Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can affect any part of the neuraxis. Many neurological conditions have been attributed to be caused by SARS-CoV-2, namely encephalopathy (acute necrotizing encephalopathy and encephalopathy with reversible splenial lesions), seizures, stroke, cranial nerve palsies, meningoencephalitis, acute disseminated encephalomyelitis (ADEM), transverse myelitis (long and short segment), Guillain-Barré syndrome (GBS) and its variants, polyneuritis cranialis, optic neuritis (ON), plexopathy, myasthenia gravis (MG), and myositis. The pathophysiology differs depending on the time frame of presentation. In patients with concomitant pulmonary disease, for instance, acute neurological illness appears to be caused by endotheliopathy and cytokine storm. Autoimmunity and molecular mimicry are causative for post-coronavirus disease 2019 (COVID-19)-sequelae. It has not yet been shown that the virus can penetrate the central nervous system (CNS) directly. This review aims to describe the disease and root pathogenic cause of the various neurological manifestations of COVID-19. We searched Pubmed/Medline and Google Scholar using the keywords “SARS-CoV-2” and “neurological illness” for articles published between January 2020 and November 2022. Then, we used the SWIFT-Review (Sciome LLC, North Carolina, United States), a text-mining workbench for systematic review, to classify the 1383 articles into MeSH hierarchical tree codes for articles on various parts of the nervous system, such as the CNS, peripheral nervous system, autonomic nervous system, neuromuscular junction, sensory system, and musculoskeletal system. Finally, we reviewed 152 articles in full text. SARS-CoV-2 RNA has been found in multiple brain areas without any histopathological changes. Despite the absence of in vivo virions or virus-infected cells, CNS inflammation has been reported, especially in the olfactory bulb and brain stem. SARS-CoV-2 genomes and proteins have been found in affected individuals’ brain tissues, but corresponding neuropathologic changes are seldom found in these cases. Additionally, viral RNA can rarely be identified in neurological patients’ CSF post hoc SARS-CoV-2 infection. Most patients with neurological symptoms do not have active viral replication in the nervous system and infrequently have typical clinical and laboratory characteristics of viral CNS infections. Endotheliopathy and the systemic inflammatory response to SARS-CoV-2 infection play a crucial role in developing neuro-COVID-19, with proinflammatory cytokine release mediating both pathological pathways. The systemic inflammatory mediators likely activate astrocytes and microglia across the blood-brain barrier, indirectly affecting CNS-specific immune activation and tissue injury. The management differs according to co-morbidities and the neurological disorder.

The coronavirus pandemic brought with it a wide range of clinical presentations. Earlier, the respiratory symptoms comprised most of the clinical picture. However, as more and more people got infected, many atypical presentations came into the limelight, especially the neurological manifestations. Spinal cord complications are widely reported, with COVID-19 associated myelitis constituting a big part. Through this report, we bring you a series of cases of COVID-19 associated myelitis to add to the already available data. We report four patients, two of whom developed longitudinally extensive myelitis (three or more vertebral segments). The other two suffered from multisegmented short-segment myelitis (less than three vertebral segments). COVID-19 myelitis can be seen during COVID-19 illness and post COVID. We aim to familiarize the medical community with this entity so that there is a minimum delay between the onset of the symptoms in the patient and the management of this complication, as the treatment is often gratifying.

Insular seizure is a rare entity. Insular spikes spread to the temporal, parietal, and frontal lobes and clinically manifest with seizure semiology specific to these areas. We report the case of a 19-year-old male patient who presented with complaints of left-sided hemimotor tonic-clonic focal seizures of the limbs occurring three times per day. Neuroimaging showed cortical-subcortical right posterior insular cortex hyperintensities on fluid-attenuated inversion recovery (FLAIR) sequence and T2-weighted MRI with no significant diffusion restriction on apparent diffusion coefficient (ADC) and no post-contrast enhancement, suggesting focal cortical dysplasia of right posterior insular cortex. Electroencephalogram (EEG) showed right frontal epileptiform activity with secondary bilateral synchrony. The patient's atypical hemimotor tonic-clonic focal seizure, the conventional video EEG showing right frontal spikes synchronizing with bilateral temporal ictal spikes, and insular cortical dysplasia on MRI led us to a diagnosis of insular epilepsy.

Hyperbaric oxygenation or hyperbaric oxygen therapy (HBOT) has a spectrum of applications in the clinical setting. It is used non-empirically in pain management, hypoxic encephalopathy and critical post-cardiac arrest care. Clinical outcome improvement varies case-by-case. We reviewed the literature for etiologies of neurological causes of chronic pain and role of HBOTin the management of chronic pain in these conditions

The location of single strategic infarcts and the cognitive impairment after a stroke reect the neuroanatomy of the brain's cognitive functions. Poststroke dementia or post-stroke cognitive impairment (PSD/PSCI) is a form of cognitive disturbance caused by cerebrovascular disease that can manifest at different times after a stroke, including during the acute phase of stroke, during the recovery phase (while motor stroke symptoms improve), or months and years later. The onset of cognitive impairment depends on the location of infarct. Infarct in certain locations have cognitive impairment as a sole presentation from the outset. Infarcts in the left frontotemporal lobes, right parietal lobe, and left thalamus are notably correlated with cognitive impairment following a stroke. In the former, patients present with complains of motor difculties as the main complain. In addition to these locations, vascular lesions in the thalamo-perforating area of the PCAmay cause dementia and other forms of severe memory loss. Abaseline (pre-morbid) and early post-stroke (early post-morbid) cognitive status should be evaluated and a protocol for the same is needed in regular clinical and ICU care facilities. MoCA assessment is commonly used for cognitive assessment. Its role in strategic infarcts is undermined as it leaves out the evaluation of symptoms corresponding to common strategic infarct locations such as the medial temporal lobe and thalami. There is a need for dedicated neuropsychological assessment score based on education level, and native-language for PSCI.