Colin Slaymaker
Background/Definition
Atypical antipsychotics refers to a class of drugs used primarily to treat psychoses, such as schizophrenia (“Atypical Antipsychotics (Psychosis)”). The class of pharmaceuticals emerged in 1958 with the development of clozapine, which became available for use in the United States in 1990 and was followed by multiple other antipsychotic medications that were meant to mimic its effects and mechanism of action (“Atypical Antipsychotics”). Today, the class of atypical antipsychotics includes 11 different medications, the most recent of which, pimavanserin, was introduced for use in the United States in 2016 (“Acadia Pharmaceuticals”). Atypical antipsychotics are designed to treat psychosis, which refers to conditions or illnesses that “affect the mind [and cause] some loss of contact with reality,” (“What is Psychosis?”), but are also used to treat acute mania and behavioral disorders in children. Common psychotic disorders and illnesses include schizophrenia, schizoaffective disorder, schizophreniform disorder, and brief psychotic disorder, characteristic symptoms of which include delusions, hallucinations, incoherent speech, and inappropriate behavior (“What is Psychosis?”).
Atypical antipsychotics are referred to often as second-generation antipsychotics, as they are different in side effect profile than other antipsychotic drugs used before the introduction of clozapine. These antipsychotics, called typical antipsychotics, first emerged in 1951, with the creation of chlorpromazine, which was noted to decrease the effects of psychosis and led to decreased “psychiatric impatient populations […] around the world,” (Shen 409) after its spread and wide usage. However, by 1954, it became clear that chlorpromazine caused extrapyramidal symptoms (EPS) as a side effect, which refer broadly to drug-induced movement disorders such as acute and tardive dyskinesia, parkinsonism, and neuroleptic malignant syndrome (Blair). A link to a website that describes the debilitating effects of Tardive dyskinesia is attached here: https://www.webmd.com/schizophrenia/tardive-dyskinesia#1. Furthermore, a video demonstrating the effects on the body of tardive dyskinesia is linked here: https://www.youtube.com/watch?v=Qf3I6t8fuA8. In the video, one can see the lack of control the woman has over her body movement.
Atypical antipsychotics differ from typical antipsychotics primarily due to the fact that they produce less of these extrapyramidal symptoms than typicals at doses high enough to control standard symptoms of psychosis (Meltzer). Furthermore, atypical antipsychotics have been shown to be more efficacious in improving cognitive function in those with psychotic conditions and to work by a different mechanism than do typical antipsychotics (Meltzer). Despite the decreased frequency and risk of extrapyramidal symptoms, atypical antipsychotics have a range of harmful side effects. Though risks for certain side effects differs by the specific drug taken, atypicals have been shown to cause weight gain and lead to higher risk of certain metabolic conditions such as diabetes, hyperlipidemia, dyslipidemia, and hyperglycemia (“Atypical Antipsychotics”). When atypical antipsychotics were first released into the market in the United States, they were marketed to be “more efficacious and have fewer and less-severe side effects than all the antipsychotic drugs [previously] introduced,” (“Atypical Antipsychotics”). However, recent studies, and court cases, such as the 1.4 billion dollar settlement Eli-Lilly reached in 2009 over false claims about olanzapine, demonstrate that many of these claims were ungrounded and that atypicals and typicals are not significantly or consistently different in their respective abilities to treat the symptoms of psychosis (Kendall 266).
Both typical and atypical antipsychotics operate as biological antagonists. To explain, typical antipsychotics are dopamine D2 antagonists, meaning that, in the brain, these drugs bind to the D2 receptors that dopamine normally binds to. By binding to these receptors, they block the ability of dopamine to bind and thus function (“Atypical Antipsychotics”). However, this antagonistic behavior is responsible for the onset of the extrapyramidal symptoms that plague users of typical antipsychotics. Atypical antipsychotics differ from typical antipsychotics in their mechanism of action by binding to both dopamine D2 receptors and serotonin 5HT2A receptors, making them serotonin-dopamine antagonists (Guzman). As overproduction of dopamine and serotonin and subsequent overbinding at these receptors is a main cause of the symptoms of schizophrenia, disallowing such binding works to alleviate these conditions (“Typical”). A video describing takeaway points in the differences between atypical and typical antipsychotics is linked here https://youtu.be/tE0ClEQxTrU (Guzman).
