Antipsychotic Drugs and Tardive Dyskinesia (TD) Resources Center
For Prescribers, Scientists, Professionals, Patients and their Families
Antipsychotic Drugs and Tardive Dyskinesia Scientific Literature
By Peter R. Breggin, MD
What is Tardive Dyskinesia?
Introduction
Tardive dyskinesia (TD) is a group of involuntary movement disorders caused by drug-induced damage to the brain and often associated with physical or emotional suffering. TD is caused by all drugs that block the function of dopamine neurons in the brain. This includes all antipsychotic drugs in common use as well as a few drugs used for other purposes. TD can vary from a disfiguring grimace to a totally disabling array of spasms and often bizarre movements of any part of the body. See the Videos section for examples of TD. Unless identified at an early stage and the offending drugs stopped, these disorders nearly always become permanent.
Antipsychotic drugs are also called neuroleptics. Prescribers often promote them in a misleading fashion as antidepressants, mood stabilizers, bipolar drugs, sleeping pills, and behavior control drugs in children. Recent ones include Risperdal (risperidone), Abilify (aripiprazole), Geodon (ziprasidone), Invega (paliperidone), Latuda (lurasidone), Rexulti (brexpiprazole), Risperdal (risperidone), Saphris (asenapine), Seroquel (quetiapine), and Zyprexa (olanzapine). Older antipsychotics include Haldol (haloperidol) and Thorazine (chlorpromazine).
For a more complete list of antipsychotic or neuroleptic drugs, go here.
In recent years, Risperdal (risperidone) has most commonly come to my attention as a medical expert, especially in harming children, and this website contains extra information about Risperdal and its manufacturer Johnson and Johnson (J&J).
As a psychiatrist, the scientific information on this website is built upon many decades of clinical experience, research, publications, educational efforts, and work as a medical expert in legal cases. Now I wish to share this information in one convenient place for TD victims and their families, for their attorneys and other medical experts, and for any citizens, scientists and professionals concerned about this worldwide epidemic of medication-induced brain damage and dysfunction.
Rates of TD are Extremely High
TD commonly begins to appear within 3-6 months of exposure to the drugs, but cases have occurred from one or two doses. The risk of getting TD is very high in all age groups, including children. It afflicts 5% to 8% per year of younger adults treated with antipsychotics. The rates are cumulative in the first few years so that by three years 15% to 24% of patients will be afflicted. Rates escalate in the age group 40-55 years old, and among those over 55 are staggering, in the range of 25%-30% per year. (For more about rates in each age group, see the Scientific Literature section, groups 1 through 3.)
Newer “Atypical” Antipsychotics Have Similar TD Rates
Drug companies have made false or misleading claims that newer antipsychotic drugs or so-called atypicals are less likely to cause TD than the older ones. Recent research, much of it from a large government study called CATIE, have dispelled this misinformation. Considering how huge the TD rates are, a small variation among drugs would be inconsequential. All the antipsychotic drugs with the possible exception of the deadly Clozaril, cause TD at tragically high rates. Since all these drugs are potent dopamine blockers, there should have been no doubt from the beginning that they would frequently cause TD. (See the Scientific Literature section, group 4.)
What TD Looks Like
TD can impair any muscle functions that are partially or wholly under voluntary control such as the face, eye muscles, tongue, neck, back, abdomen, extremities, diaphragm and respiration, swallowing, and vocal cords. Coordination and posture can be afflicted. TD can cause tremors, tics, and paresthesias (e.g., burning sensations, numbness).TD can also afflict the autonomic nervous system, especially impairing gastrointestinal functioning.
Classic Tardive dyskinesia
Classic TD involves either rapid, jerky movements (choreiform) or slower, serpentine movements (athetoid). In the extreme, a patient may look as if he or she is playing a guitar in a wild rock band. He may be unable to sit or stand straight, or be unable to control constant head bobbing. Hands and feet or fingers and toes may curl uncontrollably.
Tardive Dystonia
A second form of TD, tardive dystonia, involves painful muscle contractions or spasms, often the neck, and sometimes leading to overall rigidity of the body. (See the Scientific Literature section, group 7.)
Tardive Akathisia, Dementia and Psychosis
A third form of TD, tardive akathisia, involves psychomotor agitation, an inner torture that drives the person to move about compulsively seeking relief. Tardive akathisia can cause psychosis, a general worsening of the person’s condition and life, suicide, and violence. (See the Scientific Literature section, group 8.) There are many additional forms of TD including tardive psychosis and tardive dementia. (See the Scientific Literature section, groups 5 & 6.) The various tardive disorders can exist separately or in combination.
Masking: Antipsychotics Mask the Symptoms they Cause
Unfortunately, antipsychotic drugs not only cause TD, they mask the manifestation of the symptoms, so that the patient grows worse without initially realizing it. The TD disorder then breaks out, often amid emotional anguish from its effects, at a time with the drugs can no longer suppress it or the individual tries to withdraw from the drug.
Physical Exhaustion
Tardive dyskinesia frequently leads to exhaustion. The exhaustion is often overlooked by diagnosticians, but it grossly impairs the quality of life.
