Neuropathological investigation of cerebral white matter lesions caused by closed head injury.
In order to ascertain whether there is widespread axonal disruption of cerebral white matter in the so-called 'diffuse axonal injury' (DAI), a type of closed head injury, proposed by Adams et al. the author investigated his own cases clinicopathologically. Twenty-six male autopsied cases of head injury, aged between 19 and 84, 15 of which had sustained road traffic accidents, were examined; the others were due to falling from heights and so on. The study group all belonged to non-missile head injuries and included 12 cases of diffuse brain injury, as well as 14 cases of focal brain injury, according to the classification of Gennarelli et al. The survival time ranged from 2 h to 21 years. Formalin-fixed brains were cut coronally so as to make paraffin-embedded hemispheric sections. Then these sections were stained conventionally (HE, Bodian, Kluver-Barrera and Holzer) and immunohistochemically (GFAP) to assess axonal decrease, myelin pallor and gliosis by the use of light microscopy. In the 13 chronic cases that died more than 1 month after the accidents, the intensities of gliosis, myelin pallor and axonal decrease tended to correlate with each other. In the 13 acute cases who died less than 1 month after their accident, the degree of axonal decrease in white matter seemed to correlate with the severity of myelin pallor. Regardless of types of trauma, however, axonal retraction balls, the so-called hallmark of DAI, were found only with myelin pallor suggesting the presence of brain swelling after the injury. Therefore these findings indicate that it may be difficult to accept the notion of DAI, that is, the presence of axonal retraction balls without brain swelling. In addition, diffuse vascular injury (2 cases) as well as rarefaction of subcortical white matter (6 cases) were presented and their pathogenesis individually discussed based on a literature review.
Onaya
Mitsumoto
M
Shimofusa National Hospital, Chiba-shi, Chiba, Japan. fwgi0530@mb.infoweb.ne.jp
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D016564:Amyloid beta-Protein Precursor / Q000378:metabolism; D001369:Axons / Q000378:metabolism / Q000473:pathology*; D001929:Brain Edema / Q000000981:diagnostic imaging / Q000473:pathology; D002540:Cerebral Cortex / Q000000981:diagnostic imaging / Q000378:metabolism / Q000473:pathology*; D020833:Diffuse Axonal Injury / Q000378:metabolism / Q000401:mortality / Q000473:pathology*; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D005911:Gliosis / Q000473:pathology; D016489:Head Injuries, Closed / Q000378:metabolism / Q000401:mortality / Q000473:pathology*; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009186:Myelin Sheath / Q000473:pathology; D014057:Tomography, X-Ray Computed
D016564:Amyloid beta-Protein Precursor; D005904:Glial Fibrillary Acidic Protein