Diseases Treatment

What do doctors call this condition?

Huntington’s chorea, hereditary chorea, chronic progressive chorea, adult chorea
What is this condition?

Huntington’s disease is a hereditary disease in which degeneration of the cerebral cortex and basal ganglia cause chronic progressive chorea (involuntary movements) and mental deterioration, ending in dementia. Huntington’s disease usually strikes persons between ages 25 and 55 (the average age is 35); however, 2% of cases occur in children, and 5% as late as age 60. Death usually results 10 to 15 years after onset, from suicide, congestive heart failure, or pneumonia.
What causes it?

The cause of Huntington’s disease is unknown. Because this disease is transmitted as a genetic trait common to men and women, either sex can transmit and inherit it. Each child of a parent with this disease has a 50% chance of inheriting it; however, the child who doesn’t inherit it can’t pass it on to his or her own children.
What are its symptoms?

Onset is insidious. The person eventually becomes totally dependent, emotionally and physically, through loss of musculoskeletal control. Gradually, the individual develops progressively severe choreic movements. Such movements are rapid, often violent, and purposeless. Initially, they appear on one side and are more prominent in the face and arms than in the legs. They progress from mild fidgeting to grimacing; tongue smacking; indistinct speech; slow, writhing movements (especially of the hands) related to emotional state; and contracted neck muscles.

Ultimately, the person with Huntington’s disease develops dementia, although the dementia doesn’t always progress at the same rate as the chorea. Dementia can be mild at first but eventually severely disrupts the personality. Such personality changes include obstinacy, carelessness, untidiness, moodiness, apathy, inappropriate behavior, loss of memory and concentration, and sometimes paranoia.
How is it diagnosed?

Huntington’s disease can be detected by positron emission tomography and DNA analysis. Diagnosis is based on a characteristic clinical history: progressive chorea and dementia, onset in early middle age (35 to 40), and confirmation of a genetic link. Computed tomography scan (commonly called a CAT scan) and magnetic resonance imaging (commonly called an MRI) demonstrate brain atrophy. Molecular genetics may detect the gene for Huntington’s disease in people at risk while they’re still symptom-free.
How is it treated?

Because a cure for Huntington’s disease has not yet been found, treatment is supportive, protective, and symptomatic. Tranquilizers, as well as anti psychotics such as Thorazine, Haldol, and Tofranil, help control choreic movements. They also relieve discomfort and depression, making the person easier to manage. However, tranquilizers increase rigidity and can’t stop mental deterioration. Institutionalization is often necessary because of mental deterioration.

Osteoporosis is a chronic disease in which the mineral content of the bones progressively decreases so that the bones become brittle and are easily broken. It is linked to more than 1 million fractures of the hip, spine, and other bones each year. Vertebral bones in the spine shrink and fracture, causing a deformed spine. Bones in the wrist are also common fracture’ sites. Some 25 million Americans are affected by osteoporosis, 80% of whom are postmenopausal women. Although postmenopausal white and Asian women are at highest risk, men and women of all ages and ethnicities can be affected.

Though bones may seem hard, they are made of living cells that require calcium and vitamin D (necessary for optimum absorption of calcium) to grow and stay strong. Almost all of the body’s calcium stores are located in bone. During growth and development, bones typically receive more calcium than they give up. By age 25, when bone density peaks, calcium absorption levels off; at age 30, the bone-building process is over. This is when bone mass maintenance and calcium are especially important. If blood levels of calcium drop, the body withdraws what it needs from its bones. With adequate dietary intake of calcium, bones are spared the effects of calcium depletion that may accelerate osteoporosis.

Calcium is not the only factor associated with bone loss. Estrogen depletion during menopause triggers bone loss up to 1 % a year. By the time a woman is 80, she may have lost 30% to 40% of her bone mass. When bone-mass loss becomes excessive, it may not take even a fall to fracture bones. Simply bending over and lifting 25 pounds-a heavy bag of groceries-could cause injury. During menopause, hormone-replacement therapy in the form of estrogen supplementation is recommended for many women as protection against osteoporosis.

