Enhanced pre-frontal functional-structural networks to support postural control deficits after traumatic brain injury in a pediatric population

Traumatic brain injury (TBI) affects the structural connectivity, triggering the re-organization of structural-functional circuits in a manner that remains poorly understood. We focus here on brain networks re-organization in relation to postural control deficits after TBI. We enrolled young participants who had suffered moderate to severeTBI, comparing them to young typically developing control participants. In comparison to control participants, TBI patients (but not controls) recruited prefrontal regions to interact with two separated networks: 1) a subcortical network including part of the motor network, basal ganglia, cerebellum, hippocampus, amygdala, posterior cingulum and precuneus; and 2) a task-positive network, involving regions of the dorsal attention system together with the dorsolateral and ventrolateral prefrontal regions

Associations between brain structure and control of balance and gait in young patients with traumatic brain injury

In children and adolescents, traumatic brain injury (TBI) is a leading cause of death and permanent disability. The main causes of TBI in children are falls, sports-related injuries and motor vehicle accidents. TBI can lead to a wide range of impairments, including deficits in cognitive and motor functions as well as changes in personality. The degree of recovery of cognitive and motor skills is variable and highly unpredictable, particularly in young patients. Motor control disorders following TBI often include deficits in the control of posture and gait which can profoundly affect an individual’s mobility and independence. Although most patients regain independent stance and gait during rehabilitation, abnormalities often remain prevalent. A possible factor mediating these deficits may be weakness or strength asymmetry of leg muscles, but this has never been investigated. Therefore, the first objective of the doctoral thesis was to investigate whether muscle weakness and/or strength asymmetry are predictive of increased postural sway and abnormal spatiotemporal gait characteristics in young TBI patients (chapter 2). Postural sway was quantified in TBI patients and typically developing (TD) participants during normal standing and challenging conditions in which sensory resources (i.e. somatosensory inputs, visual inputs or both) were systemically disrupted. Findings revealed increased body sway (i.e. poorer postural control) in TBI patients as compared to TD participants. Surprisingly, this reduced performance could not only be demonstrated during conditions of compromised sensory feedback (visual, vestibular and/or somatosensory) but even during normal conditions. An electronic walkway system was used to assess gait characteristics during comfortable and fast-speed walking. During comfortable and fast gait, TBI patients walked with a lower velocity, longer double support phase and increased step length asymmetry, which are established indicators of impaired gait. Finally, TBI patients had a reduced strength and increased strength asymmetry in the investigated muscle groups of the legs. The asymmetry in muscle strength was a strong predictor of poorer balance control and a more variable and asymmetric gait. These findings illustrate the importance of muscular asymmetry as a potential marker and possible risk factor of impairments in the control of posture and gait. The second objective of the doctoral thesis was to investigate associations between impairments in gait and posture in young TBI patients and abnormalities in brain structure using different magnetic resonance imaging (MRI) techniques (chapters 3, 4 and 5). The control of gait and posture depends on an extensive neural circuitry involving cortical and subcortical grey matter (GM) areas and white matter (WM) pathways connecting these areas. In TBI patients, this network of brain regions can potentially be affected through various injury mechanisms. In the study described in chapter 3, voxel-based morphometry was used to investigate whether GM and WM volume loss in infratentorial structures (brain stem and cerebellum) can account for impairments in static and dynamic postural control in TBI. The focus on the cerebellum and brain stem was motivated by the fact that these structures are crucial for the neural control of posture and have been shown to be particularly vulnerable to primary and secondary structural consequences of brain injury. For the investigation of postural control, the participants (TBI and TD) performed a static postural control task with conditions of compromised sensory feedback as well as dynamic tests of balance control, requiring goal directed postural adjustments. Findings revealed both global volume loss (in total cerebellar GM and total infratentorial WM) as well as regional volume loss in specific WM areas (middle cerebellar peduncles, pons and midbrain). In the TBI group and across the whole group (TBI + TD participants), lower dynamic postural control performance was associated with reduced GM volume in the vermal/paravermal regions of the anterior cerebellar cortex. This is consistent with previous literature showing that these areas are important in sensorimotor processing and regulation of muscle tone to sustain upright stance. Volumetric analysis of the cerebellar cortex may therefore be a valuable prognostic marker of the chronic neural pathology which complicates rehabilitation of postural control in TBI patients. In addition, findings revealed that, across all subjects, lower volume in WM of the cerebellum and a large part of the brain stem were associated with worse dynamic and static postural control. These finding give credibility to the hypothesis that degeneration of important sensorimotor pathways in the brain stem can also be an important factor in the deterioration of postural control. In chapter 4, we used a different approach for the volumetric analysis of GM structures associated with locomotion in young TBI and TD participants. Specifically, specialized software was used to extract volumes of cortical and subcortical GM structures which have previously been reported to be involved in the neural control of human gait. Moreover, established spatiotemporal markers of gait impairments in TBI patients, including step length asymmetry, step length variability and double support time, were obtained using the same electronic walkway system as in chapter 2. It was demonstrated that compared to TD participants, TBI patients had reduced volumes in overall subcortical GM as well as in individual subcortical structures, including the hippocampus, cerebellar cortex, putamen and thalamus. Moreover, in the TBI group, volume losses in the subcortical regions were highly interrelated, indicative of a diffuse pathology in which atrophy tends to occur in combined subcortical structures. Finally, it was demonstrated, for the first time, that gait abnormalities in TBI patients were associated with reduced volume in specific cortical and subcortical GM structures which are crucial in gait control. The current results shed new light on the degenerative processes after TBI which contribute to the deficits in locomotion. A third approach for the analysis of brain structure was used in chapter 5. While the previously mentioned volumetric analyses gave a macrostructural characterization of brain areas, diffusion MRI can reveal microstructural properties of brain (white matter) tissue. In young TBI and TD participants, diffusion MRI metrics were determined in the cerebellum and cerebellar peduncles, structures known to be crucial for balance control. Findings revealed that, in TBI patients, diffusion metrics in these structures were associated with a reduced performance on static and dynamic postural control tasks. These findings are consistent with the relationships between altered cerebellar macrostructure and postural control that were found in TBI patients in chapter 2. Furthermore, this chapter included a longitudinal investigation of the brain together with a study of the behavioral metrics which pertains to the third objective of the doctoral thesis. Specifically, the objective was to investigate whether an intensive 8 week balance training program resulted in postural control improvements, and if these improvements were associated with changes in cerebellar WM microstructure. TBI patients and TD participants attended balance training, using PC-based portable balancers with real-time visual feedback. An additional control group of TD participants did not attend balance training. Moreover, diffusion MRI scans were acquired before, during (4 weeks) and at completion of training (8 weeks), together with the assessment of postural control tasks. Following training, the training groups (TBI and TD) showed significant improvements in dynamic and static postural control. These improvements were not observed in the TD group without training. Following training in TBI patients, a significant microstructural change was revealed in the inferior cerebellar peduncles. These peduncles contain fibers that carry sensory information (vestibular and somatosensory) to the cerebellum. Moreover, in both training groups, diffusion metrics in the cerebellum and/or cerebellar peduncles at baseline (before training) were predictive of the amount of performance increase after training. Finally, in TBI patients, amount of training-induced improvement on a dynamic postural control test was related to the amount of microstructural change in the inferior cerebellar peduncle. These findings emphasize the critical role of the cerebellum and associated peduncles for postural control and they provide important suggestions towards training-induced structural plasticity that may drive behavioral improvement in young TBI patients.nrpages: 175status: publishe

