Compensatory Network Research Articles

Современные проблемы морфологического изучения цитоархитектоники коры большого мозга человека в норме и при ишемии

Study of the human cortex morphology in norm and at the ischemia is due to the desire to identify common patterns and specific features of compensatory neural networks reorganization, seeking means of regulation of destructive and regenerative processes. The emergence of a large amount of information on the nervous tissue mor-phology is the need for increasing the accuracy of morphometric analysis. This requires an assessment of the overall methodological level of modern morphological studies of the human cortex. The authors analyzed the literature and their own data obtained from a morphological study of the human cortex. The main tendencies, current methodological issues and perspective directions of study the structural and functional state of neurons in norm and ischemia are presented. Great attention is paid to the immunohistochemical and morphometric methods of obtaining objective information. Currently there are methodological and methodical basis for further study of the human brain morphology. However, the total number of articles on the study of human brain morphology earned far less than the experimental works. For the fullest use of biopsy material is offered a comprehensive approach, including method of computer-aided analysis of images, immunohistochemistry, morphometry and statistical analysis.

Dynamical predictions of insular hubs for social cognition and their application to stroke.

The insular cortex (IC) is considered a rich hub for context-sensitive emotions/social cognition. Patients with focal IC stroke provide unique opportunities to study socio-emotional processes. Nevertheless, Couto et al. (2013b) have recently reported controversial results regarding IC involvement in emotion and social cognition. Similarly, patients with similar lesions show high functional variability, ranging from almost totally preserved to strongly impaired behavior. Critical evidence suggests that the variability of these patients in the above domains can be explained by enhanced neuroplasticity, compensatory processes, and functional remapping after stroke. Therefore, socio-emotional processes would depend on long-distance connections between the IC and frontotemporal regions. We propose that predictive coding and effective connectivity represent a novel approach to explore functional connectivity and assess compensatory, contralateral, and subsidiary network differences among focal stroke patients. This approach would help explain why socio-emotional performance is so variable within this population.

PO-0815 Moyamoya In Paediatric Patients

Background and aims Moyamoya disease (MMD) is an uncommon chronic progressive cerebrovascular occlusive disease of the bilateral internal carotid arteries that leads to a compensatory abnormal vascular network at the base of the brain. Reported incidence in the USA is approximately 0,086 per 100,000 patients. It can be primary or associated with other conditions. Methods Retrospective analysis of clinical files of patients diagnosed with MMD currently followed in the Paediatric Neurology ambulatory unit of Vila Nova de Gaia Hospital, Portugal. Results There are three cases of MMD, all male, two associated with neurofibromatosis type 1 (NF-1) and one case of primary MMD. All diagnosis were based on brain magnetic resonance angiography (MRA) findings: stenotic lesions in the distal carotid arteries, increased signal in the leptomeninges and perivascular spaces. Idiopathic MMD presented in an 11 year old with acute hemiparesis and disartria. Brain CT revealed an ischaemic stroke and MRA was consistent with MMD. In both cases of NF-1, MMD was diagnosed during follow up of the disease. Patients were 1 and 4 years old and were assymptomatic at time of diagnosis. In one case, neurologic symptoms developed during follow-up and revascularisation surgery was necessary. Conclusions The natural history of MMD tends to be progressive. Association between MMD and NF-1 is rare, but poses a potencial risk. In previously healthy patients who present with acute neurologic symptoms, a high index of suspicion is necessary. In both cases, prompt diagnosis and appropriate management are crucial to improve long-term prognosis.

Neurophysiological correlates of metabolic syndrome and cognitive impairment in schizophrenia: a structural equation modeling approach.

