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Developmental Neurorehabilitation, January – March 2007; 10(1): 75–81 LESSONS FROM HISTORY Flashback to the 1960s: LSD in the treatment of autism JEFF SIGAFOOS1, VANESSA A. GREEN1, CHATURI EDRISINHA2, & GIULIO E. LANCIONI3 1 School of Education, University of Tasmania, Australia, 2Department of Special Education, The University of Texas at Austin, USA, and 3University of Bari, Italy (Received 10 April 2006; revised 22 September 2006; accepted 22 September 2006) Abstract Between 1959 and 197
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Developmental Neurorehabilitation, January – March 2007; 10(1): 75–81 LESSONS FROM HISTORY Flashback to the 1960s: LSD in the treatment of autism JEFF SIGAFOOS1, VANESSA A. GREEN1, CHATURI EDRISINHA2, & GIULIO E. LANCIONI3 1School of Education, University of Tasmania, Australia, 2Department of Special Education, The University of Texas at Austin, USA, and3University of Bari, Italy (Received 10 April 2006; revised 22 September 2006; accepted 22 September 2006) Abstract Between 1959 and 1974, several groups of researchers issued reports on the use of d-Lysergic Acid Diethylamide (LSD) in the treatment of children with autism. This paper reviews that literature to consider how the authors justified these studies, as well as their methods, results, and conclusions. The justification for using LSD was often based on the default logic that other treatment efforts had failed. Several positive outcomes were reported with the use of LSD, but most of these studies lacked proper experimental controls and presented largely narrative/descriptive data. Today there is renewed interest in the use of psychedelic drugs for therapeutic purposes. While this resurgence of research has not yet included children with autism, this review of the LSD studies from the 1960s and 1970s offers important lessons for future efforts to evaluate new or controversial treatments for children with autism. Keywords:Autism, LSD Entre los an˜ os 1959 y 1974 varios grupos de investigacio´ n publicaron reportes acerca del uso de la dietilamida de a´cido lise´rgico (LSD) en el tratamiento de nin˜ os con autismo. Este artı ´culo revisa esa literatura para considerar como justifican los autores estos estudios, ası ´como sus me´todos, resultados y conclusiones. La justificacio´n para el uso del LSD se basaba generalmente en la lo´gica de que otros intentos de tratamiento habı ´an fracasado. Varios resultados positivos fueron reportados con el uso del LSD, pero la mayorı ´a de estos estudios carecı ´an de controles experimentales apropiados y presentaban ampliamente datos descriptivos/narrativos. En la actualidad existe un intere´s renovado en el uso de drogas psicode´licas con fines terape´uticos. Ya que el resurgimiento de la investigacio´ n au´ n no ha incluido a nin˜ os con autismo, esta revisio´ n de los estudios de LSD de 1960 a 1970 ofrece lecciones importantes para esfuerzos futuros que busquen evaluar tratamientos controvertidos o nuevos para nin˜ os con autismo. Palabras clave:Autismo, LSD Introduction Ever since Kanner first described autism in 1943, researchers have struggled to explain and effectively treat this perplexing disorder [1]. Various etiological theories have been proposed, ranging from Kanner’s srcinal albeit often forgotten conclusion that the condition was probably biological in srcin, to more psychoanalytic accounts [2]. A prevailing view in the 1950s and 1960s was that autism represented a childhood version of adult psychosis or schizophrenia [3]. Consistent with this conceptuali- zation, treatment was firmly rooted in the clinical psychiatry of the day. By the early 1960s, numerous biologic treatments (e.g., electric convulsive shock, sub-shock insulin, amphetamines, and antidepres- sants) had been used in an attempt to help children with autism [4]. This is a brief historical review of one such treatment; the psychedelic drug known as LSD. Between 1959 and 1974, several groups of researchers issued reports on the use of LSD in the Correspondence: Jeff Sigafoos, School of Education, University of Tasmania, Private Bag 66, Hobart, Tasmania 7001, Australia. E-mail: Jeff.Sigafoos@utas.edu.au ISSN 1751–8423 print/ISSN 1751–8431 online/07/010075–7ß 2007 Informa UK Ltd. DOI: 10.1080/13638490601106277treatment of children with autism. This paper provides a historical review and methodological critique of the use of LSD in the treatment of children with autism and related disorders. We consider the justification offered for these studies, as well as their methods, results, and conclusions. From today’s perspective, LSD might appear to be one of the more peculiar approaches to the treatment of autism with little contemporary relevance. However, there is renewed interest in the use of LSD for therapeutic purposes [5]. Once again researchers are focusing on evaluating the potential of LSD and other psychedelic drugs for treating a range of problems, such as post-traumatic stress [6] and anxiety [7]. Given this renewed