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The supplementary motor area (SMA) syndrome is a characteristic neurosurgical syndrome that can occur after unilateral resection of the SMA. Clinical symptoms may vary from none to a global akinesia, predominantly on the contralateral side, with preserved muscle strength and mutism. A remarkable feature is that these symptoms completely resolve within weeks to months, leaving only a disturbance in alternating bimanual movements. In this review we give an overview of the old and new insights from the SMA syndrome and extrapolate these findings to seemingly unrelated diseases and symptoms such as Parkinson's disease (PD) and tics. Furthermore, we integrate findings from lesion, stimulation and functional imaging studies to provide insight in the motor function of the SMA.

Background The pre‐supplementary motor area (preSMA) is a critical region within domain‐general networks involved in speech production. However, the impact of post‐stroke aphasia (PSA) on functional reorganization in this area remains unclear. Objective This study aimed to investigate alterations in functional connectivity (FC) of the preSMA in patients with PSA and their relationships with neurotransmitters and speech production recovery. Methods We conducted language assessments using the Western Aphasia Battery (WAB) on 31 patients with left hemisphere strokes at approximately 28 days and 3 months post‐stroke. Functional magnetic resonance imaging (fMRI) was performed on all PSA patients and 22 normal controls (NCs) at baseline. We compared the FC of the bilateral preSMA between the two groups. Results Compared to NCs, PSA patients exhibited decreased FC between the ipsilesional preSMA and the prefrontal‐cingulate cortex, insula, and caudate, as well as between the contralesional preSMA and the prefrontal cortex and caudate. These FC changes were significantly associated with various neurotransmitters, particularly metabotropic glutamate, kappa opioid receptor, and cannabinoid receptor. Moreover, FC between the preSMA and the prefrontal‐cingulate cortex showed negative correlation trends with changes in WAB‐AQ and WAB subtests (naming, auditory comprehension, and repetition) at the three‐month assessment. These findings were partially validated in an independent dataset (patients: N = 17; controls: N = 22). Conclusion Our results suggest that functional connections of the preSMA are disrupted in PSA patients, which may be associated with neurotransmitter activity. Our findings suggest that functional connections of the preSMA are disrupted in PSA patients, which may be associated with neurotransmitter activity, possibly serving as the predictive markers for recovery of PSA.

Motor inhibitory control implemented as response inhibition is an essential cognitive function required to dynamically adapt to rapidly changing environments. Despite over a decade of research on the neural mechanisms of response inhibition, it remains unclear, how exactly response inhibition is initiated and implemented. Using a multimodal MEG/fMRI approach in 59 subjects, our results reliably reveal that response inhibition is initiated by the right inferior frontal gyrus (rIFG) as a form of attention-independent top-down control that involves the modulation of beta-band activity. Furthermore, stopping performance was predicted by beta-band power, and beta-band connectivity was directed from rIFG to pre-supplementary motor area (pre-SMA), indicating rIFG’s dominance over pre-SMA. Thus, these results strongly support the hypothesis that rIFG initiates stopping, implemented by beta-band oscillations with potential to open up new ways of spatially localized oscillation-based interventions.

The dorsal mesial frontal cortex contains the supplementary motor area (SMA) and the pre-supplementary motor area (pre-SMA), which play an important role in action and cognition. Evidence from cytoarchitectonic, stimulation, and functional studies suggests structural and functional divergence between the two subregions. However, a microstructural map of these areas obtained in a representative sample of brains in a stereotaxic reference space is still lacking. In the present study we show that the dorsal mesial frontal motor cortex comprises two microstructurally different brain regions: area SMA and area pre-SMA. Area-specific cytoarchitectonic patterns were studied in serial histological sections stained for cell bodies of ten human postmortem brains. Borders of the two cortical areas were identified using image analysis and statistical features. The 3D reconstructed areas were transferred to a common reference space, and probabilistic maps were calculated by superimposing the individual maps. A coordinate-based meta-analysis of functional imaging data was subsequently performed using the two probabilistic maps as microstructurally defined seed regions. It revealed that areas SMA and pre-SMA were strongly co-activated with areas in precentral, supramarginal and superior frontal gyri, Rolandic operculum, thalamus, putamen and cerebellum. Both areas were related to motor functions, but area pre-SMA was involved in more complex processes such as learning, cognitive processes and perception. The here described subsequent analyses led to converging evidence supporting the microstructural, and functional segregation of areas SMA and pre-SMA, and maps will be made available to the scientific community to further elucidate the microstructural substrates of motor and cognitive control.

