Multiple Sclerosis
Thesis Statement
Multiple Sclerosis is mainly an inflammatory disorder of the brain and spinal cord in which central lymphocytic permeation leads to harm of the myelin scabbard and axons. Initially, inflammation is temporary and re-myelination occurs but is not long-lasting. Hence, the early course of disease is characterized by occurrences of neurological dysfunction that usually recover. However, over time the pathological alterations start to take over by widespread microglia activation associated with broad and constant neuro-degeneration, the clinical correlate of which is progressive growth of disability. Para-clinical investigations show abnormalities that specify the distribution of inflammatory lesions and axonal loss (MRI); hindrance of transmission in previously myelinated pathways (evoked electrophysiological potentials); and intrathecal combination of oligoclonal antibody (examination by lumbar puncture of the cerebral fluid). Multiple sclerosis is triggered by ecological dynamics in individuals with multifarious genetic-risk profiles. Licensed disease modifying agents lessen the rate of recurrence of new episodes, but do not repeal fixed insufficiencies and have questionable outcomes on the long-term accumulation of disability and disease development. They foresee that future studies in Multiple sclerosis will provide a new classification on the center of mechanisms rather than clinical empiricism, and so enlighten strategies of improved treatment at all stages of the disease.
I. Diagnosis
II. Cause
III. Environmental factor
IV. Geography of MS and migrations
V. Genetics
VI. Disease mechanisms
VII. Management and treatment
VIII. Self-Management
IX. Perceived Control
X. Past, present, and future
XI. The future of treatment
References
Falvo, D. R., (2009). Medical and Psychosocial Aspects of Chronic Illness and Disability. Jones and Bartlett.
Malachy Bishop, Michael P Frain, Molly K Tschopp. (2008). Self-Management,
Multiple Sclerosis is mainly an inflammatory disorder of the brain and spinal cord in which central lymphocytic permeation leads to harm of the myelin scabbard and axons. Initially, inflammation is temporary and re-myelination occurs but is not long-lasting. Hence, the early course of disease is characterized by occurrences of neurological dysfunction that usually recover. However, over time the pathological alterations start to take over by widespread microglia activation associated with broad and constant neuro-degeneration, the clinical correlate of which is progressive growth of disability. Para-clinical investigations show abnormalities that specify the distribution of inflammatory lesions and axonal loss (MRI); hindrance of transmission in previously myelinated pathways (evoked electrophysiological potentials); and intrathecal combination of oligoclonal antibody (examination by lumbar puncture of the cerebral fluid). Multiple sclerosis is triggered by ecological dynamics in individuals with multifarious genetic-risk profiles. Licensed disease modifying agents lessen the rate of recurrence of new episodes, but do not repeal fixed insufficiencies and have questionable outcomes on the long-term accumulation of disability and disease development. They foresee that future studies in Multiple sclerosis will provide a new classification on the center of mechanisms rather than clinical empiricism, and so enlighten strategies of improved treatment at all stages of the disease.
I. Diagnosis
II. Cause
III. Environmental factor
IV. Geography of MS and migrations
V. Genetics
VI. Disease mechanisms
VII. Management and treatment
VIII. Self-Management
IX. Perceived Control
X. Past, present, and future
XI. The future of treatment
References
Falvo, D. R., (2009). Medical and Psychosocial Aspects of Chronic Illness and Disability. Jones and Bartlett.
Malachy Bishop, Michael P Frain, Molly K Tschopp. (2008). Self-Management,
References: Falvo, D. R., (2009). Medical and Psychosocial Aspects of Chronic Illness and Disability. Jones and Bartlett.