Metabolic syndrome (MetSyn) represents a clustering of different metabolic abnormalities. MetSyn prevalence is present in approximately 25% of all adults with increased prevalence in advanced ages. The presence of one component of MetSyn increases the risk of developing MetSyn later in life and likely represents a high lifetime burden of cardiovascular disease risk. Therefore we pooled data from multiple studies to establish the prevalence of MetSyn and MetSyn component prevalence across a broad range of ethnicities. PubMed, SCOPUS and Medline databases were searched to find papers presenting MetSyn and MetSyn component data for 18–30 year olds who were apparently healthy, free of disease, and MetSyn was assessed using either the harmonized, National Cholesterol Education Program Adult Treatment Panel III (NCEP-ATPIII), American Heart Association/National Heart, Blood and Lung Institute (AHA/NHBLI), or International Diabetes Federation (IDF) definitions of MetSyn. After reviewing returned articles, 26,609 participants' data from 34 studies were included in the analysis and the data were pooled. MetSyn was present in 4.8–7% of young adults. Atherogenic dyslipidaemia defined as low high density lipoprotein (HDL) cholesterol was the most prevalent MetSyn component (26.9–41.2%), followed by elevated blood pressure (16.6–26.6%), abdominal obesity (6.8–23.6%), atherogenic dyslipidaemia defined as raised triglycerides (8.6–15.6%), and raised fasting glucose (2.8–15.4%). These findings highlight that MetSyn is prevalent in young adults. Establishing the reason why low HDL is the most prevalent component may represent an important step in promoting primary prevention of MetSyn and reducing the incidence of subsequent clinical disease.

The recovery of coordinated motor function after stroke onset has been associated with the practice of upper limb movements that required the activation of homologous muscles. This pilot study investigated whether repetitive bimanual coordinated movements enhanced upper limb corticomotor (CM) excitability and motor function poststroke. Patients practiced driving their paretic wrist through passive rhythmical flexion-extension by active flexion-extension of their unaffected wrist using purpose-built manipulanda over a 4-week period. Both preintervention and postintervention motricity was assessed using the upper limb Fugl-Meyer rating scale, and cortical maps of wrist flexor and extensor representations were derived from potentials evoked by transcranial magnetic stimulation. Five of nine subjects improved upper limb motricity in response to this novel active-passive bimanual movement therapy (APBT). Unaffected cortical map volume decreased, especially for a subgroup of five patients who had a postintervention increase in motricity. No change in unaffected map volume was revealed for the four patients who did not improve their postintervention motricity. No consistent shifts in cortical map center of gravity were revealed. These findings suggest that APBT can initiate an improvement in motricity that is accompanied by a balancing of between-hemisphere CM excitability. The findings justify the assessment of the rehabilitative effects of APBT in a homogeneous sample of patients poststroke.

We set out to answer two questions with this study: 1. Can stroke patients improve voluntary control of their paretic ankle by practising a visuo-motor ankle-tracking task? 2. Are practice effects enhanced with non-invasive brain stimulation? A carefully selected sample of chronic stroke patients able to perform the experimental task attended three data collection sessions. Facilitatory transcranial direct current stimulation (tDCS) was applied in a random order over the lower limb primary motor cortex of the lesioned hemisphere or the non-lesioned hemisphere or sham stimulation was delivered over the lesioned hemisphere. In each session, tDCS was applied as patients practiced tracking a sinusoidal waveform for 15 min using dorsiflexion-plantarflexion movements of their paretic ankle. The difference in tracking error prior to, and after, the 15 min of practice was calculated. A practice effect was revealed following sham stimulation, and this effect was enhanced with tDCS applied over the lesioned hemisphere. The practice effect observed following sham stimulation was eliminated by tDCS applied over the non-lesioned hemisphere. The study provides the first evidence that non-invasive brain stimulation applied to the lesioned motor cortex of moderate- to well-recovered stroke patients enhances voluntary control of the paretic ankle. The results provide a basis for examining whether this enhanced ankle control can be induced in patients with greater impairments and whether enhanced control of a single or multiple lower limb joints improves hemiparetic gait patterns.

