MULTIPLE SCLEROSIS

This is an autoimmune disease that results in demyelination of the white matter of the nervous system. Nerve impulses travel along the myelin coating on the outside of the nerve cells. With the disruption in the myelin on the outside of the nerve cells, the transmission of information from cell to cell within the nervous system is altered.

 

HOW IT HAPPENS?

The exact cause of MS is unknown. It may be caused by a slow acting viral infection, an autoimmune response of the nervous system, or an allergic response. Other possible causes include trauma, anoxia, toxins, nutritional deficiencies, vascular lesions, and anorexia nervosa, all of which may help destroy axons and the myelin sheath. In addition, emotional stress, overwork, fatigue, pregnancy, or an acute respiratory tract infection may precede the onset of this illness. Genetic factors may also play a part.

 

RISK FACTORS

  • AgeMS can occur at any age, but most commonly affects people between the ages of 15 and 60
  • SexWomen are about twice as likely as men are to develop MS
  • Family history –MS is also genetic in nature
  • Certain infectionsA variety of viruses have been linked to MS, including Epstein-Barr, the virus that causes infectious mononucleosis
  • RaceWhite people, particularly those of Northern European descent, are at highest risk of developing MS. People of Asian, African or Native American descent have the lowest risk
  • ClimateMS is far more common in countries with temperate climates, including Canada, the northern United States, New Zealand, southeastern Australia and Europe

 

WHAT TESTS TELL YOU?

 

Diagnosing MS may take years because of remissions. These tests help diagnose the disease

  • MRI is the most sensitive method of detecting lesions and is also used to evaluate disease progression. More than 90% of patients show lesions when this test is performed
  • CSF analysis reveals elevated immunoglobulin G levels but normal total protein levels. This elevation is significant only when serum gamma globulin levels are normal, and it reflects hyperactivity of the immune system due to chronic demyelination. The WBC count may be slightly increased
  • Evoked potential studies demonstrate slowed conduction of nerve impulses in 80% of patients
  • CT scan may disclose lesions within the brain’s white matter
  • Neuropsychological tests may help rule out other disorders
  • EEG shows abnormalities in one-third of patients

 

WHAT TO LOOK FOR?

 

 

  • UHTHOFF’S PHENOMENONis the worsening of neurologic symptoms in multiple sclerosis (MS) and other neurological, demyelinating conditions when the body gets overheated from hot weatherexercise, fever, or saunas and hot tubs. It is possibly due to the effect of increased temperature on nerve conduction.[1] With an increased body temperature, nerve impulses are either blocked or slowed down in a damaged nerve but once the body temperature is normalized, signs and symptoms may disappear or improve
  • LHERMITTE’S SIGNsometimes called the barber chair phenomenon, is an electrical sensation that runs down the back and into the limbs. In many patients, it is elicited by bending the head forward. It can also be evoked when a practitioner pounds on the posterior cervical spine while the neck is flexed; this is caused by involvement of the posterior columns.

 

Myelin plays a key role in speeding electrical impulses to the brain for interpretation. The myelin sheath is a lipoprotein complex formed of glial cells. It protects the neuron’s long nerve fiber (axon) much like the insulation on an electrical wire. Because of its high electrical resistance and weak ability to store an electrical charge, the myelin sheath permits conduction of nerve impulses from one node of Ranvier to the next.

 

Effects of injury

 

Myelin can be injured by hypoxemia, toxic chemicals, vascular insufficiency, or autoimmune responses. When this occurs, the myelin sheath becomes inflamed and the membrane layers break down into smaller components. These components become well circumscribed plaques filled with microglial elements, macroglia, and lymphocytes. This process is called demyelination

 

The damaged myelin sheath impairs normal conduction, causing partial loss or dispersion of the action potential and consequent neurologic dysfunction

THE MYELIN BREAKDOWN

TREATMENT

Treatment for multiple sclerosis (MS) aims to shorten exacerbations and, if possible, relieve neurologic deficits so the patient can resume a near-normal lifestyle.

 

DRUG OPTIONS

 

Because MS may have allergic and inflammatory causes, corticotropin, prednisone, or dexamethasone is used to reduce edema of the myelin sheath during exacerbations, relieving symptoms and hastening remissions. However, these drugs don’t prevent future exacerbations. Currently, the preferred treatment during an acute attack is a short course of methylprednisolone, with or without a short prednisone taper. Interferon beta-1a or interferon beta-1b may also be given to decrease the frequency of relapses. How these drugs achieve their effect isn’t clearly understood. Interferon beta-1b, a naturally occurring antiviral and immunoregulatory agent derived from human fibroblasts, is thought to attach to membrane receptors and cause cellular changes, including increased protein synthesis. Other useful drugs include chlordiazepoxide to mitigate mood swings, baclofen or dantrolene to relieve spasticity, and bethanechol or oxybutynin to relieve urine retention and minimize urinary frequency and urgency.

 

SUPPORTIVE MEASURES

During acute exacerbations, supportive measures include bed rest, massage, prevention of fatigue and pressure ulcers, bowel and bladder training, treatment of bladder infections with antibiotics, physical therapy, and counseling.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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