2020. 1. 31. 03:30ㆍ카테고리 없음
Clark's DAHLC role involves researching and implementing stress alleviation programs such as wellness coaching and stress management groups. Research from this work, such as a DAHLC member cohort study observing employee stress and health behaviors, published in the September 2016 Journal of Occupational and Environmental Medicine, found high stress in one-sixth of participants. While each survey year those experiencing high stress changed, having high stress was associated with negative health behaviors, such as fewer DAHLC visits, impaired mental health, poor nutritional habits and lower perceived overall health. Over time, Dr.
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Clark and colleagues began turning the paradigm to the positive, asking, 'What if, instead of trying to manage employees' negative life aspects such as stress and burnout, we looked at building positive life aspects, good things we want to see grow?' Rather than focusing solely on becoming stress-free, this wellness model targets resiliency: the ability to achieve and have a good quality of life, something that employees could work on daily. This emphasis change led to Dr. Clark's DAHLC title becoming resiliency domain leader.
A novel study Dr. Clark and colleagues noted a dearth of research on happiness's role in bolstering health care employees' workplace function. Researchers posited as individuals' happiness relates to willful choices, a study designed to boost intentionality could increase happiness and other well-being measures., a Mayo Clinic internist in Rochester, Minnesota, had designed such an intervention, Stress Management and Resiliency Training (SMART), with demonstrated effectiveness improving various quality of life domains, yet not happiness specifically. The researchers designed a study observing SMART efficacy for increasing health care worker happiness and well-being.
DAHLC members volunteered for this study — a prospective, nonrandomized, single-arm trial — and received the SMART intervention between 2013 and 2017. It involved six months' participation: three months' in-person SMART intervention and three months' post-intervention follow-up. Investigators used these tools to determine outcome at baseline, intervention end and three months' post-intervention:. Functional Assessment of Chronic Illness Therapy-Spiritual Well-Being. Gratitude Scale. Mindful Attention Awareness Scale.
Perceived Stress Scale. Subjective Happiness Survey. Satisfaction With Life Scale Researchers found statistically significant improvements in all domains, including subjective happiness, gratitude, life satisfaction, mindfulness, spiritual well-being and stress levels. They also noted strong engagement rates, indicated by few participant dropouts. Findings were published in Mayo Clinic Proceedings: Innovations, Quality & Outcomes' December 2017 issue.
Practice application Dr. Clark believes these findings also may apply in depression treatment. Many patients reported as depression worsened, their health behaviors became more negative. Therefore, part of a depression recovery plan may include a wellness intervention.
While patients can start feeling better through depression treatment, their lifestyles may have fallen apart, prompting behaviors such as missing yoga because they feel bad or eating junk food for comfort. At some recovery juncture, however, actively working on wellness and resiliency could be appropriate as part of a comprehensive depression relapse prevention plan, says Dr. To examine how resiliency programs could complement depression treatment, the Mayo Clinic Depression Center is conducting a single-arm pilot study providing SMART to patients being treated for depression, observing recovery impact and ability to benefit from SMART. For future research Dr.
Clark indicates a randomized, controlled study of increasing health care workers' happiness and additional studies investigating resilience programs for patients with depression should be explored. Though he feels stress groups are useful, Dr. Clark notes such programs aren't scalable for thousands of medical center workers, since these groups only facilitated 300 participants yearly at Mayo Clinic. To broaden the scope, he's now looking at large participant group interventions.
One possible avenue for resiliency improvement at the workplace is a wellness champions program, where individual employees volunteer to promote wellness with co-workers. This program, discussed in a 2016 issue of American Journal of Health Behavior, has demonstrated benefit and is a future research focus.
For more information Berkland BE, et al. Mayo Clinic Proceedings: Innovations, Quality & Outcomes. Clark MM, et al. Journal of Occupational and Environmental Medicine. Wieneke KC, et al.
American Journal of Health Behavior.
