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Tactile defensiveness and stereotyped behaviors.

OBJECTIVES: This study explores the constructs of stereotyped behaviors (e.g., repetitive motor patterns, object manipulations, behavioral rigidities) and tactile defensiveness as relevant to occupational therapy theory and practice and attempts to test their purported relationships in children with developmental disabilities. METHOD: Twenty-eight children with developmental disabilities and autism were assessed on eight factors of stereotyped behavior via a questionnaire and by four measures of tactile defensiveness. The subjects' scores from the questionnaire were correlated with their scores on the tactile defensiveness measures to see what, if any, relationship among these behaviors exists. RESULTS: Significant relationships emerged from the data, indicating that subjects with higher levels of tactile defensiveness were also more likely to evidence rigid or inflexible behaviors, repetitive verbalizations, visual stereotypes, and abnormal focused affections that are often associated with autism. No significant association was found between motor and object stereotypes and tactile defensiveness. These relationships could not be explained solely by maturational factors. CONCLUSION: The results suggest that clinicians should include observations of stereotyped behaviors, particularly behavioral rigidities, in conjunction with assessments of sensory defensiveness because these are related phenomena that may pose unique challenges for children with developmental disabilities and autism. Further study is needed to determine the causal mechanisms responsible for these relationships.

Adolescent↗

Sensitization of apomorphine-induced stereotyped behavior in mice is context dependent.

RATIONALE: The role of the environment in the sensitization of the stereotyped behavioral effects of apomorphine is unclear, since sensitization of this drug effect has either been difficult to demonstrate or has been shown to occur with a low but not a higher dose of apomorphine. OBJECTIVES: The present study was designed to determine whether sensitization of the stereotyped behavioral effects induced by a single dose of apomorphine is dependent on environmental context. METHODS: CF-1 mice were pretreated with apomorphine or vehicle under different environmental conditions and tested for stereotyped behavior after apomorphine challenge. Animals were scored positively for stereotyped behavior if they remained stationary and exhibited repetitive head and/or fore-limb movements, and data are reported as the percentage of mice rated as positive for stereotyped behavior. RESULTS: When mice were pretreated with 40 mg/kg apomorphine and later tested in the same environment, the dose-response curve for stereotyped behavior elicited by apomorphine was shifted threefold to the left 48 h after pretreatment, and this sensitization persisted for at least 28 days after pretreatment. Mice pretreated with apomorphine did not have higher brain levels of apomorphine after administration of the test dose of apomorphine. When the pretreatment environment was different from the test environment, mice did not exhibit sensitization to apomorphine. CONCLUSIONS: These results show that pre-exposure to a single high dose of apomorphine induces a long-lasting sensitization of apomorphine-induced stereotyped behavior that is context dependent. Since apomorphine directly activates dopamine receptors, these observations suggest that a mechanism located postsynaptic to dopamine neurons may be responsible for sensitization of stereotyped behavior.

Animals↗

Different effects of ethylketocyclazocine on phencyclidine- and N-allylnormetazocine-induced stereotyped behaviors in rats.

The effects of ethylketocyclazocine (EKC) on the stereotyped behaviors induced by intraperitoneal injection of phencyclidine (PCP) or N-allylnormetazocine (SKF 10,047) were examined. EKC markedly antagonized PCP-induced stereotyped behaviors such as sniffing, head-weaving, turning and backpedalling. On the other hand, EKC failed to antagonize SKF 10,047-induced stereotyped behaviors, which are PCP-like stereotyped behaviors, except sniffing and head-weaving at 0-15 min after the SKF 10,047 injection. PCP-induced turning and backpedalling were potentiated by pretreatment with SKF 10,047, while PCP-induced sniffing and head-weaving were not. EKC failed to affect the enhancing effect of SKF 10,047 on PCP-induced turning and backpedalling. These results suggest that part of the PCP- and SKF 10,047-induced stereotypy may be mediated by different neuronal mechanisms.

Analgesics, Opioid↗

The stereotyped behavior syndrome: a new model and proposed therapy.

