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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.

Kaya, Dilaver/0000-0002-7364-171X; Batur Caglayan, Hale/0000-0002-3279-1842; Kocaman, Ayse S/0000-0002-5621-9453; GIRAY, Semih/0000-0002-0722-3181; UZUNER, NEVZAT/0000-0002-4961-4332; Afsar, Nazire/0000-0001-8123-8560; Dalkara, Turgay/0000-0003-3943-7819; Arsava, Ethem Murat/0000-0002-6527-4139; Nazliel, Bijen/0000-0002-6148-3814 WOS: 000375144200008 PubMed: 26853139 Background: The relatively late approval of use of recombinant tissue plasminogen activator (rt-PA) for acute ischemic stroke in Turkey has resulted in obvious underuse of this treatment. Here we present the analyses of the nationwide registry, which was created to prompt wider use of intravenous thrombolysis, as well as to monitor safe implementation of the treatment in our country. Methods: Patients were registered prospectively in our database between 2006 and 2013. Admission and 24-hour National Institutes of Health Stroke Scale and 3-month modified Rankin Scale scores were recorded. A "high-volume center" was defined as a center treating 10 or more patients with rt-PA per year. Results: A total of 1133 patients were enrolled into the registry by 38 centers in 18 cities. A nearly 4-fold increase in the study population and in the number of participating centers was observed over the 6 years of the study. The mean baseline NIHSS score was 14.5 +/- 5.7, and the prevalence of symptomatic hemorrhage was 4.9%. Mortality at 3 months decreased from 22% to 11% in the 6 years of enrollment, and 65% of cases were functionally independent. Age older than 70 years, an NIHSS score higher than 14 upon hospital admission, and intracranial hemorrhage were independently associated with mortality, and being treated in a high-volume center was related to good outcome. Conclusions: We observed a decreasing trend in mortality and an acceptable prevalence of symptomatic hemorrhage over 6 years with continuous addition of new centers to the registry. The first results of this prospective study are encouraging and will stimulate our efforts at increasing the use of intravenous thrombolysis in Turkey. Turkish Neurological Society Internet-based registration was funded by the Turkish Neurological Society

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.

The aim of this study was to evaluate the computed tomography (CT) and magnetic resonance imaging findings (MRI) of asymptomatic remote cerebellar hemorrhage (RCH) at the preoperative, early postoperative, and postoperative period. A total of 983 consecutive adult patients who underwent supratentorial craniotomies were included in the study. The ethics committee approved the study. The patient's clinical records and radiological examinations were retrospectively analyzed. All patients had preoperative CT and MRI examinations, immediate postoperative CT, and postoperative MRI within 24 h. The patients with the radiological diagnosis of RCH were followed up to 5 years. Eight asymptomatic RCH cases were recruited. The prevalence of asymptomatic RCH was 0.8% in our series. RCH was unilateral in two patients and bilateral in six patients. The postoperative CT was positive in two cases. The hemorrhage presented on MRI as folial linear hypointensities in six cases. In three cases (including one mixed case), punctate hypointense spots were identified at the superior cerebellar folia. Diffuse hemorrhage in the cerebellar tonsil, subarachnoid hemorrhage, and hemorrhage in the cerebellar vermis and the ventricles were also seen. The MRI findings were stable up to 5 years. The prevalence of asymptomatic RCH is higher than previously reported. Immediate postoperative CT is usually unremarkable; however, MRI demonstrates various hemorrhagic patterns at the cerebellum other than classical "zebra sign". This condition is self-limiting and no further investigation or follow-up study is required. In the proper clinical setting, the awareness of different hemorrhagic patterns in patients with RCH would prevent unnecessary investigations.

Nonconvulsive status epilepticus (NCSE) is an enduring epileptic condition characterized by alteration in consciousness and continuous ictal discharges on the EEG. Various etiologies have been reported. We describe the case of a 66-year-old woman with altered mental status who was diagnosed with NCSE. A workup to explain the etiology revealed tuberculous meningitis (TBM) with increased cerebrospinal fluid protein and positive tuberculous DNA polymerase chain reaction and interferon-γ assay tests. She was treated according to the status epilepticus protocol with a four-drug anti-tuberculosis regimen to which she responded. TBM is a serious disease with insidious presentation and still constitutes a diagnostic challenge with its various presentations. Among the many presentations of tuberculosis, clinicians should consider NCSE.

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.

The aim of this study was to investigate aortic atheromas in stroke subgroups.Two hundred consecutive subjects had acute ischemic stroke confirmed by diffusion-weighted imaging (DWI) (195 cases) or computerized tomography (5 cases). Multidetector computed tomographic angiography (MDCTA) (16- or 64-slice) was used to detect atherosclerotic plaques in vessels. Patient data and diagnostic test results were recorded. Stroke subgroups (TOAST classification) were compared with respect to plaque features in the ascending aorta or aortic arch such as presence of at least 1 plaque, larger than 1mm thick, multiple plaques, and plaque morphology (calcific, soft, mixed and ulcerated).Of the patients, 20.3% were in the large-artery atherosclerosis (LAA), 29.4% had small artery occlusion (SAO), 23.8% had cardioembolism (CE), 6.6% had more than one potential cause found (MPC) and 19.8% had cryptogenic stroke (CS). Overall, 49.7% of patients had at least 1 plaque (any size) in the ascending aorta or aortic arch. The corresponding rates for subgroups were as follows: LAA 80%, SAO 50%, CE 44.7%, MPC 61.5% and CS 20.5% (p0.001). Subgroups also differed significantly with respect to presence of multiple plaques and plaques1mm thick. Of all plaques 93% were mixed type, of which 19% were ulcerated.Almost half of the stroke cases had atheroma in ascending aorta or aortic arch and most of them had a soft component. Subgroups LAA, SAO, and MPC had higher aortic atheroma density compared to CE and CS.

