scholarly journals MOG-antibody Related Unilateral Cerebral Cortical Encephalitis With Refractory Cephalalgia: a Case Report

2021 ◽  
Author(s):  
Ning Ren ◽  
Jing Lei ◽  
Haibao Zhu ◽  
Zilong Zhu ◽  
Jie Qin ◽  
...  
Keyword(s):  
Brain Mri ◽  
Occipital Cortex ◽  
Myelin Oligodendrocyte Glycoprotein ◽  
High Signal Intensity ◽  
Clinical Feature ◽  
High Signal ◽  
Fundus Examination ◽  
Intravenous Methylprednisolone ◽  
Refractory Headache

Abstract Background: Myelin oligodendrocyte glycoprotein (MOG) antibody positive utilateral cerebral cortical encephalitis (UCCE) comprises a new entity with heterogeneity which usually present as epilepsy. Cases with cephalalgia as the only clinical feature were rare reported. Here, We report a case with MOG antibody positive UCCE who only presented with refractory cephalalgia and had a good response to glucocorticoid. MOG antibody-related UCCE should be identified when patients present with refractory headache and it may represent benign cortical encephalitis.Case Presentation: The case of a 41-year-old woman with MOG antibody positive UCCE presented with refractory cephalalgia. Neurological examination is normal, and fundus examination suggested bilateral optic nerve head edema. Brain MRI discovered Flair hyperintense lesions in the sulci of right temporoparietal occipital cortex. MOG antibody was positive both in the serum and cerebrospinal fluid. When the patient was treated with intravenous methylprednisolone, her headache completely disappeared and brain MRI showed partly recovery. At the follow-up of 6 months after discharge, she had no relapse, serum MOG antibody was negative and the high signal intensity on Flair had completely disappeared.Conclusions: MOG antibody-positive UCCE with headache as the single clinical symptom may represent benign cortical encephalitis.

scholarly journals Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease Presenting as Recurrent and Migrating Focal Cortical Encephalitis

2020 ◽  
Vol 7 ◽  
pp. 2329048X2096617
Author(s):  
Xinran Maria Xiang ◽  
Rachel Evans ◽  
Jesus Lovera ◽  
Rashmi Rao
Keyword(s):  
Brain Mri ◽  
Occipital Cortex ◽  
Myelin Oligodendrocyte Glycoprotein ◽  
New Right ◽  
High Dose ◽  
Antibody Testing ◽  
Leptomeningeal Enhancement ◽  
The Right ◽  
Work Up ◽  
New Onset

Although pediatric myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease is increasingly well-recognized, its full clinical spectrum is still being defined. Cortical encephalitis is emerging as a distinct clinico-radiologic syndrome of adult MOG antibody-associated disease. We describe a 12-year-old girl who presented with new onset seizures and left-sided hemiparesis. Brain MRI showed edema of the right temporal-parietal-occipital cortex with associated focal leptomeningeal enhancement. Patient received high-dose corticosteroids and 21 days of acyclovir despite negative infectious work-up due to the focal nature of encephalitis. Patient remained seizure-free for 20 months before presenting with new right hemiclonic seizures with right-sided hemiparesis and edema of the left temporal-parietal cortex with associated leptomeningeal enhancement. Patient’s MOG antibody titer was 1:40. She completed high-dose corticosteroids and intravenous immunoglobulin. Our patient highlights the importance of MOG antibody testing in pediatric focal cortical encephalitis to avoid unnecessary anti-viral agents and provide more appropriate immunotherapy and a more informed prognosis.

First Clinical Experience with Anti-myelin Oligodendrocyte Glycoprotein Antibody-Positive Optic Neuritis

2020 ◽  
Vol 237 (04) ◽  
pp. 458-463 ◽  
Author(s):  
Jan Heckmann ◽  
Margarita Todorova ◽  
Stefanie Müller ◽  
Philip Julian Broser ◽  
Veit Sturm
Keyword(s):  
Visual Acuity ◽  
Optic Neuritis ◽  
Pulse Therapy ◽  
Myelin Oligodendrocyte Glycoprotein ◽  
Individual Treatment ◽  
Igg Antibodies ◽  
Intravenous Methylprednisolone ◽  
Finger Counting ◽  
The Right