Historical Context
The development of antipsychotics began with the discovery of the sedative and anesthetic-potentiating effects of promethazine (Shen 408). These discoveries prompted the beginning of research into chlorpromazine in 1950. By 1952, the antipsychotic properties of chlorpromazine were well-established, leading to its commercial release by Rhone-Poulenc under the trade name Largactil (Shen 408). Chlorpromazine’s clinical success led to a drive to discover more antipsychotic agents, leading to the production of 40 such compounds by 1990. Of these 40, 8 were available worldwide for patient use, only two of which were available in the United States (Shen 409).Despite its initial clinical success, by 1954, linkages between chlorpromazine use and EPS became recognized worldwide (Shen 409). It was estimated then that 38.9% of users of this antipsychotic agent had EPS, and by 1958, the link between EPS and increased efficacy of antipsychotic agents became undeniable to many researchers (Shen 409). To explain, at the time, many researchers believed that the more efficacious an antipsychotic was, the more likely it was to cause EPS. An image listing and describing common EPS is pictured below (Keks).
Figure 1: A description of common EPS (Keks)
These realizations led to the advent of clozapine, the first atypical antipsychotic. The discovery of clozapine began in Switzerland, where researchers at Wander Pharmaceuticals began work to disprove the link between EPS and the efficacy of antipsychotic medications. After the creation of clozapine in 1960, two clinical trials, one performed in 1966 and the other in 1971, provided confirmation that clozapine was an efficacious antipsychotic that led to no major EPS (Shen 409). Clozapine was quickly withdrawn by Wander Pharmaceuticals after its initial release, mainly due to reports of clozapine-linked agranulocytosis in Finland. Agranulocytosis is a disease that leads to a lower number of white blood cells, which is significant as it leads to an increased susceptibility to infection. In 1975, 8 patients taking clozapine died from agranulocytosis in Finland, which led to the quick withdrawal of its license to be sold in both Europe and North America (Kendall 266). Later research done in the 1990s demonstrated that the incidence of clozapine-induced agranulocytosis was between 1-2% (Lieberman et al.). After the agranulocytosis scare, clozapine was FDA-approved for use in October 1989 and began to be sold as Clozaril in the United States in February the following year. FDA-approval of clozapine was aided by the genesis of white blood cell monitoring programs, which allowed patients who began to develop agranulocytosis to stop taking the drug and often recover. In the United States, 1,800 patients took place in clinical trials of clozapine that involved monitoring programs. Of the 1,800, only 18 developed agranulocytosis, none of whom died after discontinuing clozapine use (Spolar). As the study suggested was proper, when clozapine was introduced for patient use in the United States, patients were required to take part in weekly white blood cell count measurements, titled the Clozaril Patient Management System (CPMS) (Lieberman et al). CPMS allowed researchers to monitor patients for potential risk factors of the drug and to estimate the incidence of agranulocytosis in patients taking clozapine (Lieberman et al). Though the program was discontinued in May 1991, it gave researchers an opportunity to further understand the pros and cons of a highly controversial pharmaceutical.
FDA-approval of clozapine met controversy in the United States due to its tie to agranulocytosis, but also due to the fact that the drug was not as accessible as many originally hoped. Clozaril was marketed as a pharmaceutical that could finally aid treatment-resistant patients and, due to the risk of agranulocytosis, was solely administered to such patients when it was released. However, due to its novelty at the time and its requirement of a monitoring program, the drug cost $9,000 a year (Spolar). At the time, many of those affected by treatment-resistant schizophrenia were outraged that “possibly the only drug” (Spolar) to allow them to return to normalcy had such a hefty price-tag (Spolar).
