• Published on

  • View

  • Download

Embed Size (px)


<ul><li><p>Journal of Marital and Family Therapy 1990, Vol. 16, No. 1, 59-70 </p><p>A PSYCHOEDUCATIONAL MODEL FOR WORKING WITH FAMILIES OF AUTISTIC CHILDREN* </p><p>M. Mary Konstantareas University of Toronto </p><p>Canada </p><p>Because of the well-documented effectiveness of paradigms which emphasize parental or family pathology in understanding and intervening with dysfunc- tional children, the temptation exists for applying them to other dysfunctional populations. Autism is a pervasive developmental dysfunction with life-long adverse sequelae for the child and family. This paper reviews evidence on the biological etiology of autism and other pervasive developmental deviations, and stresses the necessity forproviding an early and accurate diagnosis for the family. The adverse implications of downplaying individual pathology and concentrat- ing on parental or family dysfunction are then discussed. The natural evolution and specific components of a psychoeducational model for diagnosing autistic children and working with them and their families are then presented. Finally, some of the advantages of this multimodal, multidiscipline model in long-term work with these pervasively dysfunctional individuals and their families are considered. </p><p>A systemic approach to understanding psychopathology has had a distinct appeal to many mental health workers because it allows for a complete and balanced view of an individual's pathological behavior. Although the relative emphasis placed on individual versus family variables differs across systemic paradigms (cf. Schwartz &amp; Johnson, 19851, by and large family therapists subscribe to the notion of the identified patient (IP) (Haley, 1980). They usually see the IP as the most vulnerable family member, whose dysfunctional behavior allows the remaining members of the family to maintain their homeostatic, albeit pathological balance. In the case of schizophrenia, for example, most systemic theorists' three main assumptions are that: (a) schizophrenia is intrafamilial rather than physical; (b) the family, in a transactional way, chooses its ill members; and (c) the illness is an advantage, in that it allows the family to maintain its homeostatic balance (Terkelsen, 1983). In this conceptualization, treatment of the IP is a futile exercise since the entire family constitutes the proper intervention target. </p><p>*An earlier version of this paper was presented at the Annual Conference of the American Association for Marriage and Family Therapy, New Orleans, October 27-30, 1988. </p><p>The research discussed has been supported in part by the Ontario Mental Health Foundation, Grant No. 899-84186. </p><p>A special word of thanks to my close collaborators Dr. Leon Sloman and Miss Soula Homatidis for their constructive comments. </p><p>M. Mary Konstantareas, PhD, is Head of Research, Child and Family Studies Centre, Clarke Institute of Psychiatry and Professor, Psychology and Psychiatry, University of Toronto, 250 College Street, Toronto, Ontario, Canada M5T 1R8. </p><p>Address all correspondence to Dr. Mary Konstantareas, Clarke Institute of Psychiatry, 250 College Street, Toronto, Ontario M5T 1R8, Canada. </p><p>January 1990 JOURNAL OF MARITAL AND FAMILY THERAPY 59 </p></li><li><p>The successful application of the various schools of systemic family therapy has been well documented with a variety of psychiatric conditions (Falloon, Boyd, McGill, Williamson, Razani, MOSS, Gilderman &amp; Simpson, 1985; Gurman, Kniskern &amp; Pinsof 1986; Haley, 1980; Minuchin, 1974). In addition, family therapy research, particularly of the still limited process variety, is already well under way (Gurman, Kniskern &amp; Pinsof, 1986). Thus, there is very little question as to the relevance, viability and fairly broad spectrum of applicability of this central therapeutic paradigm. Yet, the success and acceptance of an approach does not preclude attempts a t clarifying the limits of its spheres of application. Engaging in such an activity is usually reflective of the mature stage of a paradigm. With few exceptions (Selvini-Palazzoli, Boscolo, Cecchin &amp; Prata, 1978; Selvini-Palazzoli, Cirillo, Selvini &amp; Sorrentino, 1989), family therapists have, in fact, avoided using family therapy when a member suffers from a severe disorder originating in birth or soon thereafter, such as mental retardation and autism, or other pervasive developmental deviations (PDD) (American Psychiatric Association, 1980, 1987). </p><p>However, in our work with autistic and other PDD children, we have been frequently urged, by colleagues working within the Milan approach, to view the autistic childs severe pathology as having been caused by dysfunctional intrafamilial patterns. In addition, one is still aware of clinicians trained within the psychoanalytic tradition who consider autisms causation to be at least partly psychogenic (DeMyer, Hingtgen &amp; Jackson, 1981). Thus, family work within this tradition is frequently undertaken and the childs problem is reframed as being partly a