The tardive portion of the disorder refers to a delayed reaction and the dyskinesia portion refers to abnormal movement. The delayed abnormal movements referenced are the jerky bodily movements which occur subsequent to the intake of certain medications.
Tardive dyskinesia (TD) is a collection of side effects which are brought on by the usage of antipsychotic medications which are used to treat schizophrenia, seizures, and several other types of mental health disorders. Most people who have to take these antipsychotic medications do not develop symptoms of TD, but those who do are sometimes permanently afflicted by it.
The condition is characterized by uncontrollable jerky movements of the face and body that are involuntary and inappropriate to the situation. It could be a blinking of the eyes, sticking out the tongue, and possibly even something more emphatic, like wildly waving the arms unintentionally.
TD occurs fairly often as a side effect of drugs which are used to treat seizures, for instance gabapentin, which achieves its usefulness by subduing the interaction between nerves in the brain. Any seizures which are brought on by the rapid-fire interactions between nerves would thus be prevented or delayed to a great extent – but an unfortunate side effect could also be the development of dyskinesia. While the reason for this is not understood, the dyskinesia side effects can develop weeks, months, and sometimes even years following the medication usage.
The jerkiness exhibited as dyskinesia is most commonly associated with the limbs, but in addition to legs and arms, it might also cause a victim to controllably smack their lips together, or to jerk their head repeatedly without even being aware of it. The rather severe nature of these reactions makes it essential that patients exhibiting these symptoms report them immediately to their physician, especially if they’re being treated with anti-seizure medications.
Although the disorder can occur in both genders, there is a statistical predominance among older women, for some unknown reason. The actual incidence of TD development among patients being treated for seizures or psychotic behavior hovers somewhere between 30% and 50%, so it is far from a sure thing that anti-psychotic medications will lead to tardive dyskinesia disorder.
There are some medical tests which can be administered to a patient with dyskinesia that help to determine the severity of symptoms, which may be useful over a longer period of time, for observation of any increase or decrease in symptom levels. The Abnormal Involuntary Muscle Scale (AIMS) examination is one such test which is often administered to patients who have prolonged usage of antipsychotic medications.
It is not intended to detect the presence of tardive dyskinesia, but merely to establish a scale of the symptoms for reference. As might be expected, the scale of symptoms ranges from none at all to very severe, and the examination measures involuntary muscle movement in the areas of arms, legs, trunks, and the face. It is currently one of the best methods of tracking the progression of tardive dyskinesia over time.
The symptoms of tardive dyskinesia are not life-threatening, but they can be extremely inconvenient and embarrassing, and for the most part, the victim of these involuntary jerky movements is unaware of them at the time they are being manifested. This can cause some tremendous difficulties in the workplace, or in any social circles other than the immediate family, who may understand the condition of the sufferer.
The areas of the body most commonly affected by tardive dyskinesia are the legs and the arms, but the potential exists for these kinds of involuntary movements to appear on virtually any part of the body.
People afflicted by TD have been observed blinking their eyes rapidly, chewing without being in the process of eating, smacking and puckering their lips, puffing out their cheeks, sticking their tongues out, persistently frowning without reason, and grunting without cause. Other unusual behaviors have been observed, such as the wiggling of fingers, the uncontrolled tapping of feet, flapping arms wildly about, thrusting out the pelvis, and swaying from side to side.
Depending on the types of movements exhibited by someone afflicted with TD, it can be extremely hard to work and stay active when in the throes of an episode. Episodes may be close together or may be spaced out substantially, and there’s no rhyme or reason to the severity or frequency of attacks. When an episode does occur however, the victim is almost never aware of it, and when movements have subsided after the attack, the victim is not generally aware that anything has happened.
Tardive dyskinesia is believed to be caused by the presence of low levels of a neurotransmitter known as dopamine, which occurs more frequently among patients who have been treated for at least three months with an anti-seizure medication. Another risk factor for developing TD is being a substance abuser or an alcoholic, especially since the treatment for those afflictions may call on using some of the medications that potentially trigger TD.
African-Americans and Asian-Americans are also at greater risk statistically than Caucasians, although the role that genetics plays in contracting TD has yet to be defined by science.
The specific medicines used to treat psychotic behavior and seizures fall into a category called neuroleptics, which are actually major tranquilizers used for their effectiveness in sedating troubled patients. Some medications which fall into this grouping are chlorpromazine, fluphenazine, haloperidol, perphenazine, prochlorperazine, thioridazine, and trifluoperazine.
