Journal of the neurological sciences
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Traumatic brain injury (TBI) causes deleterious critical-illness-related-corticosteroid-insufficiency (CIRCI), leading to high mortality and morbidity. However, the incidence of CIRCI following different TBI severities is not fully defined. This study was designed to investigate mechanistically the effects of injury severity on corticosteroid response and the development of CIRCI in a rat model of experimentally controlled TBI. ⋯ Second, TBI-induced CIRCI is closely correlated with injury severity. As the injury severity rises both the incidence of CIRCI and mortality surge; Third, increased level of injury severity reduces the expression of endothelial tight junction protein, aggravate BBB permeability and exacerbate the ensuing neural apoptosis in the PVN of hypothalamus. These findings indicate that increased severity of TBI aggravate the incidence of CIRCI by causing damage to tight junctions of vascular endothelial cells and increasing neuronal apoptosis in the PVN of hypothalamus.
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N-methyl-D-aspartate receptor (NMDAR) activity is increased, while GABAB receptor is downregulated in the spinal cord dorsal horn in diabetic neuropathy. In this study, we determined the interaction of NMDARs and GABAB receptors in streptozotocin (STZ)-induced diabetic neuropathy. The paw withdrawal threshold (PWT) was significantly lower in STZ-treated rats than in vehicle-treated rats. ⋯ In addition, the phosphorylated cAMP response element-binding (CREB) protein level was significantly higher in the spinal cord dorsal horn in STZ-treated rats compared with vehicle-treated rats. Intrathecal injection of baclofen significantly decreased phosphorylated CREB protein level in STZ-treated rats; an effect was blocked by CGP55845. These data suggest that activation of GABAB receptors in the spinal cord dorsal horn normalizes NMDAR expression level in diabetic neuropathic pain.
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Transcranial magnetic stimulation (TMS) has been used to evaluate neuroplastic changes in the brain in clinical trials. The purpose of this study was to establish the test-retest reliability of 4 TMS measures of corticomotor excitability - (1) resting motor threshold, (2) slope of input-output curve, (3) peak motor evoked potential amplitude, and (4) cortical silent period duration for the corticospinal projections to the first dorsal interosseous of the contralateral hand. Fourteen healthy subjects (mean age 27.4 years) and 27 subjects with stroke-induced upper limb hemiparesis (mean age 61.3 years) completed 2 repeated sessions of assessment of 1 week apart. ⋯ Measurement reliability was good (ICC ≥ 0.75) for the 4 outcome measures in healthy subjects. Contrary to the similarity in standard error of measurements in both hemispheres for outcome measures (1) to (3) in the stroke subjects, that of the cortical silent period duration was larger in magnitude in the lesioned hemisphere. The test-retest reliability coefficients determined for the four corticomotor excitability measurements allowed the estimation of 95% minimal detectable changes of these outcome variables for the respective subject group in future clinical trials.
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A boy, who had shown muscle weakness and hypotonia from early childhood and fiber type disproportion (FTD) with no dystrophic changes on muscle biopsy, was initially diagnosed as having congenital fiber type disproportion (CFTD). Subsequently, he developed cardiac conduction blocks. We reconsidered the diagnosis as possible LMNA-myopathy and found a heterozygous mutation in the LMNA gene. ⋯ Four of 23 muscular dystrophy patients with LMNA mutation also showed fiber type disproportion (FTD). Importantly, all FTD associated with LMNA-myopathy were caused by hypertrophy of type 2 fibers as compared with age-matched controls, whereas CFTD with mutations in ACTA1 or TPM3 showed selective type 1 fiber atrophy but no type 2 fiber hypertrophy. Although FTD is not a constant pathological feature of LMNA-myopathy, we should consider the possibility of LMNA-myopathy whenever a diagnosis of CFTD is made and take steps to prevent cardiac insufficiency.