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The stenting versus aggressive medical therapy for intracranial artery stenosis (SAMMPRIS) trial compared aggressive medical therapy to aggressive medical therapy and percutaneous angioplasty and stenting (PTAS) in patients with symptomatic intracranial atherosclerotic disease (ICAD; Chimowitz et al., 2011). The trial was halted when a higher 30-day rate of stroke and death was present in the PTAS compared to the aggressive medical therapy group (14.7 vs. 5.8%, p = 0.002).

ObjectiveThis study explored what worked for whom, how and under what circumstances in a community-based augmented arm rehabilitation programme that was designed to enable stroke survivors to meet their personal rehabilitation needs.DesignA mixed methods realist-informed study of data from a randomised controlled feasibility trial, comparing augmented arm rehabilitation after stroke with usual care. The analysis was designed to develop initial programme theories and refine these through triangulation of qualitative and quantitative trial data. Participants with a confirmed stroke diagnosis and stroke-related arm impairment were recruited from five health boards in Scotland. Only data from participants in the augmented group were analysed. The augmented intervention comprised evidence-based arm rehabilitation (27 additional hours over 6 weeks) including self-managed practice, and focused on individual rehabilitation needs identified through the Canadian Occupational Performance Measure (COPM). The COPM indicated to which extent rehabilitation needs were met following the intervention, the Action Research Arm Test provided data on changes in arm function, and qualitative interviews provided information about the context and potential mechanisms of action.FindingsSeventeen stroke survivors (11 males, age range 40–84 years, NIHSS median (IQR) 6 (8)) were included. Median (IQR) COPM Performance and Satisfaction scores (min.1-max.10) improved from pre-intervention 2 (5) to post-intervention 5 (7). Findings suggested that meeting rehabilitation needs was facilitated by strengthening participants’ sense of intrinsic motivation (through grounding exercises in everyday activities linked to valued life roles, and enabling them to overcome barriers to self-managed practice), and via therapeutic relationships (through trust and expertise, shared decision-making, encouragement and emotional support). Collectively, these mechanisms enabled stroke survivors to build confidence and gain mastery experience necessary to engage in new self-managed practice routines.ConclusionThis realist-informed study enabled the development of initial programme theories to explain how and in what circumstances the augmented arm rehabilitation intervention may have enabled participants to meet their personal rehabilitation needs. Encouraging participants’ sense of intrinsic motivation and building therapeutic relationships appeared instrumental. These initial programme theories require further testing, refinement, and integration with the wider literature.

It is postulated that the decreased walking speed; small, shuffling steps; and "freezing" shown by patients with Parkinson's disease could stem from an inability to tilt the body forward enough to provide sufficient forward propulsion. In two repeated-measures studies we examined whether adaptation to upward-shifting prisms, resulting in a downward after-effect, could improve gait initiation in healthy participants and patients with Parkinson's disease. Faster forward stepping followed a brief (5 min) exposure period for patients, and a longer (20 min) exposure period for age-matched controls. Backward stepping was unchanged, and adaptation to downward-shifting prisms with control participants showed no effect on forward or backward stepping. These results suggest that adaptation of arm proprioception in the vertical plane may generalize to anterior-posterior postural control, presenting new possibilities for the treatment of gait disturbance in basal ganglia disorders.

There is a complex interrelation between epilepsy and cardiac pathology, with both acute and long-term effects of seizures on the regulation of the cardiac rhythm and on the heart functioning. A specific issue is the potential relation between these cardiac manifestations and the risk of Sudden and Unexpected Death in Epilepsy (SUDEP), with unclear respective role of centrally-control ictal changes, long-term epilepsy-related dysregulation of the neurovegetative control and direct effects on the heart function. In the present review, we detailed available data about ictal cardiac changes, along with interictal cardiac manifestations associated with long-term functional and structural alterations of the heart. Pathophysiological mechanisms of these cardiac changes are discussed, with a specific focus on central mechanisms and the investigation of a possible deregulation of the central control of autonomic functions in addition to the role of catecholamine and hypoxemia on heart.

