As one type of primary brain injury, diffuse axonal injury (DAI) has specific traumatic mechanisms. The occurence of DAI is close to the loading property, loading manner, structural characteristics of skull, brain tissue and neck. This article demonstrated how the stress and strain varied in brain tissue effected by the load magnitude, load waveform, load frequency, load duration, linear acceleration, rotational acceleration, compounded linear/rotational acceleration, brain tissue, cerebral falx, cerebellar tentorium, skull and neck, and what are the relationships between these factors and the event of DAI.
Animals ; Biomechanical Phenomena ; Brain ; physiology ; Diffuse Axonal Injury ; physiopathology ; Humans ; Neck ; physiology ; Skull ; physiology ; Stress, Mechanical

Although nitric oxide (NO) plays an important role in the pathophysiological process of cerebral ischemia or severe traumatic brain injury, its contribution to the pathogenesis of moderate diffuse axonal injury (mDAI) remains to be clarified. The alterations in nitric oxide synthase (NOS) activity and the histopathological response after mDAI was investigated. Forty anesthetized Sprague-Dawley adult rats were injured with a Marmarou's weight-drop device through a Plexiglas guide tube. These rats were divided into 8 groups (control, 1 hr, 2 hr, 3 hr, 6 hr, 12 hr, 24 hr, 48 hr after trauma). The temporal pattern of apoptosis in the adult rat brain after mDAI was characterized using TUNEL histochemistry. In addition, the cDNA for NOS activity was amplified using RT-PCR. The PCR products were electrophoresed on a 2% agarose gel. eNOS activity was not detected, but nNOS activity was expressed after 3 hr and continuously 48 hr after impact, which was approximately double that of the control group at 12 and 24 hr. Subsequently, there was a decrease in activity after 48 hr. The iNOS activity increased dramatically after 12 hr and was constant for a further 12 hr followed by a dramatic decrease below the level of the control group. Significant apoptotic changes occurred 12 and 24 hr. after insult. nNOS and iNOS activity were affected after moderate diffuse axonal injury in a time-dependent manner and there was a close relation between the apoptotic changes and NOS activity. Although the nNOS activity was expressed early, its activity was not stronger th an iNOS, which was expressed later.
Animal ; *Apoptosis ; Craniocerebral Trauma/enzymology/*physiopathology ; Diffuse Axonal Injury/enzymology/*physiopathology ; Nitric-Oxide Synthase/*metabolism ; Rats ; Rats, Sprague-Dawley ; Wounds, Nonpenetrating/enzymology/*physiopathology

Traumatic brain injury (TBI) is a highly complex multi-factorial disorder. Animal models of TBI are used to elucidate primary and secondary injury mechanisms and pathophysiological changes and to provide the diagnostic and therapeutical basis for TBI. The choices of animal models depend upon the research objectives. However, various animal models have limitations. The models only can duplicate the pivotal injury mechanisms or a certain important pathophysiological course. The characteristics of human TBI can not fully be reflected by using these models. In the review, animal models of traumatic brain injury are classified as dynamic direct brain injury, indirect dynamic brain injury and combined neuro-traumatic models. Several common models are described for consideration.
Animals ; Biomechanical Phenomena ; Brain/physiopathology* ; Brain Injuries/physiopathology* ; Diffuse Axonal Injury/physiopathology* ; Disease Models, Animal ; Forensic Medicine ; Head Injuries, Closed/physiopathology* ; Head Injuries, Penetrating/physiopathology* ; Humans ; Mice ; Rats ; Reproducibility of Results