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P410-Multiple Sclerosis

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Kathleen Stanton

on 6 April 2017

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Transcript of P410-Multiple Sclerosis

Multiple Sclerosis
Definition
progressive disease which results in demyelinization of nerve pathways

myelin, fatty tissue which covers and insulates nerve fibers and assists with impulse & transmission of efferent and afferent signals

result in a variety of motor impairments resulting in nondiscriminating motor issues
Epidemiology of MS


More commonly seen later in life (20-50 years)

More common in certain ethnic groups (e.g., caucasians) and not seen in others (e.g., aborigines; Inuit)
Tertiary Symptoms
social, vocational, psychological issues that result from primary and secondary symptoms


Loss of job

Depression

Loss or poor personal relationships
Aquatics
water helps a person with weakened extremities attain greater range of motion, as the effects of gravity are essentially eliminated


Cooler water helps to dissipate any body heat that is generated by exercise, the core temperature of the body remains lower, and less overheating

To promote this positive response, water temperatures of 80° - 84°F are usually recommended BUT….
Symptoms
Primary: direct result of demyelinization
Secondary: complications that result from primary
Symptoms

disuse weakness, poor coordination
muscle imbalances
insufficient breathing
muscle tightness or spasticity
Ataxia
Skin ulcers
Category Standards
Relapsing-Remitting MS

Clearly defined disease relapses (flare-ups/exacerbations) with....


Recovery with “residual” deficit


periods between disease relapses characterized by a lack of disease progression

relapses become more severe with time
Types Continued
Primary-progressive (PP) MS:

Disease progression from onset,

No distinct relapses or remissions

Disease begins with a slow progression of neurologic deficits. Problems appear and gradually worsen over time.

Common problems include spastic paraparesis, cerebellar ataxia, urinary incontinence.
Types continued

Secondary Chronic-progressive (SP) MS:

Initial RR disease course but symptoms and attacks become steadily progressive

accumulation of neurological symptoms become more severe

remissions become more "incomplete" and shorter in nature

Transition from RR to SP may be delayed with medication
Habilitation/Treatments
Physical Therapy:Gait Training, ROM

Occupational Therapy:ADL’s

Medication:
Maintenance, reduction in attacks, reduce symptoms

interferons, corticosteriods

potassium and Vit. D

anti-tremor medication

anti-depressants

Stem cells and Plasma Rich Protein
Exercise Modifications
Timing is important…avoid exercising when person is fatigued or when it’s too hot

Uhthoff's Phenomenon-impairment of nerve conduction as a result of increased temperature

Modify “overload” adjusting intensity

Key is to pace exercise routines to conserve energy and minimize increases in core body temperature (interval approach)

Focus on trunk/shoulder/and pelvic girdle (stabilizers)

“Anti-gravity” muscles (knee extensors, hip extensors, low back)
Weakness in these areas will impair gait and require higher energy needs potentially increasing fatigue

Flexibility to address potential contractures


Keep a record of “energy profiles” for each day of exercise……record when during exercise the individual feels strongest


Have participant keep a record of “post-exercise” responses
Cognitive/Memory Changes
Memory or recall problems (frequently reported)

Memory loss seems to be confined to recent events.

Abstract reasoning and problem-solving abilities

Loss "looks like"

1-ability to analyze a situation,
2-ability to identify the salient points,
3-ability to plan a course of action, and carry it out.
Results of Demyelination

Whatever route the pathological process takes from inflammation to demyelination, the effects of loss of myelin by the nerve fibers are quite dramatic.

Saltatory conduction is much more energy efficient than nerve impulses transmitted along the entire length of the nerve fiber.

Loss of myelin results in one or all of the following:

conduction block at the site of lesion
slower conduction time along the affected nerve
increased subjective feeling of fatigue secondary to compensation for neurologic deficits
Abnormal MRI scans are found in patients with MS "eventually"....but brain lesions do not always mean an MS diagnosis.

There are three criteria for the MR diagnosis of MS (Fazekas et al.):

-Lesions in the lateral ventricles
- Lesions present in the posterior fossa
- Lesions greater than .6cm in length


History of two attacks with positive oligoclonal bands
no clinical or para clinical evidence of a disease (e.g., s/sx)
70% of these patience of abnormal MRI


History of two attacks without laboratory
abnormalities (e.g., clinical s/sx) but MR and blood work are clean



History of two attacks with evidence of one lesion
Oligoclonal bands in CSF
90% of patients have abnormal MRI
Probable MS with laboratory support
Clinically probable MS
Clinically Definite MS w/laboratory support
Benign MS

Mild infrequent sensory exacerbations with full recovery.
http://library.med.utah.edu/kw/ms/video/intension.html
Two to three times more common in women than men-is the X chromosome a factor?
1 in 750 chance of developing MS regardless
not directly inherited but increased risk-what's the genetic risk factor?
More common in countries farther from the equator (Vit D deficiency)
Types/Stages of MS
Infection....leukocyte (WBC) entry into the CNS is an early event in MS -BBB dysfunction?
Diagnostic
Criteria
Additional Evidence
Full transcript