Related Experiment Video
Updated: Aug 18, 2026

A Mouse Model of Single and Repetitive Mild Traumatic Brain Injury
Published on: June 20, 2017
The structural basis of moderate disability after traumatic brain damage
J H Adams1, D I Graham, B Jennett
1University Department of Neuropathology, Institute of Neurological Sciences, South Glasgow University Hospitals NHS Trust, 1345 Govan Road, Glasgow G51 4TF, Scotland, UK. D.Graham@clinmed.gla.ac.uk
Abstract:
The objective was to discover the nature of brain damage in survivors of head injury who are left with moderate disability. Macroscopic and microscopic examination was carried out on the brains of 20 persons who had died long after a head injury that had been treated in a neurosurgical unit. All had become independent but had various disabilities (moderate disability on the Glasgow outcome scale) Most deaths had been sudden, which had led to their referral from forensic pathologists. Post-traumatic epilepsy was a feature in 75%. An intracranial haematoma had been evacuated in 75%, and in 11 of the 15 with epilepsy. Diffuse axonal injury was found in six patients, five of the mildest type (grade 1) and one of grade 2. No patient had diffuse thalamic damage but one had a small focal ischaemic lesion in the thalamus. No patient had severe ischaemic brain damage, but three had moderate lesions which were bilateral in only one. No patient had severe cortical contusions. In conclusion, the dominant lesion was focal damage from an evacuated intracranial haematoma. Severe diffuse damage was not found, with diffuse axonal injury only mild and thalamic damage in only one patient.
More Related Videos
09:49Assessing Changes in Synaptic Plasticity Using an Awake Closed-Head Injury Model of Mild Traumatic Brain Injury
Published on: January 20, 2023
08:27Development of an Uncomplicated Mild Traumatic Brain Injury Model Modified by Weight-Drop Method and Evidenced by Magnetic Resonance Imaging
Published on: April 11, 2025
Related Concept Videos
Traumatic Brain Injury l: Introduction
Secondary Spinal Cord Injury llI: Pathophysiology