Idiopathic young-onset Fahr's disease with schizophrenia-like presentation: a case report.

This case report describes an exceptionally rare case in which a prior diagnosis of schizophrenia was later determined to be early-onset Fahr's disease, linked to a genetic mutation in the SLC20A2 gene. Initially, the patient exhibited symptoms resembling schizophrenia, including aggression and hostility, and was highly susceptible to medication side effects such as restlessness and Parkinsonism. Despite maintaining independent activities of daily living, his neurological examinations revealed hidden weakness on the left side. Following adjustments to the medication regimen, stability was achieved with residual psychotic symptoms under treatment with Risperidone 1.5mg/day, Valproic acid 1500mg/day, and Quetiapine 37.5mg/day. This case underscores the importance of conducting comprehensive imaging studies at the time of initial psychiatric diagnosis, regardless of the apparent typicality of the presentation. Additionally, it emphasizes the need for patience and adherence to the "Start Low and Go Slow" approach in medication management to minimize the risk of exacerbating psychiatric symptoms and aggression.

Vessel Wall Imaging in Angiogram-Negative Diffuse Subarachnoid Hemorrhage Reveals a Ruptured Lenticulostriate Aneurysm.

A patient presented with acute onset headache and subsequent unconsciousness. The neurologic exam showed left-sided myoclonic jerking and right flaccid hemiparalysis. Noncontrast computed tomography revealed diffuse subarachnoid hemorrhage (SAH) with acute hydrocephalus. Initial digital subtraction angiography (DSA) showed no culprit source for SAH. Repeat DSA on day 7 after initial presentation raised suspicion for left internal carotid artery ophthalmic segment and left lateral lenticulostriate artery (LSA) aneurysms. A magnetic resonance vessel wall imaging (VWI) exam was performed given the presence of multiple potential culprit aneurysms. Vessel wall enhancement around the dome of the left LSA aneurysm suggested rupture, which then facilitated treatment with surgical clipping. LSA aneurysms are exceedingly rare and challenging to treat. Given the associated high degree of morbidity, expedient diagnosis is critical to direct management. VWI could be a valuable tool for detecting ruptured aneurysms in the setting of angiogram-negative SAH.

Transcranial sonography of subcortical structures in tic/tourette disorder.

Functional neuroimaging studies demonstrate disinhibition of the cortico-striatal-thalamo-cortical circuit. However, structural imaging studies revealed conflicting results, some suggesting smaller volumes of the caudate nucleus (CN) in children with Gilles de la Tourette syndrome (TS). Here we wanted to find out whether transcranial sonography (TCS) detects alterations of raphe nuclei, substantia nigra, lenticular nucleus (LN), or CN in children with Tic disorder or TS (TIC/TS).The study included 25 treatment-naive children (age: 12.2 ± 2.5 years) with a DSM-V based diagnosis of Tic disorder or TS (10 subjects), without other psychiatric or neurologic diagnosis, and 25 healthy controls (age: 12.17 ± 2.57 years), matched for age and sex. Parental rating of behavioral, emotional abnormalities, somatic complaints and social competencies of the participants were assessed using the Child Behavior Check List (CBCL/4-18R). TCS of deep brain structures was conducted through the preauricular acoustic bone windows using a 2.5-MHz phased-array ultrasound system. Fisher's exact test and Mann-Whitney-U test were used for comparisons between TIC/TS patients and healthy volunteers. The number of participants with hyperechogenic area of left CN in the TIC/TS sample was increased, compared to the healthy control group. TIC/TS patients with hyperechogenic CN showed an increased occurrence of thought- and obsessive-compulsive problems. This TCS study revealed pathologic structural changes in CN, its higher occurrence in TIC/TS compared to healthy controls and the relation to comorbidity of thought problems. Further research should focus on the molecular cause of these alterations, probably the disturbed iron metabolism.

Globus pallidus is not independent from striatal direct pathway neurons: an up-to-date review.

