Neurodiversity: Conflicting Perspectives on Autism
by Katherine A. Cohen


First defined in the early 1940s, autism diagnosis increased dramatically in recent years, approaching 1 percent of total United States population. This paper examines the active and deliberate creation of autism as a disease and explores a reactionary neurodiversity perspective that rejects this disease status. Neurodiversity advocates contend that while autism may be a cognitive abnormality, it is not pathological and requires no cure. The controversy surrounding the status of autism as a mental disease brings to light questions concerning the construction of personhood as well as the reduction of people to symptoms. The future of the two perspectives on autism raises valuable questions with respect to the consequences of framing mental impairments as disease in a wider social perspective. 



First defined by Austrian psychiatrist and physician Leo Kanner in the early 1940s, autism was conceived as a break from schizophrenia, the early beginnings of mental disturbance rendering the disorder distinct (Wolff 2003).  Autism has since entered the American Psychiatric Association’s Diagnostic and Statistical Manual, Fourth Edition (DSM-IV) and World Health Organization’s International Classification of Diseases, Tenth Edition (ICD-10); it has expanded to include Asperger’s syndrome, a high functioning type of autism, and atypical autism, which may cause significant life-disturbance or abnormal neural function while failing to meet a satisfy diagnostic criteria for autism. This family of disorder is referred to collectively as “pervasive developmental disorders—not otherwise specified” (PDD-NOS) in the DSM-IV and ICD-10 colloquially referred to as “autism spectrum disorders” (ASD) which, while not explicitly named in the DSM, is preferred by physicians. The frequency with which these spectrum disorders are diagnosed has increased dramatically in recent years, approaching 1 percent of the total population in the United States in 2009 (American Academy of Paediatrics 2009; Baird et al. 2003).  This paper will henceforth use the terms autism and autistic to refer to all affected and all afflictions on the so-called autism spectrum, including Asperger’s syndrome.

A diagnosis of autism is usually made in early childhood, prompted by suspicions of delayed language development or abnormal interaction skills. In general, people with low-functioning autism will be unable to live independently, unable to complete basic life tasks (i.e. cooking or laundry) and unable to maintain employment. Many are unable to communicate verbally, although some are able to use laptop computers and text-to-speech devices to great effect. Those with high-functioning autism are usually considered to be of average or normal intelligence and are able to live in most respects just as the non-autistic person would. Their impairments are usually limited to social unease or aloofness; they usually prefer to concentrate social activities to arenas of mediated interaction, namely the Internet.

The paper sets out three objectives. Firstly, to examine the development of a disease conception of autism as a direct result of efforts by emergent concerned groups in the sense used by Callon and Rabeherisoa (2008) comprised mainly of the parents of autistic children.  The second objective examines the rise of the reactionary “neurodiversity movement, which promotes a disability model of autism and rejects the disease model. The final objective examines this controversy and the questions it raises about the framing of disease and illness and medical reductionism.

That autism is considered an organically originating disease is an achievement of psychology: it was originally thought to be the result of “pathological mothering” and other adverse environmental factors in early childhood (Bumiller 2009).  Research into the causes and prognosis of autism was in large part initiated as a result of publicity (awareness campaigns) and fundraising efforts by parents and teachers of autistic children. Members of this emergent concerned group are defined by their shared efforts to emphasize that a) there was something biologically unique about autistic children; b) that it was an undesirable and involuntary condition that would benefit from effective treatment and/or cure; and c) that autistic children required and were entitled to receive medically insured specialized and intensive occupational and behavioural therapy to cope with their environments (; Callon & Rabeherisoa 2008). Through online information databases and awareness campaigns, this group sought to aid and incite research into the causes of autism, predictably effective treatments and, ultimately, a cure. To present autism as the result of some organic pathology is advantageous to the extent that it legitimates for autism the same research mandate as exists for other childhood diseases-- it helps to collect a condition with a spectrum of symptom severity and presentation under one term, facilitating fundraising efforts from the previously uninformed public and support the writing of research grants necessary for medical professionals to actually conduct meaningful research.