The stereotyped behavior syndrome was induced in rats through local impairment of inhibitory GABA-ergic mechanisms in both caudate nuclei by bilateral microinjection of tetanus toxin, penicillin, or picrotoxin into the rostral part of the caudate nucleus. Intraperitoneally injected haloperidol suppressed the syndrome; this effect was dose-dependent. The same effect on the tetanus toxin-induced stereotyped behavior was produced by GABA microinjected bilaterally into the rostral part of the caudate nucleus of unrestrained rats. It was found in this model of tetanus toxin-induced stereotyped behavior that lithium chloride and diazepam can suppress the syndrome. Combined application of lithium chloride, diazepam, and haloperidol in minimal effective doses resulted in a much more complete and longer-lasting suppression of the syndrome than the separate use of these drugs. This effect is attributed to the joint specific actions of the drugs on pathogenetically interrelated components of a hyperactive determinant structure that arises in the caudate nuclei after impairment of the GABA control and this is responsible for the stereotyped behavior syndrome.

Animals↗

Stereotyped behaviors in deaf and hard of hearing children.

Stereotyped behaviors frequently cause anxiety to parents and educators, and behaviors that appear stereotyped may prompt negative reactions. There has been little research on whether deaf or hard of hearing children display such behaviors. This study surveyed 390 students aged 3-24 years attending 3 residential schools for the deaf and hard of hearing in the United Kingdom. At least 1 additional disability was reported in 79% of the students. The main findings were that: deaf and hard of hearing children without additional disabilities did not show apparently stereotyped behaviors; approximately 35% of children with additional disabilities did show such behaviors; some disabilities, in addition to hearing loss, were more likely than others to be associated with stereotyped behaviors. Implications of these findings for further research are considered with a view toward making recommendations for educational practice.

Adolescent↗

The influence of vigorous versus mild exercise on autistic stereotyped behaviors.

A major problem encountered in many autistic children is their high rate of stereotypic behavior, which has been shown to interfere with on-task responding and other appropriate behaviors. Since the experimental literature indicates that physical exercise can positively influence both appropriate and inappropriate behaviors, including the children's stereotypic behaviors, the purpose of this study was to investigate whether the specific type of exercise (i.e., mild vs. vigorous) would differentially affect subsequent stereotyped behaviors. The results demonstrated that (1) 15 minutes of mild exercise (ball playing) had little or no influence on the children's subsequent stereotyped responding, and (2) 15 minutes of continuous and vigorous exercise (jogging) was always followed by reductions in stereotyped behaviors. These results are discussed in relation to cognitive, physiological, and educational implications.

Autistic Disorder↗

Fluoxetine decreases stereotypic behavior in primates.

BACKGROUND: Primates reared in captivity may display stereotypic behaviors. These behaviors are arguably reminiscent of human obsessive-compulsive or posttraumatic symptoms, which respond to selective serotonin reuptake inhibitors (SSRIs). Captive primates with marked stereotypic behaviors were entered into a randomized controlled study of the SSRI, fluoxetine. METHODS: A sample of 10 vervet monkeys with behaviors such as marked saluting, somersaulting, weaving, or head tossing was selected. Subjects were randomized to receive fluoxetine 1 mg/kg for 6 weeks (n=5) or no treatment (n=5). A rater blind to the medication status of subjects noted the frequency of the stereotypic behaviors. RESULTS: Repeated-measures analysis of variance (RM-ANOVA) demonstrated a significant GroupxTime difference with significantly fewer stereotypic symptoms in the fluoxetine group by endpoint. At this time, three of the five fluoxetine-treated subjects (but none of the no-treatment subjects) were responders on the Clinical Global Impressions (CGI) change item (CGI < or =2). CONCLUSIONS: Stereotypic behaviors in captive vervets gradually and partially decrease in response to administration of an SSRI, paralleling research on human anxiety symptoms. Further research on animal stereotypies may be useful in providing appropriate veterinary care, and in exploring the underlying neurobiology of certain psychiatric disorders.

Animals↗

Possible mechanisms involved in the stereotyped behavior elicited by amphetamine.

