A role for humoral mechanisms in the pathogenesis of Devic's neuromyelitis optica.

  title={A role for humoral mechanisms in the pathogenesis of Devic's neuromyelitis optica.},
  author={Claudia F. Lucchinetti and Raul N Mandler and Dorian B. McGavern and Wolfgang Bruck and Gerald J. Gleich and Richard M. Ransohoff and Corinna Trebst and Brian G. Weinshenker and Dean M. Wingerchuk and Joseph E. Parisi and Hans Lassmann},
  journal={Brain : a journal of neurology},
  volume={125 Pt 7},
Devic's disease [neuromyelitis optica (NMO)] is an idiopathic inflammatory demyelinating disease of the CNS, characterized by attacks of optic neuritis and myelitis. The mechanisms that result in selective localization of inflammatory demyelinating lesions to the optic nerves and spinal cord are unknown. Serological and clinical evidence of B cell autoimmunity has been observed in a high proportion of patients with NMO. The purpose of this study was to investigate the importance of humoral… 

Figures and Tables from this paper

Neuromyelitis optica (Devic's syndrome).

Mechanisms for lesion localization in neuromyelitis optica spectrum disorders

The pathological changes observed in AQP4-antibody positive and MOG-antIBody positive NMOSD patients are strikingly similar to those found in corresponding animal models, and many mechanisms which determine lesion localization in experimental animals seem to closely reflect the human situation.

Optic Neuritis: A Model for the Immuno-pathogenesis of Central Nervous System Inflammatory Demyelinating Diseases.

Looking at the clinical and pathological features of ON in relation to other inflammatory demyelinating conditions of the CNS, namely MS and neuromyelitis optica provides an opportunity to glean common and distinct mechanisms of disease.

Neuromyelitis optica: an overview

This review discusses recent understanding of NMO with reference to epidemiology, clinical spectrum, immunopathology, diagnostic evaluation, clinical course and management, and overwhelming evidence strongly indicates that aquaporin 4 antibody has a pathogenetic role in the development of N MO and serves as a useful diagnostic and prognostic marker.

The Spectrum of Neuromyelitis Optica (NMO) in Childhood

Current clinical, pathological, and pathogenetic knowledge is reviewed with a focus on clinical presentation, neuroimaging findings, serological investigations, and treatment of children with disorders within the spectrum of central nervous system aquaporin-4 autoimmunity.

Molecular Pathogenesis of Neuromyelitis Optica

Despite rapid advances in the understanding of NMO pathogenesis, unanswered questions remain, particularly with regards to disease mechanisms in NMO IgG seronegative cases.

Comparative immunopathogenesis of acute disseminated encephalomyelitis, neuromyelitis optica, and multiple sclerosis

The clinically heterogeneous group of idiopathic inflammatory demyelinating diseases of the central nervous system is characterized by several immunopathological patterns that suggest the involvement of diverse pathogenic effector mechanisms.

Evidence for humoral autoimmunity in neuromyelitis optica

Clinical experience suggests that plasmapheresis and immunosuppressive therapies are beneficial for treatment and prevention of acute attacks but that standard MS immunomodulatory drugs may not alter the course of NMO.



Clinical, CSF, and MRI findings in Devic's neuromyelitis optica.

It is proposed that Devic's neuromyelitis optica is a distinctive disorder with some clinical, CSF, and MRI features different from those found in classic multiple sclerosis.

Neuromyelitis optica.

A systematic review of the literature using MEDLINE was conducted to better understand NMO and its associations with recognized diseases, and it is suggested that NMO does not represent a specific clinical entity.

The clinical course of neuromyelitis optica (Devic’s syndrome)

Clinical, laboratory, and imaging features generally distinguish neuromyelitis optica from MS, and patients with relapsing optic neuritis and myelitis may have neuromyeliitis opticas rather than MS.

Heterogeneity of multiple sclerosis lesions: Implications for the pathogenesis of demyelination

At a given time point of the disease, the patterns of demyelination were heterogeneous between patients, but were homogenous within multiple active lesions from the same patient, suggesting that MS may be a disease with heterogeneous pathogenetic mechanisms.

Devic's neuromyelitis optica: A clinicopathological study of 8 patients

The clinical, imaging, and laboratory features of 8 patients with Devic's neuromyelitis optica report the lack of white matter abnormalities demonstrated by magnetic resonance imaging of the head facilitates the recognition of Devic’s syndrome during life.

Devic's neuromyelitis optica during pregnancy in a patient with systemic lupus erythematosus

A 28-year-old woman who had been diagnosed as having SLE with cutaneous and articular involvement in 1987 and had signs of transverse myelitis with a sensory level at T6 associated with an optic neuropathy suggesting a Devic's syndrome during pregnancy is reported.

Matrix metalloproteinases and tissue inhibitors of metalloproteinases in cerebrospinal fluid differ in multiple sclerosis and Devic's neuromyelitis optica.

It is concluded that multiple sclerosis patients have higher MMP-9 levels in the CSF than patients with DNO, which supports the different pathological mechanisms of these diseases.

A case of neuromyelitis optica (Devic's syndrome) in systemic lupus erythematosus

An interesting case of systemic lupus erythematosus (SLE) is presented in which the clinical onset of myelopathy strongly suggested demyelinating disease, and it is questioned whether some of the cases showing necroticmyelopathy might have an autoimmune pathogenesis.

Haemorrhagic and perivenous encephalitis: a clinical-pathological review of 38 cases.

  • M. HartK. Earle
  • Medicine
    Journal of neurology, neurosurgery, and psychiatry
  • 1975
Clinical and pathological data from eight cases of acute haemorrhagic leucoencephalitis (AHL) confirm the previously documented devastating features of this disease and reveal pathological changes analogous to the pathological features of experimental allergic encephalitis (EAE).