Multiple Sclerosis Lecture 4.2 PDF

Lecture 4.2 (1.5 hours) Objectives  Epidemiology & aetiology of multiple sclerosis  Process of demyelination & its effect on neuronal transmission  Different patterns of disease process  Clinical symptoms of multiple sclerosis  Diagnostic process for multiple sclerosis  Pharmacological manage...

Lecture 4.2 (1.5 hours) Objectives  Epidemiology & aetiology of multiple sclerosis  Process of demyelination & its effect on neuronal transmission  Different patterns of disease process  Clinical symptoms of multiple sclerosis  Diagnostic process for multiple sclerosis  Pharmacological management for multiple sclerosis  Key features of physiotherapy management for people with multiple sclerosis MS – info on services  https://www.youtube.com/watch?v=fhUW3BJvVC4 (5.89) from Cleveland clinic Abu Dhabi  MS society websites (UK, US, Australia, Canada for further reading) Epidemiology  Mainly affects white races  Young  2.3 million worldwide (2016 report)  More prevalent further away from equator (? related to Vitamin D/sunlight)  Eg 140/100000 in North America  Eg 108/100000 in Europe  Eg: 2.1/100000 in Sub-Saharan Africa  Eg: 2.2/100000 in East Asia  ? in countries where MS rare, early contact with causative agent (? virus) protects population (? immunity) Epidemiology  Born in high risk area – move to low risk area 50yo)  If diagnosed over 50 year, it is usually a late stage of MS  Childhood onset rare  15% risk if relative has disease Myelin  PNS  One Schwann cell myelinates one axon  CNS  Oligodendrocytes form myelin around CNS axons  One oligodendrocyte myelinates multiple axons Pathogenesis  Demyelination results from disintegration of CNS myelin sheath due to inflammation Perivascular inflammation ↓ Myelin depletion, oligodendrocyte loss & astroglial proliferation ↓ Limited remyelination, axon loss, scar formation Pathogenesis  Most common sites of plaques (scar formation):  White boundary in cerebrum  Periventricular regions  Cerebellar white matter  Optic nerves  Cervical portion of spinal cord  Brain stem Disease process  Benign 5%  Relapsing remitting 40%  Secondary progressive 40%  Primary progressive 10-15%  (rare other clinical variants described) Relapsing remitting  Most common early clinical course  Usually converts to secondary progressive after 10 yrs Clearly defined attacks (relapses) followed by total or partial improvement in between Secondary progressive  Relapsing-remitting usually converts to this clinical pattern where no true ‘stable’ period Secondary progressive Primary progressive  Constant deterioration since initial onset Clinical patterns of MS  Rate and severity of disease progression differs among patients  20-30% still working 20-25yrs after diagnosis  The longer the delay in new symptoms after diagnosis, the more likely a benign course  Secondary progressive – older age at onset MS ‘snapshot’  1/3 quiescent phase/not significantly disabled  1/3 slowly deteriorating  1/3 stable but disabled MS diagnosis CT scan is ineffective in showing up areas of demyelination MRI: periventricular plaques MS diagnosis  Lumbar Puncture CSF shows specific changes that match up with the presence of inflammation: slightly more inflammatory cells, greater number of inflammatory proteins.  ‘oligoclonal bands’ MS Symptoms Dependent upon CNS lesion/s location  Sensory disturbance (spinal cord)  Optic neuritis  Limb weakness (often monoparesis)  Diplopia  Vertigo (vestibular)  Ataxia & tremor  Sphincter disturbance Acute exacerbation Use of anti-inflammatory drugs (steroids):  Methylprednisolone (IV)  +/- prednisolone (orally) Drug treatments – disease modifying  Avonex – interferon beta-1a  Betaferon – interferon beta-1b  Copaxone – immunomodulator, blocks myelin-specific autoimmune responses  Rebif – interferon beta-1a Symptomatic drug management  Baclofen (spasticity)  Ondansetron/dramamine (Dizziness & nausea)  Antidepressants (depression)  Anticholinergics (Bladder symptoms) Non-specific (complex) symptoms  Fatigue  Heat intolerance  Cognitive impairments Fatigue  ‘MS’ fatigue – overwhelming tiredness  Primary or secondary fatigue  Partially demyelinated axons cannot transmit fast trains of impulses  Affects 75% of people with MS  Occurs daily  Worse as day progresses  Worse in heat Fatigue Secondary fatigue:  Related to sleep deprivation eg due to nocturnal leg spasms or continence issues  Related to depression  Related to additional effort required to perform PADLs  Related to loss of ‘fitness’ due to inactivity Heat intolerance  Occurs in 60-90% of people with MS  Impaired thermoregulation (ANS)  Small increase in body temp = ↓ nerve conduction velocity (Note – may result in beneficial or adverse consequences ie may ↑ weakness but ↓ central pain) Cognitive impairment  Occurs in >50% of those with MS  Attentional deficits, both auditory and visual; subsequent memory problems, prone to euphoria, greater incidence of depression, changes in personality Physiotherapy management  Preserve musculoskeletal integrity  Preserve aerobic capacity  Manage fatigue  Optimise functional ability & mobility  Match interventions to client-focused goals  Provide equipment/aids to increase independence  Work within multidisciplinary team to ensure quality of life issues are addressed Outcome measures  Consider measures of QOL & fatigue to supplement standard neuro measures  Eg 6MWT sensitive to reduction in speed and increase in fatigue in patients with MS cf controls Physio – address impairments Spasticity Physio – address activity limitations  Physio – address participation restrictions Efficacy of physio intervention  No evidence that physio Rx increases or decreases the frequency of exacerbations Physio intervention  Increased focus on aerobic exercise early in disease process  3 x 40 mins per week of arm and leg ergometry, 10 week program  Increase in VO2 max, UL & LL strength, depression/anger scores decreased, fatigue decreased Physio intervention  5 x 30 min/week bicycle ex (4 weeks)  Increased aerobic threshold, work rate, health perception, activity level  No evidence of symptom exacerbation by physical activity Hydrotherapy  Heated pools may be poorly tolerated  Cooled pools may enable greater exercise capacity (manage thermosensitivity, reduce core body temp rise)  Buoyancy of water may limit cumulative fatigue  Water may provide resistive element for ataxia and dysmetria http://www.msaustralia.org.au/documents/MS- Practice/aquatic.pdf Benefits of strength training  Can improve muscle force production PLUS: http://www.msaustralia.org.au/documents/MS-Practice/strength.pdf Summary  Immunologically mediated inflammatory disease within CNS  Aetiology likely to be combination of environmental and genetic factors  Multiple sites of disease throughout CNS  Different clinical course patterns  Physio intervention will change relative to disease stage and symptoms  No evidence that exercise exacerbates MS  Evidence that exercise improves MS symptoms