Vitamin D and multiple sclerosis: a critica… [Acta Neurol Belg. 2012] – PubMed – NCBI

Posted on January 1, 2013 by Maurice Preter MD

Vitamin D and multiple sclerosis: a critica… [Acta Neurol Belg. 2012] – PubMed – NCBI.

Acta Neurol Belg. 2012 Dec;112(4):327-33. doi: 10.1007/s13760-012-0108-z. Epub 2012 Jul 6.

Vitamin D and multiple sclerosis: a critical review and recommendations on treatment.

Faridar A, Eskandari G, Sahraian MA, Minagar A, Azimi A.

Source

Department of Neurology, University of California, San Francisco, USA.

Abstract

Multiple sclerosis (MS) is an immune-mediated and degenerative disease of nervous system, which affects mostly young adults. Vitamin D deficiency is a well-known environmental risk factor for MS and is considerable in terms of immediate clinical implications. In addition to its classical action on regulation of bone homeostasis, vitamin D may have a potent impact on cytokine profiles and neuro-inflammation. Given the immunomodulatory effects of vitamin D and its high rate of deficiency in MS patients, prescribing vitamin D is a remarkable issue in MS. The results from several experimental and clinical studies indicate that vitamin D supplementation may ameliorate the inflammation during the relapse phase and attenuate disease progression. We present the experimental and clinical studies, which assessed the effects of vitamin D on the pathophysiology, prevalence and management of MS. The authors also discuss current recommendations on prescription of this vitamin to MS patients.

PMID:
22767049
[PubMed – in process]

LinkOut – more resources

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Current Affairs: Hillary Clinton’s Illness and Prognosis of Cerebral Venous Thrombosis

Posted on January 1, 2013 by Maurice Preter MD

 

Our classic long-term follow up of CVT. Fulltext is available here, courtesy of Stroke:

Long-term Prognosis in Cerebral Venous Thrombosis

Follow-up of 77 Patients

  1. Maurice Preter, MD;
  2. Christophe Tzourio, MD;
  3. Alain Ameri, MD;
  4. Marie-Germaine Bousser, MD

+ Author Affiliations


  1. From the Department of Neurology, Albert Einstein College of Medicine, Bronx, NY (M.P.); INSERM, U 360, Recherches Epidémiologiques en Neurologie et Psychopathologie, La Salpêtrière, Paris (C.T.); Service de Neurologie, Hôpital de Meaux, Meaux (A.A.); and Service de Neurologie, Hôpital Saint-Antoine, Paris (M.-G.B.), France.

Abstract

Background and Purpose Very little is known about the long-term outcome of patients with cerebral venous thrombosis (CVT), particularly regarding the risk of residual epilepsy and further thrombotic events. We retrospectively studied 77 patients with CVT diagnosed by angiography and/or MRI.

Methods A cohort of 77 patients aged 18 to 77 (mean, 38.5) years with CVT, evaluated from 1975 through 1990, was followed up for a mean of 77.8 months (range, 14 to 204 months; median, 63 months). Information on death, neurological status, seizures, recurrent CVT, other thrombotic events, and subsequent pregnancies was obtained from direct observation, mail questionnaire, or telephone interviews.

Results Sixty-six of 77 patients (85.7%) had no neurological sequelae during follow-up. Eleven patients (14.3%) remained neurologically impaired. Two who initially presented with isolated intracranial hypertension had blindness due to optic atrophy. The other 9 had focal signs at the time of CVT and were left with various cognitive or focal deficits. Four of 28 (14.3%) patients who had seizures at the acute stage had recurrent seizures. One of the 51 patients with lateral sinus thrombosis developed a dural arteriovenous fistula. Nine of the 77 patients (11.7%) suffered a second CVT, all but one in the first year. Noncerebral thrombotic events occurred in 11 patients (14.3%). No recurrence of CVT occurred during later pregnancies, but 1 patient had a postpartum deep vein thrombosis.

Conclusions In the present series, CVT has an essentially good long-term prognosis. The frequency of long-standing epilepsy was low, suggesting that long-term anticonvulsant treatment is not necessary in the majority of cases. A second CVT or another thrombotic episode occurred in 20% of patients, stressing the need in a minority of cases for long-term anticoagulation.

Key Words:

 

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Vitamin D deficiency treated by consuming UVB-irradiated mushrooms

Posted on December 6, 2012 by Maurice Preter MD

Vitamin D deficiency treated by consuming UVB-irradiated mushrooms.

Vitamin D deficiency treated by consuming UVB-irradiated mushrooms

Andrew Ozzard, DCH, MRCPCH, GP Registrar and Gurdip Hear, BSc, DCH, DRCOG, DFFP, MRCGP, GP Trainer

Crosby House Surgery, Slough
Gavin Morrison, MBBS, FY1

Leighton Hospital, Crewe, Cheshire
Mike Hoskin, DRCOG, MRCGP, GP Trainer
Author information ► Article notes ► Copyright and License information ►

Abstract

Deficiency of vitamin D is usually caused by dietary deficiency and/or lack of exposure to sunlight in dark skinned individuals living at northern latitudes. Simple vitamin D deficiency is commonly treated by prescribing a vitamin D containing calcium supplement. This report presents a patient who rejected this approach and instead, after researching alternative treatment options independently, opted to self-treat by consuming UVB-irradiated mushrooms. The beneficial effect of this on the patient’s plasma biochemical markers is shown. Further research into the beneficial effect of consuming UVB-irradiated mushrooms is required.