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

Prolonged status epilepticus may directly cause selective neuronal necrosis due to excitotoxic mechanisms, as observed in experimental models and described in case reports. A 36-year-old woman presented with right hemiplegia and aphasia following a generalised tonic-clonic status epilepticus of two hours duration. Accompanying serial MRI with advanced imaging techniques, EEG and histopathology of the cortical tissue of the patient were all compatible with excitotoxic neuronal necrosis. In this histopathologically-proven rare case of status epilepticus-induced excitotoxic neuronal injury, the observation of delayed cortical laminar necrosis on MRI, together with paroxysmal lateralised epileptiform discharges on the EEG, suggests that these changes may be an early sign of impending and ongoing excitotoxic neuronal injury and delayed cell death caused by glutamate release due to excessive neuronal firing in status epilepticus.

Background The location of the primary motor cortex can be detected in healthy adults using the findings of ‘T2 hypointensity’ and the ‘double layer sign’ on 3 T diffusion-weighted imaging. The aim of this study was to assess whether ischemic involvement of the primary motor cortex can be identified on 3 T diffusion-weighted imaging within six-hours after stroke onset and to evaluate whether this finding could predict clinical outcome three-months after ischemic stroke. Methods Sixty-five patients who had paralysis and ischemia of the anterior circulation underwent 3 T magnetic resonance imaging within six-hours of symptom onset. Follow-up MRI was obtained at 72 h. Anatomic localization and ischemic involvement of the primary motor cortex were evaluated on diffusion-weighted imaging by two investigators. Ischemic involvement on the primary motor cortex was classified into three grades. Ischemic lesion volumes were measured. We compared the favorable outcomes at three-months between subjects with and without ischemic involvement on the primary motor cortex using the NIHSS and modified Rankin Scale. Results Ischemic involvement on the primary motor cortex was identified in 52% of patients. Interrater agreement coefficients were 0·93 for the identification of ischemic involvement of primary motor cortex. As defined by scores on the modified Rankin Scale, among the patients with ischemic involvement of the primary motor cortex were worse than the patients without ischemic involvement of the primary motor cortex ( P = 0·01). The mean ischemic lesion volume at baseline diffusion-weighted imaging was 38·7 ± 41·7 cm3 and was 89·8 ± 93·6 cm3 at follow-up T2-WI. Ischemic involvement on the primary motor cortex (odds ratio: 14·7) was a determinant for worse outcome. Conclusions 3T diffusion-weighted imaging can identify ischemic involvement on the primary motor cortex and may provide useful information for predicting outcome during the hyperacute stage. Ischemic involvement on the primary motor cortex has a significant negative impact on recovery.

The aim of the study is to analyze diffusion tensor imaging (DTI) characteristics of the Guillain-Mollaret triangle (GMT) in patients with hypertrophic olivary degeneration (HOD) and to investigate their correlation with previously reported histopathology. DTI was performed in 10 patients diagnosed with HOD. Fractional anisotropy, apparent diffusion coefficient, axial diffusivity, and radial diffusivity were measured in the inferior olivary nucleus (IO), the central tegmental tract, the red and the dentate nuclei, and the superior cerebellar peduncle of HOD patients and compared to age, sex, and side-matched 10 neurologically normal population. The prominent finding on DTI in affected IO was an increase in radial diffusivity compatible with demyelination. While conventional magnetic resonance imaging did not show any sign of involvement in the other components of GMT, DTI demonstrated signal changes in all anatomical components of the GMT. Main DTI findings in GMT of patients with HOD were an increase in radial diffusivity representing demyelination and an increase in axial diffusivity that is reflective of neuronal hypertrophy. DTI parameters can reflect the spatiotemporal evolution of transneuronal degeneration associated with HOD in a manner consistent with the known pathologic stages of HOD.

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.

The aim of the study described here was to analyze findings in 15 cases who were admitted with nonconvulsive status epilepticus (NCSE) and whose EEGs featured atypical triphasic waves (ATWs). We also investigated whether ATWs are useful for diagnosing this condition. Mental status was assessed, and EEGs were recorded during/after the antiepileptic drug treatment. Eight patients had metabolic disorders and nine had intracranial pathology. The ATWs were unilateral focal in 5 cases and bilaterally asymmetrical focal in 10 cases. In 11 of the 15 cases, the ATWs disappeared and mental status improved after treatment. NCSE should be considered in any individual who presents in an acute confusional state and whose EEG reveals either unilateral or bilaterally asymmetric ATWs.

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.