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Sensory development is a complex process that can influence physiological and pathological factors. In laterally-eyed mammals, monocular enucleation (ME) during development and the subsequent lack of external sensory stimuli can result in permanent morphological and physiological changes. Malnutrition, especially in early life, also can cause permanent morphofunctional changes due to inadequate nutrient intake in both hemispheres. This study investigated the effects of early (postnatal day 7) ME and malnutrition during the suckling period on cortical excitability in adulthood (110-140 days of life). For this, we compared the speed propagation of cortical spreading depression in the occipital and parietal cortex of malnourished and well-nourished adult rats, previously suckled small-sized litters with three pups (L3/dam) medium-sized litters with six pups (L6/dam), and large-sized litters with twelve pups (L12/dam). The CSD velocity was augmented by the ME in the contralateral side of the removed eye in the parietal and occipital cortex. These findings suggest that visual sensory input deprivation is associated with permanent functional changes in the visual pathways, which can alter cortical excitability and lead to modifications in CSD propagation.

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Background: Interactions between the somatosensory and motor cortices are of fundamental importance for motor control. Although physically distant, face and hand representations are side by side in the sensorimotor cortex and interact functionally. Traumatic brachial plexus injury (TBPI) interferes with upper limb sensorimotor function, causes bilateral cortical reorganization, and is associated with chronic pain. Thus, TBPI may affect sensorimotor interactions between face and hand representations. Objective: The aim of this study was to investigate changes in hand-hand and face-hand sensorimotor integration in TBPI patients using an afferent inhibition (AI) paradigm. Method: The experimental design consisted of electrical stimulation (ES) applied to the hand or face followed by transcranial magnetic stimulation (TMS) to the primary motor cortex to activate a hand muscle representation. In the AI paradigm, the motor evoked potential (MEP) in a target muscle is significantly reduced when preceded by an ES at short-latency (SAI) or long-latency (LAI) interstimulus intervals. We tested 18 healthy adults (control group, CG), evaluated on the dominant upper limb, and nine TBPI patients, evaluated on the injured or the uninjured limb. A detailed clinical evaluation complemented the physiological investigation. Results: Although hand-hand SAI was present in both the CG and the TBPI groups, hand-hand LAI was present in the CG only. Moreover, less AI was observed in TBPI patients than the CG both for face-hand SAI and LAI. Conclusion: Our results indicate that sensorimotor integration involving both hand and face sensorimotor representations is affected by TBPI.

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Prolonged changes in neural activity trigger homeostatic synaptic plasticity (HSP) allowing neuronal networks to operate within functional ranges. Cell-wide or input-specific adaptations can be induced by pharmacological or genetic manipulations of activity, and by sensory deprivation. Reactive functional changes caused by deafferentation may partially share mechanisms with HSP. Acute hippocampal slices are a suitable model to investigate relatively rapid (hours) modifications occurring after denervation and explore the underlying mechanisms. As during slicing many afferents are cut, we conducted whole-cell recordings of miniature excitatory postsynaptic currents (mEPSCs) in CA1 pyramidal neurons to evaluate changes over the following 12 h. As Schaffer collaterals constitute a major glutamatergic input to these neurons, we also dissected CA3. We observed an average increment in mEPSCs amplitude and a decrease in decay time, suggesting synaptic AMPA receptor upregulation and subunit content modifications. Sorting mEPSC by rise time, a correlate of synapse location along dendrites, revealed amplitude raises at two separate domains. A specific frequency increase was observed in the same domains and was accompanied by a global, unspecific raise. Amplitude and frequency increments were lower at sites initially more active, consistent with local compensatory processes. Transient preincubation with a specific Ca2+/calmodulin-dependent kinase II (CaMKII) inhibitor either blocked or occluded amplitude and frequency upregulation in different synapse populations. Results are consistent with the concurrent development of different known CaMKII-dependent HSP processes. Our observations support that deafferentation causes rapid and diverse compensations resembling classical slow forms of adaptation to inactivity. These results may contribute to understand fast-developing homeostatic or pathological events after brain injury.

