after angioplasty and an MCA branch occlusion 6 weeks after angioplasty leading to stroke and thought to be related to endovascular trauma from the use of a 988

more rigid than necessary balloon and guidewire system. 23The only reported death as a consequence of this technique resulted from a hemorrhagic infarction in the vasospastic vascular territory 24 hours after angioplasty which was thought to be related to reperfusion hemorrhage. ~4 While concern for the possibility of an artery rupture was expressed in two of the reported series,14'32 no case of actual arterial rupture from transluminal angioplasty for vasospasm has been reported. In reviewing the cause for arterial rupture in our patient, at least six possibilities exist. First, the rupture may have occurred from a purely mechanical disruption of a structurally normal artery. Second, the rupture may have occurred from mechanical stressing of an artery, structurally altered from vasospasm. Third, inflation of the balloon may have caused torsion of the aneurysm clip with a shearing injury of the arteryaneurysm neck interface, leading to the rupture. Fourth, inflation of the balloon may have caused the clip to move more distally onto the aneurysm with subsequent exposure of the aneurysm neck, thereby providing the structural weakness predisposing to rupture. Fifth, the aneurysm clip may have induced necrosis and weakness of the arterial wall within its jaws. This alone may have

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Aneurysm rupture during angioplasty predisposed the artery-aneurysm neck interface to rupture or the inflation of the balloon may have moved the clip distally enough to expose this necrosed area of aneurysm neck to the increased transmural pressure, leading to rupture. Finally, a small portion of the aneurysm neck may have remained unclipped and provided the strt~ctural weakness predisposing to rupture. As to the first possibility, the rupture in the present case occurred at the artery-aneurysm neck interface, which can hardly be considered a structurally normal segment of artery. The same type of catheter and technique, including inflation times and volumes, that were used in our patient have been used safely without rupture in over 23 reported patients/''423 In an experimental study, human MCA segments taken at autopsy from patients who died from SAH were grafted end-toend to femoral arteries in dogs. A microballoon, similar to that used in our patient, was then inserted into the graft and inflated to a pressure of 3 atm for 1 minute. This was repeated five times, resulting in 30% dilatation of the graft. While histopathological examination of the vessels revealed compression of the intima and stretching of the internal elastic lamina and muscle layers, there was no evidence of the internal elastic membrane splitting or any other mechanical disruption caused by even this extreme amount of distention, t~ While the possibility exists that the silicone microballoon we used could lead to rupture in a structurally normal artery, it is much more likely that some preexisting structural abnormality predisposed our patient's carotid artery to rupture. Both human autopsy studies s~5 and investigations of intraoperative arterial specimens27--~9 following SAH have purported to demonstrate ultrastructural changes in arterial walls as a result of vasospasm. Alterations reported in the intima include intimal thickening from subendothelial granulation tissue or fibrosis,~~s'2~'29 while changes in the media include myonecrosis, L~increased myofibroblasts, and increased collagen content] 7 Morphological changes described in vasospastic arteries in animal models of SAH include changes in endothelial morphology, smooth-muscle cell vacuolation, smooth-muscle cell necrosis, proliferation of myointimal cells, inflammation of the adventitia, and perivascular axonal degeneration.l2-7.~-~L~9-2t.3~ The specimen in the present case revealed small scattered foci of myonecrosis and intracellular vacuolation of smooth-muscle cells within the media. These areas were not confluent and did not extend transmurally. The fact that the rupture occurred in an area without media and without any other morphological change ascribable to vasospasm suggests that ultrastructural changes in the artery wall as a result of vasospasm did not play a causative role in the arterial rupture in this case. The angioplasty procedure was recorded fluoroseopically on videotape. If balloon inflation caused torsion of the aneurysm clip, the position of the clip would have changed during inflation of fluoroscopy. The videotape was carefully reviewed after the patient died and J. Neurosurg. / Volume 74/June, 1991