Because nicotine is thought to decrease blood levels of estrogen, smoking also contributes to bone loss. Smokers go through menopause on average at least 2 years earlier than nonsmokers. Genetics may also play a role in osteoporosis. Researchers have identified an osteoporosis gene that determines how well vitamin D facilitates the absorption of calcium. People who have the gene are more resistant to absorbing available calcium. Caffeine and alcohol have also been implicated in bone loss. A recent study found that women who drank two or more cups of caffeinated coffee a day and drank no milk experienced significant loss of bone density after menopause. The effects of caffeine can be negated with consumption of milk. In the same study, coffee drinkers who drank at least one glass of milk per day had 6.5% higher bone density than the coffee only group.
Osteoporosis Treatment

The National Osteoporosis Foundation recommends several simple steps to reduce the risk of contracting this disease. First, consume adequate amounts of calcium, preferably from food. If this doesn’t work, calcium supplements are recommended. The Foundation suggests 1500 mg, which is almost double the amount given in the RDA. 25 Second, consume enough vitamin D (400 IU) to permit absorption of the calcium. Third, consider hormone-replacement therapy (estrogen) and discuss its use with your medical doctor, especially if there is a family history of osteoporosis. And fourth, participate in weight-bearing activities, such as walking, running, and weight training, to prevent bone loss. In one study, women who participated in a year-long exercise program and received daily doses of estrogen experienced a 7% increase in bone density and fared better than women on estrogen alone. Physical exercise forces bones to adapt to the stresses imposed on them, and they hypertrophy in response. Bones atrophy when they are unstressed.

People with osteoporosis can and should exercise, but the type of physical activity and the intensity of exercise must be carefully selected. Forceful contractions of muscles and high-impact activities should be avoided because they may stress the bones beyond their breaking point. Swimming, water aerobics, stationary cycling, walking, and light weight training are good starting activities for those with osteoporosis.

What do doctors call this condition?

Parkinsonism, paralysis agitans, shaking palsy
What is this condition?

Named for James Parkinson, the English doctor who wrote the first accurate description of the disease in 1817, Parkinson’s disease is a slowly progressive movement disorder that characteristically produces muscle rigidity, loss or absence of voluntary motion (akinesia), and involuntary tremors.

One of the most common crippling diseases in the United States, Parkinson’s disease affects men more often than women, and strikes 1 in every 100 people over age 60. Because of increased longevity, this amounts to roughly 60,000 new cases diagnosed annually in the United States alone.
What causes it?

Although the cause of Parkinson’s disease in unknown, studies of the brain have established that a deficiency of a neurotransmitter, dopamine, prevents brain cells from performing their normal function within the central nervous system.
Parkinsons Disease symptoms?

The cardinal symptoms of Parkinson’s disease are muscle rigidity and akinesia and an insidious tremor that begins in the fingers (unilateral “pill-roll” tremor), increases during stress or anxiety, and decreases with purposeful movement and sleep. Muscle rigidity results in resistance to passive muscle stretching, which may be uniform or jerky.

Akinesia causes the person with Parkinson’s disease to walk with difficulty, either bent backward or falling forward.

Akinesia also produces a high-pitched, monotone voice; drooling; a masklike facial expression; loss of posture control; and difficulty swallowing or speaking (or both). Occasionally, the person’s eyes are fixed upward, with involuntary tonic movements, or the eyelids are completely closed. Parkinson’s disease itself doesn’t impair the intellect, but a coexisting disorder, such as arteriosclerosis, may do so.
How is it diagnosed?

Lab tests are not usually helpful in identifYing Parkinson’s disease, so the diagnosis is based on the person’s age and history, and the characteristic clinical picture of the disease. However, a urinalysis may support the diagnosis by revealing decreased dopamine levels. A conclusive diagnosis is possible only after ruling out involutional depression, cerebral arteriosclerosis, other causes of tremor and, in people under age 30, intracranial tumors, Wilson’s disease, or toxicity from phenothiazine or other drugs.
How is it treated?

