MULTIPLE SCLEROSIS

Multiple sclerosis is an autoimmune disease, meaning its cause is an attack by the body's own
immune system. For unknown reasons, immune cells attack and destroy the myelin sheath that insulates
neurons in the brain and spinal cord. This myelin sheath, created by other brain cells called glia, speeds
transmission and prevents electrical activity in one cell from short-circuiting to another cell. Disruption of
communication between the brain and other parts of the body prevent normal passage of sensations and
control messages, leading to the symptoms of MS. The demyelinated areas appear as plaques, small round
areas of gray neuron without the white myelin covering. The progression of symptoms in MS is correlated
with development of new plaques in the portion of the brain or spinal cord controlling the affected areas.
Because there appears to be no pattern in the appearance of new plaques, the progression of MS can be
unpredictable.

Despite considerable research, the trigger for this autoimmune destruction is still unknown. At
various times, evidence has pointed to genes, environmental factors, viruses, or a combination of these.
The risk of developing MS is higher if another family member is affected, suggesting the influence of
genetic factors. In addition, the higher prevalence of MS among people of northern European background
suggests some genetic susceptibility.

The role of an environmental factor is suggested by studies of the effect of migration on the risk
of developing MS. Age plays an important role in determining this change in risk—young people in low-
risk groups who move into countries with higher MS rates display the risk rates of their new
surroundings, while older migrants retain the risk of their original home country. One interpretation of
these studies is that an environmental factor, either protective or harmful, is acquired in early life; the risk
of disease later in life reflects the effects of the early environment.

These same data can be used to support the involvement of a slow-acting virus, one that is
acquired early on but begins its destructive effects much later. Slow viruses are known to cause other
diseases, including AIDS. In addition, viruses have been implicated in other autoimmune diseases. Many
claims have been made for the role of viruses, slow or otherwise, as the trigger for MS, but as of 2001 no
strong candidate has emerged. How a virus could trigger the autoimmune reaction is also unclear. There
are two main models of virally induced autoimmunity. The first suggests the immune system is actually
attacking a virus (one too well-hidden for detection in the laboratory), and the myelin damage is an
unintentional consequence of fighting the infection. The second model suggests the immune system
mistakes myelin for a viral protein, one it encountered during a prior infection. Primed for the attack, it
destroys myelin because it resembles the previously-recognized viral invader.

Either of these models allows a role for genetic factors, since certain genes can increase the
likelihood of autoimmunity. Environmental factors as well might change the sensitivity of the immune
system or interact with myelin to provide the trigger for the secondary immune response. Possible
environmental triggers that have been invoked in MS include viral infection, trauma, electrical injury, and
chemical exposure, although controlled studies do not support a causative role.
PATHOPHYSIOLOGY:
Sensitized T cells typically cross the blood brain barrier, their function is to check the CNS for
antigens and then leave. In Multiple Sclerosis, the sensitized T cells remain in the CNS and promote the
infiltration of other agents that damage the immune system. The immune system attack leads to
inflammation that destroys the myelin sheath which normally insulates the axon and the oligodendroglial
cells that produce in the CNS. Demyelination interrupts the flow of nerve impulses and results in a variety
of manifestations depending on the nerves affected. Plaques appear on demyelinated axons, further
interrupting the transmission of impulses. Demyelinated axons are scattered irregularly throughout the
CNS. The areas most frequently affected are the optic nerves, chiasm and tracts, the cerebrum the
brainstem cerebellum, and the spinal cord. Eventually, the axon themselves begin to degenerate resulting
in permanent and irreversible damage.

SIGNS AND SYMPTOMS:

The signs and symptoms of multiple sclerosis may occur in one of three patterns:

 The most common pattern is the "relapsing-remitting" pattern, in which there are clearly
defined symptomatic attacks lasting 24 hours or more, followed by complete or almost
complete improvement. The period between attacks may be a year or more at the beginning of
the disease, but may shrink to several months later on. This pattern is especially common in
younger people who develop MS.
 In the "primary progressive" pattern, the disease progresses without remission or with
occasional plateaus or slight improvements. This pattern is more common in older people.
 In the "secondary progressive" pattern, the person with MS begins with relapses and
remissions, followed by more steady progression of symptoms.

