BACKGROUND: Acute subdural hematoma is usually associated with cerebral contusion or laceration of the bridging veins following a head injury. However, several cases of acute subdural hematoma without head injury (acute spontaneous subdural hematoma) have been reported. METHODS: Among 162 cases of acute subdural hematoma admitted to our departments between 1996 and 2003, we repoort eight cases of acute spontaneous subdural hematoma. These cases fulfilled the following criteria. 1) Head injury was either trivial or absent. 2) Neither aneurysm nor arteriovenous malformation was apparent. 3) CT scan revealed neither brain contusion nor traumatic subarachnoid hemorrhage. 4) At operation, laceration of the cortical artery was observed. In this article, we describe the clinical feature (age, sex, Glasgow Coma Scale [GCS] Score on admission, past history, CT appearance, and outcome) associated with this condition. RESULTS: Patients ranged in age from 68 to 85 years (average 74.8 years), and were comprised of 3 males and 5 females. Previous medical history included cerebral infarction in 6 of the 8 patients and myocardial infarction in 1 patient. These seven patients were taking antiplatelet manifestation. GCS on admission ranged from 4 to 13. Five of the 7 patients on antiplatelet medication had secondary insults, such as hypoxia. On CT, hematoma thickness ranged from 13.2mm to 42.5mm (average 22.6mm), and midline shift ranged from 10.0mm to 24.0mm (average 16.5mm). Neurological outcome evaluated using the Glasgow Outcome Scale was as follows, good recovery n = 2, moderate disability n = 2, severe disability n = 3, persistent vegetative state n = 1. CONCLUSION: The mechanism of acute spontaneous subdural hematoma is influenced by the presence of pre-existing cerebrovascular disease and by the use of antiplatelet agents. In such cases, the possibility of cortical arterial bleeding should be taken into account, and craniotomy should be performed.
BACKGROUND:Acute subdural hematoma is usually associated with cerebral contusion or laceration of the bridging veins following a head injury. However, several cases of acute subdural hematoma without head injury (acute spontaneous subdural hematoma) have been reported. METHODS: Among 162 cases of acute subdural hematoma admitted to our departments between 1996 and 2003, we repoort eight cases of acute spontaneous subdural hematoma. These cases fulfilled the following criteria. 1) Head injury was either trivial or absent. 2) Neither aneurysm nor arteriovenous malformation was apparent. 3) CT scan revealed neither brain contusion nor traumatic subarachnoid hemorrhage. 4) At operation, laceration of the cortical artery was observed. In this article, we describe the clinical feature (age, sex, Glasgow Coma Scale [GCS] Score on admission, past history, CT appearance, and outcome) associated with this condition. RESULTS:Patients ranged in age from 68 to 85 years (average 74.8 years), and were comprised of 3 males and 5 females. Previous medical history included cerebral infarction in 6 of the 8 patients and myocardial infarction in 1 patient. These seven patients were taking antiplatelet manifestation. GCS on admission ranged from 4 to 13. Five of the 7 patients on antiplatelet medication had secondary insults, such as hypoxia. On CT, hematoma thickness ranged from 13.2mm to 42.5mm (average 22.6mm), and midline shift ranged from 10.0mm to 24.0mm (average 16.5mm). Neurological outcome evaluated using the Glasgow Outcome Scale was as follows, good recovery n = 2, moderate disability n = 2, severe disability n = 3, persistent vegetative state n = 1. CONCLUSION: The mechanism of acute spontaneous subdural hematoma is influenced by the presence of pre-existing cerebrovascular disease and by the use of antiplatelet agents. In such cases, the possibility of cortical arterial bleeding should be taken into account, and craniotomy should be performed.