Graph representing the different types of multiple sclerosisWorld map showing that risk for MS increases with greater distance from the equator
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Multiple sclerosis

Multiple sclerosis (MS) is a chronic disease that affects the brain and spinal cord. MS can cause a variety of symptoms, including changes in sensation, visual problems, muscle weakness, depression, and difficulties with coordination and speech. Although many patients lead full and rewarding lives, MS can cause impaired mobility and disability in the more severe cases. more...

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Multiple sclerosis affects neurons, the cells of the brain and spinal cord that carry information, create thought and perception and allow the brain to control the body. Surrounding and protecting these neurons is a fatty layer known as the myelin sheath, which helps neurons carry electrical signals. MS causes gradual destruction of myelin (demyelination) and transection of neuron axons in patches throughout the brain and spinal cord, causing various symptoms depending upon which signals are interrupted. The name multiple sclerosis refers to the multiple scars (or scleroses) on the myelin sheaths. It is thought that MS results from attacks by an individual's immune system on the nervous system and is therefore categorized as an autoimmune disease.

Multiple sclerosis may take several different forms, with new symptoms occurring in discrete attacks or slowly accruing over time. Between attacks, symptoms may resolve completely, but permanent neurologic problems often persist. Although much is known about how MS causes damage, its exact cause remains unknown. MS currently does not have a cure, though several treatments are available which may slow the appearance of new symptoms. MS primarily affects adults, with an age of onset typically between 20 and 40 years, and is more common in women than in men.

Signs and symptoms

Individuals with multiple sclerosis may experience a wide variety of symptoms. The initial attacks are often transient, mild (or asymptomatic), and self-limited. They often do not prompt a health care visit and sometimes are only identified in retrospect once the diagnosis has been made based on further attacks. The most common initial symptoms reported are: changes in sensation in the arms, legs or face (33%), complete or partial vision loss (optic neuritis) (16%), weakness (13%), double vision (7%), unsteadiness when walking (5%), and balance problems (3%). Fifteen percent of individuals have multiple symptoms when they first seek medical attention. Most people find their initial MS symptoms occur over a period of hours to weeks. For some people the initial MS attack is preceded by infection, trauma or strenuous physical effort.

Other symptoms and physical findings common in multiple sclerosis are flickering eye movements (nystagmus), speech difficulties, tremor, clumsiness of the hands, abnormal muscle spasms, bladder and bowel difficulties, and sexual dysfunction. Cognitive impairments are also common, such as difficulty performing multiple tasks at once, difficulty following detailed instructions, loss of short term memory, emotional instability, and fatigue. Emotional symptoms are common and can be the normal response to having a debilitating disease or the result of damage to the nerves that generate and control emotions. The most common condition, clinical depression, is a product of both causes. Feelings such as anger, anxiety, frustration, and hopelessness are also common, and suicide is a very real threat.

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Mediastinal sarcoidosis in a patient receiving interferon-beta for multiple sclerosis
From CHEST, 10/1/05 by Sean O'Reilly

INTRODUCTION: A female with multiple sclerosis presented to pulmonary clinic with a mediastinal mass.

CASE PRESENTATION: A 52-year-old female was referred to pulmonary clinic having developed right-sided chest pain which radiated to both shoulders. The sensation was described as dull and pressure-like. The pain was pleuritic and made worse by swallowing both solids and Liquids. It was not exertional. A two week course of ibuprofen reduced, but did not eliminate the pain. There were no associated symptoms. She specifically denied cough, fevers, chills, night sweats, or weight loss. Her past medical history was significant for multiple sclerosis, diagnosed 28 years ago. The MS was well controlled with 30 mcg of weekly self-administered interferon-beta for the past three years. She had been very active, walking two miles daily without difficulty. The patient was afebrile, heart rate 84,blood pressure 126/80 in both arms respiratory rate 14, and pulse oximetry of 98% while breathing room air. There was no cervical or axillary lymphadenopathy. The lungs were clear to auscultation and heart exam was normal. Neurologic, musculoskeletal, and skin exams were unremarkable. Results of a CBC, serum chemistries, liver function tests, and serial troponins were all within normal limits. ECG showed normal sinus rhythm at a rate of 65. Chest radiograph showed a widened mediastinum and a small right pleural effusion. Computerized tomography of the chest revealed a 3cm mass in the superior mediastinum in addition to the small effusion. Positron emission tomography showed moderately intense tracer uptake in the mediastinum, corresponding to the lesion seen on CT. PPD testing was negative and a serum angiotensin converting enzyme level was normal at 20 IU/ml. Mediastinoscopy revealed multiple enlarged mediastinal and right paratracheal lymph nodes. Pathology showed non-caseating granulomas, and was consistent with sarcoidosis. Acid fast and fungal stains were negative for organisms. A diagnosis of sarcoidosis was made, possibly relating to her use of IFN-[beta]. This medication was discontinued. Repeat CT of the chest at six months demonstrated complete resolution of both the mediastinal lymphadenopathy and the right sided pleural effusion. Her MS remained stable after discontinuation of the IFN-[beta].

DISCUSSIONS: Sarcoidosis is a systemic granulomatous disease of unknown etiology. Common manifestations include hilar lymphadenopathy, pulmonary infiltrates, ocular and cutaneous lesions, although it can affect any organ system. Neurosarcoidosis rarely mimics multiple sclerosis, and this patient's clinical course was more suggestive of MS. Numerous reports have linked exogenously administered interferons to the development of sarcoidosis. The majority of cases involve patients using IFN-[alpha]; and ribavirin for chronic hepatitis C infection. Interferons are cytokine mediators involved in the early, innate immune response to viral pathogens. They are also crucial to the development of virus-specific adaptive immunity and can enhance antigen presentation to specific T cells. Type I interferons (IFN-[alpha] and IFN-[beta]) have been shown in vitro to promote Th1 cell differentiation. In sarcoidosis, an exaggerated Th1 immune response, to an unknown antigen, is thought to promote macrophage activation and result in the pathologic granulomatous response. This misdirected immune response results in tissue damage in the affected organs.

CONCLUSION: Sarcoidosis is a recognized complication of IFN-[beta] therapy. While the exact etiology of sarcoidosis remains unknown, this unusual ease provides evidence of a contributing role of interferon. The use of IFN-[beta] as a treatment for multiple sclerosis may be associated with an increased risk of sarcoidosis.

REFERENCES:

(1) Antoniou KM et al. Interferons and Their Application in the Diseases of the Lung. Chest, Jan 2003; 123:209-216.

(2) Marzouk K et al. Interferon-induced granulomatous lung disease. Current Opinion in Pulmonary Medicine 2004, 10:435-440.

(3) Sinigaglia F et al. Type I Interferons and the Th1/Th2 paradigm. Developmental and Comparative Immunology 1999. 23:657-663.

DISCLOSURE: Sean O'Reilly, None.

Sean O'Reilly MD * Alexander White MD Agustin Florian MD Tufts-New England Medical Center, Boston, MA

COPYRIGHT 2005 American College of Chest Physicians
COPYRIGHT 2005 Gale Group

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