Between 10-20% of people have a benign type of MS, meaning their symptoms progress very little over
the course of their lives.
Because plaques may form in any part of the central nervous system, the symptoms of MS vary widely
from person-to-person and from stage-to-stage of the disease. Initial symptoms often include:

 Muscle weakness, causing difficulty walking

 Loss of coordination or balance
 Numbness, "pins and needles," or other abnormal sensations
 Visual disturbances, including blurred or double vision.

Later symptoms may include:

 Fatigue
 Paralysis
 Depression
 Speech or swallowing difficulty
 Loss of bowel and bladder control
 Incontinence, constipation
 Sexual dysfunction
 Cognitive changes
Charcot’s Triad

 Nystagmus
 Intention tremor
 Scanning/staccato speech

Weakness in one or both legs is common, and may be the first symptom noticed by a person with MS.
Muscle spasticity, or excessive tightness, is also common and may be more disabling than weakness.
Double vision or eye tremor (nystagmus) may result from involvement of the nerve pathways controlling
movement of the eye muscles. Visual disturbances result from involvement of the optic nerves (optic
neutritis) and may include development of blind spots in one or both eyes, changes in color vision, or
blindness. Optic neuritis usually involves only one eye at a time and is often associated with movement of
the effected eye.
More than half of all people affected by MS have pain during the course of their disease, and many
experience chronic pain, including pain from spasticity. Acute pain occurs in about 10% of cases. This
pain may be a sharp, stabbing pain especially in the face, neck, or down the back. Facial numbness and
weakness are also common.
Cognitive changes, including memory disturbances, depression, and personality changes, are found in
people affected by MS, though it is not entirely clear whether these changes are due primarily to the
disease or to the psychological reaction to it. Depression may be severe enough to require treatment in up
to 25% of those with MS. A smaller number of people experience disease-related euphoria, or abnormally
elevated mood, usually after a long disease duration and in combination with other psychological
changes.
Symptoms of MS may be worsened by heat or increased body temperature, including fever, intense
physical activity, or exposure to sun, hot baths, or showers.

DIAGNOSTIC PROCEDURES:
 Magnetic Resonance Imaging (MRI) Scan
MRIs use magnetic waves to produce images of the brain and spinal cord. If MS is suspected, a special
contrast material (gadolinium) injection is usually at the time of the scan, as it reacts to areas of
inflammation and will "light up" when a lesion is active. This indicates that demyelination is
occurring..

This is considered the best test for diagnosing MS, as abnormal lesions appear on MRIs in over 95% of
people with MS. However, 5% of people with MS do not have abnormalities that can be detected on
an MRI (producing a false negative), and some age-related damage looks like MS lesions (producing a
false positive).

 Neurologic Exam

The doctor will be testing for the following:

o Functioning of the cranial nerves (these control the senses, as well as how you talk and swallow)
o Coordination
o Strength
 o Reflexes
o Sensation

He will do this by having you perform tasks (like touching your nose, then his finger in succession),
touching you with various instruments (and having you report a sensation or looking for a response
himself) and doing an examination of your eyes. These tests do not hurt. The entire test will probably
last about 45 minutes, but may be as long as two hours.

 Evoked Potential Testing

Three main types of evoked potential tests are used in the diagnosis of MS. Each of these tests requires
that electrodes are attached to your scalp and connected to an electroencephalograph (EEG) to record
brainwaves in response to different stimuli. The different tests are:
o Brainstem Auditory Evoked Potentials (BAEP): A series of clicks are played in each ear through
headphones.
o Visual Evoked Potentials (VEP): A series of checkerboard patterns are displayed on a screen.
o Sensory Evoked Potentials (SEP): Mild electrical shocks are administered to an arm or leg.

The doctor is looking for both the size of the response and the speed in which the brain receives the
signal. Weaker or slow signals may indicate that demyelination has occurred and that MS is a
possibility. However, this test is also not specific to MS; abnormalities could indicate another problem.
A series of all three tests could take up to two hours to complete.

DRUGS:
The three major drugs previously approved for the treatment of MS affect the course of the disease. None
of these drugs is a cure, but they can slow disease progression in many patients.

