Short Case Study
A previously healthy 34 years-old female presents for with an onset of progressive organic psycho-syndrome, dysarthria, and bilateral numbness. The medical history revealed an admission to another hospital with an acute onset of psychiatric symptoms, such as aggression, loss of energy, drowsiness, gestational hypertension, and hypothyroidism (Mahboobi et al. 388). She never used any psychoactive drugs. However, her parents had a history of colon and bronchial cancer.
Upon admission with a progressive delirium diagnosis, her vital signs were within the normal range. Even so, she demonstrated drowsiness, reduced incitement, slower formal thought, and amnestic deficiency. ECG results reveal an electrical conductivity of 7Hz. A brain MRI report shows severe lesion load, hypointensity, and multiple peri-ventricular hyper-intensities, whereas a cervical spine MRI conclusion is a central lesion (Ibid). Also, neurological results showed dysarthria, hypoesthesia, spinal ataxia, and cognition-involving disorder. Meanwhile, blood tests revealed oligoclonal bands and measles-rubella-varicella zoster reaction. Using McDonald’s criteria, the conclusion was a diagnosis of multiple sclerosis (MS), and an appropriate treatment plan initiated (Gossman et al. “Evaluation”)
- Definition of the Disease
MS is a disabling condition that affects the brain and spinal cord. Goldenberg defines the disease as an autoimmune, inflammatory neurological infection of the nervous system that attacks and destroys the myelinated axons. That is, in MS, the immune system attacks body tissues, terminating myelin, the fatty substance that protects the brain and spinal cord. Close to half a million patients in the United States suffer from the disease, subjecting approximately 50% of the patients to mobility assistance within 15 years after its onset (Ibid).
The grouping of the condition entails the use of causes and predisposing factors. The standard form associated with 85% of patients is relapsing-remitting (RR) MS. It involves flare-ups of symptoms accompanied by remission periods, following recovery (Ibid). RRMS patients may exhibit secondary progressive MS. This form of MS may worsen regardless of remission or plateaus. Primary progressive MS encompasses gradual deterioration in the condition, with no relapse remission. According to Goldenberg, approximately 10% of MS patients have experienced occasional plateaus with high resistance to MS drugs. Finally, progressive-relapsing form affects less than six percent of MS patients. The condition is progressive at the initial stages, accompanied by flare-ups of increased symptoms. There are no periods of remission.
MS is common in patients aged between 20 and 40 years old, with 1% and 2-10% detected in childhood and after age 50 years, respectively (Ghasemi et al. 1). Also, the condition is more common in women than men at a ratio of 2.5:1. While MS aetiology is unclear, it combines genetic predisposition and environmental influences (Ghasemi et al. 2).
- Cause of the Disease
The cause of MS is unclear, but it encompasses both genetic susceptibility and environmental factors. According to Ghasemi et al., the risk of developing MS is related to the amount of gene information shared in a family (4). Therefore, for monozygotic twins and dizygotic twins, the risk is 25% and 2-5%, respectively. What is more, the risk in first, second, and third-degree relatives is 2-5%, 1-2%, and 1%, respectively (4). Another group of genes associated with MS includes a range of Human Leukocyte Antigen and Interleukin (-7 and -2) receptor-alpha.
In light of environmental factors, the onset of MS is in connection with viral and bacterial agents. These agents include Epstein Barr virus, mycoplasma pneumonia, mycoplasma pneumonia, and herpes virus type 6. The individual lifestyle and behaviours that predispose to Ms include a poor diet, cigarette smoking, exposure to ultraviolet radiation and vitamin D and B12 deficiency, and body organs malfunctioning (3). For example, nitric oxide exposure can lead to lipid peroxidation and mitochondrial damage. As a result, patients may develop demyelination, axonal degeneration, and oligodendrocytes apoptosis. Exposure to carbon monoxide causes tissue oxygenation, which degenerates the primary protein of myelin. This degeneration contributes to axonal injury and high levels of CD4+ lymphocyte and microglia invasion, leading to demyelination (Ibid). In terms of diet, the risk factors include a high intake of fish, animal fat-based caloric, and linoleic acid are associated with MS.
iii. Signs and Symptoms
Myelin sheath is the coating around the brain and spinal cord. When it is damaged, nerve fibres are exposed, subsequently slowing down the electrochemical messages that travel through the nerves and damaging the nerve itself. According to Ghasemi et al. (1), the signs and symptoms of MS may vary from individual, by the course of the disease and according to the location of affected nerve fibres.
