Case reports 9 Springer-Verlag 1992 Child's Nerv Syst (1992) 8:343-346
Acute spontaneous subdural hematoma in a teenager Alpaslan Kulah 1, Nebahat Ta~demir 2, and Co~kun Fiskeci 3 1 Clinic of Neurosurgery, 2 Clinic of Neurology, and 3 Clinic of Radiology, Dicle University School of Medicine, TR-21280 Diyarbakir, Turkey Received December 27, 1990
Abstract. A teenager with a history of sudden onset of headache and vomiting is described. Computed tomography revealed an acute subdural hematoma in the right temporoparietal region, causing marked compression of the right ventricular system and a shift of midline structures to the left. N o operation was carried out because the symptoms and neurological signs were slight enough to allow monitoring by means of close clinical and neuroradiological investigations. Within 18 days the hematoma resolved spontaneously and completely. There was no history of trauma or any objective sign of trauma about the face or head, and radiography of the skull showed no fracture. We are not aware of any other report of a spontaneous subdural hematoma which did not require surgery. This feature makes our case unique. In addition, comparable cases in the literature are reviewed and the etiological possibilities of spontaneous subdural hem a t o m a are discussed.
scribed the syndrome "acute spontaneous subdural hematoma". Further review of the literature shows the rarity of this entity; in fact, few authors have reported cases of "acute spontaneous subdural h e m a t o m a " (Table 1). All of these patients required surgical evacuation because of acute progressive neurological deterioration with loss of consciousness and/or signs suggestive of tentorial herniation. The bleeding site, if identified, was usually arterial, involving one of the cortical branches of the middle cerebral artery. Most patients were middle aged, rather than young adults. There was no occurrence in the older child or adolescent. Here we report a teenager with an acute spontaneous subdural hematoma which needed no surgical treatment and resolved spontaneously and completely within 18 days. With respect to both the age of the patient and the spontaneous resolution of the h e m a t o m a we have not encountered such a case in the current literature dealing with acute spontaneous subdural hematomas.
Key words: Teenager - Computed t o m o g r a p h y - Acute spontaneous subdural h e m a t o m a - Spontaneous resolution - Sylvian region
The acute subdural hematoma is well known as a complication of craniocerebral trauma resulting in laceration or contusion of the brain and tearing of bridging veins and/ or cortical arteries [4, 9, 14, 15]. The standard surgical treatment consists of evacuation of the hematoma through burr holes or craniotomy, depending upon the consistency of the clot. In his pioneering report M u n r o [10] described a patient, without a history of head trauma, who was affected by sudden severe headache and then developed progressive weakness of the limbs due to a large right subdural hematoma. Talalla and McKissock [17] reported eight cases of acute subdural hematoma due to spontaneous rupture of a cortical artery and first deCorrespondence to: A. Kulah
Case report A 15-year-old boy was admitted to the neurological clinic of our University Hospital after being transferred to the emergency service because of the sudden onset of severe headache and vomiting. No loss of consciousness was noted. The patient denied any recent or prior trauma; this was confirmed by his family. His past medical history was uneventful. On admission he was alert and had no external evidence of head injury; he had a questionable left hemiparesis and right papilledema. Blood pressure was 110/70 mmHg and pulse rate 70/rain. The remaining findings of both the general physical and neurological examination were normal. A lumbar puncture showed an increased cerebrospinal fluid pressure and no xanthochromia. A skull radiograph did not show any abnormality. Routine blood investigations, coagulation screen, chest radiograph, and electrocardiogram were all reported to be normal. An electrocephalogram discovered temporo-occipital slowing on the left side. Two days after admission a computed tomography (CT) scan after contrast-medium enhan~ment showed a high-density mass with a concave inner margin in the right temporoparietal region, causing a marked shift of midline structures to the left and a marked compression of the right ventricular system. It was assumed that this must be an acute spontaneous subdural hematoma, as there was no associated brain edema, laceration or contusion suggestive of trau-
344 Table 1. Cases of acute spontaneous subdural hematoma reported in the literature Author
Year
No. of cases (n = 35)
Age (years)
Sex
Munro Scott
1934 1949
1 2
59 66 51
M M F
Talalla and McKissock
1971
8
61 54 57 66 54 59 72 48
M M M F M M M M
Williams
1971
1
71
M
O'Hara et al.