Efforts to this extent have been promoted most prominently by the association “Autism Speaks,” an online information database for parents and the public that also actively promotes autism awareness, raises funds for research, and encourages the participation of parents of autistic children in scientific research efforts (i.e. by providing specific reports of their child’s behaviour as it relates to autism) ( These efforts have been overwhelmingly successful; much recent research has been oriented towards brain imaging to explore the role of and abnormalities in neural networks in the autistic brain as well as genetic coding in efforts to decipher genetic mutations responsible for neural defects as well as to explore potential heredity of the condition (Nicholas et al. 2007; Soulières et al. 2009; Belmonte et al. 2004).

The “neurodiversity” movement developed in much the same way as the “disease model” group in reaction to its successful efforts to promote research and effective treatment for autism.  Proponents, a vocal minority, are united in their claims that a) autism does not require a cure; b) autism is not necessarily indicative of a reduced capacity for intelligence; and c) autism is better conceived of as a disability along the lines of deafness, in the sense that while their ability to communicate with the outside world (or, with “neurotypicals,” as the movement calls the non-autistic) is limited, their intellect and ability to comprehend their environment is not (Jurecic 2007; Wolman 2008;;  Supporters of the movement, a significant portion of whom place themselves on the autism spectrum (affectionately referring to themselves as “auties” and “aspies”) interpret the search for a “cure to autism” as a denial of personhood in to someone in an autistic (“diseased”) state. The community’s mandate for “civil rights,” as they view the acceptance and tolerance of autism as a communication disability not unlike deafness, contend that a cure for autism is at best unnecessary and at worst unethical (;; Jurecic 2007).

In spite of extensive research, the origins of autism remain obscured; searches for physical lesions of the brain have been unfruitful and the existence of responsible genetic mutations remains to be satisfactorily proven.  Due to this absence of discernable physical indicators, autistic disorders are diagnosed solely on the basis of demonstrated behaviours (Baird et al., 2003; Cox et al. 1999; Maton et al. 2007).  Although a single diagnostic schedule has not been standardized, a DSM-IV compatible diagnosis of autism may be made when a person displays deficiencies in social interaction and communication skills as well as sensory input disorders which commonly include repetitive and compulsive self-stimulation (“stimming”) and sleep and eating related abnormalities.  (Lord & Risi 1998; Baird et al. 2003).

Crucially constitutive of the debate include medical professionals (clinicians, psychiatrists, and researchers), indirectly affected non-collected laypersons (immediate family of autistics, teachers), and directly affected individuals (i.e. those on the autistic spectrum). I suggest, however, that the most important actors in shaping the debate between “disease” and “neurodiversity” models are non-human actors in the form of a) the absence of a satisfactory physical anomaly or diagnostic test for autism and b) online information forums.

The role of Internet-based information forums the establishment and maintenance of interest and activist groups on both sides of the aisle has been significant, especially for the neurodiversity contingent. The neurodiversity movement is comprised in large part of people who are themselves autistic and are unable or uncomfortable navigating and initiation more traditional information collectives, which generally requires just the sorts of communication and social skill sets those with autism characteristically lack (Lord and Risi 1998; Baird et al. 2003). 

The absence of useful information regarding the origins and prognosis of autism, as a discrete uncertainty that is one of the most important constructive elements (“actors”) of the development of the neurodiversity reaction. This lack of information is rather unique among diseases, most of which either follow a predictable trajectory or arise from a known cause or source—autism lacks both. Because the absences is in this sense unique, it’s absences is palpable enough to other involved actors that its influence can be understood to act upon the rest of the network in the same way that a more tangible actor would. Although there has been some speculation on the functional differences between neurochemistry in autistic and non-autistic brains, no unified theory has emerged.  Neither physiological and genetic determinants nor causal mutations or neural lesions have been identified in a definitive causal sense (Bumiller 2009).  Diagnostic apparatuses remain bases on behavioural observations, sometimes by untrained laypersons; the subjective nature of such diagnostic schedules remains significantly more subjective than a laboratory-tested physical diagnostic sample (Baird et al. 2003; Lord & Risi 1998; Moore & Goodson 2003; Matson et al. 2007). I suggest that this general failure of the medical research community to find universally or near-universally applicable diagnostic tools and satisfactorily validated causal mechanisms of autism, that this absence, is extremely significant in the shaping of the neurodiversity debate. 

