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Multiple Sclerosis

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Bullet Incidence
Bullet Cause
Bullet Symptoms
Bullet Progression
Bullet History
Bullet Diagnostic Tests
Bullet Review of Literature

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For CURRENT treatment modalities and testing, as well as profiles of MS patients, visit:THE WORLD OF MULTIPLE SCLEROSIS.

Recent Topics at World of Multiple Sclerosis include:

  • Pain
  • Fatigue
  • Cognitive Problems

Future Topics will include:
  • Visual disturbances
  • Spasticity
  • Bladder & bowel
  • Treatment successes and failures
  • Family responses to MS
  • Humorous incidents
  • Holidays
  • Changing attitudes and stereotypes
  • Coping strategies

The following is a Mailing List for MS found on Rootsweb. This mailing list covers all multiple sclerosis issues. To subscribe, send an email to: Just write "subscribe" in the body of your email message. There is no need to sign.



  1. Onset between 20-40 years
  2. Ratio of women to men 3:2
  3. Caucasian to Blacks 5:1
  4. Family history: Although MS occurs in families more frequently than pure chance alone would explain, no hereditary factors have been definitely associated with the disease.

  5. Upper socio-economic groups
  6. Cold, damp climate
  7. Scottish Ancestry: A study presented in the Journal of Neurology, Neurosurgery and Psychiatry on June 18, 1998 suggests that Scottish ancestry seems to be a risk factor for the development of multiple sclerosis.

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Definition: MS is a disease characterized by exacerbation and remissions caused by progressive demyelination of white matter of the brain and spinal cord. (Newest research indicates that demyelination may not be the only damage caused by MS) The sporadic patches of demyelination in the CNS induce widely disseminated and varied neurological dysfunction, often mistaken for hysteria.

Recent research based on technological advances in imaging has shed new light on this debilitating disease. MS is an infection-induced auto-immunity in a genetically predisposed host. It is an auto-immune disease whose main target is the axon fibers of the nervous system, which transmit electrical impulses throughout the body. The immune system incorrectly identifies the axon as alien to the body, and attempts to destroy it. Although this is a chronic disease, the course is an unpredictable one.

MS degeneration is continually active even in 100% functional individuals, and before the appearance of any visible symptoms. Ninety percent of patients have active disease. We now know that for every noticeable exacerbation, there will likely have been a number of silent or unnoticed exacerbations only visible on the MRI. Active MS lesions (lesions visible on the MRI) are 5-10 times more common than clinical relapses (observable exacerbation of symptoms). The disease causes axonal loss not only within plaques in the brain, but also within normal-appearing white matter outside of the demyelinating lesions. Untreated, brain volume loss may be as high as 5-10% each year. Although axonal damage and loss are the major causes of progressive disability in MS, damage to the myelin (the protective insulation surrounding nerve fibers in the central nervous system) also occurs independently of axonal damage. It is likely that tissue damage is beyond rescue by the time symptoms appear. Lesion load (the total accumulation of lesions) may be less relevant to understanding the progression of disability than measures of axonal damage visible on MRIs as brain volume reduction. A great article on MS can be found at the Multiple Sclerosis Association of King County, Washington: What's New

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Possible Causes:

