2008
DOI: 10.1002/art.23991
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Cognitive dysfunction in systemic lupus erythematosus: Past, present, and future

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Cited by 83 publications
(92 citation statements)
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“…However, axonal loss and demyelination may also result from direct antibody attack on neuronal cells, either on neuronal bodies or in the WM tracts. 2 Although SLE and MS have notable differences in etiology, there is a marked overlap concerning the CNS inflammatory and neurodegenerative nature of these 2 diseases. 3 In 1972, Fulford et al 4 first coined the term "lupoid sclerosis" when referring to patients with SLE who presented with symptoms similar to those in MS. Additionally, neuropsychological and cognitive testing revealed similarities in cognitive profiles of patients with MS and those with SLE that may be the result of similar dysfunctional CNS structures.…”
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confidence: 99%
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“…However, axonal loss and demyelination may also result from direct antibody attack on neuronal cells, either on neuronal bodies or in the WM tracts. 2 Although SLE and MS have notable differences in etiology, there is a marked overlap concerning the CNS inflammatory and neurodegenerative nature of these 2 diseases. 3 In 1972, Fulford et al 4 first coined the term "lupoid sclerosis" when referring to patients with SLE who presented with symptoms similar to those in MS. Additionally, neuropsychological and cognitive testing revealed similarities in cognitive profiles of patients with MS and those with SLE that may be the result of similar dysfunctional CNS structures.…”
mentioning
confidence: 99%
“…7,8 It is possible that these cognitive disturbances may be attributed to decreased WM integrity, the presence and extent of WM lesions, or GM damage, all of which are present in patients with MS and those with SLE. 2,3,[8][9][10] Unlike in MS, the relationship between cerebral pathology and resulting neuropsychiatric disorders in SLE is not well-established. Neuropsychiatric symptoms range from transient to chronic and are heterogeneous among patients.…”
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confidence: 99%
“…Cerebral atrophy, white matter lesions and cerebral infarction have been correlated with the severity of CD 8 ( Figure 1). An apparently normal MRI in CD may be associated with microstructural and metabolic changes in white matter tissue suggesting potentially immune-mediated myelinopathy, which is best seen by spectroscopy and other advanced MRI techniques 19 . The pathophysiology of CD remains to be fully understood and may involve vascular abnormalities, intrathecal inflammatory cytokines and BBB disruption.…”
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confidence: 99%
“…The treatment for CD remains uncertain. Identification and management of secondary or exacerbating causes of CD is recommended 19 . Patients may respond to methylphenidate or prednisone (0.5 mg/kg) 19 .…”
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confidence: 99%
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