scholarly journals 3-Tesla Study of the Spinal Cord White Matter

2009 ◽  
Vol 22 (1_suppl) ◽  
pp. 85-93
Author(s):  
L. Albini Riccioli ◽  
A.F. Marliani ◽  
M. Leonardi

Spinal cord as soon as brain, can be affected by dysmyelinating and demyelinating diseases, as Multiple Sclerosis (MS), Acute Disseminated Encephalomyelitis (ADEM), Neuromyelis Optica (NMO) and Transverse Myelitis. Investigation of the spinal cord with a high field strength MR system is hampered by the inhomogeneous magnetic field, physiological movements and the small size of the anatomical area. We describe normal and pathological neuroradiological findings in spinal cord white matter and the parameters of optimized sequences for use with the 3T MR systems.

2008 ◽  
Vol 15 (2) ◽  
pp. 180-188 ◽  
Author(s):  
CP Gilmore ◽  
JJG Geurts ◽  
N Evangelou ◽  
JCJ Bot ◽  
RA van Schijndel ◽  
...  

Background Post-mortem studies demonstrate extensive grey matter demyelination in MS, both in the brain and in the spinal cord. However the clinical significance of these plaques is unclear, largely because they are grossly underestimated by MR imaging at conventional field strengths. Indeed post-mortem MR studies suggest the great majority of lesions in the cerebral cortex go undetected, even when performed at high field. Similar studies have not been performed using post-mortem spinal cord material. Aim To assess the sensitivity of high field post-mortem MRI for detecting grey matter lesions in the spinal cord in MS. Methods Autopsy material was obtained from 11 MS cases and 2 controls. Proton Density-weighted images of this formalin-fixed material were acquired at 4.7Tesla before the tissue was sectioned and stained for Myelin Basic Protein. Both the tissue sections and the MR images were scored for grey matter and white matter plaques, with the readers of the MR images being blinded to the histopathology results. Results Our results indicate that post-mortem imaging at 4.7Tesla is highly sensitive for cord lesions, detecting 87% of white matter lesions and 73% of grey matter lesions. The MR changes were highly specific for demyelination, with all lesions scored on MRI corresponding to areas of demyelination. Conclusion Our work suggests that spinal cord grey matter lesions may be detected on MRI more readily than GM lesions in the brain, making the cord a promising site to study the functional consequences of grey matter demyelination in MS.


2014 ◽  
Author(s):  
J William Lindsey

Multiple sclerosis (MS) is a relatively common cause of neurologic symptoms and disability in young adults. The distinguishing pathologic features of MS are loss of myelin and inflammation in the central nervous system (CNS). The myelin sheath is essential for rapid conduction of nerve signals along large-diameter axons. Oligodendrocytes produce and maintain myelin in the CNS, and Schwann cells produce and maintain myelin in the peripheral nerves. In addition to MS, there are a number of related disorders causing demyelination, inflammation, or both in the CNS. This chapter discusses MS and related disorders, including neuromyelitis optica, optic neuritis, acute disseminated encephalomyelitis, transverse myelitis, Behçet syndrome, neurosarcoidosis, inherited demyelinating diseases (leukodystrophies, cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy [CADASIL]), and virus-induced demyelination (progressive multifocal leukoencephalopathy, subacute sclerosing panencephalitis). The section on MS covers epidemiology, etiology/genetics, pathogenesis, diagnosis, differential diagnosis, management, and prognosis. Figures include organization of the microenvironment of larger-diameter axons, typical magnetic resonance imaging findings in MS and neuromyelitis optica, postgadolinium images of the cervical spine in MS, and an approach to treatment of relapsing-remitting MS. Tables list MS and related disorders, distribution of neurologic deficits at the onset of MS, differential diagnosis of MS, disease-modifying therapies for relapsing-remitting MS, and selected leukodystrophies, as well as diagnostic criteria and selected symptomatic therapies for MS. This review contains 3 highly rendered figures, 7 tables, and 82 references.


2015 ◽  
Author(s):  
J William Lindsey

Multiple sclerosis (MS) is a relatively common cause of neurologic symptoms and disability in young adults. The distinguishing pathologic features of MS are loss of myelin and inflammation in the central nervous system (CNS). The myelin sheath is essential for rapid conduction of nerve signals along large-diameter axons. Oligodendrocytes produce and maintain myelin in the CNS, and Schwann cells produce and maintain myelin in the peripheral nerves. In addition to MS, there are a number of related disorders causing demyelination, inflammation, or both in the CNS. This chapter discusses MS and related disorders, including neuromyelitis optica, optic neuritis, acute disseminated encephalomyelitis, transverse myelitis, Behçet syndrome, neurosarcoidosis, inherited demyelinating diseases (leukodystrophies, cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy [CADASIL]), and virus-induced demyelination (progressive multifocal leukoencephalopathy, subacute sclerosing panencephalitis). The section on MS covers epidemiology, etiology/genetics, pathogenesis, diagnosis, differential diagnosis, management, and prognosis. Figures include organization of the microenvironment of larger-diameter axons, typical magnetic resonance imaging findings in MS and neuromyelitis optica, postgadolinium images of the cervical spine in MS, and an approach to treatment of relapsing-remitting MS. Tables list MS and related disorders, distribution of neurologic deficits at the onset of MS, differential diagnosis of MS, disease-modifying therapies for relapsing-remitting MS, and selected leukodystrophies, as well as diagnostic criteria and selected symptomatic therapies for MS.   This chapter contains 3 highly rendered figures, 7 tables, 82 references, 1 teaching slide set, and 5 MCQs.


