1. Current concepts: Diffuse axonal injury–associated traumatic brain injury 
Jay M. Meythaler, MD, JD, Jean D. Peduzzi, PhD, Evangelos Eleftheriou, PhD, Thomas A. Novack, PhD 
Archives of Physical Medicine and Rehabilitation 
Volume 82, Issue 10, Pages (October 2001)
DOI: /apmr
Copyright © 2001 American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation Terms and Conditions

2. Fig. 1
Admission CT scan of a 22-year-old man status post-MVC and a GCS admission score of 6. Note the punctate hemorrhages at the gray-white matter junction, and the internal capsule as noted by the arrows. There is also a loss of the definition of the sulci and a blurring of the gray-white matter junction indicating cerebral edema.
Archives of Physical Medicine and Rehabilitation  , DOI: ( /apmr )
Copyright © 2001 American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation Terms and Conditions

3. Fig. 2
Histopathology slides of DAI sectioned from the corpus callosum of a patient who died from a severe TBI several weeks after the initial injury. (A) Low power view (×10) of hematoxylin-eosin stain demonstrating DAI and petechial hemorrhages. (B) Higher power (×200) hematoxylin-eosin stain of axons undergoing Wallerian degeneration. (C) Silver stain of the same area indicating the axonal retraction bulbs (×200).
Archives of Physical Medicine and Rehabilitation  , DOI: ( /apmr )
Copyright © 2001 American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation Terms and Conditions

4. Fig. 3
Photograph of a gross brain, coronally sectioned, of a patient who suffered a fatal TBI from a MVC. There are numerous small punctate intracerebral hemorrhages associated with DAI within the parasagittal white matter of the cerebral cortex, corpus callosum, and the gray-white matter junction. Note the large area of damage from an intracerebral hematoma within the corpus callosum.
Archives of Physical Medicine and Rehabilitation  , DOI: ( /apmr )
Copyright © 2001 American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation Terms and Conditions

5. Fig. 4
(A) Graphic representation of force over time causing deformation in an elastic substance. Line a represents force in 1 direction such as a patient spinning in 1 direction ejected from a motor vehicle. Line b represents reciprocating force that would be similar to shaking a head back and forth, as in shaken baby syndrome After the threshold of necessary force to create deformation is reached, it is the length of time over which force is applied that determines the amount of DAI. This threshold is defined as the point where the elasticity (defined by its inherent capability to resist strain) of the substance is exceeded such that the material object will not return to its original geometric and physical shape once the force is removed. (B) Graphic representation of a cylindrical elastic substance attached to 2 different plates traveling in different directions stretching the cylinder and changing its geometric shape. Eventually it is stretched beyond the point where it will return to its original shape and function. As it is stretched beyond this point, it can exert less force or resistance impending the movement of the plates in different directions.
Archives of Physical Medicine and Rehabilitation  , DOI: ( /apmr )
Copyright © 2001 American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation Terms and Conditions

6. Fig. 5
Representation of DAI at the level of the neuron. (A) Representative cross-section of the axon, demonstrating that the predominant damage appears to occur at the nodes of Ranvier within the axon.63,64 (A) Early stage represents the normal axon at the very earliest time after injury. (A) Late stage damage to the metabolic capability of the neuron at the axon leads to a reduction in the production of ATP, which is necessary for the ion pumps to maintain neuronal homeostasis with regard to sodium (Na+), potassium (K+), calcium (Ca2+), and other ions is represented. The changes include increased intracellular levels of Ca2+ and Na+. There is disarray of the neurofilaments and breakdown of the mitochondria and microtubules. However, it is likely there is also mechanically induced damage to the dendrites as well as to the neuronal cell body. (B) Represents the neuronal membrane ion channels with receptor positions for NMDA receptor/channel AMPA receptor/channel and positions for glutamate receptors (Glu). The glutamate is released from contiguous injured or dying cells, which may be neurons or adjacent glial elements. These NMDA and AMPA channels are predominate along the dendrites, the axonal hillock, and the neuronal cell body.100 Once activated, they further increase the influx of Na and Ca ions, which, if the intracellular concentration reaches a critical level, will cause cellular death. Magnesium (Mg2+), zinc (Zn2+), phencyclidine (PCP), and glycine (Gly) represent the potential receptor antagonists that may limit Na+ and Ca2+ influx, and K+ efflux, potentially reducing the damage.
Archives of Physical Medicine and Rehabilitation  , DOI: ( /apmr )
Copyright © 2001 American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation Terms and Conditions