Introduction Multiple Sclerosis (MS) is a chronic inflammatory, demyelinating, and neurodegenerative disorder of the central nervous system (CNS) that affects the white and grey matter of the brain, spinal cord, and optic nerve. MS is one of the most common causes of non-traumatic disability among young and middle-aged adults. Direct MS-related healthcare costs are estimated to be more than $10 billion annually in the United States. As symptoms of MS are extremely variable and often quite subtle, diagnosis and management have been greatly enhanced by the use of magnetic resonance imaging (MRI). Therapies that target inflammation and slow progression of disease are available; therefore, early diagnosis and treatment are important in limiting the impact of this potentially devastating disease. Complementary approaches such as symptom management and healthy lifestyle practices also have an important role in MS care.
Definition and Disease Course There are several different forms of MS. Since these classifications were based upon clinical characteristics, they are empiric and do not reflect specific biologic pathophysiology. Nonetheless, they provide an organized framework for diagnosis and long-term management.
Approximately 85% of patients present with a relapsing-remitting MS (RRMS) disease course at onset, where symptoms appear for several days to weeks, after which they usually resolve spontaneously. After tissue damage accumulates over many years and reaches a critical threshold, about two-thirds of the patients transition to secondary progressive MS (SPMS), where pre-existing neurologic deficits gradually worsen over time. Relapses can be seen during the early stages of SPMS, but are uncommon as the disease further progresses. About 10% to 15% of patients have gradually worsening manifestations from the onset without clinical relapses, known as primary progressive MS (PPMS).
Patients with PPMS tend to be older, have fewer abnormalities on brain MRI, and generally respond less effectively to standard MS therapies. Prevalence MS affects approximately 1 million individuals in the US and 2.5 million worldwide. Initial symptoms typically occur between 20 and 50 years of age, and women have about 3 times increased likelihood of developing MS compared with men.
Although MS is more frequently seen in white than African American and Hispanic populations, the latter groups overall have poorer disease outcomes in that they accumulate disability more quickly, suggesting more destructive tissue injury in these groups. The prevalence of MS varies by location and generally increases the further one travels from the equator in either hemisphere. It remains unclear whether this altered incidence represents an environmental influence (eg, vitamin D deficiency), genetic difference, variable surveillance, or other, as yet unidentified, differences. Pathophysiology Early in the disease course, MS involves recurrent bouts of CNS inflammation that results in damage to both the myelin sheath surrounding axons as well as the axons themselves.
Histologic examination reveals foci of severe demyelination, decreased axonal and oligodendrocyte numbers, and glial scarring. The exact cause of inflammation remains unclear, but an autoimmune response directed against CNS antigens is suspected. In progressive MS, inflammation is a less defining pathological hallmark. Instead, progressive MS is characterized by neurodegeneration of the white and grey matter resulting in brain and spinal cord atrophy on a background of mild-moderate inflammation. Predominant factors driving neurodegeneration include mitochondrial dysfunction due to defective oxidative phosphorylation and nitric oxide production, resulting in a chronic state of virtual hypoxia due to unmet energy demands, and age-dependent iron accumulation in myelin and oligodendrocytes leading to oxidative tissue damage. Further research is needed to understand how these different pathologic subtypes affect prognosis and response to treatments. Currently, brain biopsy is the only method to definitively determine pathologic subtypes, but studies are underway to find blood, cerebrospinal fluid, and MRI biomarkers.
Historically, MS was classified as an inflammatory disease targeting white matter, with diagnostics and therapeutics focused on this mechanism of pathology. However, more recent imaging and histopathological studies suggest that cortical demyelination plays a crucial role in MS pathogenesis and cognitive dysfunction. Cortical demyelination is now recognized in early MS. Although some investigative MRI modalities capture some cortical involvement, including double inversion recovery sequences at 3 tesla and ultra-high field MRI, conventional MRI metrics used in clinical practice do not show these changes well.
Likewise, extensive cortical demyelination that is seen in histopathological studies is not clearly demonstrated on any current MRI modality. This pathology/imaging discordance demonstrates that we are still technologically disadvantaged in accurately assessing cortical lesion pathology in the live patient. In the past, inflammation was thought to involve only demyelination, but pathologic studies have found significant axonal pathology as well. In actively demyelinating MS lesions, an average of more than 11,000 transected axons/mm 3 were observed, while control brain tissue had less than one transected axon/mm. Significant axonal injury is also observed in cortical demyelinating lesions. Clearly, axonal injury is significant in the early stages of disease.
