Journal of neurotrauma
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Journal of neurotrauma · May 2008
Changes in corticospinal function and ankle motor control during recovery from incomplete spinal cord injury.
Little is known about the mechanisms that underlie motor recovery after incomplete spinal cord injury (iSCI) in humans. This study assessed changes in corticospinal tract (CST) function by measuring motor-evoked potentials (MEPs) and ankle motor control at 1, 3, and 6 months after acute iSCI. In 12 iSCI patients and matched controls, MEPs (evoked at 20% of maximal voluntary contraction [MVC]) were combined with a comprehensive ankle motor assessment protocol that measured ankle dorsiflexor strength (MVC, manual muscle testing, maximal movement velocity [MMV]), dexterity (the ability to accurately time ankle dorsiflexion movements) and gait (speed, walking aids). ⋯ The finding of unchanged CST conductivity, as assessed by MEP latencies in acute iSCI patients recovering motor function, is in accordance with previous studies in human SCI on this issue. The increased MEP facilitation at stable background EMG might indicate improved synchronization of the descending volley and/or responsiveness of motoneurons to supra-spinal input. The absence of a relationship between MEP amplitudes and recovery of ambulation and muscle strength implies that plastic changes in spinal neural circuits and preserved motor units might have contributed to the functional improvement.
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Journal of neurotrauma · May 2008
Androgen regulates neuritin mRNA levels in an in vivo model of steroid-enhanced peripheral nerve regeneration.
Following crush injury to the facial nerve in Syrian hamsters, treatment with androgens enhances axonal regeneration rates and decreases time to recovery. It has been demonstrated in vitro that the ability of androgen to enhance neurite outgrowth in motoneurons is dependent on neuritin-a protein that is involved in the re-establisment of neuronal connectivity following traumatic damage to the central nervous system and that is under the control of several neurotrophic and neuroregenerative factors--and we have hypothesized that neuritin is a mediator of the ability of androgen to increase peripheral nerve regeneration rates in vivo. Testosterone treatment of facial nerve-axotomized hamsters resulted in an approximately 300% increase in neuritin mRNA levels 2 days post-injury. ⋯ In a corroborative in vitro experiment, the androgen dihydrotestosterone induced an approximately 100% increase in neuritin mRNA levels in motoneuron-neuroblastoma cells transfected with androgen receptors, but not in cells without androgen receptors. These data confirm that neuritin is under the control of androgens, and suggest that neuritin is an important effector of androgen in enhancing peripheral nerve regeneration following injury. Given that neuritin has now been shown to be involved in responses to both central and peripheral injuries, and appears to be a common effector molecule for several neurotrophic and neurotherapeutic agents, understanding the neuritin pathway is an important goal for the clinical management of traumatic nervous system injuries.
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Journal of neurotrauma · May 2008
Time of hypotension and discharge outcome in children with severe traumatic brain injury.
We performed a retrospective study at a level I pediatric trauma center of patients admitted between 1998 and 2005 to determine the time after severe pediatric traumatic brain injury (TBI) that hypotension (systolic blood pressure [SBP] of <5th percentile) is most strongly associated with poor outcome. One hundred forty-six patients of <18 years of age with TBI, head Abbreviated Injury Score (AIS) of >or=3, and PICU admission Glasgow Coma Scale (GCS) score of <9 formed the analytic sample. Available SBP readings through the first 72 h after severe TBI were collected. ⋯ Poor discharge GOS was predicted by hypotension occurring during the first 6 h after injury. SBP data beyond the first 6 h did not improve our ability to predict poor discharge GOS. The first 6 h after severe pediatric TBI may represent a critical time period for either predicting or improving outcome.
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Journal of neurotrauma · May 2008
Post-operative expansion of hemorrhagic contusions after unilateral decompressive hemicraniectomy in severe traumatic brain injury.
Decompressive hemicraniectomy is commonly performed in patients with traumatic brain injury (TBI) with diffuse brain swelling or refractory raised intracranial pressure. Expansion of hemorrhagic contusions in TBI patients is common, but its frequency following decompressive hemicraniectomy has not been well established. The aim of this retrospective study was to determine the rate of hemorrhagic contusion expansion following unilateral hemicraniectomy in severe TBI, to identify factors associated with contusion expansion, and to examine whether contusion expansion is associated with worsened clinical outcomes. ⋯ Expansion of hemorrhagic contusions is common after decompressive hemicraniectomy following severe TBI. The volume of hemorrhagic contusion expansion following hemicraniectomy is strongly associated with mortality and poor outcome. Severity of initial CT findings may predict the risk of contusion expansion following hemicraniectomy, thereby identifying a subgroup of patients who might benefit from therapies aimed at augmenting the coagulation system.
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Journal of neurotrauma · May 2008
Force-dependent development of neuropathic central pain and time-related CCL2/CCR2 expression after graded spinal cord contusion injuries of the rat.
Spinal cord injury (SCI) often results in intractable chronic central pain syndromes. Recently chemokines such as CCL2 were identified as possible key integrators of neuropathic pain and inflammation after peripheral nerve lesion. The focus of the current study was the investigation of time-dependent CCL2 and CCR2 expression in relation to central neuropathic pain development after spinal cord impact lesions of 100, 150, or 200 kdyn force on spinal cord level T9 in adult rats. ⋯ While in the early post-operative time course, CCL2 and CCR2 were expressed in astroglia and granulocytes only on level T9; there was additional astroglial CCL2 expression in dorsal columns and dorsal horns above and below T9 of severely injured animals 42d after lesion. In dorsal horns (level L3-L5) of animals exhibiting chronic below-level pain CCL2 was co-expressed with transmitters and receptors that are involved in nociceptive processing like calcitonin gene-related peptide (CGRP), Substance-P, vanilloid-receptor-1, and its activated phosphorylated form. These data demonstrate lesion grade dependence of below-level pain development and suggest chemokines as potential candidates for integrating inflammation and central neuropathic pain after SCI.