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Tremor hereditary essential

Essential tremor is a neurological disorder characterized by shaking of hands (and sometimes other parts of the body including the head), evoked by intentional movements. The incidence is unknown, but is estimated to be as common as one person in 20, and it is the most common type of tremor and also the most commonly observed movement disorder. more...

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The cause of the disease is unknown (idiopathic). While no identifiable and consistent structural abnormality has been demonstrated yet to exist in the nervous system of every person with ET, prominent researchers including Elan D. Louis are searching actively for neurochemical and brain structure abnormalities that might be commonplace among people with ET. Usually the diagnosis is established on clinical grounds, but when suspicion exists, other potential sources of tremor (excessive caffeine consumption, recreational drug use, hyperthyroidism) should be excluded. Tremor intensity can worsen in response to fatigue, strong emotions, hunger, cold, or other factors and can be reduced with alcohol in approximately 50 percent of patients. However, an over-reliance on alcohol to control tremor symptoms can sometimes lead to alcohol addiction.

There is ongoing controversy as to whether ET is related to Parkinson's disease and whether essential tremor should properly be considered a kind of parkinsonism. While some research findings appear to suggest that ET patients face a greater than average chance of developing Parkinson's, those findings might be a misleading effect of the widespread difficulty that doctors experience when they try to distinguish Parkinson's symptoms from ET symptoms and arrive at a definitive diagnosis.

Members of a family known as the "Iowa Kindred" develop either parkinsonism or symptoms that are indistinguishable from ET; their pattern of inheritance is associated with PARK4.


Essential tremor is often found in more than one member of a family (familial tremor), in which case it is usually dominant in inheritance, or it may occur with no family history. Tremors can start as any age, from birth through advanced ages (senile tremor). Any voluntary muscle in the body may be affected, though it's most commonly seen in the hands and arms and slightly less commonly in the neck (causing the patient's head to shake), eyelids, larynx, tongue, trunk, and legs. A resting tremor of the hands is sometimes present, despite the common misunderstanding that a resting tremor is proof of Parkinson's Disease. ET is usually painless, although in some cases tremor of the head or neck causes pain, and writing can become painful quickly for a person with hand tremors who grips a pen tightly in a struggle to maintain control over penmanship.

ET does sometimes occur in combination with other neurological disorders such as dystonia and benign fasciculation syndrome. However, there is no clear evidence that having ET predisposes a person to one of these diseases. Conflicting research results have so far made it difficult for medical researchers to say with certainty that people with ET are more likely than the general population to experience hearing loss and a reduction or complete loss of olfaction, among a wide assortment of other non-tremor symptoms, but credible researchers have published findings to support such claims of progressive hearing loss and progressive loss of olfaction. Other published research suggests that an impaired sense of balance prevents ET patients from walking normally. It is commonly assumed among researchers that tremors are not the only symptom of ET.


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Parkinson's disease - includes related articles - Cover Story
From Nutrition Health Review, 9/22/91

The Parkinson Profile

Parkinson's disease is a disorder of the central nervous system. Its principal symptoms are tremors, rigidity of limbs, and slowness of movement of torso, hands and legs. Maintaining equilibrium of balance is difficult and stressful.

Other characteristics are: loss of facial expression, difficulty in walking, changing positions in bed, dressing, bathing, talking and bending.

Symptoms of Parkinson's disease begin insidiously, becoming apparent on one side of the body and gradually worsening.

It is not a rare disease, but because it is not contagious and not reportable, no one knows how prevalent the problem has become. According to reputable estimates, more than two million people in the United States suffer from this neurological disease.

At least one misconception has gained belief among both the public and the medical profession, that Parkinson's disease is exclusively an ailment of the elderly. Symptoms may appear at any age, but are uncommon before age 30.

Although not considered hereditary, the disease occasionally appears within families, affecting siblings, parents, and grandparents.

The cause of the disease is not known, but many people succumbed after the epidemics of encephalitis that spread around the world between 1918 and 1925. A motion picture, Awakenings, based on Dr. Oliver Sacks' book, dramatized the epidemic effectively.

Parkinson's disease is the result of degenerative changes found in the central nuclei of the brain (basal ganglia) caused by a deficiency of a chemical substance known as dopamine.

Dopamine is formed in the nerve cells to facilitate transmissions of nerve impulses (messages) between these cells and other parts of the brain.

If dopamine is lacking, there is interference with the efficient passage of nerve messages which are essential to proper functioning of the neurological system. Fortunately, several medications have been developed that can modify some of the problems that Parkinson patients suffer.

Q: How prevalent is Parkinson's disease among the population in the United States?

