Intracystic hematoma of middle fossa arachnoid cyst caused by rupture of internal carotid-posterior communicating artery aneurysm.

A 46-year-old woman was admitted with generalized convulsion and deep coma which occurred 3 weeks after sudden onset of severe headache and pyrexia. Initial computed tomography did not reveal any abnormal findings except for an arachnoid cyst in the right middle fossa. Three weeks later repeat computed tomography showed intracystic hematoma in the arachnoid cyst with uncal herniation. Angiography revealed a right internal carotid-posterior communicating artery aneurysm. The neck of the aneurysm was clipped successfully, but hemiparesis was persistent postoperatively. Angiography is required for investigation of intracystic hematoma of an arachnoid cyst, especially in the absence of head injury, to avoid delayed diagnosis of any ruptured aneurysm.

[Serum S-100B protein and neuron-specific enolase after traumatic brain injury].

OBJECTIVE: The aim of this study was to investigate S-100B protein and NSE as a serum marker of brain cell damage after traumatic brain injury. MATERIAL AND METHODS: Forty-one patients with traumatic brain injury were included in this prospective study. Venous blood samples for S-100B protein and NSE were taken after admission and on the next day. Serum levels of S-100 protein and NSE were compared with Glasgow Coma Scale score, computed tomographic findings and outcome after 3 months. RESULTS: Serum S-100B protein and NSE were significantly correlated with Glasgow Coma Scale score and outcome after 3 months. The significant correlation was found between the initial S-100B and NSE (P < 0.001). In patients without parenchymal injuries on computed tomographic scan such as epidural hematoma and concussion, the elevation of S-100B protein and NSE was observed. The initial values of S-100B and NSE in acute subdural hematomas with unfavorable outcome were significantly higher than in those with favorable outcome. Secondary increase of serum markers was associated with the presence of secondary insult such as hypoxia or hypotension, and was found to have an unfavorable outcome. CONCLUSIONS: Serum concentration and kinetics of S-100B protein and NSE provide the clinical assessment of the primary brain damage and have a predictive value for outcome after traumatic brain injury.

[A case of non-functional pituitary adenoma associated with Rathke's cleft cyst].

A very rare case of non-functional pituitary adenoma associated with Rathke's cleft cyst is reported. A 42-year-old male suffering from visual disturbance and headache was admitted. Visual acuity was 1.2 on the right and 0.5 on the left, and visual field examination showed bitemporal hemianopsia. Endocrinological study disclosed that the basal serum level of prolactin was elevated slightly to 52.6 ng/ml, whereas those of other hormones were within normal limits. MRI showed a dumbbell-shaped cystic sellar mass extending to the suprasellar region beyond the diaphragm sellae, which consisted of two isolated components around the sellar turcica. At the middle of May, the tumor was partially removed by bifrontal craniotomy. The suprasellar tumor tightly adhered to the frontal lobe and the optic nerve, the tumor was grayish cyst and cyst fluid from the suprasellar mass had the appearance of motor oil and the intrasellar tumor contained old hematoma. Histological findings revealed that the suprasellar mass was Rathke's cleft cyst and the intrasellar mass was diagnosed as pituitary adenoma (non-functional). Visual acuity was improved following surgical operation. So far twenty-three cases of pituitary adenoma associated with Rathke's cleft cysts have been reported in the literature, but there was only one case reported of a non-functional pituitary adenoma associated with a Rathke's cleft cyst. Etiology and pathogenesis of the coexistence of non-functional pituitary adenoma and Rathke's cleft cyst in the present case were not elucidated.

[Acute spontaneous subdural hematoma of arterial origin].

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.