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Neuromyelitis optica (NMO) is characterized by attacks of optic neuritis and longitudinally extensive transverse myelitis. Cases positive for aquaporin 4 antibodies are classified to NMO spectrum disorder (NMOSD) which includes cases with optic neuritis, transverse myelitis, or with brain lesions
Aquaporin 4 antibody (anti-AQP4) positive neuromyelitis optica spectrum disorder (NMOSD) is known to occur in the setting of myasthenia gravis (MG). However, comorbid MG with myelin oligodendrocyte glycoprotein antibody (anti-MOG) positive NMOSD has not been reported. We present a case of anti-MOG
Neuromyelitis optica (NMO) has a complex pathology. Clinical symptoms, derived from damage to optic nerves and spinal cord, cause optic neuritis and/or longitudinally extensive myelitis. Treatment options are limited. We assessed adrenocorticotropic hormone (ACTH) use in patients OBJECTIVE
To report the clinical and radiological features of 2 patients with neuromyelitis optica (NMO) associated with severe acute disseminating encephalomyelitis. The first patient had anti-aquaporin 4 antibodies (NMO-IgG) but no lesion enhancement, in contrast to the second patient who was
Introduction: Neuromyelitis optica spectrum disorder (NMO-SD) has been recognized for the past decade. Biomarkers such as anti-Aquaporin 4 antibodies (AQP4) and anti-Myelin Oligodendrocyte Glycoprotein (MOG) have been able to classify
Anti-aquaporin-4 antibody (NMO-IgG) is used as a diagnostic marker for neuromyelitis optica (NMO). Although the mechanism of spinal cord lesions in NMO has been investigated, that of extensive hemispheric lesions with brain edema remains unclear. Here we report a 36-year-old woman with NMO positive
BACKGROUND
The long-term effect of neuromyelitis optica (NMO) on the brain is not well established.
METHODS
After 22 years of NMO, a patient's brain was examined by quantitative T1- and T2-weighted mono- and biexponential diffusion and proton spectroscopy. It was compared to 3 cases with short-term
While spinal cord (SC) attacks of neuromyelitis optica spectrum disorder (NMOSD) are often devastating, signs predictive of their poor clinical outcome have been elusive until now, except for the delay in initiating plasma exchange (PE).We studied the Zamboni et al proposed a new hypothesis for the pathomechanisms of multiple sclerosis (MS): chronic cerebrospinal venous insufficiency (CCSVI). Using Doppler ultrasound and venograms, they found severe extracranial venous stenosis in MS patients. They suggested that a venous obstruction in the neck
Microcystic macular edema (MME) is a term used to describe pseudocystic spaces in the inner nuclear layer (INL) of the human retina. It has been noted in multiple sclerosis (MS) as well as a variety of other diseases. The processes that lead to MME formation and their change over time have yet to be
Neuromyelitis optica spectrum disorder (NMOSD) is an autoimmune disease that classically manifests as attacks of optic neuritis (ON) and transverse myelitis (TM). The prevalence, course, and severity of NMOSD vary considerably. Few studies report the neuro-ophthalmologic disease course and visual
BACKGROUND
Recently defined consensus criteria for the diagnosis of neuromyelitis optica spectrum disorders (NMOSD) allow establishing the diagnosis in patients without elevated AQP4-Ab and optic nerve involvement. According to the new extended definition, NMOSD is closely associated with extensive
A 51-year-old female with a history of rheumatoid arthritis rapidly developed anterior neck pain and paresis in the left upper and lower extremities and right lower extremity, sensory disturbance in the left upper and lower extremities, and bladder and rectal disorder. Adduction of the left eye and
Neuromyelitis optica (NMO) is an inflammatory demyelinating disorder characterized by optic neuritis and acute myelitis. A parainfectious pathogenesis may play a partial role in the development of this disorder. Several viral infections are known to cause NMO. Here we report the case of a