Autonomic Dysreflexia & Hyperreflexia Autonomic Dysreflexia Sections Autonomic Dysreflexia Mechanism of Autonomic Dysreflexia Causes of Autonomic Dysreflexia Functional Electrical Stimulation Headaches Autonomic Dysreflexia ? Autonomic Dysreflexia, also known as Hyperreflexia, is a potentially life threatening condition which can be considered a medical emergency requiring immediate attention. It occurs where the blood pressure in a person with a spinal cord injury (SCI) above T5-6 becomes excessively high due to the over activity of the Autonomic Nervous System
Beneficial Plasma Exchange Response in Central Nervous System Inflammatory Demyelination Setty M. Maga?a, BS; B.
SPECIAL SECTION: MONOCLONAL ANTIBODIES WHAT ARE MONOCLONAL ANTIBODIES (MABs)?
Sections: The Urinary System After Spinal Cord Injury Bladder Management See also: Urinary Tract Infections ? The Urinary System The Urinary System is made up of five major parts: The Kidneys The two kidneys filter waste and excess water from the blood and produce urine. Urine is being produced every minute of the day. The Ureters Each kidney has a thin, hollow tube that connects to the bladder.
The central nervous system ( CNS ) represents the largest part of the nervous system , including the brain and the spinal cord . Together with the peripheral nervous system , it has a fundamental role in the control of behavior
Aquaporin 4(AQP4) is a water channel protein strongly expressed in the central nervous system in perimicrovessel astrocyte foot processes, the glia limitans, and ependyma. Expression of AQP4 is highest at the blood-brain barrier and blood-spinal cord barrier, supporting its critical function in material transport across these structures. Recently, presence of the anti-aquaporin-4 antibody in sera has been used as an important diagnostic tool for neuromyelitis optica, suggesting a potential role in central nervous system inflammation.
The complement system is essential in the pathogenesis of inflammatory central nervous system disorders.
We present a pediatric case of recurrent optic neuritis, celiac disease, partial IgA and IgG3 deficiency in the context of anti-aquaporin-4 auto-immunity and familial IgA deficiency with celiac disease. Treatment with tacrolimus was successful in preventing disease relapses
We describe two patients with recurrent longitudinally extensive transverse myelitis (LETM) associated with human T-lymphotropic virus type I or II (HTLV-I/II) exposure, and with neuromyelitis optica (NMO) immunoglobulin G (IgG) antibody in one case. HTLV-I/II are well known retroviral agents of myelopathy and B-cell dysfunction in humans.
OBJECTIVE: Severe inflammation and astrocyte loss with profound demyelination in spinal cord and optic nerves are typical pathological features of neuromyelitis optica (NMO).
We identified the autoantibody against phosphoglycerate mutase 1 (PGAM1), which is a glycolytic enzyme, in sera from multiple sclerosis (MS) patients by proteomics-based analysis. We further searched this autoantibody in sera from patients with other neurological diseases. The prevalence of the anti-PGAM1 antibody is much higher in patients with MS and neuromyelitis optica (NMO) than in those with other neurological diseases and in healthy controls.
Background: Although neuromyelitis optica has been traditionally regarded as a disease without brain involvement, brain abnormalities are not uncommon in patients with neuromyelitis optica-related disorders.Methods: We aimed to characterize the brain magnetic resonance imaging (MRI) abnormalities in neuromyelitis optica spectrum disorder patients who are seropositive for anti-aquaporin-4 autoantibody (AQP4 Ab). Of 236 consecutive patients with inflammatory demyelinating central nervous system diseases, we retrospectively analyzed MRI characteristics of 78 patients who were seropositive for AQP4 Ab.Results: For an average observational period of 6.3 years, 62 patients (79%) had brain lesions on MRI