no movement of the aneurysm clip was revealed by fluoroscopy. It would, therefore, seem unlikely that a shearing injury' to the artery-aneurysm neck interface from clip torsion could account for the carotid rupture. The fourth and fifth possibilities were excluded by the histopathological findings. The site of crush artifact on the aneurysm neck was discrete and corresponded in size to the width of the aneurysm clip blades. There was no second crush artifact site and neither crush artifact nor cellular necrosis was present at the site of artery rupture. The most likely reason for carotid rupture in this case is that a small portion of the aneurysm neck between the aneurysm clip and the ICA remained unclipped. This small portion was without an internal elastic lamina or media and provided the structural weakness predisposing to rupture. Our conclusion is supported by the postoperative angiogram (Fig. 2) which revealed a small dilatation just proximal to the aneurysm clip, the gross pathological specimen (Fig. 3) which revealed an approximately 3-ram portion of unclipped aneurysm neck just proximal to the aneurysm clip, and the microscopic findings (Fig. 4) which showed that the rupture occurred proximal to the site of aneurysm clip crush artifact in an area of arterial wall without media or internal elastic lamina. It is not uncommon for a very. small portion of aneurysm neck to remain unclipped. This may result from poor visualization of the aneurysm neck, incomplete dissection of the aneurysm neck, fear of"kinking" the parent artery, calcification of the aneurysm neck, or other technical factors during surgery. Even if postoperative angiography shows no residual neck, the wall of the artery at the site of clipping may be structurally abnormal since a vessel lumen must often be "recreated" during clipping of an aneurysm, with part of a wide-mouthed aneurysm neck contributing to the newly formed vessel wall. If additional transmural stress is applied to these structurally weakened areas, rupture could potentially occur. It would seem prudent, therefore, to avoid performing transluminal angioplasty in the region of even an adequately clipped aneurysm. While the microballoon used in this case was small in diameter, it was 12 mm long when inflated. This length helps to distribute transmural pressure evenly over a longer distance making the dilatation safer. Unfortunately, it also means that, in order to exclude the region of aneurysm clipping from dilatation, one should not dilate the arterial segment over a 2.4-cm distance, from 12 mm proximal to 12 mm distal to the aneurysm. Since vasospasm most commonly occurs in the vessels intimately associated with the vessel of aneurysm origin, this region is often the segment most in need of dilatation.

Acknowledgments The authors thank John Moossy, M.D., for reviewing the manuscript, the medical media department at Children's Hospital of Pittsburgh for their artistic contribution, the Coroner's 989

M. E. Linskey, J. A. Horton, G. R. Rao, and H. Yonas Office of Allegheny County. Pennsylvania. for their assistance with this case, and Joan Russo tor her assistance with preparation of the manuscript. References 1. Alksne JF: Myonccrosis in chronic experimental vasospasm. Surgery 76:1-7. 1974 2. Alksne JF, Greenhoot JH: Experimental catecholamineinduced chronic cerebral vasospasm. Mvonecrosis in vessel wall. J Neurosurg 41:440-445, 1974" 3. Allen GS, Ahn HS, Preziosi TJ, eta]: Cerebral arterial spasm - - a controlled trial of nimodipine in patients with subarachnoid hemorrhage. N Engl J Med 308:619-624, 1983 4. Auer LM: Acute operation and preventive nimodipine improve outcome in patients with ruptured cerebral aneuusms. Neurosurgery 15:57-66, 1984 5. Awad IA, Carter LP, Spetzler RF, et al: Clinical vasospasm after subarachnoid hemorrhage: response to hypervolemic hemodilution and arterial hypertension. Stroke 18:365-372, 1987 6. Barnwell SL, Higashida RT, Halbach VV, et al: Transluminal angioplasty of intracerebral vessels for cerebral arterial spasm: reversal of neurological deficits after delayed treatment. Neurosurgery 25:424-429, 1989 7. Clower BR, Smith RR, Haining JL, et ah Constrictive endarteropathy following experimental subaraehnoid hemorrhage. Stroke 12:501-508. 1981 8. Conway LW, McDonald LW: Structural changes of the intradural arteries following subaraehnoid hemorrhage. J Neurosurg 37:715-723, 1972 9. Duff TA, Scott G, Feilbach JA: Ultrastructural evidence of arterial denervation following experimental subarachnoid hemorrhage. J Neurosurg 64:292-297, 1986 10. Espinosa F, Weir B, Shnitka T: Treatment of chronic cerebral vasospasm after subarachnoid hemorrhage in monkeys and electron microscopic anatomy of normal and subarachnoid hemorrhage arteries, in Wilkins RH (ed): Cerebral Vasospasm. New York: Raven Press, 1988. pp 195-210 11. Fein JM, Flor WJ, Cohan SL, et al: Sequential changes of vascular ultrastructure in experimental cerebral vasospasm. Myonecrosis of subarachnoid arteries. 3 Neurosurg 41:49-58, 1974 12. Fisher CM, Kistler JP, Davis JM: Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computerized tomographic scanning. Neurosurgery 6: 1-9, 1980 13. Heros RC, Zervas NT, Varsos VG: Cerebral vasospasm after subarachnoid hemorrhage: an update. Ann Neurol 14:599-608, 1983 14. Higashida RT, Halbach VV, Cahan LD, et al: Transluminal angioplasty for treatment of intracranial arterial vasospasm. J Neurosurg 71:648-653, 1989 15. Hughes JT, Schianchi PM: Cerebral artery spasm. A histological study at necropsy of the blood vesselsin cases of subarachnoid hemorrhage. J Neurosurg 48:515-525, 1978 16. Hunt WE, Hess RM: Surgical risk as related to time of intervention in the repair of intracranial aneurysms. J Neurosurg 28:14-20, 1968 t7. Kassell NF, Peerless SJ, Durward QJ, el al: Treatment of ischemic deficits from vasospasm with intravascular volume expansion and induced arterial hypertension. Neurosurgery 11:337-343, 1982 18, Konishi Y, Maemura E, Yokota H, et al: Treatment of cerebral vasospasm with dilation balloon catheter: basic 990

