Neuropsychological effects of interferon β‐1a in relapsing multiple sclerosis

Js, Fischer; Rl, Priore; Ld, Jacobs; Dl, Cookfair; Ra, Rudick; Rm, Herndon; Richert,; Am, Salazar; De, Goodkin; Cv, Granger; Jh, Simon; Jh, Grafman; Lezak,; Km, O'Reilly Hovey; Kk, Perkins; Barilla-Clark, Danielle; Schacter, Mark; Dw, Shucard; Al, Davidson; Ke, Wende; Dn, Bourdette; Mf, Kooijmans-Coutinho

doi:10.1002/1531-8249(200012)48:6<885::aid-ana9>3.3.co;2-t

Cited by 69 publications

(7 citation statements)

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“…Treatment type may contribute to impairment of cognitive functions in people with MS. We found that attention, memory, language, and informationprocessing speed were significantly better in patients receiving immunomodulatory drugs compared to those on immunosuppressive medications. This agreed with Fischer and colleagues, who reported that interferon Beta 1a had a significant favorable effect on attention, memory, visuospatial abilities, information processing, and problem solving [22]. Available immune-modulatory treatments for multiple sclerosis rapidly inhibit the inflammation and reduce the progression of brain atrophy, and they may also have neuro-protective properties [6].…”

Section: Discussionsupporting

confidence: 84%

Clinical predictors to cognitive impairment in multiple sclerosis patients

Elshebawy

Fahmy

Elfayoumy

et al. 2021

Egypt J Neurol Psychiatry Neurosurg

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Background Cognitive dysfunction is increasingly recognized in multiple sclerosis, even in the early phase of the disease. Multiple sclerosis patients with even mild cognitive deficits may experience greater difficulties in social contact and daily activities, irrespective of physical handicap. This study aimed to estimate clinical predictors of cognitive dysfunction in a sample of Egyptian people with MS. Results Significant worse performance in assessed cognitive scales was observed in people with MS as compared to controls. This was related to low educational level, long disease duration, initial cerebellar and motor attacks, progressive course, frequent relapses, and immunosuppressive medications. Cognitive assessment scales were significantly negatively correlated with disability measured by Expanded Disability Status Scale (EDSS) scores. Conclusion Predictors of cognitive impairment in people with MS were low educational level, longer disease duration, type of initial attack, frequent relapses, progressive form, higher clinical disability, and immunosuppressive treatment.

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Section: Discussionsupporting

confidence: 84%

Clinical predictors to cognitive impairment in multiple sclerosis patients

Elshebawy

Fahmy

Elfayoumy

et al. 2021

Egypt J Neurol Psychiatry Neurosurg

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“…Use of disease modifying therapy for multiple sclerosis has a demonstrable slowing effect on dysfunction 60. Rudick et al 61 demonstrated that patients with relapsing-remitting disease on interferon β-1a therapy had a significant reduction in the progression of brain atrophy during the second year of treatment.…”

Section: Discussionmentioning

confidence: 99%

A longitudinal study of brain atrophy and cognitive disturbances in the early phase of relapsing-remitting multiple sclerosis

Zivadinov

Sepčić

Nasuelli

et al. 2001

Journal of Neurology, Neurosurgery &Amp; Psychiatry

356

266

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Objective-(a) To establish whether the cognitive decline of the early phase of relapsing-remitting multiple sclerosis depends on the progression of the burden of disease, or on the loss of brain parenchyma, or is influenced by both; (b) to monitor the loss of brain parenchyma in the early phase of the disease; and (c) to examine its possible relation with the progression of physical disability. Methods-For 2 years 53 patients with clinically definite relapsing-remitting multiple sclerosis with disease duration 1-5 years and expanded disability status scale<5.0 at baseline were monitored. The neuropsychological performances, the psychological functioning, the neurological impairment, and the disability have been assessed at baseline and after 2 years. Patients also underwent PD/T2 and T1 weighted brain MRI. T2 and T1 lesion volumes were measured by a semiautomatic technique. Quantification of brain parenchymal volumes was obtained using a highly reproducible computerised interactive program. The relation between cognitive impairment and MRI findings has been investigated by partial correlation and stepwise multiple regression analyses excluding the eVects of age, education, anxiety, depression, and total days of steroid use. Results-In the 2 years of the study the mean change for T2 and T1 lesion volumes and brain parenchymal volumes were +1.7 ml (95% confidence interval (95% CI) 1.3-2.2, p=0.005, (29.8%); +0.2 ml, 95% CI 0.15-0.26, p=0.004, (25%); and -32.3 ml, 95% CI 24.2-42.3, p<0.0001, (2.7%), respectively. Overall, 14 patients (26.4%) were judged to be cognitively impaired at baseline and 28 (52.8%) at the end of the follow up. Of the 18 neuropsychological tests and subtests employed in the study, patients with multiple sclerosis failed 5.8 (SD 2.3) tests at the baseline and 8.4 (SD 2.9) (p<0.0001) tests at the end of the study. When the cognitive changes were examined in individual patients, five (9.4%) of them were considered cognitively improved, 33 (62.3%) remained stable, and 15 (28.3%) worsened over 2 years. T2 and T1 volume changes in improved, stable, and worsened patients did not show any significant diVerence, whereas brain parenchymal volume decrease in cognitively worsened patients was significantly greater (−66 ml (5.4%), 95% CI 37-108.9, p=0.0031). The cognitive impairment was independently predicted over 2 years only by the change of brain parenchymal volumes (R=0.51, p=0.0003). Ten patients (18.9%), who worsened by one or more points in the EDSS during the follow up period had significant decreases in brain parenchymal volumes (−99 ml (8%), 95% CI 47.6-182.3, p=0.005). At the end of the study the loss of brain parenchyma correlated significantly with change in EDSS (r= 0.59, p<0.0001). Conclusions-In the early phase of relapsing-remitting multiple sclerosis the cognitive deterioration relies more on the development of brain parenchymal volume atrophy than on the extent of burden of disease in the brain. The loss of brain parenchymal volume underlies the progressive accumulation of phy...

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“…Two‐year data from the phase III study showed that IFN β ‐1a (Avonex ® , Biogen, Inc.) was effective in slowing disability progression, reducing exacerbations, reducing disease activity as measured by magnetic resonance imaging (MRI) scans, and improving cognitive function (4, 16–19). The annual exacerbation rate calculated after 2 years of IFN β ‐1a treatment in the present study of 96 patients (mean = 0.52) is slightly lower than that observed in 85 patients from the phase III study after 2 years of IFN β ‐1a treatment (mean = 0.67) (4).…”

Section: Discussionmentioning

confidence: 99%