BACKGROUND:Qualitative data are lacking on decision making and factors surrounding changes in employment for patients with multiple sclerosis(MS). This study aimed to increase our understanding of the key symptoms and factors leading patients with MS to leave work or reduce employment.
METHODS:Adults with MS who reported leaving the workforce, reducing work hours, or changing jobs due to MS in the past 6 months were recruited from four US clinical sites. Patients participated in semistructured interviews to discuss MS symptoms and reasons for changing employment status. All interviews were transcribed and coded for descriptive analyses.
RESULTS:Twenty-seven adults (mean age = 46.3 years, mean duration of MS diagnosis = 10.9 years) with a range of occupations participated; most were white (81.5%) and female (70.4%). Physical symptoms (eg, fatigue, visual deficits) (77.8%) were the most common reasons for employment change; 40.7% of patients reported at least one cognitive symptom (eg, memory loss). Fatigue emerged as the most pervasive symptom and affected physical and mental aspects of patients’ jobs. Most patients (85.2%) reported at least two symptoms as drivers for change. Some patients reported a significant negative impact of loss of employment on their mental status, family life, and financial stability.
CONCLUSIONS:Fatigue was the most common symptom associated with the decision to leave work or reduce employment and can lead to a worsening of other MS symptoms. Comprehensive symptom management, especially fatigue management, may help patients preserve their employment status.
We know that fatigue is the number one symptom that you want some resolution to as this turns out to be of importance in most surveys. This also number one reason why you leave employment.
Inhibition of relapsing autoimmunity can sometimes curtail fatigue but we need better treatments. Likewise because we do not understand the pathology of fatigue it is difficult to model and research it.
It is probably part of a sickness behaviour due to inflammation and
so you may be interested in this work
Bonsall DR, Kim H, Tocci C, Ndiaye A, Petronzio A, McKay-Corkum G, Molyneux PC, Scammell TE, Harrington ME. Suppression of Locomotor Activity in Female C57Bl/6J Mice Treated with Interleukin-1β: Investigating a Method for the Study of Fatigue in Laboratory Animals.PLoS One. 2015; 10:e0140678.
Fatigue is a disabling symptom in patients with multiple sclerosis and Parkinson’s Disease, and is also common in patients with traumatic brain injury, cancer, and inflammatory disorders. Little is known about the neurobiology of fatigue, in part due to the lack of an approach to induce fatigue in laboratory animals. Fatigue is a common response to systemic challenge by pathogens, a response in part mediated through action of the pro-inflammatory cytokine interleukin-1 beta (IL-1β). We investigated the behavioral responses of mice to IL-1β. Female C57Bl/6J mice of 3 ages were administered IL-1β at various doses i.p. Interleukin-1β reduced locomotor activity, and sensitivity increased with age. Further experiments were conducted with middle-aged females. Centrally (directly into the CNS) administered IL-1β dose-dependently reduced locomotor activity. Using doses of IL-1β that caused suppression of locomotor activity, we measured minimal signs of sickness, such as hyperthermia (high temperatures) pain or anhedonia (as measured with abdominal temperature probes, pre-treatment with the analgesic buprenorphine and through sucrose preference, respectively), all of which are responses commonly reported with higher doses. We found that middle-aged orexin (a peptide that regulates appetite) -/- mice showed equivalent effects of IL-1β on locomotor activity as seen in wild-type controls, suggesting that orexins are not necessary for IL-1β -induced reductions in wheel-running. Given that the availability and success of therapeutic treatments for fatigue is currently limited, we examined the effectiveness of two potential clinical treatments, modafinil and methylphenidate. We found that these treatments were variably successful in restoring locomotor activity after IL-1β administration. This provides one step toward development of a satisfactory animal model of the multidimensional experience of fatigue, a model that could allow us to determine possible pathways through which inflammation induces fatigue, and could lead to novel treatments for reversal of fatigue.
Is this really fatigue?