scholarly journals Neuromyelitis Optica Spectrum Disorder Coinciding with Spinocerebellar Ataxia Type 31

2017 ◽  
Vol 9 (2) ◽  
pp. 127-130
Author(s):  
Yoshiaki Takahashi ◽  
Yasuhiro Manabe ◽  
Ryuta Morihara ◽  
Hisashi Narai ◽  
Toru Yamashita ◽  
...  
Keyword(s):  
Spinocerebellar Ataxia ◽  
Neuromyelitis Optica ◽  
Cerebellar Atrophy ◽  
Spectrum Disorder ◽  
Spinocerebellar Ataxia Type ◽  
Neuromyelitis Optica Spectrum Disorder ◽  
Inflammatory Processes ◽  
Thoracic Cord ◽  
The Brain ◽  
Cerebellar Symptoms

We report the unusual case of a 63-year-old man with spinocerebellar ataxia (SCA) type 31 who developed neuromyelitis optica spectrum disorder (NMOSD) 14 years after the onset of cerebellar symptoms. In addition to cerebellar atrophy, magnetic resonance imaging showed multiple high-intensity areas in the brain and a long thoracic cord lesion from Th1/2 to Th11. The combination of NMOSD and SCA31 is accidental. However, our case suggests that inflammatory processes could be involved in the pathogenesis of NMOSD and SCA31.

Development of extensive brain lesions following fingolimod (FTY720) treatment in a patient with neuromyelitis optica spectrum disorder

2011 ◽  
Vol 18 (1) ◽  
pp. 113-115 ◽  
Author(s):  
Ju-Hong Min ◽  
Byoung Joon Kim ◽  
Kwang Ho Lee
Keyword(s):  
Neuromyelitis Optica ◽  
Vasogenic Edema ◽  
Brain Mri ◽  
Brain Lesions ◽  
Steroid Treatment ◽  
Spectrum Disorder ◽  
Neuromyelitis Optica Spectrum Disorder ◽  
Parietal Lobes ◽  
The Right ◽  
The Brain

We report the case of a patient who developed extensive brain lesions during fingolimod (FTY720) treatment in the TRANSFORMS study. His initial diagnosis was multiple sclerosis, but after encephalopathy anti-aquaporin4 antibody (anti-AQP4 Ab) was detected, it was changed to neuromyelitis optica spectrum disorder. After treatment with fingolimod, he developed bilateral extensive brain lesions. The brain MRI showed lesions predominantly involving the right frontal and parietal lobes, with vasogenic edema and enhancement. He had residual encephalomalacia and no recurrence with steroid treatment over 3 years following withdrawal of fingolimod.

Multifrequency magnetic resonance elastography of the brain reveals tissue degeneration in neuromyelitis optica spectrum disorder

2016 ◽  
Vol 27 (5) ◽  
pp. 2206-2215 ◽  
Author(s):  
Kaspar-Josche Streitberger ◽  
Andreas Fehlner ◽  
Florence Pache ◽  
Anna Lacheta ◽  
Sebastian Papazoglou ◽  
...  
Keyword(s):  
Magnetic Resonance ◽  
Neuromyelitis Optica ◽  
Magnetic Resonance Elastography ◽  
Spectrum Disorder ◽  
Neuromyelitis Optica Spectrum Disorder ◽  
Tissue Degeneration ◽  
The Brain

scholarly journals Simultaneous new onset of neuromyelitis optica spectrum disorder in identical twins

2021 ◽  
Vol 3 (2) ◽  
pp. e000174
Author(s):  
Ivo Bekavac ◽  
Matea Matejic ◽  
Riley J Woods ◽  
John I Halloran
Keyword(s):  
Spinal Cord ◽  
White Matter ◽  
Neuromyelitis Optica ◽  
Cervical Spinal Cord ◽  
Identical Twins ◽  
Spectrum Disorder ◽  
Cerebral White Matter ◽  
Neuromyelitis Optica Spectrum Disorder ◽  
Csf Analysis ◽  
The Brain

ObjectiveTo present a case of two identical twins presenting concurrently with symptoms and subsequent initial diagnosis of neuromyelitis optica spectrum disorder (NMOSD).MethodsClinical, laboratory and MRI findings for both twins were reviewed and presented here.ResultsTwin A presented with right eye pain and subsequent blurred vision in right eye. MRI of the brain and spine demonstrated pre-chiasmal right optic nerve enhancement and T2 hyperintense lesions in the spinal cord at T7 and T9 levels. Cerebrospinal fluid (CSF) analysis was remarkable for NMO/aquaporin-4 (AQP4) fluorescence-activated cell sorting (FACS) titre of 1:32 and a serum NMO/AQP4-IgG positive titre of 1:10 000. Twin B presented with diplopia. MRI of the brain and spine demonstrated T2 hyperintense lesions in the periventricular cerebral white matter, in the periaqueductal white matter of the pons, in the midbrain and the cervical spinal cord. Neurological examination findings revealed incomplete right trochlear palsy, rotatory nystagmus, an incomplete left internuclear ophthalmoplegia and hyper-reflexia. CSF analysis was remarkable for NMO/AQP4 FACS titre of 1:256 and a serum NMO-IgG positive titre of 1:10 000. Both twins responded well to intravenous steroid therapy. There was no adverse environmental exposure present.ConclusionWe present an interesting and rare case of identical twins presenting concurrently and for the first time with NMOSD.

scholarly journals Neuromyelitis Optica Spectrum Disorder: A Case Report of Effective Combination Immunosuppressant, Corticosteroids, and Therapeutic Plasma Exchange

2019 ◽  
Vol 7 (20) ◽  
pp. 3433-3436
Author(s):  
Laura Tambunan ◽  
K. Ritarwan ◽  
K. P. Surbakti
Keyword(s):  
Magnetic Resonance ◽  
Plasma Exchange ◽  
Neuromyelitis Optica ◽  
Evoked Potential ◽  
Serum Antibody ◽  
Therapeutic Plasma Exchange ◽  
Spectrum Disorder ◽  
Resonance Spectroscopy ◽  
Neuromyelitis Optica Spectrum Disorder ◽  
The Brain

BACKGROUND: Neuromyelitis optica spectrum disorder (NMOSD) is an autoimmune disease that causes severe demyelination, especially in the optic nerve and spinal cord with typical clinical manifestations of acute optic neuritis and transverse myelitis. The symptoms can occur simultaneously or separated by a variable period. NMOSD is associated with serum aquaporin antibodies 4 immunoglobulin G (AQP4-IgG). CASE PRESENTATION: We report a case of a 22-year-old male with complaints of weakness of all four limbs, impaired vision, urinary incontinence, and dyspnea. The Expanded Disability Status Scale (EDSS) was nine. Spinal magnetic resonance imaging (MRI) showed longitudinal extensive transversal myelitis. The brain MRI showed a normal impression, whereas the brain magnetic resonance spectroscopy (MRS) examination showed a description of the mild demyelination process. The serum antibody AQP4 (AQP4-IgG) results were seronegative, the cerebrospinal fluid examination was normal, and the oligoclonal band was negative. The ophthalmoscopic examination found bilateral papillary atrophy but optical coherence tomography (OCT) was still normal. Somatosensory evoked potential and visual evoked potential examinations were abnormal. The patient was diagnosed with NMOSD and was given combination immunosuppressant therapy, corticosteroids, and therapeutic plasma exchange. The patient experienced significant improvement with EDSS decreased to six. CONCLUSION: In the case of relapsing NMOSD patient, combination therapy of immunosuppressants, corticosteroids, and TPE was used. There were significant improvements from EDSS nine to six.

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