Although severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) predominantly infects the respiratory system, several investigations have shown the involvement of the central nervous system (CNS) along the course of the illness, with encephalitis being one of the symptoms. The objective of this systematic review was to evaluate the characteristics (clinical, neuro-radiological aspects, and laboratory features) and outcomes of encephalitis in COVID-19 patients. PubMed, Scopus, and Google Scholar databases were searched from 1 December 2019 until 21 July 2022 to identify case reports and case series published on COVID-19 associated with encephalitis. The quality of the included studies was assessed by the Joanna Briggs Institute critical appraisal checklists. This systematic review included 79 studies, including 91 COVID-19 patients (52.7% male) experiencing encephalitis, where 85.6% were adults (49.3 ± 20.2 years), and 14.4% were children (11.2 ± 7.6 years). RT-PCR was used to confirm 92.2% of the COVID-19 patients. Encephalitis-related symptoms were present in 78.0% of COVID-19 patients at the time of diagnosis. In these encephalitis patients, seizure (29.5%), confusion (23.2%), headache (20.5%), disorientation (15.2%), and altered mental status (11.6%) were the most frequently reported neurologic manifestations. Looking at the MRI, EEG, and CSF findings, 77.6%, 75.5%, and 64.1% of the patients represented abnormal results. SARS-CoV-2-associated or -mediated encephalitis were the most common type observed (59.3%), followed by autoimmune encephalitis (18.7%). Among the included patients, 66.7% were discharged (37.8% improved and 28.9% fully recovered), whereas 20.0% of the reported COVID-19-positive encephalitis patients died. Based on the quality assessment, 87.4% of the studies were of high quality. Although in COVID-19, encephalitis is not a typical phenomenon, SARS-CoV-2 seems like a neuropathogen affecting the brain even when there are no signs of respiratory illness, causing a high rate of disability and fatality.

Following brain injury, development of hippocampal sclerosis often led to the temporal lobe epilepsy which is sometimes resistant to common anti-epileptic drugs. Cellular and molecular changes underlying epileptogenesis in animal models were studied, however, the underlying mechanisms of kainic acid (KA) mediated neuronal damage in rat hippocampal neuron cell culture alone has not been elucidated yet. Embryonic day 18 (E-18) rat hippocampus neurons were cultured with poly-L-lysine coated glass coverslips. Following optimisation, KA (0.5 μM), a chemoconvulsant agent, was administered at three different time-points (30, 60 and 90 min) to induce seizure in rat hippocampal neuronal cell culture. We examined cell viability, neurite outgrowth density and immunoreactivity of the hippocampus neuron culture by measuring brain derived neurotrophic factor (BDNF), γ-amino butyric acid A (GABAA) subunit α-1 (GABRA1), tyrosine receptor kinase B (TrkB), and inositol trisphosphate receptor (IP3R/IP3) levels. The results revealed significantly decreased and increased immunoreactivity changes in TrkB (a BDNF receptor) and IP3R, respectively, at 60 min time point. The current findings suggest that TrkB and IP3 could have a neuroprotective role which could be a potential pharmacological target for anti-epilepsy drugs.

Visual cognitive function is important to build up executive function in daily life. Perception of visual Number form (e.g., Arabic digit) and numerosity (magnitude of the Number) is of interest to cognitive neuroscientists. Neural correlates and the functional measurement of Number representations are complex occurrences when their semantic categories are assimilated with other concepts of shape and colour. Colour perception can be processed further to modulate visual cognition. The Ishihara pseudoisochromatic plates are one of the best and most common screening tools for basic red-green colour vision testing. However, there is a lack of study of visual cognitive function assessment using these pseudoisochromatic plates. We recruited 25 healthy normal trichromat volunteers and extended these studies using a 128-sensor net to record event-related EEG. Subjects were asked to respond by pressing Numbered buttons when they saw the Number and Non-number plates of the Ishihara colour vision test. Amplitudes and latencies of N100 and P300 event related potential (ERP) components were analysed from 19 electrode sites in the international 10-20 system. A brain topographic map, cortical activation patterns and Granger causation (effective connectivity) were analysed from 128 electrode sites. No major significant differences between N100 ERP components in either stimulus indicate early selective attention processing was similar for Number and Non-number plate stimuli, but Non-number plate stimuli evoked significantly higher amplitudes, longer latencies of the P300 ERP component with a slower reaction time compared to Number plate stimuli imply the allocation of attentional load was more in Non-number plate processing. A different pattern of asymmetric scalp voltage map was noticed for P300 components with a higher intensity in the left hemisphere for Number plate tasks and higher intensity in the right hemisphere for Non-number plate tasks. Asymmetric cortical activation and connectivity patterns revealed that Number recognition occurred in the occipital and left frontal areas where as the consequence was limited to the occipital area during the Non-number plate processing. Finally, the results displayed that the visual recognition of Numbers dissociates from the recognition of Non-numbers at the level of defined neural networks. Number recognition was not only a process of visual perception and attention, but it was also related to a higher level of cognitive function, that of language.

Background: Previous studies from animal models have shown that pre-synaptic NMDA receptors (preNMDARs) are present in the cortex, but the role of inhibition mediated by preNMDARs during epileptogenesis remains unclear. In this study, we wanted to observe the changes in GABAergic inhibition through preNMDARs in sensory-motor and visual cortical pyramidal neurons after pilocarpine-induced status epilepticus. Methods: Using a pilocarpine-induced epileptic mouse model, sensory-motor and visual cortical slices were prepared, and the whole-cell patch clamp technique was used to record spontaneous inhibitory post-synaptic currents (sIPSCs). Results: The primary finding was that the mean amplitude of sIPSC from the sensory-motor cortex increased significantly in epileptic mice when the recording pipette contained MK-801 compared to control mice, whereas the mean sIPSC frequency was not significantly different, indicating that post-synaptic mechanisms are involved. However, there was no significant presynaptic inhibition through preNMDARs in the acute brain slices from pilocarpine-induced epileptic mice. Conclusion: In the acute case of epilepsy, a compensatory mechanism of post-synaptic inhibition, possibly from ambient GABA, was observed through changes in the amplitude without significant changes in the frequency of sIPSC compared to control mice. The role of preNMDAR-mediated inhibition in epileptogenesis during the chronic condition or in the juvenile stage warrants further investigation.