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Prediction of Neurological Impairment in Cervical Spondylotic Myelopathy using a Combination of Diffusion MRI and Proton MR Spectroscopy.
Ellingson, BM, Salamon, N, Hardy, AJ, Holly, LT
PloS one. 2015;(10):e0139451
Abstract
PURPOSE In the present study we investigated a combination of diffusion tensor imaging (DTI) and magnetic resonance spectroscopic (MRS) biomarkers in order to predict neurological impairment in patients with cervical spondylosis. METHODS Twenty-seven patients with cervical spondylosis were evaluated. DTI and single voxel MRS were performed in the cervical cord. N-acetylaspartate (NAA) and choline (Cho) metabolite concentration ratios with respect to creatine were quantified, as well as the ratio of choline to NAA. The modified mJOA scale was used as a measure of neurologic deficit. Linear regression was performed between DTI and MRS parameters and mJOA scores. Significant predictors from linear regression were used in a multiple linear regression model in order to improve prediction of mJOA. Parameters that did not add value to model performance were removed, then an optimized multiparametric model was established to predict mJOA. RESULTS Significant correlations were observed between the Torg-Pavlov ratio and FA (R2 = 0.2021, P = 0.019); DTI fiber tract density and FA, MD, Cho/NAA (R2 = 0.3412, P = 0.0014; R2 = 0.2112, P = 0.016; and R2 = 0.2352, P = 0.010 respectively); along with FA and Cho/NAA (R2 = 0.1695, P = 0.033). DTI fiber tract density, MD and FA at the site of compression, along with Cho/NAA at C2, were significantly correlated with mJOA score (R2 = 0.05939, P < 0.0001; R2 = 0.4739, P < 0.0001; R2 = 0.7034, P < 0.0001; R2 = 0.4649, P < 0.0001). A combination biomarker consisting of DTI fiber tract density, MD, and Cho/NAA showed the best prediction of mJOA (R2 = 0.8274, P<0.0001), with post-hoc tests suggesting fiber tract density, MD, and Cho/NAA were all significant contributors to predicting mJOA (P = 0.00053, P = 0.00085, and P = 0.0019, respectively). CONCLUSION A linear combination of DTI and MRS measurements within the cervical spinal cord may be useful for accurately predicting neurological deficits in patients with cervical spondylosis. Additional studies may be necessary to validate these observations.
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Occipital C1-C2 neuromodulation decreases body mass and fat stores and modifies activity of the autonomic nervous system in morbidly obese patients--a pilot study.
Sobocki, J, Herman, RM, Fraczek, M
Obesity surgery. 2013;(5):693-7
Abstract
BACKGROUND Autonomic and vagal neuromodulation has been suggested for the treatment of morbid obesity. Occipital nerves remain in close anatomical relation to vagal nerve roots at the entrance to medulla oblongata. The aim of the study was to evaluate the effect of C1-C2 occipital neuromodulation on autonomic activity, body mass, and composition. METHODS Five obese patients were included in the study (three women and two men, BMI 43-49, average age 43.3, range 24-55). Two electrodes were placed bilaterally in the C1-C2 region subcutaneously under local anesthesia. Stimulation was started 24 h after implantation and continued for 8 weeks. Patients activated stimulators for 12 h every day and turned the stimulators off at night. No other treatment including diet or change in lifestyle was introduced during the study. The following parameters were evaluated: body mass (0, 4th, and 8th week), body composition (bioimpedance study), food intake, quality of life, and heart rate variability (HRV) (0 and 8th week). RESULTS No adverse events were observed in this group. One patient reported amelioration of constipation and one reported two incidents of salivation. The average body mass decrease was 5.6 kg in 4 weeks and 8.7 kg in 8 weeks. Body composition study showed a 2-month decrease in body fat of 7.9 kg on average. HRV revealed increased parasympathetic tone (LF/HF 4.4 ± 4.3 SD vs. 1.6 ± 1.7 SD). CONCLUSIONS C1-C2 occipital stimulation seems being capable of decreasing body mass and affecting a positive shift in body composition and significantly increases the activity of the autonomic nervous system.
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The effect of an energy drink containing glucose and caffeine on human corticospinal excitability.