In a variety of animals, amphetamine administration produces an increase in locomotor behavior and an induction of repetitive, stereotyped behaviors. There is now considerable evidence to suggest that the induction of stereotyped behaviors is accomplished, in part, by alterations in catecholaminergic transmission in the central nervous system. By recording the spontaneous activity of neurons in the rat brain substantia nigra, reticular formation, basal ganglia, and elsewhere during systemic administration of amphetamine and related drugs, or during administration by means of microinfusions directly into these brain regions, relationships may be drawn between the biochemical and behavioral effects of these drugs and drug-induced changes in neuronal activity in the central nerovous system. Current evidence, for example, suggests that amphetamine produces an inhibition of neuronal activity in the neostriatum and pars compacta of the substantia nigra by means of dopamine released from dopaminergic terminals in the neostriatum and dopaminergic dendrites in the substantia nigra respectively. In addition, current evidence suggests the possibility of a GABA-mediated functional antagonism between excitatory cortical and/or thalamic input to the neostriatum and dopaminergic input from the substantia nigra which could be involved in the apparently mutually exclusive occurrence of amphetamine-induced locomotion and stereotyped behaviors that follow amphetamine administration. Such evidence may also have relevance to a variety of behavioral disorders involving the basal ganglia and catecholaminergic transmission in the central nervous system.

Amphetamine↗

Stereotypic behavior and heart rate in pigs.

Heart rate responses to feeding of both loose-housed and tethered sows, some of which engaged in persistent behavioral stereotypies, were recorded telemetrically in order to determine if stereotypic behavior occurs in response to, and serves to reduce increased sympathetic nervous activity. Heart rates rose in response to feeding (after which stereotypic behavior is most common) and this was greater for tethered sows. This response was partly blocked by a beta-adrenoreceptor antagonist (carazolol), but not by naloxone, although the latter tended to lead to overall increases in heart rate. Thus long-term tethering of sows leads to greater sympathetic nervous responses to feeding. No consistent relationships were found between heart rate and the performance of stereotypic behavior. In Experiment 1, using sows tethered for 6-8 months, neither basal heart rates nor heart rates following naloxone or carazolol differed between high- and low-stereotyping sows. In Experiment 2, using sows tethered for 1-2 months, high-stereotyping sows had lower basal heart rates than low-stereotyping sows. Marked reductions in heart rate caused by a beta-adrenoreceptor blocker did not lead to any change in stereotypic behavior, and preventing stereotypic behavior led to a reduction not an increase in heart rates. The results suggest that stereotypies are performed in situations where heart rate is high, but they provide no evidence that stereotypies reduce this heart rate.

Adrenergic beta-Antagonists↗

Effects of ovariectomy, castration, and chronic lithium chloride treatment on stereotyped behavior in rats.

The effects of ovariectomy, castration, and chronic lithium chloride treatment on stereotyped behavior (SB) induced by apomorphine (APO) (0.3--0.6 mg/kg) were investigated in rats. Duration of stereotyped behavior (interval between APO injection and termination of SB) increased in ovariectomized rats compared to female control rats. Castration had no effect on the duration of stereotyped behavior. On the other hand, ovariectomized rats that were treated chronically with LiCl (2mEq/kg daily) showed no difference in duration of stereotyped behavior compared to female controls chronically treated with LiCl. Neither treatment group showed a significantly altered intensity of stereotyped behavior compared with the appropriate control. These findings are consistent with the hypothesis that estrogen deficit contributes to a greater incidence of neuroleptic-induced tardive dyskinesia in postmenopausal women than in men of comparable age. Furthermore, LiCl may attenuate the symptoms associated with increased postsynaptic dopamine receptor sensitivity following ovariectomy.

Animals↗

Effects of histamine agents on methamphetamine-induced stereotyped behavior and behavioral sensitization in rats.

In this study, effects of histamine (HA) agents on methamphetamine (METH)-induced stereotyped behavior and behavioral sensitization were examined in rats. Pretreatment with a precursor of HA, L-histidine (750mg/kg), significantly inhibited the METH (3 mg/kg)-induced stereotyped behavior, whereas pretreatment with an inhibitor of HA synthesis, alpha-fluoromethylhistidine (FMH) (100 mg/kg), an H1 antagonist pyrilamine (5 mg/kg) or an H2 antagonist zolantidine (5 mg/kg) enhanced it. The inhibitory effect of L-histidine on METH-induced stereotyped behavior was significantly blocked by coadministration of pyrilamine and zolantidine, indicating that the effect is mediated through H1 and H2 receptors. Moreover, chronic treatment with METH (3 mg/kg) significantly enhanced stereotyped behavior at the rechallenge with METH (1 mg/kg). Chronic treatment with L-histidine (750 mg/kg) plus METH inhibited the METH-induced argumentation of stereotyped behavior, while that with FMH (100 mg/kg), pyrilamine (5 mg/kg) or zolantidine (5 mg/kg) potentiated it. These findings suggest that the HA neuron system has an inhibitory role in METH-induced stereotyped behavior and behavioral sensitization.

