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Multiple Sclerosis

MultipleSclerosis

MultipleSclerosis

1.0Introduction

MultipleSclerosis is a disease affecting the nervous system, andsystematically the myelin sheath surrounding the nerve cells in thebrain and nervous system. This inflammation or sclerosis leads to afunctional and anatomical breakdown of areas of the nervous system incontrol of different physical and psychological body functions(Compston&amp Coles, 2008).This affect is associated with disruptions in the way the bodyfunctions and the symptoms are in form of a wide range of physical,psychiatric and mental malfunctions. A disease showing genetic,racial as well as geographical preferences, MS affects close to 2.5million people globally spread in definite clusters (Miller&amp Leary, 2007).This paper will discuss MS from both the anatomical perspective (theform and extent of physical affect on various body parts, especiallythe brain cells) and the physiological affect (mainly the physicallyevident symptoms, the functional alterations of parts of organs inthe body, and the progression symptoms as the patient ages). It willalso explore the standard of care of relapse management, especiallywith regard to oral and intravenous methylprednisolone.

2.0Anatomy of

Theimmediately observable physical changes in a MS patient are lesions,or sclera in their myelin sheath. The most common attack area forthese lesions is the white matter of various nervous cells includingthe ones in the optic nerve, spinal cord and brain stem. The basalganglia are also often affected (Compston&amp Coles, 2008).A typical microscopic examination of nerve tissues of a patientsuffering from MS shows discoloration as well as appearance of scars,or depletion of myelin substance, in their myelin sheaths. At thebase of the myelin sheath is a layer of cells responsible forgeneration of the thin fatty tissue which is the myelin. Theselesions destroy the oligodendrocytes, thereby limiting the formationof the sheath that is responsible for electric conductivity of thenerve cells (Compston&amp Coles, 2008).In younger patients whose MS has not reached a critical stage, theoligodendrocytes are still able to generate a new layer of myelin,though each time with a little less success. This leads to theadvancement of the disease with age, and patients become graduallymore incapacitated by the disease, depending on the particularregions mainly attacked (Compston&amp Coles, 2008).

Asremyelination progressively becomes less effective, the scars formand extend to the axons, which also become destroyed (Miller&amp Leary, 2007).Another common method of MS formation and progression is through thediffusion of lymphocytes into the brain tissue through a dilapidatedbrain-blood barrier. This barrier is usually not porous enough forbody defense cells, or lymphocytes, to pass. However, in conditionswhere disease affects the integrity of the barrier, it may becometemporarily permeable for the lymphocytes, and chances exist that thestructural weakness may heal leaving the white blood cells inside thebrain (Compston&amp Coles, 2008).The lymphocytes, stranger to the brain environment, may fail torecognize the myelin sheath in brain cells and attack it. The neteffect is further breakdown of myelin and the possible breakdown ofaxons too (Stadelmann&amp Brück 2004).

Fordiagnosis of MS, either of two methods is normally used. The firstmethod relies on multiple experiences of neurologic symptoms typicalof the disease. In such a case, normally, the patient is questionedregarding the nature and frequency of their experiences, and thephysician can then eliminate all other causes and reach a diagnosisof MS. When a patient has complained of only one or just a fewepisodes of neurologic signs, the examining doctor may have to relyon scans, especially the Magnetic Resonance Imaging (MRI) to scanareas of the brain for areas of plaques or demyelination (Miller&amp Leary, 2007).

3.0 effect on other Body Organs

MShas effects on multiple other body organs including the centralnervous system, visual system, speech system, throat, sensationsystems, the alimentary canal, and the urinary system.

