Loading presentation...

Present Remotely

Send the link below via email or IM


Present to your audience

Start remote presentation

  • Invited audience members will follow you as you navigate and present
  • People invited to a presentation do not need a Prezi account
  • This link expires 10 minutes after you close the presentation
  • A maximum of 30 users can follow your presentation
  • Learn more about this feature in our knowledge base article

Do you really want to delete this prezi?

Neither you, nor the coeditors you shared it with will be able to recover it again.


Stephen Eikermann

No description

Stephen Eikermann

on 15 August 2014

Comments (0)

Please log in to add your comment.

Report abuse

Transcript of Stephen Eikermann

Multiple Sclerosis
Spasticity: r/o coexisting condit.
PT, OT, Remove noxious stim, ROM, positioning,
cryo, casting, rhizotomy, tenotomy, optimize bowel
& bladder function

Baclofen 2.5-5mg BID (BZDs 1-2mg BID)
Dantrolene .5mg/kg BID Tizanidine
Clonidine .1mg patch x 7 d
Rehabilitation – Symptom Mgmt

Cyclophosphamide (modest improvement)
Azathioprine (mixed results)
Methotrexate (AE: mucosa ulcers, GI abnorm)

Mitoxantrone – IV Ig 3 mo, antineoplastic


Corticosteroids: Short bursts 1000mg/d IV x4-7d, 2 wk PO
AE: GI disturb, fluid, mood, electrolyte, insomnia, acne, Hgly, HTN (Long term: HTN, Osteoporosis, DM, Cataracts)

Disease Altering: “A, B, C’s”
Avenox = Interferon-A = 6 million units IM Q week
AE: flu-like, myalgia, fever, chills, asthenia
18% reduction in relapse rate

Betaseron = Inf-B = 8 million units SQ QOD
AE: Flu-like, increase LFTs, low WBC, myalgia, injxn necr
30% reduction in relapse rate

Copaxone = Inf-C = SQ injection Q day
AE: flushing, injxn site reaction, self-lim chest tightness
32% reduction in relapse rate

“Lesions scattered in time and space”
Neuro deficits in 2+ areas, 2+ points in time, lasting >24 hrs, separated by 1-6 months
No two symptoms explained by single lesion
Supported by diagnostic data**


Myokymia, deafness,
tinnitus, vertigo, V, dysphag.
1) Relapsing-Remitting
2) Benign
3) Progressive-Relapsing
4) Primary progressive
5) Secondary progressive
6) Malignant

Infectious: Very slow viral process

Minimal Record of Disability (MRD): FS, ISS, ESS

-Kurtzke Functional Status (FS) - 8 areas tested
0 – normal
4 – severe disability, but ambulates
8 – bedbound
10 – death
Scoring Systems
Resistive Exercises:
Prevent deconditioning, disuse atrophy, mm weakness
Increase endurance, multiple periods of rest

Sensory Disturbance Pain Syndrome:
TENS, PT, OT,Neurontin, Tegretol, TCA, Dilantin, Capsaicin

Fatigue Prevention:
Keep Cool & Calm, Cooler temp for swimming, heat delays conduction
R/O anemia/depression/hypothyroidism/medication induced
Amantadine 100-200mg Qday

Spastic Bladder: Ditroban, Pro-Banthine, Levsin, Tolterodine,Antichol.
Urinary Retention: Flowmax, Alpha antag, Self-Caths

Constipation: Bowel Regimen important

MRI: Greatest Sensetivity for MS Dx
Multifocal areas of increased intensity on T2 weighted images  Abnormal in 85% cases
Ovoid plaques in periventricular white matter
Enhancement with gadolinium may precede deficits
May visualize subclinical lesions

CT Scan:
Not effective for brainstem, cerebellum and optic nerve
Cerebral atrophy MC sign


Sensory Evoked Potentials

Prolongation of absolute peak or interpeak latency

Diagnostic Data

Not Pathognomonic
New Symptom Not Always New Lesion*


Rapidly progressive, Motor (ataxia/tremor) is 1st sign, not ambulatory, higher relapse rate, high disability

Prognostic Factors

Exact cause remains unknown

Females > Males 2:1, Whites >>> Blacks/Asians

Stephen Eikermann, DO
Friday, August 15th 2014
Corpus Christi Medical Center
Progressive inflammatory disease of white matter resulting in plaques over time through subsequent exacerbations and remissions.