Animals↗

Dextrorotatory opioids induce stereotyped behavior in Sprague-Dawley and Dark Agouti rats.

Dextromethorphan and dextrorphan elicited a stereotyped behavioral syndrome in rats indistinguishable from that produced by PCP and other non-competitive NMDA antagonists. The rank order of potency for the induction of stereotyped behavior in male Sprague-Dawley rats was: MK-801>PCP>(+/-)cyclazocine>dextrorphan>(+/-)ketamine>dextromethorphan. These behavioral potencies were significantly correlated (0.91; P<0.05) with their respective affinities for high affinity [3H]dextrorphan-labelled NMDA receptors in rat forebrain membranes. To address the propensity of dextromethorphan to induce stereotyped behavior, dextrorotatory-opioid induced stereotypies were investigated in female Dark Agouti and female Sprague-Dawley rats. The female Dark Agouti lacks CYP2D1, the cytochrome P450 enzyme which catalyses the oxidative O-demethylation of dextromethorphan to dextrorphan. No differences were observed in either potency or time to peak effect for dextromethorphan to induce stereotyped behavior in the rat strains, suggesting that the affinity of dextromethorphan for NMDA receptors adequately accounts for its ability to induce stereotyped behavior. Female Dark Agouti rats were, however, more sensitive to the effects of dextrorphan, which may reflect differences in the ability of this strain to metabolize dextrorphan. We find no evidence to suggest that dextromethorphan produces a behavioral syndrome in rats that is distinct from that induced by dextrorphan. The commonality between the pharmacologic profiles of these compounds suggests that the abuse potential of dextromethorphan containing antitussive preparations is related to the non-competitive NMDA antagonist activity of dextromethorphan and its metabolites.

Alcohol Oxidoreductases↗

Stereotypic behavior as a reinforcer: effects and side effects.

This study assessed the effects and side effects of using stereotypic behavior as a consequence for correct responding with two autistic children. The children were cued through a model to engage in stereotypic behavior contingent upon correct responses in task-training sessions. This instructional arrangement produced increases in the percent of correct responses. Measures of the stereotypic behavior used as a reinforcer, other stereotypic behaviors, and appropriate behaviors were collected during daily 5-minute free operant settings before and after the task-training sessions. No replicable, systematic changes in the percent of intervals in which subjects engaged in those side effect measures were noted. Thus, a new method for delivering stereotypic behavior as a reinforcer was investigated and produced reinforcing effects; the rate of that behavior in free operant settings was not adversely affected.

Child↗

Effects of single and long-term administration of nifedipine on nociception and stereotyped behavior of rats.

In the present investigation, nociception and stereotyped behavior were evaluated in 3-month old male Wistar rats after a single nifedipine dose (2.5 and 5.0 mg/kg, ip, 1 h before testing, 6-7 rats per group for stereotypy studies and 15 animals per group for nociception experiments) or after long-term nifedipine treatment (2.5 mg/kg, ip, twice daily for 30 days, with testing performed 72 or 96 h after the last injection, 7 rats per group for stereotypy studies and 14-16 animals per group for nociception experiments). Stereotypy was induced with 2.5 mg/kg amphetamine, ip, and nociception was measured by the tail-immersion test. Administration of a single nifedipine dose did not modify nociception or amphetamine-induced stereotypy (with a mean +/- SEM tail-withdrawal latency of 4.5 +/- 0.5 s for control, 4.4 +/- 0.3 s for 2.5 mg/kg nifedipine and 4.7 +/- 0.7 s for 5.0 mg/kg nifedipine and with mean +/- SEM sum of stereotypy scores of 32.5 +/- 1.6 for control, 29.1 +/- 1.0 for 2.5 mg/kg nifedipine and 29.1 +/- 1.6 for 5.0 mg/kg nifedipine). Withdrawal from long-term nifedipine treatment did not affect stereotyped behavior (with mean +/- SEM sum of stereotypy scores of 28.7 +/- 1.6 for control and 30.7 +/- 1.3 for nifedipine-treated rats) but significantly increased tail-withdrawal latencies (with a mean +/- SEM tail-withdrawal latency of 4.1 +/- 0.3 s for control and 6.4 +/- 0.6 s for nifedipine-treated rats). Therefore, long-term nifedipine treatment induced plastic modifications in nociception but not in stereotyped behavior.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Stereotyped behavior correlates better than ataxia with phencyclidine-receptor interactions.