A: It is estimated that more than 40% of the people suffering from the disease have not been identified. Either they don't know they are afflicted, or they do not seek treatment. Many who have been diagnosed as Parkinsonians do not have the disease.

A survey conducted by the pharmaceutical industry suggests that only 250,000 people in the United States are receiving medication specifically for Parkinson's disease, although more than a million, it is assumed, should be in treatment.

Q: Is there a particular test that can implicate the disease?

A: A specific test has not been developed. Usually diagnosis is based on neurological examination, which covers evaluation of symptoms which are most apparent, such as trembling of the blims when they are at rest, muscular stiffness, resistance to passive movement, and lack or slowness of body movement.

Q: Few diseases have remained medical mysteries for so long a period. Many conditions have changed during the past 175 years. What do we have in common with our ancestors that could be the cause?

A: The disorder was first described in England by James Parkinson, who called it "the shaking palsy." Tremor, however, is not always present, nor is there real paralysis.

Prior to Dr. Parkinson's identification of the disease, both literature and folklore referred to "possessed" individuals who may have been suffering from Parkinsonian symptoms. Also, because the average lifespan seldom extended beyond what we consider middle age, few lived long enough to be stricken.

If the "meat-eater's disease" belief has any validity, the cannibalism theory (see page 4) may provide some clues. Pollution, although prevalent in other forms in the past, has been implicated as a source of health problems. The use of aluminum, recreational drugs, tobacco and physical damage to the brain can add credence to the theory that Parkinson's disease now appears more frequently in younger people. Viruses and toxins have always plagued humanity.

Q: Does the Parkinson patient feel great pain from the ailment?

A: Pain is not usual in Parkinson's disease. When patients complain of pain, it may be from other sources, such as arthritis, strain and stress of exerting affected limbs, difficulty in chewing and swallowing, and general depression.

Q: The theory that implicates a slow virus infection to be the cause of Parkinson's disease was popular among scientists 20 years ago; does it have credence today?

A: That supposition is practically ignored at present. Attempts were made to test the theory by transmitting suspected viruses from a patient to test subjects; the project failed to prove the assumption.

Q: Is Parkinson's disease inherited or contagious?

A: No investigations have ever determined that the ailment is hereditary or can be passed on through contact.

Q: Is sexual activity always affected?

A: In most patients sexual ability is not affected, although the condition may hamper freedom of movement.

Since L-dopa (levedopa) medication has become widely publicized, there have been rumors about its heightening effects on sexual desire and potency. Because L-dopa has marvelous effects upon physical and mental powers for many patients, the exhilaration of well-being felt may help renew interest in sex.

Q: How successful has surgery proved to be in alleviating the problems of Parkinson's disease?

A: Mexican surgeons reported dramatic improvement in two patients who had cells surgically removed from their adrenal glands and transplanted to the brain. The same type of procedure was performed later in the United States upon 19 patients with only modest improvement.

In several patients, complications developed after surgery. Two suffered strokes and another lapsed into coma. The surgeons concluded that surgery is not ready for general use. (C.G. Goetz, et al., New England Journal of Medicine 320:337, Feb. 1989.)

Q: Medications for the treatment of Parkinson's disease have been around for more than a century. How different are the new ones?

A: In the latter part of the 19th century, belladonna alkaloids were introduced for the treatment of Parkinson's disease. Since then, other derivatives have been tried, but at their best no more than 20% improvement was achieved.

The discovery of dopamine deficiency in the brains of patients with Parkinson's disease led to the development of levedopa (L-dopa), a substance than can increase the levels of dopamine in the brain. Levodopa proved to be the most dramatic breakthrough in the history of Parkinson's disease therapy.

Q: Since high doses of mercury can cause neurological disease, is it likely that mercury amalgam fillings may be the cause of Parkinson's disease?

A: Mercury amalgam used in dental fillings is not a bio-available organic mercurial and is unlikely to result in neurological symptoms, says Juan R. Sanchez-Ramos, M.D., a professor of neurology at Miami School of Medicine.

Q: Since loss of mobility is part of the Parkinsonian problem, and pneumonia and urinary tract infections are linked to threatening immobility, what preventive measures can be taken?

A: Because these are probable complications, most specialists monitor the patient's need for some form of exercise. A nutrition-oriented physician would probably prescribe supplementation of vitamin E for respiratory health and vitamin C to keep the pH levels of the urine on the acid side. Vitamin C has been used successfully in the treatment of urinary infections.

Q: Observers of patients suffering from Parkinson's diseases have noted that symptoms rise and fall: walking is more difficult at times, tremors increase, fatigue is greater, grimacing increases. Is there an answer to such inconsistency?