1973
2
59 60
M M
O'Brien etal.
1974
2
61 57
M M
Buruma and Sande
1979
1
55
M
Byun and Patel
1979
2
37 57
F M
Yamanaka etal.
1981
1
48
M
Arai
1983
1
Hesselbrock etal.
1984
1
50 51
F M
McDermott eta1.
1984
5
Yanai etal. Tokoro etal.
1985 1988
1 2
53 55 65 45 54 40
M M M F M M
53 45
M M
Stephenson and Gibson
1989
3
64 67 66
M M M
Jacome and Yanez
1989
1
65
M
1
15
M
Current report
ma and no gross evidence of vascular malformation was found. The rest of the brain appeared normal (Fig. 1). Two days later the control CT scan, without administration of contrast medium, supported the presumptive diagnosis of an acute spontaneous subdural hematoma (Fig. 2). Therefore, the patient was transferred to the neurosurgical clinic. At the time of transfer he was alert, but continued to complain of a moderate headache which was decreasing in intensity. Neurological examination showed no lateralizing signs; however, the right papilledema still persisted. Because of the trivial symptoms and signs, which had been decreasing, no surgical evacuation was carried out. The patient was monitored by means of close clinical and neurological investigations. Eighteen days later a control CT scan showed that the hematoma had resolved completely and the ventricular system had expanded to its normal size and site (Fig. 3). Prior to discharge the patient underwent angiography of both carotid arteries, which did not reveal any abnormality. He was discharged in excellent condition, free of symptoms and complaints. Six months after discharge, a repeat angiogram to study potential external or internal carotid contributions to a tumor or a vascular malformation revealed no cause for the hemorrhage.
Discussion
A c u t e s p o n t a n e o u s subdural h e m a t o m a has been infrequently reported in the literature [I - 3, 5, 8 - 1 3 , 1 6 - 1 8 , 2 0 - 2 2 ] . We have collected 35 cases f r o m the literature, including o u r o w n case (Table 1). There was an unexplained male p r e p o n d e r a n c e (80%) [7]. M o s t patients were middle-aged rather than y o u n g adults a n d the average age was 57 years, ranging f r o m 37 to 72. Unlike o u r patient, w h o was aged 15 years, no patient in this series was u n d e r 30 years o f age. This m i g h t be explained by the increasing n u m b e r o f risk factors during the course o f life which m a y possibly lead to the d e v e l o p m e n t o f an acute s p o n t a n e o u s h e m a t o m a . H o w ever, age-related brain a t r o p h y , which causes the stretching o f bridging veins, should n o t be cited as being a possible factor contributing to the predilection o f old patients developing acute s p o n t a n e o u s subdural hem a t o m a s because in 26 patients (87%), whose bleeding points were k n o w n , an arterial origin was f o u n d to be responsible. Scott [13] described a n u m b e r o f these risk factors: infection, systemic metabolic factors, hypertension, h e m o r r h a g i c diathesis, vascular m a l f o r m a t i o n , bleeding f r o m a tumor, and chronic alcoholism. H y p e r tension and alcohol abuse have also been reported by several other a u t h o r s as being the m o s t c o m m o n risk factors [1, 8, 16-22]. In our case, hypertension and alcohol abuse were out o f the question and no evidence o f an a n e u r y s m or other vascular anomalies was seen on neuroradiological examination. W h a t e v e r the causative mechanism o f an acute s p o n a n e o u s subdural h e m a t o m a , no cause in o u r patient could be established with certainty as reported by other a u t h o r s in some o f their cases [3, 5, 7, 10, 12, 13, 17]. In all previously reported cases o f acute s p o n t a n e o u s subdural h e m a t o m a , in c o n t r a s t to o u r case, the crani o t o m y or burr holes were required because o f the sudden onset o f life-threatening neurological deterioration and in 26 o f a total o f 34 patients and arterial source in the region o f the sylvian fissure was f o u n d either at operation or at a u t o p