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TD Resources Center – Scientific Literature

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This section contains scientific literature on tardive dyskinesia (TD)

 

 

(1) Tardive dyskinesia (TD) rates in adults are very high. Note the “authoritative” sources that confirm high rates, including the American Psychiatric Association (see documents labelled APA). TD occurs in young adults up to age 40 at a rate of at least 58% per year, accumulating with a risk of 20%24% after four years (American Psychiatric Association, 1992, pp. 67-8; Chouinard et al., 1988 for the higher rate; Wojcieszek, 1998). TD annual rates rise steeply for middle-aged people: “For a 40-year-old patient, the risk is 18% at 2 years [9% per year] and 30% at 4 years” (Wojcieszek, 1998, p. 220). In patients older than age 45 years, “the cumulative incident of TD after neuroleptic exposure is 26%, 52%, and 60% after 1, 2, and 3 years, respectively (Wojcieszek, 1998, p. 220).

 

(2) TD rates in the elderly are astronomical. Tardive dyskinesia in the elderly is one of the worst medical catastrophes. In controlled clinical trials, rates for the elderly for TD exceed 20% per year, and accumulate year after year. In addition to the Black Box Warnings about increase mortality in elderly patients for all antipsychotic drugs, the risk to patients is enormously greater than any possible benefit. Numerous studies confirm even more tragically high rates of TD in people 55 and older: 41% in 24 months (Yassa et al., 1988); 35% in 20.7 months (Yassa et al., 1992); and 26% in 12 months (Jeste et al., 1993). The elderly may develop tardive dyskinesia after 2 weeks exposure (Saltz et al., 1991) and probably after a day or two in my clinical experience.

 

(3) TD rates in children are similar or higher than in adults. In one of my earliest medical books (P. Breggin, Psychiatric Drugs: Hazards to the Brain, Springer, 1983), I marshaled evidence for the first time about the high risk of tardive dyskinesia in children. Since then, “authorities” routinely admit that it is risk, but too many negligent prescribers act as if it is not. Estimated TD prevalence rates in children vary widely but are generally very high at “8%-51% of antipsychotic-treated children and adolescents” (Cozza et al., 2003). p. 1422).

 

(4) Scientific studies confirm that “atypical” antipsychotic drugs cause typical extrapyramidal reactions (EPS) and TD. In addition to the scientific studies, Full Prescribing Information are provided for Risperdal, Abilify and Saphris to show that they block dopamine type 2 neurons and that they are considered to cause TD by the FDA. Indeed, all so-called atypicals are dopamine blockers and therefore they cause TD. For example, J&J (Johnson & Johnson), their medical consultants, and scientifically alert prescribers from the beginning should have known that Risperdal (as well as other so-called atypicals) would cause tardive dyskinesia at a high rate. From the beginning, the FDA-approved Risperdal label or Full Prescribing Information stated that Risperdal was an “antagonist” (blocker) with “high affinity” for “Dopamine Type 2 (D2).” That is, Risperdal is a potent blocker of D2 neurons and therefore would inevitably cause TD. Similarly, Abilify’s label states that the drug “exhibits high affinity for dopamine D2…” A new drug Saphris has similar observations and all three have warnings about TD.   In addition to the studies cited in this group, see group (10) below with more than two dozen reports of tardive dyskinesia caused by Risperdal published prior to 2005.

 

(5) Permanent brain damage and dysfunction, including cognitive dysfunction, dementia, tardive psychosis, and atrophy (shrinkage) of brain tissue with cell death caused by antipsychotic drugs. Brain atrophy can occur early in treatment even before TD develops. I was among the first to warn about the risk of antipsychotic drug-induced dementia and atrophy of the brain in my 1983 book, Psychiatric Drugs, and I have continued to document this risk in my most recent textbooks, Brain-Disabling Treatments in Psychiatry (2008) and Psychiatric Drug Withdrawal (2013). These drastic, tragic outcomes are the result of the extreme neurotoxicity of the antipsychotic drugs.

 

(6) Antipsychotic drugs especially damage the basal ganglia where the dopamine neurons originate. Tardive dyskinesia results from the permanent hypersensitivity and proliferation of these neurons as a compensatory reaction to the suppression and dysfunction caused by the antipsychotic drugs. A rudimentary knowledge of the function of the basal ganglia informs us that the dopaminergic nerves in the basal ganglia provide a main nerve trunk into the frontal lobes, as well as affecting the temporal lobes and other regions of the brain involved with memory, cognition, and all the higher human functions. It is no surprise, therefore, that tardive dyskinesia, a manifestation of damage to dopaminergic neurons, also causes cognitive deficits and even dementia. Here are a few of many scientific studies of the complex functions of the basal ganglia and the dopaminergic neurons that originate in them.

 

(7) Tardive Dystonia is a variant of tardive dyskinesia (TD) that has been recognized for decades in the scientific literature. It shares many basic characteristics with TD in general, except it is characterized by tension and spasms in the muscles, and can be very painful. Some of the articles in this section will make comparisons to “classic TD” and some will discuss the rates.