MS patients may exhibit numbness or weakness in either one or more limbs. Typically, symptoms alternate on one side of the body. Electric shock sensations are also familiar with particular neck movements, for example bending forward of the neck, also known as Lhermitte sign (Gossman “History and Physical”). Patients may experience tremors, poor coordination, and unsteady gait. Visual problems are also associated with MS. For example, a patient may have either partial or complete vision loss, which alternates from one eye to another accompanied by painful eye movements. Besides, an individual may experience blurry vision and prolonged double vision. Gossman et al. elaborate that poor vision is related to the afferent pupillary defect, an abnormality of the pupil that affects its ability to respond to light (“History and Physical”). Internuclear ophthalmoplegia encompassing abnormal eye movement that results from the medial longitudinal fasciculus demyelinating lesion (“History and Physical”). People with MS also exhibit slurred speech, dizziness, fatigue, depression, sleep problems, sexual, bladder and bowel dysfunction and vertigo.
- Diagnosis and Differentiation Process
MS does not have a single diagnostic test (Goldenberg 175; Gossman et al. “Evaluation”). However, Goldenberg, present three criteria for diagnosis based on evidence. The first one is space dissemination criterion, which involves at least two varying lesions/plaques/scars in the white matter of the central nervous system. The second criterion concentrates on time; which comprises at least two separate episodes in the disease course. The latter approach involves inflammation; this entails the analysis of cerebrospinal fluid that occurs due to inflammation in the CNS (175).
Diagnosing the autoimmune, inflammatory neurological infection of the central nervous system is primarily clinical, which depends on the manifestations of neurological signs and symptoms consequent of white matter lesions. However, an accurate diagnosis of MS requires taking the patient’s medical history and neurological tests, that include various imaging techniques, such as MRI, LP and CSF analysis, blood sample tests and evoked potentials (Ghasemi et al. 4). Laboratory technicians use MRI to identify the formation and damage of scar/plaque tissue in the CNS (Appendix Fig. 1). What is more, conducting a CSF analysis for immunoglobulin-gamma- and myelin-based determinations are diagnostically useful. Blood sample tests for vitamin deficiency detection are considered diagnostically expedient for detecting MS. A careful examination and evaluation of the eye, in particular, Babinski’s reflexes would suffice.
Several criteria are used to distinguish MS from other conditions that manifest similar neurological signs and symptoms. Huang et al., identify McDonald criteria, which focuses on demonstrating lesions disseminated in space and time excluding the alternative diagnosis (3165). The differentiation is achieved by combining paraclinical assessments through a series of imaging and lab tests. Currently, MS diagnosis largely depends on MRI scanning. While gadolinium is used as a contrast agent to highlight lesions, MRI highlights ongoing plaque destructions (3165). Early accurate detection of MS provides the opportunity to develop an effective treatment plan for patients.
Several criteria are in use to distinguish MS from other conditions that manifest similar neurological signs and symptoms. Huang et al., identify McDonald criteria, which focuses on demonstrating lesions disseminated in space and time excluding the alternative diagnosis (3165). The differentiation is by combining paraclinical assessments through a series of imaging and lab tests. Currently, MS diagnosis mainly depends on MRI scanning. While gadolinium is used as a contrast agent to highlight lesions, MRI highlights ongoing plaque destructions (3165). Early accurate detection of MS provides the opportunity to develop an effective treatment plan for patients
- Treatment
Multiple sclerosis does not have a cure. Even so, various treatment strategies can speed recovery from MS-related attacks, alter its course, and manage subsequent symptoms. The primary goal of treating MS involves using therapies to prevent damaged areas (Gossman, “Treatment/Management”). During the 1990s, MS treatments were injectable, but medical and pharmacological advancements influenced the introduction of oral and infusion therapies. Primarily, modern therapies target the most common form of the disease – relapsing-remitting therapies. By 2017, the European Medicines Agency and US Food and Drug Administration approved the first therapy for primary progressive MS (“Treatment/Management”).
Disease-modifying agents are used in therapy to shorten the duration of acute exacerbations, curtail their frequency, and provide symptomatic relief. According to Goldenberg (177), disease-modifying treatments include intravenous dexamethasone and brief corticosteroids to maintain functioning and improve quality of life. The FDA and EMA have also licensed 12 products to control MS symptoms (Appendix Fig. 2). First-line therapy medication for relapsing-remitting MS includes Interferon-β-1a variants and Glatiramer (177). These drugs are efficient in curtailing the relapse rate, delaying neurological disability progression, and reducing the severity of ameliorating relapse. Dimethyl fumarate reduces the relapse rate by nearly 50% (178).
- Prognosis
Estimates show that close to half a million patients in the US suffer from the disease, subjecting approximately 50% of the patients to mobility assistance within 15 years after its onset (Goldenberg 175). Accordingly, more than half of the patients depend on walking aid or are on wheelchairs. Depression and suicide rate among MS patients is statistically higher compared to the general population (Ghasemi et al. 2). However, estimating the average longevity among MS patients remains a challenge considering that the disease varies with individuals. According to Huang et al., poor prognosis is mainly due to the advanced age of patients and an increased number of relapses in the early stages (3164). The most common reasons for MS patients’ death are secondary, compromised swallowing, challenges in breathing, chronic urinary tract infections, and immobility.