s y [21]. N i n e o f 34 cases did n o t survive the insult. In early studies the majority o f deaths occurred before the a d v e n t o f C T [10, 17]. Several hypotheses have been p r o p o s e d to explain the development o f these s p o n t a n e o u s subdural h e m a t o m a s . J a c o m e and Yanez [7] described a patient with acute s p o n t a n e o u s subdural h e m a t o m a apparently p r o d u c e d by straining while lifting a heavy weight. T h e y f o u n d no source o f bleeding at surgery. However, they suspected that the rupture o f bridging dural veins while p e r f o r m i n g the Valsalva m a n e u v e r on h e a v y lifting caused the bleed. The m o s t widely s u p p o r t e d hypothesis was p u t f o r w a r d by Vance [19], w h o examined a u t o p s y material f r o m cases o f subdural h e m a t o m a and f o u n d arterial ruptures which were either due to the avulsion o f twigs that traversed the subdural space f r o m surface cortical arteries to the d u r a m a t e r or to the rupture o f cortical vessels at the origin o f a fragile arterial twig, especially a right-angled branch, which is a point o f potential weakness which he termed a "fire h o u s e " rupture. O ' B r i e n et al. [11] s u p p o r t e d his histopathological findings by showing microscopic deft-
345
Fig. 1A, B. Computed tomography (CT) scan after contrast-medium enhancement shows a high-density mass which had a concave inner margin in the right temporoparietal region (arrows) with a marked shift of midline structures to the left Fig. 2. Two days after admission plain CT scan showing an acute spontaneous subdural hematoma in the right temporoparietal area (arrows). Midline shift with collapse of the right lateral ventricle is still evidient. There is no associated brain laceration, edema or contusion suggestive of trauma Fig. 3. Eighteen days later plain CT scan shows that the hematoma resolved completely and the ventricular system expanded to its normal size and site
ciency in the wall of the affected artery corresponding to the origin in a branch on the lateral cerebral surface near the sylvian fissure. In our case, there was no visual evidence of an arterial twig at the bleeding point. The hematoma was also located in the temporoparietal region, on the lateral cerebral surface, covering the Sylvian fissure. This anatomically weak point might have caused rupture by a sudden motion of the brain, not severe enough to be considered trauma [28], or by other unexplained etiology [3, 5, 10, 13, 17]. In our patient the acute s p o n t a n e o u s subdural hem a t o m a caused a marked compression effect on the brain, but that did not produce any severe neurological deficits which could have required an immediate surgical intervention. In contrast to all of the 34 cases previously reported in the literature, a complete spontaneous resolution without re-rupture and catastrophic deterioration occurred in our patient. This might be attributable to the age of our patient and his having had better cerebral parenchyma resistance against the expansion of the spontaneous subdural hematoma. As H o w a r d III [6] suggested, acute subdural hematoma volumes in old patients were on average more than four times larger and caused twice the a m o u n t of midline shift as those of young patients. The pathophysiology of acute subdural hematoma varies with age, and mortality rates were more than four times higher in older patients than in younger ones. That might also be applicable to the spontaneous acute subdural hematoma, making it reasonable to consider that
acute spontaneous subdural hematoma might be an agedependent clinical entity which can also have a better outcome in older children than in adults or the elderly. With the sudden onset of symptoms (usually headache and vomiting) the possibility of a spontaneous subdural hematoma should also be kept in mind even if the patient is a teenager without a previous history of head trauma or without any severe neurological deficit.