Known as the ABC drugs, Avonex and Betaseron are forms of the immune system protein beta interferon,
while Copaxone is glatiramer acetate (formerly called copolymer-1). All three have been shown to reduce
the rate of relapses in the relapsing-remitting form of MS. Different measurements from tests of each
have demonstrated other benefits as well: Avonex may slow the progress of physical impairment,
Betaseron may reduce the severity of symptoms, and Copaxone may decrease disability. All three drugs
are administered by injection

Two major clinical studies were completed that focused on the question of whether disease-modifying
therapy known to slow the disease, can postpone the development of clinically definitive MS in high risk
patients. Data presented at the annual meeting of the American Academy of Neurology in May, 2000,
highlighted the different effects of interferon therapy when it was initiated at the earliest recognizable
stages of MS versus later. Previous studies with interferon beta-1b (Betaseron) and interferon beta-1a
(Avonex, Rebif) clearly demonstrated benefits in patients with relapsing forms of MS. Moreover,
previous treatment with High-dose corticosteroids also delays, but does not prevent the ultimate
development of MS. The encouraging message from the CHAMPS study in the United states and the
ETOMS study in Europe is that early intervention can reduce the probability of developing clinically
definitive MS.
Although the ABC drugs stop relapses and may keep patients in relatively good health for the short-term,
their long-term success has not been proven and they don't work well for patients who have reached a
steadily progressive stage of MS. In the meantime, new approaches to using current therapies are being
researched especially using combinations of different types of agents when one agent alone is not
effective. Clinical trials are now evaluating the safety and efficacy of combining cyclophosphamide
(Cytoxan) and methylprednisolone (Medrol) in patients who do not respond to the ABC drus, and of
adding mitoxantrone (Novantrone), prednisone (Prelone), azathioprine (Imuran), or methotrexate
(Rheumatrex) to betainterferon for further benefit.

In addition, Miloxzantrone HCI (novantrone), a drug approved for cancer treatment, has been approved
for treating patients with advanced or chronic multiple scelerosis. In clinical trials, mitoxantrone reduced
the number of relapse episodes and slowed down the disease. Reserved for progressive forms of MS, it is
given intravenously by a doctor to help maintain mobility and reduce the number of flare-ups. However,
there are serious side effects with the drug including heart problems, nausea, and hair thinning.

The Diet:

The Paleolithic diet is a dietary regime which some people believe to be effective in
treating multiple sclerosis. The diet was first popularised by film writer Roger MacDougall. MacDougall
was diagnosed with MS in 1953. His condition progressed steadily until he changed his diet to one which
is essentially the same as what is now called the Paleolithic diet.

Paleolithic diet:

 No foods that contains gluten. This means avoiding all cereals - wheat, barley, rye and oats - and
foodstuffs containing them such as:
o breakfast cereals
o pasta
o bread
o beer, whisky and many other alcoholic beverages
o cakes, biscuits and other foods containing flour
 No foods that contain dairy produce:
o liquid milk and cream
o butter
o cheese
 Low sugars, in particular, no refined sugar. MacDougall recommends using honey and fruit
sugars to sweeten food.
 Low animal fats. High unsaturated fats. This means avoiding beef, pork, lamb, goose and duck.
Wild and free-range meats are preferred to meats that come from modern agriculture.
 No foods to which you are allergic.
 Vitamin and mineral supplements to counter any deficiencies. MacDougall put together this list
for his own use:
o Vitamin Bl: 25 mg
o Vitamin B2: 15 mg
 o Vitamin B6: 75 mg
o Vitamin B12: 250 mcg
o Vitamin C: 300 mg
o Vitamin E: 200 iu
o Chlorine Bitartrate: 120 mg
o Calcium Gluconate: 900 mg
o Calcium-D-Pantothente: 150 mg
o Folic Acid: 200 mcg
o Lecithin from flax: 300 mg
o Magnesium Carbonate: 900 mg
o Nicotinamide: 500 mg
o Inositol: 120 mg

Nowadays, many people with MS would add a form of Vitamin D, called 1,25-dihydroxyvitamin
D3, to this list.

NURSING MANAGEMENT:
1. Provide emotional and psychological support for the patient and family.

2. Increase patient comfort with massages and relaxing baths.

3. Administer medications as needed.

4. Promote emotional stability. Help the patient establish a daily routine to maintain optimal functioning.

5. Keep bedpan or urinal readily accessible because the need to void is immediate.

6. Encourage adequate fluid intake and regular urination.

7. Watch for adverse reactions to administered medications.

8. Monitor bowel and bladder function during hospitalization.

9. Assess patient’s neurologic status for deficits.

10. Educate the patient nad her family about this chronic disease.

11. Emphasize the importance of exercise.

12. Teach the patient about bowel and bladder training if necessary.