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1. |
Preface |
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Mental Retardation and Developmental Disabilities Research Reviews,
Volume 1,
Issue 2,
1995,
Page 87-88
Travis Thompson,
Stephen R. Schroeder,
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ISSN:1080-4013
DOI:10.1002/mrdd.1410010202
出版商:John Wiley&Sons, Inc.
年代:1995
数据来源: WILEY
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2. |
Functional assessment and intervention in community settings |
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Mental Retardation and Developmental Disabilities Research Reviews,
Volume 1,
Issue 2,
1995,
Page 89-93
Jeffrey R. Sprague,
Robert H. Horner,
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摘要:
AbstractFunctional assessment has emerged as an important strategy for designing effective interventions for serious problem behavior. A comprehensive functional assessment identifies the behavior of concern, stimuli correlated with the onset and maintenance of the behavior, features of the setting in which the behavior occurs, and behaviors (typically communication) that may serve to replace the problem behavior. We present a historical and modern context for functional assessment and, in juxtaposition to this, discuss the purposes of functional assessment as a tool for researchers and practitioners. We review the current range of functional assessment applications, emphasizing the strengths and limitations of each; propose needed extensions of existing functional assessment methods; and discuss the critical role of functional assessment in designing effective community‐based behavioral interventions. © 1995 Wiley‐Liss,
ISSN:1080-4013
DOI:10.1002/mrdd.1410010203
出版商:John Wiley&Sons, Inc.
年代:1995
数据来源: WILEY
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3. |
Biological setting events for self‐injury |
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Mental Retardation and Developmental Disabilities Research Reviews,
Volume 1,
Issue 2,
1995,
Page 94-98
Edward G. Carr,
Christopher E. Smith,
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摘要:
AbstractSelf‐injurious behavior typically occurs in response to specific antecedent stimuli that predict the occurrence of such desirable consequences of the behavior as obtaining attention from others, escaping aversive situations, and securing preferred foods, objects, and activities. Setting events constitute an additional controlling variable, altering the probability that a specific antecedent stimulus will evoke self‐injury. We discuss the influence of several biological factors, including menses, otitis media, fatigue, allergies, and constipation, that may serve as setting events. We also present a model which suggests that these events alter the functional properties of the antecedent stimuli that control self‐injurious behavior, thereby strengthening the specific consequences that maintain the behavior. One implication of this model is the likelihood that effective intervention will have to have multiple components, addressing both the biological and environmental variables that control the behavior. A second implication is that greater collaboration between medical and psychological or educational practitioners will be necessary in order to address the multiple factors that affect self‐injury. © 1995 Wiley
ISSN:1080-4013
DOI:10.1002/mrdd.1410010204
出版商:John Wiley&Sons, Inc.
年代:1995
数据来源: WILEY
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4. |
Rodent models of mental retardation: Self‐injury, aberrant behavior, and stress |
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Mental Retardation and Developmental Disabilities Research Reviews,
Volume 1,
Issue 2,
1995,
Page 99-103
Richard E. Tessel,
Stephen R. Schroeder,
Christopher J. Stodgell,
Pippa S. Loupe,
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摘要:
AbstractThis paper reviews the research on three animal models related to self‐injurious behavior (SIB), stereotypy, and aggression and their susceptibility to stress. These studies support the importance of stress and differences in organic dysfunction in the etiology, maintenance, and topography of SIB and their relationship to stereotypy and aggression. Several organic risk factors associated with mental retardation also increase the susceptibility to manifestation of SIB and related behaviors. © 1995 Wiley‐Liss,
ISSN:1080-4013
DOI:10.1002/mrdd.1410010205
出版商:John Wiley&Sons, Inc.
年代:1995
数据来源: WILEY
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5. |
Bio‐behavioral diagnosis and treatment of self‐injury |
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Mental Retardation and Developmental Disabilities Research Reviews,
Volume 1,
Issue 2,
1995,
Page 104-110
F. Charles Mace,
Joyce E. Mauk,
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摘要:
AbstractSelf‐injurious behavior(SIB) in individuals with mental retardation is a severe behavioral disorder that has significant social and medical consequences. Although considerable research evidence indicates that SIB can be maintained by either environmental contingencies or biologic conditions, integrative diagnostic and treatment models have yet to be developed. We have piloted a bio‐behavioral diagnostic and treatment model to classify and subtype cases of SIB, leading to the selection of specific behavioral or pharmacologic treatments. A functional analysis defines SIB as operant, possibly biologic, or mixed operant and possibly biologic. Subtyping within these classes is based on the delineation of specific operant functions and the clinical characteristics of the individual patient. Our preliminary research suggests that this empirical decision‐making model can lead to specific treatments that are effective and that reduce the incidence of nonresponders to behavioral intervention and medication. © 1995 Wiley‐L
ISSN:1080-4013
DOI:10.1002/mrdd.1410010206
出版商:John Wiley&Sons, Inc.
