Traumatic Axonal Injury in the Spinal Cord Evoked by Traumatic Brain Injury

Czeiter, Endre; Pál, József; Kövesdi, Erzsébet; Bukovics, Péter; Lückl, János; Dóczi, Tamás; Büki, András

doi:10.1089/neu.2007.0331

Cited by 28 publications

(22 citation statements)

References 20 publications

(8 reference statements)

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“…The presence of TAI in the CC, internal capsule, optic tracts, cerebral and cerebellar peduncles, and the long tracts in the brainstem was consistent with previous studies that showed axonal pathology in similar locations in the original Marmarou model (Czeiter et al, 2008;Kallakuri et al, 2003;Marmarou et al, 1994;Rafols et al, 2007;Stone et al, 2001). Our results also showed that the extent of TAI was significantly greater at 2.25 m than at 1.25 m, which agrees with a preliminary study by Kallakuri and associates (2003), showing that TAI in the CC was most severe in the 2-m group, and mildest in the 1-m group.…”

Section: Traumatic Axonal Injury Quantificationsupporting

confidence: 90%

“…Most previous studies assessed TAI level based on drop height (Czeiter et al, 2008;Sawauchi et al, 2004;Vagnozzi et al, 2005), but did not quantify the mechanical response of the head. Results from our current study showed that in spite of minimal variations in impactor velocity, biomechanical responses in the rat head can vary widely within the same drop height.…”

Section: Biomechanical Parametersmentioning

confidence: 99%

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Quantitative Relationship between Axonal Injury and Mechanical Response in a Rodent Head Impact Acceleration Model

Zhang

Kallakuri

et al. 2011

Journal of Neurotrauma

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A modified Marmarou impact acceleration model was developed to study the mechanical responses induced by this model and their correlation to traumatic axonal injury (TAI). Traumatic brain injury (TBI) was induced in 31 anesthetized male Sprague-Dawley rats (392±13 g) by a custom-made 450-g impactor from heights of 1.25 m or 2.25 m. An accelerometer and angular rate sensor measured the linear and angular responses of the head, while the impact event was captured by a high-speed video camera. TAI distribution along the rostro-caudal direction, as well as across the left and right hemispheres, was determined using β-amyloid precursor protein (β-APP) immunocytochemistry, and detailed TAI injury maps were constructed for the entire corpus callosum. Peak linear acceleration 1.25 m and 2.25 m impacts were 666±165 g and 907±501 g, respectively. Peak angular velocities were 95±24 rad/sec and 124±48 rad/sec, respectively. Compared to the 2.25-m group, the observed TAI counts in the 1.25-m impact group were significantly lower. Average linear acceleration, peak angular velocity, average angular acceleration, and surface righting time were also significantly different between the two groups. A positive correlation was observed between normalized total TAI counts and average linear acceleration (R(2)=0.612, p<0.05), and time to surface right (R(2)=0.545, p<0.05). Our study suggested that a 2.25-m drop in the Marmarou model may not always result in a severe injury, and TAI level is related to the linear and angular acceleration response of the rat head during impact, not necessarily the drop height.

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Section: Traumatic Axonal Injury Quantificationsupporting

confidence: 90%

Section: Biomechanical Parametersmentioning

confidence: 99%

Quantitative Relationship between Axonal Injury and Mechanical Response in a Rodent Head Impact Acceleration Model

Zhang

Kallakuri

et al. 2011

Journal of Neurotrauma

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“…In spite of the fiber damage observed in the left thoracic CST at 4 weeks post injury, there was no evident decrease in motor performance of the left hindlimb on the horizontal ladder. However, this lack of measurable motor deficits produced by secondary damage has been reported previously (Czeiter et al, 2008;Iizuka et al, 1989). Also, in a clinical setting, spinal cord-injured patients, as well as stroke patients, usually recover gradually, although secondary tissue damage is known to occur in a delayed fashion (Ishida and Tominaga, 2002).…”

