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PubMed1992

Repetitive behaviors in chronically institutionalized schizophrenic patients.

Repetitive dysfunctional behaviors (e.g., polydipsia, bulimia, hoarding, mannerisms) are frequently observed in chronically institutionalized schizophrenics, cause significant morbidity and are readily reproduced in animal models. The goal of this study was to assess the frequency and severity of these behaviors. Thirty-two chronic schizophrenics on an extended treatment unit were rated on the Elgin Behavioral Rating Scale, which includes eight repetitive behaviors and eight positive and negative symptoms. Forty-seven percent of the patients exhibited at least one severe, or 2 moderate, repetitive behaviors, while 63% exhibited at least one severe or 2 moderate positive or negative symptoms. The mean total score (+/- SD) on the eight repetitive behaviors (10.3 +/- 6.1) was about 2/3 that for the eight positive and negative symptoms (15.3 +/- 8.9, t = 4.1, p = .0001). Interrater reliability for the repetitive behaviors was similar to that for the positive and negative symptoms. Repetitive behaviors were positively related to male gender, white race and total length of hospitalization. Repetitive dysfunctional behaviors are frequently observed and can be reliably rated in chronically institutionalized schizophrenics.

Adult↗
PubMed1990

Optically active benzamides as predictive tools for mapping the dopamine D2 receptor.

Substituent variations on the pyrrolidinyl nitrogen of sulpiride, a selective D2 dopamine antagonist, showed that in vitro and in vivo activities are concentrated in the (S) optical series for N-alkyl analogs and in the (R) series for N-benzyl analogs. To account for these unusual structure-activity relationships, a pharmacophoric model was built from the crystallographic structure of (-)piquindone and extended to 14 other D2 antagonists. This model considers the lone pair orientation of the basic nitrogen rather than its spatial location. Two distinct active conformations for benzamides were defined, corresponding to the (S) and (R) series. An extended pharmacophore is then proposed involving four main anchoring areas: (i) an aromatic site Ar1, (ii) a tertiary nitrogen with its lone pair orthogonal to the Ar1 plane, (iii) a dipole delta 1 coplanar to the Ar1 ring and (iv) three sites for the N-substituent, including a small hydrophobic pocket and two different aromatic binding sites Ar2 and Ar3. To probe the predictive value of this model, structures were designed and several compounds were synthesized and tested as inhibitors of [125I]iodo-sulpiride binding to rat striatal membranes and as antagonists of apomorphine-induced stereotyped behavior in mice.

Animals↗
PubMed2006

Monozygotic twins with Asperger syndrome: differences in behaviour reflect variations in brain structure and function.

A pair of monozygotic twins discordant for symptoms of Asperger syndrome was evaluated at the age of 13.45 years using psychometric, morphometric, behavioural, and functional imaging methods. The lower-functioning twin had a smaller brain overall, a smaller right cerebellum, and a disproportionately large left frontal lobe, and manifested almost no differential activation between distractors of high and low-congruence with target visual stimuli. The higher-functioning twin manifested a typically autistic pattern of anterior deactivation and posterior hyperactivation in response to incongruent distractors, overlaid with a typically normal pattern of activation of superior frontal cortex. The morphometric results are consistent with known correlations between brain structure and behaviour in autism, and the physiological results suggest correspondences between structure and function.

Adolescent↗
PubMed2006

Development and temporal organization of compulsive checking induced by repeated injections of the dopamine agonist quinpirole in an animal model of obsessive-compulsive disorder.

Rats treated chronically with the dopamine D2/D3 receptor agonist quinpirole develop locomotor sensitization and exhibit compulsive checking of specific places in an open-field arena, a behavioral profile that may represent an animal model of obsessive-compulsive disorder. However, it is not known how compulsive checking develops across quinpirole injections nor whether checking behavior possesses a particular temporal structure. Male rats received quinpirole (0.5mg/kg, twice weekly x 10) or an equivalent regimen of saline and were placed in a large open field for 55 min where their behavior was digitally tracked for subsequent analysis of checking behavior using existing and newly developed computer software. Results showed that the measures of compulsive checking did not follow a singular profile across injections: some remained constant and others changed monotonically reaching their near-maximum levels after about 5-7 quinpirole injections. Moreover, results showed that checking behavior was organized into bouts of checking, with the number of bouts, as well as the rate of checking within a bout, increasing across injections to reach near maximal levels after about 5-7 administrations of quinpirole. Finally, quinpirole-treated rats showed a paucity of long inter-bout intervals. These results suggest that (a) compulsive checking emerges from the operation of at least two underlying processes: a regulated process and a process of sensitization that intensifies the performance of checking behavior; and (b) quinpirole treatment may attenuate a sense of satiety that could underlie the compulsive nature of checking. Finally, because key variables measured using the newly developed algorithms showed the expected profile, the present study provides validation for the use of this methodology for the analysis of checking behavior.

