Legal Medicine 16 (2014) 92–94

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Case Report

Traumatic basal subarachnoid hemorrhage suspected to have been caused by contrecoup cerebellar contusions: A case report Takako Sato a,⇑, Kento Tsuboi a, Masakatsu Nomura a, Misa Iwata a, Shuntaro Abe a, Akiyoshi Tamura a, Hitoshi Tsuchihashi a, Hajime Nishio b, Koichi Suzuki a a b

Department of Legal Medicine, Osaka Medical College, Takatsuki, Japan Department of Legal Medicine, Hyogo College of Medicine, Nishinomiya, Japan

a r t i c l e

i n f o

Article history: Received 12 November 2013 Received in revised form 20 December 2013 Accepted 22 December 2013 Available online 1 January 2014 Keywords: Traumatic basal subarachnoid hemorrhage Traumatic cerebellar contusions Contrecoup injury

a b s t r a c t Traumatic cerebellar hemorrhagic contusions are infrequent, and the pathogenic mechanism involves a coup injury that is associated with motor vehicle accidents in most cases. Traumatic basal subarachnoid hemorrhage (TBSAH) is commonly reported after blunt trauma to the neck or unrestricted movement of the head, and the source of the hemorrhage is most frequently identified in the vertebrobasilar arteries. A 55-year-old woman who was addicted to alcohol was found dead in her bed. She had a bruise on the left side of her posterior parietal region, and autopsy revealed massive subarachnoid hemorrhage at the base of the brain; the hematoma was strongly attached to the right lower surface of the cerebellar hemisphere. No ruptured cerebral aneurysms, arteriovenous malformations or vertebrobasilar artery leakage were detected. Hemorrhagic cerebellar contusions were regarded as the source of the TBSAH. This is the first report of TBSAH suspected to have been caused by contrecoup cerebellar contusions. Ó 2013 Elsevier Ireland Ltd. All rights reserved.

1. Introduction

2. Case report

Traumatic cerebellar hemorrhagic contusions and hematomas are rare, with a reported incidence of approximately 0.39–0.82% of all head injuries [1–5]. The most frequent mechanism of injury involves coup injury following direct trauma to the occiput [6,7]. Subarachnoid hemorrhage (SAH) at the base of the brain usually results from a nontraumatic cause such as aneurysm rupture or vascular malformation. However, trauma is also a well-known cause of basal SAH, and differentiation between traumatic and nontraumatic basal SAH is a crucial medico-legal issue. Traumatic basal SAH (TBSAH) is commonly reported after blunt trauma to the neck or unrestricted movement of the head. The vast majority of TBSAH is associated with rupture of vertebrobasilar arteries without associated brain contusion or skull fracture [8–12]. We herein report an autopsy case of TBSAH suspected to have been caused by contrecoup cerebellar contusions in a female alcoholic victim following a fall to the floor. To our knowledge, no similar cases with autopsy details have been described in the forensic literature.

2.1. Clinical history

⇑ Corresponding author. Address: Department of Legal Medicine, Osaka Medical College, Takatsuki 569-8686, Japan. Tel.: +81 726 831221; fax: +81 726 846515. E-mail address: [email protected] (T. Sato). 1344-6223/$ - see front matter Ó 2013 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.legalmed.2013.12.004

A 55-year-old woman began to drink large amounts of alcohol when her daughter got married 4 years previously. She was diagnosed with hypertension and alcohol-related liver dysfunction. At 54 years of age, she developed a staggering gait, and she often fell to the floor. One winter night, she was found dead in the right lateral decubitus position in her bed. We assumed at the time of the forensic autopsy that about 3 days had passed since her death.

2.2. Autopsy findings Her height was 160 cm and weight was 60 kg, and she was slightly putrefactive. Autopsy revealed generalized bruising on the trunk and extremities. There were subcutaneous hematomas (14  14 cm) on left side of her posterior parietal region; no skull fractures or subdural hematomas were observed (Fig. 1). The cerebellum seemed to be atrophic. There was a massive amount of SAH at the base of the brain, and a small amount of SAH was found at the bilateral poles of the temporal lobes (Fig. 2A). The right cerebellar hemisphere was substantially softer than the left one, and clotted blood was tenaciously adhered to the right basal surface of the cerebellum. Her brain weighed 1357 g, including clotted blood at the cerebellum. There were no ruptured cerebral

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2.3. Microscopic findings

Fig. 1. External (A) and subcutaneous (B) injury to the left side of the posterior temporal region.

