Nystagmus – Involuntary Movt ofeyes,fast (may be: side-side, up-down, rotary)*Termed as “sclerosis in plaques”
Epidemiology Ratio of 2:1, > in women Affects white population Areas of frequencies: High - N. US & Europe, S. Canada & AUS, New Zealand -rates of 30-80 /100k pop. Medium - S. US & Europe, rest of AUS -rates of 10-25 / 100k pop.
Etiology Precise theory is Unknown Widely accepted theory: autoimmune dse. Induced by viral/other infectious agents (33%). In particular, herpes V. - I (oral),II (genital),IV & chlamydial pneumonia > young adults bet. 20 – 40
f/hx st – 15% (1 degree relative) 3-5 % fraternal co-twinm, but rises to 26% for identical co-twin.
Pathophysiology Immune response triggers the prod. Of T – lymphocytes, macrophages, and antibodies (IgG). Antigen is activated producing autoimmune cytotoxic effects w/in the CNS.
BBB fails & myelin synthesized T- lymphocytes enter & attack the myelin sheath surrounding the nerves. Eventually oligodendrocytes becomes involved.
Demyelinated areas eventually become filled w/ fibrous astrocytes and undergo gliosis. Axonal loss varies from 10-20% (milder forms), and as much as 80%(severe) Primarily affects white matter early, w/ lesions of gray matter in advance cases.
Main patterns of disease progression are recognized: RELAPSING AND REMITTING MS – lesion often occurs in diff. parts of the CNS at diff. times SECONDARY PROGRESSIVE MS – char. by initial RRMS course, followed by progression at a variable rate that may also include occasional relapses & minor remissions.
PRIMARY PROGRESSIVE MS – in w/c there is little or no recovery from relapse. With a cumulative disability PROGRESSIVE – RELAPSING – char. by progressive dse. From onset but w/o clear acute relapses that may that may or may not have some recovery ; commonly seen in people who develop the dse. After 40 yrs. Of age.
Benign MS - fully functl in all neurological system 15 yrs. After onset. - affects 20% of cases Malignant MS (Marburg Variant) - rare dse. Course, char. by rapid onset & almost continual progression leading to significant disability / death w/ short time after onset.
Exacerbating factors Viral/bacterial infections (cold, UTI) Dse. of major organs-hepa,asthma Stress (major - divorce, death, minor- exhaustion,dehydration) Pseudoexacerbation*sx/s tend to get worse with heat (eg.In the bath or during hot weather) –Uthoffs phenomenon
Differential Dx.Investigationsno diagnostic test but the clinical suspicionis suported by the ff. Three tests: MRI CSF Evoked Potentials- visual evoked potentials (VEPs)- Somatosensory Evoked Potentials(SSEPs)- Brainstem Auditory Evoked Potentials(BAEPs)
prognosis 74 % survives after 25 of onset of symtoms. Minority are still in the workforce after 10 yrs. Onset. 15 yrs. – 50% uses asst. devices 20 yrs. - 50% requires w/c
Prognostic Factors Symptoms Course of dse. Age-younger > 40 yrs. old Neurological findingd at 5 years MRI findings
Medical Mx. Dse. Modifying agents - interferons (interferon beta – 1b, inteferon beta 1a) -reduce relapse by about 30 % Glatiramer acetate & novatrone -clogs T – cell receptors. Limited lifetime dose to prevent heart problems.
Mx. of Relapse & symptoms Corticosteroid therapy – treat acute disease relapse,shortening duration of episodes. - 1000 mg/day, IV (3-5 days) followed by dosage of oral medication over a period of 10 days,5-6 weeks ACTH- long term supression of the immune system, alone/with steriods
Clinical manifestation of inactivity Psychosocial – anxiety/depression Neuromuscular – dec. sensory input, motor control, poor coordination Renal – inc. urinary infections, renal calculi Cardiovascular – inc. HR, thrombophlebitis, OHPN Integumentary – skin atrophy,decubiti Respiratory – inc. resp. infection Digestive – anorexia, constipation Musculoskeletal- osteoporosis, atrophy
Preventive intervention includes: -Primary prevention -Secondary prevention -Tertiary prevention Compensatory inervention Maintetnance Therapy – series of occassional ,clinical, educational and admiinistrative services defined to maintain the Pxs current level of function.
Standardized tests & measures Expanded Disability Status Scale (EDSS) (Kurtyze, 1955) Minimum Record of Disability (MRD) (Intl. Federation of MS Soceities, 1985) Modified Fatigue Impact Scale (Fisk et. al.,1994) MS Functional Composite (MSFC) MS Quality of Life – 54 MS Quality of Life inventory (MSQLI) Functional Exam. Of the MS (FAMS) Multiple Sclerosis Impact Scale (MSIS-29)
Goals & outcomes Impact of pathology/pathophysiology is reduced Impact of impairment is reduced Improved ability to perform physical actions, tasks, activities Reduced disability assoc w/ chronic illness Improved health status & quality of life Enhanced px./client satisfaction
PT Interventions Mx. of Sensory Deficits & Skin Care Mx. of Pain Exercise Training
strength and conditioning Prescription based on four interralated elements: -Freq. Of exercise -Intensity of exercise -Type of exercise -Time/Duration
Guidelines Exerise session should be alternate (non endurance).optimal time such as morning. Submaximal exercise (moderate intensities 50 – 70% MVC)well tolerated,maximal(not) Resistance training modes Circuit training Balance exercise w/ rest periods
Progression Precautions Functional training activities Group exercise outcome measures
Cardiovascular conditioning (Guidelines for clinical exercise testing) Performance measure
Examples half-lying:hip & knee flexion & extension each limb, foot flat on mat Sitting: alternate foot placing to a specified target (floor markings) Standing: up & down to a specified count Walking: sideways or forward to a specified count (floor marking)