We aimed to investigate the brain functional substrate underlying relationships between metabolic syndrome (MetS) and cognitive impairment in schizophrenia. In this cross-sectional study, we collected socio-demographic, clinical, anthropometric, blood, and cognition data and performed brain 99mTc-ECD-SPECT imaging of cerebral blood flow in patients with schizophrenia. Patients were grouped according to the absence or presence of MetS. Whole-brain perfusion SPECTs were compared at voxel level between these two groups, and voxel-wise interregional correlation was performed to compare functional connectivity (voxel level significance of p<0.005, uncorrected; p<0.05 for the cluster, uncorrected; using SPM8). A structural equation model (SEM) was applied to examine the relationships between brain perfusion, connectivity between brain areas, and cognition. Of the 55 patients, 17 had MetS. They performed significantly worse than patients without MetS on tests of executive functions (processing speed p=0.005 for TMT-A; and reactive flexibility p=0.014 for TMT-B), attention (D2 attention task p=0.007), and memory (California Verbal Learning Test p=0.039). In comparison to patients without MetS, those with MetS exhibited significant hypoperfusion within the left orbital prefrontal cortex and greater functional connectivity from this left frontal cluster within the left insula and middle/superior frontal gyrus. SEM confirmed the effect on executive functions of brain hypoperfusion and of increased connectivity, suggesting possible compensatory networks in patients with MetS. Our study identifies the brain functional impact of MetS on cognition, with orbital prefrontal impairment and possible compensatory networks.

Compensatory neural fuzzy network with symbiotic particle swarm optimization for temperature control

This study proposes a symbiotic particle swarm optimization (SPSO) algorithm for compensatory neural fuzzy networks (CNFN). The CNFN model using compensatory fuzzy operators makes fuzzy logic systems more adaptive and effective. The proposed SPSO algorithm adopts a multiple swarm scheme that uses each particle to represent a single fuzzy rule and each particle in each swarm evolves separately to avoid falling into a locally optimal solution. Additionally, the SPSO embeds the symbiotic evolution scheme in a specific particle swarm optimization (PSO) to accelerate the search and increase global search capacity. Finally, the proposed CNFN with SPSO (CNFN-SPSO) method is applied to control a water bath temperature system. Results of this study demonstrate the effectiveness of the proposed CNFN-SPSO method.

Compensatory cerebral motor control following presumed perinatal ischemic stroke

CaseA fifteen year-old left-handed girl presented with right-sided focal motor seizures. Neuroimaging showed a large left hemisphere lesion compatible with a middle cerebral artery stroke of presumed perinatal origin. She was not previously diagnosed with a motor deficit, although neurological examination now revealed that it required more attention to use the affected right hand during both unimanual and bimanual movements. MethodsAs perinatal stroke provides unique insight in plasticity of the brain, we performed functional and diffusion brain imaging showing reduction of pyramidal efferents from the affected hemisphere and extensive compensatory bilateral brain activations during right hand movements. ResultsThe activated compensatory network was extensive, comprising regions involved in higher-order motor control and visuospatial attention, now recruited during simple right unimanual and bimanual antiphase movements. DiscussionThis pre-existing network for simple movements that healthy subjects only need to recruit for more complex motor actions, enabled our patient to perform simple right-handed movements.

Compromised frontocerebellar circuitry contributes to nonplanning impulsivity in recovering alcoholics.

Degradation of frontocerebellar circuitry is a principal neural mechanism of alcoholism-related executive dysfunctions affecting impulse control and cognitive planning. We tested the hypothesis that alcoholic patients would demonstrate compromised dorsal anterior cingulate cortex (dACC) -cerebellar functional connectivity when adjusting their strategies to accommodate uncertain conditions and would recruit compensatory brain regions to overcome ineffective response patterns. Twenty-six alcoholics and 26 healthy participants underwent functional MRI in two sequential runs while performing a decision-making task. The first run required a response regardless of level of ambiguity of the stimuli; the second run allowed a PASS option (i.e., no response choice), which was useful on ambiguous trials. Healthy controls demonstrated strong synchronous activity between the dACC and cerebellum while planning and executing a behavioral strategy. By contrast, alcoholics showed synchronous activity between the dACC and the premotor cortex, perhaps enabling successful compensation for accuracy and reaction time in certain conditions; however, a negative outcome of this strategy was rigidity in modifying response strategy to accommodate uncertain conditions. Compared with the alcoholic group, the control group had lower nonplanning impulsiveness, which correlated with using the option PASS to respond in uncertain conditions. These findings suggest that compromised dACC-cerebellar functional circuitry contributes to recruitment of an alternative network-dACC-premotor cortex- to perform well under low-risk, unambiguous conditions. This compensatory network, however, was inadequate to enable the alcoholics to avert making poor choices in planning and executing an effective behavioral strategy in high-risk, uncertain conditions.