Despite the risks of agranulocytosis, clozapine was incredibly successful as “[clozapine] was useful not only for treating positive symptoms (such as hallucinations, delusions, disorganized behavior, and disorganized speech) associated with schizophrenia but also for treating negative symptoms (such as severe social withdrawal, inactivity, apathy, affective flattening, and poverty of thought),” (Shen 410). Furthermore, the discovery and introduction of clozapine into the pharmaceutical market destroyed the previously commonly-held notion that the efficacy of an antipsychotic was linked to its tendency to cause EPS (Shen 410). Ultimately, the remarkable success of clozapine led to the creation of many other atypical antipsychotics, created to mimic the mechanisms and effects of clozapine. During the 1990s, as other atypicals were produced, atypicality of antipsychotics was defined by, “a clinical profile with a low propensity to induce EPS and with efficacy for the negative symptoms of schizophrenia,” (Shen 410). Atypical antipsychotics manufactured and sold after the release of clozapine include risperidone in 1993, olanzapine in 1996, quetiapine in 1997, ziprasidone in 2001, aripiprazole in 2002, paliperidone in 2006, iloperidone and asenapine in 2009, and lurasidone in 2010 (“Atypical Antipsychotics”). Pimavanserin was also FDA-approved in 2016 for treatment of Parkinson’s Disease-derived psychosis (“Acadia Pharmaceuticals”). The genesis of multiple new atypical antipsychotics during this time period was not only significant as it gave many individuals the opportunity to take antipsychotics without high risk of EPS, but also because it led to a large rise in sales of antipsychotics. Before risperidone was introduced to the market in 1993, antipsychotic drugs totaled less than a billion dollars in sales worldwide. Furthermore, atypical antipsychotics, which referred to only clozapine at the time, only made up a small portion of these sales (“Atypical Antipsychotics”). However, after risperidone and other atypicals were introduced, “Over the next decade, atypical antipsychotic drugs captured more than 90 percent of the [antipsychotic] market, and worldwide sales of these compounds mushroomed to more than $10 billion,” (“Atypical Antipsychotics”). By 2011, antipsychotics totaled $28 billion worldwide, and even became the fifth-largest selling drug class in the world (“Atypical Antipsychotics”).
Despite the large initial success of atypical antipsychotics, recent research has dampened the excitement regarding them. After the creation of atypicals, pharmaceutical companies led heavily directed marketing efforts that praised the ability of these drugs to reduce both the negative and positive symptoms of schizophrenia and other forms of psychosis (“Atypical Antipsychotics”). However, studies done throughout the late 2000s and early 2010s have shown that, “there [are] no important differences between any of the antipsychotics in terms of clinical or cost-effectiveness,” (Kendall 268). The only exceptions to this rule are that clozapine is more efficacious in treating treatment-resistant schizophrenics and that olanzapine may be more efficacious in treating psychosis than other medications. An image of the chemical structures of clozapine and olanzapine is pictured below (Vang et al.). However, no evidence has emerged that atypical antipsychotics are significantly better or worse as a class at treating psychosis than typical antipsychotics, giving reason to end the distinction between atypicals and typicals (Kendall 268).
Figure 2: The chemical structures of two atypical antipsychotics, olanzapine and clozapine (Vang)
Pharmaceutical companies, in their efforts to market atypicals, emphasized the safety of these new drugs as compared to typical antipsychotics. However, it was later revealed, through multiple court cases, that these companies consciously declined to release data that demonstrates that these pharmaceuticals can be just as dangerous (“Atypical Antipsychotics”). Though pharmaceutical companies did succeed in creating some antipsychotics with less risk of EPS and agranulocytosis, atypical antipsychotics have a side effect profile that includes serious diseases such as diabetes, and many atypicals still have high risk for EPS (Kendall 268). These realizations led to a slew of lawsuits against pharmaceutical companies, including a $515 million settlement by Bristol-Myers Squibb in 2007, a $1.4 billion settlement by Eli-Lilly in 2009, and a $520 million settlement by AstraZeneca in 2010. As Tim Kendall, a researcher at the Royal College of Psychiatrists, states, “The story of the atypical antipsychotics is a tale of the triumph of profit over patient benefit, of marketing over ethics,” (Kendall 266). An image detailing the side effect profiles of individual typical and atypical antipsychotics is shown below (Keks).