Oligodendrocytes make up myelin of white matter
Outcome: 85% have normal life expectancy, 2/3 don’t
require ambulatory assistance in 10 years after dx
Suicide Rate: 7.5x higher, 70% with neuropsych issues
Pregnancy: Decreases relapses, no change long term
Increased incidence in high SES
Age: 20-50, If migrate to tropical climate by 15 y/o than chances decrease
Geographic: Canada, N. Eu, N. USA >> S. Eu, S. USA > Equator (30-80 >> 4-6 > 1)
Genetic Factors:
Family hx (siblings > children)

MHC on Chromosome 6
T-Cells cross BBB to areas of inflammation and cause destruction
Onset: sensory optic neuritis
Longer remissions
Bladder &
Bowel Dysfunction (#1)
Fatigue (#2)
Visual Disturbance:
optic neuritis, diplopia, nystagmus, INO

Weakness (#3)

Speech Disturbance (dysarthria)
Ataxia, intention tremor
Sensory abnormalities,
paresthesias, prorioception

Weakness and spasticity
Cognitive, Memory, Learning, Emotional, Depress.
-Functional Independence Measure
13 motor, 5 cognitive - scored 1-7
Lhermitte’s Sign
Passive neck flexion - (+) Electric Shock
Increased sensitivity of myelin to stretch/traction
UMN Signs
Hyperreflexive MSR and Plantar Responses
Spasticity (CST)
Decreased Sensation (DC)
Cerebrospinal Fluid (CSF) Analysis

Increased Protein (25% myelin basic)
Oligoclonal IgG bands (highest sensitivity), IgG, WBC
Visual Evoked Potentials

High sensitivity along with MRI

P100 Latency is abnormal
Slowing secondary to plaques
Pontine absence or delay of waves in 55%
Brainstem Auditory Evoked Response (BAER)
Dz Altering
7: Complete I 6: Mod-I 5: Supervision 4: Min Contact assistance 3: Mod Assist 2: Max Assist 1: Total Assist 0: None
Assist Devices:
Orthotics, Cockup splints
0 No increase in tone
1 Slight increase in muscle tone, manifested by a catch and release or minimal resistance at the
end of the ROM when the affected part(s) is moved in flexion or extension
1+ Slight increase in muscle tone, manifested by a catch, followed by minimal resistance
throughout the remainder (less than half) of the ROM
2 More marked increase in muscle tone through most of the ROM, but affected part(s) easily
3 Considerable increase in muscle tone, passive movement difficult
4 Affected part(s) rigid in flexion or extension
From Katz RT. Spasticity. In: O’Young B, Young MA, Stiens SA. PM&
Optic Neuritis: in 1/4 of MS patients, if lasting > 24h
-IV Methylprednisolone 1000mg / d

Aunt Minnie

Neurology 43: 548, 1993
MS patients are much more likely to have antibodies against the potassium channel KIR4.1 (NEJM 367: 115, 2012. )

Vast majority of patients are EBV-positive; Epidemiology 11: 220, 2000
Epidemiology 11: 220, 2000
NEJM: 367, 115: 2012
Mitoxantrone, a topoisomerase II inhibitor familiar from cancer chemotherapy, is a dangerous medication used for aggressive MS: Neurology 74: 1463 & 1822, 2010.
Neurology 74: 1463 & 1822, 2010.
DEVIC'S NEUROMYELITIS OPTICA is an aggressive demyelinating disease with retrobulbar neuritis and large lesions in the spinal cord (i.e., blindness and paralysis). The cause is an IgG antibody (NMO-Ig) directed against aquaporin-4, on the feet of astrocytes (Arch. Neuro. 63: 964 & 1398, 2006),
ACUTE DISSEMINATED ENCEPHALOMYELITIS: (much more than in common multiple sclerosis -- Brain 133: 333, 2010). --> post-infectious encephalomyelitis" is a rare disease that tends to follow (by a few days to 2 weeks) one of the "childhood diseases" (infamously measles and even worse the old smallpox and neural-based rabies vaccines) or one of the old-fashioned immunizations with lots of impurities (especially rabies).

There is altered sensorium and/or movement, and both gray and white matter lesions and/or a very large lesion. Coma rapidly develops; many patients die, but most recover with little or no residual difficulty. In fatal cases, there is striking demyelinization around the blood vessels
Ann. Neurol. 33: 18, 1993 (by Dr. Kepes at K.U.)
Full transcript