interest it would seem timely to re-evaluate the literature from the initial era of LSD experimentation on children with autism. Doing so may highlight important lessons that should be considered when designing research to evaluate new or controversial treatments. In addition, because few of our contemporaries seem aware that research of this nature had once been conducted, we thought a review of this literature might not only be of interest to readers, but also stimulate thoughtful reflection on contemporary autism practice, which is littered with unproven, ineffective, and possibly harmful treatments [8]. Background: Albert Hofmann’s problem child In 1943 the Swiss chemist Albert Hofmann accidentally discovered the psychedelic properties of LSD [9]. The manner is which this discovery was made is a classic illustration of the role and value of serendipity in scientific discoveries so well docu- mented by Gest [10]. Briefly, in 1938 Hofmann produced the substance known as LSD or more technically LSD-25, so called because it was ‘the twenty-fifth substance in this series of lysergic acid derivatives’ [9, section 1.3]. It was thought that this new drug might have some potential as a circulatory and respiratory stimulant, but initial animal tests were rather uninteresting and so the project was discontinued. Five years later, Hofmann synthesized some more LSD for further testing. In the process he accidentally absorbed enough of the substance to produce the perceptual distortions for which the drug is so infamous. He reported feeling restless, dizzy, and having an extremely stimulated imagina- tion consisting of a stream of ‘fantastic pictures, extraordinary shapes with intense kaleidoscopic play of colors.’ [9, section 1.4]. These feelings and sensations, he noted, were not unpleasant. Shortly after this accident he deliberately ingested a very small amount of the substance (0.25 milli- gram) to confirm that LSD-25 was in fact respon- sible for the strange effects he had experienced a few days earlier. Within 40 minutes he began to experi- ence similar symptoms, but this time the effect was not so pleasant. Instead he found the sensations to be rather more disturbing and intense. A few additional self-experiments by Hofmann and collea- gues confirmed that LSD was indeed an incredibly powerful intoxicant even in extremely small dosages. Impressed by these powerful effects, Hofmann’s employer, Sandoz, approved further trials to estab- lish its toxicity and physiological effects. In 1947, Stoll published the results of what appears to be the first human trial, which involved 16 healthy volun- teers and 6 patients with schizophrenia [11]. He reported that the drug produced ‘very impressive disturbances of perception and visual hallucinations’ (p. 279), but also appeared to induce vegetative-like states and some motor control problems. Stoll took some LSD himself, extending Hoffman’s precedence of self-experimentation. (Parenthetically, while no substitute for the randomized controlled trial, self- experimentation has a legitimate role in treatment evaluation and may enable researchers to gain some understanding of the effects of any treatment that they seek to use with children. Gandevia [12] outlined several methodological and ethical issues that need to be considered in self-experimentation.) Under the influence of LSD, Stoll initially enjoyed the condition and felt rather euphoric. But his euphoria soon turned to depression, which lingered for several days. Depression aside, Hofmann and others at Sandoz agreed that Stoll’s trial had demonstrated some clinical potential for LSD. It was soon marketed as an experimental drug for the study of psychosis and as a possible facilitator of psychotherapy. They made the drug freely available to researchers and medical personnel for such experimental and clinical pur- poses. Several autism researchers were among those who made use of the newly available substance. The Autism/LSD studies The first public reports on the use of LSD in the treatment of children occurred in 1959 at a conference in Princeton New Jersey [13]. The conference was devoted to the use of LSD in psychotherapy and included several independent references to its use with autistic-schizophrenic children. A summary published the following year included comment on five such studies [13]. As noted by Rhead [14], while these initial reports 76 J. Sigafoos et al.lacked critical detail, the results were considered ‘quite promising in a number of cases.’ (p. 93). A more formal study by Freedman, Ebin, and Wilson appeared in print two years later [15]. It is worth considering the Freedman et al. study in some detail because their methodological approach is fairly typical to that of many subsequent LSD studies. Freedman et al. gave LSD to 12 ‘autistic schizo- phrenic’ children. The sample consisted of 10 boys and 2 girls who ranged from 5 years 11 months to 11 years 10 months of age. Varying dosages of LSD (either 50, 100 or 200mg) were given on one or two occasions. The drug was administered orally as the child arrived at school in the morning. The children were continually observed for the next several hours with ‘Careful notes... taken of all physiological and mental changes...’ (p. 39). The researchers noted that the signs of LSD inebriation became apparent within 15–30 min with the effect lasting 4–5 hours. Physiologically not too much happened. Some children became flush and their pupils dilated, but neither pulse nor blood pressure showed much change. Behaviourally, the effects varied. Three children were said to show evidence of catatonia (e.g., strange, fixed position of hands, bizarre postures, waxy flexibility of arms). None of the children ate their lunch until the drug wore off. Freedman et al.’s narrative description of the children’s behaviour under LSD includes refer- ence to increased physical contact, disappearance of physical mannerisms, and development of what were interpreted as new bodily sensations. These appar- ently new bodily sensations were evidenced by the fact that ‘...all but four of the children were observed to repeatedly stroke or move a particular area – most often the lips or mouth’ (p. 41). Psychic effects were also noted, including rapid moods swings ‘from extreme elation to extreme depression’, increased anxiety, and signs of both auditory and visual hallucinations (p. 41). The authors were primarily interested in evaluating whether LSD might promote speech, but the ‘hoped for change from muteness to speech did not occur’ (p. 44). Considering their results in light of previous research on adults with schizophrenia, the authors found ‘little hope for its [i.e., LSD’s] success in the treatment of children’ (p. 44). Despite Freedman et al.’s pessimistic conclusion, the pace of LSD research accelerated over the next few years. Their less than promising results were countered by assertions that children respond differently to psychedelic agents than adults. Children were not only said to show fewer medica- tion side effects, but they also developed tolerance more slowly and thus could receive larger doses [4]. The emerging journal literature soon included a good number of studies [4,15–21]. By 1969, the volume of literature was sufficient to warrant a systematic review [22]. However, this initial era of legitimate LSD experimentation was already coming to a close by the time this first review was published in 1969. Faced with increasing hysteria and negative publicity stemming from recreational misuse, Sandoz stopped the production and distribution of LSD in 1965 [9]. In the USA, researchers could still obtain supplies from the National Institutes of Mental Health, but the numerous bureaucratic hurdles discouraged research [5]. The last studies to examine the effects of LSD in the treatment of children with autism appeared in the early 1970s [19,21] and the second, more comprehensive review of the literature appeared in 1977 [14]. Thirty years have now lapsed since Rhead’s comprehensive review of research on LSD as a treatment for children with autism and related disorders [14]. From this historical vantage point, and given the renewed interest in psychedelic drugs for therapeutic purposes [5], it would seem timely to re-examine the initial wave of Autism/LSD studies. Consideration of the justification for — and the methods, results, and conclusions of — these studies may offer important lessons for future generations of researchers and clinicians. Justification for the LSD studies The primary justification offered for the Autism/ LSD studies was based on the logic of default. Simply put, nothing much seemed to work very well, so why not try LSD. Simmons et al. [20], for example, employed this logic for their first LSD study. After listing the range of treatments that had been tried up to that point, they correctly noted that: ‘In many instances successful treatment has been largely absent or limited to isolated behavioural changes’ (p. 1201). All seven studies included in the first systematic review of the literature [22] were justified on the grounds that ‘all known forms of treatment had been attempted without success’ (p. 46). Bender, Goldschmidt, and Siva Sanker [4] were more selective in their application of this logic. They recruited 14 children for an LSD trial on the basis of the fact that these particular children had received ‘a variety of treatments with inadequate response’ (p. 172). Presumably other children were excluded from the study because of their adequate response to some other form of treatment. This selectivity implies that LSD was not the treatment of choice and suggests a hesitancy to employ such a potent medication. Bender and her colleagues were in fact LSD in the treatment of autism 77‘... extremely cautious when first using the drug, even obtaining parents’ consent’ [23, p. 85]. It should be noted that this brief statement was the only mention of ethical issues among these LSD studies. In the main, ethical issues and parental consent were simply never mentioned. It is therefore unclear if the