Humiliation
TD commonly causes humiliation with social withdrawal. The emotional suffering in the form of shame, loneliness and isolation cannot be exaggerated.
Catastrophic Impact on the Brain, Mind and Lifespan
TD also leads to shortened lifespan and frequently causes cognitive dysfunction and dementia. Antipsychotic drugs, without or without TD, can cause shrinkage (atrophy) of the brain and take years of the victim’s life. (See the Scientific Literature section, groups 5 and 6.) Most people with TD are also afflicted with a loss of cognitive functioning.
Educating Clinicians, Patients and Families
Clinicians, patients and families must be able recognize the symptoms of TD in order to identify potential TD and to take appropriate action in stopping the medication. All health care providers must be prepared to educate patients and their families about the dangers of tardive dyskinesia.
Overlooked and Confusing Signs of TD
TD can afflict one muscle group such as the tongue or fingers or it can affect many muscle groups. It can cause a generalized hypertension or rigidity of the entire musculature of the body. It can manifest itself in varying ways at varying times. Like most or all neurological disorders, manifestations of TD vary enormously depending on the individual’s general physical condition and mental condition. It often improves during relaxation and worsens during stress, fatigue, illness, or lack of sleep. Although it can make it difficult to fall asleep, it usually disappears when the individual falls asleep.
TD symptoms may change from one muscle group to another over a period of minutes, days, weeks or even months or years. In the beginning, TD may afflict the tongue and eye muscles. Years later, it may change to afflicting the neck and shoulders and not the tongue and eyes. One set of symptoms may grow worse over the years, another set may grow less severe, and yet others may appear. Sometimes, TD symptoms first appear months or years after the last drug exposure. When symptoms of TD have been present for several weeks or months, the disorder, while commonly changing its manifestations, rarely disappears entirely.
TD frequently causes severe exhaustion, even when limited to one area, such as the jaw, neck, or feet. Victims often fail to report exhaustion or fatigue unless they are asked, and then it may turn out to be a dominant part of the disability that vastly limits their activities, such as walking, doing housework or visiting.
Especially in the dystonic forms, the pain can be very severe, and the physical stress can cause serious orthopedic problems, including erosion of the cervical spine from muscle spasms in the neck or claw-like joint distortions due to flexion contractures of the hands or feet.
Many people try to cover up their TD by making their movements look intentional. A person who grimaces may pretend to be smiling. An individual whose arm rises uncontrollably may make it look as if he or she is stroking or combing their hair with their hand. They may not be aware of what they are doing.
Patients and Diagnosticians Fail to Recognize Symptoms
Individuals frequently have little or no perception or understanding of the severity of their tardive dyskinesia. Typically, abnormal tongue movements go unnoticed, even while the individuals are aware of biting their tongue or the inner side of their cheeks, or having difficulty articulating or swallowing. Even more gross abnormal movements can be ignored, especially if they are not physically painful. This failure to recognize TD in oneself has been described in the scientific literature section, and may be an aspect of what I call medication spellbinding or intoxication anosognosia—the failure to recognized drug intoxication and other harms associated with psychoactive substances. It is probably related to frontal lobe dysfunction caused by drugs.
Without being grossly apparent to the untrained eye, TD can interfere with balance, walking, running, playing, and gross and fine motor coordination. Commonly, the individuals cannot clap their hands, patty cake, drum their fingers or write in a rapid and coordinated manner. Children suffering from TD frequently experience these disabilities, along with postural difficulties. Out of difficulty, fatigue or embarrassment, children stop playing as much.
Doctors, including neurological consultants, frequently fail to do thorough TD examinations or to accept the possibility that patients have TD. (See the Scientific Literature section, group 14.) A careful, informed physical examination of a patient, lasting at least 30 minutes, will frequently disclose more symptoms than reported to the doctor by the individual or the family, such as a curling of the tongue on extension from the mouth or while lying in the open mouth, a mildly spastic gait, or difficulty with balance on quick turns. Hand movements, such as curling fingers, may become more obvious while the individual is walking. Blinking may appear when the individual is focusing on something else such as writing a sentence or reading aloud. Slow movements may be more difficult than rapid ones, so that the individual has greater difficulty walking slowly than walking rapidly, which may give the misimpression of exaggerating their problem. Climbing stairs often displays difficulties not apparent when walking on flat surface.
Neuroleptic Malignant Syndrome (NMS)
NMS is caused by antipsychotic drugs and other dopamine blockers but is not considered a form of tardive dyskinesia. However, if the individual survives NMS, residual symptoms can include anything associated with TD. Approximately 20% of patients will die if the disorder is not recognized, the offending drug stopped, and supportive measures instituted. (See the Scientific Literature section, group 9.)
The classic signs of neuroleptic malignant syndrome are (1) fever, (2) rigidity or any other extrapyramidal reaction (including a wide variety of abnormal movements and spasms, Parkinsonism and TD-like symptoms), (3) altered mental status, and (4) autonomic dysfunction, such as rapid respirations, elevated pulse, unstable blood pressure, chills, sweating, and incontinence.
