Brain Disorder or Dysfunction: Multiple Sclerosis

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The consequences of demyelination for salutatory conduction explain many clinical and laboratory features of multiple sclerosis. Symptoms of multiple sclerosis fluctuate immensely, both from patient to patient and over time in one patient. Individuals diagnosed with MS are unable to perform their daily activities. Within the cerebrum, we can perceive symptoms of cognitive impairments with signs of deficiency in attention, reasoning, early executive functioning, and late dementia as well as feelings of depression and dysfunction in motor and sensory systems (Compston & Coles, 2002). Motor symptoms comprise of weakness, tremors, spasticity, ataxia which is loss of balance or incoordination, and speech disabilities. Within the

optic nerve, unilateral loss of vision occurs with relative afferent pupillary dysfunction while the cerebellum and cerebellar pathway experience postural and action tremors and balance impairments due to limb incoordination and gait ataxia. Impairments to the brainstem, spinal

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cord, and other parts of the central nervous system are compromised as MS progresses in the individuals’ bodies. Sensory symptoms comprise of the feeling of pins and needles, numbness,

feelings of tightness or solidity (paresthesias), and, sometimes, sharp pains respond to baclofen. Visual symptoms include blurred or double vision, nystagmus (involuntary eye movements), and, on occasion, blindness, which is almost always temporary (Keegan & Noseworthy, 2002). Urinary symptoms are common due the bladder dysfunction, as are frequent urinary tract infections responds to oxybutynin. Energy problems include a lack of energy, easily fatigued, and lack of endurance, particularly in the presence of heat and humidity (Compston & Coles, 2002). Damaged nerve fibers have an intensely weakened tolerance for heat. Demyelinated nerve fibers consume additional energy for impulses to be conducted and so individuals become more fatigued easily than with normal fibers (Keegan & Noseworthy, 2002). Muscles become deteriorated as a result in the reliance on stronger muscles, which gets exhausted faster.

The progression of the disease differs from one person to another like symptoms, and may fluctuate over time in the same person. There are three principal evolvements the disease may undertake: a benign course, concerning a limited amount of early, mild attacks followed by nearly complete remission, producing little or no disability; an exacerbating- remitting course with additional early attacks with less likely to achieve complete remission succeeding in some disability, followed by long periods of stability; and a progressive course comprising of a gradual and ongoing advancement of the disease with no remission (Hafler et al., 2005; Murray, 2006). It

is has been studied that very seldom does MS advance to a progressive state that leads to death, but the underlying impediments and infections from MS will cause death but not the disease itself. The symptoms of MS may arise quickly within minutes or days, or gradually throughout

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periods of weeks, while new symptoms may accumulate and old ones may resurface and intensify. The beta interferons are utilized to diminish the rate of relapses in multiple sclerosis

due to the propensity of viruses to arise and trigger the relapse (Compston & Coles, 2002). Azathioprine inhibits lymphocyte proliferation by inhibiting purine synthesis, and probably has similar efficacy to the beta interferons, although the trial data were obtained in a less rigorous manner and reported more candidly (Compston & Coles, 2002, p. 1226). Mitoxantrone prevents DNA repair and synthesis in dividing and non-dividing cells through the hindrance of DNA topoisomerase II, which is theoretically more toxic than the beta interferons, but has a US license for the management of aggressive relapsing disease. Corticosteroids attached to their cytoplasmic receptors, penetrate the cell nucleus and inhibit the transcription of proinflammatory cytokines, such as interleukin 1, interleukin 2, tumor necrosis factor- (TNF-) and proinflammatory enzymes, including collagenase, elastase, and plasminogen activator. These anti-inflammatory effects have long been used for acute treatment of multiple sclerosis relapses which prevents the increase in the attributes of the disability in relapse. Fixed neurological deficits in multiple sclerosis are best accomplished by a multidisciplinary team, concentrating to physical therapies, psychosomatic, and social intermediations augmented by medical treatments. The assistances of intense inpatient therapy endure the length of therapy by up to 9 months especially for spasticity and sphincter dysfunction (Compston & Coles, 2002). The aim of treatment to inhibit the disability through progression by the implication is that positive results of the European [pic 2][pic 3]

Betaferon study could have arisen through reduction in accumulation of disability dependent on relapse rather than an effect on disability due to disease progression (Compston & Coles, 2002, p. 1228).

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References

- Carlson, N. R. (2013). Physiology of behavior (11th Ed.). Boston, MA: Pearson.

- Compston, A., & Coles, A. (2002). Multiple sclerosis. The Lancet, 359, 1221-1231.

- Hafler, D. A., Slavik, J. M., Anderson, D. E., O’Connor, K. C., De Jager, P., Baecher-

Allen, C. (2005). Multiple sclerosis. Immunological Reviews, 204, 208-231.

- Hafler, D. A. (2004). Multiple sclerosis. The Journal of Clinical Investigation, 113(6),

788-794.

- Keegan, B. M. & Noseworthy, J. H. (2002). Multiple sclerosis. Annual Review of

Medicine, 53, 285-302.

- Murray, T. J. (2006). Diagnosis and treatment of multiple sclerosis, BMJ, 332, 525-527.

- Silverthorn, D. U. (2010). Human physiology: An integrated approach (5th Ed.). San

Francisco, CA: Pearson.

Running head: MULTIPLE SCLEROSIS

Brain disorder or dysfunction: Multiple sclerosis

Liza George

University of Houston-Clear