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In animal models, prolonged exposure (2 h) to high-level noise causes an irreparable damage to the synapses between the inner hair cells and auditory nerve fibers within the cochlea. Nevertheless, this injury does not necessarily alter the hearing threshold. Similar findings have been observed as part of typical aging in animals. This type of cochlear synaptopathy, popularly called "hidden hearing loss," has been a significant issue in neuroscience research and clinical audiology scientists. The results obtained in different investigations are inconclusive in their diagnosis and suggest new strategies for both prognosis and treatment of cochlear synaptopathy. Here we review the major physiological findings regarding cochlear synaptopathy in animals and humans and discuss mathematical models. We also analyze the potential impact of these results on clinical practice and therapeutic options.

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Unilateral brachial plexus injury (BPI) impairs sensory and motor functions of the upper limb. This study aimed to map in detail brachial plexus sensory impairment both in the injured and the uninjured upper limb. Touch sensation was measured through Semmes-Weinstein monofilaments at the autonomous regions of the brachial plexus nerves, hereafter called points of exclusive innervation (PEIs). Seventeen BPI patients (31.35 years±6.9 SD) and 14 age-matched healthy controls (27.57 years±5.8 SD) were tested bilaterally at six selected PEIs (axillary, musculocutaneous, median, radial, ulnar, and medial antebrachial cutaneous [MABC]). As expected, the comparison between the control group and the brachial plexus patients' injured limb showed a robust difference for all PEIs (p ≤ 0.001). Moreover, the comparison between the control group and the brachial plexus uninjured limb revealed a difference for the median (p = 0.0074), radial (p = 0.0185), ulnar (p = 0.0404), and MABC (p = 0.0328) PEIs. After splitting the sample into two groups with respect to the dominance of the injured limb, higher threshold values were found for the uninjured side when it occurred in the right dominant limb compared to the control group at the median (p = 0.0456), radial (p = 0.0096), and MABC (p = 0.0078) PEIs. This effect was absent for the left, non-dominant arm. To assess the effect of the severity of sensory deficits observed in the injured limb upon the alterations of the uninjured limb, a K-means clustering algorithm (k = 2) was applied resulting in two groups with less or more severe sensory impairment. The less severely affected patients presented higher thresholds at the median (p = 0.0189), radial (p = 0.0081), ulnar (p = 0.0253), and MABC (p = 0.0187) PEIs in the uninjured limb in comparison with the control group, whereas higher thresholds at the uninjured limb were found only for the median PEI (p = 0.0457) in the more severely affected group. In conclusion, an expressive reduction in touch threshold was found for the injured limb allowing a precise mapping of the impairment caused by the BPI. Crucially, BPI also led to reduced tactile threshold in specific PEIs in the uninjured upper limb. These new findings suggest a superordinate model of representational plasticity occurring bilaterally in the brain after a unilateral peripheral injury.

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Sensory-motor integration models have been proposed aiming to explain how the brain uses sensory information to guide and check the planning and execution of movements. Sensory neuronopathy (SN) is a peculiar disease characterized by exclusive, severe and widespread sensory loss. It is a valuable condition to investigate how sensory deafferentation impacts brain organization. We thus recruited patients with clinical and electrophysiological criteria for SN to perform structural and functional MRI analyses. We investigated volumetric changes in gray matter (GM) using anatomical images; the microstructure of WM within segmented regions of interest (ROI), via diffusion images; and brain activation related to a finger tapping task. All significant results were related to the long disease duration subgroup of patients. Structural analysis showed hypertrophy of the caudate nucleus, whereas the diffusion study identified reduction of fractional anisotropy values in ROIs located around the thalamus and the striatum. We also found differences regarding finger-tapping activation in the posterior parietal regions and in the medial areas of the cerebellum. Our results stress the role of the caudate nucleus over the other basal ganglia in the sensory-motor integration models, and suggest an inhibitory function of a recently discovered tract between the thalamus and the striatum. Overall, our findings confirm plasticity in the adult brain and open new avenues to design neurorehabilitation strategies.

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Synaptic plasticity is the process by which long-lasting changes take place at synaptic connections. The phenomenon itself is complex and can involve many levels of organization. Some authors separate forms into adaptations that have positive or negative consequences for the individual. It has been hypothesized that an increase in the number of synapses may represent a structural basis for the enduring expression of synaptic plasticity during some events that involve memory and learning; also, it has been suggested that perforated synapses increase in number after some diseases and experimental situations. The aim of this study was to analyze whether dopamine depletion induces changes in the synaptology of the corpus striatum of rats after the unilateral injection of 6-OHDA. The findings suggest that after the lesion, both contralateral and ipsilateral striata exhibit an increased length of the synaptic ending in ipsilateral (since third day) and contralateral striatum (since Day 20), loss of axospinous synapses in ipsilateral striatum and a significant increment in the number of perforated synapses, suggesting brain plasticity that might be deleterious for the spines, because this type of synaptic contacts are presumably excitatory, and in the absence of the modulatory effects of dopamine, the neuron could die through excitotoxic mechanisms. Thus, we can conclude that the presence of perforated synapses after striatal dopamine depletion might be a form of maladaptive synaptic plasticity.