NMS is frequently called “rare” but some studies show it occurs in up to 3% of hospitalized patients, making it a very common and yet potentially crippling or deadly disorder. The common idea that patients must show “rigidity” is false, but most show some sign of neurological impairment typically found in patients exposed to antipsychotic drugs. The idea that patients can be “carefully” restarted on the drug is a prescription for disaster.
NMS should be viewed as a disorder that occurs in many shapes and varying intensities. It can become chronic, especially if the offending agent or aggravating drugs are continued.
The NMS diagnosed is frequently missed or dismissed. I have been a medical expert in a number of cases where doctors have failed to diagnose NMS and severely harmed their patients by continuing the causative drug. Any patient on antipsychotic drugs or other dopamine blockers should be thoroughly evaluated for NMS if they develop a fever, changes in heart rate or pulse, any of various neurological symptoms, or new or worsened mental dysfunction. Even an unrelated physical disorder, especially infections such as pneumonia, should raise the question of whether an underlying NMS caused the vulnerability.
More about the Heavy Toll of TD
TD commonly ruins the lives of the afflicted individuals as well as the lives of those who love and care for them.
TD can lead to demoralizing chronic pain, such as teeth grinding and tongue biting, and dystonic spasms of the neck, hands or feet.
TD is typically stigmatizing, leading to demoralization, humiliation, and social isolation. Loudly grinding teeth, squinting eye spasms or rapid blinking, abnormal speech, or facial grimaces can ruin an individual’s confidence and cause social withdrawal. Those who are afflicted will often be shy and embarrassed about discussing how ashamed they are to appear in front of friends or strangers.
TD commonly leads to full disability, so that the victim cannot work, whether or not the associated psychiatrists and neurologists consider it disabling. It commonly disrupts intimate relationships on every level. The individual often becomes irritable and less affectionate, causing additional suffering to family and loved ones.
Concentration and attention can be impaired by the stress of TD, by abnormal movements that are distracting, and by mental disability caused by the associated brain dysfunction. Victims often report difficulty relaxing enough or positioning themselves well enough to easily or comfortably read and watch television. Hobbies such as cooking, sewing, golfing, fishing and hiking may become impossible.
Signs of related brain injury include impairments of attention, concentration, and memory. Especially in more severe or long-lasting cases, there can be signs of dementia and psychosis (tardive dementia and tardive psychosis, see the Scientific Literature section, groups 5 and 6). Individuals may become highly anxious and paranoid. Distrust of all physicians and healthcare providers is a natural consequence of the betrayal felt by TD victims.
The millions of cases in the US result in inestimable costs to society.
Tardive Dyskinesia Legal Cases including many cases since 2018 |
Observations on Recovery from Tardive Dyskinesia
Although most tardive dyskinesia (TD) cases are permanent, many people experience a partial or even whole recovery from TD symptoms gradually over months and years. At present, no medical approaches are consistently useful and many drug interventions can worsen the condition.
Botox can alleviate some dystonic spasms but has its limitations. I have found that it is usually most helpful for patients to stop all psychoactive substances, although some patients benefit from the judicious use of sedatives like benzodiazepines to calm their nervous system or analgesic medications to relieve the pain associated with dystonia.
I try to help people focus on the basics of healthy living, including good nutrition, moderate exercise, and worthwhile activities and relationships. In my clinical practice, I have found that individuals do best by also seeking their own preferred alternative approaches including massage, acupuncture, mindfulness training, yoga, Chinese medicine, various exercise routines, and non-psychoactive supplements.
When individuals want psychotherapy, I often emphasize spiritual coaching, along with the more common therapeutic emphasis on self-insight. If possible, I work with a couple or family to help each member deal with the stresses associated with TD and to maintain or develop the quality of their love relationship.
I have been able to help some individuals find new internal strengths, revitalizing old aspirations or ideals, and building loving relationships. I have seen people live surprisingly satisfying lives as they learn to focus their minds on more productive ways of thinking, feeling and acting, in a manner I describe in my book Guilt, Shame and Anxiety: Understanding and Overcoming Negative Emotions. However, in making these observations, I want to emphasize that my success depends more on my patient than on my therapy. Also, a substantial number of people do improve over time as a natural course of the disorder, and I encourage hope for this eventuality, while improving one’s overall health and emotional outlook.
Meanwhile, I am trying my best to stop my colleagues from prescribing these toxic chemicals and I urge people to avoid starting on them. If an individual is taking them, when at all possible it is best to carefully taper off them with as much personal and professional support as possible as I describe in my book, Psychiatric Drug Withdrawal.
Antipsychotic Drugs and Tardive Dyskinesia Scientific Literature
| WARNING: Psychiatric drugs are not only dangerous to take, they are also dangerous to withdraw from. Withdrawal from psychiatric drugs, including antipsychotic drugs, should be done cautiously with professional supervision.Please see my book, Peter R. Breggin, MD, Psychiatric Drug Withdrawal: A Guide for Prescribers, Therapists, Patients and their Families. |
