Tardive dyskinesia (TD) and Parkinson’s disease are both movement disorders, and both have causes related to the neurotransmitter chemical called dopamine. Dopamine takes signals from the brain to certain parts of the body, regulating their function. Both diseases can be the result of medication side effects. Though Parkinson’s disease may be congenital (not caused by drugs), only in extremely rare cases is tardive dyskinesia congenital. Tardive dyskinesia is usually caused by certain drugs.
In the human brain, dopamine works on five types of dopamine receptors. It is produced in several parts of the brain. Though dopamine is available as an intravenous medication, it only acts on the sympathetic nervous system when given as a drug, producing a higher heart rate and increased blood pressure. Dopamine given as a drug, however, cannot cross the blood-brain barrier, and so cannot affect the central nervous system.
Inside the brain, dopamine is associated with the brain’s “reward” system, causing a feeling of enjoyment and increasing motivation. It is released by rewarding experiences like sexual activity, food, drugs, and even normally neutral stimuli that become associated with activation of the brain’s reward system. Drugs like cocaine, amphetamines, and nicotine directly or indirectly cause an increase of dopamine levels in one of the brain’s reward pathways, and this may help explain the addictive nature of these drugs.
Though TD may “look like” Parkinson’s disease, the two conditions are different. While people with TD have great difficulty being still, those with Parkinson’s disease actually lose some ability to move, and experience symptoms like muscular stiffness along with their tremors and shaking. Parkinson’s also causes secondary symptoms like impaired speech and difficulty swallowing.
Tardive dyskinesia symptoms include facial “tics” like repeated grimacing or eye blinking, as well as arm movements, finger fluttering, restless legs, and toe tapping. Sometimes the torso and hips can be involved in TD symptoms too. The movements associated with TD tend to be more fluid and less “jerky” than the spasms associated with Parkinson’s disease. Symptoms of TD may disappear when a patient sleeps or is otherwise at rest, and may get worse when a patient is under stress, but this is not the case with Parkinson’s.
The key to both these conditions is dopamine. Drugs used to treat certain mental illnesses block receptors that receive certain brain signals transmitted by dopamine. The drugs are known as dopamine antagonists. With TD (as well as with Parkinson’s disease), insufficient amounts of dopamine are produced, or the chemicals and receptors do not function together properly. This can cause some patients taking antipsychotic drugs to develop symptoms that resemble those of Parkinson’s disease. But true Parkinson’s disease most often results from genetic predisposition.
Tardive dyskinesia treatment may be similar to treatment for Parkinson’s disease. Neither condition is considered curable, though both can be managed. TD has been known to go into spontaneous remission in patients who stop taking a symptom-causing drug after only having been on it for a short period. For cases that do not go into remission, the condition may be managed by a combination of a drug called Levdopa as well as other drugs that make dopamine work better.