A TSK-Type-Based Self-Evolving Compensatory Interval Type-2 Fuzzy Neural Network (TSCIT2FNN) and Its Applications

In this paper, a Takagi-Sugeno-Kang (TSK)-type-based self-evolving compensatory interval type-2 fuzzy neural network (FNN) (TSCIT2FNN) is proposed for system modeling and noise cancellation problems. A TSCIT2FNN uses type-2 fuzzy sets in an FNN in order to handle the uncertainties associated with information or data in the knowledge base. The antecedent part of each compensatory fuzzy rule is an interval type-2 fuzzy set in the TSCIT2FNN, where compensatory-based fuzzy reasoning uses adaptive fuzzy operation of a neural fuzzy system to make the fuzzy logic system effective and adaptive, and the consequent part is of the TSK type. The TSK-type consequent part is a linear combination of exogenous input variables. Initially, the rule base in the TSCIT2FNN is empty. All rules are derived according to online type-2 fuzzy clustering. For parameter learning, the consequent part parameters are tuned by a variable-expansive Kalman filter algorithm to the reinforce parameter learning ability. The antecedent type-2 fuzzy sets and compensatory weights are learned by a gradient descent algorithm to improve the learning performance. The performance of TSCIT2FNN for the identification is validated and compared with several type-1 and type-2 FNNs. Simulation results show that our approach produces smaller root-mean-square errors and converges more quickly.

Association between auditory P300, psychopathology, and memory function in drug-naïve schizophrenia

The aim of this study was to explore memory deficits and psychopathology and their relationships with P300 in drug-naïve patients with schizophrenia. The Positive and Negative Syndrome Scale (PANSS) and the Wechsler Memory Scale—Revised were administered. Auditory event-related potentials elicited by an oddball paradigm were obtained. After controlling for age, sex, the results showed a statistically significant negative correlation between the total PANSS score and P300 amplitude at the parietal position (r = −0.66, p < 0.05). Moreover, visual memory was significantly positively correlated with P300 amplitude at the parietal position (r = 0.67, p < 0.05). After controlling for the duration of illness, the above correlations remained statistically significant. The correlation between P300 and the severity of psychopathology was reconfirmed in drug-naïve patients with schizophrenia. A possible contribution of memory decompensation in P300 among drug-naïve patients with schizophrenia may be considered, and the compensatory or Default Model Network might be a possible explanation of this association.

Pathomechanisms and compensatory efforts related to Parkinsonian speech.

Voice and speech in Parkinson's disease (PD) patients are classically affected by a hypophonia, dysprosody, and dysarthria. The underlying pathomechanisms of these disabling symptoms are not well understood. To identify functional anomalies related to pathophysiology and compensation we compared speech-related brain activity and effective connectivity in early PD patients who did not yet develop voice or speech symptoms and matched controls. During fMRI 20 PD patients ON and OFF levodopa and 20 control participants read 75 sentences covertly, overtly with neutral, or with happy intonation. A cue-target reading paradigm allowed for dissociating task preparation from execution. We found pathologically reduced striato-prefrontal preparatory effective connectivity in early PD patients associated with subcortical (OFF state) or cortical (ON state) compensatory networks. While speaking, PD patients showed signs of diminished monitoring of external auditory feedback. During generation of affective prosody, a reduced functional coupling between the ventral and dorsal striatum was observed. Our results suggest three pathomechanisms affecting speech in PD: While diminished energization on the basis of striato-prefrontal hypo-connectivity together with dysfunctional self-monitoring mechanisms could underlie hypophonia, dysarthria may result from fading speech motor representations given that they are not sufficiently well updated by external auditory feedback. A pathological interplay between the limbic and sensorimotor striatum could interfere with affective modulation of speech routines, which affects emotional prosody generation. However, early PD patients show compensatory mechanisms that could help improve future speech therapies.

