To elucidate whether a relationship exists between the site of trauma and severity of acute hyperextension spinal cord injury without bone damage, we examined the clinical features of 25 male and 10 female patients aged 13 to 88 years. None of the patients had vertebral damage such as fracture and dislocation. The site of impact was classified as the buccal, forehead, or mandibular region. The neurological findings were assessed according to Frankel's classification at admission and at follow up after 3 months or more to assess outcome. Eleven patients suffered trauma in the buccal region, one patient in Frankel's grade B, three in grade C, and seven in grade D at admission. All 11 of these patients showed an improvement of one grade or more to an outcome of C in one patient, D in one, and E in nine. Trauma occurred at the forehead region in 18 patients, four in grade B, 10 in grade C, and four in grade D. Improvement was seen at follow up by one grade or more to C in one patient, D in 10, and E in seven. Trauma occurred at the mandibular region in six patients, four in grade B and two in grade C. Four of these patients showed improvement of one grade or more to grade B in one, grade C in four, and grade E in one. Overall, seven patients had poor outcomes, five of whom suffered trauma to the mandibular region, indicating that impact to the mandibular region tends to have an unfavorable clinical outcome. Our findings indicate that the site of trauma greatly influences the severity of hyperextension spinal cord injury.

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The incidences of arterial dissection of the vertebral artery (VA) of aortic origin and VA of subclavian artery origin were determined. The origins of the left and right VAs were confirmed by angiography in 860 and 717 patients, respectively. Left VA of aortic origin was found in 21 patients (6 females and 15 males) but no right VA of aortic origin was found. Left VA of left subclavian artery origin was found in 837 patients and right VA of right subclavian artery origin in 717 patients. Arterial dissection of the VA occurred in 17 patients (6 females and 11 males), four patients with left VA of aortic origin, seven with left VA of left subclavian artery origin, four with right VA of right subclavian artery origin, and two with bilateral VAs of subclavian artery origin. Left VA of aortic origin (4 of 21 patients) was associated with a significantly higher incidence of VA dissection than left VA of left subclavian artery origin and right VA of right subclavian artery origin (p < 0.001). Left VA of aortic origin is associated with a predilection for VA dissection in comparison to VA of subclavian artery origin.

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Asymptomatic small hemorrhages were identified in hypertensive patients by T₂*-weighted gradient echo magnetic resonance (MR) imaging to investigate the relationship between hypertensive intracerebral hemorrhage and asymptomatic minute hemorrhages. Forty-eight patients with hypertensive intracerebral hemorrhage or cerebral infarction with hypertension (these diseases were defined as stroke) were treated in National Defense Medical College from April 1998 to February 2000. All patients had no past history of stroke or head injury, underwent MR imaging within 6 months of the stroke attack, were aged from 40 to 80 years, and had no diagnosis of aneurysm, angioma, or moyamoya disease. Patients were divided into the infarction group and hemorrhage group. All foci over 2 mm in size appearing as hypointense on T₂*-weighted MR imaging and unrelated to stroke areas were defined as minute hemorrhages. There were no significant differences between the two groups with respect to sex, age, and history of diabetes mellitus. The incidence of minute hemorrhages in the hemorrhage group (21/26) was greater than in the infarction group (9/22, p < 0.01). The incidence of minute hemorrhages in the basal ganglia (18/26) was greater in the hemorrhage group than in the infarction group (4/22, p < 0.001). Symptomatic intracerebral hemorrhage may be preceded by asymptomatic minute hemorrhage.

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Two child and three elderly patients underwent craniotomy for organized and/or partially calcified chronic subdural hematomas (CSHs). The characteristic feature of magnetic resonance imaging was a heterogeneous web-like structure in the hematoma cavity. Both children had undergone one side subduroperitoneal shunt for bilateral CSHs when infants. As a result, the opposite hematoma cavities persisted and developed into calcified CSHs after a couple of years. All three elderly patients with senile brain atrophy showed various systemic complications such as cerebral infarction, diabetes mellitus, leg ulceration, cirrhosis, and bleeding tendency. Craniotomy for removal of the hematoma and calcification achieved good results in all patients. Subdural space created by shunt, craniotomy, or brain atrophy and persisting for a certain period, and additional various brain damage such as microcirculatory disorder, meningitis, encephalitis, or premature delivery may be important in generating calcified or organized CSH.