Does a Comparison View Improve the Reliability of Staging Wrist Osteoarthritis?

Background: Radiological grading of wrist osteoarthritis associated with scaphoid nonunion advanced collapse (SNAC) can be difficult. A comparison radiograph of the contralateral healthy wrist and an educational training in the various SNAC stages may improve reliability. Our purposes were to evaluate the difference in the reliability: (1) between observers who rate SNAC wrists with and without a comparison radiograph; and (2) between observers who receive training prior to ratings and those who do not. Methods: In this cross-sectional survey study, 82 fully trained orthopedic or hand surgeons rated anteroposterior radiographs of 19 patient wrists following a scaphoid nonunion based on SNAC stages 0 to 4. Observers were randomized online in 4 groups: one group rated unilateral views without training, a second group unilateral views with training, a third group bilateral views without training, and a fourth group bilateral views with training. Training included a 1-page clarification of the SNAC stages. Interobserver agreement was calculated using kappa statistics. Results: There was no significant difference between agreement between observers who rated unilateral radiographs (κ = 0.55) and who rated bilateral radiographs (κ = 0.58) (P =.14), nor between agreement between observers who received training (κ = 0.59) and who did not (κ = 0.54) (P =.058). Conclusions: The use of an additional comparison view and/or training does not seem to be clinically relevant in SNAC staging. There is room for improvement in the way we assess patients with SNAC wrists

Regional gray matter volume loss is associated with gait impairments in young brain-injured individuals

Traumatic brain injury ( TBI ) often leads to impairments in gait performance. However, the underlying neurostructural pathology of these gait deficits is poorly understood. We aimed to investigate regional gray matter ( GM ) volume in young moderate-to-severe TBI participants ( n = 19; age 13 years 11 months ±3 years 1 month ), compared with typically developing ( TD ) participants ( n = 30; 14 years 10 months ±2 years 2 months ), and assess whether reduced volume was related to impaired gait performance in TBI participants. Cortical and subcortical GM structures involved in the neural control of gait were selected as regions of interest ( ROIs ) and their volume was extracted using Freesurfer. Moreover, established spatiotemporal markers of gait impairments in TBI participants, including step length asymmetry, step length variability, and double support time, were obtained using an electronic walkway. Compared with TD participants, TBI participants showed increased double support time, step length asymmetry, and step length variability, suggesting a reduced gait control. Secondly, in TBI participants, reduced volumes were demonstrated in overall subcortical GM and individual subcortical ROIs, including the hippocampus, cerebellar cortex, putamen, and thalamus. Moreover, in the TBI group, volume losses in subcortical ROIs were highly inter-correlated, indicating that atrophy tends to occur in combined subcortical structures. Finally, it was demonstrated, for the first time, that gait abnormalities in TBI subjects were associated with reduced volume in specific GM structures, including the hippocampus, thalamus, and the cerebellar, superior frontal, paracentral, posterior cingulate, and superior parietal cortices. The present study is an important first step in the understanding of the neurostructural pathology underlying impaired gait in TBI patients