Forensic Sciace Znte-rnatimal, 49 (1991) 113-120 Elsevier Scientific Publishers Ireland Ltd. 113 DISSECTION OF THE ANTERIOR AND MIDDLE CEREBRAL ARTERY WITH FATAL ISCHEMIA FOLLOWING KICKS TO THE HEAD* HORST P. SCHMITT and ERICH MILTNER Znstitut fir (F.R.G.) Neumpathologie and Znstitut fir Rechtsmedizin, University of Heidelberg, Heidelberg (Received November 3rd, 1990) (Accepted December 13th, 1990) Summary A 19-year-old male received kicks to his head in the course of a fight with other young people. On admission to hospital he became drowsy and developed a hemiparesis and a facial paralysis on the right. After 3-4 days of continuous improvement the patient suddenly fell unconscious again and died on the seventh day after the trauma due to an increase of the intracranial pressure. Neuropathologic examination revealed an extensive dissection of the wall of the left anterior and middle cerebral artery. The age of the recurring infarction in the dependent areas of blood supply corresponded to the biphasic clinical course. Key words: Blunt head trauma; Cerebral arterial dissection; Stroke Introduction Laminar dissection of cerebral arteries is a well-known form of vascular lesion which is often of traumatic origin [8,10,18,20,21,25,27,30,35,41,44,53,55,56] but may also occur spontaneously, with and/or without preceding vascular disease such as inflammation and others [1,3,4,6,7,9,11,17,19,21,22,33,34,38-40,44,50,53]. Traumatic or mechanical origin of cerebral arterial dissection has been reported under various conditions, such as traffic accidents [18,25,27,43,49], sports and fight injuries [10,25,30,48,52,55,56], and manipulation of the cervical spine [2,14-16,23,26,29,31,32,46,47,51]. In the observations reported in the literature, the vertebro-basilar arteries were most frequently involved [8,10,14-16,26, 31,32,46-48,561 followed by the carotid arteries and their branches [2,29,30,35,37,45,49,55]. The laminar arterial dissection is, as a rule, followed by intramural bleeding, often with the formation of an intramural hematoma in the dissected space. The *Dedicated to Professor Dr. Gtinter Ule, Director emeritus of the Institute of Neuropathology of the University of Heidelberg on the occasion of his 70th birthday. Correspondence to: H.P. Schmitt, Institut ftir Neuropathologie der Universitat Heidelberg, Im Neuenheimer Feld 220, 6900 Heidelberg 1, F.R.G. 0379-0738/91/$03.66 0 1991 Elsevier Scientific Publishers Printed and Published in Ireland Ireland Ltd. 114 hematoma may compress the vascular lumen, thus causing ischemia in the dependent territories of blood supply [2,5-7,10,13,28,44,54]. Here we report the observation of a surprisingly extensive laminar arterial dissection in the brain of a young man who had received kicks to his head. Case Report A 18year-old normally constituted drunken male became involved in a fight with other youngsters. Witnesses said that he had fallen down and received kicks to his head. He had to be admitted to the hospital where he arrived in a drowsy state and exhibited facial paralysis and hemiparesis on the right. On general examination he did not show any signs of traumatic impact to his body or head; he only exhibited two bite-lesions of his tongue. To pain stimuli he answered with extension spasms on the right and non-coordinated reactions on the left. He could only breathe with respirator support. Hematologic studies revealed a leukocytosis of 14 000/n-L All other findings were normal. CT scans obtained shortly after the admission only showed brain edema of unknown origin. However, 1 day later control scans revealed signs of ischemic infarction in the left frontal lobe, centered to the supply territories of the left anterior and middle cerebral artery. Some further hypodense foci were found in the left temporo-parietal region. Doppler sonographic examination of the cephal-ad vessels did not provide evidence of vascular occlusion. In addition, the results of an ultrasound echocardiography rendered cardiogenic embolism unlikely. From the third day on, after admission, his condition improved significantly; he became alert and could breathe spontaneously. However, on the sixth day he suddenly deteriorated again, fell unconscious and exhibited signs of raised intracranial pressure. CT scans revealed severe edema of the left cerebral hemisphere with a shift of the midline structures to the right. The intracranial pressure rise could