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1 Multiple sclerosis What is the etiology of MS? It is a demyelinating disease affecting only the white matter. Pathologically produces multiple plaques of various age in different locations, especially in periventricular white matter. Lesions initially evoke an inflammatory response with monocytes and lymphocytic perivascular cuffing, but with age settle down to glial scars. Epidemiology of MS? Usual onset is 10-59 year, with the greatest peak between ages 20-40. Female/male ratio: 1,5:1. In Hungary the prevalence is 65-80/100000. Clinical course of MS? The disease can present in different forms, such as primary progressive, relapsing remitting, relapsing progressive and secondary progressive phenotypes. Initially the recovery can be complete, later after the attacks residual signs can remain. 1/3 of the patients will be bed-ridden, 1/3 will have severe symptoms but can live self-sufficiently, 1/3 will have only mild symptoms. Most important symptoms? generalized fatigue sensory symptoms Lhermitte’s sign central neuropathic pain from focal demyelination (e.g., trigeminal neuralgia) optic neuritis nystagmus ataxia 2 Bell’s palsy vertigo dysdiadochokinesis saccadic speech paresis hyperreflexia pyramidal signs bladder hyperreflexia or hyporeflexia euphoria or depression Differential diagnosis of MS: What kind of investigations should be done when you suspect MS? MRI, CSF (routine + oligoclonal bands), VEP, BAEP, ENG, ophthalmology (visus, fundus, CFF, visual field). How can magnetic resonance imaging (MRI) diagnose MS? MRI shows abnormalities in approximately 80% of patients with MS. Subcortical periventricular white matter abnormalities that characterise MS may occur in a variety of other settings, including some subjects who appear to be normal. For this reason, reliance on the MRI can lead to an overdiagnosis of MS. Axial T2-weighted MRI of the brain shows typical confluent, deep white matter signal intensities characteristic of MS. What is the prognosis of MS? MS varies greatly, not only in its symptoms and clinical course, but also in its prognosis. Although not a fatal disease, there is a slight statistical shortening of lifespan as a result of secondary complications that 3 can afflict severe sufferers of MS, such as aspiration pneumonia, decubitus ulcers, urinary tract infections, and falls. As a general rule, approximately one-third of patients with MS will do well throughout their life, never accumulating any significant disability. Another one-third will accumulate neurologic deficits sufficient to impair their activities, but not serious enough to prevent them from leading a normal life — holding a job, raising a family, etc. The final third of people with MS become disabled, requiring a walker, a wheelchair, or even total care. What is the role of steroids in MS? Immunosupression Stabilise blood-brain barrier Anti-inflammatory Enhance nerve conduction What is the best treatment for fatigue in MS? Amantadine has been shown to be useful for eliminating fatigue, usually in doses of 100 mg/ day. Another helpful drug is pemoline, a mild stimulant, which can be given in doses of 18.75 mg /day. What is the best treatment for motor deficits in MS? Unfortunately, little can be done to restore muscle strength. However, spasticity often improves with the use of baclofen in doses of 60 mg or more a day. Dantrolene and diazepam are also useful oral antispasticity agents, although their side effects made them less attractive as first-line drugs. Physical therapy can also minimise spasticity. What is the best treatment for urologic problems in MS? The most common problem is a hyperreflexic bladder with a small capacity, early detrusor contraction, urinary frequency, and urgency. It can be 4 managed with medications such as oxybutinin, propantheline or hyoscyamine. More rarely, there is a flaccid bladder, which may require self-catheterisation. How would you treat the psychological problems in MS? For depression SSRI, especially for patients with fatigue should be given. Tricyclics may be useful for patients with neuropathic pain or insomnia. What are the guidelines in the therapy of MS? IV or PO methylprednisolone or corticotrophin (ACTH) are beneficial for acute relapses. Interferon beta-1a or interferon beta-1b reduces relapse rates and may delay development of neurological disability in patients with active relapsing/remitting course. Copolymer 1 also reduces exacerbations by one-third and has few side effects. Azathioprine has modest effect on relapse.
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