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 ◽  
...  
2019 ◽  
Vol 7 (20) ◽  
pp. 3433-3436
Author(s):  
Laura Tambunan ◽  
K. Ritarwan ◽  
K. P. Surbakti

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.


2017 ◽  
Vol 9 (2) ◽  
pp. 127-130
Author(s):  
Yoshiaki Takahashi ◽  
Yasuhiro Manabe ◽  
Ryuta Morihara ◽  
Hisashi Narai ◽  
Toru Yamashita ◽  
...  

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.


2015 ◽  
Vol 72 (7) ◽  
pp. 815 ◽  
Author(s):  
Stephane Kremer ◽  
Felix Renard ◽  
Sophie Achard ◽  
Marco A. Lana-Peixoto ◽  
Jacqueline Palace ◽  
...  

2011 ◽  
Vol 18 (1) ◽  
pp. 113-115 ◽  
Author(s):  
Ju-Hong Min ◽  
Byoung Joon Kim ◽  
Kwang Ho Lee

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.


Sign in / Sign up

Export Citation Format

Share Document