Olfactory dysfunction (OD) is a recognized symptom of the severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) and is independently associated with neurodegenerative disorders. Moreover, the central nervous system manifestations in patients infected with the coronavirus‐2019 (COVID‐19) have demonstrated cognitive decline and neuropsychiatric manifestations. Hence, OD in COVID‐19 necessitates perusal of its mechanism and available treatment options to avert possible development of neurocognitive sequelae of the pandemic. The article presents a literature review organized from the published information about olfactory training (OT) for OD during COVID‐19. The methodology comprised retrieval of available literature from database searches and subsequent scrutinization of relevant information. Inferentially, injury to the sustentacular cells, possessing angiotensin‐converting enzyme 2 (ACE‐2) receptors, is an important mechanism causing OD in COVID‐19. Olfactory dysfunction may be prolonged in severe cases of anosmia predisposing to neurodegenerative and cognitive impairment in COVID‐19 infection. Olfactory training demonstrates an effective treatment for OD based on human and animal‐derived evidence through recent studies. It curtails the progression of OD, besides inducing neural rearrangement and changes in functional connectivity in patients receiving OT. Additionally, contemporary reports support that the administration of OT for COVID‐induced anosmia is effective and encompasses no significant adverse effects. The present review highlights the prominence of olfactory training as a recommended intervention for OD in COVID‐19. This review can guide the clinicians in curbing neurological repercussions of COVID besides enhancing cognitive rehabilitation through olfactory training.
Background. Migraine headache may have a substantial bearing on the brain functions and rhythms. Electrophysiological methods can detect changes in brain oscillation. The present work examined the frequency band power through quantitative electroencephalogram (qEEG) and density spectral array (DSA) to elucidate the resting state neuronal oscillations in migraine. Methods. Clinical details were inquired, and EEG was recorded in migraineurs and healthy controls. The acquired data were analyzed to determine power spectral density values and obtain DSA graphs. The absolute and relative powers for the alpha, theta, and delta frequencies in frontocentral, parieto-occipital, and temporal regions were determined. A correlation of significant EEG findings with clinical features of migraine was sought. Results. Forty-five participants were enrolled in the study. The spectrum analysis revealed an increase in the relative theta power ( P < .001) and a reduction in relative alpha power ( P < .001) in the observed cortical areas among the migraineurs as compared to the healthy controls. Relative delta power was increased over the frontocentral region ( P = .001), slightly more on the symptomatic side of the head. In addition, frontocentral delta power had a moderate positive correlation (r = .697, n = 22, P = .000) with migraine severity. Conclusion. The study supports the evidence of a neuronal dysfunction existing in the resting state during the ictal phase of migraine. qEEG can reveal these aberrant oscillations. Utility of DSA to depict the changes in brain activity in migraine is a potential area for research. The information can help formulate new therapeutic strategies towards alteration in cortical excitability using brain stimulation techniques.
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