Specterman, M, Bhuiya, A, Kuppuswamy, A, Strutton, PH, Catley, M, Davey, NJ
Physiology & behavior. 2005;(5):723-8
Abstract
Glucose- and caffeine-containing energy drinks are said to influence the cognitive and cellular function within the brain. In this study, we have used the size of motor-evoked potentials (MEPs) produced in response to transcranial magnetic stimulation (TMS) of the motor cortex as an index of corticospinal excitability after ingestion of Lucozade and control drinks of glucose-containing or caffeine-containing carbonated water or carbonated water alone. With local ethical approval and informed consent, 10 healthy volunteers took part; surface electromyographic (EMG) recordings were taken from the thenar muscles of the dominant hand. In each assessment, 15 TMS stimuli were delivered over the motor cortex at an intensity of 1.1 T. Six subjects ingested a 380-ml bottle of carbonated Lucozade drink containing 68 g of glucose and 46 mg caffeine. Four subjects took part in three control trials drinking: (A) carbonated water with caffeine, (B) carbonated water with glucose and (C) carbonated water alone. Assessments were made before and at 30-min intervals after each drink. Mean fasting blood glucose concentrations and mean areas of MEPs rose after the Lucozade, remaining elevated for 90 min. Similar rises in MEP areas were seen in trials after drinking carbonated water with caffeine or with glucose, but not after drinking carbonated water alone. No change was seen in the M-wave evoked by electrical stimulation of the ulnar nerve. We conclude that Lucozade can affect the size of MEPs to activation of the motor cortex with fixed-intensity TMS. The underlying mechanism is likely to relate to the combined effects of caffeine and glucose on the brain.
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Spinal prostaglandin formation and pain perception following thoracotomy: a role for cyclooxygenase-2.
McCrory, C, Fitzgerald, D
Chest. 2004;(4):1321-7
Abstract
STUDY OBJECTIVE Prostaglandins (PGs) generated in the spinal cord may play a major role in pain perception. Consequently, the suppression of spinal cyclooxygenase (COX) and PG formation may contribute to the analgesic effect of nonsteroidal anti-inflammatory drugs (NSAIDs) in pain following surgery. Which isoform of COX is responsible for postsurgical pain and, consequently, should be targeted, is unclear. DESIGN Prospective randomized blinded study. SETTING University teaching hospital. PATIENTS Thirty patients undergoing thoracotomy for lobectomy were recruited. INTERVENTIONS Patients were randomized to receive the COX-2 selective inhibitor nimesulide, 100 mg orally twice daily, or ibuprofen (nonselective), 400 mg orally three times daily, in an open-label study. In addition, there was a randomized control group that received no NSAIDs. Cerebrospinal fluid (CSF) was analyzed for 6-keto-PGF(1)alpha, the principle metabolite of prostacyclin. COX-1 and COX-2 activity was determined by measuring serum thromboxane (TX) B(2) and endotoxin-induced PGE(2) generation in whole blood. MEASUREMENTS Pain perception was measured by visual analog scores, and blinded assessment of opioid analgesic requirements and expiratory peak flow measurements were performed. RESULTS At the doses used, nimesulide was selective for COX-2, while ibuprofen was nonselective based on serum TXB(2) levels. The mean (+/- SEM) levels of 6-keto-PGF(1)alpha in CSF increased following surgery from 32 +/- 4.9 to 127 +/- 29 pg/mL (p < 0.001), and this was suppressed by nimesulide (49 +/- 9.3 pg/mL; p = 0.0025) but not by ibuprofen (122 +/- 35 pg/mL). Pain scores (p < 0.001), morphine requirement (p = 0.0175), and the fall in peak expiratory flow rate (p < 0.001) were significantly lower in the nimesulide group. CONCLUSIONS Increases in spinal PG synthesis after thoracotomy are repressed by a selective COX-2 inhibitor. This suggests that the inducible COX-2 mediates central PG synthesis, which may be important in the generation of pain, as the use of nimesulide also resulted in significant decreases in postoperative pain perception.
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Intrathecal release of nitric oxide in Alzheimer's disease and vascular dementia.
Tarkowski, E, Ringqvist, A, Blennow, K, Wallin, A, Wennmalm, A
Dementia and geriatric cognitive disorders. 2000;(6):322-6
Abstract
A growing body of evidence points out the potential role of inflammatory mechanisms in the pathophysiology of brain damage in dementia. We have recently demonstrated that patients with Alzheimer's disease (AD) and vascular dementia (VaD) display an intrathecal production of proinflammatory cytokines. TNF-alpha, one of these cytokines, leads to the production of nitric oxide (NO), a potent inflammatory mediator, by induction of inducible NO synthase. The aim of the present study was to investigate the intrathecal levels of nitrate, one of the main metabolites of NO, and to relate its levels to the degree of intellectual impairment, in patients with AD and VaD. Twenty patients with early AD and 26 patients with VaD were analyzed with respect to cerebrospinal fluid levels of nitrate by gas chromatography/mass spectrometry. Interestingly, in patients with AD but not VaD, the intrathecal levels of nitrate were significantly and inversely correlated (r = -0.68, p = 0.002) to the degree of intellectual impairment. Our study demonstrates an inverse correlation between the intrathecal levels of nitrate and the degree of cognitive impairment in patients with AD, suggesting a neuroprotective effect of NO in AD.