This absence opens the door for speculation into the nature of autism as a disease that ethically should be cured. The absence shapes the perspectives that can be taken of autism; it is necessary to the development of the conception of autism as an impediment of communication but not of intellect. At the same time, this absence of information serves as a mandate for further research to the medical (disease) perspective.  Because the absence of information exists, the need for an emphasis on research into causes and cures exists, and this goal requires the rigid categorization of autism as a disorder or disease to secure support for expensive studies.

The handbooks of psychiatric medicine, the DSM-IV and ICD-10, conceive autism as a mental disorder in the disease model, that is to say, among its basic operation assumption on the nature of autism is the idea that the state of autism is fundamentally abnormal and undesirable, and ethics require that every effort be made to alleviate symptoms and lessen the disabilities resulting from autism. The most widely used diagnostic schedules for diagnosing autism in children are the Autism Diagnostic Interview-Revised (ADI-R), and the Childhood Autism Rating Scale (CARS) (Lord & Risi 1998). In all cases, the schedules rely on the observation of behaviour the potentially autistic over a discrete period of time by parents in a home setting or professionals in a clinical setting. Although the results of one test are usually upheld by the other, the underlying ambiguity of terminology and ultimate subjectivity inherent in both assessments 

A distinction in the autism diagnosis is generally made between high-functioning autism (also called Asperger’s syndrome, though the term seems to be falling out of favour) and low-functioning (not otherwise qualified) autism.  In this nomenclature, functioning refers to the ability of neurons to communicate interregional, rather than the ability of the autistic person to function in everyday life (Belmonte et al. 2004; Soulières et al. 2009). Cleavage between the two is generally made on the capacity of the autistic to communicate with his environment in a coherent and coherent fashion. This communication deficiency may include impairment or retardation of early childhood verbal language acquisition, a lack of comprehension of non-verbal communication skills (i.e. instrumental pointing), and regression of communicative ability at any age (Baird et al. 2003). In the majority of cases, this deficit in communication and inability to interact with outside environment is thought to cause or correlate with below average intelligence (Dawson et al. 2007).

The disease model has the advantages of implicitly encouraging and facilitating research into the origins and (lately) the genetic bases of autism.  There is evidence that intensive therapies and small-group special education classes may be beneficial to the skill acquisition and refinement of autistic children (Eikeseth et al. 2002). By establishing autism as a collection of pathological brain abnormalities, people defined as autistic may be entitled to certain privileges or services (i.e. in the school systems) that would not otherwise be justifiably necessary nor likely provided. An agreed upon disease category is essential to the accumulation and dissemination of relevant information in therapeutic and research settings (Rosenberg 2002).

It is important to note that while the neurodiversity movement opposes the conception of autism as a disease, it does not oppose the categorization the categorization of people as autistic, as this confers a sense of disability or of characteristic features (c.f. deafness and homosexuality). The conception of autism as a disease is rejected because such a status implies the idea that an autistic person is “sick” (Rosenberg 2002). They argue that autistic mind, while deficient in some respects, also allows a unique and advantageous cognitive perspective.

Opponents of the disease model of autism cite the tumultuous journey of homosexual through the conferences of the APA, that most regrettable blemish on the DSM’s résumé, as a reminder that validation by the authoritative bodies does not necessarily confer accuracy of designation. Homosexuality as a metal state was once widely considered by the medical community to be a potentially curable mental disease and stood in the DSM as such, until, under pressure from activist groups and relevant lobbyist groups, it was voted out of the Manual in the 1970s (Silverstein 2008). This case emphasizes both the construction-through-consensus of mental illness and represents a precedent for a mental disease to be reconceived as simply a benign difference (Atkinson 1995).  The neurodiversity movement hold the ultimate goal of reinventing autism to be perceived as a disability in the model of deafness or blindness, where special accommodations are necessary for communication but a “cure” per se is neither required nor necessarily desirable.

