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Currently, transcranial stimulation for CVA treatment is based on the interhemispheric rivalry model. This model has proven to have many anomalies, necessitating a new paradigm. Spontaneous recovery from post-CVA hemiplegia has an ontogenetic pattern. We reanalyzed the 2008 longitudinal London study and found that cortical disinhibition is the mechanism for ontogenetic CVA recovery. We propose that transcranial stimulation with 10 Hz rTMS or anode electrical microstimulation can produce CVA recovery similar to spontaneous recovery. (Acta Med Colomb 2022; 47. DOI:https://doi.org/10.36104/amc.2022.2466).

Actualmente la aplicación de la estimulación transcraneal para el tratamiento del ACV se realiza con base en el modelo de rivalidad interhemisférica. Este modelo ha mostrado muchas anomalías que hacen necesario un nuevo paradigma. La recuperación espontánea de la hemiplejia post-ACV tiene patrón ontogénico. Reanalizamos el estudio longitudinal de Londres 2008 y encontramos que su propuesta corresponde al mecanismo de recuperación ontogénica del ACV. Planteamos que la estimulación transcraneal, utilizando EMTr a 10 Hz o microestimulación eléctrica anódica, podría recuperar el ACV de manera similar a la recuperación espontánea. (Acta Med Colomb 2022; 47. DOI:https://doi.org/10.36104/amc.2022.2466).

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Objective: The purpose of this study was to determine the intra- and interexaminer reliability, concurrent validity, and responsiveness of the applied kinesiology manual muscle test (AK-MMT) to discriminate gluteus medius muscle strength and latency. Methods: A cross-sectional and methodological study was conducted in 38 participants using electromyography, electrogoniometry, and hand-held dynamometry to measure latency, angular displacement, and muscle force during the assessment of the gluteus medius by AK-MMT. Inter- and intrarater reliability of 2 examiners with different levels of experience were obtained using the intraclass correlation coefficient. Muscle force, latency, and joint angular displacement were compared between groups (facilitated vs inhibited). Latency and angular displacement also were compared within groups by using the Wilcoxon paired test. For the concurrent validity of the AK-MMT in classifying an inhibited muscle as weak, the receiver operating characteristic curve was conducted. Results: Intra- and interexaminer reliability for the facilitated vs inhibited classifications based on AK-MMT presented good results, with intraclass correlation coefficient > 0.86. For the inhibited group, force and peak force were significantly lower and joint displacement significantly greater. The receiver operating characteristic curve showed an area under the curve of 0.743, demonstrating that the test has concurrent validity (P = .001) to discriminate muscle force. The Wilcoxon paired test showed a significant delay in latency of the inhibited gluteus medius group (0.10 s vs 0.18 s, P = .007) when compared with the facilitated one. Conclusion: In this study, we found good intra- and interexaminer reliability and concurrent validity for the AK-MMT to determine differences in gluteus medius muscle force. Although the paired data showed a different latency time between groups, the hypothesis of prolonged latency in muscles classified as inhibited by AK-MMT still needs further investigation.

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Abstract A patient with chronic brainstem CVA sequelae received one cycle of magnetic stimulation to treat her dysphagia and serendipitously obtained a minimal improvement in her axial movement. Two additional cycles gave her improved postural control and then distal movement, preceded by a display of ipsilateral and contralateral motor evoked potentials, respectively. Magnetic stimulation at 10 Hertz produces cortical disinhibition and reopens the critical neurodevelop ment periods. The ontogenic pattern of hemiplegia recovery in this patient may be explained by an increased and rejuvenated brain plasticity due to critical period reopening through cortical disinhibition. (Acta Med Colomb 2022; 47. DOI:https://doi.org/10.36104/amc.2022.2253).

Resumen Una paciente con secuelas crónicas de un ACV del tallo cerebral recibió un ciclo de estimulación magnética para el manejo de la disfagia y, por serendipia obtuvo mejoría leve del movimiento axial. Dos ciclos adicionales le permitieron mejoría del control postural y luego la aparición de movimiento distal, precedidos por la visualización de los potenciales evocados motores ipsilateral y contralateral, respectivamente. La estimulación magnética a 10 Hertz produce desinhibición cortical y reabre los periodos críticos del neurodesarrollo. Es posible, que el patrón ontogénico de recuperación de la hemiplejía en esta paciente se explique por el incremento y rejuvenecimiento de la plasticidad cerebral debido a la reapertura de los periodos críticos, por medio de la desinhibición cortical. (Acta Med Colomb 2022; 47. DOI:https://doi.org/10.36104/amc.2022.2253).