This review focuses on the use of resting-state functional magnetic resonance imaging data to assess functional connectivity in the human brain and its application in intractable epilepsy. This approach has the potential to predict outcomes for a given surgical procedure based on the pre-surgical functional organization of the brain. Functional connectivity can also identify cortical regions that are organized differently in epilepsy patients either as a direct function of the disease or through indirect compensatory responses. Functional connectivity mapping may help identify epileptogenic tissue, whether this is a single focal location or a network of seizure-generating tissues. This review covers the basics of connectivity analysis and discusses particular issues associated with analyzing such data. These issues include how to define nodes, as well as differences between connectivity analyses of individual nodes, groups of nodes, and whole-brain assessment at the voxel level. The need for arbitrary thresholds in some connectivity analyses is discussed and a solution to this problem is reviewed. Overall, functional connectivity analysis is becoming an important tool for assessing functional brain organization in epilepsy.

Over the last 30 years, the functions (and dysfunctions) of the sensory-motor circuitry have been mostly conceptualized using linear modelizations which have resulted in two main models: the "rate hypothesis" and the "oscillatory hypothesis." In these two models, the basal ganglia data stream is envisaged as a random temporal combination of independent simple patterns issued from its probability distribution of interval interspikes or its spectrum of frequencies respectively. More recently, non-linear analyses have been introduced in the modelization of motor circuitry activities, and they have provided evidences that complex temporal organizations exist in basal ganglia neuronal activities. Regarding movement disorders, these complex temporal organizations in the basal ganglia data stream differ between conditions (i.e., parkinsonism, dyskinesia, healthy control) and are responsive to treatments (i.e., l-DOPA, deep brain stimulation). A body of evidence has reported that basal ganglia neuronal entropy (a marker for complexity/irregularity in time series) is higher in hypokinetic state. In line with these findings, an entropy-based model has been recently formulated to introduce basal ganglia entropy as a marker for the alteration of motor processing and a factor of motor inhibition. Importantly, non-linear features have also been identified as a marker of condition and/or treatment effects in brain global signals (EEG), muscular activities (EMG), or kinetic of motor symptoms (tremor, gait) of patients with movement disorders. It is therefore warranted that the non-linear dynamics of motor circuitry will contribute to a better understanding of the neuronal dysfunctions underlying the spectrum of parkinsonian motor symptoms including tremor, rigidity, and hypokinesia.

General and central nervous system anatomy and physiology in children is different to that of adults and this is relevant to traumatic brain injury (TBI) and spinal cord injury. The controversies and uncertainties in adult neurotrauma are magnified by these differences, the lack of normative data for children, the scarcity of pediatric studies, and inappropriate generalization from adult studies. Cerebral metabolism develops rapidly in the early years, driven by cortical development, synaptogenesis, and rapid myelination, followed by equally dramatic changes in baseline and stimulated cerebral blood flow. Therefore, adult values for cerebral hemodynamics do not apply to children, and children cannot be easily approached as a homogenous group, especially given the marked changes between birth and age 8. Their cranial and spinal anatomy undergoes many changes, from the presence and disappearance of the fontanels, the presence and closure of cranial sutures, the thickness and pliability of the cranium, anatomy of the vertebra, and the maturity of the cervical ligaments and muscles. Moreover, their systemic anatomy changes over time. The head is relatively large in young children, the airway is easily compromised, the chest is poorly protected, the abdominal organs are large. Physiology changes-blood volume is small by comparison, hypothermia develops easily, intracranial pressure (ICP) is lower, and blood pressure normograms are considerably different at different ages, with potentially important implications for cerebral perfusion pressure (CPP) thresholds. Mechanisms and pathologies also differ-diffuse injuries are common in accidental injury, and growing fractures, non-accidental injury and spinal cord injury without radiographic abnormality are unique to the pediatric population. Despite these clear differences and the vulnerability of children, the amount of pediatric-specific data in TBI is surprisingly weak. There are no robust guidelines for even basics aspects of care in children, such as ICP and CPP management. This is particularly alarming given that TBI is a leading cause of death in children. To address this, there is an urgent need for pediatric-specific clinical research. If this goal is to be achieved, any clinician or researcher interested in pediatric neurotrauma must be familiar with its unique pathophysiological characteristics.