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Demyelinating disease

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Demyelinating disease
SpecialtyNeurology Edit this on Wikidata

A demyelinating disease is any disease of the nervous system in which the myelin sheath of neurons is damaged.[1] This impairs the conduction of signals in the affected nerves, causing impairment in sensation, movement, cognition, or other functions depending on which nerves are involved.

The term describes the effect of the disease, rather than its cause; some demyelinating diseases are caused by genetics, some by infectious agents, some by autoimmune reactions, and some by unknown factors. Organophosphates, a class of chemicals which are the active ingredients in commercial insecticides such as sheep dip, weed-killers, and flea treatment preparations for pets, etc., will also demyelinate nerves.

Neuroleptics can cause demyelination.[2]

Signs and Symptoms

Symptoms that present in demyelinating diseases are different for each condtion. Below is a list of symptoms that can present in a person with a demyelinating disease[3]:

  • Ocular paralysis
  • Impaired muscle coordination
  • Weakness (muscle)
  • Loss of sensation
  • Impaired vision
  • Neurological symptoms
  • Unsteady gait
  • Spastic paraparesis
  • Incontinence
  • Hearing problems
  • Speech problems

Causes

Some demyelinating diseases are caused by genetics, some by infectious agents, some by autoimmune reactions, and some by unknown factors.

Diagnosis

Below are various methods/techniques used to diagnose Demyelinating Diseases.

Oftentimes unreliable because changes observed during an MRI assess changes in proton density. “Spots” can occur as a result of changes in brain water content[4]

Treatment

Treatment typically involves improving the patient's wuality of life by the management of symptoms or slowing the rate of demyelination. Treatment can include medication, lifestyle changes (i.e. quit smoking, adjusting daily schedules to include rest periods and dietary changes), counselling, relaxation, physical exercise, patient education and, in some cases, deep brain thalamic (see Thalamus) stimulation (in the case of Tremors). [4]

Treatments are patient specific and depend on the symptoms that present with the disorder as well as the progression of the condition.

Prognosis

Prognosis depends on the condition itself. Some conditions such as Multiple sclerosis depend on the subtype of the disease and various attributes of the patient such as age, sex, initial symptoms and the degree of disability the patient experiences. [5] Life expectancy in Multiple sclerosis patients is 5 to 10 years lower than unaffected people. [6] Other conditions such as Central pontine myelinolysis have about a third of patients recover and the other two thirds experience varying degrees of disability [7]. There are cases, such as Transverse myelitis where the patient can begin recovery as early as 2 to 12 weeks after the onset of the condition.

Epidemiology

Incidence of demyelinating diseases vary from disorder to disorder. Some conditions, such as Tabes dorsalis appear predominantly in males and begins in mid-life. Optic neuritis on the other hand, occurs preferentially in females typically between the ages of 30 and 35.[8]. Other conditions such as Multiple sclerosis vary in prevalence depending on the country or population. [9] This condition can appear in children as well as adults. [10]

More information can be obtained on the wiki pages for these disorders. See “Types of Demyelinating Diseases”

Types of Demyelinating Diseases

Demyelinating diseases of the central nervous system include:

Demyelinating diseases of the peripheral nervous system include:

Research

Research is being conducted in a variety of very specific areas. The focus of this research is aimed at gaining more insight into how demyelinating disorders affect the Central Nervous System and Peripheral Nervous System[11][12][13][14][15], develop and how these disorders are affected by various external inputs[16][17][18][19][20] . Much of the research is targeted towards learning about the mechanisms by which these disorders function in an attempt to develop therapies and treatments for individuals affected by these conditions.

Insights:

Currently it is believed that N-cadherin plays a role in the myelination process. Experimentation has shown that N-cadherin plays an important role in producing a remyelination-facilitating environment[21]. It has been shown in animal models that there is a direct correlation between the amount of myelin debris present and the degree of Inflammation observed[22].

The effects of various environmental inputs:

Experimentation has shown that manipulating the levels of Thyroid hormone can be considered as a strategy to promote remyelination and prevent irreversible damage in Multiple sclerosis patients[23]. N-cadherin agonists (see Agonist) have been identified and observed to stimulate Neurite growth and cell migration, key aspects of promoting axon growth and remyelination after injury or disease[24]. It has been shown that intranasal (see Insufflation) administration of aTf (apotransferrin, see Transferrin) can protect myelin and induce remyelination[25].

  • Much of the research presented in this section has been conducted in 2012 and represents very new information about demyelinating diseases and potential therapies for them.