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Abstract Stress is a contributing factor to painful temporomandibular disorders (TMD). Nevertheless, the underpinnings of this relationship are not fully understood. Objective To investigate the effects of acute mental stress on conditioned pain modulation (CPM) in TMD patients compared with healthy individuals. Methodology Twenty women with chronic myofascial TMD diagnosed according to the RDC/TMD and 20 age-matched healthy women had the CPM assessed before and after a stressful task using the Paced Auditory Serial Addition Task (PASAT) in a single session. Subjective stress response was assessed with the aid of visual analog scale (VAS). Pressure pain threshold (PPT) on masseter muscle was the test stimulus (TS) and immersion of the participant's hand on hot water was the conditioning stimulus (CS) - CPM-sequential paradigm. Results Healthy individuals reported PASAT are more stressful when compared with TMD patients and the stress task did not affect the CPM in neither group. Nonetheless, a negative correlation was observed between change in CPM and change in TS from baseline to post-stress session, which indicates that the greater the increase in PPT after the stress task, the greater was the decrease in CPM magnitude. The correlation was strong for healthy controls (r=- 0.72, p<0.001) and moderate for TMD patients (r=- 0.44, p=0.047). Conclusions The correlation between the change in CPM and the TS change following the stress task may possibly indicate an overlapping pathway between stress-induced analgesia/hyperalgesia and descending pain inhibition.

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RESUMEN: La percepción del dolor resulta de múltiples y dinámicos mecanismos en el sistema nervioso central (SNC) y periférico que inhiben o facilitan el estímulo y respuesta nociceptiva. Sin embargo, la principal capacidad de modulación esta a cargo del SNC. Los estímulos nociceptivos son detectados por terminaciones nerviosas libres de neuronas periféricas que sinaptan con neuronas aferentes secundarias de la médula espinal. Luego estas fibras decusan para formar las vías nociceptivas ascendentes. Una vez alcanzadas las estructuras subcorticales, se activan las neuronas del tálamo, quienes envían el estímulo hacia la corteza somatosensorial, desencadenando la percepción consciente del dolor y activando el sistema inhibitorio descendente. Para que la modulación nociceptiva se realice, es necesaria la participación de diversas sustancias o neurotransmisores que conectan áreas del SNC especializadas. Por lo tanto, el objetivo de este estudio fue realizar una revisión de la literatura respecto de los mecanismos que participan en los procesos de modulación central del dolor.

SUMMARY: Pain perception results from multiple and dynamic mechanisms in the central nervous system (CNS) and peripheral nervous system that inhibit or facilitate stimulation and nociceptive response. However, neuromodulation is mainly a function of the CNS. Nociceptive stimulus is detected by peripheral neurons receptors that synapse with the secondary afferent neurons of the spinal cord. These fibers cross to conform the ascending nociceptive pathways. Once the subcortical structures are reached, the thalamus`s neurons are activated; the thalamus send the stimulus to the somatosensory cortex, triggering the conscious perception of pain and activating the descending inhibitory system. For the nociceptive modulation to be carried out, the participation of various substances or neurotransmitters that connect specialized CNS areas is necessary. Therefore, the aim of this study was to review the literature regarding the mechanisms involved in central pain modulation processes.

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Background: Diverse forms of long-term potentiation (LTP) have been described, but one of the most investigated is encountered in the glutamatergic synapses of the hippocampal cornu Ammonis (CA1) subfield. However, little is known about synaptic plasticity in wildlife populations. Laboratory animals are extremely inbred populations that have been disconnected from their natural environment and so their essential ecological aspects are entirely absent. Proechimys are small rodents from Brazil's Amazon rainforest and their nervous systems have evolved to carry out specific tasks of their unique ecological environment. It has also been shown that long-term memory duration did not persist for 24-h in Proechimys, in contrast to Wistar rats, when both animal species were assessed by the plus-maze discrimination avoidance task and object recognition test. Methods: In this work, different protocols, such as theta burst, single tetanic burst or multiple trains of high frequency stimulation (HFS), were used to induce LTP in hippocampal brain slices of Proechimys and Wistar rats. Results: A protocol-independent fast decay of early-phase LTP at glutamatergic synapses of the CA1 subfield was encountered in Proechimys. Long-term depression (LTD) and baseline paired-pulse facilitation (PPF) were investigated but no differences were found between animal species. Input/output (I/O) relationships suggested lower excitability in Proechimys in comparison to Wistar rats. Bath application of d-(-)-2-amino-5-phosphonopentanoicacid (D-AP5) and CNQX prevented the induction of LTP in both Proechimys and Wistar. However, in marked contrast to Wistar rats, LTP induction was not facilitated by the GABAA antagonist in the Amazon rodents, even higher concentrations failed to facilitate LTP in Proechimys. Next, the effects of GABAA inhibition on spontaneous activity as well as evoked field potentials (FPs) were evaluated in CA1 pyramidal cells. Likewise, much lower activity was detected in Proechimys brain slices in comparison to those of the Wistar rats. Conclusions: These findings suggest a possible high inhibitory tone in the CA1 network mediated by GABAA receptors in the Amazon rodents. Currently, neuroscience research still seeks to reveal molecular pathways that control learning and memory processes, Proechimys may prove useful in identifying such mechanisms in complement to traditional animal models.

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