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A 67-year-old female with a history of hypertension and cerebral infarction presented with subarachnoid hemorrhage (SAH) (Hunt and Kosnik grade 4). Brain computed tomography (CT) revealed a clot dominantly on the right (Fisher's classification Group 4). Cerebral angiography showed funnel-shaped widenings at the origins of the bilateral posterior communicating arteries. The maximum diameter of the widening was greater than 3 mm, so this widening was called an enlarged infundibular widening. Angiography showed a small bulge protruding posterolaterally from the wall of the right enlarged infundibular widening, and the right posterior communicating artery arose from the apex of the enlarged infundibular widening. Based on the findings of the brain CT and cerebral angiography, the diagnosis was SAH due to rupture of the right enlarged infundibular widening. Approximately 12 hours after the onset, the clot was evacuated through the right pterional approach. Bleeding from the small bulge of the right enlarged infundibular widening occurred intraoperatively, so a right-angled ring clip was applied parallel to the right internal carotid artery to obliterate the rupture point. Postoperatively, she was discharged without neurological deficit, and follow-up CT showed no other new infarction. We recommend clipping rather than wrapping or coating for similar cases of ruptured enlarged infundibular widening.

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A 45-year-old male presented with an extremely rare case of symmetrical kissing aneurysms located at the both ends of the anterior communicating artery. Angiography and three-dimensional computed tomography (3D-CT) angiography clearly showed the relationship of the kissing aneurysms. The aneurysms were clipped through the right pterional approach. Temporary clipping of the anterior cerebral arteries for 5 minutes was required to gain enough operative space. The patient was discharged without neurological deficits. 3D-CT angiography, magnetic resonance angiography, or rotatory digital subtraction angiography may be useful for detecting kissing aneurysms, but the most important issue is awareness of this unusual condition.

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An 81-year-old female presented with a giant aneurysm of the distal anterior cerebral artery (A₃) which grew from a small saccular aneurysm to a huge aneurysm within 36 months before manifesting as a mass lesion. The thrombosed portion of the aneurysm showed growth, whereas the aneurysmal cavity did not change in size. Computed tomography and magnetic resonance imaging showed new bleeding in the thrombosed portion. Hemorrhage into the thrombus and/or aneurysmal wall might have caused the aneurysmal growth. She refused surgery and was discharged with no deficits. Distal anterior cerebral artery aneurysm which shows neuroimaging signs of growth requires regular follow up as such lesions may become giant before manifesting clinical symptoms.

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A 26-year-old female with idiopathic moyamoya disease developed chest pain with concomitant ST depression on electrocardiography. Coronary angiography detected no stenotic lesions in the epi- cardial coronary arteries. The clinical diagnosis was vasospastic angina pectoris. She was medicated with calcium antagonists, which reduced the frequency of chest pain episodes. Angina pectoris is a rare occurrence in young patients with moyamoya disease. Coronary artery disease and moyamoya disease may have common etiological factors.

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A 57-year-old male presented with a frontal bone defect associated with a middle meningeal arteriovenous fistula (AVF) manifesting as headache. The patient had a history of head injury 19 years previously. Skull radiography and computed tomography demonstrated a left frontal bone defect. Left external carotid angiography demonstrated a middle meningeal AVF at the frontal region, at the same location as the bone defect. The AVF was fed by the bilateral middle meningeal and left deep temporal arteries, and drained by the superior sagittal and ipsilateral cavernous sinuses. The minor feeding artery, the left deep temporal artery, was embolized with polyvinyl alcohol particles, then 0.4 ml of a 1:3 mixture of n-butyl cyanoacrylate and lipiodol was injected from the left middle meningeal artery. Follow-up angiography 3 months after the embolization revealed complete obliteration of the fistula. The bone defect may have been caused by erosion of the frontal bone by the pulsating effect of the feeding and draining vessels of the fistula, or by inadequate nutrition to the bone tissue because of the arteriovenous shunt.

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A 20-year-old male presented with symptoms of isolated neurosarcoidosis including epilepsy. Magnetic resonance imaging disclosed multiple enhanced right temporal and frontal lesions. Cerebrospinal fluid examination identified mild lymphocytic pleocytosis, and histological examination of a stereotactic brain biopsy specimen demonstrated noncaseating granulomas, so fungal or other inflammatory or granulomatous diseases were excluded. The diagnosis was cerebral sarcoidosis, despite the absence of systemic manifestations. Corticosteroid therapy improved his neurological state and radiological findings. Neurosarcoidosis is a well-recognized occurrence in systemic sarcoidosis, but diagnosis may be difficult in the absence of extracerebral manifestations.

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