Clinicopathological Study of Diffuse Axonal Injury in Head Trauma.
- Author:
Young Gwi SHIN
1
;
Min Cheol LEE
;
Young Jik LEE
;
Chang Soo PARK
;
Jae Hyoo KIM
;
Moon Sun PARK
Author Information
1. Department of Neurosurgery, Eulji Medical College, Korea.
- Publication Type:Original Article
- Keywords:
Clinicopathological study;
Head trauma;
Diffuse axonal injury
- MeSH:
Amyloid;
Autopsy;
Axons;
Brain;
Brain Edema;
Brain Stem;
Corpus Callosum;
Craniocerebral Trauma*;
Dendrites;
Diagnosis;
Diffuse Axonal Injury*;
Glasgow Coma Scale;
Head Injuries, Closed;
Head*;
Humans;
Magnetic Resonance Imaging;
Neurons;
Unconsciousness
- From:Journal of Korean Neurosurgical Society
1997;26(6):755-763
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
To delineate the clinicopathological features of diffuse axonal injury in patients with diffuse cerebral injury, we reviewed 19 cases from a series of 726 brain autopsies performed during a recent ten-year period. The criteria for inclusion were loss of consciousness for more than 6 hours in closed head injury patients, and no development of a space-occupying lesion within 7 days of injury. The injury was more prevalent in males(70.6%), and in patients aged between 10 and 50 years(82.4%). The main cause was traffic accident(82.4%), and the patients, Glasgow coma scale score on admission after injury was between 3 and 7. CT or MRI performed within the first 7 days of injury disclosed either one or combined focal lesions in the cerebral white matter, corpus callosum and brain stem in 66.7% of cases, and no identifiable lesion in 33.3%. Axonal swellings are the histologic hallmark of diffuse axonal injury in closed head trauma. In this study, careful brain dissection and neuropathologic studies demonstrated these swellings in all autopsy brains. The immunohistochemical stain for neurofilament proteins(68kD, 160/200kD) is the most sensitive marker of axonal swelling, especially when a patient survives more than 12 hours after injury. However, a neurofilament protein(160/200kD) is also expressed in a few normal pyramidal neurons and axial dendrites. Bielschowsky stain also clearly delineates axonal swellings in patients who have survived more than 2 days after injury. Cerebral edema and the appearance of amyloid body are easily identifiable by Luxol fast blue-PAS stain. In patients who survive for 6 months after injury, axonal swellings are hardly identifiable; about 25% of cases are diagnosed by neuropathologic examination only. The above data indicate that for the diagnosis of diffuse axonal injury, careful gross examination and neuropathologic studies are important.