not be managed. On the seventh day no further brain activity could be registered by electroencephalography. Respirator treatment was stopped on the eighth day, when he showed clear signs of coma depasse. General medico-legal examination revealed only some slight, several days-old excoriations of his elbows and a minor bleeding into the left temporal muscle. Further, a recent thrombotic occlusion of the jugular veins and a purulent tracheobronchitis were found. Neuropathologieal Findings On gross inspection his brain (1240 g) showed flattening of the gyri and narrowing of the sulci. The coloration of the cortical grey matter varied considerably from pale-white to dark-brownish, in particular in the fronto-parietal region of the left hemisphere. The latter exhibited clear features of recent ischemic infarction with hemorrhage of the left basal ganglia (putamen and dorsal part of the 2 4 (‘Wf 0~6 WuasaJdaJ mq !u!qs SVd (I W.I~CI@ siuasa~daJ ieq fuosa!~ WA mgse[r~ 3‘~) .passaJduroD s! (7) uaum[ m[nxeh aql ‘(a‘s) s!se~sowaq lua3al pue (a) stop p%uue.w! dq papualsrp s! axds paljass!p aql wpaur aql uroy paqxgap s! eu!rue~ Dgsv[a [ewalu! ayl .(v) LJal-Ie pxqaJa3 .xo!-laiuo aql pue (~$8) rCla)JB p=qaJas alpp!tu $Jal ayl Jo saq3ueJq ~0 uog3assfp Jtm!ruE~ (a*) w$!u&! pxeq aql u! a%qxouraq lua3al ql!M UO!JDJ~J~! Iwqala3 +uaqx! am3y (v) 1 %.J 116 internal capsule) (Fig. 1A). The midbrain appeared symmetrically compressed with numerous recent secondary bleedings in the tegmentum and in the pons. The cerebellum showed signs of acute tonsillar herniation with hemorrhagic softening of the tonsillar tips. The basal cerebral arteries were slightly hypoplastic. Light microscopically, recent neuronal palloring was found in the supply territories of the left anterior and middle cerebral artery, mostly still without any glial reaction. Only in some places a slight to moderate glio-mesenchymal proliferation had occurred indicating a longer duration of the damage in these areas. Microscopic cross sections of the left anterior and middle cerebral artery in the interhemispheric cleft and the Sylvian fissure displayed a striking laminar dissection of their walls, the intima and elastic laminar being detached from the media (Figs. lB,C). The three major branches of the middle cerebral artery in the Sylvian fissure all showed this kind of damage. The dissection extended from the origin of the anterior and middle cerebral artery to the small peripheral branches. Finally, the trunc of the left internal carotid artery was also involved. The space between the internal elastic lamina and the media was markedly distended by the formation of an intramural hematoma which compressed the vascular lumen. The intramural bleeding was predominantly acute without any cellular reactions from the vessel wall. Only in some of the dissected peripheral vascular branches an early cellular response to the damage and intramural clot formation could be observed. In addition to the laminar dissection, the origin of the left middle cerebral artery also showed single transversal ruptures of the intima and the internal elastic lamina. Microscopic examination did not reveal any signs of a pre-existing vascular disorder, such as inflammation, fibro-muscular dysplasia, firbo-elastosis or others. Comments A 19-year-old alcohol-intoxicated male had sustained kicks to his head in the course of a fight with other young people. Thereafter, he had to be admitted to the hospital where he had exhibited clinical symptoms of a left-sided ischemic cerebral infarction in the supply territories of the internal carotid artery. After a short interval of improvement throughout the first 5 days after admission, he rapidly deteriorated again on the sixth day due to a rise of the intracranial pressure. He died on the eighth day after admission. As the cause of the cerebral infarction a surprisingly extensive laminar dissection of his left anterior and middle cerebral artery, beginning in the trunk of the internal carotid artery and extending peripherally into small arterial branches, could be demonstrated. The lumina of the involved vessels had been compressed due to the formation of an intramural hematoma in the space between the internal elastic lamina and the media. Microscopic examination disclosed that in some areas the ischemic infarction of the left hemisphere was already some days old as indicated by glio-mesenchymal reaction to