Cigarette Smokers - Tardive Dyskinesia Risk Factors

Since 1964, it has been established that the movement disorder identified as tardive dyskinesia is the result of side effects of psychoactive drugs developed for the treatment of schizophrenia and other mental illnesses. The use of such medications in the United States dates from 1954, when the predecessor of modern pharmaceutical corporate giant GlaxoSmithKline obtained the rights to a drug developed in Europe, called chloropromazine, which it marketed at home as Thorazine.

These drugs are known as anti-psychotics or neuroleptics. These operate by suppressing the body's dopamine receptors, interfering with electrochemical signals between the brain and various cells in the body. Theoretically, these drugs target a specific type of dopamine receptor that controls emotional response and lower cognitive functions related to particular behaviors. However, they appear to be less selective than researchers had hoped; these drugs affect dopamine receptors involved in voluntary muscle control as well, causing the tics and spasms associated with tardive dyskinesia.

Drugs developed between the early 1950s and the 1970s are classified as "typical" medications and are usually (A) less expensive and (B) more likely to result in the symptoms of tardive dyskinesia.

"Atypical" drugs are those of the "second generation" of psychoactive drugs developed after 1970. These are also known to cause symptoms of tardive dyskinesia, however the onset is usually later.

Tardive Dyskinesia and Substance Abuse

Patients treated with neuroleptic medication run a three-in-ten chance of developing symptoms of tardive dyskinesia, which can linger long after the medication responsible has been discontinued; in many cases, the damage is permanent. Research has identified a number of characteristics however that are common to most of the 30 percent of patients who do develop symptoms. One such characteristic is substance abuse, particularly alcohol and tobacco.

Tobacco and Dopamine Receptors

Some of the most recent research on the connection between cigarette smoking and tardive dyskinesia has been conducted by Dr. John Brasic at the Johns Hopkins School of Medicine. He has determined that nicotine - the psychoactive chemical in tobacco - magnifies the affects of neuroleptic medications, causing these dopamine inhibitors to be metabolized at a higher rate and in larger amounts - essentially, causing a overdose.

Interestingly, other studies have indicated that people suffering from schizophrenia (for which neuroleptic drugs are prescribed) smoke cigarettes at a rate that is as much as 300 percent that of the general public. In addition, these patients tend to smoke more heavily. In a study carried out in Scotland in the late 1990s, researchers suggested that smoking is a subconscious attempt by schizophrenics to self-medicate, as nicotine also increases the release of dopamine. Significantly, this study also found that when a patient started smoking at an early age, there was a correspondingly early onset of schizophrenia, particularly among female patients.

One of the conclusions of the Scottish study was that cigarette smoking interfered with the action of neuroleptic drugs. The end result is that greater dosages of the drugs were required in order to achieve the same benefits. It is known that symptoms of tardive dyskinesia are more likely among patients that have taken larger amounts of a given antipsychotic drug for a longer period of time.

This study has been confirmed by others. A Pakistani research paper published in 2005 noted that "some studies have found that smokers experience more tardive dyskinesia than nonsmokers."

Understanding the mechanisms of dopamine inhibitors and how these interact with nicotine, it is not surprising that the use of tobacco should be related to tardive dyskinesia in certain patients.

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