Striatal projection neurons, which are classified into two groups-direct and indirect pathway neurons, play a pivotal role in our understanding of the brain's functionality. Conventional models propose that these two pathways operate independently and have contrasting functions, akin to an "accelerator" and "brake" in a vehicle. This analogy further elucidates how the depletion of dopamine neurons in Parkinson's disease can result in bradykinesia. However, the question arises: are these direct and indirect pathways truly autonomous? Despite being distinct types of neurons, their interdependence cannot be overlooked. Single-neuron tracing studies employing membrane-targeting signals have shown that the majority of direct pathway neurons terminate not only in the output nuclei, but also in the external segment of the globus pallidus (GP in rodents), a relay nucleus of the indirect pathway. Recent studies have unveiled the existence of arkypallidal neurons, which project solely to the striatum, in addition to prototypic neurons. This raises the question of which type of GP neurons receive these striatal axon collaterals. Our morphological and electrophysiological experiments showed that the striatal direct pathway neurons may affect prototypic neurons via the action of substance P on neurokinin-1 receptors. Conversely, another research group has reported that direct pathway neurons inhibit arkypallidal neurons via GABA. Regardless of the neurotransmitter involved, it can be concluded that the GP is not entirely independent of direct pathway neurons. This review article underscores the intricate interplay between different neuronal pathways and challenges the traditional understanding of their independence.

Idiopathic basal ganglia calcification presenting with obsessive-compulsive symptoms: A case report.

Background: Idiopathic basal ganglia calcification (IBGC), also known as Farh's disease, is a rare neurodegenerative disorder characterized by calcification of the basal ganglia and other brain regions. This disease usually occurs in middle-aged patients and presents with various neurological and psychiatric symptoms. The exact prevalence is unknown; however, population genomic data analysis suggests a prevalence of at least 4.5/10,000 to 3.3/1000, indicating that the disease is more common than previously thought and remains underdiagnosed. Case Presentation: We report the case of a middle-aged Japanese man who attempted suicide twice because of obsessive-compulsive ideation caused by trivial triggers. The patient's psychiatric symptoms resolved relatively quickly after hospitalization, and imaging and genetic testing led to a diagnosis of IBGC. Conclusion: This case report illustrates the importance of including IBGC in the differential diagnosis of psychiatric symptoms that initially develop in middle-aged patients.

Opioid Overdose-Induced Diffusion Restriction in the Bilateral Basal Ganglia Revealed on Brain Imaging.

Opioid misuse and addiction have led to an opioid epidemic in the United States, with widespread effects on the healthcare system. Opioid-induced cardiovascular morbidity and mortality effects have been extensively described in past literature; however, neurological effects have been described less frequently.  Here, we describe a case of a female patient who presented to our center after being found unresponsive with magnetic resonance imaging (MRI), revealing bilateral basal ganglia diffuse restriction hyperintensities secondary to a diagnosis of opioid overdose.  Opioid overdose-induced bilateral basal ganglia diffusion restriction has only been described infrequently in the literature. Recognizing the associated imaging findings as a potential consequence of opioid overdose is important to avoid unnecessary workups for ischemic stroke.

Subthalamic control of impulsive actions: insights from deep brain stimulation in Parkinson's disease.

Control of actions allows adaptive, goal-directed behaviour. The basal ganglia, including the subthalamic nucleus, are thought to play a central role in dynamically controlling actions through recurrent negative feedback loops with the cerebral cortex. Here, we summarize recent translational studies that used deep brain stimulation to record neural activity from and apply electrical stimulation to the subthalamic nucleus in people with Parkinson's disease. These studies have elucidated spatial, spectral and temporal features of the neural mechanisms underlying the controlled delay of actions in cortico-subthalamic networks and demonstrated their causal effects on behaviour in distinct processing windows. While these mechanisms have been conceptualized as control signals for suppressing impulsive response tendencies in conflict tasks and as decision threshold adjustments in value-based and perceptual decisions, we propose a common framework linking decision-making, cognition and movement. Within this framework subthalamic deep brain stimulation can lead to suboptimal choices by reducing the time that patients take for deliberation before committing to an action. However, clinical studies have consistently shown that the occurrence of impulse control disorders is reduced, not increased, after subthalamic deep brain stimulation surgery. This apparent contradiction can be reconciled when recognizing the multifaceted nature of impulsivity, its underlying mechanisms and modulation by treatment. While subthalamic deep brain stimulation renders patients susceptible to making decisions without proper forethought, this can be disentangled from effects related to dopamine comprising sensitivity to benefits vs. costs, reward delay aversion and learning from outcomes. Alterations in these dopamine-mediated mechanisms are thought to underlie the development of impulse control disorders, and can be relatively spared with reduced dopaminergic medication after subthalamic deep brain stimulation. Together, results from studies using deep brain stimulation as an experimental tool have improved our understanding of action control in the human brain and have important implications for treatment of patients with Neurological disorders.

