RESUMEN
PURPOSE: Multiple sclerosis (MS) patients whose first demyelinating event is optic neuritis have been claimed to display a milder disease course and reduced physical disability. Our aim was to investigate the impact of the clinical features of the first clinical episode on cognitive disability and sleep dysfunction in MS. METHODS: A total of 26 (10 with optic neuritis as the first clinical event) MS patients were recruited. A comprehensive sleep study was performed, and a panel of tests were administered to examine cognitive and motor performance. Serum levels of sleep-related mediators orexin-A and melatonin were measured by enzyme-linked immunosorbent assay. Subjective sleep quality was evaluated by Pittsburgh sleep quality test, and daytime excessive sleepiness was tested by Epworth sleepiness scale. RESULTS: MS patients with the first clinical episode of optic neuritis and patients with at least one optic neuritis attack exhibited increased daytime sleepiness, higher sleep efficiency and NREM duration and lower total wake time. Patients with a history of optic neuritis obtained more favorable scores in neuropsychological tests measuring executive functions and complex attention as compared to those who had never experienced optic neuritis. Melatonin and orexin-A levels were lower in patients with optic neuritis onset. The higher no. of optic neuritis attacks was associated with reduced wake time and higher symbol digit modalities test scores. CONCLUSIONS: Having a history of optic neuritis is associated with improved sleep quality and executive functions but increased daytime sleepiness. Reduction of orexin-A and melatonin levels might be one of the underlying mechanisms.
Asunto(s)
Disfunción Cognitiva/etiología , Esclerosis Múltiple/complicaciones , Neuritis Óptica/complicaciones , Trastornos del Sueño-Vigilia/etiología , Sueño/fisiología , Adulto , Biomarcadores/metabolismo , Disfunción Cognitiva/metabolismo , Disfunción Cognitiva/fisiopatología , Progresión de la Enfermedad , Ensayo de Inmunoadsorción Enzimática , Femenino , Humanos , Masculino , Melatonina/metabolismo , Esclerosis Múltiple/diagnóstico , Esclerosis Múltiple/etiología , Esclerosis Múltiple/metabolismo , Pruebas Neuropsicológicas , Neuritis Óptica/diagnóstico , Neuritis Óptica/metabolismo , Estudios Prospectivos , Trastornos del Sueño-Vigilia/fisiopatologíaRESUMEN
The interplay between the immune system, sleep dysfunction and cognitive impairment participates in the progression of disability in multiple sclerosis (MS). Our aim was to identify molecular pathways and B cell associated with separate components of MS disability. Benign MS, non-benign MS patients and healthy controls were recruited. Patients underwent polysomnography and cognitive studies. Microarray and bioinformatics analysis performed using peripheral blood mononuclear cell samples identified B cell-associated genes with the most significantly altered expression. Expression levels of these genes were validated by real-time PCR and peripheral blood cell subsets were examined by flow cytometry. Putative correlations among clinical and laboratory parameters were investigated by correlation network analysis. Sleep and cognitive functions were equally impaired in BMS and NBMS. BMS patients showed significantly reduced memory B cell and increased regulatory B cell percentages than NBMS patients. Among genes that were selected by bioinformatics, levels of BLK, BLNK, BANK1, FCRL2, TGFB1 and KCNS3 genes were significantly different among study subgroups. Correlation network analysis showed associations among physical-cognitive disability and sleep dysfunction measures of MS versus expression levels of selected genes. BMS and NBMS differ by physical disability but not cognitive and sleep dysfunction. Different components of disability in MS are associated with peripheral blood B cell ratios and B cell related gene expression levels. Thus, it is likely that altered B cell functions participate in the progression of disability in MS.
Asunto(s)
Linfocitos B Reguladores , Disfunción Cognitiva , Esclerosis Múltiple , Trastornos del Sueño-Vigilia , Cognición , HumanosRESUMEN
Sjögren's syndrome (SS) may be complicated by neurological manifestations. We herein report three women (age range 26-60 years old) who all presented with limbic encephalitis (LE) as the predominant clinical feature 3 months to 15 years after the diagnosis of SS. The 26-year-old patient also developed acute motor axonal neuropathy one week after autoimmune encephalitis. All three patients showed contrast-enhanced MRI lesions and inflammatory cerebrospinal fluid findings, while not displaying any anti-neuronal antibodies and showing a remarkable response to immunotherapy. SS is often overlooked when the symptoms are mild. Therefore, in LE cases with no identifiable cause, serological screening for rheumatologic disorders is recommended.
Asunto(s)
Encefalitis Límbica/líquido cefalorraquídeo , Encefalitis Límbica/diagnóstico por imagen , Síndrome de Sjögren/líquido cefalorraquídeo , Síndrome de Sjögren/diagnóstico por imagen , Adulto , Biomarcadores/líquido cefalorraquídeo , Encefalopatías/complicaciones , Femenino , Humanos , Encefalitis Límbica/complicaciones , Imagen por Resonancia Magnética , Persona de Mediana Edad , Síndrome de Sjögren/complicacionesRESUMEN
Since some neurological disorders present with increased body-mass index (BMI) and cerebrospinal fluid (CSF) oligoclonal bands (OCB), obesity-induced inflammation has been previously speculated in formation of OCB. We investigated the association between BMI, OCB formation and clinical features of MS in 120 patients with relapsing remitting multiple sclerosis (RRMS), a disease with high OCB positivity incidence. Thirty RRMS patients had BMI≥30 and 100 patients displayed CSF OCB. OCB positive and negative patients had comparable BMI and weight values. Disease duration, annual attack number and EDSS were not correlated with BMI and body weight. Patients with normal and high BMI did not significantly differ by means of OCB positivity, gender, annual attack number, disease duration and EDSS scores. Our results argue against a possible role of obesity in OCB formation. Moreover, obesity does not appear to influence disability and clinical progression of MS patients.