Compensatory neural fuzzy networks with rule-based cooperative differential evolution for nonlinear system control

This study presents a rule-based cooperative differential evolution (RCDE) learning algorithm to optimize the parameters of a compensatory neural fuzzy network (CNFN) for solving control problems. CNFN uses the compensatory degree for fuzzy reasoning to dynamically adjust fuzzy operators that can make the fuzzy system more adaptive and effective. RCDE decomposes the fuzzy system into multiple rule-based subpopulations where each subpopulation represents a fuzzy rule set, and each individual within each subpopulation evolves by differential evolution (DE) separately. The proposed RCDE uses cooperative behavior among multiple subpopulations for combining their information and building the complete fuzzy system to accelerate the search and increase global search capacity. Finally, the experimental results show that the proposed RCDE method better approximates the global optimal solution and has a faster convergence rate than the other methods.

Compensatory networks to counteract the effects of ageing on language

BackgroundWord-retrieval difficulties are a common consequence of healthy ageing and are associated with a reduction in asymmetrical recruitment of the dorsolateral prefrontal cortex (DLPFC), although the significance of this reduction has not yet been clarified. Using repetitive transcranial magnetic stimulation (rTMS) it has been demonstrated that an asymmetrical involvement of the DLPFC during action naming in young subjects, whereas bilateral involvement was shown in elderly participants. By using rTMS during a naming task in a group of elderly subjects, the aim of the present work was to investigate whether the magnitude of DLPFC asymmetry (left–right rTMS effect) during action naming correlates with task performance, proving the presence of a compensation strategy in some but not all elderly participants. MethodsWe aimed to test if there was a correlation between DLPFC asymmetry (left–right rTMS effect) and naming performance in a group of elderly subjects. ResultsThe results show that rTMS affects action naming differently according to individual naming ability. In particular, the predominance of a left vs. right DLPFC effect was observed only in the low-performing older adults, while an asymmetric reduction was selectively shown in the high-performing group. Interestingly, high-performing older adults also displayed better performances on a phonemic fluency test. ConclusionThe present data suggest that successful ageing is linked to less prefrontal asymmetry, an efficient strategy for counteracting age-related declines in cognitive function.

Metabolic Networks Underlying Cognitive Reserve in Prodromal Alzheimer Disease: A European Alzheimer Disease Consortium Project

This project aimed to investigate the metabolic basis for resilience to neurodegeneration (cognitive reserve) in highly educated patients with prodromal Alzheimer disease (AD). Sixty-four patients with amnestic mild cognitive impairment who later converted to AD dementia during follow-up, and 90 controls, underwent brain (18)F-FDG PET. Both groups were divided into a poorly educated subgroup (42 controls and 36 prodromal AD patients) and a highly educated subgroup (48 controls and 28 prodromal AD patients). Brain metabolism was first compared between education-matched groups of patients and controls. Then, metabolism was compared between highly and poorly educated prodromal AD patients in both directions to identify regions of high education-related metabolic depression and compensation. The clusters of significant depression and compensation were further used as volumetric regions of interest (ROIs) in a brain interregional correlation analysis in each prodromal AD subgroup to explore metabolic connectivity. All analyses were performed by means of SPM8 (P < 0.001 uncorrected at peak level, P < 0.05 false discovery rate-corrected at cluster level; age, sex, Mini-Mental State Examination score, and center as nuisance). Highly educated prodromal AD patients showed more severe hypometabolism than poorly educated prodromal AD patients in the left inferior and middle temporal gyri and the left middle occipital gyrus (ROI depression). Conversely, they showed relative hypermetabolism in the right inferior, middle, and superior frontal gyri (ROI compensation). The sites of compensation, mainly corresponding to the right dorsolateral prefrontal cortex (DLFC), showed wide metabolic correlations with several cortical areas in both hemispheres (frontotemporal cortex, parahippocampal gyrus, and precuneus) in highly educated prodromal AD patients but not in poorly educated prodromal AD patients. To provide evidence on whether these metabolic correlations represent preservation of the physiologic networks of highly educated control subjects (neural reserve) or rather the recruitment of alternative networks (neural compensation), or a combination of the two, we performed metabolic connectivity analysis of the DLFC in highly educated controls as well. The correlation sites of right DLFC partly overlapped those of highly educated prodromal AD patients but were less extended. The present findings suggest that highly educated prodromal AD patients can cope better with the disease thanks to neural reserve but also to the recruitment of compensatory neural networks in which the right DLFC plays a key role.