3.1Central Nervous System

TheCNS is spread throughout the brain and backbone. This system isresponsible for multiple sense and coordination functions, as well asregulation of the body’s internal environment. Some of the adverseeffects normally evident due to MS neurologic symptoms in the nervoussystem include intermittent or continuous unstable moods, occasionalor long term depression which worsens progressively as the patientages, problems with thought or logic structures ( or cognitiveimpairment), fatigue among others (Rog, 2009). Generally, thesymptoms so experienced differ from individual to individual, and inseverity or frequency of occurrence. Electric Sensations in the backare also evidenced for a significant number of patients (Miller&amp Leary, 2007).For some patients, there could be one prevalent symptom affecting aparticular body system, and the frequency of this affect may becontinuous, often or rare- but severity and frequency has shown atendency of worsening as one ages. Typically, a MS patient willnormally live to adulthood, and have normal development in comparisonto the wider population. However, the later years of this conditionare often marked by mild to severe handicap, with the life expectancyof MS patients being 5-15 years shorter than the averagepopulation’s.

3.2The Visual System

MScan cause very adverse affects in the visual system. Some of thesymptoms may include Diplopia, optic Neuritis and Nystagmus. Diplopiais the perception of double images of the same object due either tothe inability of both eyes to focus properly, or due to neuromusculardisorders such as those posed by degeneration of myelin in brain andnervous system cells (Phillips2007).As expected, double vision comes with impaired focus and loss ofbalance, which may also lead to secondary complications such asnausea and dizziness (Rog, 2009). Optical Neuritis is the severeaffect, usually leading to blindness, caused by optic nerveinflammation. This inflammation is typical to the one caused bymyelin damage and axon vulnerability seen in MS patients, and theloss of vision, as well as other predisposing symptoms of OpticalNeuritis, maybe intermittent or complete (Lee &amp Brazis, 2011). Statistics indicate that half of MS cases will develop this symptomat some point in life, making optical neuritis a diagnosing symptom.

Tomost patients, Optical Neuritis presents itself as sudden blurred andpainful vision, and sometimes complete loss of sight (Lee &ampBrazis, 2011). Pain, however, is not a prevalent accompanying sign,with about 60% of patients not stating perception of pain in theearly development of MS. Nystagmus on the other hand presents in mostcases as involuntary eye movement, usually accompanied by blurredmotion sensation, or inability to coordinate movement. This conditionis typically caused by the lack of coordination and control in theregion of brain controlling eye movement. Disorders of the CNS areone of the most prevalent causes of Nystagmus, as well as drugs use.The condition has a treatment, especially in cases where its cause isrelated to removable conditions (Poser&amp Brinar 2004).Nystagmus caused by MS related complications, however, may have anenduring quality, and sometimes last the patient’s entire life.

3.3Speech and Throat Systems

Themost prevalent MS related affect on the speech mechanism isDysarthria, a medical condition characterized by the impairment ofspeech production muscles. Its most common diagnosing symptom isinability to pronounce words (Poser&amp Brinar 2004).In its extreme case, it can aggravate into Anarthria, the completeloss of speech. Lack of coordination of the speech-motor systems isthe causal factor of this disease, and the degeneration of brainnervous system responsible for speech is responsible for the failure(Rog, 2009). Dysphagia, a throat related disease, is characterized byswallowing difficulty. Typically, the patient only experiences lackof swallowing sensation, but usually without pain.

3.4Musculoskeletal Systems

TheMS induced symptoms affecting the musculoskeletal system includemuscle coordination problems, convulsive muscle problems and seizures(Lee &amp Brazis, 2011). Muscle weakness is a problem affecting themuscles where coordination by the nervous system is dysfunctional.Spasms and convulsions may also be evident in the muscles. Ataxia, orthe lack of coordinated muscle movement, may also be observed. Thesensation of pain is prevalent especially in the musculoskeletalsystem due to MS invasions (Rog, 2009).

3.5Bowel and Excretory System

Thechemical balance in the digestive system is subject to control by thenervous-system. The lack of proper coordination and balance controlby the brain may lead to adverse effects in the bowel system such asincontinence, diarrhea or constipation. In this regard, patients withMS may experience bowel problems from time to time.

3.6Urinary System

Aswith the bowel system, the urinary system is also controlled by thebrain. For this reason, the lack of proper controls by the brainregarding the urinary system may lead to certain adverse problemssuch as the lack of ability to hold or contain urine, or retention ofurine, or very frequent urination. Therefore, MS can be said to havea profound, overwhelming effect on bodily functions (Rog, 2009).

