Modifiable factors influencing relapses and disability in multiple sclerosis.

Posted on January 16, 2013 by Maurice Preter MD

Mult Scler. 2010 Jul;16(7):773-85. doi: 10.1177/1352458510367721. Epub 2010 May 18.

Modifiable factors influencing relapses and disability in multiple sclerosis.

D’hooghe MB, Nagels G, Bissay V, De Keyser J.

Source

National Center For Multiple Sclerosis, Melsbroek, Belgium. marie.dhooghe@ms-centrum.be

Abstract

A growing body of literature indicates that the natural course of multiple sclerosis can be influenced by a number of factors. Strong evidence suggests that relapses can be triggered by infections, the postpartum period and stressful life events. Vaccinations against influenza, hepatitis B and tetanus appear to be safe. Surgery, general and epidural anaesthesia, and physical trauma are not associated with an increased risk of relapses. Factors that have been associated with a reduced relapse rate are pregnancy, exclusive breastfeeding, sunlight exposure and higher vitamin D levels. A number of medications, including hormonal fertility treatment, seem to be able to trigger relapses. Factors that may worsen progression of disability include stressful life events, radiotherapy to the head, low levels of physical activity and low vitamin D levels. Strong evidence suggests that smoking promotes disease progression, both clinically and on brain magnetic resonance imaging. There is no evidence for an increased progression of disability following childbirth in women with multiple sclerosis. Moderate alcohol intake and exercise might have a neuroprotective effect, but this needs to be confirmed.

PMID:

20483884

[PubMed – indexed for MEDLINE]

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Fingolimod treatment for multiple sclerosis patients What do we do with varicella?

Posted on January 16, 2013 by Maurice Preter MD

Fingolimod treatment for multiple sclerosis patie… [Ann Neurol. 2011] – PubMed – NCBI.

Ann Neurol. 2011 Oct;70(4):673-4; author reply 674. doi: 10.1002/ana.22605.

Fingolimod treatment for multiple sclerosis patients What do we do with varicella?

Winkelmann A, Loebermann M, Reisinger EC, Hartung HP, Zettl UK.

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PMID:
22028236
[PubMed – indexed for MEDLINE]

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Melanoma occurring during treatment with fingo… [Arch Dermatol. 2011] – PubMed – NCBI

Posted on January 16, 2013 by Maurice Preter MD

Arch Dermatol. 2011 Aug;147(8):991-2. doi: 10.1001/archdermatol.2011.212.

Melanoma occurring during treatment with fingolimod for multiple sclerosis: a case report.

Conzett KB, Kolm I, Jelcic I, Kamarachev J, Dummer R, Braun R, French LE, Linnebank M, Hofbauer GF.

PMID:

21844470

[PubMed – indexed for MEDLINE]

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Delayed fingolimod-associated asystole. [Mult Scler. 2011] – PubMed – NCBI

Posted on January 16, 2013 by Maurice Preter MD

Mult Scler. 2011 Nov;17(11):1387-9. doi: 10.1177/1352458511410344. Epub 2011 Jun 7.

Delayed fingolimod-associated asystole.

Espinosa PS, Berger JR.

Source

North Oaks Neurology, Hammond, LA, USA. ps.espinosa@gmail.com

Abstract

Oral fingolimod (Gilenya) is a sphingosine-1-phosphate-receptor modulator that prevents the egress of lymphocytes from lymph nodes. Fingolimod reduces relapses and delays disability progression in patients with relapsing forms of multiple sclerosis (MS). We report a patient with MS who developed asystole and sustained bradycardia 21 hours after the first dose of fingolimod.

PMID:

21652609

[PubMed – indexed for MEDLINE]

Publication Types, MeSH Terms, Substances

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via Delayed fingolimod-associated asystole. [Mult Scler. 2011] – PubMed – NCBI.

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25-Hydroxyvitamin D, dementia, and cerebrovascular… [Neurology. 2010] – PubMed – NCBI

Posted on January 15, 2013 by Maurice Preter MD

Neurology. 2010 Jan 5;74(1):18-26. doi: 10.1212/WNL.0b013e3181beecb7. Epub 2009 Nov 25.

25-Hydroxyvitamin D, dementia, and cerebrovascular pathology in elders receiving home services.

Buell JS, Dawson-Hughes B, Scott TM, Weiner DE, Dallal GE, Qui WQ, Bergethon P, Rosenberg IH, Folstein MF, Patz S, Bhadelia RA, Tucker KL.

Source

Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, 711 Washington St., Boston, MA 02111, USA.

Abstract

BACKGROUND:

Vitamin D deficiency has potential adverse effects on neurocognitive health and subcortical function. However, no studies have examined the association between vitamin D status, dementia, and cranial MRI indicators of cerebrovascular disease (CVD).

METHODS:

Cross-sectional investigation of 25-hydroxyvitamin D [25(OH)D], dementia, and MRI measures of CVD in elders receiving home care (aged 65-99 years) from 2003 to 2007.

RESULTS:

Among 318 participants, the mean age was 73.5 +/- 8.1 years, 231 (72.6%) were women, and 109 (34.3%) were black. 25(OH)D concentrations were deficient (<10 ng/mL) in 14.5% and insufficient (10-20 ng/mL) in 44.3% of participants. There were 76 participants (23.9%) with dementia, 41 of which were classified as probable AD. Mean 25(OH)D concentrations were lower in subjects with dementia (16.8 vs 20.0 ng/mL, p < 0.01). There was a higher prevalence of dementia among participants with 25(OH)D insufficiency (< or =20 ng/mL) (30.5% vs 14.5%, p < 0.01). 25(OH)D deficiency was associated with increased white matter hyperintensity volume (4.9 vs 2.9 mL, p < 0.01), grade (3.0 vs 2.2, p = 0.04), and prevalence of large vessel infarcts (10.1% vs 6.9%, p < 0.01). After adjustment for age, race, sex, body mass index, and education, 25(OH)D insufficiency (< or =20 ng/mL) was associated with more than twice the odds of all-cause dementia (odds ratio [OR] = 2.3, 95% confidence interval [CI] 1.2-4.2), Alzheimer disease (OR = 2.5, 95% CI 1.1-6.1), and stroke (with and without dementia symptoms) (OR = 2.0, 95% CI 1.0-4.0).

CONCLUSIONS:

Vitamin D insufficiency and deficiency was associated with all-cause dementia, Alzheimer disease, stroke (with and without dementia symptoms), and MRI indicators of cerebrovascular disease. These findings suggest a potential vasculoprotective role of vitamin D.

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25-hydroxyvitamin D, dementia, and cerebrovascular pathology in elders receiving home services. [Neurology. 2010]

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