Introduction and Pathophysiology Introduction Spasticity has been defined as an increase in muscle tone due to hyperexcitability of the stretch reflex and is characterized by a velocity-dependent increase in tonic stretch reflexes. [1] Spasticity usually is accompanied by paresis and other signs, such as increased stretch reflexes, collectively called the upper motor neuron syndrome. Paresis particularly affects distal muscles, with loss of the ability to perform fractionated movements of the digits
OBJECTIVE: To investigate an association between serum B cell activating factor of TNF family (BAFF) levels and anti-aquaporin-4 (AQP4) antibody titers in patients with neuromyelitis optica (NMO) after rituximab treatment. BACKGROUND: Anti-AQP4 antibodies are present in approximately 70% of NMO patients. Such antibodies are probably pathogenic and the titers are elevated during relapse as compared with those in remission.
In neuromyelitis optica (NMO), B-cell autoimmunity to aquaporin-4 (AQP4) has been shown to be essential. However, the role of T cells remains ambiguous
Neuromyelitis optica (NMO) is a severe inflammatory CNS disorder of putative autoimmune aetiology, which predominantly affects the spinal cord and optic nerves. Recently, a highly specific serum reactivity to CNS microvessels, subpia and Virchow–Robin spaces was described in patients with NMO [called NMO–IgG (NMO–immunoglobulin G)]
OBJECTIVE: To describe a patient with neuromyelitis optica (NMO) whose aquaporin 4 (AQP4) antibody levels increased following treatment with interferon beta. DESIGN: Prospective clinical and laboratory case report. SETTING: Institutional referral center for multiple sclerosis (MS)