Representation of rhythmic chunking in striatum of mice executing complex continuous movement sequences.

We used a step-wheel system to examine the activity of striatal projection neurons as mice practiced stepping on complexly arranged foothold pegs in this Ferris-wheel-like device to receive reward. Sets of dorsolateral striatal projection neurons were sensitive to specific parameters of repetitive motor coordination during the runs. They responded to combinations of the parameters of continuous movements (interval, phase, and repetition), forming "chunking responses"-some for combinations of these parameters across multiple body parts. Recordings in sensorimotor cortical areas exhibited notably fewer such responses but were documented for smaller neuron sets whose heterogeneity was significant. Striatal movement encoding via chunking responsivity could provide insight into neural strategies governing effective motor control by the striatum. It is possible that the striking need for external rhythmic cuing to allow movement sequences by Parkinson's patients could, at least in part, reflect dysfunction in such striatal coding.

Clinical characteristics of post-stroke basal ganglia aphasia and the study of language-related white matter tracts based on diffusion spectrum imaging.

BACKGROUND: Stroke often damages the basal ganglia, leading to atypical and transient aphasia, indicating that post-stroke basal ganglia aphasia (PSBGA) may be related to different anatomical structural damage and functional remodeling rehabilitation mechanisms. The basal ganglia contain dense white matter tracts (WMTs). Hence, damage to the functional tract may be an essential anatomical structural basis for the development of PSBGA. METHODS: We first analyzed the clinical characteristics of PSBGA in 28 patients and 15 healthy controls (HCs) using the Western Aphasia Battery and neuropsychological test batteries. Moreover, we investigated white matter injury during the acute stage using diffusion magnetic resonance imaging scans for differential tractography. Finally, we used multiple regression models in correlation tractography to analyze the relationship between various language functions and quantitative anisotropy (QA) of WMTs. RESULTS: Compared with HCs, patients with PSBGA showed lower scores for fluency, comprehension (auditory word recognition and sequential commands), naming (object naming and word fluency), reading comprehension of sentences, Mini-Mental State Examination, and Montreal Cognitive Assessment, along with increased scores in Hamilton Anxiety Scale-17 and Hamilton Depression Scale-17 within 7 days after stroke onset (P < 0.05). Differential tractography revealed that patients with PSBGA had damaged fibers, including in the body fibers of the corpus callosum, left cingulum bundles, left parietal aslant tracts, bilateral superior longitudinal fasciculus II, bilateral thalamic radiation tracts, left fornix, corpus callosum tapetum, and forceps major, compared with HCs (FDR < 0.02). Correlation tractography highlighted that better comprehension was correlated with a higher QA of the left inferior fronto-occipital fasciculus (IFOF), corpus callosum forceps minor, and left extreme capsule (FDR < 0.0083). Naming was positively associated with the QA of the left IFOF, forceps minor, left arcuate fasciculus, and uncinate fasciculus (UF) (FDR < 0.0083). Word fluency of naming was also positively associated with the QA of the forceps minor, left IFOF, and thalamic radiation tracts (FDR < 0.0083). Furthermore, reading was positively correlated with the QA of the forceps minor, left IFOF, and UF (FDR < 0.0083). CONCLUSION: PSBGA is primarily characterized by significantly impaired word fluency of naming and preserved repetition abilities, as well as emotional and cognitive dysfunction. Damaged limbic pathways, dorsally located tracts in the left hemisphere, and left basal ganglia pathways are involved in PSBGA pathogenesis. The results of connectometry analysis further refine the current functional localization model of higher-order neural networks associated with language functions.