Abstract Background Antibodies against myelin oligodendrocyte glycoprotein (MOG-IgG) have been consistently found in a range of demyelinating disorders. In this context, MOG-IgG-associated optic neuritis (ON) has been suggested as a new subset of optic neuropathy. However, clinical manifestations and distinctive characteristics have only rarely been described. Patients and Methods A retrospective case series of three patients with MOG-IgG-associated ON. Clinical morphological features using imaging techniques are presented. Results Three patients (8-year-old boy, 28-year-old female, 48-year-old male) were included. An 8-year-old boy suffered from a bilateral ON with severe visual loss. The best-corrected visual acuity (BCVA) was 0.05 in the right eye and finger counting in the left eye. The patient had a previous episode of acute disseminated encephalomyelitis (ADEM) with a right abducens nerve palsy. Visual acuity recovered after repeated cycles of intravenous methylprednisolone pulse therapy and 10 cycles of plasma exchange. During the last follow-up, BCVA was 0.9 in the right eye and 0.8 in the left eye. A 28-year-old female presented with a bilateral ON. Her BCVA was 0.5 in the right eye and 0.8 in the left eye. She fully recovered with pulse methylprednisolone therapy (1000 mg/d) with tapering after the second cycle and had a BCVA of 1.0 during the last follow-up visit. A 48-year-old male suffered from a relapsing bilateral ON. At first presentation, BCVA was 0.1 in the right eye and finger counting in the left eye. BCVA fully recovered after each pulse therapy with intravenous methylprednisolone (two cycles). Since the first relapse, the patient has been receiving long-term immunosuppression with rituximab. Despite rituximab and low-dose oral prednisone, the patient had another relapse with a left ON. After a third cycle with intravenous methylprednisolone, he partially recovered. BCVA at last follow-up was 1.0 in the right and 0.8 in the left eye. Conclusions MOG-IgG antibodies have been identified in different acquired demyelinating syndromes. The patients reported had an ADEM followed by bilateral ON, an isolated bilateral ON, and a relapsing bilateral ON. Individual treatment strategies led to substantial visual recovery in all patients. We recommend inclusion of MOG-IgG antibodies in the diagnostic workup at least after the first recurrence of ON since they can serve as a diagnostic and potential prognostic tool and might lead to specific therapeutic recommendations.

Asymptomatic Carotid T1-High-Intense Plaque as a Risk Factor for a Subsequent Cerebrovascular Ischemic Event

2017 ◽  
Vol 43 (5-6) ◽  
pp. 250-256 ◽  
Author(s):  
Yoshitaka Kurosaki ◽  
Kazumichi Yoshida ◽  
Hitoshi Fukuda ◽  
Akira Handa ◽  
Masaki Chin ◽  
...  
Keyword(s):  
Risk Factor ◽  
Signal Intensity ◽  
High Signal Intensity ◽  
High Signal ◽  
Asymptomatic Carotid ◽  
Ischemic Event ◽  
Cox Regression Analysis ◽  
Carotid Mri ◽  
Cerebrovascular Events

Background: Intraplaque hemorrhage, detected as a high-signal intensity on carotid MRI, is also strongly associated with ischemic events in symptomatic patients. However, in asymptomatic patients, the relationship of the T1-high intense plaque and the subsequent stroke is not clear. The aim of this study is to test the hypothesis that asymptomatic carotid T1-high intense plaque is a risk factor for a subsequent cerebrovascular ischemic event. Methods: Of the 1,353 consecutive patients, who underwent head and carotid MRI as part of their annual medical check-up, the imaging quality of 13 was poor and 150 did not present for follow-up examination, thus leaving 1,190 subjects for evaluation. Of the 1,190 patients, 96 patients had findings of high-signal intensity on carotid MRI and 1,094 patients did not. Cerebrovascular events were retrospectively evaluated. Results: During a mean follow-up period of 53 months, 4 patients with high-signal intensities on carotid MRI (4%) and 3 with no findings (0.3%) had a cerebrovascular ischemic event, with the occurrences significantly higher in the high-signal-intensity group. (p < 0.01) Cox regression analysis indicated that the presence of the high-intense plaque on carotid MRI (hazard ratio [HR] 4.2; 95% CI 1.0-17.1; p = 0.04), age (HR 1.1; 95% CI 1.0-1.2; p = 0.003), and diabetes mellitus (HR 7.2; 95% CI 1.8-27.4; p = 0.004) were associated with the occurrence of subsequent ischemic cerebrovascular events. Conclusions: Asymptomatic carotid T1-high-intense plaque might be a potential high-risk factor for a subsequent cerebrovascular ischemic event.

