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Objective:Central nervous system involvement in patients with coronavirus disease-2019 (COVID-19) is associated with increased morbidity and mortality. The assessment of neurological symptoms in patients with critical illnesses, who are mechanically ventilated under deep sedation is challenging, which means doctors could be unaware of such symptoms until patients reach the weaning stage. Thus, this study aimed to identify potential prognostic predictors for COVID-19-related impaired consciousness in patients with critical illnesses.Materials and Methods:This retrospective, multicenter, and observational cohort study was conducted among patients with COVID-19 who were admitted to the intensive care units of five hospitals between March 11, 2020, and September 18, 2020. The patient population was analyzed in two groups-cases with impaired consciousness and cases without impaired consciousness.Results:Patients with impaired consciousness were found to be significantly younger (p=0.001) and to exhibit significantly more laboratory abnormalities, such as high ferritin (p=0.003), C-reactive protein (p=0.001), procalcitonin (p=0.019), and D-dimer (p=0.001) levels. Additionally, pathological magnetic resonance imaging findings were detected in 14 of 29 (48%) patients with impaired consciousness.Conclusion:All patients with severe COVID-19 should be screened for signs of hyperinflammation due to the associated risk of neurological complications. The early detection of at-risk cases and the prompt initiation of specific treatment should result in better disease outcomes.

Dincer, Alp/0000-0001-9158-8353; Afsar, Nazire/0000-0001-8123-8560; KAYA, DILAVER/0000-0002-7364-171X; Yildirim, Duzgun/0000-0002-5411-229X; Sarikaya, Zeynep Tugce/0000-0002-1352-7667; Dogan, Lerzan/0000-0002-1456-4072; Korkmazer, Bora/0000-0001-7015-365X; Mammadov, Orkhan/0000-0001-7648-2948 WOS:000574262800006 PubMed ID: 32384020 [No abstract available]

Highlights. • Severely ill COVID-19 patients failing to regain consciousness or showing agitation during the ventilation weaning period require thorough neurological assessment. • Brain magnetic resonance imaging and cerebrospinal fluid examination are required to determine the extent of central nervous system involvement. • Neurological involvement during COVID-19 infection can be immune mediated. • Plasmapheresis can be beneficial in COVID-19 patients with autoimmune encephalitis., Severe SARS-CoV-2 (COVID-19) infection has the potential for a high mortality rate. In this paper, we report the results of plasmapheresis treatment in a series of severely ill patients with COVID-19–related autoimmune meningoencephalitis in the Intensive Care Unit ICU.

Background Patients with the syndrome of headache with neurological deficits and lymphocytosis (HaNDL) typically present with recurrent and temporary attacks of neurological symptoms and cerebrospinal fluid lymphocytosis. Aim and methods To identify potential HaNDL‐associated antibodies directed against neuronal surface and/or synapse antigens, sera of four HaNDL patients and controls were screened with indirect immunohistochemistry, immunofluorescence, cell-based assay, radioimmunoassay, protein macroarray and enzyme-linked immunosorbent assay (ELISA). Results Although HaNDL sera did not yield antibodies to any of the well-characterized neuronal surface or synapse antigens, protein macroarray and ELISA studies showed high-titer antibodies to a subunit of the T-type voltage-gated calcium channel (VGCC), CACNA1H, in sera of two HaNDL patients. Conclusion Our results support the notion that ion channel autoimmunity might at least partially contribute to HaNDL pathogenesis and occurrence of neurological symptoms.