Histological examination revealed contusions, numerous hemorrhages, and destruction of nerve tissue at the right basal surface of the cerebellum (Fig. 3). Berlin blue staining of the contused region was negative. Although the number of Purkinje cells was only mildly decreased, deformation of Purkinje cells and loss of granular cells were evident. With respect to the cerebrum, petechial hemorrhage in the periaqueductal region of the brain stem was not observed. The presence or absence of petechial hemorrhage, neuronal loss, or gliosis could not be investigated because of the damage to the mammillary bodies by clotted blood. No cardiomyocyte hypertrophy or disarray was observed in her heart. Mild interstitial fibrosis was detected, but inflammatory cell infiltration was not detected. The dominant finding in the liver was severe steatosis with a slight degree of accompanying portal and perivenular fibrosis. A few inflammatory cell infiltrations and no Mallory bodies were observed. 2.4. Toxicological findings Her blood alcohol concentration was 2.024 mg/ml, and drug screening results by gas chromatography/mass spectrometry were negative.

3. Discussion

Fig. 2. Massive SAH at the base of the brain (A). Clotted blood was tenaciously adhered to the right basal surface of the cerebellum. The vertebrobasilar arteries were intact (B).

aneurysms or arteriovenous malformations. We particularly examined the vertebrobasilar arteries, but found no tears (Fig. 2B). Her heart weighed 416 g and appeared hypertrophic. The left ventricular wall width was 1.5 cm. The inner surface of the coronary arteries was slightly atherosclerotic, but showed no signs of stenosis. Her liver weighed 2348 g and showed macroscopic evidence of fatty liver. No other underlying structural diseases were present that could have caused or contributed to her death.

The victim was estimated to have fallen to the floor and suffered a bruise to the left side of her posterior parietal region. Contusions of the contralateral cerebellar hemisphere were assumed to have resulted in massive basal SAH. Intracerebellar hemorrhage rarely occurs in association with traumatic head injury [1–5]. The large majority of supratentorial cerebral contusions are related to the impact of the brain against the bony surfaces of the anterior and middle fossa or the falx on the contralateral side of the bruise. This mechanism (contrecoup) is less likely to occur in the posterior fossa because of the physical confinement of its content. The most frequently considered mechanism is a direct injury to the occiput, where coup injury is often accompanied by skull fracture [6,7]. Sato et al. reported that the cause injury was most frequently traffic accidents; however, d’ Avella stated that the cause was almost equally divided between motor vehicle accidents and backward falls or direct blows to the occiput at home or in the workplace [3,5]. Although there are a

Fig. 3. Contused area of the right basal surface of the cerebellum (arrows) after formalin fixation (A). Histological examination showing contusions with numerous areas of hemorrhage and destruction of nerve tissue. (B) Hematoxylin and eosin staining, original magnification 12.5.

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few reports on contrecoup intracerebellar hemorrhage, they involve delayed traumatic intraparenchymal hematomas [13,14]. TBSAH is a life-threatening form of intracranial bleeding known to be primarily associated with rupture of the vertebrobasilar arteries following minor blunt-force injury to the head and neck [8–12]. In the present case, no vascular lesions were detected in the vertebrobasilar arteries; however, clotted blood was adhered to the basal surface of the cerebellar contusion, indicating the source of the SAH. Chen et al. reported a case of TBSAH possibly originating from hemorrhagic cerebellar contusions due to a fist blow to the neck. In their case, because the cerebellar contusion site was ipsilateral to the blow, coup injury was suggested [15]. In our case, although the victim suffered a bruise to the left side of the posterior parietal region, a right-sided cerebellar contusion was detected. The mechanism of injury was suspected to be contrecoup. At autopsy, her cerebellum appeared atrophic. We speculated that a decrease in the volume of the cerebellum might have been associated with the occurrence of the contusion. Because the cerebellum is usually relatively packed into the posterior fossa, it is immovable at the time of an impact to the head. In our case, however, the atrophic cerebellum might have enabled the formation of a contralateral contusion as a supratentorial injury. The victim had problems with alcohol, and it is well known that cerebellar atrophy is commonly associated with alcoholism [16]. Quantitative pathological studies have shown a loss of Purkinje cells in the vermis (average reduction of 43%) correlated with clinical ataxia/ unsteadiness [17]. Her gait disturbance was severe. Although the reduction in the number of Purkinje cells was mild, deformation of Purkinje cells and loss of granular cells in her vermis were evident. In conclusion, we herein report the first case of fatal TBSAH suspected to have been associated with a contrecoup cerebellar contusion without vertebrobasilar vascular insults. Cerebellar atrophy due to alcoholism may have been deeply involved in the mechanism of her cause of death. References [1] Takeuchi S, Wada K, Takasato Y, Masaoka H, Hayakawa T, Yatsushige H, et al. Traumatic hematoma of the posterior fossa. Acta Neurochir Suppl 2013;118:135–8.