Analysis of Variance↗
PubMed2006

Animal models of restricted repetitive behavior in autism.

Restricted, repetitive behavior, along with deficits in social reciprocity and communication, is diagnostic of autism. Animal models relevant to this domain generally fall into three classes: repetitive behavior associated with targeted insults to the CNS; repetitive behavior induced by pharmacological agents; and repetitive behavior associated with restricted environments and experience. The extant literature provides potential models of the repetitive behavioral phenotype in autism rather than attempts to model the etiology or pathophysiology of restricted, repetitive behavior, as these are poorly understood. This review focuses on our work with deer mice which exhibit repetitive behaviors associated with environmental restriction. Repetitive behaviors are the most common category of abnormal behavior observed in confined animals and larger, more complex environments substantially reduce the development and expression of such behavior. Studies with this model, including environmental enrichment effects, suggest alterations in cortical-basal ganglia circuitry in the development and expression of repetitive behavior. Considerably more work needs to be done in this area, particularly in modeling the development of aberrant repetitive behavior. As mutant mouse models continue to proliferate, there should be a number of promising genetic models to pursue.

Animals↗
PubMed2004

Cerebellar function in autism: functional magnetic resonance image activation during a simple motor task.

BACKGROUND: The cerebellum is one of the most consistent sites of neuroanatomic abnormality in autism, yet it is still unclear how such pathology impacts cerebellar function. In normal subjects, we previously demonstrated with functional magnetic resonance imaging (fMRI) a dissociation between cerebellar regions involved in attention and those involved in a simple motor task, with motor activation localized to the anterior cerebellum ipsilateral to the moving hand. The purpose of the present investigation was to examine activation in the cerebella of autistic patients and normal control subjects performing this motor task. METHODS: We studied eight autistic patients and eight matched normal subjects, using fMRI. An anatomic region-of-interest approach was used, allowing a detailed examination of cerebellar function. RESULTS: Autistic individuals showed significantly increased motor activation in the ipsilateral anterior cerebellar hemisphere relative to normal subjects, in addition to atypical activation in contralateral and posterior cerebellar regions. Moreover, increased activation was correlated with the degree of cerebellar structural abnormality. CONCLUSIONS: These findings strongly suggest dysfunction of the autistic cerebellum that is a reflection of cerebellar anatomic abnormality. This neurofunctional deficit might be a key contributor to the development of certain diagnostic features of autism (e.g., impaired communication and social interaction, restricted interests, and stereotyped behaviors).

Adolescent↗
PubMed2005

Neural correlates of executive function in autistic spectrum disorders.

BACKGROUND: Some clinical characteristics of high-functioning individuals with autistic spectrum disorder (ASD) such as repetitive stereotyped behaviors, perseveration, and obsessionality have been related to executive function (EF) deficits, more specifically to deficits in inhibitory control and set shifting and mediating frontostriatal neural pathways. However, to date, no functional imaging study on ASD has investigated inhibition and cognitive flexibility and no one has related EF brain activation to brain structure. METHODS: We compared brain activation (using functional magnetic resonance imaging) in 10 normal intelligence adults with ASD and 12 healthy control subjects during three different EF tasks: 1) motor-inhibition (GO/NO-GO); 2) cognitive interference-inhibition (spatial STROOP); and 3) set shifting (SWITCH). Using voxel-based morphometry, we investigated if cortical areas which were functionally different in people with ASD were also anatomically abnormal. RESULTS: Compared with control subjects, ASD individuals showed significantly increased brain activation in 1) left inferior and orbital frontal gyrus (motor-inhibition); 2) left insula (interference-inhibition); and 3) parietal lobes (set shifting). Moreover, in individuals with ASD, increased frontal gray matter density and increased functional activation shared the same anatomical location. CONCLUSIONS: Our findings suggest an association between successful completion of EF tasks and increased brain activation in people with ASD, which partially may be explained by differences in brain anatomy.

Adolescent↗
PubMed2005

Disorganized rhythm and synchrony: early signs of autism and Rett syndrome.

