Abstract-Robotics is rapidly emerging as a viable approach to enhance motor recovery after disabling stroke. Current principles of cognitive motor learning recognize a positive relationship between reward and motor learning. Yet no prior studies have established explicitly whether reward improves the rate or efficacy of robotics-assisted rehabilitation or produces neurophysiologic adaptations associated with motor learning. We conducted a 3 wk, 9-session clinical pilot with 10 people with chronic hemiparetic stroke, randomly assigned to train with an impedance-controlled ankle robot (anklebot) under either high reward (HR) or low reward conditions. The 1 h training sessions entailed playing a seated video game by moving the paretic ankle to hit moving onscreen targets with the anklebot only providing assistance as needed. Assessments included paretic ankle motor control, learning curves, electroencephalograpy (EEG) coherence and spectral power during unassisted trials, and gait function. While both groups exhibited changes in EEG, the HR group had faster learning curves (p = 0.05), smoother movements (p = 0.05), reduced contralesional-frontoparietal coherence (p = 0.05), and reduced left-temporal spectral power (p = 0.05). Gait analyses revealed an increase in nonparetic step length (p = 0.05) in the HR group only. These results suggest that combining explicit rewards with novel anklebot training may accelerate motor learning for restoring mobility.Clinical Trial Registration: ClinicalTrials.gov; NCT01072032; "Cortical and biomechanical dynamics of ankle robotics training in stroke"; http://www.clinicaltrials.gov/ct2/show/NCT01072032
In this study, we used manual delineation of high-resolution magnetic resonance imaging (MRI) to determine the spatial and temporal characteristics of the cerebellar atrophy in spinocerebellar ataxia type 2 (SCA2). Ten subjects with SCA2 were compared to ten controls. The volume of the pons, the total cerebellum, and the individual cerebellar lobules were calculated via manual delineation of structural MRI. SCA2 showed substantial global atrophy of the cerebellum. Furthermore, the degeneration was lobule-specific, selectively affecting the anterior lobe, VI, Crus I, Crus II, VIII, uvula, corpus medullare, and pons, while sparing VIIB, tonsil/paraflocculus, flocculus, declive, tuber/folium, pyramis, and nodulus. The temporal characteristics differed in each cerebellar subregion: 1) Duration of disease: Crus I, VIIB, VIII, uvula, corpus medullare, pons, and the total cerebellar volume correlated with the duration of disease; 2) Age: VI, Crus II, and flocculus correlated with age in control subjects; 3) Clinical scores: VI, Crus I, VIIB, VIII, corpus medullare, pons, and the total cerebellar volume correlated with clinical scores in SCA2. No correlations were found with the age of onset. Our extrapolated volumes at the onset of symptoms suggest that neurodegeneration may be present even during the presymptomatic stages of disease. The spatial and temporal characteristics of the cerebellar degeneration in SCA2 are region-specific. Furthermore, our findings suggest the presence of presymptomatic atrophy and a possible developmental component to the mechanisms of pathogenesis underlying SCA2. Our findings further suggest that volumetric analysis may aid in the development of a non-invasive, quantitative biomarker.
PURPOSE To compare glioblastoma and brain metastases using T1-weighted dynamic contrast-enhanced (DCE)-MRI perfusion technique. METHODS 26 patients with glioblastoma and 32 patients with metastatic brain lesions with no treatment who underwent DCE-MRI were, retrospectively, analyzed. DCE perfusion parameters Ktrans and Vp were calculated for the whole tumor. Signal intensity time curves were quantified by calculating the area under the curve (AUC) and the logarithmic slope of the washout phase to explore the heterogeneous tumor characteristics. RESULTS Glioblastoma did not differ from all brain metastases in Ktrans (P = .34) or Vp (P = .47). Glioblastoma and melanoma metastases differed from hypovascular metastases in AUC and log slope of the washout phase of the signal intensity time curve (P < .05); however, glioblastoma and melanoma metastases did not differ from each other (AUC: P = .78, Log slope: P = .77). Glioblastoma and melanoma metastases differed from hypovascular metastases in the ratio of Voxelneg/Voxelpos (P< .03); however, they did not differ from each other. Glioblastoma and melanoma metastases differed from each other in Voxelneg_threshold at higher negative log slope threshold. CONCLUSION DCE-MRI showed that it has a potential to differentiate glioblastomas, melanoma metastases and hypovascular brain tumors. Logarithmic slope of the washout phase and AUC of the signal intensity time curve were shown to be the best discriminator between hypervascular and hypovascular neoplasms.
a b s t r a c tPurpose: To investigate the relationship between abdominal chemoradiation (CRT) for locally advanced cancers and bone mineral density (BMD) reduction in the vertebral spine. Materials and methods: Data from 272 patients who underwent abdominal radiation therapy from January 1997 to May 2015 were retrospectively reviewed. Forty-two patients received computed tomography (CT) scans of the abdomen prior to initiation and at least twice after radiation therapy. Bone attenuation (in Hounsfield unit) (HU) measurements were collected for each vertebral level from T7 to L5 using sagittal CT images. Radiation point dose was obtained at each mid-vertebral body from the radiation treatment plan. Percent change in bone attenuation (D%HU) between baseline and post-radiation therapy were computed for each vertebral body. The D%HU was compared against radiation dose using Pearson's linear correlation. Results: Abdominal radiotherapy caused significant reduction in vertebral BMD as measured by HU. Patients who received only chemotherapy did not show changes in their BMD in this study. The D%HU was significantly correlated with the radiation point dose to the vertebral body (R = À0.472, P < 0.001) within 4-8 months following RT. The same relationship persisted in subsequent follow up scans 9 months following RT (R = À0.578, P < 0.001). Based on the result of linear regression, 5 Gy, 15 Gy, 25 Gy, 35 Gy, and 45 Gy caused 21.7%, 31.1%, 40.5%, 49.9%, and 59.3% decrease in HU following RT, respectively. Our generalized linear model showed that pre-RT HU had a positive effect (b = 0.830) on determining post-RT HU, while number of months post RT (b = À0.213) and radiation point dose (b = À1.475) had a negative effect. A comparison of the predicted versus actual HU showed significant correlation (R = 0.883, P < 0.001) with the slope of the best linear fit = 0.81. Our model's predicted HU were within ±20 HU of the actual value in 53% of cases, 70% of the predictions were within ±30 HU, 81% were within ±40 HU, and 90% were within ±50 HU of the actual post-RT HU. Four of 42 patients were found to have vertebral body compression fractures in the field of radiation. Vertebral body insufficiency and compression fractures are most commonly caused by osteoporosis, an age-related and systemic skeletal disorder characterized by compromised bone strength and low bone mineral density [1]. Although, most fractures are asymptomatic, the degree of BMD loss, location of the fracture, and secondary osteoporosis from underlying medical condition including chemotherapy may make an asymptomatic, stable fracture more prone to progressive collapse causing pain, loss of mobility, and spinal cord compression [2]. The overall morbidity of vertebral body compression fractures is significant, and women diagnosed with compression fractures have a 15% higher mortality rate than matched controls [3].Irradiation of normal, non-malignant bone results in small vessel damage leading to microcirculatory occlusion, marrow hypocellularity from death of osteo...
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