References 1. Arai H (1983) Acute hypertensive subdural hematoma from arterial rupture shortly after the onset of cerebral subcortical hemorrhage: leakage of contrast medium during angiography. Stroke 14:281-285 2. Buruma ()JS, Sande J Jr (1979) Bilateral acute spontaneous subdural hematoma. A case report. Clin Neurol Neurosurg 79:211 214 3. Byun HS, Patel PP (t979) Spontaneous subdural hematoma of arterial origin. Report of two cases. Neurosurgery 5:611-613 4. Fell DA, Fitzgerald S, Moiel RH, Caram P (1975) Acute subdural hematomas. Review of 144 cases. J Neurosurg 42:37-42 5. Hesselbrock R, Sawaya R, Means ED (1984) Acute spontaneous subdural hematoma. Surg Neurol 21:363-366 6. Howard MA III, Gross AS, Dacey RG, Winn HR (1989) Acute subdural hematomas: an age-dependent clinical entity. J Neurosurg 71:858-863 7. Jacome DE, Yanze GF (1989) Subdural hematoma upon straining. J Neurol Neurosurg Psychiatry 52:134 8. McDermott M, Fleming JPR, Vanderlinden RG, Tucker WS (i 984) Spontaneous arterial subdural hematoma. Neurosurgery 14:13-18
346 9. McLaurin RL, Tutor FT (1961) Acute subdural hematoma. Review of ninety cases. J Neurosurg 18:61-67 10. Munro D (1934) The diagnosis and treatment of subdural hematoma: a report of sixty-two cases. N Engl J Med 210:11451160 11. O'Brien PK, Norris JW, Tator CH (1974) Acute subdural hematoma of arterial origin. J Neurosurg 41:435-439 12. O'Hara H, Takaku A, Suzuki J (1973) Acute spontaneous subdural hematoma. Report of two cases. No To Shinkei 25: 591596 13. Scott M (1949) Spontaneous nontraumatic subdural hematoma. JAMA 141:596-602 14. Seeling JM, Becket DP, Miller JD (1981) Traumatic acute subdural hematoma. Major mortality reduction in comatose patients treated within four hours. N Engl J Med 304:1511-1518 15. Shenkin HA (1982) Acute subdural hematoma. Review of 39 consecutive cases with high incidence of cortical artery rupture. J Neurosurg 57:254-257
16. Stephenson G, Gibson M (1989) Acute spontaneous subdural hematoma of arterial origin. Br J Neurosurg 3:225-228 17. Talalla A, McKissock W (1971) Acute spontaneous subdural hemorrhage: an unusual form of cerebrovascular accident. Neurology 21:19-25 18. Tokoro K, Nakajima F, Yamataki A (1988) Acute spontaneous subdural hematoma of arterial origin. Surg Neuro129:159-163 19. Vance BM (1950) Ruptures of surface blood vessels on cerebral hemispheres as a cause of subdural hemorrhage. Arch Surg 61: 992-1006 20. Williams B (1971) Subdural hematoma of arterial origin. Lancet I: 1074-1075 21. Yamanaka M, Chikuie S, Sasaki U (1981) Acute spontaneous subdural hematoma. A case report. No Shinkei Geka 9:12071221 22. Yanai Y, Kohno N, Mitsui T (1985) Acute spontaneous subdural hematoma of arterial origin. Surg Neurol 23:417-420
Acute spontaneous subdural hematoma in a teenager Alpaslan Kulah 1, Nebahat Ta~demir 2, and Co~kun Fiskeci 3 1 Clinic of Neurosurgery, 2 Clinic of Neurology, and 3 Clinic of Radiology, Dicle University School of Medicine, TR-21280 Diyarbakir, Turkey Received December 27, 1990
Abstract. A teenager with a history of sudden onset of headache and vomiting is described. Computed tomography revealed an acute subdural hematoma in the right temporoparietal region, causing marked compression of the right ventricular system and a shift of midline structures to the left. N o operation was carried out because the symptoms and neurological signs were slight enough to allow monitoring by means of close clinical and neuroradiological investigations. Within 18 days the hematoma resolved spontaneously and completely. There was no history of trauma or any objective sign of trauma about the face or head, and radiography of the skull showed no fracture. We are not aware of any other report of a spontaneous subdural hematoma which did not require surgery. This feature makes our case unique. In addition, comparable cases in the literature are reviewed and the etiological possibilities of spontaneous subdural hem a t o m a are discussed.
scribed the syndrome "acute spontaneous subdural hematoma". Further review of the literature shows the rarity of this entity; in fact, few authors have reported cases of "acute spontaneous subdural h e m a t o m a " (Table 1). All of these patients required surgical evacuation because of acute progressive neurological deterioration with loss of consciousness and/or signs suggestive of tentorial herniation. The bleeding site, if identified, was usually arterial, involving one of the cortical branches of the middle cerebral artery. Most patients were middle aged, rather than young adults. There was no occurrence in the older child or adolescent. Here we report a teenager with an acute spontaneous subdural hematoma which needed no surgical treatment and resolved spontaneously and completely within 18 days. With respect to both the age of the patient and the spontaneous resolution of the h e m a t o m a we have not encountered such a case in the current literature dealing with acute spontaneous subdural hematomas.