Intracranial calcifications associated with factors related and unrelated to atherosclerosis in older people: A community dwelling cohort study.

The cause of intracranial calcification is not fully understood. The aim of the current study was to identify factors associated with intracranial calcification and to determine whether these factors differ in calcification of different sites. A total of 404 community-dwelling people aged 65 or older were included in the study. All subjects underwent brain computed tomography (CT), blood tests, and a Mini-Mental State Examination (MMSE). Intracranial calcifications were scored using CT. Stepwise regression analysis was performed to examine factors associated with intracranial calcification, with each calcification score used as a dependent variable. Independent variables included age, gender, hemoglobin A1c (HbA1c), dyslipidemia, estimated glomerular filtration rate (eGFR), blood pressure, body mass index (BMI), smoking, serum iron, ferritin, and intact parathyroid hormone (PTH). Stepwise regression analysis detected male gender as a predictor of pineal gland calcification and intact PTH as a predictor of basal ganglia calcification. Age and lifestyle diseases were identified as predictors of calcification of the falx cerebri, internal carotid arteries, and vertebral arteries. These results indicate that the mechanisms of calcifications of the pineal gland and basal ganglia might differ from that of artery calcification, and that causes of intracranial calcification might be classified using factors that are and are not related to atherosclerosis.

Investigation of the mechanism of action of deep brain stimulation for the treatment of Parkinson's disease.

Parkinson's disease (PD) is a severe, progressive, neurological disorder. PD is not a single disease, but rather resembles a syndrome. PD includes two types of pathogenesis (i.e., classical PD and new PD). Clinically, PD patients present with a range of motor symptoms including decreased spontaneous movement, bradykinesia, muscle rigidity, changes in speech, and resting tremors. PD patients also often exhibit non-motor symptoms such as fatigue, sleep disorders, and emotional and mental health disturbances. Deep brain stimulation (DBS) performed in clinical neurosurgery has demonstrated considerable efficacy in the treatment of dyskinesia that occurs in PD patients. However, the specific neural mechanism of DBS remains unknown and is limited by several shortcomings that have hampered the popularization and development of the procedure. To address this issue, this study established a theoretical model of DBS for PD to investigate and understand the mechanism of DBS using several artificial intelligence (AI) algorithms. This model was used to investigate both classical PD and unheard-of new PD. The research described in this paper was as follows: a single neuron was used to establish a theoretical model of the basal ganglia circuit and to simulate the characteristic indicators of the potential release of the basal ganglia circuit in both normal and PD states. The state of the deep brain electrical stimulation in PD was then analyzed to identify the critical electrical stimulation index and the optimal target. We showed that the use of AI algorithms such as particle swarm optimization and other AI algorithms was beneficial for more detailed exploration and understanding of the mechanisms of DBS compared to those used in previous studies. This discovery may lead to advances in DBS technology and provide better treatment options for neurological diseases such as PD.

Neurochemistry and circuit organization of the lateral spiriform nucleus of birds: A uniquely nonmammalian direct pathway component of the basal ganglia.

