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Pathophysiological mechanisms of oromandibular dystonia.
Manzo, N, Ginatempo, F, Belvisi, D, Defazio, G, Conte, A, Deriu, F, Berardelli, A
Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology. 2022;:73-80
Abstract
Oromandibular dystonia (OMD) is a rare form of focal idiopathic dystonia. OMD was clinically identified at the beginning of the 20th century, and the main clinical features have been progressively described over the years. However, OMD has several peculiarities that still remain unexplained, including the high rate of oral trauma, which is often related to the onset of motor symptoms. The purpose of this paper was to formulate a hypothesis regarding the pathophysiology of OMD, starting from the neuroanatomical basis of the masticatory and facial systems and highlighting the features that differentiate this condition from other forms of focal idiopathic dystonia. We provide a brief review of the clinical and etiological features of OMD as well as neurophysiological and neuroimaging findings obtained from studies in patients with OMD. We discuss possible pathophysiological mechanisms underlying OMD and suggest that abnormalities in sensory input processing may play a prominent role in OMD pathophysiology, possibly triggering a cascade of events that results in sensorimotor cortex network dysfunction. Finally, we identify open questions that future studies should address, including the effect of abnormal sensory input processing and oral trauma on the peculiar neurophysiological abnormalities observed in OMD.
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Cortical stimulation in aphasia following ischemic stroke: toward model-guided electrical neuromodulation.
Beuter, A, Balossier, A, Vassal, F, Hemm, S, Volpert, V
Biological cybernetics. 2020;(1):5-21
Abstract
The aim of this paper is to integrate different bodies of research including brain traveling waves, brain neuromodulation, neural field modeling and post-stroke language disorders in order to explore the opportunity of implementing model-guided, cortical neuromodulation for the treatment of post-stroke aphasia. Worldwide according to WHO, strokes are the second leading cause of death and the third leading cause of disability. In ischemic stroke, there is not enough blood supply to provide enough oxygen and nutrients to parts of the brain, while in hemorrhagic stroke, there is bleeding within the enclosed cranial cavity. The present paper focuses on ischemic stroke. We first review accumulating observations of traveling waves occurring spontaneously or triggered by external stimuli in healthy subjects as well as in patients with brain disorders. We examine the putative functions of these waves and focus on post-stroke aphasia observed when brain language networks become fragmented and/or partly silent, thus perturbing the progression of traveling waves across perilesional areas. Secondly, we focus on a simplified model based on the current literature in the field and describe cortical traveling wave dynamics and their modulation. This model uses a biophysically realistic integro-differential equation describing spatially distributed and synaptically coupled neural networks producing traveling wave solutions. The model is used to calculate wave parameters (speed, amplitude and/or frequency) and to guide the reconstruction of the perturbed wave. A stimulation term is included in the model to restore wave propagation to a reasonably good level. Thirdly, we examine various issues related to the implementation model-guided neuromodulation in the treatment of post-stroke aphasia given that closed-loop invasive brain stimulation studies have recently produced encouraging results. Finally, we suggest that modulating traveling waves by acting selectively and dynamically across space and time to facilitate wave propagation is a promising therapeutic strategy especially at a time when a new generation of closed-loop cortical stimulation systems is about to arrive on the market.
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Astroglial Isopotentiality and Calcium-Associated Biomagnetic Field Effects on Cortical Neuronal Coupling.
Martinez-Banaclocha, M
Cells. 2020;(2)
Abstract
Synaptic neurotransmission is necessary but does not sufficiently explain superior cognitive faculties. Growing evidence has shown that neuron-astroglial chemical crosstalk plays a critical role in the processing of information, computation, and memory. In addition to chemical and electrical communication among neurons and between neurons and astrocytes, other nonsynaptic mechanisms called ephaptic interactions can contribute to the neuronal synchronization from different brain regions involved in the processing of information. New research on brain astrocytes has clearly shown that the membrane potential of these cells remains very stable among neighboring and distant astrocytes due to the marked bioelectric coupling between them through gap junctions. This finding raises the possibility that the neocortical astroglial network exerts a guiding template modulating the excitability and synchronization of trillions of neurons by astroglial Ca2+-associated bioelectromagnetic interactions. We propose that bioelectric and biomagnetic fields of the astroglial network equalize extracellular local field potentials (LFPs) and associated local magnetic field potentials (LMFPs) in the cortical layers of the brain areas involved in the processing of information, contributing to the adequate and coherent integration of external and internal signals. This article reviews the current knowledge of ephaptic interactions in the cerebral cortex and proposes that the isopotentiality of cortical astrocytes is a prerequisite for the maintenance of the bioelectromagnetic crosstalk between neurons and astrocytes in the neocortex.
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Why is glycine cleavage system segmentally expressed in radial glia?
Sato, K
Journal of theoretical biology. 2019;:17-19
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Thalamocortical network: a core structure for integrative multimodal vestibular functions.