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Later in the disease course, gradual progression of disability is observed. However, there is significantly less active inflammation during this period, so clinical progression may arise instead from degenerative changes. Nonetheless, oligodendrocyte progenitor cells capable of remyelinating axons have been observed even in white matter plaques from patients with chronic MS.
This observation suggests that the potential for remyelination persists even very late in the disease course, which is an encouraging indicator for possible therapeutic targets at this late stage of disease. Current concepts of the pathophysiology of MS are illustrated in. In the preclinical phase, patients may develop lesions characteristic of MS visible on MRI before they phenotypically manifest symptoms, known as radiologically isolated syndrome. In a different scenario, patients may develop MS symptoms compatible with inflammatory demyelination without other characteristic lesions on MRI. This phenomenon is called clinically isolated syndrome. On average, patients with RRMS experience clinical relapses every 1 to 2 years.
Serial MRI studies show that lesions develop up to 10 to 20 times more frequently than clinical relapses Thus, although RRMS appears to have clinically active and quiescent periods, inflammatory lesions are developing and evolving almost continuously. A current hypothesis states that overt progression of disability, which marks the transition from RRMS to SPMS, occurs when ongoing irreversible tissue injury exceeds a critical threshold beyond which the nervous system can no longer compensate. It is thought that at this point the disease has primarily transitioned to a neurodegenerative condition with neurologic deterioration independent of ongoing inflammation, although superimposed inflammation can continue to cause additional injury. An important implication of this hypothesis is that the accumulation of irreversible tissue damage limits the potential for anti-inflammatory disease modifying therapies (DMTs) when used in the progressive stage of the disease. To be maximally effective, DMTs should be started early in patients with RRMS before permanent disability develops. Overall, an incomplete understanding of progressive MS pathogenesis has slowed the development of effective therapies and requires further inquiry. Signs and Symptoms MS can cause a wide variety of neurologic symptoms since it can affect numerous areas of the brain, optic nerve, and spinal cord.
Characteristic lesions are located in the periventricular and juxtacortical regions, in addition to the brainstem, cerebellum, spinal cord, and optic nerve. Disease localized to the spinal cord may cause partial or complete transverse myelitis, involving sensory or motor changes involving 1 or both sides of the body. Lhermitte’s phenomenon is a nonspecific symptom whereby flexion of the neck causes an electrical-like shooting sensation that extends into the arms or down the back. It is thought to arise from partially demyelinated tissue, whereby mechanical stimulation leads to axonal activation.
Other common symptoms of MS often stemming from spinal cord lesions include bladder and bowel dysfunction. Posterior fossa (eg, brainstem and cerebellum) involvement may present as diplopia, dysphagia, altered sensation or weakness of the face, or ataxia. Inflammation of the optic nerve (optic neuritis) usually presents as blurry vision with painful eye movements, and is often an early clinical manifestation of RRMS. Of all the lesions in MS, cerebral lesions are the most common but cause the fewest symptoms early in MS. Most cerebral lesions are not located in eloquent regions and so are thus clinically silent and identified only by brain MRI.
Very large cerebral lesions may present with weakness or numbness and rarely may cause aphasia or other cortical dysfunction. Cerebral and cortical lesions may also cause subtle symptoms, such as cognitive impairment, fatigue, and affective disorders like depression. Although these symptoms are not uncommon in patients with MS, they are also nonspecific and can be seen in a multitude of disorders. Symptoms of a clinical relapse typically arise over hours to days, worsen over several weeks, and then gradually subside over several weeks or months.
Residual enduring neurologic symptoms are common. The gradual progression of progressive MS can manifest as worsening myelopathy causing asymmetric limb weakness, ataxia, spasticity, and bladder/bowel and sexual dysfunction; impaired mobility; impaired motor dexterity; and cognitive impairment. Diagnosis There are no pathognomonic clinical, laboratory, or imaging findings in MS. The diagnosis ultimately is a clinical decision based on weighing the factors that support the diagnosis against those that fail to support it or point to the possibility of an alternative diagnosis. The Schumacher criteria from 1965 capture the essence of the diagnosis of MS: CNS lesions disseminated in space and time and the elimination of alternative diagnoses. These core diagnostic characteristics remain relevant today. The International Panel on MS Diagnosis criteria, also called the McDonald criteria, are diagnostic criteria for MS that incorporate the clinical characteristics and MRI features.