A: The severity of symptoms may parallel the individual's emotions, becoming more pronounced during times of anxiety, tension and unhappiness. Symptoms are less evident when the individual is relaxed and relatively contented.

Q: How significant has electroconvulsive shock therapy been in treating Parkinson's disease?

A: Electroshock therapy is principally used to treat Parkinson patients who have severe depression. One report noted that of seven patients who were given seven electroshock treatments, four showed improvement (for about six months), as reported in the American Journal of Psychiatry (November 1989). A serious side effect of electroconvulsive shock therapy is permanent partial loss of memory.

Q: One compelling theory implicates neurotoxins in the premature death of brain cells. Can an oversupply of glutamate, usually a normal chemical produced in the brain, prove to be dangerous in the form of monosodium glutamate, a flavor enhancer widely used in prepared foods?

A: The theory of neurotoxins is sound. Recent studies have shown that two "normal" chemicals, aspartate and glutamate, when present in abnormal quantities, can contribute to damaged brain cells and can cause the complex symptoms of Parkinson's disease.

No conclusive evidence, however, has been gathered to prove that MSG, often added to processed foods, is responsible for neurotoxic damage, although several researchers are earnestly pursuing that theory.

Q: Many patients using L-dopa show high levels of uric acid in their blood. Should such individuals avoid a high purine diet?

A: L-dopa causes a false and misleading elevation of uric acid by a computerized laboratory evaluation. Other methods for evaluation are more reliable. The physician should specify testing by the uricase technique.

Q: Are victims of Parkinsonism also subject to mental confusion and dementia?

A: Although many patients suffer from dementia, it is not necessarily part of the disease. It has been estimated that only 15% to 20% of Parkinson patients have dementia. It is important not to confuse the slow responses of patients with true dementia. Many anti-Parkinsonian medications increase confusion and cause hallucinations or even outright psychosis in patients.

Q: Long-term usage of levodopa has been reported to be less than fully effective, with complications sometimes occurring. Are there other drugs that have some promise?

A: The latest development in drug thereapy involves the combined use of levodopa and carbidopa. The combination is marketed under the trade name of Sinemet.

Carbidopa prevents levodopa from being metabolized in the gut, liver and other tissues so that blood levels of levodopa remain high, permitting more of it to reach the brain.

Consequently, the combined medication's value is important because less levodopa is required to be taken and particular side effects of levodopa therapy are avoided. Nausea and vomiting are reduced.

Other drugs, such as Parlodel (bromocriptine), Permax (pergolide) and Eldepryl (deprenyl), have been reported to be effective in people with advanced cases of Parkinson's disease.

Q: Besides the usual antidepressant drugs prescribed for alleviation of psychiatric problems that Parkinson's disease patients endure, are there specific agents that show promise?

A: Exciting advances are being made in determining the part that serotonin, a natural brain chemical, plays in depression associated with the disease. Parkinson patients have low levels of serotonin; experimental therapy is being conducted to replace the amount of serotonin lost in an effort to restore that chemical's balance in the brain.

Q: Can vitamin-mineral supplements treat or prevent Parkinson's disease?

A: The entire range of vitamins and minerals is necessary for the functional integrity of the brain and nervous system.

Especially important are the B vitamins (thiamine, niacin, pyridoxine, folic acid, vitamin B12, and biotin). The inclusion of vitamins A, C, and E is essential because of the antioxidant functions that these vitamins provide.

Minerals such as zinc, calcium, magnesium, and potassium are necessary to preserve the integrity of muscles and bone mass. Large doses of vitamins D and A are to be avoided, although substituting beta carotene for vitamin A can avoid toxic overload of that vitamin.

The use of octacosanol has been investigated by Lazarus A. Orkin, M.D., of the National Parkinson Foundation (Miami, Florida). His observations indicate that the vitamin seems to have alleviated the need for large doses of L-dopa when taken together. Dr. Orkin quotes the work of Dr. Hemut Prahl, the Executive Director of the Dynatron Research Foundation in Madison, Wisconsin. Dr. Prahl believes the vitamin has beneficial effects upon membranes of neurons. (From the Parkinson Report, 2nd Quarter 1991.)

Q: Which drugs can contribute to these side effects?

A: Tranquilizers, some antihypertensive drugs (medications for reducing high blood pressure), such as reserpine, a-methyldopa, or some calcium-channel blockers, gastrointestinal drugs (which oppose dopamine production), toxins such as carbon monoxide, methanol exposure, and cyanide gas inhaled. Other medications that can cause pseudo-Parkinsonism are: Prolixin, Permitil, Trilaphon, Navane, and Haldol.

COPYRIGHT 1991 Vegetus Publications
COPYRIGHT 2004 Gale Group

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