Background Cognitive manifestations associated with the severity of a novel coronavirus (COVID-19) infection are unknown. An early detection of neuropsychological manifestations could modify the risk of subsequent irreversible impairment and further neurocognitive decline. Methods In our single-center cohort study, we included all consecutive adult patients, aged between 20 and 60 years old with confirmed COVID-19 infection. Neuropsychological assessment was performed by the same trained neuropsychologist from April, 22nd through June 16th, 2020. Patients with previous known cognitive impairment, any central nervous system or psychiatric disease were excluded. Demographic, clinical, pharmacological and laboratory data were extracted from medical records. Results Thirty-five patients met inclusion criteria and were included in the study. Patients presenting headache, anosmia, dysgeusia, diarrhea and those who required oxygen therapy had lower scores in memory, attention and executive function subtests as compared to asymptomatic patients. Patients with headache and clinical hypoxia scored lower in the global Cognitive Index (P ​= ​0.002, P ​= ​0.010). A T score lower than 30 was observed in memory domains, attention and semantic fluency (2 [5.7%]) in working memory and mental flexibility (3 [8.6%]) and in phonetic fluency (4 [11.4%]). Higher scores in anxiety and depression (P ​= ​0.047, P ​= ​0.008) were found in patients with cognitive complaints. Conclusions In our cohort of COVID-19 patients neurologic manifestations were frequent, including cognitive impairment. Neurological symptoms during infection, diarrhea and oxygen therapy were risk factors for neurocognitive impairment. Cognitive complaints were associated with anxiety and depression.

A 69-year-old otherwise healthy woman presented to our clinic with irradiated cervical pain, imbalance, and motor weakness and numbness in the left hand, which had been ongoing for 7 days. Eight days before the onset of these symptoms, she had fever and dry cough. On admission, her neurologic examination showed right facial and left hand hypoesthesia, subtle left hand interosseous weakness, and general hyperreflexia. MRI of the brain was normal, whereas spinal cord images (figure 1, A and D) showed T2hyperintensity extending from the medulla oblongata to C7, involving most of the cord with diffuse patchy enhancing lesions, suggesting acute transverse myelitis. Extensive diagnostic workup was performed, showing negative results in blood test for infectious, autoimmune diseases (including myelin oligodendrocyte glycoprotein and aquaporin-4 antibodies), and other potential causes such as vitamin deficits or antiphospholipid syndrome.

The new criteria increase the estimates, but NMOSD remains as a rare disease. The differences in age- and sex-specific estimates highlight the importance of the serologic classification.

Background and Purpose— Remote parenchymal hemorrhage (rPH) after intravenous thrombolysis with recombinant tissue-type plasminogen activator may be associated with cerebral amyloid angiopathy, although supportive data are limited. We aimed to investigate risk factors of rPH after intravenous thrombolysis with recombinant tissue-type plasminogen activator. Methods— This is an observational study of patients with ischemic stroke who were treated with intravenous thrombolysis with recombinant tissue-type plasminogen activator and were included in a multicenter prospective registry. rPH was defined as any extraischemic hemorrhage detected in the follow-up computed tomography. We collected demographic, clinical, laboratory, radiological, and outcome variables. In the subset of patients who underwent a magnetic resonance imaging examination, we evaluated the distribution and burden of cerebral microbleeds, cortical superficial siderosis, leukoaraiosis, and recent silent ischemia in regions anatomically unrelated to the ischemic lesion that caused the initial symptoms. We compared patients with rPH with those without rPH or parenchymal hemorrhage. Independent risk factors for rPH were obtained by multivariable logistic regression analyses. Results— We evaluated 992 patients (mean age, 74.0±12.6 years; 52.9% were men), and 408 (41%) of them underwent a magnetic resonance imaging. Twenty-six patients (2.6%) had a rPH, 8 (0.8%) had both rPH and PH, 58 (5.8%) had PH, and 900 (90.7%) had no bleeding complication. Lobar cerebral microbleeds (odds ratio, 8.0; 95% confidence interval, 2.3–27.2) and recent silent ischemia (odds ratio, 4.8; 95% confidence interval, 1.6–14.1) increased the risk of rPH. Conclusions— The occurrence of rPH after intravenous thrombolysis with recombinant tissue-type plasminogen activator in patients with ischemic stroke is associated with lobar cerebral microbleeds and multiple ischemic lesions in different regions.