RESUMEN
There is a requirement for an objective method to determine a safe level of low-level military occupational blast, having recognised it can lead to neurological damage. The purpose of the current study was to evaluate the effect of artillery firing training on the neurochemistry of frontline soldiers using two-dimensional (2D) COrrelated SpectroscopY (2D COSY) in a 3-T clinical MR scanner. Ten men considered to be of sound health were evaluated before and after a week-long live firing exercise in two ways. Prior to the live fire exercise, all participants were screened by a clinical psychologist using a combination of clinical interviews and psychometric tests, and were then scanned with 3-T MRI. The protocols included T1- and T2-weighted images for diagnostic reporting and anatomical localisation and 2D COSY to record any neurochemical effects from the firing. No changes to the structural MRI were recorded. Nine substantive and statistically significant changes in the neurochemistry were recorded as a consequence of firing training. Glutamine and glutamate, glutathione, and two of the seven fucose-α (1-2)-glycans were significantly increased. N-acetyl aspartate, myo-inositol + creatine, and glycerol were also increased. Significant decreases were recorded for the glutathione cysteine moiety and tentatively assigned glycan with a 1-6 linkage (F2: 4.00, F1: 1.31 ppm). These molecules are part of three neurochemical pathways at the terminus of the neurons providing evidence of early markers of disruption to neurotransmission. Using this technology, the extent of deregulation can now be monitored for each frontline defender on a personalised basis. The capacity to monitor early a disruption in neurotransmitters, using the 2D COSY protocol, can observe the effect of firing and may be used to prevent or limit these events.
RESUMEN
Response to pain therapy is currently by patient self-report. We demonstrate that by evaluating the neurochemistry of a patient, using two-dimensional Correlated SpectroscopY (2D COSY) in a 3T MRI scanner, response to therapy can be recorded. A chronic temporomandibular joint (TMJ) pain patient was evaluated by a pain physician specializing in temporomandibular disorders (TMD), and by 2D COSY, before, and 6 days after treatment with Botulinum Toxin A. Prior to treatment the self-reported pain score was 8/10 and reduced to 0/10 within 24 h of treatment. The neurochemistry of the patient prior to treatment was typical of chronic pain. In particular, the Fuc-α(1-2) glycans were affected. Following treatment, the substrates, α-L Fucose, were elevated and the Fuc-α(1-2) glycans repopulated. The depletion of the molecule assigned the glutathione cysteine moiety, with chronic pain, is indicative of a Glutathione redox imbalance linked to neurodegeneration. This new approach to monitor pain could help discriminate the relative contributions in the complex interplay of the sensory and affective (emotional suffering) components of pain leading to appropriate individualized pharmaceutical drug regimens.