Key words: Teenager - Computed t o m o g r a p h y - Acute spontaneous subdural h e m a t o m a - Spontaneous resolution - Sylvian region
The acute subdural hematoma is well known as a complication of craniocerebral trauma resulting in laceration or contusion of the brain and tearing of bridging veins and/ or cortical arteries [4, 9, 14, 15]. The standard surgical treatment consists of evacuation of the hematoma through burr holes or craniotomy, depending upon the consistency of the clot. In his pioneering report M u n r o [10] described a patient, without a history of head trauma, who was affected by sudden severe headache and then developed progressive weakness of the limbs due to a large right subdural hematoma. Talalla and McKissock [17] reported eight cases of acute subdural hematoma due to spontaneous rupture of a cortical artery and first deCorrespondence to: A. Kulah
Case report A 15-year-old boy was admitted to the neurological clinic of our University Hospital after being transferred to the emergency service because of the sudden onset of severe headache and vomiting. No loss of consciousness was noted. The patient denied any recent or prior trauma; this was confirmed by his family. His past medical history was uneventful. On admission he was alert and had no external evidence of head injury; he had a questionable left hemiparesis and right papilledema. Blood pressure was 110/70 mmHg and pulse rate 70/rain. The remaining findings of both the general physical and neurological examination were normal. A lumbar puncture showed an increased cerebrospinal fluid pressure and no xanthochromia. A skull radiograph did not show any abnormality. Routine blood investigations, coagulation screen, chest radiograph, and electrocardiogram were all reported to be normal. An electrocephalogram discovered temporo-occipital slowing on the left side. Two days after admission a computed tomography (CT) scan after contrast-medium enhan~ment showed a high-density mass with a concave inner margin in the right temporoparietal region, causing a marked shift of midline structures to the left and a marked compression of the right ventricular system. It was assumed that this must be an acute spontaneous subdural hematoma, as there was no associated brain edema, laceration or contusion suggestive of trau-
344 Table 1. Cases of acute spontaneous subdural hematoma reported in the literature Author
Year
No. of cases (n = 35)
Age (years)
Sex
Munro Scott
1934 1949
1 2
59 66 51
M M F
Talalla and McKissock
1971
8
61 54 57 66 54 59 72 48
M M M F M M M M
Williams
1971
1
71
M
O'Hara et al.
1973
2
59 60
M M
O'Brien etal.
1974
2
61 57
M M
Buruma and Sande
1979
1
55
M
Byun and Patel
1979
2
37 57
F M
Yamanaka etal.
1981
1
48
M
Arai
1983
1
Hesselbrock etal.
1984
1
50 51
F M
McDermott eta1.
1984
5
Yanai etal. Tokoro etal.
1985 1988
1 2
53 55 65 45 54 40
M M M F M M
53 45
M M
Stephenson and Gibson
1989
3
64 67 66
M M M
Jacome and Yanez
1989
1
65
M
1
15
M
Current report
ma and no gross evidence of vascular malformation was found. The rest of the brain appeared normal (Fig. 1). Two days later the control CT scan, without administration of contrast medium, supported the presumptive diagnosis of an acute spontaneous subdural hematoma (Fig. 2). Therefore, the patient was transferred to the neurosurgical clinic. At the time of transfer he was alert, but continued to complain of a moderate headache which was decreasing in intensity. Neurological examination showed no lateralizing signs; however, the right papilledema still persisted. Because of the trivial symptoms and signs, which had been decreasing, no surgical evacuation was carried out. The patient was monitored by means of close clinical and neurological investigations. Eighteen days later a control CT scan showed that the hematoma had resolved completely and the ventricular system had expanded to its normal size and site (Fig. 3). Prior to discharge the patient underwent angiography of both carotid arteries, which did not reveal any abnormality. He was discharged in excellent condition, free of symptoms and complaints. Six months after discharge, a repeat angiogram to study potential external or internal carotid contributions to a tumor or a vascular malformation revealed no cause for the hemorrhage.