Because there’s no cure for Parkinson’s disease, the primary aim of treatment is to relieve symptoms and keep the person functional as long as possible. Treatment consists of drugs, physical therapy and, in severe cases unresponsive to drugs, neurosurgery.

Drug therapy usually includes Larodopa, a dopamine replacement that’s most effective during early stages of the disease. It’s given in increasing doses until symptoms are relieved or side effects appear. Because side effects can be serious, a combination drug­Sinemet-is frequently given. When Larodopa proves unsuitable, alternative drug therapy includes anticholinergics, such as Artane; antihistamines, such as Benadryl; and Symmetrel, an antiviral agent. Eldepryl, an enzyme-inhibiting agent, allows conservation of dopamine and enhances the therapeutic effect of Larodopa.

When drug therapy fails, stereotactic neurosurgery may be an alternative. In this procedure, electrical coagulation, freezing, radioactivity, or ultrasound is used to inactivate a small, specific portion of the brain to prevent involuntary movement. This is most effective in young, otherwise healthy people with unilateral tremor or muscle rigidity. However, neurosurgery can only relieve symptoms.

Individually planned physical therapy complements drug treatment and neurosurgery to maintain normal muscle tone and function
What can a person with Parkinson’s disease do?

• If you have difficulty eating, eat frequent small meals to increase your caloric intake.

• To help establish a regular bowel elimination routine, drink plenty of fluids and eat high-fiber foods.

• If you have trouble moving from a standing to a sitting position, consider installing an elevated toilet seat.

• If you have excessive tremors, you may achieve partial control of your body by sitting on a chair and using its arms to steady yourself.

• Remember that fatigue may cause you to depend more on others.

• As instructed by your doctor, use proper positioning to help prevent bed sores and contractures .

• If you’re taking Larodopa, follow your doctor’s instructions on which foods to avoid (such as multivitamin preparations and fortified cereals) .

• Take household safety measures to prevent accidents.

• For more information, contact the National Parkinson Foundation or the United Parkinson Foundation.

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What do doctors call this condition?

Multiple neuritis, peripheral neuritis, peripheral neuropathy, polyneuritis

What is this condition?

This disorder involves degeneration of peripheral nerves supplying the distal muscles of the extremities. It results in muscle weakness with sensory loss and atrophy as well as decreased or absent deep tendon reflexes. Although peripheral nerve degeneration can occur at any age, incidence is highest in men between ages 30 and 50. Because onset is usually subtle, a person may compensate by overusing unaffected muscles; however, the disease may begin rapidly with severe infection and chronic alcohol intoxication. If the cause can be identified and eliminated, the prognosis is good.

What causes it?

Causes of peripheral nerve degeneration include:

• chronic intoxication (with ethyl alcohol, arsenic, lead, carbon disulfide, benzene, phosphorus, and sulfonamides)

• infectious diseases (meningitis, diphtheria, syphilis, tuberculosis, pneumonia, and mumps)

• metabolic and inflammatory disorders (gout, diabetes, rheumatoid arthritis, polyarteritis nodosa, and lupus)

• nutritional disorders (beriberi and other vitamin deficiencies, and malnourishment) .

What are its symptoms?

The signs and symptoms of peripheral nerve degeneration develop slowly, and the disease usually affects the motor and sensory nerve fibers. The condition typically produces flaccid paralysis, wasting, loss of reflexes, pain of varying intensity, loss of ability to perceive vibratory sensations, and numbness, tingling, increased sensitivity to pain or touch, or anesthesia in the hands and feet. Deep-tendon reflexes are diminished or absent, and atrophied muscles are tender or hypersensitive to pressure or palpation. Footdrop may also be present. Skin manifestations include glossy red skin and decreased sweating. Many people with the disease have a history of clumsiness and complain of frequent vague sensations.

How is it diagnosed?

The person’s history and physical exam reveal characteristic distribution of motor and sensory deficits. Electromyography may show a delayed action potential if peripheral nerve degeneration impairs motor nerve function.

How is it treated?