We used diverse methods to characterize the role of avian lateral spiriform nucleus (SpL) in basal ganglia motor function. Connectivity analysis showed that SpL receives input from globus pallidus (GP), and the intrapeduncular nucleus (INP) located ventromedial to GP, whose neurons express numerous striatal markers. SpL-projecting GP neurons were large and aspiny, while SpL-projecting INP neurons were medium sized and spiny. Connectivity analysis further showed that SpL receives inputs from subthalamic nucleus (STN) and substantia nigra pars reticulata (SNr), and that the SNr also receives inputs from GP, INP, and STN. Neurochemical analysis showed that SpL neurons express ENK, GAD, and a variety of pallidal neuron markers, and receive GABAergic terminals, some of which also contain DARPP32, consistent with GP pallidal and INP striatal inputs. Connectivity and neurochemical analysis showed that the SpL input to tectum prominently ends on GABAA receptor-enriched tectobulbar neurons. Behavioral studies showed that lesions of SpL impair visuomotor behaviors involving tracking and pecking moving targets. Our results suggest that SpL modulates brainstem-projecting tectobulbar neurons in a manner comparable to the demonstrated influence of GP internus on motor thalamus and of SNr on tectobulbar neurons in mammals. Given published data in amphibians and reptiles, it seems likely the SpL circuit represents a major direct pathway-type circuit by which the basal ganglia exerts its motor influence in nonmammalian tetrapods. The present studies also show that avian striatum is divided into three spatially segregated territories with differing connectivity, a medial striato-nigral territory, a dorsolateral striato-GP territory, and the ventrolateral INP motor territory.

Focal Seizures in a Patient With Chronic Basal Ganglia Calcifications Secondary to Idiopathic Primary Hypoparathyroidism.

Patients with hypoparathyroidism can present with concurrent basal ganglia calcifications (BGCs). The exact pathogenesis is unknown, although it is thought to relate to calcium-phosphate deposition from chronic hypocalcemia and hyperphosphatemia. We present the case of a 65-year-old man with known idiopathic primary hypoparathyroidism and concurrent extensive BGC. Thirty years after diagnosis, he presented with focal seizures despite a decade of stable intracranial calcifications on imaging. Serum calcium, phosphate, 25-hydroxyvitamin D, and parathyroid hormone levels were well controlled during this period. He was commenced on lifelong levetiracetam with subsequent seizure remission. Given the scarcity of literature surrounding focal seizures and BGC, it is essential to raise awareness in this area.

Wilson's Disease in an Early Adolescent: Classic Magnetic Resonance Imaging Findings.

Wilson's disease (WD), alternatively termed hepatolenticular degeneration, represents a rare autosomal recessive disorder typified by disrupted copper metabolism, culminating in copper accumulation across various organs. WD commonly manifests with early-onset liver cirrhosis, with notable involvement of the central nervous system, particularly impacting the midbrain and basal ganglia. This case report delineates the clinical presentation of an early adolescent female with WD, accentuating classical magnetic resonance imaging (MRI) findings. These MRI findings, which include the "face of a giant panda sign" and the "Face of a miniature panda sign," are pivotal for expeditious diagnosis. Recognition of these classical signs underscores the indispensable role of MRI in elucidating the neurological dimensions of WD.

Linking Striatal Dopaminergic Asymmetry with Personality Traits: Insights from Gambling Disorder.

The role of dopamine in the pathophysiology of gambling disorder (GD) remains incompletely understood, with disparate research findings concerning presynaptic and postsynaptic structures and dopaminergic synthesis. The aim of this study was to investigate potential correlations between striatal dopamine transporter (DAT) lateralization and asymmetry index, as assessed by 123I-FP-CIT SPECT, and temperamental traits, as measured by Cloninger's Temperament and Character Inventory (TCI), in GD subjects. Significant associations were found between DAT binding asymmetries in the caudate and putamen and the temperamental dimensions of harm avoidance and novelty seeking. Specifically, high novelty seeking scores correlated with increased DAT binding in the left caudate relative to the right, whereas higher harm avoidance scores corresponded to increased DAT binding in the right putamen relative to the left. These observations potentially imply that the asymmetry in DAT expression in the basal ganglia could be an outcome of hemispheric asymmetry in emotional processing and behavioural guidance. In summary, our study provides evidence supporting the relationship between DAT asymmetries, temperamental dimensions and GD. Future investigations could be directed towards examining postsynaptic receptors to gain a more comprehensive understanding of dopamine's influence within the basal ganglia circuit in disordered gambling. If confirmed in larger cohorts, these findings could have substantial implications for the tailoring of individualized neuromodulation therapies in the treatment of behavioural addictions.

Aperiodic components of local field potentials reflect inherent differences between cortical and subcortical activity.

