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Objetivo: Describir la fisiopatología de las manifestaciones neurológicas por infección con COVID-19. Método: Revisión sistemática de 22 articulos relacionados con el objetivo de investigación, procedentes de la base de datos PubMed. Resultados: Dentro de las manifestaciones clínicas del COVID-19 en el SNP, se hallaron en los reportes clínicos, disminución parcial de la capacidad de percibir olores, denominada hiposmia y reducción total de la misma, denominada anosmia, así mismo otros pacientes o en los mismos que reportaron el anterior síntoma, refirieron haber perdido la capacidad para distinguir sabores, así la hipogeusia, y la ageusia también iban de la mano con la hiposmia. Conclusión: Se ha demostrado que el SARS-CoV-2 tiene un tropismo por las células del sistema nervioso, lo cual significaría una afectación al sistema nervioso que demás puede ser afectado por la tormenta de citoquinas, que a su vez pueden desarrollar un daño directo al parénquima neuronal.
Objective: To describe the pathophysiology of neurological manifestations due to infection with COVID-19. Methods: Systematic review of 22 articles related to the research objective, from the PubMed database. Results: Among the clinical manifestations of COVID-19 in the PNS, in the clinical reports, partial reduction of the ability to perceive odors, called hyposmia and total reduction of the same, called anosmia, as well as other patients or in the same patients who reported the previous symptom, reported having lost the ability to distinguish flavors, thus hypogeusia and ageusia also went hand in hand with hyposmia. Conclusion: SARS-CoV-2 has been shown to have a tropism for nervous system cells, which would mean an affectation to the nervous system that can be further affected by the cytokine storm, which in turn can develop direct damage to the neuronal parenchyma.
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Objective To establish a multi-drug resistant model of temporal lobe epilepsy,and to observe the changes of γ-aminobutyric acid (GABA) receptor expression in the hippocampal tissues so as to explore its effects in pharmacoresistant epileptogenesis.Methods One hundred rats were selected to prepare the amygdaloid kindled model of epilepsy by chronic stimulation of amygaloid basal lateral nucleus.After the kindled model of epilepsy was prepared successfully(n =52),pharmacoresistant epileptic rats were selected according to their response to the phenobabital and phenytoin.The selected pharmacoresistant epileptic rats (n =8)were sacrificed and the hippocampus was removed to determine the GABA receptor expression,and the same number of pharmacosensitive epileptic rats was used as control.Results The pharmacoresistant epileptic rats displayed degenerative and necrotic hippocampal neurons.The arrangement of hippocampal neurons was disordered,and the structural characteristics of the arrangement of the hippocampal neurons disappeared.The gray values of GABAA-positive neurons in the hippocampal tissues (141.15 ± 14.72) increased significantly compared with the pharmacosensitive epileptic rats (92.56 ± 5.17; t =3.380,P =0.006).Western blot method demonstrated that the band of GABAA became narrowed and thin.The relative quantity of GABAA in the hippocampal tissues (0.38 ± 0.08) decreased significantly as compared with the pharmacosensitive epileptic rats (0.88 ± 0.18).A significant difference was observed (t =5.420,P =0.002).Conclusions GABA receptor expression might be decreased in the hippocampal tissues of pharmacoresistant epileptic rats.It might play a certain role in the formation of pharnmacoresistant epilepsy.
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Objective To establish a multi-drug resistant model of temporal lobe epilepsy,and then the sodium current of pyramidal neurons in CA1 areas of the hippocampus was used as as index to observe the effect of hippocampal stimulation on pharmacoresistant epileptic rats.Methods Eighty Wistar rats were selected to prepare an amygdaloid kindled model of epilepsy by chronic stimulation of amygaloid basal lateral nucleus.When the kindled model of epilepsy was prepared successfully,the pharmacoresistant epileptic rats were selected according their response to phenobabital and phenytoin.The selected pharmacoresistant epileptic rats were divided into a hippocampal stimulation group (HS group) and a pharmacoresistant control group (PR group).A low-frequency hippocampal stimulation was performed in the HS group,while the PR group received sham stimulation.The whole-cell recording technique by patch-clamp was used to observe the changes of sodium current of hippocampal pyramidal neurons after the hippocampal stimulation.Results Compared with the PR group,the pharmacoresistant epileptic rats in HS group underwent low-frequency stimulation for 2 weeks showed that the amygdale stimulus-induced seizures were decreased (2.32 ± 0.38 in HS group and 4.45 ± 0.42 in PR group,t =84.600,P =0.000) and the parameters of the after-discharges were improved significantly.In HS group,the peak current shifted towards depolarization,the sodium channels were difficult to activate,and were more susceptible to inactivation.Moreover,the recovery time after the sodium channel inactivation was slower in HS group ((17.9 ±0.6) s) than in PR group((16.3 +0.3) s,t =-25.420,P =0.000).Conclusions Hippocampal stimulation may inhibit the sodium channel current of pyramidal neurons in CA1 areas of hippocampus.The mechanism of hippocampal stimulation in the treatment of pharmacoresistant epilepsy might be achieved partly by inhibiting the sodium channel current so as to decrease the excitability of hippocampal neurons.