Brandt, T, Dieterich, M
Current opinion in neurology. 2019;(1):154-164
Abstract
PURPOSE OF REVIEW To apply the concept of nonreflexive sensorimotor and cognitive vestibular functions and disturbances to the current view of separate right and left thalamocortical systems. RECENT FINDINGS The neuronal modules for sensorimotor and cognitive functions are organized in so-called provincial hubs with intracommunity connections that interact task-dependently via connector hubs. Thalamic subnuclei may serve not only as provincial hubs but also in higher order nuclei as connector hubs. Thus, in addition to its function as a cortical relay station of sensory input, the human thalamus can be seen as an integrative hub for brain networks of higher multisensory vestibular function. Imaging studies on the functional connectivity have revealed a dominance of the right side in right-handers at the upper brainstem and thalamus. A connectivity-based parcellation study has confirmed the asymmetrical organization (i.e., cortical dominance) of the parieto-insular vestibular cortex, an area surrounded by other vestibular cortical areas with symmetrical (nondominant) organization. Notably, imaging techniques have shown that there are no crossings of the vestibular pathways in between the thalamic nuclei complexes. Central vestibular syndromes caused by lesions within the thalamocortical network rarely manifest with rotational vertigo. This can be explained and mathematically simulated by the specific coding of unilateral vestibular dysfunction within different cell systems, the angular velocity cell system (rotational vertigo in lower brainstem lesions) in contrast to the head direction cell system (directional disorientation and swaying vertigo in thalamocortical lesions). SUMMARY The structural and functional separation of the two thalamic nuclei complexes allowed a lateralization of the right and left hemispheric functions to develop. Furthermore, it made possible the simultaneous performance of sensorimotor and cognitive tasks, which require different spatial reference systems in opposite hemispheres, for example, egocentric manipulation of objects (handedness) and allocentric orientation of the self in the environment by the multisensory vestibular system.
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NEURAL CONTROL OF SWALLOWING.
Costa, MMB
Arquivos de gastroenterologia. 2018;(Suppl 1):61-75
Abstract
BACKGROUND Swallowing is a motor process with several discordances and a very difficult neurophysiological study. Maybe that is the reason for the scarcity of papers about it. OBJECTIVE It is to describe the chewing neural control and oral bolus qualification. A review the cranial nerves involved with swallowing and their relationship with the brainstem, cerebellum, base nuclei and cortex was made. METHODS From the reviewed literature including personal researches and new observations, a consistent and necessary revision of concepts was made, not rarely conflicting. RESULTS AND CONCLUSION Five different possibilities of the swallowing oral phase are described: nutritional voluntary, primary cortical, semiautomatic, subsequent gulps, and spontaneous. In relation to the neural control of the swallowing pharyngeal phase, the stimulus that triggers the pharyngeal phase is not the pharyngeal contact produced by the bolus passage, but the pharyngeal pressure distension, with or without contents. In nutritional swallowing, food and pressure are transferred, but in the primary cortical oral phase, only pressure is transferred, and the pharyngeal response is similar. The pharyngeal phase incorporates, as its functional part, the oral phase dynamics already in course. The pharyngeal phase starts by action of the pharyngeal plexus, composed of the glossopharyngeal (IX), vagus (X) and accessory (XI) nerves, with involvement of the trigeminal (V), facial (VII), glossopharyngeal (IX) and the hypoglossal (XII) nerves. The cervical plexus (C1, C2) and the hypoglossal nerve on each side form the ansa cervicalis, from where a pathway of cervical origin goes to the geniohyoid muscle, which acts in the elevation of the hyoid-laryngeal complex. We also appraise the neural control of the swallowing esophageal phase. Besides other hypotheses, we consider that it is possible that the longitudinal and circular muscular layers of the esophagus display, respectively, long-pitch and short-pitch spiral fibers. This morphology, associated with the concept of energy preservation, allows us to admit that the contraction of the longitudinal layer, by having a long-pitch spiral arrangement, would be able to widen the esophagus, diminishing the resistance to the flow, probably also by opening of the gastroesophageal transition. In this way, the circular layer, with its short-pitch spiral fibers, would propel the food downwards by sequential contraction.
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The processing of food stimuli in abnormal eating: a systematic review of electrophysiology.
Wolz, I, Fagundo, AB, Treasure, J, Fernández-Aranda, F
European eating disorders review : the journal of the Eating Disorders Association. 2015;(4):251-61
Abstract
To update the knowledge about attentional processing of food stimuli, a systematic review of electrophysiological studies was conducted using PubMed, PsychInfo and Web of Knowledge (2000-2014). Twenty-one studies were included into a qualitative synthesis. Presentation of food and control pictures was used to analyze event-related potentials related to sensory processing and motivated attention. Results show consistent attentional bias towards food pictures compared with neutral pictures for patient and control groups. Group comparisons between individuals with abnormal-eating and healthy-eating participants were more inconsistent. Results suggest that temporal differences in the millisecond range are essential for the understanding of visual food processing. In obesity, early attention engagement to food is followed by relatice disengagement. Loss of control eating, as well as external and emotional eating, are associated with a sustained maintenance of attention towards high-caloric food. There is a lack of studies in anorexia nervosa, bulimia nervosa and binge eating disorder.