  1. Slow-acting virus
  2. Autoimmune response to nervous system
  3. Inherited predisposition
  4. Allergic response to infectious agent
  5. Known precipitating factors include:
    • Emotional/Physical stress
    • Chilling
    • Fatigue
    • Heat, fever (fever can trigger dysphagia)
    • Pregnancy
    • Acute respiratory infection
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  1. Influenza-like symptoms
  2. May vary from day to day
  3. May wax and wane with no predictable pattern
  4. May be bizarre and difficult for the patient to describe
  5. In most patients, visual problems and sensory impairment, such as numbness and tingling, are the first signs
  6. Ocular:
    • Optic neuritis: inflammation of optic nerve with or without pain
    • Diplopia: double vision. Both eyes are used but not in focus
    • Opthalmoplegia: paralysis of ocular muscles
    • Blurred vision, narrowing of visual field (tunnel vision), scotomas (blind spots)
    • Nystagmus: constant, involuntary eye movements
    • Dimness of vision
  7. Muscle Dysfunction:
    • Weakness
    • Paralysis (monoplegia to quadriplegia)
    • Spasticity
    • Hyper-reflexia
    • Intention tremor
    • Ataxia (muscular incoordination)
    • Increased deep tendon reflexes
    • + Babinski; gait disturbances; unusual fatigability of limbs
  8. Urinary:
    • Incontinence
    • Frequency, urgency
    • Frequent UTI's (infection)
  9. Emotional/intellectual:
    • Mood swings
    • Irritability
    • Euphoria
    • Depression
    • Lack of attention
    • Lack of judgment
    • Changes in Cognitive Function. For further reading
  10. Parasthenia: Facial paresthesia; numbness and weakness; clumsiness; sensory changes, blunting of sensation; feelings of "tightness" of skin, as though wearing a tight girdle.

  11. Dysphagia: difficulty swallowing
  12. Dysarthria: stammering, imperfect speech
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  1. In early stages of disease, attacks take hours or days to develop; however, later the onset may occur within seconds.
  2. Attacks that last less than 2-3 days generally don't produce marked neurological deficits.
  3. Symptoms that haven't disappeared within 3 months are unlikely to disappear completely.
  4. If patient is over 30 at onset, the disease will more likely follow a slow, progressive course than the attack-remission pattern characteristic of younger patients.

  5. With each subsequent attack, chances that the resulting deficit will disappear spontaneously, decrease.
  6. The more frequent the attacks during the first 2 years, the graver the outlook.
  7. During first 10-15 years, repair within CNS of the myelin sheath appears after each attack. Eventually the CNS is no longer able to repair destructive cycle and a steady downhill course follows.

  8. With use of MRI to follow course of disease, it appears that many areas are constantly involved that are asymptomatic; therefore, the attack-remission pattern may not be a valid assessment.

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  1. Accurate history is essential to rule out a differential diagnosis.
  2. Do symptoms worsen with fever? Although the myelin sheath may be damaged with sclerotic plaques, nerve fibers may still function well under normal conditions; however, even a .01 degree rise in body temperature can disrupt them.

  3. In early stages of MS symptoms may increase, or new ones appear when taking a hot bath, or having been out in the heat, and then return to normal as body temperature decreases.

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Diagnostic Tests:

  1. Spinal tap:
    • IgG/albumin ratio of CSF (cerebral spinal fluid)
    • Oligoclonal bands
  2. VER (Visual Evoked Response)
  3. BAER (Brainstem Auditory Evoked Response)
  4. CT Scan: May show increased tissue density of white matter as normal tissue is replaced by sclerotic tissue.
  5. MRI: (Magnetic Resonance Imaging) Protons, which are charged cellular particles are tagged, using magnetic field and radio signals from frequency transmitter. They scramble the protons into signals that can be mapped. Protons in body all have specific environment and magnetic properties. Their signal strength can be mapped by position. Gadolinium DTPA is used to enhance MRI.

No single symptom or absence of positive test results can point to or eliminate the diagnosis of MS. The only real clue is multiplicity of attacks, and a pattern of exacerbation and remission of symptoms that involve multiple deficits of the Central Nervous System.

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Review of Older Literature:
I. Neurology; July 1988, Vol. 38, No. 7, supplement 2; "Rationale for Immunomodulating Therapies of Multiple Sclerosis"

p5; Overview of the rationale for immunomodulating therapies in MS; Robert P. Lisak, MD: To date, four distinct characteristics of MS lesions have been identified:

  1. Inflammation, resulting in vascular abnormalities and edema
  2. Destruction of myelin and occasionally other neurological components through infiltration by macrophages.
  3. Astrocytic proliferation and scarring
  4. Decreased conduction within CNS. It is not known what controls rate of progression or whether there is any potential for significant repair. It is not known which specific changes are responsible for exacerbation and remission.

p82; "The Use of MRI In Evaluation of Clinical Trial", by David W. Paty, MD:

There is poor correlation between number and size of lesions seen pathologically or by MRI compared with duration of disease; however, experience now suggests that MRI is most effective technique available today for objective evaluation of MS lesions during life.