Effective treatment consists of supportive measures to relieve pain, adequate bed rest, and physical therapy, as needed. Most important, however, the underlying cause must be identified and corrected. For instance, it’s essential to identify and remove the toxic agent, correct nutritional and vitamin deficiencies (the person needs a high-calorie diet rich in vitamins, especially the B-complex group), or counsel the person to avoid alcohol.
What can a person with peripheral nerve degeneration do?

• Rest frequently and avoid using the affected arm or leg. To avoid bed sores, use a foot cradle. To prevent contractures, use splints, boards, braces, or other orthopedic appliances

• After the pain subsides, passive range-of-motion exercises or massage may be beneficial. The doctor may recommend electrotherapy for nerve and muscle stimulation.

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What is this Condition?

Gout is a metabolic disease marked by localized deposits of uric acid salts that are normally excreted through the kidneys. The deposits cause painfully arthritic joints. Gout usually strikes the feet and legs of men over age 30 and women past menopause. In elderly people, it is linked to other diseases.

Though gout may disappear for years between attacks, it can lead to disability or crippling. Fortunately, most people get better with treatment.

What Causes Gout?

Although the exact cause is unknown, gout seems linked to a genetic defect in metabolism, which causes overproduction and retention of uric acid. Too much uric acid leads to urate deposits in the joints or tissues, causing local damage. Secondary gout, linked to other conditions (such as obesity, diabetes, high blood pressure, sickle cell anemia, and kidney disease) or to drug therapy, produces similar harmful substances.

Another condition, called pseudogout, or chondrocalcinosis, causes arthritic pain too, but for different reasons.

What are its Symptoms?

Gout develops in four stages (asymptomatic, acute, intercritical, and chronic) that produce the following findings:

• In asymptomatic gout, urate levels rise in the blood but produce no symptoms. Later, gout may cause high blood pressure or show up in severe back pain.

• The first acute attack strikes suddenly and peaks quickly, causing extreme pain in one or only a few joints. Affected joints feel hot, tender, inflamed, and look dusky red or bruised. The joint of the big toe usually becomes inflamed first, then the instep, ankle, heel, knee, or wrist joints. Some attacks pass quickly and then come back at irregular intervals. Severe attacks may last for days or weeks.

• Intercritical periods are the symptom-free intervals between gout attacks. Most people have a second attack within 6 months to 2 years, but others are symptom-free for 5 to 10 years. Those delayed attacks can strike untreated people with longer-lasting, severe pain in several joints, sometimes all at once and sometimes in one joint after another.

• Eventually, chronic gaur sets in. This final, continuous stage shows up in persistently painful joints, with large urate deposits in the cartilage, membranes between the bones, tendons, and soft tissue. Deposits form primarily in arms and legs and, rarely, in organs, such as the kidneys and heart lining.

The skin over the deposits may develop sores and release a chalky, white material or pus. Chronic inflammation and urate deposition progress to further restrict movement and harm the person’s general health, possibly including formation of kidney stones.

How is it diagnosed?

The doctor can find evidence of gout in fluid taken from an inflamed joint or a deposit and by checking the level of uric acid in the blood. In chronic gout, X-rays show damage to the cartilage and bones.

How is it Treated?

The doctor first tries to stop the pain and prevent complications by suggesting bed rest and protection for the painful joints. Hot or cold packs and pain relievers may help with mild attacks. For more severe attacks and chronic gour, treatment may include the following:

• drugs to reduce inflammation, including Colsalide, Butazolidin, and Indocin, and injections of corticosteroids or corticotropin

• slower-acting drugs to reduce the uric acid level in the blood, including Zyloprim, Colsalide, Benemid, and Anturane

• diet changes, primarily to avoid alcohol and some rich foods; obese people should try to lose weight because the extra weight puts more stress on painful joints.

• surgery to improve joint function or correct deformities. Deposits must be opened and drained if they become infected or ulcerated. Deposits can also be cut out to prevent ulceration, improve the joint’s appearance, or make it easier to wear shoes or gloves.