 

(8) Tardive Akathisia is a variant of tardive dyskinesia that has a powerful emotional component. An inner agitation that feels like being tortured from the inside out drives people to keep moving in a vain effort to find relief. Attempts to describe these feelings often impress hasty diagnosticians as evidence for delusions and hallucinations. Many such patients end up getting more of the drug that is driving them over the edge. The movements vary from running and pacing to tapping feet, wringing hands or squirming. I have seen people contain them for a while with great effort. Other people end up with the agitated feeling, even though they have not been or are no longer feelings driven to move about. Although little is written about it, I have found that paresthesias (abnormal feelings in the skin) often go along with akathisia, including crawling and burning sensations that may at times be felt inside the mouth as well. This condition is caused by both SSRI antidepressants and antipsychotic drugs. Among the antidepressants, Paxil may be a special offender. Among the antipsychotic drugs, Abilify is far the clear leader in causing it. The Full Prescribing Information for Abilify, found in this section, even calls it “common.” So does an Abilify advertisement contained here. Akathisia always worsens a person’s condition and can lead to psychosis, violence, and suicide. These dreadful outcomes from both SSRIs and antipsychotic drugs were recognized in the APA’s Diagnostic and Statistical Manual of Mental Disorders found in this section.

 

(9) Neuroleptic Malignant Syndrome (NMS). Although neuroleptic malignant syndrome (NMS) is not a form of TD, if the individuals survive, NMS can leave them with a wide variety of symptoms associated with TD, including abnormal movements and cognitive changes. The classic symptoms of neuroleptic malignant syndrome are (1) fever; (2) abnormal movements, such as rigidity, Parkinsonism, and TD-like reactions; (3) worsening mental status, and (4) autonomic nervous system dysfunction, such as rapid respirations, elevated pulse, unstable blood pressure, chills, sweating, and incontinence. However, in my clinical experience and confirmed in the literature (Levinson and Simpson, 1986, see below), NMS or NMS-like disorders caused by antipsychotic drugs can have many variable forms, intensities and durations. These drug-induced disorders, with or without a fever, must be recognized and the medications removed in order to prevent serious and potentially lasting harm.

I was probably the first scientist to observe that an acute case of NMS is indistinguishable from an acute episode of an epidemic called lethargic encephalitis that was recognized during the First World War and spread during the following decade (see my 1993 article in this section).

 

(10) Reports of Risperdal-induced TD published prior to 2005. One of the false claims made the defense in lawsuits pertaining to Risperdal and TD, as well as to other “atypical” antipsychotic drugs, is that there was no way for the drug company, its consultants, or prescribers to have known early on that so-called atypicals would cause TD. This section contains nearly two dozen clinical reports of Risperdal-induced TD published before 2005, including several cases involving children.

 

(11) James McCracken recently testified for the defense in a malpractice case involving tardive dyskinesia in a child. The case, in which I was an expert for the plaintiffs, was settled in trial shortly before I was scheduled to testify. Here are scientific articles jointly authored by McCracken favoring Risperdal for children with autism. These articles also mention some of his affiliations with drug companies; other times he avoids listing them. Check with Dr. Breggin for more information in this regard.

 

(12) Criminal and civil fines imposed on Johnson and Johnson, or J&J, (and subsidiary Janssen) for false marketing of Risperdal, leading to massive off-label, negligent use for children and the elderly, and all age ranges in general. J & J secretly and illegally paid Harvard psychiatrists Joseph Biederman, Thomas Spencer, and Timothy Wilens to promote Risperdal to children for the invented diagnosis of childhood bipolar disorder (Sarchet, 2011; Yu, 2011). This caused a forty times increase in children diagnosed with bipolar disorder between 1994 and 2003 (Moreno et al., 2007).

 

(13) Standards of care for preventing TD in children, adults and the elderly are well-documented. Here are a few psychiatric sources that are particular useful from the American Psychiatric Association. Of special interest are three publications from the American Geriatric Society (AGS) concerning the Beers Criteria for medication use in the elderly, which make clear that antipsychotic drugs should be “avoided” in treating the elderly. This folder contains a Beers Criteria article from 2012 and 2015. A second 2012 article intended for the public provides an excellent summary.

 

(14) Physicians too often fail to recognize or document TD. Neurologists, who often depend on psychiatrists for referrals, will often go to extremes to avoid actually diagnosing a patient with TD. I have seen cases in which everything in the patient’s history and clinical findings indicate TD but the consultant psychiatrist or neurologist refuses to make the specific diagnosis. Here are two articles about non-recognition of TD within psychiatry.

 

(15) Dr. Peter Breggin’s work. The best sources of my current research on these subjects are in two of my more recent books, Psychiatric Drug Withdrawal (2013) and Brain-Disabling Treatments in Psychiatry, Second Edition (2008). I am also including a few of my articles that deal with antipsychotic drug adverse effects, including tardive dyskinesia, tardive psychosis and tardive dementia.

 

 

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 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.