This book offers a fundamental new theory of motor cortex organization: the rendering of the movement repertoire onto the cortex. The action repertoire of an animal is highly dimensional, whereas the cortical sheet is two-dimensional. Rendering the action space onto the cortex therefore results in a complex pattern, explaining the otherwise inexplicable details of motor cortex organization. This book includes a complete history of motor cortex research from its discovery to the present, a discussion of the major issues in motor cortex research, and an account of recent experiments that led to the book's “action map” view. Though focused on motor cortex, the book includes a range of topics from an explanation of how primates put food in their mouths, to the origins of social behavior such as smiling and laughing, to the mysterious link between movement disorders and autism.

Error monitoring is a critical cognitive function that enables the detection of deviations from intended goals and the initiation of corrective actions. Two influential theoretical frameworks propose distinct mechanisms underlying this process: conflict detection and reinforcement learning. The conflict detection account emphasizes the recognition of incompatible response tendencies, while reinforcement learning models focus on predicting error likelihood and updating expectations based on outcomes. Disentangling the contributions of these mechanisms remains challenging, as errors frequently involve both heightened response conflict and unexpected results. The present study aimed to differentiate these mechanisms using functional magnetic resonance imaging (fMRI) in the stop-signal task. Forty-four participants completed the task, during which response conflict intensity (reflected in stop-signal delay, SSD) and error expectancy (indexed by stop-response interval, SRI) were assessed. fMRI data were analyzed to investigate how these measures relate to neural activity associated with error processing. The results revealed that both SSD and SRI influenced post-error slowing. However, only SSD—reflecting response conflict—was significantly associated with error-related brain activity, particularly in the pre-supplementary motor area and superior frontal gyrus. These findings support the conflict detection theory, emphasizing the central role of response conflict in the neural mechanisms underlying inhibitory control failures.

Tourette syndrome (TS) is a neurodevelopmental condition characterised by tics, which are stereotyped movements and/or vocalisations. Tics often cause difficulties in daily life and many with TS express a desire to reduce and/or gain control over them. No singular effective treatment exists for TS, and while pharmacological and behavioural interventions can be effective, the results are variable, and issues relating to access, availability and side effects can be barriers to treatment. Consequently, over the past decade, there has been increasing interest into the potential benefits of non-invasive brain stimulation (NIBS) approaches. This systematic review highlights work exploring NIBS as a potential treatment for TS. On balance, the results tentatively suggest that multiple sessions of stimulation applied over the supplementary motor area (SMA) may help to reduce tics. However, a number of methodological and theoretical issues limit the strength of this conclusion, with the most problematic being the lack of large-scale sham-controlled studies. In this review, methodological and theoretical issues are discussed, unanswered questions highlighted and suggestions for future work put forward.

Supplementary motor area (SMA) syndrome is a surgery‐related complication that commonly occurs after removing SMA glioma, and needs weeks to recover. However, susceptible factors of patients suffering from SMA syndrome remain unknown. Graphic theory was applied to reveal topological properties of sensorimotor network (SMN) by processing resting‐state functional magnetic resonance images in 66 patients with SMA gliomas. Patients were classified into SMA and non‐SMA groups based on whether they suffered from SMA syndrome. We collected recovery time and used causal mediation analysis to find association between topological properties and recovery time. Compared with the non‐SMA group, higher vulnerability (left: p = .0018; right: p = .0033) and lower fault tolerance (left: p = .0022; right: p = .0248) of the whole SMN were found in the SMA group. Moreover, higher nodal properties of lesional‐hemispheric cingulate cortex (nodal efficiency: left, p = .0389; right, p = .0169; nodal vulnerability: left, p = .0185; right, p = .0085) and upper limb region of primary motor cortex (PMC; nodal efficiency: left, p = .0132; right, p = .0001; nodal vulnerability: left, p = .0091; right, p = .0209) were found in the SMA group. Nodal efficiency and nodal vulnerability of cingulate cortex and upper limb region of PMC were important predictors for SMA syndrome occurring and recovery time prolonging. Neurosurgeons should carefully deal with upper limb region of PMC and cingulate cortex, and protect them if these two region were unnecessary to damage during SMA glioma resection.