the damage. This was in agreement with the first onset of the clinical 117 symptoms (drowsiness, right-sided hemiparesis) a few hours after the fight when he had received the kicks to his head. Correspondingly, some small peripheral arterial branches already showed a slight cellular response to the damage of their wall, while in the majority the vascular dissection was still non-reactive, indicating a short duration of the damage. This corresponded with the fact that the major part of the left-sided cerebral infarction was also still non-reactive and at most 2 days old. It is noteworthy that compared with the thorough arterial dissection, the deceased had only exhibited minor superficial signs of blunt impact to his body and head. Recent bleeding into the left temporal muscle was the only alteration found at autopsy, which indicated the mechanical impact to his head. Nevertheless, the immediate timely relation between the kicks to his head and the onset of clinical symptoms, together with the absence of pre-existing vascular disease do not leave any doubts that the extensive arterial dissection was of traumatic origin. The absence of superficial contusion marks could later be explained by the fact that the aggressor had worn jogging shoes with a soft sole. However, in general, the lack of external evidence of head injury despite severe intracranial vascular change is not so unusual. Dratz and Woodhall [12] described an observation very similar to the present one. In a young lady aged 21, a dissecting aneurysm of the left internal carotid, and the middle and anterior cerebral arteries had occurred due to blunt head trauma from a traffic accident. She also had not exhibited any external signs of head injury. The vascular dissection had separated the internal elastic lamina from the media. The same was true for the observations of de Veer et al. [54], Line11 et al. [28], Brenner and Was1 [5] and Duman et al. [13]. In some of these observations signs of external head injury had also been missing. Like in our observation, vascular occlusion due to the formation of an intramural hematoma followed by cerbral infarction had occurred at intervals ranging from 1 h to several days. In the present observation it could be derived from the microscopic findings that obviously at first only minor damage to the cerebral arteries had occurred as a cause of the older parts of the left-sided ischemic infarction, from which the patient first seemed to recover until the sixth day after admission to the hospital. At that time the major arterial dissection must have occurred as a second, spontaneous event causing the recent infarction which resulted in death due to severe brain swelling. In the reviewed literature we scarcely found reports of traumatically induced cerebral arterial dissection of an extent similar to that in the present observation. Dissections of comparable extent have mostly been observed in pre-existing vascular disease, such as fibro-muscular dysplasia, where they may even occur spontaneously [3,22,38,39]. Traumatic laminar arterial dissection may be interpreted as a “splitting-off effect” due to laminar shear stress. This means the occurrence of a laminar disconnection of the layers of the arterial wall due to their different moments of inertia. As a result, on sudden acceleration of the head with rotation and side-bending the laminae will become shifted against each other. This may result in dissection of the mural layers, e.g. disconnection of the elastic lamina from the media or 118 the media from the adventitia etc. In addition, transversal rupture of mural layers may occur due to stretching. Nedwich [36] and Ritchie [42] emphasized that on mechanical impact to the head of alcohol-intoxicated individuals the ethanol-dependent dilation of the vasa vasorum may favor the formation of an intramural hematoma in the dissected vascular space. In addition, the limitation of defense reactions and reflexes in ethanol-intoxication may contribute significantly to the occurrence of a laminar arterial dissection. By the analysis of 31 observations of traumatic cerebral arterial rupture, Krauland [24] could demonstrate that in alcohol-intoxicated individuals vascular lesions resulting in death may already occur due to minor non-penetrating head trauma, even without external signs of injury. Such observations may suggest that in the present observation the alcohol-intoxication of the victim may have played a significant role in the origin of the thorough intracranial arterial dissection. The observation reported may serve as a further example in that, a lack of external evidence of head injury after closed trauma does not exclude the occurrence of severe damage to intracranial arteries which may result in either subarachnoid hemorrhage [10,24,25] or vascular occlusion with stroke [5-7, 13,28,29,54,55]. References 1 2 3 4 5 6 J. Atom, J. Matiaa-Guiu, L. Pa&%, M. Molins, F. Romero and A. Codina, Spontaneous dissection of intracraniaJ vertebral artery: clinical recovery with conservative treatment. 