Quantitatively Measured Infrapatellar Fat Pad Signal Intensity Alteration is Associated with Joint Effusion-Synovitis in Knee Osteoarthritis

2021 ◽  
Author(s):  
Guangfeng Ruan ◽  
Yan Zhang ◽  
Zhaohua Zhu ◽  
Peihua Cao ◽  
Xiaoshuai Wang ◽  
...  
Keyword(s):  
Signal Intensity ◽  
High Signal Intensity ◽  
Joint Effusion ◽  
Infrapatellar Fat Pad ◽  
High Signal ◽  
Fat Pad ◽  
Knee Oa ◽  
Suprapatellar Pouch ◽  
Intensity Region

Abstract Background: Abnormal infrapatellar fat pad (IPFP) plays a detrimental role in knee osteoarthritis (OA) by producing pro-inflammatory cytokines. IPFP may interact with synovium because of their adjacent anatomical positions; however, whether abnormal IPFP can contribute to effusion-synovitis in knee OA is unclear.Methods: Among 255 knee OA patients, IPFP signal intensity alteration represented by four measurement parameters [standard deviation of IPFP signal intensity (IPFP sDev), upper quartile value of IPFP high signal intensity region (IPFP UQ (H)), ratio of IPFP high signal intensity region volume to whole IPFP volume (IPFP percentage (H)), and clustering factor of IPFP high signal intensity (IPFP clustering factor (H))] was measured quantitatively at baseline and two-year follow-up using magnetic resonance imaging (MRI). Effusion-synovitis of the suprapatellar pouch and other cavities were measured both quantitatively and semi-quantitatively as effusion-synovitis volume and effusion-synovitis score at baseline and two-year follow-up using MRI. Mixed-effects models were used to assess the associations between IPFP signal intensity alteration and effusion-synovitis over two years.Results: In multivariable analyses, all four parameters of IPFP signal intensity alteration were positively associated with total effusion-synovitis volume and effusion-synovitis volumes of the suprapatellar pouch and of other cavities over two years (all P＜0.05). They were also associated with the semi-quantitative measure of effusion-synovitis except for IPFP percentage (H) with effusion-synovitis in other cavities. Conclusion: Quantitatively measured IPFP signal intensity alteration is positively associated with joint effusion-synovitis in people with knee OA, suggesting that IPFP signal intensity alteration may contribute to effusion-synovitis and a coexistent pattern of these two imaging biomarkers could exist in knee OA patients.

scholarly journals Abnormal High Signal Intensity Discovered in Eye Lenses in Routine Brain MRI; Correlation with Ophthalmologist Examination

2017 ◽  
Vol 15 (1) ◽  
Author(s):  
Amin Abolhasani Foroughi ◽  
Mohammad Hossein Nowroozzadeh ◽  
Ali Khorsand ◽  
Masoume Nazeri ◽  
Masoud Yasemi ◽  
...  
Keyword(s):  
Signal Intensity ◽  
Brain Mri ◽  
High Signal Intensity ◽  
High Signal

scholarly journals Postinfectious Anti–Myelin Oligodendrocyte Glycoprotein Antibody Positive Optic Neuritis and Myelitis

2017 ◽  
Vol 32 (12) ◽  
pp. 996-999 ◽  
Author(s):  
J. P. Vieira ◽  
J. Sequeira ◽  
M. J. Brito
Keyword(s):  
Optic Nerve ◽  
Brain Mri ◽  
Optic Chiasm ◽  
Myelin Oligodendrocyte Glycoprotein ◽  
Intravenous Methylprednisolone ◽  
Human Herpes Virus ◽  
Visual Acuity Loss ◽  
Polymerase Chain ◽  
Magnetic Resonance Imaging Mri ◽  
Aquaporin 4 Antibody

We report the case of a 9-year-old girl admitted with fever, headache, and a cerebrospinal fluid lymphocytic pleocytosis. Polymerase chain reaction was positive for human herpes virus 6. She subsequently developed ataxia and bilateral loss of vision. Magnetic resonance imaging (MRI) showed bilateral optic nerve lesions with extension to optic chiasm and a short-segment myelitis. Serologic studies were positive for Borrelia burgdorferi IgM. Anti–aquaporin 4 antibody was negative and anti–myelin oligodendrocyte glycoprotein antibody (MOG) positive. After intravenous methylprednisolone, ceftriaxone, and intravenous immunoglobulin, her vision slowly recovered. The patient was discharged with only mild visual acuity loss, 1 month after admission. Brain MRI was repeated later and was normal and MOG assay became negative. In our view, this patient suffered from a postinfectious, anti-MOG–mediated, spinal cord and optic nerve demyelination.