Autism research has been overwhelmingly focused on examination of the neurochemical/neuroelectric activity by means of PET (positron emission topography) and fMRI (functional magnetic resonance imaging) brain scans. What is known is that this chemistry, the “connected-ness” of one “specialized region” of the brain to another within the context of an overarching whole. (see: Panksepp 1979; Belmonte et al. 2008; Just et al. 2004; Soulières et al. 2009). Results of these scans have been able to establish that there is a perceivable and measurable difference in the neural activity of autistic and non-autistic normal brains (Dichter et al. 2009; Soulières et al. 2009). This is as far as technology has been able to empirically establish; brain imaging is unable to establish or test for causes of neural-activity difference nor can it decipher the relationship between brain activity and the specific symptoms an autistic will exhibit. Recent studies have also attempted to explore the role of genetic elements in the development and heredity of these functional neural abnormalities (Nicholas et al. 2007).

Mainstream theories of autism are fragmented and many, mainly attempts to examine the physical structure and anatomy, neurochemistry, neural network function and central coherence of information interpretation cerebral areas (Belmonte et al. 2008).  A common underlying hypothesis is that (by whatever mechanism) certain parts of the brain responsible for the processing of information into comprehensible mental image or understanding of a situation that are normally in contact with each other, are not in communication in the autistic brain (ibid 2008; Dichter et al. 2009).

Laurent Mottron of the Université de Montreal proposes a theory of the processing of information in an autistic brain that concludes that while information is processed differently than in a non-autistic brain, capacity for intelligent thought is not diminished and may in some domains be superior to that of the average non-autistic (Mottron et al. 2006).  His initial ideas are the end results of a case study and comparative analysis of savant, E.C., who possessed superior graphic drawing skills alongside deficient social skills characteristic of high-functioning autistics (Mottron & Belleville 1993). Savants are people who score on the autistic scale, having at least a mild incapacity for communication, while simultaneously presenting a genius or master level in a certain discipline (i.e. mathematical algorithms or music). E.C. had scored +5 on the Rimland Behaviour scale, a behaviour-based evaluation for autism diagnosis widely used at the time; the average score of a non-autistic person on the same scale is -20 (ibid. 1993).  Through observation of the differences in performances between E.C. and non-autistic subjects on a variety of spatial information comprehension tasks as well as through analysis of E.C. method’s of drawing, the study suggests that E.C.’s mind, unlike the non-autistic mind does not exhibit a preference for “global” form of visual information. In other words, when the unaffected brain interprets visual information it can decipher between “local” information (i.e. keys on a flute) and “global” information (i.e. the flute as a whole), and will generally prefer the global form. To use the example of a flute, when prompted to draw the instrument, a non-autistic person would generally begin by drawing the body of the flute, then adding the keys and other piece details later; E.C. in contrast, would draw the keys of the flute in succession, the body of the flute appearing only as its outline intersects with the outline of the keys (Mottron & Belleville 1993). The study does not attempt to create a generalizable theory, but does tentatively suggest that whatever causes the global-local abnormalities in E.C.’s processing of visual information may also be at the root of his other (characteristically autistic) social impairments and other compulsive and/or repetitive behaviours (ibid. 1993).

Mottron and his colleagues later refined their model of hierarchization deficit in information comprehension in autistic brains versus non-autistic brains with their “enhanced perceptual functioning” (EPF). EPF represents a break from the prevailing Weak Central Coherence theory of the autistic brain that hypothesize regions of the brain responsible for language have fewer and weaker connections within the region and with other brain regions that non-autistic brains (i.e. those with normal functional capacity) and that affected brains lack a centralized comprehension disallowing an ability to conceptualize coherent “wholes” from pieces of information (Happé & Frith 2006; Mottron et al. 2006; Just et al. 2004; Belmont et al. 2004).  The final revision of the EPF model suggests that early and low-order perception takes precedence in the autistic brain: in tasks requiring social behaviour, the primary perceptual regions of the brain (occipital or occipital-temporal lobes) is relatively over stimulated, while the parts of the brain dedicated to “higher-order tasks,” like imagining a particular situation from a different perspective, (the fusiform face area) are relatively less active than in the brain of a non-autistic person exposed to the same situation.  The EPF model also reinforces the global-local hierarchization inversion discussed above with respect to Mottron’s case study of the savant E.C. (Mottron et al. 2006).

