Are movement disorders and sensorimotor injuries pathologic synergies? When normal multi-joint movement synergies become pathologic

The intact nervous system has an exquisite ability to modulate the activity of multiple muscles acting at one or more joints to produce an enormous range of actions. Seemingly simple tasks, such as reaching for an object or walking, in fact rely on very complex spatial and temporal patterns of muscle activations. Neurological disorders such as stroke and focal dystonia affect the ability to coordinate multi-joint movements. This article reviews the state of the art of research of muscle synergies in the intact and damaged nervous system, their implications for recovery and rehabilitation, and proposes avenues for research aimed at restoring the nervous system’s ability to control movement

Democratizing Neurorehabilitation:How Accessible are Low-Cost Mobile-Gaming Technologies for Self-Rehabilitation of Arm Disability in Stroke?

Motor-training software on tablets or smartphones (Apps) offer a low-cost, widely-available solution to supplement arm physiotherapy after stroke. We assessed the proportions of hemiplegic stroke patients who, with their plegic hand, could meaningfully engage with mobile-gaming devices using a range of standard control-methods, as well as by using a novel wireless grip-controller, adapted for neurodisability. We screened all newly-diagnosed hemiplegic stroke patients presenting to a stroke centre over 6 months. Subjects were compared on their ability to control a tablet or smartphone cursor using: finger-swipe, tap, joystick, screen-tilt, and an adapted handgrip. Cursor control was graded as: no movement (0); less than full-range movement (1); full-range movement (2); directed movement (3). In total, we screened 345 patients, of which 87 satisfied recruitment criteria and completed testing. The commonest reason for exclusion was cognitive impairment. Using conventional controls, the proportion of patients able to direct cursor movement was 38-48%; and to move it full-range was 55-67% (controller comparison: p>0.1). By comparison, handgrip enabled directed control in 75%, and full-range movement in 93% (controller comparison: p<0.001). This difference between controllers was most apparent amongst severely-disabled subjects, with 0% achieving directed or full-range control with conventional controls, compared to 58% and 83% achieving these two levels of movement, respectively, with handgrip. In conclusion, hand, or arm, training Apps played on conventional mobile devices are likely to be accessible only to mildly-disabled stroke patients. Technological adaptations such as grip-control can enable more severely affected subjects to engage with self-training software

Mechanisms and Perspectives of Post-Stroke Depression: Neuroanatomical Substrates, Incentive Motivation, and Emotional Processing

Post-stroke depression (PSD) is a prevalent affective condition after a stroke, which can impair functional and motor rehabilitation. The present dissertation and the included studies aim to further our understanding of how different mechanisms after stroke affect the emergence and maintenance of depressive symptoms on different pathological levels. For this, three separate studies were executed using several methodological applications, including different lesion-symptom mapping approaches, experimental task designs with different behavioral parameters, interviews, and test batteries. Study 1 investigated the link between anatomical brain lesions and specific PSD symptoms in a large stroke sample using a support-vector regression lesion-symptom mapping approach. Rather than treating depression as a single global score, lesion locations contributing to distinct PSD symptom domains were identified and analyzed. Study 2 examined the relationship between motor impairment and incentive motivation early after stroke and PSD symptoms, specifically motivational deficits. We were specifically interested in whether differences in motivation for physically demanding tasks could predict the development of PSD in patients with residual motor impairments. As disrupted emotion processing abilities can deteriorate social relationships and promote and maintain depressive symptoms study 3 examined emotion processing deficits after stroke and their relationship with PSD. Taken together, our findings contribute to a further understanding of the pathophysiology of PSD and how psychological and neurological influences interact in the development, maintenance, and treatment of depression after stroke. This should help to advance personalized therapeutic approaches and alleviate the burden of PSD characteristics for patients and caregivers

A review of brain circuitries involved in stuttering.

