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Stephen Eikermann

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Stephen Eikermann

on 15 August 2014

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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

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

Mitoxantrone – IV Ig 3 mo, antineoplastic

Immunosupression

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
Treatment

“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**

Diagnosis

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

Patterns
Infectious: Very slow viral process
Definition

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
Ritalin

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

Imaging

Sensory Evoked Potentials


Prolongation of absolute peak or interpeak latency


Diagnostic Data


Not Pathognomonic
New Symptom Not Always New Lesion*

Signs

>35
Male
Polysymptomatic
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
Etiology

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
Socioeconomic:
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)
?
Pathogenesis
Genetic Factors:
Family hx (siblings > children)

MHC on Chromosome 6
Immunologic:
T-Cells cross BBB to areas of inflammation and cause destruction
<35
Monosymptomatic
Sudden
Onset: sensory optic neuritis
Ambulates
Longer remissions
GOOD PROGNOSIS
BAD PROGNOSIS
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)
TREATMENT
Dz Altering
Sources
Cuccarillo
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:
Walker
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
moved
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.)
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