"With knowledge there is long life. You are the messengers to other people who have cancer or other chronic diseases, and they're suffering because they don't know. So if you know that there is another treatment that works as good or even beyond the standard treatment, I would encourage you to save they're life because that's why i'm here too."

- M.A. Nezami M.D.

Multiple Sclerosis

The other devastating neurodegenerative disorder is Multiple Sclerosis.


MS derived its name from the multiple scarred areas in the brain termed plaques.  The acute lesion in MS is characterized by perivenular cuffing and tissue infiltration by mononuclear cells predominantly T lymphocytes and macrophages.  As the lesion evolves, demyelination occurs, with macrophages and microglial cells scavenging the myelin debris.  Proliferation of astrocytes lead to scar formation. 


 The most common initial symptoms of MS include weakness in one or more limbs, blurring of vision secondary to optic neuritis, sensory disturbances, diplopia and ataxia. CSF abnormalities include mononuclear cell pleocytosis, elevation of total Ig, and the presence of oligoclonal Ig. Evoked response testing may reveal slowed or abnormal conduction in visual, auditory, somatosensory , or motor pathways.  On MRI, periventricular lesions may be found on T2 weighted MRI brain scans. However, no clinical sign or diagnostic test finding is unique for MS. 


Conventional treatment may be for symptomatic management, or focused to arrest the disease with chemotherapeutic drugs, depending on the pattern of MS. 


Our concept of the disease would be different in the sense that we focus in conjunction with the pathogenesis of the disorder on immune imbalance involved in etiology of the disease, for example Vit D is involved in pathogenesis and exacerbations of the disease. Also TH1/ TH2 immune response and cytokines are involved. Heavy metals and infectious diseases can also trigger the immune reaction which leads to antibody production and damage/ cross reaction with normal cells/ neurons in this case producing myelin sheath.


Management depends on the cause and we don't treat patients with MS with synthetic medicine. We put that in the hands of Neurologists and honestly with all the side effects they cause and lack of the cost effectiveness in most of the cases, patients desire to discontinue them even against out advise. Please refer to www.medhyperbaric.com for further information in regards to usage of Hyperbaric oxygen therapy (HBO)for neurodegenerative disorder, such as MS.


Following is a case report that we are in the process of submitting to the medical gjournal for publication and I include that here for your review. What is left unsaid here is that this case was finally diagnosed with Lyme's disease and treated  accordingly. It is very interesting that neuroborreliosis mimics the MRI findings as well as clinical manifestations of MS!




CASE REPORT:


A 48 year old female diagnosed with multiple sclerosis (MS) by the local neurologist based on clinical findings and MRI results with white matter changes indicating MS. Patient was refered to our clinic with chief complaint of weakness and numbness in her left foot and ankle.  Physical examination revealed left foot drop and decreased sensation in left ankle and foot, unsteady gait and positive Rhomberg test. The patient’s extended disability status scale was 6.5 (Constant bilateral assistance (Cane, Crutches) required to walk about 20 meters without resting) and her fatigue severity scale was 5.2. Previous labs indicated vitamin D2 level of 20 and DHEA of 67.  It is noteworthy that neurologist reported that “there was no expected clinical improvement in her current condition despite treatment”.  Medical history was positive for Hoshimotos thyroiditis and MS, PSH was C section X one and family history was positive for MI, HTN and diabetes. Patient was perimenopausal and was experiencing irregular periods along with insomnia. Her medications included. daily Copaxone® injections, vitamin D3 1.25 mg/day and thyroid medication.


Investigations: The patient underwent a full laboratory studies.  Post challenge testing with dimercaptosuccinic acid for urine heavy metals produced essentially normal results, except for mild elevation in lead levels.  Hematology revealed CBC, Met 15, thyroid stimulating hormone and thyroid panel all within normal limits. Thrombopoetin was increased to 305 and anti thyroglobulin antibody was 150 indicating Hoshimotos thyroiditis.  Metabolic studies indicated high methyl malonate (methylation cofactor marker) indicating the need for vitamin B12, increased alpha keto –B- methyl valerate and low 5 hydroxy indole acetate (neurotransmitter metabolism marker), and high ethyl malonate (fatty acid metabolism) indicating the need for carnitine and vitamin B2.  Saliva testing indicated increased morning cortisol (31.7 nM).


Targeted Metabolic Treatments: Based on the testing discussed above, a supplement regimen along with IV treatments for nutritional deficiencies and metabolic abnormalities was initiated. The regimen included “Neuroprotect-Hope”. This product contains N-acetyl-cysteine (NAC), acetyl-L-carnitine, thiamine, niacin, riboflavin (vitamin B2), vitamins B6 and B12, folic acid and grape seed extract. NAC is used to facilitate detoxification and carnitine along with the B vitamins were administered based on the above lab reports. Patient also received IV treatments with vitamin C, H2O2, amino acids and DMSO.


Response to Treatment: The patient was monitored during weekly clinic visits. Dramatic improvement was observed 8 weeks following initiation of treatment with the above regimen. After 4 weeks of treatment, the patient’s foot drop, numbness and her ability to walk showed improvement; she stopped using the cane was reported to be independently ambulating without aid or rest for about 100 meters.  The initial Expanded Disability Status Scale of 6.5 improved to 5.5.  The patient stopped using Copaxone® against our advice and continued improving clinically.