Revisions were made in 2005, 2010, and most recently in 2017 as a reflection of an increased understanding of the natural history of MS and improved MRI techniques. The latest version of the McDonald criteria (2017) simplifies the diagnostic process and allows earlier diagnosis. A diagnosis of clinically definite multiple sclerosis requires fulfillment of dissemination in space and time.
Dissemination in space is defined as 1 or more T2-hyperintense lesions in more than 1 characteristic location of MS, which includes the periventricular, juxtacortical, and infrantentorial regions (eg, brainstem and cerebellum), and spinal cord. Cerebrospinal-fluid restricted oligoclonal bands can be used as paraclinical support for an early diagnosis of MS.
The 2016 magnetic resonance imaging in multiple sclerosis (MAGNIMS) criteria now include the optic nerve as 1 of the characteristic locations fulfilling an MS diagnosis, though it still remains separate from the McDonald criteria. Dissemination in time is defined as 1) the simultaneous presence of a gadolinium-enhancing (GdE) and non-enhancing lesion at any time on initial MRI or 2) a new T2-hyperintense or GdE lesion on follow-up MRI with reference to a baseline scan, irrespective of the timing of the baseline MRI. Table 1: Summary of the 2017 McDonald Criteria Clinical presentation Additional findings needed for MS diagnosis ≥ 2 clinical attacks and objective clinical evidence of ≥ 2 lesions None; however, magnetic resonance imaging (MRI) is typically obtained to both exclude other diagnoses and stage the severity of disease. In 2013, an international panel of MS experts proposed changes to the classification of MS to more effectively characterize the disease course.
One of the changes included the categorization of disease as either manifesting active inflammation (‘active’) or no active inflammation (‘non-active’) based on new clinical relapses or new T2 or GdE MRI lesions or in combination within the past year. Another change was the categorization of disease based on the presence or absence of continued gradual clinical decline (with progression or without progression). These disease classifications were intended to provide a clearer conceptualization of progressive MS and its differentiation from active inflammation. Although the diagnosis of MS cannot be based on MRI alone, typical MRI lesions in the periventricular and juxtacortical regions, as well as the brainstem, cerebellum, and spinal cord can raise the suspicion of MS, warranting further diagnostic workup or monitoring. MRI is typically obtained at the time of diagnosis to both exclude other diagnoses and stage the severity of disease. Patients with a typical history of MS without typical MRI findings are highly unusual and should prompt consideration of an alternative diagnosis. Treatment Strategies Management of MS requires multiple therapeutic approaches.
The current goals of MS management involve the treatment of acute relapses, prevention of new disease activity and disability progression, management of symptoms that affect quality of life, and adherence to a healthy lifestyle. Acute Relapse Several studies have found that treatment with corticosteroids can shorten the length of relapses and may even improve long-term outcomes. A typical regimen is 500 mg to 1,000 mg of intravenous methylprednisolone with or without a tapering dose of oral prednisone over several weeks. The standard protocol at the Cleveland Clinic is intravenous methylprednisolone 1,000 mg daily for 3 to 5 days, followed by a 12-day prednisone taper (60 mg daily, decreasing by 20 mg every 4 days). Evaluation of a relapse should include a search for precipitating factors such as fever, upper respiratory illness, or bladder infection. For patients who do not respond sufficiently to corticosteroids or who do not tolerate corticosteroids, adrenocorticotropic hormone or plasma exchange can be considered. Disease-Modifying Therapies for Relapsing MS: Treatment Targets and Therapeutic Strategies After the acute relapse is treated, consideration should be given to use of DMTs, which primarily target the inflammatory, demyelinating aspects of the disease.
A list of DMTs for MS approved by the U.S. Food & Drug Administration (FDA) is presented in.