Objectives: The aim of the study was to analyze the etiology, treatment and clinical and electroencephalographic features in adult patients with nonconvulsive status epilepticus (NCSE). Methods: We retrospectively evaluated all consecutive patients with NCSE admitted to our hospital between 2006 and 2010. Patient data and diagnostic test results were recorded. The following treatment protocol was used: 1) Diazepam 10 mg, 2) Phenytoin (18 mg/kg), 3) Midazolam (0.1-0.6 mg/kg/h), and 4) Thiopental (3-5 mg/kg/h) i.v. infusion. The groups were structured according to the necessity of treatment. Group 1 (n: 31): NCSE was treated with diazepam and phenytoin; and Group 2 (n: 7): NCSE was treated with midazolam or thiopental. Group 2 was also defined as refractory status epilepticus (RSE).Results: We studied 38 episodes in 35 adults (16 men, 19 women; median age: 61.8 years). Of the patients, 84.2% had a history of epilepsy, 44.7% had structural disorders, 13.2% had metabolic disorders, 18.4% had systemic infections, 15.8% had encephalitis, and 5.3% had antiepileptic drug withdrawal. In patients, 65.8% of them exhibited focal and 34.2% exhibited generalized status epilepticus discharges on EEGs. RSE occurred in approximately 18% of patients and was not associated with etiology, history of epilepsy, and clinical or electroencephalographic features. Conclusion: The majority of our patients had a history of epilepsy. Of the patients, 18% had RSE. There was no significant correlation among the treatment groups with respect to etiology, history of epilepsy, and clinical or electroencephalographic features.

Delayed administration of vascular endothelial growth factor (VEGF) promotes functional recovery after focal cerebral ischemia. However, early intravenous injection of VEGF increases blood–brain barrier (BBB) leakage, hemorrhagic transformation and infarct volume whereas its application to cortical surface is neuroprotective. We have investigated whether or not early intracerebroventricular administration of VEGF could replicate the neuroprotective effect observed with topical application and the mechanism of action of this protection. Mice were subjected to 90 mins middle cerebral artery (MCA) occlusion and 24 h of reperfusion. Vascular endothelial growth factor (8 ng, intracerebroventricular) was administered 1 or 3 h after reperfusion. Compared with the vehicle-treated (intracerebroventricular) group, VEGF decreased the infarct volume along with BBB leakage in both treatment groups. Neurologic disability scores improved in parallel to the changes in infarct volume. Independently of the decrease in infarct size, VEGF also reduced the number of TUNEL-positive apoptotic neurons. Phospo-Akt levels were significantly higher in ischemic hemispheres of the VEGF-treated mice. Contrary to intracerebroventricular route, intravenous administration of VEGF (15 μg/kg) enhanced the infarct volume as previously reported for the rat. In conclusion, single intracerebroventricular injection of VEGF protects brain against ischemia without adversely affecting BBB permeability, and has a relatively long therapeutic time window. This early neuroprotective action, observed well before recovery-promoting actions such as angiogenesis, possibly involves activation of the PI-3-Akt pathway.

Infectious-immunogenic mechanisms have been proposedfor the pathogenesis of the syndrome of transient headacheand neurological deficits with cerebrospinal fluid lympho-cytosis (HaNDL) [1]. To investigate this assumption, weperformed immunohistochemistry and Western blot studieswith sera and cerebrospinal fluid (CSF) of two HaNDLpatients. Serum and CSF IgGs of both patients showedstrong reactivity with the nuclei of rat central nervoussystem (CNS) cells and proteins extracted from neuro-blastoma cells. This reactivity was not observed withsamples of a sporadic hemiplegic migraine (SHM) patientand 12 migraine patients used as controls. The CNSbinding pattern of HaNDL IgG was easily distinguishablefrom that of other well-known anti-neuronal nuclear anti-bodies (ANNA) such as anti-Hu, anti-Ri, and anti-nuclearantibody (ANA). The presence of an anti-neuronal immuneresponse may support the autoimmune hypothesis as apathogenic factor for HaNDL and should be furtherinvestigated in larger series.To show the presence of a possible autoimmuneresponse in this syndrome, sera and CSF of two HaNDLpatients were investigated for anti-neuronal antibodies.Serum/CSF of a SHM patient, sera from 12 migraine, 2anti-Hu, 2 anti-Ri, 34 ANA positive patients and 30 healthyindividuals were used as controls. All headache patientsfulfilled the clinical criteria established by The Interna-tional Headache Society [2].Transient headache and neurological deficits with cere-brospinalfluidlymphocytosispatientswere35-(H1)and38-year-old (H2) men presenting with three episodes of throb-bing headache, dysphasia/dysarthria, marching righthemiparesis and hemihypoesthesia (H1 only) lasting for 2–9 h. Their CSF revealed increased lymphocytes [496/mm

