NeuroImage
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Non-impact blast-related mild traumatic brain injury (mTBI) appears to be present in soldiers returning from deployments to Afghanistan and Iraq. Although mTBI typically results in cognitive deficits that last less than a month, there is evidence that disrupted coordination of brain activity can persist for at least several months following injury (Thatcher et al., 1989, 2001). In the present study we examined whether neural communication may be affected in soldiers months after blast-related mTBI, and whether coordination of neural function is associated with underlying white matter integrity. ⋯ For blast injured (i.e., blast-related mTBI) soldiers we found that EEG phase synchrony was associated with the structural integrity of white matter tracts of the frontal lobe (left anterior thalamic radiations and the forceps minor including the anterior corpus callosum). Analyses revealed that diminished EEG phase synchrony was not the consequence of combat-stress symptoms (e.g., post-traumatic stress and depression) and commonly prescribed medications. Results provide evidence for poor coordination of frontal neural function after blast injury that may be the consequence of damaged anterior white matter tracts.
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The objective of the study was to examine whether deep brain stimulation (DBS) of the subthalamic nucleus (STN), the globus pallidus internus (GPi), and/or the ventralis intermedius thalamic nucleus (Vim) was associated with making patients angrier pre to post-surgical intervention. ⋯ STN and GPi DBS for Parkinson's disease were associated with significantly higher anger scores pre- to post-DBS as compared to Vim for essential tremor. Anger score changes in STN and GPi patients seem to be associated with microelectrode passes, suggesting that it may be a lesional effect. PD patients with longer disease duration may be particularly susceptible, and this should be kept in mind when discussing the potential of DBS surgery for an individual patient. Essential tremor patients who on average have much longer disease durations did not get angrier. The changes in anger scores were not related to LED change or dopamine agonist use. Whether the induction of anger is disease-specific or target-specific is not currently known; however, our data would suggest that PD patients implanted in STN or GPi are at a potential risk. Finally, on closer inspection of the COMPARE DBS data, VAMS anger scores did not change on or off DBS, suggesting that anger changes may be more of a lesional effect rather than a stimulation induced one (Okun et al., 2009).
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The symptoms of primary blast-induced mTBI, posttraumatic stress disorder and depression overlap. Evidence of an organic basis for these entities has been scarce and controversial. ⋯ The most salient findings observed were (1) the peak pressures (P(max)) in the brain, elicited from the blast from the firing of military weapons (P(max) 23-45 kPa), have a similar magnitude as that registered in air close to the head. Corresponding measurements during the detonation pulse from explosives under water show a P(max) in the brain, which is only 10% of that in water outside the head. (2) The rise time of the pressure curve is 10 times longer in the brain as compared with the blast in air outside the head during firing of military weapons. (3) The lower frequencies in the blast wave appear to be transmitted more readily to the brain than the higher frequencies. (4) When animals are exposed to low levels of blast, the blast wave appears mostly transmitted directly to the brain during air exposure, not via the thorax or abdomen. (5) Low levels of blast cause brain edema, as indicated by increased bioelectrical impedance, an increase in the intracranial pressure, small brain hemorrhages and impaired cognitive function.
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Research in blast-induced lung injury resulted in exposure thresholds that are useful in understanding and protecting humans from such injury. Because traumatic brain injury (TBI) due to blast exposure has become a prominent medical and military problem, similar thresholds should be identified that can put available research results in context and guide future research toward protecting war fighters as well as diagnosis and treatment. At least three mechanical mechanisms by which the blast wave may result in brain injury have been proposed-a thoracic mechanism, head acceleration, and direct cranial transmission. ⋯ There is a subset of blast conditions likely to result in TBI due to head acceleration and/or a thoracic mechanism without concomitant lung injury. These results can be used to guide experimental designs and compare additional data as they become available. Additional data are needed before actual probabilities or severity of TBI for a given exposure can be described.
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Although the exact number of affected individuals is unknown, it has been estimated that approximately 20% of U. S. veterans of Operations Enduring Freedom (OEF) and Iraqi Freedom (OIF) have experienced mild traumatic brain injury (mTBI) (i.e., concussion), which is defined as a brief loss or alteration of consciousness from a blow or jolt to the head. Blast exposure is among the most common causes of concussion in OEF-OIF warriors. ⋯ MDD relative to non-MDD individuals showed greater activity during fear matching trials in the amygdala and other emotion processing structures, lower activity during fear matching trials in emotional control structures such as the dorsolateral prefrontal cortex and lower fractional anisotropy (FA) in several white matter tracts including the superior longitudinal fasciculus (SLF). Greater depressive symptom severity correlated negatively with FA in the SLF. These results suggest a biological basis of MDD in OEF-OIF veterans who have experienced blast-related concussion, and may contribute to the development of treatments aimed at improving the clinical care of this unique population of wounded warriors.