Keywords: food irradiation, vitamin D, vitamin D deficiency
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ADJUVANT USE OF THE KETOGENIC DIET FOR THE TREATMENT OF MALIGNANT BRAIN TUMORS INHIBITS CYCLOOXYGENASE-2 EXPRESSION AND REDUCES TUMOR-ASSOCIATED EDEMA

Posted on December 3, 2012 by Maurice Preter MD

53. Basic Science

Title: ADJUVANT USE OF THE KETOGENIC DIET FOR THE TREATMENT OF MALIGNANT BRAIN TUMORS INHIBITS CYCLOOXYGENASE-2 EXPRESSION AND REDUCES TUMOR-ASSOCIATED EDEMA

Author: Adrienne C Scheck PhD
Co-authors Eric C. Woolf, Gregory Turner, Vikram D. Kodibagkar, Rohini Vidya Shankar, Mark C. Preul, Mohammed G. Abdelwahab, Julie A. Charlton. Phoenix, AZ Keywords: glioma, edema, cyclooxygenase 2, mouse model

Malignant gliomas are uniformly fatal despite treatment including surgery, chemotherapy and radiation. One source of morbidity is brain edema caused by tumor growth and/or treatment. This can have a variety of sequelae including headaches, seizures and steroid dependence. We previously used a bioluminescent intracranial mouse model of malignant glioma to demonstrate that a ketogenic diet (KD) extends survival following tumor implantation, and potentiates the therapeutic effects of radiation and chemotherapy. The KD also prevents the increased expression of Cyclooxygenase 2 (COX2) seen in tumors from animals fed standard rodent chow (SD). COX2 is a mediator of inflammation and we hypothesize that KD is reducing tumor-associated edema through its inhibition and concomitant downstream effects. Bioluminescence is a quantitative measure of live tumor cells and we have found that animals maintained on KD have more tumor-associated bioluminescence when they succumb! to their disease than do animals maintained on SD. Survival is a function of overall tumor burden consisting of the tumor and peritumoral edema. The increased bioluminescence in tumor from animals fed KD suggests that the diet may be reducing the contribution of peritumoral edema to the overall tumor burden. Taken together, our data demonstrates that metabolic alteration not only affects tumor bioenergetics, it alters the expression of genes involved in other aspects of tumor growth and therapy response. The adjuvant use of KD for brain tumor therapy may improve the patients’ quality of life in addition to extending survival.

Supported by Students Supporting Brain Tumor Research and Arizona Biomedical Research Commission.

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A PET AND MRI APPROACH TO STUDY BRAIN GLUCOSE AND KETONE METABOLISM DURING AGING AND ALZHEIMER’S DISEASE.

Posted on December 3, 2012 by Maurice Preter MD

52.
Title A PET AND MRI APPROACH TO STUDY BRAIN GLUCOSE AND KETONE METABOLISM DURING AGING AND ALZHEIMER’S DISEASE.

Author: Alexandre Courchesne-Loyer, MSc1,2,
Co-Authors: Christian A. Castellano, PhD1,2, Scott Nugent, BSc1,2, Maggie Roy, MSc1,2, Mélanie Fortier, MSc1, Sébastien Tremblay, PhD1,4, Éric Turcotte MD4, Tamas Fulop MD, PhD1,3, Stephen C. Cunnane, PhD1,2,3,

(1) Research Center on Aging, Sherbrooke, QC, Canada
(2) Department Physiology and Biophysics, Université de Sherbrooke, QC, Canada
(3) Department of Medicine, Université de Sherbrooke, QC, Canada
(4) Department of Radiobiology and Nuclear Medicine, Université de Sherbrooke, QC, Canada

Key words: PET, ketone, Alzheimer’s

Background: Lower brain glucose uptake can be present before the onset of aging- associated cognitive deterioration and may increase the risk of Alzheimer’s disease (AD). Ketones are the brain’s main alternative energy substrates to glucose. We have developed the positron emission tomography (PET) tracer – [11C]-acetoacetate ([11C]-AcAc) – to study brain ketone metabolism in humans. Our goal was to assess whether deteriorating brain fuel uptake affects uptake of any brain fuel or is specific to glucose. This approach might also be informative about how ketogenic treatments improve cognition in AD and mild cognitive impairment.

Methods: Healthy elderly (65-85 y; n=15) and young adults (18-30 y; n=15), and 8 patients with mild AD underwent a dual tracer brain PET protocol with [11C]-AcAc followed by [18F]-FDG. Cerebral metabolic rates of AcAc (CMRAcAc) and glucose (CMRg) were calculated using an image-derived input function with correction for brain atrophy.

Results: Compared to young adults, CMRAcAc in the healthy elderly was 20-25% lower in specific brain regions, notably the superior frontal cortex and cingulate (p<0.01); CMRg in the elderly was also 15-20% lower in the caudate, thalamus and frontal cortex (p<0.01). Different brain regions had lower CMRg and CMRAcAc in AD than in the elderly.

Conclusion: Both major brain fuels are affected in aging and in AD but differently depending on the brain regions. We are developing protocols with ketogenic pharmaceuticals/nutriceuticals in order to sustainably induce mild ketonemia to determine whether it can correct or bypass deteriorating brain glucose uptake, thereby hopefully reducing the risk of cognitive decline. Financial support from CRC, CIHR, CFI, FRQS, CFQCU and the Université de Sherbrooke.

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