Osteopetrosis, or Albers-Schonberg disease, is a rare hereditary disease characterized by osteoclast dysfunction and consequent diminished bone resorption and disturbed bone building and remodeling, resulting in abnormally dense and brittle bones. Bone marrow failure, pathologic fractures, and neurologic deficits are common. Osteopetrosis is diagnosed on radiographs. Patients have generalized osteosclerosis, and radiographs may show evidence of fractures. We report a case of cerebral hemorrhage and multiple sclerosis associated with the benign adult form of osteopetrosis.

BACKGROUND AND PURPOSE: During the hyperacute phase of stroke, multiple hypointense vessels were identified specifically in the ischemic territory on gradient-echo T2{*}-weighted MR images (GRE-T2{*} WI) at 3T. The area was named a ``region of multiple hypointense vessels (RMHV).{''} The aim of this study was to assess the usefulness of RMHV for the diagnosis of acute ischemic stroke (AIS) and to establish the relationship of this finding to other MR imaging studies. MATERIALS AND METHODS: Twenty patients with AIS underwent MR imaging at 3T consisting of GRE-T2{*}, diffusion-weighted images (DWI), and perfusion-weighted images (PWI) within 6 hours of symptom onset and follow-up images at 72 hours. RMHV was defined as an area containing multiple hypointense vessels strictly in the region of the ischemic territory on GRE-T2{*}. The RMHV volume on GRE-T2{*}, initial ischemic lesion volumes on DWI, PWI maps, and on follow-up images were measured and compared with the RMHV volume. RESULTS: RMHV on GRE-T2{*} was identified in 20 patients. There was no significant difference between the ischemic lesion volumes on mean transit time (247.3 +/- 88.1 mL), time-to-peak (228.6 +/- 88.8 mL), cerebral blood flow (200.6 +/- 89.7 mL), RMHV on GRE-T2{*} (214.4 +/- 86 mL), and the infarct volume at 72 hours (210.3 +/- 90.4 mL) (P = .975). CONCLUSIONS: RMHV on GRE-T2{*} can be used as a supportive imaging finding for the diagnosis of hyperacute ischemic stroke. RMHV volume provides information that is in accordance with the infarct volume at 72 hours and the data supplied by PWI.

Even though stroke is known to be a common cause of status epilepticus (SE), the types of stroke or SE that may be associated are not yet clearly defined. The aims of this study were to assess the timing and type of SE in stroke patients and to observe the effects of stroke and the type of SE on the response to treatment and mortality.From May 1998 to May 2001 a total of 121 patients were admitted with SE. Among these, 30 cases (24.8%) of poststroke SE were identified and evaluated. There were 20 early-onset, and 10 late-onset SE. All stroke types were evenly distributed within the early-onset group, whereas only ischaemic stroke was found in the late-onset group. Posterior cerebral artery (PCA) infarcts were significantly more common within the latter (P: 0.0017).Nonconvulsive SE (NCS) was more frequent than convulsive SE (CS) in the early-onset group (P: 0.0352). There was a delay in the time-to-treatment for NCS compared to CS (P: 0.0007). Without, however any effect on the rate of response to first step treatment (intravenous diazepam and phenytoin; P: 0.6334). Thirteen patients died (43.3%) during hospitalisation. Disability was significantly associated with higher mortality in the early-onset group (P: 0.0201). As a conclusion, NCS seems to be an important issue in stroke, thus requiring a high degree of suspicion in an acute stroke setting to avoid further neuronal injury and morbidity.