THE CONTUSION INDEX: A REAPPRAISAL IN HUMAN AND EXPERIMENTAL NON‐MISSILE HEAD INJURY

Abstract

A previously described method of quantifying cerebral contusions in man (the contusion index) caused by non-missile head injury has been modified and applied to a larger series of cases, and used to assess contusions in experimental head injuries. The initial findings in man have been confirmed, viz. that contusions are most severe in the frontal and temporal lobes; that contusions may be entirely absent in a patient dying as a result of a head injury; that there is no correlation between the severity of contusions and the nature of the injury; that the concept of contrecoup must continue to be questioned; that contusions are more severe in patients who have a fracture of the skull in comparison to those who do not; that contusions are more severe in patients who do not experience a lucid interval than in those who do; and that contusions are less severe in patients with diffuse axonal injury than in those who do not have diffuse axonal injury. The distribution of contusions in subhuman primates is similar to that seen in man, and they occur more frequently with short duration than with long duration acceleration.

Neuropathology of the vegetative state after head injury

“…This index takes into account the depth and extent of surface contusions in various parts of the brain: zero means that there were no contusions, a contusion index in the twenties indicates moderately severe contusions, while one of more than 37 indicates severe contusions. 9 DiVuse axonal injury was graded as described previously, 10 11 and in this series was always of the more severe grades-either grade 2 with a focal lesion in the corpus callosum or grade 3 with a similar lesion also in the dorsolateral sector of the rostral brainstem. The focal lesions that are not apparent macroscopically are not diYcult to identify on microscopic examination, although it may be necessary to examine several levels of the corpus callosum.…”

Lateralized Response of Dynorphin A Peptide Levels after Traumatic Brain Injury

“…TBI causes pronounced atrophy and dysfunction of cortical and sub-cortical structures, including the hippocampus, thalamus, and striatum (Adams et al, 1985;Anderson et al, 1996Anderson et al, ,2005Baldwin et al, 1997;Bramlett et al, 1997;Colicos et al, 1996;Dietrich et al, 1994;Pierce et al, 1998;Shin et al, 2011;Soares et al, 1995;Thompson et al, 2010). Because the frontal cortex, hippocampus, and striatum additionally express moderate to high levels of dynorphins they were chosen for analysis.…”

“…Massive neuronal damage and cell loss occur in the cerebral cortex, hippocampus, and substantia nigra following experimental and clinical TBI (Adams et al, 1985;Anderson et al, 2005;Baldwin et al, 1997;Dietrich et al, 1994;Soares et al, 1995). Neuronal damage and degeneration in the hippocampus and thalamus correlate with the severity of post-traumatic motor dysfunction and cognitive deficits.…”

Effects of a Small Acute Subdural Hematoma following Traumatic Brain Injury on Neuromonitoring, Brain Swelling and Histology in Pigs

“…From each coordinate, 2 sections were stained with HE and analyzed for brain damage using a lesion index (LI) [for detailed description, see [19]]. The LI is derived by adding several injury parameters – such as intracerebral bleeding (ICB, values range: 0–3), subarachnoid hemorrhage (SAH, 0–2), intensity of edema (0–3) and surface contusion (0–1) – to the Contusion Index [28], which grades pyknotic and eosinophilic neurons (e.g. dead or dying cells) by depth and extent (range from 0–12: injury depth 1–4 and injury extent 1–3).…”