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BACKGROUND: Facial chronic neuropathic pain (FCNP) is a disabling clinical entity, its incidence is increasing within the chronic pain population. There is indication for neuromodulation when conservative treatment fails. Motor cortex stimulation (MCS) has emerged as an alternative in the advanced management of these patients. The aim of this work is to review the worldwide literature on MCS for FCNP. METHODS: A PubMed search from 1990 to 2012 was conducted using established MeSH words. A total of 126 relevant articles on MCS focused on chronic pain were selected and analysed. Series of cases were divided in (1) series focused on MCS for FCNP, and (2) MCS series of FCNP mixed with other chronic pain entities. RESULTS: A total of 118 patients have been trialed for MCS for FCNP, 100 (84.7%) pursued permanent implantation of the system, and 84% of them had good pain control at the end of the study. Male: female ratio was about 1:2 in the whole group of studies; mean age was 58 years (range, 28-83), and mean pain duration was 7 years (range, 0.6-25). Four randomized controlled studies have been reported, all of them not focused on MCS for FCNP. The most common complication was seizure followed by wound infection. Preoperative evaluation, surgical techniques, and final settings varied among the series. CONCLUSION: MCS for FNCP is a safe and efficacious treatment option when previous managements have failed; however, there is still lack of strong evidence (larger randomized controlled multicentre studies) that MCS can be offered in a regular basis to FNCP patients.

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En la medida que crece la población y aumenta el número de personas de la tercera edad con trastornos de la visión, se necesita cada vez más hacer conciencia del Síndrome de Charles Bonnet entre los oftalmólogos, psiquiatras y neurólogos. El propósito de la presente revisión es ofrecer una visión actualizada sobre sus aspectos clínicos, fisiopatológicos, epidemiológicos junto con las estrategias de manejo más razonables. Para ello se emprendió una búsqueda exhaustiva de la literatura más relevante, con el fin de comprender estos aspectos. El síndrome de Charles Bonnet es una entidad subreportada y subdiagnosticada que aparece en personas de la tercera edad, visualmente comprometidas. Estos pacientes por lo general tienen un estado cognoscitivo intacto aunque algunos autores sostienen que puede ser más frecuente en casos de deterioro cognoscitivo leve. Su fisiopatología aún es tema de debate pero las teorías mas aceptadas, hasta el momento, son la teoría de la denervación y el fenómeno de liberación. Los reportes de casos aislados señalan la posibilidad de intervenciones farmacológicas. Sin embargo, asegurar al paciente y tratar la patología visual son las piezas principales del tratamiento, no obstante, se necesitan más investigaciones que permitan aumentar las opciones terapéuticas eficaces.

As population grows, the number of older people with impaired vision does too.That is why ophthalmologists, psychiatrists and neurologists urgently require familiarization with the most important characteristics of Charles Bonnet syndrome. The purpose of this review is to give an update on its clinical aspects, pathophysiology, epidemiology and more reasonable management strategies of this syndrome. Accordingly, we carried out an exhaustive search of the relevant literature, in order to understand these issues. Charles Bonnet syndrome is a sub reported and sub diagnosed entity in visually impaired older people. These patients usually have an intact mental status although some authors claim that may be more common in cases of mild cognitive impairment. Its pathophysiology is still debated but most accepted theories are “the deafferentation theory” and “the phenomenon of liberation”. Isolated case reports point to the possibility of pharmacological interventions, however reassuring the patient and treating visual diseases are the main parts of treatment, more research is needed to allow the possibility of effective treatment options.

