Introduction
Multiple sclerosis (MS) is a chronic inflammatory demyelinating disorder of the central nervous system (CNS), which is typified by progressive neurological disability and is perceived to be autoimmune in nature and scope (Burgess, 2011). The presenting neurological disability often occurs as a direct consequence of permanent axonal damage (Meehan, 2011). This paper reviews the pathophysiology, diagnosis and treatment for MS.
Pathophysiology of MS
To date, the exact pathophysiology of MS remains poorly understood; however, it is universally established “…that it is an autoimmune response, which plays an important part in both its onset and its subsequent clinical course” (Ward-Abel & Burgoyne, 2008, p. 212). Irrespective of what the preliminary cause is for MS, available literature demonstrates that a surge of immune-related activity arises once the immune system becomes affected, eventually leading to the production of inflammatory lesions throughout the CNS followed by sustained fatigue (Meehan, 2011; Besharat et al, 2011).
The inflammation is not only the hallmark of MS but it’s the causative agent which triggers damage to the CNS as it occurs in the wrong place at the wrong time. While in the general population inflammation is considered a healthy autoimmune response, the opposite is true in MS as such inflammation leads to a typical clinical case of exacerbations of neurological symptoms and, eventually, failure of neurological functionality (Ward-Abel & Burgoyne, 2008).
Although the fundamental disease process of MS is complex and the precise pathogenesis still difficult to comprehend, it is assumed that the immune system malfunctions and commences a sustained “…attack against the myelin that surrounds the axons and the oligodendrocytes that produce it; a process known as demyelination” (Ward-Abel & Burgoyne, 2008, p. 212).
This process results in plaques and lesions developing along the myelin cover, effectively impairing nerve transmission and, eventually, generating an intricate array of neurological indications including visual loss, bladder and bowel failure, mobility difficulties, ataxia, fatigue, tremor, sexual disorientation and shifts in cognition (Ward-Abel & Burgoyne, 2008).
Although there exists proof in a subset of the population who has experienced demyelination that unprompted remyelination of injured nerves can occur, available literature shows that it is only a small percentage of the population who can make the turnaround (Ward-Abel & Burgoyne, 2008).
It follows that patients are unable to achieve complete recovery of function in the absence of proper regeneration and remyelination of nerves, leading to sustained accumulation of disability (Burgess, 2011). Consequently, “…as MS evolves it will typically cause damage in multiple areas within the CNS, not only by the process of acute demyelination but also because it leads to axonal loss, degeneration and brain atrophy” (Ward-Abel & Burgoyne, 2008, p. 212).
In disease patterns, it is noted that majority of patients diagnosed with MS primarily experience an inflammatory course of the syndrome with relapses and remissions of neurological symptoms occurring with spontaneous regularity and varying severity (Burgess, 2011). Over time and for most patients, this pattern of syndrome activity shifts and relapses become less recurrent but more dangerous, “…probably because the level of inflammation has been replaced by neuronal degeneration resulting in gradual but progressive disability” (Ward-Abel & Burgoyne, 2008, p 213).
In a small subset of the population, particularly in adults, the disease pattern will be principally degenerative from the onset; these patients will experience progressive neurological destruction but with no definite clinical relapses.
Diagnosis of MS
There is no definitive test or diagnosis for MS (Meehan, 2011), primarily due to its transient nature of presenting symptoms. However, general practitioners (GPs) should evaluate the patient’s clinical history to determine the rate of relapses, while neurologists should perform neurological examinations such as magnetic resonance imaging (MRI), electro-encephalographic (EEG) recording, and cerebro-spinal fluid (CSF) assessment to confirm inflammatory episodes in different areas of the CNS (Burgess, 2010; Meehan, 2011).
A diagnosis of MS is confirmed in these disease activities are detected and in the absence of any other better explanation. However, there must be evidence of inflammatory experiences in diverse areas of the CNS and relapse lasting more than 24 hours and occurring after at least one month of stability (Burgess, 2011).
Treatment for MS
Although there is currently no cure available for the treatment of MS (Ward-Abel & Burgoyne, 2008), experts argue relapses can be contained through the use of high-dose steroid treatment and disease-modifying therapies (Burgess, 2011). Steroid treatments are effective in reducing acute inflammation associated with the disease but do not alter the outcome of the condition.
Disease modifying therapies (DMTs) such as natalizumab and Avonex not only reduce the frequency, duration and severity of relapse but are well tolerated by patients (Burgess, 2011; Meehan, 2011).
Reference List
Besharat, M.A., Pourhosein, R., Rostami, R., & Bazzazian, S. (2011). Perfectionism and fatigue in multiple sclerosis. Psychology & Health, 26(4), 419-432.
Burgess, M. (2010). Diagnosing multiple sclerosis: Recognizing symptoms and diagnostic testing. British Journal of Neuroscience Nursing, 6(3), 112-115.
Burgess, M. (2011). Improving relapse management in multiple sclerosis: A Nurse-led model. British Journal of Neuroscience Nursing, 7(1), 441-444.
Meehan, M. (2011). The MS nurse’s role in managing natalizumab therapy in patients with relapsing-remitting MS. British Journal of Neuroscience Nursing, 6(8), 392-396.
Ward-Abel, N., & Burgoyne, T. (2008). The importance of the immune response in multiple sclerosis, part 1: Pathophysiology. British Journal of Neuroscience Nursing, 4(5), 212-217.