A new hybrid intelligent control algorithm for a seven-link biped walking robot

In recent years, many studies on bipedal walking robots and control algorithms have been conducted. However, different conditions and circumstances that have to be taken into account make the control of biped walking robots a big challenge. This paper proposes the implementation of a new hybrid intelligent control approach for a seven-link biped walking robot to track the specified trajectory based on a compensatory neurofuzzy network and fuzzy controller. This algorithm consists of two main parts: the feedforward compensator includes an integrated compensatory neurofuzzy network for identification of the inverse dynamics model which attempts to cancel the dynamics of the robot, and the feedback controller which includes a Mamdani-type fuzzy controller to compensate the modeling error and the effect of noise on the system. Moreover, a new style of membership functions distribution for fuzzy controller with noise reduction capability is proposed and its influence on the performance of the robot under noise-free and noisy conditions is investigated. Simulations performed on a biped robot illustrate the methods and their performance. The results confirm the high tracking capability and effectiveness of the proposed control approach.

Caucasian Familial Moyamoya Syndrome With Rare Multisystemic Malformations

Moyamoya disease is an idiopathic progressive steno-occlusive disorder of the intracranial arteries located at the base of the brain. It is associated with the development of compensatory extensive network of fine collaterals. Moyamoya disease is considered syndromic when certain genetic or acquired disorders such as polycystic kidney disease, neurofibromatosis, or meningitis are also present. Although the genetic contribution in moyamoya is indisputable, its cause and pathogenesis remain under discussion. Herein, we report a rare occurrence of moyamoya syndrome in two European Caucasian siblings in association with unusual multisystemic malformations (polycystic kidney disease in one, and intestinal duplication cyst in the other). The karyotype was normal. No mutation in the RFN213 gene was found, and none of the HLA types linked to moyamoya disease or described in similar familial cases were identified. By describing these multisystemic associations, polycystic kidney disease for the second time, and intestinal malformation for the first time in the literature, our report expands the phenotypic variability of moyamoya syndrome. The coexistence of disparate malformations among close relatives suggests an underlying common genetic background predisposing to structural or physiological abnormalities in different tissues and organs.

Functional magnetic resonance imaging of chronic dysarthric speech after childhood brain injury: reliance on a left-hemisphere compensatory network

Severe and persistent speech disorder, dysarthria, may be present for life after brain injury in childhood, yet the neural correlates of this chronic disorder remain elusive. Although abundant literature is available on language reorganization after lesions in childhood, little is known about the capacity of motor speech networks to reorganize after injury. Here, we examine the structural and functional neural correlates associated with chronic dysarthria after childhood-onset traumatic brain injury. Forty-nine participants aged 12 years 3 months to 24 years 11 months were recruited to the study: (i) a group with chronic dysarthria (n = 17); matched for age and sex with two control groups of (ii) healthy control subjects (n = 17); and (iii) individuals without dysarthria after traumatic brain injury (n = 15). A high-resolution 3D T(1)-weighted whole-brain data set was acquired for voxel-based morphometry analyses of group differences in grey matter. Functional magnetic resonance imaging was used to localize activation associated with speaking single words (baseline: listening to words). Group differences on voxel-based morphometry revealed widespread grey matter reductions in the dysarthric group compared with healthy control subjects, including in numerous speech motor regions bilaterally, such as the cerebellum, the basal ganglia and primary motor cortex representation of the articulators. Relative to the non-dysarthric traumatic brain injury group, individuals with dysarthria showed reduced grey matter bilaterally in the ventral sensorimotor cortex, but this reduction was concomitant with increased functional activation only in the left-hemisphere cluster during speech. Finally, increased recruitment of Broca's area (Brodmann area 45, pars triangularis) but not its right homologue, correlated with better speech outcome, suggesting that this 'higher-level' area may be more critically involved with production when associated motor speech regions are damaged. We suggest that the bilateral morphological abnormalities within cortical speech networks in childhood prevented reorganization of speech function from the left- to right-hemisphere. Rather, functional reorganization involved over-recruitment of left-hemisphere motor regions, a reorganization method that was only partly relatively effective, given the presence of persisting yet mild speech deficits. The bilateral structural abnormalities found to limit functional reorganization here, may also be critical to poor speech prognosis for populations with congenital, degenerative or acquired neurological disorders throughout the lifespan.

