scholarly journals Neuromyelitis optica with linear enhancement of corpus callosum in brain magnetic resonance imaging with contrast: a case report

2015 ◽  
Vol 9 (1) ◽  
Author(s):  
Mohammad Ali Sahraian ◽  
Abdorreza Naser Moghadasi ◽  
Mahsa Owji ◽  
Hoda Naghshineh ◽  
Alireza Minagar
2010 ◽  
Vol 16 (10) ◽  
pp. 1229-1236 ◽  
Author(s):  
Woojun Kim ◽  
Min Su Park ◽  
Sang Hyun Lee ◽  
Su-Hyun Kim ◽  
In Ja Jung ◽  
...  

Background: Although neuromyelitis optica has been traditionally regarded as a disease without brain involvement, brain abnormalities are not uncommon in patients with neuromyelitis optica-related disorders. Methods: We aimed to characterize the brain magnetic resonance imaging (MRI) abnormalities in neuromyelitis optica spectrum disorder patients who are seropositive for anti-aquaporin-4 autoantibody (AQP4 Ab). Of 236 consecutive patients with inflammatory demyelinating central nervous system diseases, we retrospectively analyzed MRI characteristics of 78 patients who were seropositive for AQP4 Ab. Results: For an average observational period of 6.3 years, 62 patients (79%) had brain lesions on MRI. Twenty-four patients (31%) had brain MRI abnormalities at the onset of disease, and 35 (45%) had symptomatic brain involvement. Characteristic brain MRI abnormalities were classified into five categories: (1) lesions involving corticospinal tracts (e.g. posterior limb of internal capsule and cerebral peduncle (44%); (2) extensive hemispheric lesions likely due to vasogenic edema (29%); (3) periependymal lesions surrounding aqueduct and the third and fourth ventricles (22%); (4) periependymal lesions surrounding lateral ventricles (40%); and (5) medullary lesions, often contiguous with cervical lesions (31%). Fifty-four patients (69%) showed at least one kind of brain abnormality among the five characteristic MRI lesions. Ten patients showed gadolinium-enhancing lesions, which were characterized by multiple patchy enhancing patterns with blurred margins. Conclusions: In central nervous system AQP4 autoimmunity, brain MRI abnormalities were more common than is generally appreciated and were characterized by their unique localization and configuration.


2020 ◽  
pp. 197140092095382
Author(s):  
Emiliano Ruiz Romagnoli ◽  
Manuel Perez Akly ◽  
Luis A Miquelini ◽  
Jorge A Funes ◽  
Cristina H Besada

Hereditary spastic paraplegias are an uncommon group of monogenic diseases that include 79 types of genetic disorders. The most frequent cause of recessive hereditary spastic paraplegia is a mutation in the spastic paraplegia gene type 11 followed by type 15. This group is usually associated with non-specific clinical features like cognitive decline and may precede the progressive weakness and spasticity of lower limbs. The magnetic resonance imaging hallmark of hereditary spastic paraplegia is thinning of the spinal cord. However, brain magnetic resonance imaging may provide relevant clues for specific hereditary spastic paraplegia subtypes, and thinning of the corpus callosum has been described as the most frequent abnormality in almost one-third of recessive hereditary spastic paraplegias. Moreover, a characteristic abnormality affecting the forceps minor of the corpus callosum has been recently reported as the “ears of the lynx” sign and is highly suggestive of type 11 and 15 hereditary spastic paraplegias. We report a patient who was diagnosed with hereditary spastic paraplegia type 11 by exome genetic testing, presenting the ears of the lynx sign in the first magnetic resonance imaging assessment.


2007 ◽  
Vol 14 (2) ◽  
pp. 248-251 ◽  
Author(s):  
JA Cabrera-Gómez ◽  
A. Saiz-Hinarejos ◽  
F. Graus ◽  
A. González-Quevedo ◽  
R. Rodríguez-Rojas ◽  
...  

We studied cranial magnetic resonance imaging (MRI) lesions in three women with acute attacks of recurrent longitudinally extensive transverse myelitis (r-LETM), recurrent-optic neuritis (r-ON) and r-LETM-CNS. Neuromyelitis Optica -immunoglobulin (IgG) antibody was positive in all cases. Brain MRI (1.5 Tesla) was performed according to protocol from consortium MS centre. We described the cranial lesions in brain MRI of acute relapses. These lesions were different from MS, most had an asymptomatic course which disappeared with time, protocol from consortium of MS centre criteria for brain MRI and seropositivity of NMO-IgG are useful tools for differentiate acute lesions of NMO/MS. Multiple Sclerosis 2008; 14: 248—251. http://msj.sagepub.com


2019 ◽  
Vol 72 (11-12) ◽  
pp. 375-378
Author(s):  
Svetlana Ruzicka-Kaloci ◽  
Marija Stamenkovic ◽  
Zeljko Zivanovic ◽  
Aleksandar Jovanovic ◽  
Tamara Rabi-Zikic ◽  
...  

Introduction. Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy is the most common monogenic disease of small blood vessels. It commonly presents with repeated epi?sodes of brain ischemia leading to progressive subcortical vascular dementia, migraine attacks and mood disorders. Case Report. A 46-year-old male patient was admitted with clinical presentation of stroke. The neurological examination revealed mild divergent strabismus and a left homonymous hemianopia. Brain magnetic resonance imaging showed subacute infarction in the region of the posterior cerebral artery to the right, as well as similar lesions in the splenium of the corpus callosum, numerous mostly confluent and some discrete T2-weighted/fluid attenuated inversion recovery hyperintense lesions of the centrum semiovale, corona radiata, frontoparietal subcortex, capsula externa, periventricularly at the level of occipital and temporal horns of lateral chambers bilaterally, and small punctiform lesions in the region of the corpus callosum. The magnetic resonance angiography findings were normal. The patient?s brother underwent neurological examination at the age of 42 due to severe headaches, double vision, confusion, and numbness in the right arm. The magnetic resonance imaging of the endocranium showed multifocal confluent ischemic lesions predominantly in the frontal and temporal lobes, as well as focal microangiopathic changes in the gangliocapsular regions bilaterally in the brainstem and cerebellum. In agreement with the patient and his brother, genetic analyses were performed in both of them, and a mutation in exon 3 of the neurogenic locus notch homolog protein 3 gene was confirmed (c.505C > t, p.R169C). Conclusion. Although there is no causal therapy, it is very important to diagnose cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy in order to implement measures to prevent cerebrovascular diseases in both patients and their family members.


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