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El síndrome de Charles Bonnet se caracteriza por alucinaciones visuales que se presentan en personas con una pérdida de visión severa y, generalmente, enpersonas de edad avanzada, con un estado mental normal. En este artículo se analizan las características de este síndrome, como la etiología, la fisiopatología y el diagnóstico diferencial, y se dan conocer criterios de diagnóstico para tener en cuenta en la práctica diaria, en especial para los optómetras, quedeben estar familiarizados con los signos y síntomas de este síndrome, ya que este grupo de pacientes casi siempre acude primero a la consulta optométrica. Aunque la condición se hizo pública en la comunidad médica hace más de doscientos años atrás, es muy poco diagnosticada por el desconocimiento existente sobre ella. En la práctica optométrica, se debe sospechar del síndrome de Charles Bonnet, especialmente en los grupos de pacientes que presentan alucinaciones visuales y debilidad visual o ceguera, evitando un diagnóstico psiquiátrico equivocado.

The Charles Bonnet Syndrome is characterized by visual hallucinations that occur in people with severe sight loss and usually in elderly people with a normal mental state. This article discusses the characteristics of this syndrome as the etiology, pathophysiology and differential diagnosis, and is known diagnostic criteria for consideration in daily practice. Especially for optometrists be who sould be familiar with the signs and symptoms of this syndrome, as this group of patients almost always come first to consult optometrists. Even though the condition was published in the medical community for over 200 years ago, it has been rarely diagnosed due to the lack of knowledge about it. In optometric practice, it is suspected Charles Bonnet Syndrome especially in this age group with visual hallucinations and visual weakness or blindness, avoiding a psychiatric diagnosis wrong.

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A Odontalgia Atípica (OA) é uma entidade clínica importante, pois a dor é neuropática por desaferentação e ocorre “no dente”, porém não é “dor de dente”. É caracterizada por dor em um dente ou dor em um sítio onde um dente foi extraído, com ausência de sinais clínicos ou radiográficos que acusem uma doença. Muitas vezes por insistência dos pacientes o tratamento endodôntico é realizado, mas não ocorre alívio da dor. Assim, tratamentos invasivos continuam sendo realizados incluindo retratamento endodôntico, apicetomia e finalmente a extração do dente. Sendo uma enfermidade que pode trazer alguma dificuldade diagnóstica para o cirurgião-dentista, o conhecimento de suas características se torna necessário. Deste modo, este artigo apresenta uma revisão de literatura sobre esta entidade, onde são abordados os seguintes tópicos: epidemiologia e sinais clínicos, critérios de diagnóstico, etiologia, diagnóstico diferencial e abordagens terapêuticas.

The Atypical Odontalgia (AO) it is an important clinical entity, because the pain is neuropatic for deafferentation and it happens “in the tooth”, however it is not “toothache.” It is characterized by pain in a tooth or pain in a ranch where a tooth was extracted, with absence of clinical signs or radiographics that accuse a disease. A lot of times for the patients’ insistence the endodontic treatment is accomplished, but it doesn’t happen relief of the pain. Like this, invasives treatments continue being accomplished including endodontic retreatment, apicectomy and finally the extraction of the tooth. Being an illness that can bring some diagnostic difficulty for the surgeon-dentist, the knowledge of their characteristics becomes necessary. This way, this article presents a literature revision on this entity, where the following topics are approached: epidemiology and clinical signs, diagnosis criteria, aetiology, differential diagnosis and therapeutic approaches.

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The present study aimed at understanding the regulation of AMPA-type glutamate receptors (GluRs) and nicotinic acetylcholine receptors (nAChRs) during experimentally-induced neurodegeneration in the chick visual system. Immunohistochemistry, in situ hybridization, and RNAse protection techniques were used to verify the expression of GluR and nAChR subunits at several periods after deafferentation, ranging from 1 to 30 days. The results indicate that GluR1 and 2 expression changes in a biphasic way after deafferentation, decreasing after the shortest survival periods (1-4 days) and increasing afterwards. These effects clearly involve regulation of gene expression, as verified by in situ hybridization and RNAse protection. The regulation of the α2, α4, α5, and β2 nAChR subunits after deafferentation, on the other hand, exhibited a pattern that was exactly the opposite, with an early increase followed by a consistent decrease of expression until 30 days postlesion. Furthermore, nAChR changes were not apparently due to gene expression regulation, but instead by up-regulation/ down-regulation at a protein level. These results suggest that neurotransmitter receptors undergo differential plastic changes after deafferentation in the nervous system and contribute data to their possible role in neurodegeneration and neuroprotection processes.

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