Discussion: Vitamin B12 is a key nutrient factor supporting myelin formation. Acquired B12 deficiency and inborn errors in its metabolism are recognized causes of CNS demyelination, so its deficiency in MS would be expected to contribute to progression. Early studies of B12 status in MS produced conflicting results, but improved testing techniques confirmed B12 levels that were lower in the CSF of MS patients, if not always lower in the serum. For more than 30 years, clinicians have been reporting consistent clinical improvement of MS symptoms following B12 injections. Many integrative physicians routinely prescribe intramuscular injections of B complex with B12 and folic acid to their MS patients, reportedly with improvement. Immune-suppressive steroids or cyclophosphamide can produce comparable results, but with severe adverse side effects.
 
Studies in mice indicate that antioxidants such as grape seed extract  may block the progression of MS. Grape seed extract is the primary commercial source of a group of powerful antioxidants known as oligomeric proanthocyanidins (OPCs), also generically called pycnogenol, a class of flavonoids. Laboratory studies have indicated OPCs are much more effective than vitamin C and vitamin E in neutralizing free oxygen radicals, which contribute to organ degeneration and aging in humans. The primary sources of OPCs are pine bark extract and grape seed extract.
 
L-carnitine increases mitochondrial producion of ATP and plays an important role in lipid metabolism and energy production. It is important for mitochondrial function and the transport of fatty acids into the mitochondria for beta-oxidation and energy production. In one study patients affected with MS with low serum carnitine levels were given 3-6 g/day of L-carnitine for three months. After three months, serum carnitine levels had returned to normal, and 63% of the patients reported an improvement in fatigue. N-acetyl-carnitine is a more bioavailable form than L-carnitine.


In animal studies NAC has been indicated to play an important role in controlling the inflammation associated with neurodegenerative process in MS, and encephalitis by increasing interleukin IL-10. These observations indicate that NAC treatment may be of therapeutic value in MS against the inflammatory disease process associated with the infiltration of activated mononuclear cells into the CNS.


Conclusion: It is  important to  examine patients with multiple sclerosis thoroughly for any signs of inflammation which may lead to myelin damage and neurodegeneration. The case described above suggest the need for future research in the area of nutritional intervention in patients with neurodegenerative disorders. In one study, 12 percent of affected patients with MS experienced malabsorption of vitamin B12.  Metabolic testing indicated that nutritional interventions can improve the clinical and laboratory findings in this population.
Although future studies are required to elucidate the quantitative effect of nutritional supplements on subjective symptoms, this case strongly suggests that intervention with dietary supplements may result in positive, objectively measurable outcomes.


References
        1.          Hauser SL, Goodkin DE. Multiple Sclerosis and other demyelinating diseases. In: Harrison‘s Principles of Internal Medicine. 2409-2419.
 2.          Lovblad K, Ramelli G, et al. Retardation of myelination due to dietary vitamin B12 deficiency: cranial MRI findings. Pediatr Radiol 1997 Feb 27(2):155-158 1997.
 3.     Gupta JK, Ingegno AP, Cook AW, et al. Multiple sclerosis and malabsorption. Am J Gastroenterol 1977;68:560-565.
4.          Reynolds EH. Multiple sclerosis and vitamin B12 metabolism. J Neuroimmunol 1992;40:225-230. Kira J, Tobimatsu S, Goto I. Vitamin B12 metabolism and massive-dose methyl vitamin B12 therapy in Japanese patients with multiple sclerosis. Intern Med (Tokyo) 1994;33:82-86.
 5.          Preuss, H., et al. 2000. Effects of niacin-bound chromium and grape seed proanthocyanidin extract on the lipid profile of hypercholesterolemic subjects: A pilot study. J.Med, 31, 227–246.
6.          Antioxidants in multiple sclerosis: do they have a role in therapy? Carlson NG, Rose JW.GRECC, VASLCHCS, Department of Neurobiology and Anatomy, University of Utah, Salt Lake City, Utah, USA.


7.          Immunopharmacol Immunotoxicol. 2009;31(1):13-29.Antioxidant therapy in multiple sclerosis. Mirshafiey A, Mohsenzadegan M. Department of Immunology, Tehran University of Medical Sciences, Iran. mirshafiey@tums.ac.ir
        8.          The role of oxidative stress in the pathogenesis of multiple sclerosis: the need for effective antioxidant therapy. Gilgun-Sherki Y, Melamed E, Offen D.


Laboratory of Neurosciences, Felsenstein Medical Research Center, The Sackler School of Medicine, Tel Aviv University, Petach Tikva 49100, Israel.


        9.           L-carnitine supplementation for multiple sclerosis-related fatigue. Townsend Letter: The Examiner of Alternative Medicine Article date: January 1, 2007 Gaby, Alan R.


        10.      Zh Nevrol Psikhiatr Im S S Korsakova. 2002;Suppl:72-5. New approaches to antioxidant therapy in multiple sclerosis, Odinak MM, Bisaga GN, Zarubina IV.




         11.       J Autoimmune Dis. 2005; 2: 4.

              Published online 2005 May 3. doi: 10.1186/1740-

PMCID: PMC1097751

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