2005 ◽  
Vol 11 (6) ◽  
pp. 735-738 ◽  
Author(s):  
M Nakamura ◽  
M Endo ◽  
K Murakami ◽  
H Konno ◽  
K Fujihara ◽  
...  

We report a case of neuromyelitis optica (NMO) with a large cerebral lesion. The patient had an episode of fever and consciousness disturbance with a tumefactive frontal white matter lesion at age 43, and then repeated bilateral optic neuritis and transverse myelitis until she died at age 63. Histopathological examinations revealed that marked tissue destruction, cavities and inflammatory changes typical of NMO were seen in the cerebrum as well as the optic nerves and spinal cord. This is the first autopsied case of NMO with a tumefactive cerebral lesion that later became cavitary.


1947 ◽  
Vol 85 (1) ◽  
pp. 131-140 ◽  
Author(s):  
Isabel M. Morgan

By subcutaneous injection of central nervous tissue emulsified with adjuvants according to Freund's technique it has been possible to induce in the majority of monkeys an acute disseminated encephalomyelitis which is interpreted as an isoimmunization to CNS tissue. Positive reactions occurred only in response to CNS tissue containing white matter; i.e., cerebral white matter, spinal cord (whether normal or poliomyelitis-infected), and cortical "gray" matter (with an estimated 10 per cent contamination with white matter). No reaction occurred when peripheral nerve or kidney suspension or saline alone was injected with adjuvants. The perivascular and extravascular infiltration induced was confined to the CNS.


2015 ◽  
Author(s):  
J William Lindsey

Multiple sclerosis (MS) is a relatively common cause of neurologic symptoms and disability in young adults. The distinguishing pathologic features of MS are loss of myelin and inflammation in the central nervous system (CNS). The myelin sheath is essential for rapid conduction of nerve signals along large-diameter axons. Oligodendrocytes produce and maintain myelin in the CNS, and Schwann cells produce and maintain myelin in the peripheral nerves. In addition to MS, there are a number of related disorders causing demyelination, inflammation, or both in the CNS. This chapter discusses MS and related disorders, including neuromyelitis optica, optic neuritis, acute disseminated encephalomyelitis, transverse myelitis, Behçet syndrome, neurosarcoidosis, inherited demyelinating diseases (leukodystrophies, cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy [CADASIL]), and virus-induced demyelination (progressive multifocal leukoencephalopathy, subacute sclerosing panencephalitis). The section on MS covers epidemiology, etiology/genetics, pathogenesis, diagnosis, differential diagnosis, management, and prognosis. Figures include organization of the microenvironment of larger-diameter axons, typical magnetic resonance imaging findings in MS and neuromyelitis optica, postgadolinium images of the cervical spine in MS, and an approach to treatment of relapsing-remitting MS. Tables list MS and related disorders, distribution of neurologic deficits at the onset of MS, differential diagnosis of MS, disease-modifying therapies for relapsing-remitting MS, and selected leukodystrophies, as well as diagnostic criteria and selected symptomatic therapies for MS.   This chapter contains 3 highly rendered figures, 7 tables, 82 references, 1 teaching slide set, and 5 MCQs.


2020 ◽  
Vol 6 (3) ◽  
pp. 20200098
Author(s):  
Mohamed Abdelhady ◽  
Ahmed Elsotouhy ◽  
Surjith Vattoth

Spinal cord imaging findings in COVID-19 are evolving with the increasing frequency of neurological symptoms among COVID-19 patients. Several mechanisms are postulated to be the cause of central nervous system affection including direct virus neuroinvasive potential, post infectious secondary immunogenic hyperreaction, hypercoagulability, sepsis and possible vasculitis as well as systemic and metabolic complications associated with critical illness. Only a few case reports of spinal cord imaging findings are described in COVID-19, which include transverse myelitis, acute disseminated encephalomyelitis and post-infectious Guillain Barre’ syndrome. We are describing a case of myelitis which, to the best of our knowledge, is the first reported case of myelitis in COVID-19.


Author(s):  
Lilley Kate ◽  
◽  
Sudarshini Ramanathan ◽  
Russell C Dale ◽  
Fabienne Brilot ◽  
...  

The existence of antibodies to myelin oligodendrocyte glycoprotein (MOG) in some patients with CNS demyelinating disease has been recognised for 30 years, but their clinical utility as biomarkers, and potential pathogenicity in humans has only become apparent in the past 15 years. The advent of more precise live cell-based assays for antibody detection in serum and cerebrospinal fluid (CSF) has greatly refined the clinical phenotype of demyelinating diseases associated with MOG antibodies. Distinct patterns of MOG antibody associated disorder (MOGAD) include acute disseminated encephalomyelitis (ADEM) in children; and overlap with neuromyelitis optica spectrum disorders (including classical Devic’s presentations), optic neuritis, transverse myelitis, and focal encephalitis in both children and adults. A number of other rare presentations have also been described. Here we summarise what is currently known of the pathophysiology, clinical presentation and management of MOGAD.


2019 ◽  
Vol 62 (3) ◽  
pp. 123-126
Author(s):  
Iveta Chroustová ◽  
Miroslav Mareš ◽  
Leoš Ungermann ◽  
Edvard Ehler

Antibodies against myelin oligodendrocyte glycoprotein cause inflammatory lesions of central myelin – in optic nerves, of the brainstem, and spinal cord. There are characteristic changes of CNS white matter, protein-cytological association in cerebrospinal fluid, MOG IgG antibodies, a very important differential diagnosis and a relatively mild course.


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