Application of MRI to assess lesions in MS still in infancy. Initial attempts involved looking repeatedly at same patients over periods of time. Many lesions which appear gradually disappear or diminish over several months. Time course of development of large new lesions shows them becoming maximum in size over a four week period, then decreasing in size or disappearing over following ten weeks.

Lesions tend to get smaller over disease course while ventricle size increases. II Neurology; May 1986 Vol. 36:

p703: Editorial on Multiple Sclerosis Treatments; Labe C. Scheinberg, MD, and Stanley Van den Noort, MD - overview:
....In patients with moderate disability, small increments of pathology may produce disproportunate decrements of function. Small lesions in one critical focus, such as the spinal chord, may produce major symptoms, while large lesions in another site, such as the cerebrum, go unrecognized by patient and physician. Spontaneous healing and the functional plasticity of the nervous system can produce marked improvement over time.

For the patient who is at risk of developing multiple sclerosis because of geographic and remote genetic factors, there is nothing that would prevent this. For the patient who has advanced chronic disease with long established severe impairments, it is unlikely that present curative efforts would be of value, since these are usually immunoregulatory. For therapy to be effective in the latter group, it would have to produce resolution of the glial scars and remyelination--highly unlikely at present.

....Finally, physicians are traditionally concerned only with impairment as reflected by neurologic examination (in multiple sclerosis, this is largely based on function in gait). Little attention has been paid to disability in the activities of daily living or handicap measured by employment and social involvement. The impairment scores (Kutrzke EDSS) fluctuate greatly according to time of day, season, mood, fatigue, and concurrent illness, and unfortunately even with neurologists experienced in scoring.

Medical-Surgical Nursing
Concepts & Clinical Practices
The C.V. Mosby Co., 1987 Edition

"The recent discovery of slow viruses in association with frequent findings of an increase of IgG in spinal fluids of patients with MS lend credence to the theory of virus and autoimmunity as causative factors. Multiple foci of demyelination are distributed randomly in white matter of the brain stem, spinal cord, optic nerves, and cerebrum. During the demyelination process the myelin sheath and sheath cells are destroyed, but there is early sparing of the axon cylinder. The outer myelin sheath in the spinal cord neuronal pathway is often compared with the insulation of an electric wire. Its destruction causes interruption or distortion of the impulses so that it is slowed or blocked. There is evidence of partial healing in areas of degeneration, which accounts for the transitory nature of early symptoms. In late stages the degeneration may extend to gray areas of the spinal cord and limit healing.

Because of the wide distribution of areas of degeneration, there is a greater variety of signs and symptoms in MS than in other neurological diseases. These sporadic patches of demyelination induce widely varied neurological dysfunction, often mistaken for hysteria. The scarring that occurs at the degenerative lesions as well as the increasing sites provides the name "disseminated sclerosis".

MS is a chronic, remitting, and relapsing disease. The majority of people recover from early episodes. Usually there are acute exacerbations and remissions that may last for a year or more, although eventually exacerbations recur."

II. Washington University School of Medicine
Protein Implicated In Multiple Sclerosis
May 13th, 1998

Scientists may have found a protein that is responsible for the damage to nerves in multiple sclerosis. Their findings were published in the April issue of the Journal of Neuroimmunology, 1998; main author was John L. Trotter, M.D. The protein, called myelin proteolipid protein or PLP has been shown to trigger MS symptoms when injected into animals. For further reading visit Science Daily.

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Web Author: Dianne Elizabeth, 1999
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Web Site: Dianne Elizabeth's Family History, Created July 17th, 1999
Page Title: Multiple Sclerosis
Page Created: June 11th, 2000
Revised: August 14th, 2008