Spinal Dural AVF Two Cases with MRI Follow-up

1998 ◽  
Vol 4 (1_suppl) ◽  
pp. 207-212
Author(s):  
S. Nishi ◽  
N. Hashimoto ◽  
I. Nakahara ◽  
T. Iwama ◽  
M. Sawada ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Early Diagnosis ◽  
Signal Intensity ◽  
High Signal Intensity ◽  
Gait Disturbance ◽  
Diagnosis And Treatment ◽  
High Signal ◽  
Common Trunk ◽  
Spinal Dural Arteriovenous Fistula

Spinal dural arteriovenous fistula (d-AVF) is one of the arteriovenous malformations that are treatable by surgery or embolization. We present two cases treated by embolization and stress the necessity of early diagnosis and treatment, and the usefulness of T2WI on MRI for follow-up after embolization. One was a 51-year-old man who presented with gait disturbance and sphincter dysfunction. MRI revealed diffuse swelling on T1WI, and intramedullary high signal intensity on T2WI. A spinal d-AVF was found through tiny radicullomeningeal arteries via the right Th12 intercostal artery that drained into engorged retromedullary veins. The spinal d-AVF was embolized with 50% NBCA. Six months after the embolization, he was able to go back to his job, T2WI showed disappearance of the high signal intensity, which was confirmed at angiography one year after the embolization. The other case was a 62-year-old man who presented with sensory disturbance and gait disturbance, MRI showed the same findings, without the flow voids on them in case 1. The high signal area in the central spinal cord was thought to be syringomyelia, in which a syrinx-subarachnoid shunt was tried in vain. On the surface of the spinal cord, abnormally engorged and tortuous vessels were found. The syrinx was not confirmed. An angiogram showed a spinal d-AVF fed by the radicullomeningeal artery through a common trunk of the Th11/12 intercostal arteries with drainage into the retromedullary vein. The spinal d-AVF was embolized. Six months after the embolization, T2WI showed a decrease of high intensity areas. Early diagnosis and treatment are important for the prognosis of spinal d-AVF, T2WI may be the best way to check for recurrence.

Long-term seizure outcomes after pediatric temporal lobectomy: does brain MRI lesion matter?

2019 ◽  
Vol 24 (2) ◽  
pp. 200-208
Author(s):  
Ravindra Arya ◽  
Francesco T. Mangano ◽  
Paul S. Horn ◽  
Sabrina K. Kaul ◽  
Serena K. Kaul ◽  
...  
Keyword(s):  
Repeated Measures ◽  
Mixed Model ◽  
Linear Mixed Model ◽  
Hippocampal Sclerosis ◽  
Brain Mri ◽  
Temporal Lobectomy ◽  
Seizure Freedom ◽  
Seizure Onset

OBJECTIVEThere is emerging data that adults with temporal lobe epilepsy (TLE) without a discrete lesion on brain MRI have surgical outcomes comparable to those with hippocampal sclerosis (HS). However, pediatric TLE is different from its adult counterpart. In this study, the authors investigated if the presence of a potentially epileptogenic lesion on presurgical brain MRI influences the long-term seizure outcomes after pediatric temporal lobectomy.METHODSChildren who underwent temporal lobectomy between 2007 and 2015 and had at least 1 year of seizure outcomes data were identified. These were classified into lesional and MRI-negative groups based on whether an epilepsy-protocol brain MRI showed a lesion sufficiently specific to guide surgical decisions. These patients were also categorized into pure TLE and temporal plus epilepsies based on the neurophysiological localization of the seizure-onset zone. Seizure outcomes at each follow-up visit were incorporated into a repeated-measures generalized linear mixed model (GLMM) with MRI status as a grouping variable. Clinical variables were incorporated into GLMM as covariates.RESULTSOne hundred nine patients (44 females) were included, aged 5 to 21 years, and were classified as lesional (73%), MRI negative (27%), pure TLE (56%), and temporal plus (44%). After a mean follow-up of 3.2 years (range 1.2–8.8 years), 66% of the patients were seizure free for ≥ 1 year at last follow-up. GLMM analysis revealed that lesional patients were more likely to be seizure free over the long term compared to MRI-negative patients for the overall cohort (OR 2.58, p < 0.0001) and for temporal plus epilepsies (OR 1.85, p = 0.0052). The effect of MRI lesion was not significant for pure TLE (OR 2.64, p = 0.0635). Concordance of ictal electroencephalography (OR 3.46, p < 0.0001), magnetoencephalography (OR 4.26, p < 0.0001), and later age of seizure onset (OR 1.05, p = 0.0091) were associated with a higher likelihood of seizure freedom. The most common histological findings included cortical dysplasia types 1B and 2A, HS (40% with dual pathology), and tuberous sclerosis.CONCLUSIONSA lesion on presurgical brain MRI is an important determinant of long-term seizure freedom after pediatric temporal lobectomy. Pediatric TLE is heterogeneous regarding etiologies and organization of seizure-onset zones with many patients qualifying for temporal plus nosology. The presence of an MRI lesion determined seizure outcomes in patients with temporal plus epilepsies. However, pure TLE had comparable surgical seizure outcomes for lesional and MRI-negative groups.

Sign in / Sign up

Export Citation Format

Share Document