ECTRIMS eLearning

NMOSD and related autoantibody CNS disorders
ECTRIMS Learn. siva a. 10/10/18; 231851; 108
aksel siva
aksel siva
Contributions
Abstract

Abstract: 108

Type: Educational Session

Abstract Category: N/A

The differential diagnosis of MS is wide and includes either clinical, or imaging or both clinical and imaging mimickers. Among of these other primary neuro-inflammatory disorders that involve the central nervous system, Neuromyelitis optica spectrum disorders (NMOSD) and related inflammatory astrocytopathies as well as other antibody associated atypical neuroinflammatory syndromes present a major diagnostic challenge as both the clinical and imaging findings may closely mimic MS. Since, their prognosis and treatments are different from MS, a misdiagnosis may have hazardous consequences! Optic neuritis, myelopathies, brainstem and some cerebral syndromes are often among the clinical manifestations that patients present at their initial episodes of MS, NMOSD&MOG-antibody related CNS inflammatory-demyelinating syndromes. Although that longitudinally extensive spinal cord, optic nerve and corpus callosum lesions on MRI rise the possibility of NMOSD more, this may not be always the case and in a significant number of patients with NMOSD the MRI findings may mimic MS. The same clinical and imaging challenges are also seen in MOG-Ab related syndromes. However, the clinical course, associated symptomatology, the cerebrospinal findings and most importantly the AQP4-IgG and MOG-IgG serology are the clinical and laboratory tools to be used in the differential. But the seronegative NMOSD and MOG patients, and the probability of false positive and negative test results should also be kept in mind.
There are some other recently described antibody associated neuroautoimmune diseases such as anti-NMDAR-encephalitis and variant disorders. Although that the clinical manifestations at onset of these disorders are more likely to include an encephalopathy with seizures and that their MRI may not mimic MS, there have been now a number of such cases that developed in people with MS which should keep us alert for such a probability! Besides, in a few patients with anti-NMDAR-encephalitis a clinico-radiological syndrome consistent with demyelination may occur concomitantly or later.
In summary NMOSD and related autoantibody CNS disorders are among the major group disorders of which physicians should always consider in the differential diagnosis of MS or vice versa. The clinical features and the imaging findings may overlap but the CSF and antibody-serology findings may be of assistance in distinguishing these disorders to a certain extent.
Disclosure: Received honoraria and consultation fees from Novartis, Genzyme, Bayer, Biogen Idec, Merck Serono; Genzyme, Tevaand Roche; received travel and registration coverage for attending several national or international congresses or symposia, from Merck Serono, Biogen Idec/Gen Pharma of Turkey, Novartis, Teva; Genzyme and Roche.

Abstract: 108

Type: Educational Session

Abstract Category: N/A

The differential diagnosis of MS is wide and includes either clinical, or imaging or both clinical and imaging mimickers. Among of these other primary neuro-inflammatory disorders that involve the central nervous system, Neuromyelitis optica spectrum disorders (NMOSD) and related inflammatory astrocytopathies as well as other antibody associated atypical neuroinflammatory syndromes present a major diagnostic challenge as both the clinical and imaging findings may closely mimic MS. Since, their prognosis and treatments are different from MS, a misdiagnosis may have hazardous consequences! Optic neuritis, myelopathies, brainstem and some cerebral syndromes are often among the clinical manifestations that patients present at their initial episodes of MS, NMOSD&MOG-antibody related CNS inflammatory-demyelinating syndromes. Although that longitudinally extensive spinal cord, optic nerve and corpus callosum lesions on MRI rise the possibility of NMOSD more, this may not be always the case and in a significant number of patients with NMOSD the MRI findings may mimic MS. The same clinical and imaging challenges are also seen in MOG-Ab related syndromes. However, the clinical course, associated symptomatology, the cerebrospinal findings and most importantly the AQP4-IgG and MOG-IgG serology are the clinical and laboratory tools to be used in the differential. But the seronegative NMOSD and MOG patients, and the probability of false positive and negative test results should also be kept in mind.
There are some other recently described antibody associated neuroautoimmune diseases such as anti-NMDAR-encephalitis and variant disorders. Although that the clinical manifestations at onset of these disorders are more likely to include an encephalopathy with seizures and that their MRI may not mimic MS, there have been now a number of such cases that developed in people with MS which should keep us alert for such a probability! Besides, in a few patients with anti-NMDAR-encephalitis a clinico-radiological syndrome consistent with demyelination may occur concomitantly or later.
In summary NMOSD and related autoantibody CNS disorders are among the major group disorders of which physicians should always consider in the differential diagnosis of MS or vice versa. The clinical features and the imaging findings may overlap but the CSF and antibody-serology findings may be of assistance in distinguishing these disorders to a certain extent.
Disclosure: Received honoraria and consultation fees from Novartis, Genzyme, Bayer, Biogen Idec, Merck Serono; Genzyme, Tevaand Roche; received travel and registration coverage for attending several national or international congresses or symposia, from Merck Serono, Biogen Idec/Gen Pharma of Turkey, Novartis, Teva; Genzyme and Roche.

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