parental, mainly maternal, rejection or mismanagement of the child. </p><p>One of the aims of this paper is to provide a rationale for avoiding the temptation of using a family systems paradigm or a psychoanalytic conceptualization with these families, no matter how appealing we find it in our work with genuinely dysfunctional families. There may, indeed, be cases where the IP is, in fact, the member of the family who has unwittingly chosen to play out his or her pathology or where parents are, in fact, rejecting or mismanaging the child. This is not to deny that families with autistic children are not as susceptible to dysfunction as other families, and may not benefit from a systemic form of intervention or other input at some point in their evolution as a family. It is, rather, to stress that it is not family dysfunction or parental rejection which can lead to a condition as catastrophic and pervasive as autism. Although family or parental pathology may also be present, such pathology may be secondary or reactive to the stress and special non-normative adaptations members of the childs family may have to make (cf. Bristol &amp; Schopler, 1983; DeMyer, 1979; Konstantareas &amp; Homatidis, 1988). In such cases, parsimony would require that attempts be first directed at amelio- rating the childs condition. </p><p>A body of rapidly accumulating evidence has, in fact, been progressively more clearly pointing to a biological etiology in autism and other PDDs. To substantiate this point, a brief overview of this evidence will be presented, followed by an outline of a number of adverse implications which may accrue to a family if their autistic child is not promptly diagnosed. In this respect, any model of intervention which de-emphasizes appropriate individual diagnosis and reframes the problem as due to parental or family dysfunction will be unhelpful to the family. We shall, finally, present the elements of a psychoeducational model of dealing with autistic children and their families which also adopts a systemic orientation, but one in which the influence of the childs pathology on the rest of the family assumes a central role. </p><p>EVIDENCE ON THE BIOLOGICAL CAUSATION OF AUTISM Historically, although Kanner succinctly differentiated autism from schizophrenia </p><p>of childhood as early as 1943, the term autism continued to be used interchangeably </p><p>60 JOURNAL OF MARITAL AND FAMILY THERAPY January 1990 </p></li><li><p>with such other labels as symbiotic psychosis, infantile psychosis and schizophrenia of childhood (Rutter, 1978). More crucially, until relatively recently, the presence of overt neurologic dysfunction such as seizures or EEG abnormalities, for most clinicians, precluded the diagnosis of autism (Eisenberg, 1966). Children with hard and soft) signs of neurologic damage were considered as either brain damaged or mentally retarded. By contrast, autistic children were thought to be of normal intelligence. Such children, according to the prevailing thinking, apparently chose not to display, or were unable to reveal, their masked abilities because of the poor socioaffective reception they received from their parents, particularly by the mothers (Bettelheim, 1967). Thus, the children were thought to be biologically intact but psychologically impaired. Treatment under this conceptualization consisted of providing the autistics with competent and warm mother substitutes. Current evidence has shown that, given proper assessment devices and sensitive handling by the examining psychologist, autistic children can be tested. However, as many as 80% of them receive scores within the range of retardation (DeMyer et al., 1981). Moreover, when they do have the cognitive capacity, they do perform to the best of their ability. Interestingly, cognitive ability appears to be one of the best prognostic indicators of outcome (DeMyer, Barton, DeMyer, Norton, Allen &amp; Steele, 1973; Konstantareas, 1987). </p><p>Autistic children, however, are not merely intellectually impaired the way mentally retarded children are. They also present with three clusters of symptoms over and above their cognitive delays: (a) severe impairment in socioaffective functioning and reciprocal social interaction, expressed in impaired imitation, abnormal social play and poor peer interaction; (b) qualitative impairment in verbal and nonverbal communication, reflected in mutism, impoverished language, poor speech production and stereotypical and bizarre use of language and imaginative activity; and (c) a markedly restricted repertoire of activities and interests manifested in stereotyped body movements, distress upon environmental change and an insistence upon following routines. </p><p>That these pervasive dysfunctions are not likely to be due to psychosocial factors has been cogently presented elsewhere (cf. DeMyer et al., 1981; Rutter &amp; Schopler, 1987). Suffice it to say that severe environmental deprivation has been linked to a variety of psychiatric disorders, but not to autism. As well, the parents of autistic children produce other, perfectly competent offspring