Bedia Samanci

Evidence for potential involvement of pro-inflammatory adipokines in the pathogenesis of idiopathic intracranial hypertension.

Background Although specific role players are currently unknown, contribution of inflammatory mediators has been suggested in the pathophysiology of idiopathic intracranial hypertension (IIH), which is a disease more prevalent in obese female individuals of childbearing age. We aimed to investigate the levels of adipokines and cytokines to demonstrate possible markers for inflammation that participate in IIH pathophysiology and their association with clinical features of IIH. Methods IIH patients, diagnosed according to the revised criteria, and age-, gender- and body mass index (BMI)-matched healthy controls were enrolled in this study. Serum samples were evaluated for insulin-like growth factor 1, insulin, nesfatin, adiponectin, interleukin (IL)-1β, IL-6, IL-8, leptin, plasminogen activator inhibitor type-1, resistin, tumour necrosis factor-alpha (TNF-α) and monocyte chemotactic protein 1 via enzyme-linked immunosorbent assay or multiplex immunoassays. Results IL-1β level was significantly higher (p = 0.012), and IL-8 and TNF-α levels were significantly lower in the IIH group (p < 0.001 and p = 0.008, respectively) compared to the control group. There were no correlations between the cytokine/adipokine levels and age, BMI, disease duration, and cerebrospinal fluid oligoclonal bands. There were also no significant differences in cytokine and adipokine levels between IIH patients regarding visual impairment. However, statistically significant differences were found between IIH patients with relapse versus healthy controls regarding IL-1β (p = 0.007), IL-8 (p = 0.001) and TNF-α (p = 0.017) levels. Other investigated cytokines and adipokines showed no significant alterations in IIH patients investigated in the remission period. Conclusion Altered serum levels of IL-1β, IL-8 and TNF-α seem to be associated with IIH pathogenesis, and these cytokines may be used as prognostic markers in IIH to predict relapse.

Late onset aura may herald cerebral amyloid angiopathy: A case report

Background Although migraine usually begins in the early decades of life, late onset of migraine with aura is occasionally observed and can occur without headache, causing confusion in the differential diagnosis. Case report A 72-year-old man presented with recurrent episodes of visual aura lasting for 20 minutes. These episodes had started at 57 years of age and were only once accompanied by a severe headache. Magnetic resonance imaging revealed changes in the periventricular white matter, left occipital haemorrhage and subcortical haemosiderin deposits, compatible with cerebral amyloid angiopathy. Previous treatment with antiplatelet drugs was discontinued. His episodes of visual aura stopped on treatment with lamotrigine and add-on treatment with verapamil. Conclusion In patients with a late onset of migraine aura, doctors must consider other under-recognized causes of transient neurological symptoms, such as cerebral amyloid angiopathy. Blood-sensitive magnetic resonance imaging sequences are the best tool for the early detection of an underlying pathology and therefore treatment with antiplatelet/anticoagulant drugs should be avoided as this may increase the risk of haemorrhage.

Neuronal autoantibodies in patients with Rasmussen's encephalitis.

Rasmussens encephalitis (RE) is a rare disease with unknown pathophysiology. To disclose whether anti-neuronal autoimmunity participates in the aetiology of RE, various neuronal autoantibodies (NAAbs) were investigated in sera of patients with RE and controls. The study included five patients who fulfilled the RE diagnostic criteria (clinical, EEG, and MRI findings) as the patient group, and 50 multiple sclerosis patients and 50 healthy subjects as the control groups. Sera were evaluated for various NAAbs by radioimmunoassay or cell-based assays. All sera were also screened for uncharacterized antibodies to neuronal cell surface or synapse antigens by indirect immunofluorescence using hippocampal cell cultures. The mean age at onset of seizures was 8.3±3.4 years (range: 4-13.5) and mean follow-up time was 11.2±5.4 years (range: 5-19). All patients had unihemispheric atrophy of the cerebral cortex and epilepsia partialis continua. Two of the patients had moderate cognitive impairment, while the others were severely affected, as shown by neuropsychological testing. NAAb positivity was not detected in any of the patients. Immune aetiology is thought to have a role in RE, but the responsible players have not yet been elucidated. Our extensive antibody screening in a small number of patients does not support the presence of antigen-specific anti-neuronal autoimmunity in RE pathophysiology.

THE EFFECT OF CSF AMYLOID BETA CONCENTRATIONS ON MEMORY PERFORMANCE OF THE INDIVIDUALS WITH SUBJECTIVE COGNITIVE IMPAIRMENT

Vera M. Mendes, Naomi De Roeck, Javier S aez-Valero, Eduard A. Struys, Kees WJ. van Uffelen, Eugeen Vanmechelen, Ulf Andreasson, Charlotte E. Teunissen, Alzheimer Center and Department of Neurology, Amsterdam Neuroscience, VU University Medical Center, Amsterdam, Netherlands; Institute Born-Bunge, Wilrijk, Belgium; Instituto de Neurociencias de Alicante, Universidad Miguel Hern andez-CSIC, Sant Joan d’Alacant, Spain; VUmc, Amsterdam, Netherlands; Institute Born-Bunge, University of Antwerp, Antwerp, Belgium; Reference Center for Biological Markers of Dementia, Institute Born-Bunge, University of Antwerp, Antwerp, Belgium; VU University Medical Center, Amsterdam, Netherlands; VU University Medical Center Amsterdam, Amsterdam, Netherlands; Universidad Miguel Hern andez-CSIC, Alicante, Spain; University of Coimbra, Coimbra, Portugal; Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal; Reference Center for Biological Markers of Dementia, Laboratory of Neurochemistry and Behavior, Institute Born-Bunge, University of Antwerp, Antwerp, Belgium; Instituto de Neurociencias de Alicante, Universidad Miguel Hern andez-CSIC, Sant Joan d’Alacant, Spain; Department of Biochemistry, VU University Medical Center, Amsterdam Neuroscience, Amsterdam, Netherlands; ADx NeuroSciences NV, Technologiepark, Ghent, Belgium; Institute of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, M€olndal, Sweden; Neurochemistry Laboratory and Biobank, Department of Clinical Chemistry, Amsterdam Neuroscience, VU University Medical Center, Amsterdam, Netherlands. Contact e-mail: c.teunissen@vumc.nl