The importance of Mottron’s and his colleague’s suggestions are in the fact that they operate under the assumptions that while the neural structure and comprehension structure in the autistic brain is dissimilar to a non-autistic brain, it does not necessarily suggest inferiority; the studies often emphasizes the advantages of autistic subjects in particular cognitive tasks nor do they recommend treatment (Mottron & Belleville 1993; Mottron et al. 2006).

This debate over the status of autism as a disease raises important theoretical questions over the importance of disease framing and medical reductiontionism. For the sake of simplicity, the disease model must in many respects consider autistics as a homogenous group defined principally by their condition.  The danger here is that people are reduced to “being” their condition, to the extent that “autism” as a discrete entity becomes the what is studied and treated; therapies are prescribed to symptoms rather than to human patients (Epstein 2007, ch. 7).  Within the neurodiversity movement, a primary issue is the idea of legitimate “personhood” (Wolman 2008;  Proponents of the neurodiversity model argue that the disease model of autism assumes that an autistic mind is “damaged” in such a way that an autistic’s intelligence is disregarded or deemphasized autism as a disease in the sense that such a diagnosis implies a reduction of communication skills, independent living skills, and depressed intelligence

The neurodiversity movement has also raised questions about the role of diagnosis in the construction (or destruction) of personhood.  They argue that a diagnosis of autism is (wrongly) assumed to correlate with reduced intelligence and limited perception and comprehension of environment. These assumptions reduce autistic persons to their inabilities; a person with autism becomes simply autism as a removed entity. Carlos Novas and Nikolas Rose (2000) have written about the growing tendency of the medical community to reduce a person to their genetic makeup, the idea of somatic individuality, wherein people are born “genetically at risk;” the fateful mutation lies not just in their genes but contaminates their whole personhood. Proponents of the neurodiversity movement fear that an emphasis on an “autism disease” reduces an autistic child to his defective mental hardwiring (;; Wolman 2008).  Videos by mainstream autism awareness group Autism Speaks present autism as a separate entity, an enemy that must be fought[1].  Opponents of Autism speaks and the disease model contend that the focus on autism as an interloper in the minds of affected children ignores the benefits of alternate perspectives autism can provide and the exceptional talents that sometimes result.

 To what extent is the reductionism resulting from framing techniques used by Autism Speaks and similar organizations unavoidable? Is this a case of “hate the game, not the player?”  The medical world, including health insurance policy and government-mandated benefits, operates within an evidence based medicine (EBM) framework. EBM strives to objectify information produced in clinical trials and to consolidate and verify (through controlled trials) experiential and clinical knowledge, in doing so attempting to discover the most effective and efficient treatments. It has been argued that this emphasis on clinical trials, guidelines, and overall efficiency removes the patient from his disease; the disease and the doctors act in the same world while the patient remains in the lay arena (Mykhalovskiy &Weir 2004).  Research must operate within this arena of EBM; research grants must be written to focus on a discrete medical entity. Within the framework of evidence-based medicine, a disease framework may be necessary to initiate and carryout research on autism.

In conclusion, both the now-mainstream model of autism as a disease and the newer reactionary neurodiversity movement are the result of efforts from similarly constructed but differently oriented emergent concerned groups (Callon & Rabeharisoa 2008). Internet communication fora and information databases for laypersons as well as the absence of conclusive answers about the origins and characteristics of autism as a disorder are integral actors in shaping both the concerned groups themselves and the shape given to their causes. The emerging controversy surrounding the status of autism as a mental disease brings to light questions of personhood and reductionism of people to their pathologies and/or symptoms. The future of the two perspectives on autism will be a fruitful arena for insight into the consequences of a disease-framework in mental illness. 



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