Multiple Sclerosis Diagnosis, Treatment, Disability

J. Scott Pritchard, DO

NADE National Training Conference - 2011

HistoryOther clinical names- -encephalomyelitis disseminata -disseminated sclerosisFirst described by Jean-Martin Charcot in 1868 Charcots triadAnecdotal histories suggest the disease has been recognized since 1200 - HalldoraFirst well documented case Sir Frederick D' Estes personal diary 1822 - 1846

Inflammatory auto-immune disease affecting the fatty myelin sheaths of the brain/spinal cord axonsDemyelination and remyelinationScarring Sclerosis (plaques/lesions)Loss of conduction electrical signalGenetic, environmental and infectious etiologies have been suggestedProgressive and incurable

Great Mimic

The initial symptoms are varied, vague and extremely difficult to link to a specific cause Numbness, tingling, muscle weakness, changes in cognition, nystagmus, optic neuritis, diplopia, difficulty swallowing or speaking, unexplained fatigue or depressionSymptoms often increased with stress or increased heat (Uhthoffs phenomenon) exercise or environmental

Physical examination

Often very non-focal. Mild motor weakness. Non-dermatomal sensory lossLhermittes phenomenonOptic NeuritisINO-intranuclear ophthalmoplegiaMyelopathy-seen with transverse myelitisMotor weakness. Fatigability of muscles with activity. Generalized fatigueSpasticity Ashworth scale zero to four (severe)AtaxiaMMSE

Clinical testing

SSEP/VEP - evoked potentials+CSF for increased IgG synthesis and oligoclonal bandsMRI-brain/spinal cord w/gadoliniumMcDonald s criteria-clinical, laboratory and radiographic evidenceNPSMyelin Basic Protein- CSF NMO antibodies

Classification of MS

Relapsing-remitting-periods of clinical worsening that resolves with time. However, baseline function is not restoredSecondary progressive (galloping MS)Primary progressive-later onset w/minimal recoveryProgressive relapsing-progressive decline with superimposed attacks (Devics dz)

TreatmentThe goal of all therapies is slow disease progression. Inflammation Solu-MedrolImmunomodulation Avonex/Rebif, Betaseron, Copaxone (ABC therapies)Antineoplastics Mitoxantrone Monoclonal AB - Natalizumab (Tysabri)

New Treatments

Extavia- Interferon -genericCladribine- antineoplasticRituximab- biologic agent-antineoplasticMyelin Basic Protein SupplementOral therapies recently released 1. Ampyra Improves gait in RR MS 2. BG 12 - RRMS 3. Gilenya decreases freq/severity

Disability

25 foot walk test- normal- 5 seconds- men - 6 seconds- womenEDSS-Expanded Disability Status Scale Steps from 0-10-Inviduals 1.0-4.5 are fully ambulatory. 5.0-9.5-increasing ambulatory impairment. 10-Death A claimant with an EDSS of 5.0 or > would typically be disabled.

Listings

11.09 A - Reference listing to 11.04 B11.09 B - Reference to listings 2.02,2.03,2.04 and 12.02 11.09 C Reproducible, substantial motor weakness w/repetitive use or movement

SSR 96 8pDI 24510.057

Sustainability of an RFC consider the functional impact of fatigue and pain

Is the claimant able to sustain a 40 HR work week?

Case Studies57 y/o clt. 1970- numbness of the face and double vision. 1982-RLE numbness that spread to the LLE not relieved by surgery.1983 OS visual loss w/Lhermittes phenomenon. Subsequent years intermittent numbness, diplopia. 1993 major exacerbation with difficulty walking. These episodes progressed to present. She reports mild impairment to mobility and ADLs. Profound fatigue.

#262 y/o clt. Onset of symptoms 1997. On Copaxone from 1998-2002. Four courses of Mitoxantrone. 2002-2003. Progressive weakness and fatigue. Last major relapse 2005. MRIs document increasing plaque burden in the thoracic cord. 25 foot walk-11 seconds with a walkerProgressive weakness in the afternoon

#354 y/o clt onset of R optic neuritis followed by L hemiparesisDeep demyelinating lesion R hemisphere and cervical spine at C3Weakness occurs after walking 10-15 minutesSpasticity of the LUE/LLE and 3/5 motorWide based gait and decreased RAM LUE

#4

38 y/o clt initial bout of optic neuritis at age 26. No other symptoms/clinical findings until the acute onset of mid-thoracic and abdominal pain. MRI documents a T12 lesion in the spinal cord A complete work-up rules out all other etiologies for her pain. Dx neuropathic pain secondary transverse myelitis at T12 All modalities to relieve pain were ineffective.

Thank YOU !!!!

Acknowledgements

Movies from the Neurologic Exam and PediNeurologic Exam were used with the permission of Paul d. Larsen, MD., University of Nebraska Medical Center and Suzanne S. Stensass, PhD. University of Utah School of Medicine. Additional materials were drawn from resources provided by Alejandro Stern, Stern Foundation, Buenos Aires, Argentina, Kathleen Digre, MD., University of Utah

and Daniel Jacobson, MD., Marshfield Clinic, Wisconsin. The movies are licensed under a Creative Commons Attribution-Non-commercial ShareAlike 2.5 license

*