Cortico-basal ganglia and cortico-cerebellar circuits in Parkinson's disease: Pathophysiology or compensation?

The basal ganglia and the cerebellum are anatomically and functionally linked to the cerebral cortex through a series of well-established circuits. The disruption of dopaminergic projections in Parkinson's disease (PD) leads to an imbalance within these circuits, leading to motor and cognitive symptoms. The cortico-cerebellar (CC) network has often been viewed as a compensatory network, helping the dysfunction of the cortico-basal ganglia (CBG) circuits in PD. However, evidence for this compensatory role is scarce; most changes in cerebellar activity could equally be attributed to pathophysiological changes underlying PD. This paper will review the anatomy, interaction and function of the CBG and CC circuits, the pathophysiological, metabolic, and functional changes observed in PD, as well as the effect of levodopa and deep brain stimulation on these changes. We will use this framework to discuss the pathophysiological and compensatory mechanisms behind CBG and CC circuit activity in PD.

Pediatric Moyamoya disease

Background:Moyamoya disease (MMD) is a progressive cerebrovascular occlusive disease of the bilateral internal carotid arteries that leads to a compensatory abnormal vascular network at the base of the brain. Its average annual incidence 0.54 per 100,000 population but it is the most common pediatric cerebrovascular disease in East Asia. The reported incidence in USA is approximately 0.086 per 100,000 patients.Case Report:We present a case of Moyamoya disease that was to detected in a 7-year-old female who presented with transient altered mental status.Conclusions:Moyamoya disease can be diagnosed if history, physical exam and brain imaging is highly suspicious. Conventional angiography remains the gold standard for diagnosis and aids in surgical planning for patients with suspected Moyamoya disease.

A16 Defining predictors of disease

Since 2008 TRACK-HD has chronicled the earliest stages of the neurodegenerative disease processes in premanifest and mild to moderately symptomatic individuals who carry the Huntington9s disease expansion mutation. TRACK-HD was designed to observe natural disease progression in premanifest and early stage HD with the aim to establish sensitive and specific clinical and biological markers of disease progression. Such markers potentially serve as a basis for eventually defining outcome measures for future disease-modifying therapeutic trials. We recently reported longitudinal effect sizes for disease-progression in early stage Huntington9s disease over 24 months. Some of these 24 month data will be presented in this talk in more detail, including insights into what we have learnt about predictors of Huntington9s disease progression in both premanifest and early stage subjects. Analysis of the 36 month data is ongoing; this new data will also be presented including a range of novel clinical measures that now show significant change in the premanifest group over this period. We have also identified baseline predictors of disease progression which may help enrichment for future disease-modifying clinical trials. We are also now in a position to model progression in a range of functional and imaging measures across the spectrum of disease. Finally I will briefly introduce our new study – Track-On HD – which aims to identify neural compensatory networks that may occur in the premanifest phase of neurodegeneration in HD. This study will test the hypothesis that functional reorganisation of networks may precede widespread structural loss in premanifest HD, and that symptom onset may reflect a decompensation of these neural compensatory networks.

Modifications on the hydrogen bond network by mutations of Escherichia coli copper efflux oxidase affect the process of proton transfer to dioxygen leading to alterations of enzymatic activities

CueO has a branched hydrogen bond network leading from the exterior of the protein molecule to the trinuclear copper center. This network transports protons in the four-electron reduction of dioxygen. We replaced the acidic Glu506 and Asp507 residues with the charged and uncharged amino acid residues. Peculiar changes in the enzyme activity of the mutants relative to the native enzyme indicate that an acidic amino acid residue at position 506 is essential for effective proton transport. The Ala mutation resulted in the formation of a compensatory hydrogen bond network with one or two extra water molecules. On the other hand, the Ile mutation resulted in the complete shutdown of the hydrogen bond network leading to loss of enzymatic activities of CueO. In contrast, the hydrogen bond network without the proton transport function was constructed by the Gln mutation. These results exerted on the hydrogen bond network in CueO are discussed in comparison with proton transfers in cytochrome oxidase.