In 1998, the Guidelines Committee on the Management of Severe Head Injury was established by the Japan Society of Neurotraumatology, and performed a critical review of national and international studies published over the past 10 years. The guidelines were first published in 2000 based on the results of this literature review and the Committee consensus, and the 2nd revised edition was published in 2006. This English version of the 2nd edition of the guidelines is intended to promote its concepts and use worldwide.
Diffusion tensor imaging (DTI) has recently evolved as valuable technique to investigate diffuse axonal injury (DAI). This study examined whether fractional anisotropy (FA) images analyzed by statistical parametric mapping (FA-SPM images) are superior to T2*-weighted gradient recalled echo (T2*GRE) images or fluid-attenuated inversion recovery (FLAIR) images for detecting minute lesions in traumatic brain injury (TBI) patients. DTI was performed in 25 patients with cognitive impairments in the chronic stage after mild or moderate TBI. The FA maps obtained from the DTI were individually compared with those from age-matched healthy control subjects using voxel-based analysis and FA-SPM images (p < 0.001). Abnormal low-intensity areas on T2*GRE images (T2* lesions) were found in 10 patients (40.0%), abnormal high-intensity areas on FLAIR images in 4 patients (16.0%), and areas with significantly decreased FA on FA-SPM image in 16 patients (64.0%). Nine of 10 patients with T2* lesions had FA-SPM lesions. FA-SPM lesions topographically included most T2* lesions in the white matter and the deep brain structures, but did not include T2* lesions in the cortex/near-cortex or lesions containing substantial hemosiderin regardless of location. All 4 patients with abnormal areas on FLAIR images had FA-SPM lesions. FA-SPM imaging is useful for detecting minute lesions because of DAI in the white matter and the deep brain structures, which may not be visualized on T2*GRE or FLAIR images, and may allow the detection of minute brain lesions in patients with post-traumatic cognitive impairment.
A 42-year-old male presented with a rare case of delayed aneurysmal formation of the intracranial ophthalmic artery after closed head injury manifesting as subarachnoid hemorrhage. Initial magnetic resonance angiography revealed no aneurysmal formation, but angiography 7 days after the injury demonstrated an intracranial ophthalmic artery aneurysm. Follow-up computed tomography angiography demonstrated enlargement of the aneurysm. The aneurysm was successfully treated by surgical resection. Histological examination revealed that the aneurysm was a pseudoaneurysm. Traumatic intracranial aneurysm (TICA) is rare and usually occurs in the peripheral arteries of the cerebral circulation or the basal portion of the internal carotid artery. The present case shows that failure to demonstrate an aneurysm on the initial angiography in the acute stage does not exclude the presence of traumatic aneurysm. This case clearly shows the time course of development of a TICA of the ophthalmic artery after closed head injury.
A 47-year-old man presented to our hospital after suffering transient loss of consciousness and falling to the floor. On admission, his Glasgow Coma Scale score was 11 (E3V3M5), and he exhibited restlessness. Blood examination revealed hyperthyroidism. Computed tomography showed slight traumatic subarachnoid hemorrhage. He developed fever and tachycardia, and was diagnosed with thyroid crisis. Magnetic resonance imaging showed a brain contusion in the right frontal lobe, and encephalopathy signs in the right frontal and insular cortex. Immunocytochemical examinations suggested Hashimoto's disease, and hormone examinations revealed plasma levels were undetectably low of adrenocorticotropic hormone (ACTH) and low of cortisol. Pituitary stimulation tests showed inadequate plasma ACTH and cortisol response, consistent with isolated ACTH deficiency (IAD). The final diagnosis was IAD associated with Hashimoto's disease. Hydrocortisone replacement therapy was continued, and the patient was nearly free from neurological deficits after 18 months. The neuroimaging abnormalities gradually improved with time.