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Objective: To compare the abnormalities shown by magnetic resonance imaging of the brain in three clinically distinct groups of patients with multiple sclerosis, and to correlate the extent of abnormality with the degree of clinical disability in the three groups.
Design: All patients underwent magnetic resonance imaging and full neurological examination, and their disability was scored according to the expanded Kurtzke disability state scale.
Setting: National Hospital for Nervous Diseases (Multiple Sclerosis NMR Research Group).
Patients: Three groups of patients with confirmed multiple sclerosis were studied: 12 patients with minimal disability despite a long (greater than 10 years) duration of illness (benign multiple sclerosis), 16 who had developed progressive disability after a relapsing and remitting course (secondary progressive multiple sclerosis), and 13 who had had progressive disability from the onset of the disease (primary progressive multiple sclerosis).
Main Outcome Measures: Number and size of lesions in 17 anatomically defined sites; total lesion load, estimated with an arbitrary scoring system weighted for the size of lesions; and disability score.
Results: Magnetic resonance imaging showed that all 41 patients had abnormalities. These were extensive in the groups with secondary progressive and benign disease compared with the group with primary progressive disease. The lesions in the patients with secondary progressive disease were larger and more confluent than those in the two other groups (p = 0.007). Most lesions (85%) in the patients with primary progressive disease were under 5 mm in diameter; this percentage was higher than that in the two other groups (p = 0.032). Consequently the patients with primary progressive disease had the lowest mean lesion load (36.7); that in the patients with benign disease was 52.7 and that in the patients with secondary progressive disease 64.6 (p = 0.05). No correlation existed between disability and total lesion load. The distribution of brain lesions and of detectable lesions of the spinal cord, and the frequency of cortical atrophy, were similar in all groups.
Conclusions: No relation was found between the degree of clinical disability and the extent of abnormality shown by magnetic resonance imaging: patients with clinically benign disease often had extensive abnormalities and those with primary progressive disease had surprisingly few lesions. Though magnetic resonance imaging increases knowledge of the disease process in multiple sclerosis and is invaluable in diagnosis, it is not helpful in predicting disability in individual patients.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1662448 | PMC |
http://dx.doi.org/10.1136/bmj.300.6725.631 | DOI Listing |
Mult Scler
September 2025
Department of Neurology with Friedrich Baur Institute, LMU University Hospital, LMU Munich, Munich, Germany.
Description of a patient with multiple sclerosis (MS) who underwent immunotherapy with ocrelizumab and suffered a severe course of tick-borne encephalitis (TBE): A 33-year-old man presented with acute cerebellitis with tonsillar herniation. The initial suspected diagnosis of TBE was confirmed after a significant diagnostic delay, likely caused by negative serological testing due to B-cell depletion from ocrelizumab treatment for underlying MS. TBE diagnosis was made using polymerase chain reaction (PCR) and oligo-hybrid capture metagenomic next-generation sequencing (mNGS) of cerebral spinal fluid and brain biopsy samples which yielded a near-full length TBE Virus (TBEV) genome.
View Article and Find Full Text PDFMult Scler
September 2025
Department of Neurology, Medical University of Vienna, Vienna, Austria; Comprehensive Center for Clinical Neurosciences and Mental Health, Medical University of Vienna, Vienna, Austria.
Neuroinflammation has emerged as a central and dynamic component of the pathophysiology underlying a wide range of neurodegenerative disorders, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, Huntington's disease, and multiple sclerosis. Far from being a secondary consequence of neuronal damage, inflammatory processes (mediated by microglia, astrocytes, peripheral immune cells, and associated molecular mediators) actively shape disease onset, progression, and symptomatology. This review synthesizes current knowledge on the cellular and molecular mechanisms that govern neuroinflammatory responses, emphasizing both shared and disease-specific pathways.
View Article and Find Full Text PDFCell Death Differ
September 2025
Department of Neurology, China National Clinical Research Center for Neurological Diseases, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.