MISSED EVOLUTION OF DEMYELINIZING BRAIN LESIONS DURING SUPPLEMENTATION WITH NATURAL COMPOUNDS: A Case Report.

Main Article Content

Isabella Panfoli http://orcid.org/0000-0002-6261-1128 Silvia Ravera Daniela Calzia Cesare Santi

Abstract

Multiple sclerosis (MS) is an autoimmune inflammatory diseaseof the central nervous systemwhite matter, whose pathogenesis is incompletely understood. Plaques of demyelination are typically found in the periventricular and subcortical white matter. Evolution in space and time of new lesions form an initial Magnetic Resonance Imaging (MRI) report of demyelinating nature is not unusual, and it allows to formulate the diagnosis.  

We describe the case of a woman in her late forties who presented with, and after performing a cranial MRI showing multiple small lesions suggestive of  inflammatory demyelinating nature. An oral daily integration of diet with natural compounds (i.e. galactose, Coenzyme Q10and ferrous sulphate) was started. After 2 months of such supplementation numbness had disappeared fatigue and central symptoms had sensibly ameliorated. A follow-up brain MRI was completed 6 months in wellness, showed that multifocal lesions were unchanged, even though enhanced by gadolinium. Data are discussed in consideration of the presence of an aerobic metabolism in myelin and of the implication of galactose as a preferential substrate for hexose 6-phosphate dehydrogenase recently reported in myelin. We discuss the evolution of the condition and missing the diagnosis of MS, and the possible neuroprotective role of theoral dietary integration. Today, the patient has not any central symptom, is still under follow-up and treatment with the cited compounds and remains in a stationary condition.

Article Details

How to Cite
PANFOLI, Isabella et al. MISSED EVOLUTION OF DEMYELINIZING BRAIN LESIONS DURING SUPPLEMENTATION WITH NATURAL COMPOUNDS: A Case Report.. Medical Research Archives, [S.l.], v. 3, n. 9, may 2016. ISSN 2375-1924. Available at: <https://esmed.org/MRA/mra/article/view/491>. Date accessed: 28 mar. 2024.
Keywords
bioenergetics; biochemistry; neuroscience
Section
Case Reports

References

1. Matthews PM, et al. (2016) A practical review of the neuropathology and neuroimaging of multiple sclerosis. Pract Neurol. doi:10.1136/practneurol-2016-001381.
2. Koch-Henriksen N, Sørensen PS (2010) The changing demographic pattern of multiple sclerosis epidemiology. Lancet Neurol 9(5):520–32.
3. Kwon JY, Kim JY, Jeong JH, Park KD (2008) Multiple sclerosis and peripheral multifocal demyelinating neuropathies occurring in a same patient. J Clin Neurol 4(1):51–7.
4. Morelli A, Ravera S, Calzia D, Panfoli I (2012) Impairment of heme synthesis in myelin as potential trigger of multiple sclerosis. Med Hypotheses 78(6):707–710.
5. Polman CH, Wolinsky JS, Reingold SC (2005) Multiple sclerosis diagnostic criteria: three years later. Mult Scler 11(1):5–12.
6. Ge Y (2006) Multiple Sclerosis: The Role of MR Imaging. AJNR Am J Neuroradiol 27(6):1165–1176.
7. Filippi M, et al. (2016) MRI criteria for the diagnosis of multiple sclerosis: MAGNIMS consensus guidelines. Lancet Neurol 15(3):292–303.
8. Rovira A, León A (2008) MR in the diagnosis and monitoring of multiple sclerosis: an overview. Eur J Radiol 67(3):409–14.
9. D’haeseleer M, et al. (2015) Cerebral hypoperfusion: a new pathophysiologic concept in multiple sclerosis? J Cereb Blood Flow Metab 35(9):1406–10.
10. Broadwater L, et al. (2011) Analysis of the mitochondrial proteome in multiple sclerosis cortex. Biochim Biophys Acta 1812(5):630–41.
11. Ravera S, et al. (2009) Evidence for aerobic ATP synthesis in isolated myelin vesicles. Int J Biochem Cell Biol 41(7):1581–1591.
12. Ravera S, et al. (2015) Oxidative stress in myelin sheath: The other face of the extramitochondrial oxidative phosphorylation ability. Free Radic Res:1–36.
13. Ravera S, et al. (2015) Support of Nerve Conduction by Respiring Myelin Sheath: Role of Connexons. Mol Neurobiol. doi:10.1007/s12035-015-9216-0.
14. Ravera S, et al. (2009) Evidence for aerobic ATP synthesis in isolated myelin vesicles. Int J Biochem Cell Biol 41(7):1581–1591.
15. Ravera S, Panfoli I, Aluigi MG, Calzia D, Morelli A (2011) Characterization of Myelin Sheath F(o)F(1)-ATP synthase and its regulation by IF(1). Cell Biochem Biophys 59(2):63–70.
16. Ravera S, et al. (2013) Oxydative phosphorylation in sciatic nerve myelin and its impairment in a model of dysmyelinating peripheral neuropathy. J Neurochem 126(1):82–92.
17. Ravera S, et al. (2013) Tricarboxylic acid cycle-sustained oxidative phosphorylation in isolated myelin vesicles. Biochimie. doi:S0300-9084(13)00212-5 [pii]10.1016/j.biochi.2013.07.003.
18. Bartolucci M, Ramoino P, Calzia D, Traverso C, Panfoli I. RS (2014) Oxydative Metabolism in Optic Nerve Myelin: New Perspectives in Hereditary Optic Neuropathies. Clin J Ophthalmol 1(1):in press.
19. Morelli A, Ravera S, Panfoli I (2011) Hypothesis of an Energetic Function for Myelin. Cell Biochem Biophys. doi:10.1007/s12013-011-9174-8.
20. Fukunaga M, et al. (2010) Layer-specific variation of iron content in cerebral cortex as a source of MRI contrast. Proc Natl Acad Sci U S A 107(8):3834–9.
21. Todorich B, Pasquini JM, Garcia CI, Paez PM, Connor JR (2009) Oligodendrocytes and myelination: the role of iron. Glia 57(5):467–78.
22. Wu L-L, et al. (2008) Effect of perinatal iron deficiency on myelination and associated behaviors in rat pups. Behav Brain Res 188(2):263–70.
23. Sfagos C, et al. (2005) Serum ferritin, transferrin and soluble transferrin receptor levels in multiple sclerosis patients. Mult Scler 11(3):272–5.
24. Olson AL, Pessin JE (1996) Structure, function, and regulation of the mammalian facilitative glucose transporter gene family. Annu Rev Nutr 16:235–56.
25. HARTSTEIN J, ULETT GA (1957) Galactose treatment of multiple sclerosis; a preliminary report. Dis Nerv Syst 18(7 Part 1):255–8.
26. Salkovic-Petrisic M, et al. (2014) Long-term oral galactose treatment prevents cognitive deficits in male Wistar rats treated intracerebroventricularly with streptozotocin. Neuropharmacology 77:68–80.
27. Alcina A, et al. (2010) Hexose-6-phosphate dehydrogenase: a new risk gene for multiple sclerosis. Eur J Hum Genet 18(5):618–20.
28. Ravera S, Bartolucci M, Calzia D, Morelli A, Panfoli I (2015) Galactose and Hexose 6–Phosphate Dehydrogenase Support the Myelin Metabolic Role. PARIPEX-Indian J Res IV(IX):397–400.
29. Rovira A, Auger C, Alonso J (2013) Magnetic resonance monitoring of lesion evolution in multiple sclerosis. Ther Adv Neurol Disord 6(5):298–310.