1. Neural. Neurosurg. Psychiat., 49 (1986) 599-600. R.A. Beatty, Dissecting hematoma of the internal carotid artery following chiropractic cervical manipulation. J. Trauma., 17 (1977) 248-249. J. Bellot, R. Gherardi, J. Poirier et al., Fibromuscular dysplasia of cervico-ophthalmic arteries with multiple dissections and a carotid-cavernous fistula: a pathological study. Stroke, 16 (1985) 255-261. J. Bogousslavsky, P.C. Gates, A.J. Fox and H.J.M. Bamett (1986) Bilateral occlusion of vertebral artery: Clinical patterns and long-term prognosis. Neurology, 36 (1986) 1309-1315. H. Brenner and H. Wasl, Fin Fall von tijdlich verlaufendem HirnarterienverschluB als aheinige Folge einer Scb~delprellung. Zbl. Chir., 85 (1960) 201&2016. L.R. Caplan, C.K. Zarins and M. Hanmatti, Spontaneous dissection of the extracranial vertebral arteries. Stroke, 16: 103&1038. L.R. Caplan, G.D. Baquis, M.S. Pessin, J. D’Alton, L.S. Adelman, L.D. Dewitt, K. Ho, D. Izukawa and E.S. Kwan, Dissection of the intracranial vertebral artery. Neurology, 38 (1988) 868-877. S. Carpenter, Injury of neck as cause of vertebral artery thrombosis. J. Neurosurg., 18 (1961) 849-853. J. Chiras, S. Marciano, V. Vega Molina et al., Spontaneous dissecting aneurysm of the extracranial vertebral artery (20 cases). Neuroradiology, 27 (1985) 327-333. D.L. Contostavlos, Massive subarachnoid hemorrhage due to laceration of the vertebral artery associated with fracture of the transverse process of the atlas. J. Forensic Sci., 16 (1971) 4@-56. J.H. Deck, Pathology of spontaneous dissection of intracranial arteries. Can. J. Neural. Sci., 14 (1987) 88-91. H.M. Dratz and B. Woodhall, Traumatic dissecting aneurysm of left internal carotid, anterior cerebral and middle cerebral arteries. J. Neuropathol. Exp. Neural., 6 (1947) 28629 1. S. Duman and J.W. Stephen (1963) Post-traumatic middle cerebral artery occlusion. Neurology, 13 (1963) 613-616. R. Dumas and 0. Guard, Les accidents vasculaires du tronc cerebral survenant a la suite des manipulations cervicales. Ann. Med. Phys., 23 (1979) 62-71. 119 15 J.W. Dume, G.N. Conacher, M. Khangure and C.G. Harper, Dissecting aneurysms of the vertebral arteries following cervical manipulation: a case report. J. Neurol. Neurosurg. Psychiatr.. 50 (1987) 349-353. 16 J.D. Easton and D.G. Sherman, Cervical manipulation and stroke. Stroke, 8: 594-597. 17 C.M. Fischer, R.C. Ojemann and G.H. Roberson, Spontaneous dissection of the cervical internal carotid artery. Can. J. Neural. Sci., 5 (1978) 9-19. 18 A.S. Fleischer, J.M. Patton and G.T. Findall, Cerebral aneurysms of traumatic origin. Surg. Neurol., 4 (1975) 233-239. 19 R.G. Hart and J.D. Easton, Dissection of Cervicaland Cerebral Arteries in Cerebro-Vascular Disease, WB Saunders, Philadelphia, 1983. 20 T.H. Hoffmann, D.J. Richardson and L.M. Flint, Intimal disruption of major cerebral vasculature following blunt trauma. Surgery, 87 (1980) 4414. 21 F.E. Jackson, The traumatic cranial and intracranial aneurysms. In P.J. Vinken and G.W. Bruyn (eds.), Handbook of Clinical Nerurology, Vol 24, North Holland, Amsterdam, Oxford, 1976, pp 381-398. 22 K.P. Kalyanaraman and P.W. Elwood, Fibromuscular dysplasia of intracranial arteries causing multiple intracranial aneurysms. Hum. Parhoi., 11 (1980) 481-484. 23 M.B. Katirji, O.M. Reinmuth and R.E. Latschaw, Stroke due to vertebral artery injury. Arch. Neurol., 42 (1985) 242-248. 24 25 26 27 28 29 30 31 32 33 34 35 36 W. Krauland, The traumatic subarachnoidal hemorrhage (ger). Z. Rechtsmed.. 