The interaction of phencyclidine, dexoxadrol, their analogs and stereoisomers with phencyclidine receptors was compared to their ability to induce stereotyped behavior and ataxia after i.c.v. administration to rats. The order of potency for binding to phencyclidine receptors revealed that among the stereoisomers of phencyclidine derivatives, the (+) isomer was more potent than the (-) isomer. A similar order of potency of phencyclidine derivatives and degree of stereoselectivity was seen in the assays for stereotyped behavior and phencyclidine receptor interactions, which resulted in a good correlation between the relative potencies for binding to phencyclidine receptors and inducing stereotyped behavior. However, the order of potency for induction of ataxia and the stereoselectivity was different than that seen in the assays for phencyclidine receptor interactions and stereotyped behavior. A comparison of relative potencies for binding to phencyclidine receptors to induction of ataxia still resulted in a good fit to a straight line, but the line did not intersect the origin, indicating that a non-phencyclidine receptor component is also involved in mediating ataxia. Dextrorphan and 2-methyl-3,3-diphenyl-3-propylamine were equipotent as phencyclidine in phencyclidine receptor and behavioral assays. The order of potency for interacting with phencyclidine receptors and inducing phencyclidine-like behavior by the isomers of cyclazocine were opposite to that of other phencyclidine analogs. Also, the order of potency for induction of ataxia by the isomers of N-allylnormetazocine was opposite to that for phencyclidine receptor interactions. Ethylketocyclazocine did not induce any stereotyped behavior or ataxia, indicating that it is unlikely that a kappa opioid receptor interaction plays a role in mediating ataxia. Furthermore, stereotyped behavior and ataxia were not due to interactions with mu, kappa or delta opioid receptors as naloxone did not antagonize the behavioral effects of phencyclidine, (-)cyclazocine or (-)N-allylnormetazocine. These results indicate that stereotyped behavior is mediated by phencyclidine receptors, whereas ataxia is mediated by more than just phencyclidine receptors.

Animals↗

Repetitive stereotyped behaviors.

This paper points to factors that determine whether repetitive stereotyped behavior occur in the behavior repertoire. The analysis pits an "intrinsic oscillator" mechanism against a "self-stimulation" theory and chooses to emphasize the latter. The paper accounts for the repetitive and rhythmic nature of stereotypy by suggesting that repetition in a rhythmic way is the most efficient way of self-stimulation. It proposes that rhythm may be a reinforcement in at least some cases. It raises the question of whether control of stimulation by the person is a necessary condition for maintaining stereotypy. The paper recognizes the possibility that stereotyped behaviors may have their origin in the common repetitive behaviors of infancy but emphasizes that pathological stereotypy may involve more than immature repetition. It suggests that there is reason to believe that early intervention to prevent pathological stereotyped behavior might be effective but that we do not know much about how stereotypies get started.

Animals↗

Low doses of corticotropin-releasing factor potentiate amphetamine-induced stereotyped behavior.

Corticotropin-releasing factor (CRF) is a 41-amino acid polypeptide that is critically involved in the activation of the hypothalamic-pituitary adrenal axis during stress. In addition, it has been suggested that extrahypothalamic CRF may be important in initiating behavioral responses to stressful events. In the present experiment, we examined the effects of central administration of CRF on amphetamine-induced stereotyped behavior. Amphetamine-induced stereotyped behavior has been considered as a behavioral strategy to cope with excessive arousal. Low doses of CRF (0.02 and 0.1 micrograms), administered into the lateral ventricle (ICV), were shown to potentiate amphetamine (4.0 mg/kg; SC)-induced stereotyped behavior, as measured by the Creese and Iversen rating scale and behavioral observations. These low doses of CRF specifically enhanced the tendency for rats to sniff with their heads down 20 min after injection, and induced licking behavior later during testing. In contrast, the rats treated with a higher dose of CRF (0.5 micrograms, ICV) showed more locomotor activity throughout the test, but did not differ from the saline-treated animals in the intensity of amphetamine-induced stereotyped behavior.

Amphetamine↗