stud5 of percutancous transluminal angioplasty, in Wilkins RH (ed): Cerebral Vasospasm. New York: Raven Press. 1988, pp 509-511 19. Liszczak TM, Varsos VG, Black PM, et al: Cerebral arterial constriction after experimental subarachnoid hemorrhagc is associated with blood components within the arterial wall. J Neurosurg 58:18-26, 1983 20. Mayberg MR, Houser OW, Sundt TM Jr: Ultrastructnral changes in feline arterial endothelium followingsubarachnoid hemorrhage. J Neurosurg 48:49-57, 1978 21. Mayberg MR, Liszczak TM, Black PM, et ah Acute structural changes in feline cerebral arteries after subarachnoid hemorrhage, in Wilkins RH (ed): Cerebral Vasospasm. New York: Raven Press, 1988, pp 231-246 22. McKissock W, Paine KWE, Walsh LS: An analysis of the results of treatment of ruptured intracranial aneurysms. A report of 722 consecutive cases. J Neurosurg 17: 762-776, 1960 23. Newell DW, Eskridge JM, Mayberg MR, et al: Angiop]asty for the treatment of symptomatic vasospasm following subaraehnoid hemorrhage. J Neurosurg 71: 654-660, 1989 24. Sahs AL, Nishioka H, Turner JC, et al: Cooperative Study of Intracranial Aneurysms and Subarachnoid Hemorrhage. A long term prognostic study. Arch Neurol 41: 1140-1147, 1984 25. Seiler RW, Grolimund P, Zurbruegg HR: Evaluation of the calcium-antagonist nimodipine for the prevention of vasospasm after aneurysmal subarachnoid haemorrhage. A prospective transcranial Doppler ultrasound study. Acta Neuroehir 85:7-16, 1987 26. Seiler RW, Reulen HJ, Huber P, et al: Outcome of aneurysmal subarachnoid hemorrhage in a hospital population: a prospective study including early operation, intravenous nimodipine, and transcranial Doppler ultrasound. Neurosurgery 23:598-604, 1988 27. Smith RR, Clower BR, Grotendorst GM, et al: Arterial wall changes in early human vasospasm. Neurosurgery 16:171-176, 1985 28. Smith RR, Clower BR, Honma Y, et al: The constrictive angiopathy of subarachnoid hemorrhage: an immunopathological approach, in Wilkins RH (ed): Cerebral Vasospasm. New York: Raven Press, 1988, pp 247-252 29. Someda K, Morita K, Kawamura Y, et al: Intimal change following subarachnoid hemorrhage resulting in prolonged arterial luminal narrowing. Neurol Med Chir 19: 83-93, 1979 30. Tanaba Y, Sakata K, Yamada H, et al: Cerebral vasospasm and ultrastructural changes in cerebral arterial wall. An experimental study. J Neurosurg 49:229-238, 1978 31. Vasos VG, Liszczak TM, Han DH, et al: Delayed cerebral vasospasm is not reversible by aminophylline, nifedipine, or papaverine in a "two-hemorrhage" canine model. J Neurosurg 58:11-17, 1983 32. Zubkov YN, Nikiforv BM, Shustin VA: Balloon catheter technique for dilatation of constricted cerebral arteries after aneurysmal SAH. Acta Neuroehir 70:65-79, 1984

Manuscript received June 27, 1990. This work was supported in part by the Pathology Education and Research Foundation, Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania. Address reprint requesls to. Mark E. linskey, M.D., Department of Neurological Surgery, 9402 Presbyterian-University Hospital, 230 Lothrop Street, Pittsburgh, Pennsylvania 15213.

J. Neurosurg. / Volume 74/June, 1991

Fatal rupture of the intracranial carotid artery during transluminal angioplasty for vasospasm induced by subarachnoid hemorrhage. Case report.

The authors report the clinical course, radiographic findings, and gross and microscopic pathology of a patient with fatal rupture of the supraclinoid...
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