Pain, Depression, and Quality of Life in Neuromyelitis Optica Spectrum Disorder: A Cross-Sectional Study of 166 AQP4 Antibody-Seropositive Patients.

Objectives: To evaluate prevalence, clinical characteristics, and predictors of pain, depression, and their impact on the quality of life (QoL) in a large neuromyelitis optica spectrum disorder (NMOSD) cohort.

Methods: We included 166 patients with aquaporin-4-seropositive NMOSD from 13 tertiary referral centers. Patients received questionnaires on demographic and clinical characteristics, PainDetect, short form of Brief Pain Inventory, Beck Depression Inventory-II, and Short Form 36 Health Survey.

[Pain in multiple sclerosis and neuromyelitis optica spectrum disorders].

Multiple sclerosis and neuromyelitis optica spectrum disorders are autoimmune inflammatory diseases of the central nervous system, which can lead to a multitude of neurological complaints and pain syndromes. Pain may be an acute symptom during disease exacerbation as well as a chronic symptom, whereby the latter sometimes substantially reduces the quality of life. The etiology of pain is very heterogeneous but the rapid differential diagnostic classification is decisive in order to be able to initiate a differentiated treatment strategy.

Natalizumab promotes activation and pro-inflammatory differentiation of peripheral B cells in multiple sclerosis patients.

Background: In the past, multiple sclerosis (MS) medications have been primarily designed to modulate T cell properties. Based on the emerging concept that B cells are equally important for the propagation of MS, we compared the effect of four commonly used, primarily T cell-targeting MS medications on B cells.

Methods: Using flow cytometry, we analyzed peripheral blood mononuclear cells (PBMC) of untreated (n = 19) and dimethyl fumarate (DMF; n = 21)-, fingolimod (FTY; n = 17)-, glatiramer acetate (GA; n = 18)-, and natalizumab (NAT; n = 20)-treated MS patients, focusing on B cell maturation, differentiation, and cytokine production.

Glucocorticoid Therapy of Multiple Sclerosis Patients Induces Anti-inflammatory Polarization and Increased Chemotaxis of Monocytes.

Multiple Sclerosis (MS) is an autoimmune disease of the central nervous system (CNS), characterized by the infiltration of mononuclear cells into the CNS and a subsequent inflammation of the brain. Monocytes are implicated in disease pathogenesis not only in their function as potential antigen-presenting cells involved in the local reactivation of encephalitogenic T cells but also by independent effector functions contributing to structural damage and disease progression. However, monocytes also have beneficial effects as they can exert anti-inflammatory activity and promote tissue repair.

The major brain endocannabinoid 2-AG controls neuropathic pain and mechanical hyperalgesia in patients with neuromyelitis optica.

Recurrent myelitis is one of the predominant characteristics in patients with neuromyelitis optica (NMO). While paresis, visual loss, sensory deficits, and bladder dysfunction are well known symptoms in NMO patients, pain has been recognized only recently as another key symptom of the disease. Although spinal cord inflammation is a defining aspect of neuromyelitis, there is an almost complete lack of data on altered somatosensory function, including pain.

Rebound of disease activity after withdrawal of fingolimod (FTY720) treatment.

Background: The oral sphingosine-1-phosphate receptor modulator fingolimod (FTY720) was recently approved for the treatment of relapsing-remitting multiple sclerosis. To date, data about a possible recurrence of disease activity after discontinuation of fingolimod treatment are scarce.

Objective: To describe a patient who discontinued fingolimod treatment after a local malignant melanoma was diagnosed.

De-escalation from natalizumab in multiple sclerosis: recurrence of disease activity despite switching to glatiramer acetate.

Natalizumab (NAT) is an effective therapy for relapsing-remitting multiple sclerosis (MS), but is associated with an increased risk of progressive multifocal leucoencephalopathy after 2 years therapy. Thus, NAT treated patients often decide to stop NAT therapy after 2 years. Reports on recurrence of disease activity after NAT discontinuation are controversial.

Managing non-paraneoplastic Lambert-Eaton myasthenic syndrome: clinical characteristics in 25 German patients.

In about 40% of patients LEMS is not a paraneoplastic phenomenon (NT-LEMS). Several clinical aspects important to these patients remain open, especially the question when a LEMS can definitely be diagnosed as NT-LEMS. Here we describe a series of 25 German NT-LEMS patients regarding their clinical characteristics, duration of symptoms, value of serological markers, paraneoplastic antibodies and FDG-PET/CT.

Favorable response to rituximab in a patient with anti-VGCC-positive Lambert-Eaton myasthenic syndrome and cerebellar dysfunction.

Lambert-Eaton myasthenic syndrome (LEMS) is an autoimmune disease that is characterized by impaired transmission across the neuromuscular junction due to autoantibodies directed against the presynaptic voltage-gated calcium channels (VGCC-ab). Clinical symptoms are usually characterized by proximal muscle weakness and mild dysautonomia. In some patients there are signs of cerebellar dysfunction as well, usually associated with cancer.

Cross-reactive T-cell receptors in tumor and paraneoplastic target tissue.

Background: According to established criteria, paraneoplastic encephalomyelitis with adrenal neuroblastoma comprises a definite paraneoplastic neurologic syndrome.

Objective: To detect T-cell clones that cross-react against antigens shared between tumor and nervous system.

Design: Case study.

Lambert-eaton myasthenic syndrome differential reactivity of tumor versus non-tumor patients to subunits of the voltage-gated calcium channel.

Objective: Lambert-Eaton myasthenic syndrome (LEMS) is an autoimmune disease in which the transmission across the neuromuscular junction is disturbed by autoantibodies directed against the presynaptic P/Q-type voltage-gated calcium channels (VGCC). LEMS is paraneoplastic (T-LEMS) in about 60% of patients mostly associated with a small cellular lung carcinoma (SCLC), but occurs spontaneously without a tumor in 40% (NT-LEMS). In most cases neurologic symptoms appear before tumor diagnosis, but there is as yet no clear specific serologic marker to distinguish between NT- and T-LEMS.