In Other Animals

Demyelinating diseases/disorders have been found worldwide in various animals. Some of these animals include mice, pigs, cattle, hamsters, rats, sheep, Siamese kittens, and a number of dog breeds (including Chow Chow, Springer Spaniel, Dalmatian, Samoyed, Golden Retriever, Lurcher, Bernese Mountain Dog, Vizsla, Weimaraner, Australian Silky Terrier, and mixed breeds) [26][27]

See Also

References

  1. ^ "demyelinating disease" at Dorland's Medical Dictionary
  2. ^ Konopaske GT, Dorph-Petersen KA, Sweet RA; et al. (2008). "Effect of chronic antipsychotic exposure on astrocyte and oligodendrocyte numbers in macaque monkeys". Biol. Psychiatry. 63 (8): 759–65. doi:10.1016/j.biopsych.2007.08.018. PMC 2386415. PMID 17945195. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  3. ^ "Symptoms of Demyelinating Disorders - Right Diagnosis." Right Diagnosis. Right Diagnosis, 01 Feb 2012. Web. 24 Sep 2012.
  4. ^ a b c d e f g Freedman, Mark S (2005). Advances in Neurology Volume 98: Multiple Sclerosis and Demyelinating Diseases. Philadelphia: Lippincott Williams & Wilkins. p. 112. ISBN 0781751705. Cite error: The named reference "Freedman" was defined multiple times with different content (see the help page).
  5. ^ Weinshenker BG (1994). "Natural history of multiple sclerosis". Ann. Neurol. 36 (Suppl): S6–11. doi:10.1002/ana.410360704.
  6. ^ Compston A, Coles A (2008). "Multiple sclerosis". Lancet. 372 (9648): 1502–17. doi:10.1016/S0140-6736(08)61620-7. {{cite journal}}: Unknown parameter |month= ignored (help)
  7. ^ Abbott R, Silber E, Felber J, Ekpo E (2005). "Osmotic demyelination syndrome". BMJ. 331 (7520): 829–30. doi:10.1136/bmj.331.7520.829. PMC 1246086. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  8. ^ Rodriguez M, Siva A, Cross SA, O'Brien PC, Kurland LT (1995). "Optic neuritis: a population-based study in Olmsted County, Minnesota". Neurology. 45 (2): 244–50. PMID 7854520.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  9. ^ Rosati G (2001). "The prevalence of multiple sclerosis in the world: an update". Neurol. Sci. 22 (2): 117–39. doi:10.1007/s100720170011. {{cite journal}}: Unknown parameter |month= ignored (help)
  10. ^ Compston A, Coles A (2008). "Multiple sclerosis". Lancet. 372 (9648): 1502–17. doi:10.1016/S0140-6736(08)61620-7. {{cite journal}}: Unknown parameter |month= ignored (help)
  11. ^ Hochmeister, S.; Romauch, M; Bauer, J; Seifert-Held, T; Weissert, R; Linington, C; Hurtung, H.P.; Fazekas, F; Storch, M.K. (2012). "Re-expression of n-cadherin in remyelinating lesions of experimental inflammatory demyelination". Experimental Neurology. 237: 70–77. {{cite journal}}: Cite has empty unknown parameter: |month= (help)
  12. ^ Clarner, T.; Diederichs, F.; Berger, K.; Denecke, B.; Gan, L.; Van Der Valk, P.; Beyer, C.; Amor, S.; Kipp, M. (2012). "myelin debris regulates inflammatory responses in an experimental demyelination animal model and multiple sclerosis lesions". GLIA. 60: 1468–1480. {{cite journal}}: Cite has empty unknown parameter: |month= (help)
  13. ^ Newcombe, J.; Eriksson, B.; Ottervald, J.; Yang, Y.; Franzen, B. (2005). "Extraction and proteomic analysis of proteins from normal and multiple sclerosis postmortem brain". Journal of Chromatography B. 815: 119–202. {{cite journal}}: Cite has empty unknown parameter: |month= (help)
  14. ^ Silverstroff, L.; Batucci, S.; Pasquini, J.; Franco, P. (2012). "Cuprizone-induced demyelination in the rat cerebral cortex and thyroid hormone effects on cortical remyelination". Experimental Neurology. 235: 357–367. {{cite journal}}: Cite has empty unknown parameter: |month= (help)
  15. ^ Palumbo, S.; Toscano, C.D.; Parente, L.; Weigert, R.; Bosetti, F. (2012). "The cyclooxygenase-2 pathway via the pge₂ ep2 receptor contributes to oligodendrocytes apoptosis in cuprizone-induced demyelination". Journal of Neurochemistry. 121: 418–427. {{cite journal}}: Cite has empty unknown parameter: |month= (help)