Stuttering has been the subject of much research, nevertheless its etiology remains incompletely understood. This article presents a critical review of the literature on stuttering, with particular reference to the role of the basal ganglia (BG). Neuroimaging and lesion studies of developmental and acquired stuttering, as well as pharmacological and genetic studies are discussed. Evidence of structural and functional changes in the BG in those who stutter indicates that this motor speech disorder is due, at least in part, to abnormal BG cues for the initiation and termination of articulatory movements. Studies discussed provide evidence of a dysfunctional hyperdopaminergic state of the thalamocortical pathways underlying speech motor control in stuttering. Evidence that stuttering can improve, worsen or recur following deep brain stimulation for other indications is presented in order to emphasize the role of BG in stuttering. Further research is needed to fully elucidate the pathophysiology of this speech disorder, which is associated with significant social isolation

Neural correlates of laughter and humour

Although laughter and humour have been constituents of humanity for thousands if not millions of years, their systematic study has begun only recently. Investigations into their neurological correlates remain fragmentary and the following review is a first attempt to collate and evaluate these studies, most of which have been published over the last two decades. By employing the classical methods of neurology, brain regions associated with symptomatic (pathological) laughter have been determined and catalogued under other diagnostic signs and symptoms of such conditions as epilepsy, strokes and circumspect brain lesions. These observations have been complemented by newer studies using modern non‐invasive imaging methods. To summarize the results of many studies, the expression of laughter seems to depend on two partially independent neuronal pathways. The first of these, an ‘involuntary' or ‘emotionally driven' system, involves the amygdala, thalamic/hypo‐ and subthalamic areas and the dorsal/tegmental brainstem. The second, ‘voluntary' system originates in the premotor/frontal opercular areas and leads through the motor cortex and pyramidal tract to the ventral brainstem. These systems and the laughter response appear to be coordinated by a laughter‐coordinating centre in the dorsal upper pons. Analyses of the cerebral correlates of humour have been impeded by a lack of consensus among psychologists on exactly what humour is, and of what essential components it consists. Within the past two decades, however, sufficient agreement has been reached that theory‐based hypotheses could be formulated and tested with various non‐invasive methods. For the perception of humour (and depending on the type of humour involved, its mode of transmission, etc.) the right frontal cortex, the medial ventral prefrontal cortex, the right and left posterior (middle and inferior) temporal regions and possibly the cerebellum seem to be involved to varying degrees. An attempt has been made to be as thorough as possible in documenting the foundations upon which these burgeoning areas of research have been based up to the present tim

Evidence for early physiotherapy after acute stroke: a scoping review

Neuroscience evidence indicates that early rehabilitation can guarantee better outcomes and quicker cortical re-organization after lesion. Although there are some studies related to the acute stroke physiotherapy intervention, it seems that few consider the evidence that link neuroplasticity and neurorehabilitation. Therefore, understanding the current state of the art of physiotherapy intervention is vital to potentialize the intervention so the enhance neuroplastic window is properly explored. To analyze the physiotherapy's intervention on acute stroke patients, so it reveals the underlined evidence for the selection of the approach and if the neurophysiological mechanisms are associated. This scoping review's methodology follows the Joanna Briggs Institue. A main search was conducted across Pubmed, PEdro and Web of science in December 2020, including only studies in Portuguese or English. Studies included focused on the concept of physiotherapy's intervention in a population of adult acute stroke patients, in an acute care context. Were identified 14 categories of interventions in 37 studies. 62% of studies didn't give any justification for the choic of method and the ones who did, weren't focused on neurophysiological knowledge. A wide range of interventions was found in which only 38% showed justifications that were considered insufficient and imprecise

Thalamic Stroke: An Opportunity to Study the Brain Mechanisms of Sleep–Wake and Cognition

The thalamus, and its projections to the cerebral cortex, are crucial for regulating sleep rhythms, such as sleep spindles, and for maintaining arousal and sleep homeostasis. Moreover, they play a significant role in memory, executive functioning, and attention. Altered thalamocortical circuitry caused by vascular lesions affects sleep&ndash;wake architecture and may contribute to cognitive deficits observed in thalamic stroke patients. This review summarizes the biology of the thalamus and current knowledge regarding the impact of thalamic circuitry on sleep regulation and cognition, drawing from clinical and pre-clinical studies. Furthermore, deep brain stimulation and transcranial magnetic stimulation are discussed as possible therapeutic approaches targeting thalamic circuits. Understanding the role of the thalamus in sleep and cognition opens new avenues for developing novel therapeutic strategies to improve sleep and cognitive functions in affected individuals