The long term utilization of certain anti-psychotic medications and drugs can induce a condition known as tardive dyskinesia (TD). The disorder is characterized by the presence of abnormal, repetitive and uncontrollable movements that develop slowly over a period of time in the affected individual-this condition can arise out of long term utilization of drugs that are used for the treatment of conditions like schizophrenia and many other related psychiatric disorders by a person. The condition is known by the term "tardive"-translated into "late"; this is appropriate because the disorder is a late onset secondary problem that can only occur in an individual following the long-term use of many drugs used in the treatment of extreme psychological conditions. Some of these drugs include chlorpromazine - Thorazine, the drug thioridazine - also marketed as Mellaril, and the drug trifluoperazine - known as Stelazine. The second name of the condition "Dyskinesia" can be translated into meaning" abnormal movement" or abnormal motions-since such problems characterize the condition.
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An affected individual's quality of life and normal behaviour is severely affected by the symptomatic and uncontrollable movements that are typical during TD. The problem with tardive dyskinesia is that the disorder is often of a permanent nature and persist long after the use of the drug has been discontinued by the person, however; this need not be true in all patients and in some cases the symptoms may gradually diminish in intensity after the person stops taking the medication. The prevention of this condition is crucial since many of the conventional treatments available for tardive dyskinesia often give very unsatisfactory results. For this reason and to avoid the development of the disorder, all patients who are required to undergo psychotic drug treatment must be made to discontinue the use of such drugs as soon as the dosage period is over, and it is equally important that all people requiring antipsychotic drugs be given the lowest effective dose possible during prescription.
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Any of the muscle groups in the body can be affected, however the more typical symptoms of TD can include repetitive and involuntary movements-called tics, which can most often occur on the facial muscles and the tongue, and are evident in displays such as lip smacking carried out involuntarily by the patient. Unconscious actions such as moving the legs back and forth are also often apparent. Eating and walking may be disturbed and all the symptoms may be mild or severe in manifesting themselves; thus determining the severity of the condition.
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The severity of tardive dyskinesia has been found to be reducible in a number of studies by supplements of the vitamin E in all types of patients with sever or milder manifestations of the disorder. The use of the vitamin E and a placebo was conducted during a double-blind trial on two groups of people with tardive dyskinesia, each of these groups were randomly assigned supplements of the vitamin E - at dosage levels of 800 IU per day for two weeks and followed later by 1,600 IU per day or they were assigned the placebo, since it was a controlled trial the assignments were random with periodic checks. It was found that involuntary movements in the affected individuals were much more readily and significantly lowered by the vitamin E when compared to the action of the placebo. While all large dosages of the vitamin E must be made under supervision from a medical professional, a recent uncontrolled study of 20 TD affected people suggested that the dosage level of 1,600 IU for the vitamin E every day could be the optimal amount as far a supplements of this vitamin are concerned. The ability of supplements of vitamin E in reducing the severity of tardive dyskinesia has also been reported by other studies on different groups of patients. However, the beneficial effects of the vitamin were not observed and reported in two studies carried out in a controlled setting on patients afflicted with TD. This may not necessarily disprove the efficacy of the vitamin E in the treatment of TD as the majority of the individuals who took part in these two studies were already receiving neuroleptics for a period of at least ten years, this is relevant because the effectiveness of vitamin E supplements has been shown in other research to be the greatest when it is initiated within the first five years from the date on which treatments using neuroleptics is begun.
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Treatments for tardive dyskinesia have also included supplements of choline and lecithin. This is however contested as conflicting results have been found for the use of these compounds in the treatment of TD-several studies have shown that a beneficial effect exist from supplementation using these compounds, while several other researches have reported variable improvement or non-existent effects on the status of test subjects. This was tested during the course of a small double blind trial lasting for two-weeks, here the test subjects with TD were administered 25 grams of lecithin two times each day, and a controlled group was prescribed a matching placebo at the same time and for a similar duration. The test subjects who were given lecithin all expressed significant improvement in the nature of the symptoms associated with TD.
A natural precursor compound for choline is a substance known as dimethylaminoethanol-DMAE in short. The treatment of the symptoms due to TD using DMAE is reported by some studies to be about as effective as a placebo, however, this is disputed by other sources gleaned form preliminary data, and these suggest that DMAE could decrease TD symptoms, and lead to an effective remedy of the condition.
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Another interesting aspect is that fully developed tardive dyskinesia can possibly be reversed by supplements of the mineral manganese at 60 mg dosages as suggested by one doctor; this doctor also claims that administering the trace mineral manganese at dosage regimes of 15 mg per day can effectively prevent the development of TD in an individual. The use and effectiveness of manganese supplements with regard to this treatment methodology has also been reported by many other researchers who have conducted trials of other groups of patients.
The use of the oil of the evening primrose (EPO) in the effective treatment of tardive dyskinesia has also been reported by many other researchers. Only minor and clinically insignificant results were however observed during the course of a double-blind study, here supplementation was carried out using EPO - at dosage rates of 12 capsules given every day - the results obtained were insignificant.
The inability of the body to metabolize the amino acid phenylalanine has been linked to TD during one preliminary research-this needs confirmatory studies. The reduction of excess phenylalanine in such individuals can possibly be achieved though the use of supplemental forms of the many other branched-chain amino acids - or BCAA, these can include amino acids such as valine and isoleucine, and also leucine, these can supplant accumulated levels of phenylalanine and aid in the treatment process of the tardive dyskinesia affected individual. The effects of BCAA supplements was observed and studied during the course of one trial, here the researchers studied the effects of these supplements in people with tardive dyskinesia - the dosage regimens were fixed at about 150 mg per 2.2 pounds body weight per test subject, and this was variably increased even up to 209 mg per 2.2 pounds body weight. The supplements were usually taken in the period immediately following breakfast and in one hour before lunch time and one hour before dinner; the supplemental period was two weeks in total. The supplemental form of the BCAA combination had an effective mixture of equal parts of valine and isoleucine but included about 33% more of leucine. The results were positive at least six people experienced about a 58% reduction in the symptoms, the total test subjects were nine in number; all of them in addition had at least a 38% decrease in the frequency of symptoms.
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