Figure 3: A list of typical and atypical antipsychotics and the frequency of their side effects (Keks)
In recent years, the use of atypical antipsychotics for off-label uses has risen considerably (McKean). For instance, studies have estimated that $4-5 billion of the $13 billion spent per year in the United States on atypical antipsychotics is due to off-label uses (McKean). Furthermore, “the off-label use of quetiapine accounted for 17% of the total annual cost for all [atypicals] in New Zealand in 2010,” (McKean). Off-label uses of atypical antipsychotics include post-traumatic stress disorder, anxiety, depression, and drug and alcohol abuse (McKean). The new prevalence of atypical antipsychotics for off-label uses creates a situation in which physicians must balance the benefits of taking the medications for their patients with the cons of the multiple devastating side effects than can arise as a result of taking these medications.
Controversy
Atypical antipsychotics have been plagued by controversy throughout the 28 years they have been approved for use in the United States. When clozapine was first introduced, it was met heavily with outrage due to its high cost, totaling $9,000 a year for patients who wished to take it as a result of mandatory white blood cell monitoring programs (Spolar). Furthermore, after the initial clinical success of clozapine, subsequent pharmaceuticals were marketed as more efficacious at treating the symptoms of psychosis, especially cognitive impairment, and as safer drugs with less risk for EPS (“Atypical Antipsychotics”). “Many psychiatrists, especially researchers closely connected to the drug industry, claimed that the emergence of the atypicals was a revolution in schizophrenia treatment and research comparable to the introduction of the original antipsychotic, chlorpromazine,” (Kendall 267). Atypical antipsychotics were marketed as a new hope for many treatment resistant patients and eventually as a better option than typical antipsychotics, yet later research demonstrated that the creation and subsequent introduction of atypical antipsychotics into the market was, “not the story of clinical discovery and progress; it [was] the story of fabricated classes, money and marketing,” (Kendall 268). Though atypical antipsychotics are generally less likely to cause EPS and work by a different mechanism, recent research has shown that atypicals, as a class, are no more efficacious in treating psychosis than typical antipsychotics. Furthermore, they have their own side effect profile, including harmful metabolic side effects such as heightened risk of diabetes and hyperlipidemia (“Atypical Antipsychotics”).
The discussion of atypical antipsychotics brings another large controversy into play: whether the benefits of these medications outweigh the harmful risks posed by the side effect profile. In 2012, the United States Congress created a policy that allows for the expedited release and approval of certain pharmaceuticals that represent a “breakthrough therapy” (Ellis). In 2016, the FDA approved a new atypical antipsychotic, pimavanserin, sold under the trade name Nuplazid by Acadia Pharmaceuticals (Ellis). When Nuplazid was in clinical trials, individuals such as Brendan Tyne, whose mother is afflicted with psychosis as a result of Parkinson’s Disease, regarded the FDA’s slow approval process as painstaking and plead with the FDA to hasten its process. Tyne’s motivation was to help his mother return to a life of normalcy, which he believed that only Nuplazid would allow her to do (Ellis). After its release, sales of Nuplazid reached over $100 million in 2017, but this increase in sales was earmarked by the fact that the FDA received over 1,000 reports from patients taking Nuplazid that the medication had done little to help with their hallucinations and delusions. The situation is worsened when it is considered that, since the drug’s release, 700 drug-related deaths were reported to the FDA, with Nuplazid as the only suspect in 500 of these cases (Ellis). The breakthrough therapy designation has not changed the fact that a medication must be effective with acceptable risk to be approved, but has simply led to a decline in the amount of evidence needed to approve medications with the “breakthrough” designation (Darrow et al.). Proponents of the system, such as Tyne, argue that the program allows earlier access and the potential of progress to patients who would otherwise have no solution to their ailments. Members of the FDA committee that approved Nuplazid cited that they voted for the medication’s approval as they believed the benefits outweighed the risks of the medication and that families affected by the haunting symptoms of psychosis would be willing to take the risks to help their loved ones (Ellis). However, other members of this committee, even some of whom voted for approval of Nuplazid, were “not convinced […] that the benefits outweighed the risks,” (Ellis) and plead to the FDA to, “consider a large observational study [to] ensure that, once it goes into real-world use, that the benefits will outweigh the risks,” (Ellis). The director of the FDA committee that approved Nuplazid, Dr. Paul Andreason, even stated that the slew of reported deaths and adverse reactions to Nuplazid was exactly what he expected to happen. Furthermore, “investigators have reported that drugs receiving faster reviews have more spontaneous reports of drug-related adverse events” (Darrow et al.).
