Multiple Sclerosis

Diagnosis, Treatment, Disability

J. Scott Pritchard, DO
NADE National Training
Conference - 2011

History
Other clinical names-encephalomyelitis disseminata
-disseminated sclerosis
First described by Jean-Martin Charcot in
1868 Charcots triad
Anecdotal histories suggest the disease
has been recognized since 1200 - Halldora
First 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 axons
Demyelination and remyelination
Scarring Sclerosis (plaques/lesions)
Loss of conduction electrical signal
Genetic, environmental and infectious
etiologies have been suggested
Progressive 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 depression
Symptoms often increased with stress or
increased heat (Uhthoffs phenomenon)
exercise or environmental

Physical examination
Often very non-focal. Mild motor weakness.
Non-dermatomal sensory loss
Lhermittes phenomenon
Optic Neuritis
INO-intranuclear ophthalmoplegia
Myelopathy-seen with transverse myelitis
Motor weakness. Fatigability of muscles with
activity. Generalized fatigue
Spasticity Ashworth scale zero to four
(severe)
Ataxia
MMSE

Clinical testing
SSEP/VEP - evoked potentials
+CSF for increased IgG synthesis and
oligoclonal bands
MRI-brain/spinal cord w/gadolinium
McDonald s criteria-clinical, laboratory
and radiographic evidence
NPS
Myelin Basic Protein- CSF
NMO antibodies

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

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

New Treatments

Extavia- Interferon -generic

Cladribine- antineoplastic
Rituximab- biologic agent-antineoplastic
Myelin Basic Protein Supplement
Oral therapies recently released
1. Ampyra Improves gait in RR MS
2. BG 12 - RRMS
3. Gilenya decreases freq/severity

Disability
25 foot walk testnormal- 5 seconds- men
- 6 seconds- women
EDSS-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 B
11.09 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 8p
DI 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 Studies
57 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.

#2
62 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 walker
Progressive weakness in the afternoon

#3
54 y/o clt onset of R optic neuritis
followed by L hemiparesis
Deep demyelinating lesion R
hemisphere and cervical spine at C3
Weakness occurs after walking 10-15
minutes
Spasticity of the LUE/LLE and 3/5 motor
Wide 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 midthoracic 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-Noncommercial ShareAlike 2.5 license