Discussion
A c u t e s p o n t a n e o u s subdural h e m a t o m a has been infrequently reported in the literature [I - 3, 5, 8 - 1 3 , 1 6 - 1 8 , 2 0 - 2 2 ] . We have collected 35 cases f r o m the literature, including o u r o w n case (Table 1). There was an unexplained male p r e p o n d e r a n c e (80%) [7]. M o s t patients were middle-aged rather than y o u n g adults a n d the average age was 57 years, ranging f r o m 37 to 72. Unlike o u r patient, w h o was aged 15 years, no patient in this series was u n d e r 30 years o f age. This m i g h t be explained by the increasing n u m b e r o f risk factors during the course o f life which m a y possibly lead to the d e v e l o p m e n t o f an acute s p o n t a n e o u s h e m a t o m a . H o w ever, age-related brain a t r o p h y , which causes the stretching o f bridging veins, should n o t be cited as being a possible factor contributing to the predilection o f old patients developing acute s p o n t a n e o u s subdural hem a t o m a s because in 26 patients (87%), whose bleeding points were k n o w n , an arterial origin was f o u n d to be responsible. Scott [13] described a n u m b e r o f these risk factors: infection, systemic metabolic factors, hypertension, h e m o r r h a g i c diathesis, vascular m a l f o r m a t i o n , bleeding f r o m a tumor, and chronic alcoholism. H y p e r tension and alcohol abuse have also been reported by several other a u t h o r s as being the m o s t c o m m o n risk factors [1, 8, 16-22]. In our case, hypertension and alcohol abuse were out o f the question and no evidence o f an a n e u r y s m or other vascular anomalies was seen on neuroradiological examination. W h a t e v e r the causative mechanism o f an acute s p o n a n e o u s subdural h e m a t o m a , no cause in o u r patient could be established with certainty as reported by other a u t h o r s in some o f their cases [3, 5, 7, 10, 12, 13, 17]. In all previously reported cases o f acute s p o n t a n e o u s subdural h e m a t o m a , in c o n t r a s t to o u r case, the crani o t o m y or burr holes were required because o f the sudden onset o f life-threatening neurological deterioration and in 26 o f a total o f 34 patients and arterial source in the region o f the sylvian fissure was f o u n d either at operation or at a u t o p s y [21]. N i n e o f 34 cases did n o t survive the insult. In early studies the majority o f deaths occurred before the a d v e n t o f C T [10, 17]. Several hypotheses have been p r o p o s e d to explain the development o f these s p o n t a n e o u s subdural h e m a t o m a s . J a c o m e and Yanez [7] described a patient with acute s p o n t a n e o u s subdural h e m a t o m a apparently p r o d u c e d by straining while lifting a heavy weight. T h e y f o u n d no source o f bleeding at surgery. However, they suspected that the rupture o f bridging dural veins while p e r f o r m i n g the Valsalva m a n e u v e r on h e a v y lifting caused the bleed. The m o s t widely s u p p o r t e d hypothesis was p u t f o r w a r d by Vance [19], w h o examined a u t o p s y material f r o m cases o f subdural h e m a t o m a and f o u n d arterial ruptures which were either due to the avulsion o f twigs that traversed the subdural space f r o m surface cortical arteries to the d u r a m a t e r or to the rupture o f cortical vessels at the origin o f a fragile arterial twig, especially a right-angled branch, which is a point o f potential weakness which he termed a "fire h o u s e " rupture. O ' B r i e n et al. [11] s u p p o r t e d his histopathological findings by showing microscopic deft-
345
Fig. 1A, B. Computed tomography (CT) scan after contrast-medium enhancement shows a high-density mass which had a concave inner margin in the right temporoparietal region (arrows) with a marked shift of midline structures to the left Fig. 2. Two days after admission plain CT scan showing an acute spontaneous subdural hematoma in the right temporoparietal area (arrows). Midline shift with collapse of the right lateral ventricle is still evidient. There is no associated brain laceration, edema or contusion suggestive of trauma Fig. 3. Eighteen days later plain CT scan shows that the hematoma resolved completely and the ventricular system expanded to its normal size and site
ciency in the wall of the affected artery corresponding to the origin in a branch on the lateral cerebral surface near the sylvian fissure. In our case, there was no visual evidence of an arterial twig at the bleeding point. The hematoma was also located in the temporoparietal region, on the lateral cerebral surface, covering the Sylvian fissure. This anatomically weak point might have caused rupture by a sudden motion of the brain, not severe enough to be considered trauma [28], or by other unexplained etiology [3, 5, 10, 13, 17]. In our patient the acute s p o n t a n e o u s subdural hem a t o m a caused a marked compression effect on the brain, but that did not produce any severe neurological deficits which could have required an immediate surgical intervention. In contrast to all of the 34 cases previously reported in the literature, a complete spontaneous resolution without re-rupture and catastrophic deterioration occurred in our patient. This might be attributable to the age of our patient and his having had better cerebral parenchyma resistance against the expansion of the spontaneous subdural hematoma. As H o w a r d III [6] suggested, acute subdural hematoma volumes in old patients were on average more than four times larger and caused twice the a m o u n t of midline shift as those of young patients. The pathophysiology of acute subdural hematoma varies with age, and mortality rates were more than four times higher in older patients than in younger ones. That might also be applicable to the spontaneous acute subdural hematoma, making it reasonable to consider that
acute spontaneous subdural hematoma might be an agedependent clinical entity which can also have a better outcome in older children than in adults or the elderly. With the sudden onset of symptoms (usually headache and vomiting) the possibility of a spontaneous subdural hematoma should also be kept in mind even if the patient is a teenager without a previous history of head trauma or without any severe neurological deficit.