These are all drugs which have been traditionally used in the treatment of psychotic behavior, although there are others which have also been used effectively. Some of the more recently developed antipsychotic medications show less tendency to trigger dyskinesia, but they are not without their own set of risks.
In addition to the antipsychotic and anti-seizure medications, there are other kinds of drugs used for other conditions which can also trigger TD, for instance metoclopramide, which is used to treat gastroparesis. Some anti-depressant drugs are also known to induce TD in patients, for example amitriptyline, fluoxetine, phenelzine, sertraline and trazodone. Some drugs such as levodopa, which is used to treat Parkinson’s disease, are also known to occasionally trigger TD. Phenobarbital and phenytoin are two other medications which can potentially produce the symptoms of dyskinesia in a patient being treated for some other medical condition.
The best treatment for tardive dyskinesia is to prevent it altogether, and that means paying close attention to any involuntary movements you experience after having taken antipsychotic or anti-seizure medications. The problem with this is that the disorder does not necessarily develop within a time frame that allows you to naturally associate it with the actual cause, which was the medication.
The only way to be sure about the detection of symptoms is to monitor yourself after having taken any kind of anti-seizure medications, and to consult with your doctor about it as well. If the kinds of involuntary movements associated with TD do appear relatively soon after taking an anti-seizure medication, you need to point this out to your doctor immediately. Most likely your doctor would then prescribe some other kind of effective medication which may not trigger the symptoms of your original prescription.
Some of the newest antipsychotics and anti-seizure medications do appear less likely to trigger tardive dyskinesia, but in any case the observance of involuntary jerky movements should not be allowed to go unchecked. If attention is not given to this condition very quickly, there’s a chance that the disorder can become permanent in the victim, and when that happens there is very little in the way of treatment that can help.
The Food and Drug Administration (FDA) does not approve any medicines whatsoever for the treatment of tardive dyskinesia, but there are a few which have demonstrated at least some capability to diminish the severity of bodily movements. These include amantadine, clonazepam, and tetrabenazine. In addition to these somewhat effective prescription drugs, some people put their faith in home remedies such as ginkgo biloba, melatonin, vitamin B6, and vitamin E, although the medical benefits of these supplements have not been proven.
As previously mentioned, there are no known methods of prevention for tardive dyskinesia once it has been contracted, so the only course of action which really has an impact on prevention is avoiding the causes of dyskinesia.
In terms of the population and the people at greatest risk of contracting the disorder, it is of course not possible to defer older age or of being female in gender. The one avenue of potential effectiveness in avoiding dyskinesia is in the area of the antipsychotic and anti-seizure medications which are known to be the primary triggers for the disorder.
In discussing the treatment options for dyskinesia, it was previously stated that there are a group of typical treatment medications (chlorpromazine, fluphenazine, haloperidol, perphenazine, etc.) and a group of atypical treatment medications (botulinum toxin valbenazine and tetrabenazine), which have been used with success in dealing with psychotic behavior and seizures.
It has been demonstrated rather clearly that the atypical group of medications does not have the same tendency or severity of symptoms in those cases where dyskinesia does result as a side effect of treatment. It has also been shown that those patients being treated with medications from the typical grouping of drugs show improvement in the severity of their symptoms after switching to an atypical drug. Medications from this atypical grouping have been tried with varying levels of success, including a complete resolution in a few cases, to the other end of the spectrum, where no effect at all was observed.
This does not constitute prevention of course, but in the absence of any truly effective preventive measures, it is at least a course of action potentially effective for those afflicted. In most cases, patients who are experiencing psychotic behavior or regular seizures cannot be taken off their medications altogether without the risk of the original psychotic behavior returning in full force. Therefore, avoidance of the antipsychotics is not generally an option, and that leaves switching to an atypical medication as the only feasible solution which does not degrade the patient’s general health.
In the area of attempting to lessen the severity of symptoms experienced with dyskinesia, it has been shown to be somewhat effective to experiment with the dosage of antipsychotic medication given to a particular patient. If a balance can be reached where the psychotic behavior is still being effectively managed, and the symptoms of dyskinesia are also reduced, it may be possible to lower the dosage of the antipsychotic medication in order to prevent the worst dyskinesia symptoms.