Coronavirus disease 2019 (COVID-19) is a highly infectious pandemic caused by a novel coronavirus called severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). It frequently presents with unremitting fever, hypoxemic respiratory failure, and systemic complications (e.g., gastrointestinal, renal, cardiac, and hepatic involvement), encephalopathy, and thrombotic events. The respiratory symptoms are similar to those accompanying other genetically related beta-coronaviruses (CoVs) such as severe acute respiratory syndrome CoV (SARS-CoV) and Middle East Respiratory Syndrome CoV (MERS-CoV). Hypoxemic respiratory symptoms can rapidly progress to Acute Respiratory Distress Syndrome (ARDS) and secondary hemophagocytic lymphohistiocytosis, leading to multi-organ system dysfunction syndrome. Severe cases are typically associated with aberrant and excessive inflammatory responses. These include significant systemic upregulation of cytokines, chemokines, and pro-inflammatory mediators, associated with increased acute-phase proteins (APPs) production such as hyperferritinemia and elevated C-reactive protein (CRP), as well as lymphocytopenia. The neurological complications of SARS-CoV-2 infection are high among those with severe and critical illnesses. This review highlights the central nervous system (CNS) complications associated with COVID-19 attributed to primary CNS involvement due to rare direct neuroinvasion and more commonly secondary CNS sequelae due to exuberant systemic innate-mediated hyper-inflammation. It also provides a theoretical integration of clinical and experimental data to elucidate the pathogenesis of these disorders. Specifically, how systemic hyper-inflammation provoked by maladaptive innate immunity may impair neurovascular endothelial function, disrupt BBB, activate CNS innate immune signaling pathways, and induce parainfectious autoimmunity, potentially contributing to the CNS complications associated with SARS-CoV-2 infection. Direct viral infection of the brain parenchyma causing encephalitis, possibly with concurrent neurovascular endotheliitis and CNS renin angiotensin system (RAS) dysregulation, is also reviewed.

Hippocampal atrophy and a history of absence of generalized tonic clonic seizures were the sole predictors of 2-year remission, and only for medial temporal resections.

A substantial proportion of localization-related epilepsy may not become clearly intractable for many years after onset. This is especially true of epilepsy of childhood and early adolescent onset. If prospective studies confirm these findings and the underlying mechanisms behind these associations become understood, this raises the possibility of considering interventions that might interrupt such a process and some day prevent some forms of epilepsy from becoming intractable.

Summary: Purpose: To determine the intracranial EEG features responsible for producing the various ictal scalp rhythms, which we previously identified in a new EEG classification for temporal lobe seizures.Methods: In 24 patients, we analyzed simultaneous intracranial and surface ictal EEG recordings (64 total channels) obtained from a combination of intracerebral depth, subdural strip, and scalp electrodes.Results: Four of four patients with Type 1 scalp seizure patterns had mesial temporal seizure onsets. However, discharges confined to the hippocampus produced no scalp EEG rhythms. The regular 5-to 9-Hz subtemporal and temporal EEG pattern of Type l a seizures required the synchronous recruitment of adjacent inferolateral temporal neocortex. Seizure discharges confined to the mesiobasal temporal cortex produced a vertex dominant rhythm (Type lc) due to the net vertical orientation of dipolar sources located there. Ten of 13 patients with Type 2 seizures had inferolateral or lateral, temporal neocortical seizure onsets. Initial cerebral ictal activity was typically a focal or regional, low voltage, fast rhythm (20-40 Hz) that was often associated with widespread background flattening. Only an attenuation of normal rhythms was reflected in scalp electrodes. Irregular 2-to 4-Hz cortical ictal rhythms that commonly followed resulted in a comparably slow and irregular scalp EEG pattern (Type 2a). Type 2C seizures showed regional, periodic, 1-to 4-Hz sharp waves following intracranial seizure onset. Seven patients had Type 3 scalp seizures, which were characterized by diffuse slowing or attenuation of background scalp EEG activity. This resulted when seizure activity was confined to the hippocampus, when there was rapid seizure propagation to the contralateral temporal lobe, or when cortical ictal activity failed to achieve widespread synchrony.Conclusions: Type 1, 2, and 3 scalp EEG patterns of temporal lobe seizures are not a reflection of cortical activity at seizure onset. Differences in the subsequent development, propagation, and synchrony of cortical ictal discharges produce the characteristic scalp EEG rhythms. Key Words: EEG (intracrania1)-ECoG-EpilepsySeizures-Temporal lobe.Several studies report ictal scalp EEG to be reliable in localizing the side of seizure origin in patients with temporal lobe epilepsy being evaluated for surgery (1,2). However, scalp EEG patterns are usually not considered to be specific enough to localize seizure onsets to sublobar regions within the temporal lobe. The distinction between seizures that arise from mesial temporal structures versus lateral temporal cortex, for example, is clinically important, because patients with the former will often have their seizures eliminated by standard temporal lobectomies, whereas patients with neocortical disease may need invasive monitoring to tailor a resection (3).Accepted January 24, 1997. Address correspondence and reprint requests to Dr. J. S. Ebersole at Neurology Service, VA Medical Center, West Haven, CT 06516, U.S.A.We developed ...