parents had ever been consulted or informed about the use of LSD in the treatment of their children. In fairness to the investigators, it should be noted that this situation was not unique to research involving LSD, but rather reflects the fact that in the 1960s and 1970s, procedures for obtaining ethical clearance and parental consent were not as formalized as today. Even if ethical clearance and parental consent had been obtained, it is not necessarily the case that researchers would have included these details in the formal write-up of their results. Ethical issues aside, the logic of default leaves much to be desired as a process for making treatment decisions. Evidence-based practice dic- tates that treatment recommendations should be based on the best available evidence and less on the trial and error approach associated with the logic of default [24]. Still, the logic of default was compelling at the time. Back then, 30–40 years ago, most children with autism did not respond very well to the range of treatments that had been attempted. Effective, evidence-based treatments simply did not exist. None of the biologic (e.g., electric convulsive shock, sub-shock insulin, amphetamines, antidepres- sants) or psychoanalytic treatments had met with much success and behavioural intervention was in its infancy. Today the situation is vastly different. Effective, evidence-based procedures exist for addressing many of the core behavioural deficits and excesses that define autism [25]. The most effective procedures are behavioural in orientation and based on the principles of applied behaviour analysis [26]. Indeed, early and intensive application of behavioural treatment can lead to dramatic improvement in intellectual and adaptive behaviour functioning for some children with autism [27,28]. While individuals will vary in response to such treatment, the consistently positive results from well-designed behavioural interventions make it the treatment of choice for children with autism. Given today’s solid empirical support for behav- ioural interventions, the logic of default can no longer be used to justify research with controversial treatments. A higher standard must be expected in any such research programmes that might be initiated in the future. It is not enough to compare a novel approach to no treatment or to a placebo. Rather the new approach should be compared to some well-established procedure [29], provided of course that well-established alternatives do in fact exist. In the case of autism, well-established, empirically-supported treatments exist in the form of behaviourally-based interventions. Any future research into the effects of psychedelics — or any controversial treatment for that matter — should therefore at some point include comparisons with a well-designed behavioural programme. The researchers and the research settings Several independent teams of researchers were involved in the LSD studies that followed Freedman et al.’s pioneering work [15]. Lauretta Bender and her colleagues completed the most extensive research programme in this area, which was reported in a series of papers published between 1962 and 1969 [4,17,18,23]. In the course of this programme, a total of 89 children (aged 6 to 15 years) received LSD. As Rhead noted, ‘Some children were ultimately treated with daily doses of 150g for periods as long as two years’ (p. 94). The setting for this research programme was the Creedmore State Hospital in New York. Bender’s work appeared to have served as the inspiration for another prominent research team led by James Q. Simmons and his colleagues at ULCA [19–21]. This team also conducted their research in an institutional setting. Apart from these two teams with fairly extensive research programmes, the other studies appear to have been isolated projects [e.g., 15,16]. While it is unclear if these various research- ers were in direct communication with one another, citation analysis shows clearly that these indepen- dent teams were certainly aware of each other’s work. For example, Bender et al’s first paper in 1962 [4], referenced Freedman et al. [15]. Later, in 1966, Simmons et al. [20] referenced both Freedman et al. [15] and Bender et al. [4]. In fact, Simmons et al. [20] indicated that because of the difficulty of assessing the reliability of Bender’s work there was a need to develop more objective criteria and employ better experimental designs to evaluate LSD. Their subsequent studies certainly represent a methodolo- gical improvement over the approaches used in prior studies, as described in the next section. Methodological limitations, results, and conclusions of the LSD studies The vast majority of the Autism/LSD studies had serious methodological flaws. In most cases, depen- dent variables were neither operationally defined nor objectively measured [4,15–18,23]. Experimental control was generally nonexistent in that most of the protocols involved an open trial with the drug 78 J. Sigafoos et al.
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