87 (1981) l-18. W. Krauland, Die Verletzungen der intrakraniellen Schlagadern, Springer, Berlin, Heidelberg, New York, 1982. B.R. Krueger and H. Okazaki, Vertebral-basilar distribution infarction following chiropractic cervical manipulation. Mayo Clin. Proc., 55 (1980) 322-332. W. Lewin, Vascular lesions in head injuries. Br. J. Surg., 55 (1968) 321-331. E.A. Line11and M.J. Tom, Traumatic arterial lesions and cerebral thrombosis. Can. Med. Assoc. J., 81 (1959) 808-813. S.S. Lyness and A.D. Wagman, Neurological deficit following cervical manipulation. Surg. Neural., 2 (1974) 121-124. J.-P. Malin, H. Becker and J. Abicht, Bilateral traumatic extracranial aneurysms of the internal carotid artery with delayed brain infarction. .I. Neurol., 232 (1985) 316317. J.L. Mas, M.G. Bousser, D. Hasboun and D. Laplane, Extracranial vertebral artery dissections: a review of 13 cases. Stroke, 18 (1987) 1037-1047. J.L. Mas, D. Henin, M.G. Bousser, F. Chain and J.J. Hauw, Dissecting aneurysm of the vertebral artery and cervical manipulation: A case report with autopsy. Neurology, 38 (1988) 512-515. B. Mokri, T.M. Sundt, Q.W. Houser and D. Piepgras, Spontaneous dissection of the cervical internal carotid artery. Ann. Neurol., 19 (1986) 126-138. B. Mokri, W. Homer, B.A. Sandok and D.G. Piepgras, Spontaneous dissections of the vertebral arteries. Neurology, 38 (1988) 886885. D.S. Murray, Post-traumatic thrombosis of the internal carotid and vertebral arteries after nonpenetrating injuries of the neck. Br. J. Surg., 44 (1957) 556-561. A. Nedwich, H. Haft, M. Tellem and L. Kaufmann, Dissecting aneurysms of cerebral arteries. Arch. Neural., 9 (1963) 477481. 37 38 P.F. New and K.J. Momose, Traumatic dissection of the internal carotid artery at the atlanto-axial level, secondary to non-penetrating injury. Radiology, 93 (1969) 41-49. B. Pasquier, A. N’Golet, D. Pasquier, M. Panh, P. Coudre and J. Gouzet, Himodissection vertebrobasilaire: un observation anatomoclinigue avec fibrodysplasie de I’arttre verttbrale gauche. Semin. Hop. Paris, 55 (1979) 487-488. 39 40 41 P. Pilz and H.J. Hartjes, Fibromuscular dysplasia and multiple dissecting aneurysms of intracranial arteries. Stroke, 7 (1976) 393-398. P. Pilz and P. Erhart, Aneurysma dissecans des Halsteils der Arteria vertebral is im Rahmen einer generalisierten nekrotisierenden Angiitis. Wia. Med. Wschr., 127 (1977) 64-67. A.L. Rhoton, F.E. Jackson, J. Gleve and C.T. Rumbaugh, Congenital and traumatic intracranial aneurysm. Ciba Clin. Symp., 29 (1977) l--40. 120 42 G. Ritchie, Dissecting aneurysm of the left internal carotid and middle cerebral arteries. Wis Med. J., 60 (1961) 556558. 43 K.-S. Satemus, Die Verletzung von Halswirbelsilule und von Halsweichteilen. In H. Junghanns (eds.), Stuttgart, 1979. 0. Sate, J.F. Baacom and J. Logothetis, Intracranial dissecting aneurysm.J. Neurosurg., 35 (1971) 483-487. B.M. Schermann and W.S. Tucker, Bilateral traumatic thrombosis of the internal carotid arteries in the neck: a case report with review of the literature. Neurosurgery, 10 (1982) 751-753. K.P. Schellhas, R.E. Latschaw, L.R. Wendling and L.H.A. Gold, Vertebrobasilar injuries following cervical manipulation. J. Am. Med. Assoc., 244 (1980) 1450-1453. H.P. Schmitt, Anatomical structure of the cervical spine with reference to the pathology of manipulation complications. J. Man. Med., (1990) (in press). R.C. Schneider, H.H. Gosch, J.A. Taren, D.J. Ferry Jr. and M.J. Jerva, Blood vessel trauma following head and neck injuries. Clin. Neurosurg., 19 (1972) 312-354. U. Schultz, M. Kiitemeyer, A. Kern and W. Hepp, Traumatic occlusion of both internal carotid arteries. J. Neurol.. 231 (1984) 233-236. H.J. Senter and M. Sat-war, Nontraumatic dissecting aneurysm of the vertebral artery. J. Neurosurg., 56 (1982) 128-130. D.G. Sherman, R.G. Hart and J.D. Easton, Abrupt change in head position and cerebral infarction. Stroke, 12 (1981) 2-6. B.F. Sorensen, Bow hunter’s stroke. Neurosurgery, 2 (1978) 259-261. W.E. Stehbens, Dissecting aneurysms of the cerebral arteries. In: Pathology of the Cerebra/ Vessels, Mosby, Saint Louis, 1972. LA. de Veer and J. Browder, Post-traumatic cerebral thrombosis and infarction. Report of a case and discussion of its bearing on the problem of intermediate and delayed post-traumatic apoplexy. J. Neuropathol. Exp. Neural., 1 (1942) 2&31. S. Yamada, G.W. Kindt and J.R. Youmans, Carotid artery occlusion due to nonpenetrating injury. J. Trauma, 7 (1967) 333-342. J. Ziegan, Inneschichtrig einer Himbasisschlagader mit nachfolgender tijdlicher Thrombose als Folge eines Faustschlages. Mschr Unfallheilk, 72 (1969) 282-294. Die Wirbeisiiule in Forschung und Praxis, Bd 84, Hippokrates, 44 45 46 41 48 49 50 51 52 53 54 55 56