Ultimately, in the FDA’s creation of the “breakthrough therapy” designation, there has arose a controversy between those who believe that it is necessary to provide those ailed by devastating conditions with the medications necessary to help them as soon as possible and those who believe that the hastened review process is not extensive enough to fully guarantee the safety of the medication. Given the gravity of the symptoms of psychosis and the fact that antipsychotic medications are the last hope of many for a return to normalcy (Ellis), the process of hastened review by breakthrough therapy is directly related to the approval process of atypical antipsychotics. This topic is especially relevant considering the fact that Acadia Pharmaceuticals is attempting to widen the amount of conditions that Nuplazid is approved to treat, and the company’s attempts to approve Nuplazid for dementia-related psychosis have also received the “breakthrough” label (Ellis). The FDA is currently doing more research on the safety of Nuplazid.
Relation to Politics of Health
Atypical antipsychotics relate to politics of health through the concept of pharmaceuticalization, as described by Simon J. Williams. According to Williams, “pharmaceuticalization denotes the translation or transformation of human conditions, capabilities, and capacities into opportunity for pharmaceutical intervention,” (Williams et al 20). Williams goes on to say that these opportunities for pharmaceutical intervention extend beyond the medical world, giving people opportunities to use pharmaceuticals to enhance their lives. Pharmaceuticalization is related to atypical antipsychotics in the advent of the increase of atypicals for off-label uses. According to John Abraham, a medical anthropologist at the University of Sussex, “Pharmaceuticalization is also driven by industry promotion and advertising of individual drug products to the medical profession for established medical conditions, whether on- or off-label,” (Abraham 609). Abraham goes on to discuss how Zyprexa, the trade name for olanzapine, has been marketed in recent years for the use of dementia and Alzheimer’s, despite the fact that there is no research to back up claims of olanzapine’s efficacy in treating such conditions (Abraham 609). Furthermore, off-label usage of all atypical antipsychotics has grown, with reports that off-label usage accounted for $4-5 billion of the $13 billion spent nationally on atypical antipsychotics (McKean). Ultimately, atypical antipsychotics represent an example of pharmaceuticalization, as drug companies have treated human conditions, such as schizophrenia and psychosis, as opportunities for pharmaceutical intervention. Furthermore, when it is considered that these same companies have begun to market their medications for off-label conditions, it can be understood that these companies are treating conditions that are perhaps only tangentially linked to psychosis as further opportunities for pharmaceutical intervention and financial gain. Given the fact that similar trends to the evolution of Zyprexa are seen in the use of quetiadine in New Zealand and multiple other antipsychotics in the United States (McKean), atypical antipsychotics represent a clear example of pharmaceuticalization due to their increased usage in human conditions that they are not directly designed to treat.
Atypical antipsychotics are also related to politics of health through the concept of scientific knowledge production. Scientific knowledge production is the process, through research, by which information is gained on the qualities, effectiveness, and any other useful knowledge on a particular topic. The concept was introduced in the context of the Black Panther Party, who did research on sickle cell anemia at the People’s Sickle Cell Anemia Research Foundation throughout the 1970s, and used the knowledge produced to disseminate information of the condition to African-Americans throughout the United States (“Spin Doctors” 116). Scientific knowledge production is related to atypical antipsychotics given the controversy that has occurred in producing and disseminating knowledge about the efficacy and side effects of atypical antipsychotics. To explain, during the advent of atypicals, pharmaceutical companies led heavily directed marketing efforts that claimed that atypical antipsychotics were more efficacious in treating psychosis, could treat “core symptoms of schizophrenia untouched by first-generation antipsychotic drugs,” (“Atypical Antipsychotics”), and were even much safer than typical antipsychotics. However, later research demonstrated that not only was there no significant difference in the efficacy of atypical and typical antipsychotics as a class in treating psychosis, but that atypical antipsychotics have a dangerous side effect profile all their own (Kendall 267). Especially when it is considered that pharmaceutical companies withheld information about the negative side effects of atypicals (“Atypical Antipsychotics”), it can be seen that atypical antipsychotics are an example in which marketing and finance trumped true scientific knowledge production (Kendall 268).
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