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Our aim was to clarify the incidence and risk of acute symptomatic seizures in people with coronavirus disease 2019 . This multicenter retrospective study enrolled people with COVID-19 from January 18 to February 18, 2020 at 42 government-designated hospitals in Hubei province, the epicenter of the epidemic in China; Sichuan province; and Chongqing municipality. Data were collected from medical records by 11 neurologists using a standard case report form. A total of 304 people were enrolled, of whom 108 had a severe condition. None in this cohort had a known history of epilepsy. Neither acute symptomatic seizures nor status epilepticus was observed. Two people had seizurelike symptoms during hospitalization due to acute stress reaction and hypocalcemia, and 84 (27%) had brain insults or metabolic imbalances during the disease course known to increase the risk of seizures. There was no evidence suggesting an additional risk of acute symptomatic seizures in people with COVID-19. Neither the virus nor potential risk factors for seizures seem to be significant risks for the occurrence of acute symptomatic seizures in COVID-19. K E Y W O R D Sacute symptomatic seizures, COVID-19, epilepsy, SARS-CoV-2 2 | LU et aL.

Expression of bone morphogenetic protein 4 (BMP4) in adipocytes of white adipose tissue (WAT) produces "white adipocytes" with characteristics of brown fat and leads to a reduction of adiposity and its metabolic complications. Although BMP4 is known to induce commitment of pluripotent stem cells to the adipocyte lineage by producing cells that possess the characteristics of preadipocytes, its effects on the mature white adipocyte phenotype and function were unknown. Forced expression of a BMP4 transgene in white adipocytes of mice gives rise to reduced WAT mass and white adipocyte size along with an increased number of a white adipocyte cell types with brown adipocyte characteristics comparable to those of beige or brite adipocytes. These changes correlate closely with increased energy expenditure, improved insulin sensitivity, and protection against diet-induced obesity and diabetes. Conversely, BMP4-deficient mice exhibit enlarged white adipocyte morphology and impaired insulin sensitivity. We identify peroxisome proliferator-activated receptor gamma coactivator 1-α (PGC1α) as the target of BMP signaling required for these brown fat-like changes in WAT. This effect of BMP4 on WAT appears to extend to human adipose tissue, because the level of expression of BMP4 in WAT correlates inversely with body mass index. These findings provide a genetic and metabolic basis for BMP4's role in altering insulin sensitivity by affecting WAT development.oth white adipose tissue (WAT) and brown adipose tissue (BAT) function in the energy homeostasis of humans and other mammals. WAT stores energy in form of triglycerides during periods of excessive caloric intake for later use when energy demand exceeds intake (1). In contrast, brown adipose tissue (BAT) uses "stored triglycerides" to generate energy in the form of heat, most notably when environmental temperature falls (2).The excessive accumulation of body fat in WAT is the result of both hypertrophy and hyperplasia of white adipocytes (3). Such changes give rise to insulin resistance, type-2 diabetes, and an inflammatory response, thus implicating white adipocytes in the etiology of these conditions (4, 5). In contrast, promotion of BAT activities helps prevent genetic obesity, insulin resistance, and diabetes (6).Unlike the expansive mass of brown adipocytes in the interscapular region, brown adipose tissue mass in the normal adult human is proportionally smaller and previously was believed to be functionally less important. Recently, however, by using [18F]-2-fluoro-D-2-deoxy-D-glucose PET, metabolically active regions were detected in the cervical, supraclavicular, axillary, and paravertebral regions of adult human subjects (7-9). The metabolically active areas were found to consist of an admixture of brown-like adipocytes in WAT (10) which increase dramatically following cold exposure or treatment with antidiabetic drugs, thiazolidinediones, or adrenergic activators (11-13). These cells recently have been designated as "beige" (14) or "brite" (15, 16) cells derived from ...

Objective:To investigate new-onset neurologic impairments associated with coronavirus disease 2019 (COVID-19).Methods:A retrospective multicenter cohort study conducted between 18 January and 20 March 2020 including people with confirmed COVID-19 from 56 hospitals officially designated in three Chinese regions; data were extracted from medical records. New-onset neurologic events as assessed by neurology consultants based on manifestations, clinical examination and investigations, in which critical events included disorders of consciousness, stroke, CNS infection, seizures and status epilepticus.Results:We enrolled 917 people with average age 48.7 years and 55% were male. The frequency of new onset critical neurologic events was 3.5% (32/917) overall and 9.4% (30/319) among those with severe or critical COVID-19. These were impaired consciousness (n=25) or/and stroke (n=10). The risk of critical neurologic events was highly associated with age above 60 years and previous history of neurological conditions. Non-critical events were seen in less than 1% (7/917), including muscle cramp, unexplained headache, occipital neuralgia, tic and tremor. Brain CT in 28 people led to new findings in nine. Findings from lumbar puncture in three with suspected CNS infection, unexplained headache or severe occipital neuralgia were unremarkable.Conclusions:People with COVID-19 aged over 60 and neurologic comorbidities were at higher risk of developing critical neurologic impairment, mainly impaired consciousness and cerebrovascular accidents. Brain CT should be considered when new-onset brain injury is suspected, especially in people under sedation or showing an unexplained decline in consciousness. Evidence of direct acute insult of SARS-COV-2 to the CNS is still lacking.