Information flow in brain networks is reflected in local field potentials that have both periodic and aperiodic components. The 1/fχ aperiodic component of the power spectra tracks arousal and correlates with other physiological and pathophysiological states. Here we explored the aperiodic activity in the human thalamus and basal ganglia in relation to simultaneously recorded cortical activity. We elaborated on the parameterization of the aperiodic component implemented by specparam (formerly known as FOOOF) to avoid parameter unidentifiability and to obtain independent and more easily interpretable parameters. This allowed us to seamlessly fit spectra with and without an aperiodic knee, a parameter that captures a change in the slope of the aperiodic component. We found that the cortical aperiodic exponent χ, which reflects the decay of the aperiodic component with frequency, is correlated with Parkinson's disease symptom severity. Interestingly, no aperiodic knee was detected from the thalamus, the pallidum, or the subthalamic nucleus, which exhibited an aperiodic exponent significantly lower than in cortex. These differences were replicated in epilepsy patients undergoing intracranial monitoring that included thalamic recordings. The consistently lower aperiodic exponent and lack of an aperiodic knee from all subcortical recordings may reflect cytoarchitectonic and/or functional differences. SIGNIFICANCE STATEMENT: The aperiodic component of local field potentials can be modeled to produce useful and reproducible indices of neural activity. Here we refined a widely used phenomenological model for extracting aperiodic parameters (namely the exponent, offset and knee), with which we fit cortical, basal ganglia, and thalamic intracranial local field potentials, recorded from unique cohorts of movement disorders and epilepsy patients. We found that the aperiodic exponent in motor cortex is higher in Parkinson's disease patients with more severe motor symptoms, suggesting that aperiodic features may have potential as electrophysiological biomarkers for movement disorders symptoms. Remarkably, we found conspicuous differences in the aperiodic parameters of basal ganglia and thalamic signals compared to those from neocortex.

Rethinking dopamine-guided action sequence learning.

As opposed to those requiring a single action for reward acquisition, tasks necessitating action sequences demand that animals learn action elements and their sequential order and sustain the behaviour until the sequence is completed. With repeated learning, animals not only exhibit precise execution of these sequences but also demonstrate enhanced smoothness and efficiency. Previous research has demonstrated that midbrain dopamine and its major projection target, the striatum, play crucial roles in these processes. Recent studies have shown that dopamine from the substantia nigra pars compacta (SNc) and the ventral tegmental area (VTA) serve distinct functions in action sequence learning. The distinct contributions of dopamine also depend on the striatal subregions, namely the ventral, dorsomedial and dorsolateral striatum. Here, we have reviewed recent findings on the role of striatal dopamine in action sequence learning, with a focus on recent rodent studies.

Efficacy of high thiamine dosage in treating patients with biotin thiamine responsive basal ganglia disease: a two case reports.

BACKGROUND: Biotin-thiamine-responsive basal ganglia disease (BTBGD) is a rare, autosomal recessive neurometabolic disorder caused by mutations in the SLC19A3 gene and characterized by recurrent sub-acute episodes of encephalopathy. Patients with BTBGD have classical neuroimaging findings and a dramatic response to high doses of thiamine. OBJECTIVE: To highlight the advantages of administering a higher dose of thiamine for patients with BTBGD who have not shown improvement with the standard recommended dosage. RESULTS: Herein, we report on two Saudi girls with classical clinical and radiological findings of BTBGD. Hallmark symptoms in these patients included an acute onset of ataxia, tremor, slurred speech, dystonia, and dysphagia. The initial routine laboratory workups were unremarkable. Brain magnetic resonance imaging revealed extensive hyperintense signals in the bilateral basal ganglia, which suggested the diagnosis of a BTBGD. Hence started empirically on biotin 10 mg/kg/day and thiamine 40 mg/kg/day, but there was no noticeable improvement. After increasing the thiamine to 75 mg/kg/day the patients started to improve significantly. Genetic testing was requested and came positive for the mutation of the SLC19A3 gene. After two months of initiating the management, thiamine was reduced to 30 mg/kg/day. Subsequent follow-ups showed complete improvement in their condition with no apparent long-term sequel or relapse. CONCLUSION: we conclude that administration of thiamine at a dosage of up to 40 mg/kg/day may not be sufficient in treating certain patients with BTBGD. Thus, considering a significantly higher dosage could potentially contribute to achieving remission.