Section: Discussionmentioning

confidence: 94%

Secondary Damage in the Spinal Cord after Motor Cortex Injury in Rats

Weishaupt

Silasi²,

Colbourne³

et al. 2010

Journal of Neurotrauma

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When neurons within the motor cortex are fatally injured, their axons, many of which project into the spinal cord, undergo wallerian degeneration. Pathological processes occurring downstream of the cortical damage have not been extensively studied. We created a focal forelimb motor cortex injury in rats and found that axons from cell bodies located in the hindlimb motor cortex (spared by the cortical injury) become secondarily damaged in the spinal cord. To assess axonal degeneration in the spinal cord, we quantified silver staining in the corticospinal tract (CST) at 1 week and 4 weeks after the injury. We found a significant increase in silver deposition at the thoracic spinal cord level at 4 weeks compared to 1 week post-injury. At both time points, no degenerating neurons could be found in the hindlimb motor cortex. In a separate experiment, we showed that direct injury of neurons within the hindlimb motor cortex caused marked silver deposition in the thoracic CST at 1 week post-injury, and declined thereafter. Therefore, delayed axonal degeneration in the thoracic spinal cord after a focal forelimb motor cortex injury is indicative of secondary damage at the spinal cord level. Furthermore, immunolabeling of spinal cord sections showed that a local inflammatory response dominated by partially activated Iba-1-positive microglia is mounted in the CST, a viable mechanism to cause the observed secondary degeneration of fibers. In conclusion, we demonstrate that following motor cortex injury, wallerian degeneration of axons in the spinal cord leads to secondary damage, which is likely mediated by inflammatory processes.

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“…While there was no striking evidence for the presence of DAI, Strich came to the realization that extended degeneration of axons over a time period after the trauma was responsible for the high rate of mortality. The pathologic term DAI was established after Strich published her findings; later, it was agreed that DAI was a multipart pathology in that not only does the initial trauma cause severe damage, but also secondary factors such as biochemical cascades, edema, and hypoxia also contribute to the pathology as a whole [85,86]. It was in the early 1980s where the official term, DAI, was introduced and accepted worldwide as a pathology which played a key integral role in the posttraumatic development of the patient [87].…”

Section: The History Behind Daimentioning

confidence: 99%

Diffuse Axonal Injury: A Devastating Pathology

Ordookhanian¹,

Tsai²,

Kaloostian³

et al. 2018

Traumatic Brain Injury - Pathobiology, Advanced Diagnostics and Acute Management

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Traumatic brain injury (TBI) also known as intracranial injury is the result of a lesion within the brain due to an external force. Common forms of TBI result from falls, violence, and/or vehicle crashes; the classification of this pathology is dependent on the severity of the lesion as well as the mechanism of trauma to the head. One of the most common onsets of traumatic brain injuries result from mild to severe lesions to the white matter tracts of the brain called diffuse axonal injury (DAI); however, additional forms of TBI's can present in non-penetrating forms. Penetrating forms of TBI's such as trauma to the head via a foreign object do also contribute to the many millions of TBI cases per year, but we will not discuss these traumatic injuries as in depth within this chapter. The onset of diffuse axonal injury will vary on a per-patient basis from mild to severe, based on a standardized neurological examination rated on the Glasgow Coma Scale (GCS), which indicates the severity of brain damage present. While there is a spectrum of severity for DAI patients, a concussion is typically observed within a larger majority of patients in addition to other overwhelming trauma.

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Traumatic Axonal Injury in the Spinal Cord Evoked by Traumatic Brain Injury

Cited by 28 publications

References 20 publications

Quantitative Relationship between Axonal Injury and Mechanical Response in a Rodent Head Impact Acceleration Model

Quantitative Relationship between Axonal Injury and Mechanical Response in a Rodent Head Impact Acceleration Model

Secondary Damage in the Spinal Cord after Motor Cortex Injury in Rats

Diffuse Axonal Injury: A Devastating Pathology

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