Few studies have investigated the effects of repeated sessions of transcranial direct current stimulation (tDCS) combined with concurrent cognitive training on improving response inhibition, and the findings have been heterogeneous in the limited research. This study investigated the long-lasting and transfer effects of 10 consecutive sessions of multitarget anodal HD-tDCS combined with concurrent cognitive training on improving response inhibition compared with multitarget stimulation or training alone. Ninety-four healthy university students aged 18-25 were randomly assigned to undergo different interventions, including real stimulation combined with stop-signal task (SST) training, real stimulation, sham stimulation combined with SST training, and sham stimulation. Each intervention lasted 20 min daily for 10 consecutive days, and the stimulation protocol targeted right inferior frontal gyrus (rIFG) and pre-supplementary motor area (pre-SMA) simultaneously with a total current intensity of 2.5 mA. Performance on SST and possible transfer effects to Stroop task, attention network test, and N-back task were measured before and 1 day and 1 month after completing the intervention course. The main findings showed that the combined protocol and the stimulation alone significantly reduced stop-signal reaction time (SSRT) in the post-intervention and follow-up tests compared to the pre-intervention test. However, training alone only decreased SSRT in the post-test. The sham control exhibited no changes. Subgroup analysis revealed that the combined protocol and the stimulation alone induced a decrease in the SSRT of the low-performance subgroup at the post-test and follow-up test compared with the pre-test. However, only the combined protocol, but not the stimulation alone, improved the SSRT of the high-performance subgroup. The transfer effects were absent. This study provides supportive evidence for the synergistic effect of the combined protocol, indicating its superiority over the single intervention method. In addition, the long-term after-effects can persist for up to at least 1 month. Our findings also provide insights into the clinical application and strategy for treating response inhibition deficits.

Tics are unique from most movement disorders, in that they are partially suppressible. As part of the inhibitory motor network, the pre-supplementary motor area is engaged in motor control and may be involved in tic physiology. We used dual-site transcranial magnetic stimulation to assess inhibitory connectivity between right pre-supplementary motor area and left primary motor cortex, which has previously been demonstrated in healthy adults. We also used diffusion tensor imaging to investigate white matter connectivity in children with chronic tics. Twelve children with chronic tic disorder and fourteen typically developing controls underwent MRI with diffusion tensor imaging indices analysis followed by single and paired-pulse transcranial magnetic stimulation with conditioning pulse over the right pre-supplementary motor area followed by left motor cortex test pulse. Neurophysiologic and imaging data relationships to measures of tic severity and suppressibility were also evaluated in tic patients. Pre-supplementary motor area-mediated inhibition of left motor cortex was present in healthy control children but not in chronic tic disorder participants. Less inhibition correlated with worse tic suppressibility (ρ = − 0.73, p = 0.047). Imaging analysis showed increased fractional anisotropy in the right superior longitudinal fasciculus, corpus callosum, corona radiata and posterior limb of the internal capsule (p < 0.05) in tic participants, which correlated with lower self-reported tic suppressibility (ρ = − 0.70, p = 0.05). Physiologic data revealed impaired frontal-mediated motor cortex inhibition in chronic tic participants, and imaging analysis showed abnormalities in motor pathways. Collectively, the neurophysiologic and neuroanatomic data correlate with tic suppressibility, supporting the relevancy to tic pathophysiology.