Biomedical subjects

Satoru Morooka

Publications and source records attributed to Satoru Morooka.

3 recordsLinked to original sources

PubMed2005

[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.

Analysis of Variance↗

PubMed2004

[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.

Aged↗

PubMed2003

[Progressive brain injury].

The aim of this study was to evaluate the clinical manifestations and prognostic factors of progressive brain injury following trauma. We reviewed the records of 779 patients with head injury who had an admission Glasgow Coma Scale of 9 or more; 70 (7.0%) developed progressive brain injury as evidenced on serial CT scans. Of these 70 patients, 19 (27.1%) had a subdural hematoma, 19 (27.1%) an epidural hematoma, 16 (22.9%) a cerebral contusion, 13 (18.6%) an intracerebral hematoma, and 3 (4.3%) a diffuse brain swelling. Three months after injury, 36 (51.4%) patients died, 2 (2.9%) were left in a vegetative state and 23 (32.9%) had a favorable outcome. The appearance of progressive brain injury was associated with patient age, admission Glasgow Coma Scale, injury mechanisms, skull fracture and hemorrhagic lesions on the initial CT scan. Patients with the extracerebral lesions deteriorated 4 hours after injury, whereas those with intracerebral lesions deteriorated 8 hours after injury. The outcome based on Glasgow Outcome Scale was significantly associated with age, type of intracranial lesion, Glasgow Coma Scale following deterioration, the mechanism of injury and surgical treatment. It is concluded that early repeated CT scan is indicated in patients with risk factors of developing progressive brain injury.

Adult↗