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Objective To investigate whether there are different effects of electric stimulation of vagus nerve,peripheral nerve(sciatic nerve and trigeminal nerve),and motor cortex on pentylenetetrazol (PTZ)induced convulsion in rats.Methods The vagus nerve and sciatic nerve were exposed in rats.The stimulation electrodes were placed on the vagus nerve,sciatic nerve,trigeminal nerve,and motor cortex,respectively.After electric stimulation,PTZ(50 mg/kg)was intraperitoneally injected into the rats.The pattern and latency of the convulsion seizure were observed and recorded.Results Racine's grade Ⅰ-Ⅴ grade convulsion seizure Was present in 9 rats(9/10)in the control group after the injection of PTZ.However,this intensity Was reduced to Ⅰ-Ⅲ grade differentially in all the rats by electric stimulation of the vagus nerve(5/10)or peripheral nerve(6/10 and 5/10).Furthermore,in the group of rats stimulated at motor cortex,there Was completely no convulsion.On the other hand,when pathological changes appeared in cortex or hippocampus(i.e.epileptic model was set up by 7 weeks stimulation),the same stimulation of motor cortex was not able to inhibit the convulsion seizure induced by injection of PTZ and all these rats showed Ⅳ-Ⅴ grade seizure(10/10).Conclusions In physiological condition,all of the four types of stimulation differentially reduced intensity of convulsion seizure triggered by PIZ injection and motor cortex stimulation has the best effect.However.when rats were in pathological status and epileptic nidus appeared in their brains.stimulatiion of motor cortex has no effect on PTZ induced convulsion seizure.
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Objective To investigate the dynamic changes of adenosine receptors, A1 (A1R) and A2a (A2aR) in the brain from the acute to chronic phase after kindling and to explore the correlation between seizure and expression level of A1R and A2aR. MethodsRats were randomly selected into the testing model, reference and normal control groups.Testing rats were kindled by lithium choride-pilocarpine, reference rats were treated with saline, and no treatment was given in normal control group. The dynamic expression of A1R and A2aR were detected by RT-PCR, immunofluorescence staining and Western blot at time-points of 24 hours, 1 month and 6 months post-kindling. Results In the acute phase of 24 hours after kindling, the A1R expression level (mRNA level was (1. 1483 ±0. 1182); Western blot result was ( 0. 7872± 0. 0621 ) ; immunofluorescence staining count was ( 76. 17 ± 4. 62 )/HP) was increased and A2aR (mRNA level was (0. 8338±0. 0572) ; Western blot result was (0. 2098 ±0. 0257) ; immunofluorescence staining count was (43. 83 ± 5. 12 )/HP) was decreased.The results showed statistically difference compared with the reference and normal groups (P< 0. 05 ). In the later chronic phase of 1 month and 6 months after kindling, the expression level of A1R was decreased and A2aR was increased. These data revealed statistically significant difference (P <0. 01 ). Furthermore, the comparison of the results in 1 month and 6 months after kindling found that the expression of AIR was lower in 6 months (mRNA level was (0. 5682 ±0. 0443) ; Western blot result was (0. 7749 ±0. 0262) ; immunofluorescence staining count was (38. 50 ±4. 81 )/HP) than in 1 month and that of A2aR was higher in 6 months (mRNA level was (1. 2169±0. 0332) ; Western blot result was (0. 7080 ±0. 0371 ); immunofluorescence staining count was (114. 50 ± 4. 04)/HP). The differences were statistical significant (t = - 19. 02--13.28, P < 0. 05). ConclusionsThe expressions of A1R and A2AR during and after kindling presents a bidirectional change. In the acute phas the expression of AR is regulated to suppress seizures. While in the chronic phase, the repeated seizures result in the change of A1R and A2aR expression in the opposite direction. This mechanism plays an important role in refractory seizures.