4.0MS Standard of Care for Acute relapse: Oral versus IntravenousMethylprednisolone

Multiplesclerosis has no known cure so far. However, various medical as wellas therapeutic interventions have been shown to successfully manageits symptoms. The particular method applied depends on the recurrencepattern of the symptoms (Lee &amp Brazis, 2011). Broadly, recurrencecan be either be relapse –remitting ( typical of patients withbenign MS) where sudden seizures are followed by long periods ofremission, or progressive- relapsing ( in patients with malignant MS)in which the symptoms are progressive with no definite times ofremission. Acute Relapse is therefore an occurrence defined bysudden, strong manifestations of the MS symptoms. The management ofacute relapsing is done using various medication applied throughdifferent methods (Poser&amp Brinar 2004).

4.1Methylprednisolone

Methylprednisoloneis an anti-inflammatory corticosteroid used for the treatment of awide range of symptoms. It has been known to aid in recovery ofsensory and nervous impairments of varying intensities.

4.2Standard of care: Oral versus Intravenous injections

Anarticle published in the Journal of Neurology, Neurosurgery andPsychiatry, 1993, documented the results of a study done to checkwhether there was any significant difference in efficiency orside-effects when the drug was given orally or via injection. Thefigure below shows the study preparation

(Burtonet. al, 2012)

Thestudy found no significant differences in terms of efficiency oradverse effects between the two methods. In agreement, an articlepublished by the Department of Neurosciences, University of Calgaryregarding the efficiency differences in the two methods showed thatwhile both methods were comparably efficient at the same dosagelevels, the patient’s reaction time to them seemed only to dependon the age of patient, as well as the week of treatment (Burton et.al, 2012). A similar study published in the Neurology Journalregarding the oral versus intravenous administration of the drug didnot find any efficiency difference between the two methods, and inconclusion suggested that oral administration is just an effectivesubstitute for intravenous injection (Martinelli,V. et.al, 2009).

Therefore,the choice of introduction method of methylprednisolone should onlybe based on patient condition, and not on severity of symptoms, ageof patient or progress stage. In cases where the patient is unable toretain the drug once orally administered, an intravenous injectionshould be used to introduce it in their system, but in acute relapsecases where patient is able to orally admit the drug, either of themethods are applicable (Martinelli,V. et.al, 2009).

References

Alam,S. et.al (1993). Methylprednisolone in multiple sclerosis: acomparison of oral with intravenous therapy at equivalent high dose.JNeurol Neurosurg Psychiatry1993 56: 1219-1220

Burton,M et. al. (2012). Oral versus intravenous steroids for treatment ofrelapses in multiple sclerosis. CochraneDatabase SystRev. 2012 Dec 1212: CD006921

CompstonA, &amp Coles, A. (2008). &quotMultiple sclerosis&quot. Lancet372(9648): 1502–17.

Lee,A. &amp Brazis, P. (2011). ClinicalPathways in Neuro-Ophthalmology: An Evidence-Based Approach.Thieme.

Martinelli,V. et.al (2009). Ashort-term randomized MRI study of high-dose oral vs intravenousmethylprednisolone in MS.NeurologyDecember 1, 2009 vol.73 no.22 1842-1848

MillerDH, Leary SM (2007). &quotPrimary-progressive multiple sclerosis&quot.LancetNeurol6(10): 903–12

PhillipsPH. (2007). Treatment of diplopia. SeminNeurol.27(3): 288–98

Poser,M. &amp Brinar V. (2004). &quotDiagnostic criteria for multiplesclerosis: an historical review&quot. ClinNeurol Neurosurg106(3): 147–58

Rog,D. (2009). MultipleSclerosis.Class Publishing Ltd

Stadelmann,C., &amp Brück W. (2004). &quotLessons from the neuropathology ofatypical forms of multiple sclerosis&quot. Neurol.Sci.25(Suppl 4): S319–22.