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 riskyoung people in lowrisk 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:
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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:
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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:

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

Charcots Triad y y y 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:
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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 o o Functioning of the cranial nerves (these control the senses, as well as how you talk and swallow) Coordination Strength

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Reflexes 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. y 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:
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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

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Vitamin B6: 75 mg Vitamin B12: 250 mcg Vitamin C: 300 mg Vitamin E: 200 iu Chlorine Bitartrate: 120 mg Calcium Gluconate: 900 mg Calcium-D-Pantothente: 150 mg Folic Acid: 200 mcg Lecithin from flax: 300 mg Magnesium Carbonate: 900 mg Nicotinamide: 500 mg 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 patients 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.