References 1. Arai H (1983) Acute hypertensive subdural hematoma from arterial rupture shortly after the onset of cerebral subcortical hemorrhage: leakage of contrast medium during angiography. Stroke 14:281-285 2. Buruma ()JS, Sande J Jr (1979) Bilateral acute spontaneous subdural hematoma. A case report. Clin Neurol Neurosurg 79:211 214 3. Byun HS, Patel PP (t979) Spontaneous subdural hematoma of arterial origin. Report of two cases. Neurosurgery 5:611-613 4. Fell DA, Fitzgerald S, Moiel RH, Caram P (1975) Acute subdural hematomas. Review of 144 cases. J Neurosurg 42:37-42 5. Hesselbrock R, Sawaya R, Means ED (1984) Acute spontaneous subdural hematoma. Surg Neurol 21:363-366 6. Howard MA III, Gross AS, Dacey RG, Winn HR (1989) Acute subdural hematomas: an age-dependent clinical entity. J Neurosurg 71:858-863 7. Jacome DE, Yanze GF (1989) Subdural hematoma upon straining. J Neurol Neurosurg Psychiatry 52:134 8. McDermott M, Fleming JPR, Vanderlinden RG, Tucker WS (i 984) Spontaneous arterial subdural hematoma. Neurosurgery 14:13-18
346 9. McLaurin RL, Tutor FT (1961) Acute subdural hematoma. Review of ninety cases. J Neurosurg 18:61-67 10. Munro D (1934) The diagnosis and treatment of subdural hematoma: a report of sixty-two cases. N Engl J Med 210:11451160 11. O'Brien PK, Norris JW, Tator CH (1974) Acute subdural hematoma of arterial origin. J Neurosurg 41:435-439 12. O'Hara H, Takaku A, Suzuki J (1973) Acute spontaneous subdural hematoma. Report of two cases. No To Shinkei 25: 591596 13. Scott M (1949) Spontaneous nontraumatic subdural hematoma. JAMA 141:596-602 14. Seeling JM, Becket DP, Miller JD (1981) Traumatic acute subdural hematoma. Major mortality reduction in comatose patients treated within four hours. N Engl J Med 304:1511-1518 15. Shenkin HA (1982) Acute subdural hematoma. Review of 39 consecutive cases with high incidence of cortical artery rupture. J Neurosurg 57:254-257
16. Stephenson G, Gibson M (1989) Acute spontaneous subdural hematoma of arterial origin. Br J Neurosurg 3:225-228 17. Talalla A, McKissock W (1971) Acute spontaneous subdural hemorrhage: an unusual form of cerebrovascular accident. Neurology 21:19-25 18. Tokoro K, Nakajima F, Yamataki A (1988) Acute spontaneous subdural hematoma of arterial origin. Surg Neuro129:159-163 19. Vance BM (1950) Ruptures of surface blood vessels on cerebral hemispheres as a cause of subdural hemorrhage. Arch Surg 61: 992-1006 20. Williams B (1971) Subdural hematoma of arterial origin. Lancet I: 1074-1075 21. Yamanaka M, Chikuie S, Sasaki U (1981) Acute spontaneous subdural hematoma. A case report. No Shinkei Geka 9:12071221 22. Yanai Y, Kohno N, Mitsui T (1985) Acute spontaneous subdural hematoma of arterial origin. Surg Neurol 23:417-420