[2] D’Avella D, Cacciola F, Angileri FF, Cardali S, La Rosa G, Germano A, et al. Traumatic intracerebellar hemorrhagic contusions and hematomas. J Neurosurg Sci 2001;45:29–37. [3] Sato K, Hinokuma K, Matsuzawa Y, Takehara S, Uemura K, Ninchoji T, et al. Clinical study of traumatic cerebellar contusion. No Shinkei Geka 1987;15:1285–9. [4] Nagata K, Ishikawa T, Ishikawa T, Shigeno T, Kawahara N, Asano T, et al. Delayed traumatic intracerebellar hematoma: correlation between the location of the hematoma and the pre-existing cerebellar contusion – case report. Neurol Med Chir (Tokyo) 1991;31:792–6. [5] D’Avella D, Servadei F, Scerrati M, Tomei G, Brambilla G, Angileri FF, et al. Traumatic intracerebellar hemorrhage: clinicoradiological analysis of 81 patients. Neurosurgery 2002;50:16–25 [discussion 25–7]. [6] Yokota H, Kobayashi S, Yamakawa K, Tsuji Y, Yajima K, Nakazawa S, et al. Traumatic cerebellar injury. Neurotraumatology 1982;5:259–67. [7] Hamasaki T, Yamaki T, Yoshino E, Higuchi T, Horikawa Y, Hirakawa K. Traumatic posterior fossa hematoma. No To Shinkei 1987;39:1083–90. [8] Ro A, Kageyama N, Hayashi K, Shigeta A, Fukunaga T. Non-traumatic rupture of the intracranial vertebral artery of a man found dead in a severe car accident – histopathological differentiation by step-serial sections. Leg Med (Tokyo) 2008;10(2):101–6. [9] Dowling G, Curry B. Traumatic basal subarachnoid hemorrhage. Report of six cases and review of the literature. Am J Forensic Med Pathol 1988;9:23–31. [10] Gray JT, Puetz SM, Jackson SL, Green MA. Traumatic subarachnoid haemorrhage: a 10-year case study and review. Forensic Sci Int 1999;105(1):13–23. [11] Kibayashi K, Ng’walali PM, Hamada K, Honjyo K, Hamada K, Tsunenari S. Traumatic basal subarachnoid hemorrhage due to rupture of the posterior inferior cerebellar artery – case report. Neurol Med Chir (Tokyo) 2000;40(3):156–9. [12] Salvatori M, Kodikara S, Pollanen M. Fatal subarachnoid hemorrhage following traumatic rupture of the internal carotid artery. Leg Med (Tokyo) 2012;14(6):328–30. [13] Zuccarello M, Cervellini P, Pardatscher K, Iavicoli R, Andrioli GC, Fiore DL. Delayed traumatic cerebellar haematoma. Case report. Acta Neurochir (Wien) 1980;54(3–4):265–70. [14] Olin MS, Young HA, Schmidek HH. Contrecoup intracerebellar hemorrhage: report of a case. Neurosurgery 1980;7:271–3. [15] Chen JH, Ishikawa T, Michiue T, Maeda H. Cerebellar contusions as a possible cause of traumatic basal subarachnoid hemorrhage: a case report. Leg Med (Tokyo) 2010;12:97–9. [16] Torvik A, Torp S. The prevalence of alcoholic cerebellar atrophy. A morphometric and histological study of an autopsy material. J Neurol Sci 1986;75(1):43–51. [17] Baker KG, Harding AJ, Halliday GM, Kril JJ, Harper CG. Neuronal loss in functional zones of the cerebellum of chronic alcoholics with and without Wernicke’s encephalopathy. Neuroscience 1999;91(2):429–38.

Traumatic basal subarachnoid hemorrhage suspected to have been caused by contrecoup cerebellar contusions: a case report.

Traumatic cerebellar hemorrhagic contusions are infrequent, and the pathogenic mechanism involves a coup injury that is associated with motor vehicle ...
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