GNN-based structural information to improve DNN-based basal ganglia segmentation in children following early brain lesion.

Analyzing the basal ganglia following an early brain lesion is crucial due to their noteworthy role in sensory-motor functions. However, the segmentation of these subcortical structures on MRI is challenging in children and is further complicated by the presence of a lesion. Although current deep neural networks (DNN) perform well in segmenting subcortical brain structures in healthy brains, they lack robustness when faced with lesion variability, leading to structural inconsistencies. Given the established spatial organization of the basal ganglia, we propose enhancing the DNN-based segmentation through post-processing with a graph neural network (GNN). The GNN conducts node classification on graphs encoding both class probabilities and spatial information regarding the regions segmented by the DNN. In this study, we focus on neonatal arterial ischemic stroke (NAIS) in children. The approach is evaluated on both healthy children and children after NAIS using three DNN backbones: U-Net, UNETr, and MSGSE-Net. The results show an improvement in segmentation performance, with an increase in the median Dice score by up to 4% and a reduction in the median Hausdorff distance (HD) by up to 93% for healthy children (from 36.45 to 2.57) and up to 91% for children suffering from NAIS (from 40.64 to 3.50). The performance of the method is compared with atlas-based methods. Severe cases of neonatal stroke result in a decline in performance in the injured hemisphere, without negatively affecting the segmentation of the contra-injured hemisphere. Furthermore, the approach demonstrates resilience to small training datasets, a widespread challenge in the medical field, particularly in pediatrics and for rare pathologies.

Premotor cortical beta synchronization and the network neuromodulation of externally paced finger tapping in Parkinson's disease.

Parkinson's disease (PD) is characterized by the disruption of repetitive, concurrent and sequential motor actions due to compromised timing-functions principally located in cortex-basal ganglia (BG) circuits. Increasing evidence suggests that motor impairments in untreated PD patients are linked to an excessive synchronization of cortex-BG activity at beta frequencies (13-30 Hz). Levodopa and subthalamic nucleus deep brain stimulation (STN-DBS) suppress pathological beta-band reverberation and improve the motor symptoms in PD. Yet a dynamic tuning of beta oscillations in BG-cortical loops is fundamental for movement-timing and synchronization, and the impact of PD therapies on sensorimotor functions relying on neural transmission in the beta frequency-range remains controversial. Here, we set out to determine the differential effects of network neuromodulation through dopaminergic medication (ON and OFF levodopa) and STN-DBS (ON-DBS, OFF-DBS) on tapping synchronization and accompanying cortical activities. To this end, we conducted a rhythmic finger-tapping study with high-density EEG-recordings in 12 PD patients before and after surgery for STN-DBS and in 12 healthy controls. STN-DBS significantly ameliorated tapping parameters as frequency, amplitude and synchrony to the given auditory rhythms. Aberrant neurophysiologic signatures of sensorimotor feedback in the beta-range were found in PD patients: their neural modulation was weaker, temporally sluggish and less distributed over the right cortex in comparison to controls. Levodopa and STN-DBS boosted the dynamics of beta-band modulation over the right hemisphere, hinting to an improved timing of movements relying on tactile feedback. The strength of the post-event beta rebound over the supplementary motor area correlated significantly with the tapping asynchrony in patients, thus indexing the sensorimotor match between the external auditory pacing signals and the performed taps. PD patients showed an excessive interhemispheric coherence in the beta-frequency range during the finger-tapping task, while under DBS-ON the cortico-cortical connectivity in the beta-band was normalized. Ultimately, therapeutic DBS significantly ameliorated the auditory-motor coupling of PD patients, enhancing the electrophysiological processing of sensorimotor feedback-information related to beta-band activity, and thus allowing a more precise cued-tapping performance.