年代:1995
数据来源: WILEY
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6. |
Model for reduced brain dopamine in Lesch‐Nyhan syndrome and the mentally retarded: Neurobiology of neonatal‐6‐hydroxydopamine‐lesioned rats |
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Mental Retardation and Developmental Disabilities Research Reviews,
Volume 1,
Issue 2,
1995,
Page 111-119
George R. Breese,
Hugh E. Criswell,
Gary E. Duncan,
Sheryl S. Moy,
Kevin B. Johnson,
Dean F. Wong,
Robert A. Mueller,
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摘要:
AbstractSelf‐injurious behavior (SIB) remains a serious problem among the mentally retarded because no known pharmacological agents block this behavior. This symptom is especially severe in Lesch‐Nyhan syndrome (LNS), a genetic disorder associated with HPRT deficiency. Because the prominent neurobiological deficit in LNS is a loss of dopaminergic neurons, reduction of dopamine with 6‐hydroxydopamine (6‐OHDA) in rats during their development is proposed as a model of the dopamine deficiency in LNS and in mentally retarded individuals with SIB who may have this neurotransmitter deficiency. In behavioral testing of this model, dopamine agonists that activate D1‐dopamine receptors induced SIB in adult rats with neonatal 6‐OHDA‐dopamine lesions, a change not seen in rats lesioned as adults. SIB also has been observed when muscimol is microinjected into the substantia nigra reticulata (SNR) of the neonatal‐6‐OHDA lesioned rats. D1‐dopamine antagonists, as well as NMDA antagonists, have been found to block the SIB induced by L‐DOPA in these neonatally lesioned rats. In addition to the reduced dopamine, LNS patients also have an increased striatal serotonin content, as do rats neonatally lesioned with 6‐OHDA. Activation of serotonergic receptors with m‐chlorophenylpiperazine has increased oral activity in neonatal‐6‐OHDA‐lesioned rats; destruction of serotonin‐containing neurons has blocked this effect caused by a D1‐dopamine agonist. These data suggest that serotonin and corresponding serotonin receptors contribute to dysfunctions in the neonatal‐6‐OHDA‐lesioned model. This work provides background support for the hypothesis that neonatal reduction of dopamine results in increased vulnerability to SIB as a result of adaptation within a neural circuit in the brain involving D1‐dopamine receptors, the SNR, and glutamate‐and serotonin‐containing neurons. Functional mapping in neonatally lesioned rats using14C‐2‐deoxyglucose (2‐DG) uptake and Fos‐like immunoreactivity (Fos‐L1) has implicated the SNR, entopeduncular nucleus, globus pallidus, and subthalamic nucleus in the action of a D1‐dopamine agonist. In addition, a generalized increase in Fos‐L1, but not 2‐DG uptake, is also induced in the striatum by a D1‐dopamine agonist. The action of CGS‐19755 and MK‐801, NMDA antagonists, on the accumulation of Fos‐L1 in the striatum induced by a D1‐dopamine agonist also has been examined. Whereas CGS‐19755 blocked the increase in striatal Fos‐L1 induced by the D1‐dopamine agonist, MK‐801 did not. Because both drugs block SIB in the rat model, these findings suggest that the glutamatergic neuronal system that contributes to SIB is not associated with the striatum. The research being undertaken with the model of neonatal dopa‐mine reduction may suggest new therapeutic approaches to the SIB observed in developmental disorders
ISSN:1080-4013
DOI:10.1002/mrdd.1410010207
出版商:John Wiley&Sons, Inc.