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GABA estimation in the brains of children on the autism spectrum: measurement precision and regional cortical variation.
Gaetz, W, Bloy, L, Wang, DJ, Port, RG, Blaskey, L, Levy, SE, Roberts, TP
NeuroImage. 2014;:1-9
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Abstract
(1)H magnetic resonance spectroscopy ((1)H MRS) and spectral editing methods, such as MEGA-PRESS, allow researchers to investigate metabolite and neurotransmitter concentrations in-vivo. Here we address the utilization of (1)H MRS for the investigation of GABA concentrations in the ASD brain, in three locations; motor, visual and auditory areas. An initial repeatability study (5 subjects, 5 repeated measures separated by ~5days on average) indicated no significant effect of reference metabolite choice on GABA quantitation (p>0.6). Coefficients of variation for GABA+/NAA, GABA+/Cr and GABA+/Glx were all of the order of 9-11%. Based on these findings, we investigated creatine-normalized GABA+ ratios (GABA+/Cr) in a group of (N=17) children with autism spectrum disorder (ASD) and (N=17) typically developing children (TD) for Motor, Auditory and Visual regions of interest (ROIs). Linear regression analysis of gray matter (GM) volume changes (known to occur with development) revealed a significant decrease of GM volume with Age for Motor (F(1,30)=17.92; p<0.001) and Visual F(1,16)=14.41; p<0.005 but not the Auditory ROI (p=0.55). Inspection of GABA+/Cr changes with Age revealed a marginally significant change for the Motor ROI only (F(1,30)=4.11; p=0.054). Subsequent analyses were thus conducted for each ROI separately using Age and GM volume as covariates. No group differences in GABA+/Cr were observed for the Visual ROI between TD vs. ASD children. However, the Motor and Auditory ROI showed significantly reduced GABA+/Cr in ASD (Motor p<0.05; Auditory p<0.01). The mean deficiency in GABA+/Cr from the Motor ROI was approximately 11% and Auditory ROI was approximately 22%. Our novel findings support the model of regional differences in GABA+/Cr in the ASD brain, primarily in Auditory and to a lesser extent Motor but not Visual areas.
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[Neuronal dysfunction in multiple sclerosis].
Mizuno, T
Rinsho shinkeigaku = Clinical neurology. 2014;(12):1066-8
Abstract
The precise mechanisms of cortical damage in multiple sclerosis (MS) remain unknown. Microglia, the resident immune cells in the central nervous system (CNS), are involved in the chronic neuroinflammation in MS cortical lesions. Microglia produce various inflammatory cytokines such as IFN-γ and IL-β, reactive oxygen species, and glutamate. IL-β secretion is induced by NLRP3. ROS is induced by GM-CSF-producing Th17 cells. Glutamate is released via gap junctions. These molecules exert neurotoxicity. Meanwhile, damaged neurons produce fractalkine and FGF-2, which suppress microglial activation and enhance microglial neuroprotection through anti-inflammatory and anti-oxidant effect. Fractalkine accelerates microglial clearance of neuronal debris via inducing the release of MFG-E8. FGF-2 induces microglial migration through the FGFR3-Wnt-ERK signaling pathway. These molecules suppress microglial neuroinflammation, and enhance neuroprotection, which may give us clues for future therapeutic strategy cortical damage in MS.
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10.
Impaired GABAergic neurotransmission in schizophrenia underlies impairments in cortical gamma band oscillations.
McNally, JM, McCarley, RW, Brown, RE
Current psychiatry reports. 2013;(3):346
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Abstract
Impairment of cortical circuit function is increasingly believed to be central to the pathophysiology of schizophrenia (Sz). Such impairments are suggested to result in abnormal gamma band oscillatory activity observed in Sz patients, and likely underlie the psychosis and cognitive deficits linked to this disease. Development of improved therapeutic strategies to enhance functional outcome of Sz patients is contingent upon a detailed understanding of the mechanisms behind cortical circuit development and maintenance. Convergent evidence from both Sz clinical and preclinical studies suggests impaired activity of a particular subclass of interneuron which expresses the calcium binding protein parvalbumin is central to the cortical circuit impairment observed. Here we review our current understanding of the Sz related cortical circuit dysfunction with a particular focus on the role of fast spiking parvalbumin interneurons in both normal cortical circuit activity and in NMDA receptor hypofunction models of the Sz disease state.