  16. ^ Burden-Gulley, S.M.; Gates, T.J.; Craig, S.E.L.; Gupta, M.; Brady-Kalnay, S.M. (2010). "Stimulation of n-cadherin-dependint neurite outgrowth by small molecule peptide mimetic agonists of the n-cadherin hav motif". Peptides. 31: 842–849. {{cite journal}}: Cite has empty unknown parameter: |month= (help)
  17. ^ Sherafat, M.A.; Heibatollahi, M.; Mongabadi, S.; Moradi, F.; Javan, M.; Ahmadiani, A. (2012). "Electromagnetic field stimulation potentiates endogenous myelin repair by recruiting subventricular neural stem cells in an experimental model of white matter demyelination". Journal of Molecular Neuroscience. 48: 144–153. {{cite journal}}: Cite has empty unknown parameter: |month= (help)
  18. ^ Clausi, M.G.; Paez, P.M.; Campagnoni, A.T.; Pasquini, L.A.; Pasquini, J.M.; Ahmadiani, A. (2012). "Intranasal administration of atf protects and repairs the neonatal white matter after a cerebral hypoxic-ischemic event". GLIA. 60: 1540–1554. {{cite journal}}: Cite has empty unknown parameter: |month= (help)
  19. ^ Gasperini, C.; Ruggieri, S. (2012). "Development of oral agent in the treatment of multiple sclerosis- how the first available oral therapy, fingolimod will change therapeutic paradigm approach". Drug Design, Development and Therapy. 6: 175–186. {{cite journal}}: Cite has empty unknown parameter: |month= (help)
  20. ^ Ransohoff, R.M.; Hower, C.L.; Rodriquez, M. (2005). "Growth factor treatment of demyelinating disease- at last, a leap into the light". Trends in Immunology. 23 (11): 512–516. {{cite journal}}: Cite has empty unknown parameter: |month= (help)
  21. ^ Hochmeister, S.; Romauch, M; Bauer, J; Seifert-Held, T; Weissert, R; Linington, C; Hurtung, H.P.; Fazekas, F; Storch, M.K. (2012). "Re-expression of n-cadherin in remyelinating lesions of experimental inflammatory demyelination". Experimental Neurology. 237: 70–77. {{cite journal}}: Cite has empty unknown parameter: |month= (help)
  22. ^ Clarner, T.; Diederichs, F.; Berger, K.; Denecke, B.; Gan, L.; Van Der Valk, P.; Beyer, C.; Amor, S.; Kipp, M. (2012). "myelin debris regulates inflammatory responses in an experimental demyelination animal model and multiple sclerosis lesions". GLIA. 60: 1468–1480. {{cite journal}}: Cite has empty unknown parameter: |month= (help)
  23. ^ Silverstroff, L.; Batucci, S.; Pasquini, J.; Franco, P. (2012). "Cuprizone-induced demyelination in the rat cerebral cortex and thyroid hormone effects on cortical remyelination". Experimental Neurology. 235: 357–367. {{cite journal}}: Cite has empty unknown parameter: |month= (help)
  24. ^ Burden-Gulley, S.M.; Gates, T.J.; Craig, S.E.L.; Gupta, M.; Brady-Kalnay, S.M. (2010). "Stimulation of n-cadherin-dependint neurite outgrowth by small molecule peptide mimetic agonists of the n-cadherin hav motif". Peptides. 31: 842–849. {{cite journal}}: Cite has empty unknown parameter: |month= (help)
  25. ^ Clausi, M.G.; Paez, P.M.; Campagnoni, A.T.; Pasquini, L.A.; Pasquini, J.M.; Ahmadiani, A. (2012). "Intranasal administration of atf protects and repairs the neonatal white matter after a cerebral hypoxic-ischemic event". GLIA. 60: 1540–1554. {{cite journal}}: Cite has empty unknown parameter: |month= (help)
  26. ^ Merck Sharp & Dohme Corp (2011). "The Merck Vetrinary Manual – Demyelinating Disorders: Introduction". Merck Vetrinary Manual. Retrieved 2012-10-30.
  27. ^ "Johnson RT. DEMYELINATING DISEASES. In: Institute of Medicine (US) Forum on Microbial Threats; Knobler SL, O'Connor S, Lemon SM, et al., editors. The Infectious Etiology of Chronic Diseases: Defining the Relationship, Enhancing the Research, and Mitigating the Effects: Workshop Summary. Washington (DC): National Academies Press (US)". NCBI. 2004. Retrieved 2012-10-30.
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