年代:1995
数据来源: WILEY
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7. |
Clinical trials of D1and D2dopamine modulating drugs and self‐injury in mental retardation and developmental disability |
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Mental Retardation and Developmental Disabilities Research Reviews,
Volume 1,
Issue 2,
1995,
Page 120-129
Stephen R. Schroeder,
Ron G. Hammock,
James A. Mulick,
Johannes Rojahn,
Philip Walson,
Will Fernald,
Patricia Meinhold,
Geeta Saphare,
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摘要:
AbstractWe review the rationale for conducting clinical trials of D1and D2dopamine modulators for self‐injurious behavior (SIB) among people with mental retardation and developmental disabilities. We include a brief history of the relevant behavioral research on SIB, the psychopharmacology of neuroleptic drugs for SIB, pharmacotherapy for SIB based on dopamine function, treatment for SIB with neuroleptics, SIB and dopamine supersensitivity, and the D1dopamine hypothesis and SIB. We also present controlled case studies of the use of clozapine to treat chronic, refractory SIB in three individuals with profound mental retardation. One was a dramatic responder at 225 mg per day; one was a partial responder at 300 mg per day; and one showed a decrease in stereotypy, but not SIB, at 100 mg per day. Studies from rats, monkeys, and humans support the hypothesis that the D1dopamine receptor system in the nigrostriatal pathway of the basal ganglia plays a key role in SIB in some cases. © 1995 Wiley‐Liss,
ISSN:1080-4013
DOI:10.1002/mrdd.1410010208
出版商:John Wiley&Sons, Inc.
年代:1995
数据来源: WILEY
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8. |
Opiate mechanisms in self‐injury |
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Mental Retardation and Developmental Disabilities Research Reviews,
Volume 1,
Issue 2,
1995,
Page 130-136
Curt A. Sandman,
William P. Hetrick,
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摘要:
AbstractSelf‐injuring behavior is among the most unmanageable, expensive, destructive, and unpredictable behaviors exhibited by human beings. Interventions that included punishment or restraint were among the most successful for acute control of SIB. Both painful shock and restraint stimulate release of the body's own opiates into the bloodstream. These powerful agents, which possess analgesic and addictive properties, are more potent than morphine. Based on these observations, two versions of the opiate hypothesis have evolved to explain SIB. The analgesia hypothesis suggests that high‐circulating levels of β‐endorphin (βE) in individuals with SIB reduces the perception of pain. With the experience of pain reduced, individuals inflict self‐harm as a form of stimulation. The addiction hypothesis presumes that the release of opiates after “pain” or SIB produces pleasure. As a consequence, individuals exhibiting SIB become addicted to their own opiate system. The strongest link between SIB and the opiate hypotheses is the finding that opiate receptor blockers attenuate and sometimes eliminate this behavior. In addition to providing a possible treatment for some SIB individuals, these findings suggest that a specific opiate system, βE andmureceptor, is disregulated (by elevated levels of opiates, abnormally sensitive opiate receptors, or uncoupling of co‐released peptides). Recent studies have found that βE was elevated after an SIB episode, but that co‐released peptides such as ACTH were not. Selective release of βE after SIB provides evidence that endogenous opiates have a direct association with SIB. This association supports speculation that endogenous opiates maintain SIB. ©
ISSN:1080-4013
DOI:10.1002/mrdd.1410010209
出版商:John Wiley&Sons, Inc.
年代:1995
数据来源: WILEY
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9. |
Self‐injurious behavior as endogenous neurochemical self‐administration |
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Mental Retardation and Developmental Disabilities Research Reviews,
Volume 1,
Issue 2,
1995,
Page 137-148
Travis Thompson,
Frank Symons,
Dawn Delaney,
Cindy England,
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摘要:
AbstractThe compulsive and deeply disturbing character of self‐injurious behavior (SIB) makes it one of the most difficult behavior problems to understand scientifically and treat clinically. We review evidence implicating endogenous opioid peptides and the neurotransmitter dopamine in SIB. Next, we describe similarities between the self‐administration of cocaine and morphine by laboratory animals and self‐injury by people with mental retardation. We discuss shared behavioral and neurochemical properties that suggest common mechanisms that may be responsible for both the persistent, damaging behavior patterns characteristic of some forms of SIB and the addictive self‐administration of cocaine and morphine. Multifaceted treatment approaches are explored, based on a better understanding of underlying mechanisms. © 1995 Wiley
ISSN:1080-4013
DOI:10.1002/mrdd.1410010210
出版商:John Wiley&Sons, Inc.
年代:1995
数据来源: WILEY
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10. |
Masthead |
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Mental Retardation and Developmental Disabilities Research Reviews,
Volume 1,
Issue 2,
1995,
Page -
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PDF (86KB)
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ISSN:1080-4013
DOI:10.1002/mrdd.1410010201
出版商:John Wiley&Sons, Inc.
年代:1995
数据来源: WILEY
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