Journal of neurotrauma
-
Journal of neurotrauma · Nov 2012
Decreased spinothalamic and dorsal column medial lemniscus-mediated function is associated with neuropathic pain after spinal cord injury.
Neuropathic pain (NP) after spinal cord injury (SCI) can significantly and negatively affect quality of life and is often refractory to currently available treatments. In order to find more effective therapeutic avenues, it would be helpful to identify the primary underlying pathophysiological mechanisms in each individual. The aim of the present study was to assess the relationship between the presence and severity of NP after SCI and measures of somatosensory function mediated via the dorsal column medial lemniscal (DCML) pathway and the spinothalamic tract (STT). ⋯ Our results suggest that both impaired STT and DCML-mediated function are necessary for the development of NP after SCI. However, within the SCI-NP group, greater NP severity was associated with greater sensitivity to thermal stimuli below the LOI. This finding concurs with other studies suggesting that STT damage with some sparing is associated with NP.
-
Journal of neurotrauma · Nov 2012
The influence of pain on cerebral functioning after mild traumatic brain injury.
More than 75% of patients with mild traumatic brain injury (MTBI) report chronic pain whose potential detrimental effects on cognitive recovery need to be identified. The objective of this study was to investigate the relationship between pain, performance on a working memory task, gray matter density, and mid-dorsolateral prefrontal cortex (mid-DLPFC) activation in subjects with a MTBI. For comparison purposes, we performed identical correlation analyses with a group of subjects without MTBI who sustained sports injuries. ⋯ Gray matter density measures were independent of pain level. This study showed that behavioral performance and cerebral functioning are affected by pain after a MTBI. Moreover, this study suggests that pain, cognition, and cerebral functioning interactions could not easily be generalized from one clinical population to another.
-
Journal of neurotrauma · Nov 2012
Neuron-specific enolase, but not S100B or myelin basic protein, increases in peripheral blood corresponding to lesion volume after cortical impact in piglets.
A peripheral indicator of the presence and magnitude of brain injury has been a sought-after tool by clinicians. We measured neuron-specific enolase (NSE), myelin basic protein (MBP), and S100B, prior to and after scaled cortical impact in immature pigs, to determine if these purported markers increase after injury, correlate with the resulting lesion volume, and if these relationships vary with maturation. Scaled cortical impact resulted in increased lesion volume with increasing age. ⋯ Even with allometric scaling of blood volume and a uniform mechanism of injury, NSE had only a fair to poor predictive value. In a clinical setting, where the types of injuries are varied, more investigation is required to yield a panel of serum markers that can reliably predict the extent of injury. Allometric scaling may improve estimation of serum marker release in pediatric populations.
-
Journal of neurotrauma · Nov 2012
Multivariate outcome prediction in traumatic brain injury with focus on laboratory values.
Traumatic brain injury (TBI) is a major cause of morbidity and mortality. Identifying factors relevant to outcome can provide a better understanding of TBI pathophysiology, in addition to aiding prognostication. Many common laboratory variables have been related to outcome but may not be independent predictors in a multivariate setting. ⋯ A worse outcome related to increasing osmolarity may warrant further study. Importantly, hemoglobin was not found significant when adjusted for post-resuscitation GCS as opposed to an admission GCS, and timing of GCS can thus have a major impact on conclusions. In total, laboratory variables added an additional 1.3-4.4% to pseudo R².
-
Journal of neurotrauma · Nov 2012
Deficits in social behavior emerge during development after pediatric traumatic brain injury in mice.
The pediatric brain may be particularly vulnerable to social deficits after traumatic brain injury (TBI) due to the protracted nature of psychosocial development through adolescence. However, the majority of pre-clinical studies fail to assess social outcomes in experimental pediatric TBI. The current study evaluated social behavior in mice subjected to TBI at post-natal day (p)21. ⋯ Together these findings reveal reduced social interaction and a tendency towards increased aggression, which evolves across development to adulthood. This emergence of aberrant social behavior, which parallels the development of other cognitive deficits in this model and behaviors seen in brain-injured children, is consistent with the hypothesis that the full extent of deficits is not realized until the associated skills reach maturity. Thus, efficacy of therapeutics for pediatric TBI should take into account the time-dependent emergence of abnormal behavioral patterns.