and, thus far, no evidence has been provided on psychiatric deviance in the parents (DeMyer er al., 1981). More importantly, there is considerable research pointing to biological causation present, usually since birth. In brieE </p><p>1. As determined by MZ-DZ twin comparisons, a subgroup of autistic children appear to have inherited their autism (Folstein &amp; Rutter, 1977; Ritvo, Spence, Freeman, Mason-Brothers &amp; Marazita, 1985; Steffenburg, Gillberg, Hellgren, Andersson, Gill- berg, Jakobsson &amp; Bohman, 1989). </p><p>2. The developmental histories of autistic children are more likely to contain pre- conception, prenatal and perinatal complications, with particular elevation of maternal viral infection during the first trimester of embryogenesis (Chess, 1977; Deykin &amp; MacMahon, 1980) and mid-trimester bleeding (Torrey, Hersh &amp; McCabe, 1975). </p><p>3. Neonatal complications, notably encephalitis and other viral infections, also feature prominently in these childrens early histories. In fact, DeLong, Beau and Brown (1981), reported an acquired reversible autistic syndrome after acute encephalopathy in three otherwise normal children who were 5-, 7.5- and 11-years old at the illness onset, an age well beyond the period for diagnosing autism. </p><p>4. Autism has been found to coexist with a variety of structural, metabolic, func- tional and other abnormalities of the central nervous system (CNS) such as Downs syndrome, Phenylketonuria (PKU), Moebius syndrome, Gilles de la Tourette, tuberous </p><p>January 1990 JOURNAL OF MARITAL AND FAMILY THERAPY 61 </p></li><li><p>sclerosis, lactic acidosis and neurofibromatosis, among others (See Coleman &amp; Gillberg, 1985, for review). </p><p>Finally, with rapid advances in imaging technologies in recent years, some tantaliz- ing new findings have emerged, such as, the significant underdevelopment of the cerebel- lum in nonretarded autistic individuals through the use of magnetic resonance imaging (Bauman &amp; Kemper, 1985). In sum, autism is currently viewed as the final behavior pathway for a variety of biological insults to the CNS. </p><p>This evidence, on a biologic etiology, is further supported by the relative effective- ness of systematic interventions based on social learning theory and operant condition- ing attempting to assist these pervasive delayed and dysfunctional children. First, Lovaas, Berberich, Perloff and Schaeffer (1966) taught autistic children to speak, relying on imitation and reinforcement. This was the first breakthrough in the treatment of autistic children who had hitherto been either institutionalized, along with the mentally retarded, or found themselves in the back wards of psychiatric facilities. Although a breakthrough of sorts, it also heralded the beginning of asking parents and families of autistic children to become active co-therapists. In fact, in a follow-up of their original work, Lovaas, Koegel, Simmons and Long (1973) clearly demonstrated the greater gains achieved when the parents participated in treatment. Thus, parents were frequently called upon to engage in the 24-hour care required in dealing with severely disturbed, tantruming, self-abusing or aggressive autistic children. More recently, Lovaas (1987) reported on the success of early intervention with preschoolers urging clinicians to start early and to rely on extensive daily training. Because as many as 50% of autistic children remain mute or minimally verbal, despite extensive speech training efforts, an alternative to speech-only training was independently initiated by members of our team (Webster, McPherson, Sloman, Evans &amp; Kuchar, 1973) and by therapists a t The Michael Reese Hospital (Creedon, 1973). Simultaneous communication training combines signs and speech, and has been shown to be effective with autistic children (Remington &amp; Clarke, 1983), but, more specifically, the nonverbal and concomitantly lower functioning subgroup (Carr, 1979; Konstantareas, Oxman &amp; Webster, 1977). Insofar as communica- tion is the cornerstone to any skill acquisition, speech-only or simultaneous communica- tion training are the two main paradigms to treatment along with extensive efforts to manage and control, through behavior modification, occupational therapy, imitation training, etc., some of the more difficult and visible symptoms autistic children present. </p><p>In sum, over a span of almost 30 years, extensive research on the etiology of autism and its treatment have led clinicians and researchers to conclude that autism is a lifelong, severe dysfunction due to subtle, and at times clear-cut neurologic sequelae and that it requires early and competent identification and prompt intervention to remedy pervasive deficits. </p><p>ADVERSE IMPLICATIONS OF AVOIDING INDIVIDUAL DIAGNOSIS </p><p>Let us now see how any approach which deflects attention to parental or family contributions can potentially have adverse implications for the autistic child and his or her family. To enumerate some of the possible negative concomitants: </p><p>1. Not providing...</p></li></ul>


View more >