Implicit and explicit memory systems for motor skills compete with each other during and after motor practice. Primary motor cortex (M1) is known to be engaged during implicit motor learning, while dorsal premotor cortex (PMd) is critical for explicit learning. To elucidate the neural substrates underlying the interaction between implicit and explicit memory systems, adults underwent a randomized crossover experiment of anodal transcranial direct current stimulation (AtDCS) applied over M1, PMd or sham stimulation during implicit motor sequence (serial reaction time task, SRTT) practice. We hypothesized that M1-AtDCS during practice will enhance online performance and offline learning of the implicit motor sequence. In contrast, we also hypothesized that PMd-AtDCS will attenuate performance and retention of the implicit motor sequence. Implicit sequence performance was assessed at baseline, at the end of acquisition (EoA), and 24 h after practice (retention test, RET). M1-AtDCS during practice significantly improved practice performance and supported offline stabilization compared with Sham tDCS. Performance change from EoA to RET revealed that PMd-AtDCS during practice attenuated offline stabilization compared with M1-AtDCS and sham stimulation. The results support the role of M1 in implementing online performance gains and offline stabilization for implicit motor sequence learning. In contrast, enhancing the activity within explicit motor memory network nodes such as the PMd during practice may be detrimental to offline stabilization of the learned implicit motor sequence. These results support the notion of competition between implicit and explicit motor memory systems and identify underlying neural substrates that are engaged in this competition.

Magnetic stimulation of human primary motor cortex (M1) paired with electrical stimulation of a peripheral motor nerve has been used to produce a lasting modulation of corticomotor (CM) excitability. This 'paired associative stimulation' (PAS) protocol has been used to induce bidirectional changes in excitability in upper limb CM pathways. The present study tested the hypothesis that temporally dependent PAS applied to the common peroneal nerve during the swing phase of walking would induce bidirectional changes in CM excitability consistent with the Hebbian principle of activity-dependent plasticity. Fourteen subjects with no known neurological disorder participated in two data collection sessions each. PAS was delivered as a single block of 120 pairs of stimuli delivered in a 10 min period during treadmill walking at 4.0 km h −1 . Changes in CM excitability were assessed by examining the size of motor potentials evoked by transcranial magnetic stimulation prior to and following PAS. Tibialis anterior motor-evoked potentials amplitude increased to 121% over baseline when the magnetic stimulus was delivered over M1 after the estimated arrival time of the afferent volley in sensorimotor cortex and decreased to 83% of baseline when the magnetic stimulus was delivered prior to the estimated afferent volley arrival. This extent of modulation was undiminished following a further 10 min period of walking without stimulation. The temporal nature of the bidirectional effects following PAS, their rapid evolution and subsequent persistence supported the study's hypothesis and were similar to the effects described by others in quiescent muscles of the upper limb.

Balanced transcallosal inhibition sustains symmetrical corticomotor excitability and assists the performance of bimanual voluntary movements. After stroke, transcallosal inhibition becomes asymmetric. This finding raised the notion that reducing poststroke asymmetry in transcallosal inhibition might prime the motor system before training and lead to improvements in walking recovery. In this study, we examined three neuromodulatory protocols applied during walking to determine if they could increase ipsilesional and decrease contralesional motor excitability in patients with chronic stroke. Inhibitory repetitive transcranial magnetic stimulation and inhibitory paired associative stimulation were applied to the contralesional motor system, and facilitatory anodal transcranial direct current stimulation was applied to the ipsilesional motor system. We tested the bilateral modulatory effects of each stimulation protocol on the tibialis anterior, medial gastrocnemius, medial hamstrings, and vastus lateralis of nine patients with chronic stroke. All stimulation protocols increased paretic limb and decreased nonparetic limb motor excitability. There was no statistical difference in the extent of modulation between these stimulation protocols. This result suggests these three protocols are promising candidate priming mechanisms for testing the hypothesis in a future study that reducing the poststroke asymmetry of between-hemisphere motor excitability will enhance the effect of gait therapy.

Background-Because we are interested in non-invasive transcranial brain stimulation as an adjuvant to post-stroke walking therapy, we applied direct current stimulation (tDCS) preferentially to either the left or right lower limb motor cortex (M1) in two separate sessions and assessed the resulting modulation in both cortices.

What are the neuroplastic mechanisms that allow some stroke patients to regain high quality control of their paretic leg, while others do not? One theory implicates ipsilateral corticospinal pathways projecting from the non-lesioned hemisphere. We devised a new transcranial magnetic stimulation protocol to identify ipsilateral corticospinal tract conductivity from the non-lesioned hemisphere to the paretic limb in chronic stroke patients. We also assessed corticospinal tract degeneration using diffusion tensor imaging and used an ankle tracking task to assess lower limb motor control. We found greater tracking error during antiphase bilateral ankle movement for patients with strong conductivity from the non-lesioned hemisphere to paretic ankle than those with weak or no conductivity. These findings suggest that, instead of assisting motor control, contributions to lower limb motor control from the non-lesioned hemisphere of some stroke survivors may be maladaptive.