We interpret early age-related developments in intentions and socially responsive behaviour with data from home videos of infants who later develop autism or Rett syndrome. Detailed evidence is given from a micro-analytic study of videos of monozygotic twin girls at 11 months, one of whom became autistic in the second year. Changes in this twin's attention, motor tonus, initiative and emotion reduce her prospective control of movements and her anticipations in awareness compared to her sister. These changes were reflected in the child's asynchronous social behaviour, which frustrated the father's attempts to support her attempts to walk, share toys, or play a game, confusing his anticipations, and this further reduced mutual attention and joint activity. Observations of the development of girls with Rett syndrome in the first year reveal changes in motor coordination, attention and communicative initiative, indicative of a failure of intrinsic core brain regulations of neural development and conscious activity. Notwithstanding that the two conditions show clear differences in both brain growth and early development of skills and sociability, the first signs of autism and Rett syndrome have important similarities. We conclude with recommendations for an approach to early diagnosis and treatment, applicable for the whole range of developmental brain disorders, including Rett syndrome and autism, that attempts to identify residual capacities for sympathetic motivation and collaborative learning-an approach that deliberately tries to support weakened rhythmic impulses for motor, perceptual and communicative functions in the growing infant brain.

Attention↗
PubMed2004

Glutamate N-methyl-D-aspartate and dopamine receptors have contrasting effects on the limbic versus the somatosensory cortex with respect to amphetamine-induced neurodegeneration.

The roles that glutamate N-methyl-D-aspartate (NMDA) and dopamine D1-like and D2-like receptors play in the cortical neurotoxicity occurring in rats exposed to multiple doses of amphetamine (AMPH) for 2 days was evaluated. Neurodegeneration in rats that did not become hyperthermic during AMPH exposure was quantified by counting isolectin B4-labeled phagocytic microglia and Fluoro-Jade (F-J)-labeled neurons in the somatosensory parietal cortex, piriform cortex and posterolateral cortical amygdaloid nucleus (PLCo). The NMDA receptor antagonist, dizocilpine (0.63 mg/kg day) blocked AMPH-induced neurodegeneration in the somatosensory cortex. However, it did not affect degeneration in the piriform cortex and PLCo indicating that limbic degeneration was not NMDA-mediated. The dopamine antagonists, eticlopride (D2/3, 0.25 mg/kg day) and SCH-23390 (D1, 0.25 mg/kg day), blocked the stereotypic behavior and neurodegeneration in the somatosensory cortex. However, eticlopride had a lesser protective effect in the limbic regions. As well, the dopamine D2/D3 agonist quinpirole (1.5 mg/kg day) protected against cortical neurodegeneration when it was given during AMPH exposure and continued until sacrifice. The dopamine D1 agonist (SKF-38393, 12.5 mg/kg day) had no significant effect on neurodegeneration. These data indicate that there are significant differences in NMDA and dopamine D2 modulation of AMPH-induced neurodegeneration in the somatosensory cortex compared to the limbic cortices, and limbic cortical degeneration is not necessarily dependent on excessive stimulation of NMDA receptors as it is in the somatosensory cortex. Although excessive dopamine receptor stimulation during amphetamine exposure may trigger the neurodegenerative processes, continued D2 stimulation after AMPH exposure is neuroprotective in the cortex.

Amphetamine↗
PubMed2005

Preliminary evidence for reduced social interactions in Chakragati mutants modeling certain symptoms of schizophrenia.

Rodent models of schizophrenia provide powerful experimental tools for elucidating certain manifestations of the brain disease. The chakragati (ckr) mouse mutant, for instance, reproduces aberrant neuroanatomical and behavioral phenotypes observed in the corresponding human condition. To further investigate the utility of this mouse in the context of social behavior, we compared spontaneous behavioral activity and social interactions recorded during the subjective night among wild-type, heterozygous, and homozygous ckr mice. We found that both heterozygous and homozygous ckr animals failed to show appropriate norms of social behavior, including proximity, approach, huddling, and anogenital investigation in response to novel conspecifics. We further found that the anatomical distribution, topography, and connectivity of the neuropeptides oxytocin and vasopressin in the anterior hypothalamus did not differ among wild-type, heterozygous, or homozygous ckr animals. These latter findings suggest that although oxytocin and vasopressin influence social behavior, connectivity of such cells may not be phenotypically relevant for the observed social deficits seen in heterozygous and homozygous ckr mice. Collectively, ckr mice and their heterozygote kin are valuable experimental tools for pre-clinical studies involving disruptions of social behavior (e.g., social withdrawal).

Animals↗
PubMed2006

Paradoxical effects of very low dose MK-801.

Systemic injection of the noncompetitive NMDA (N-methyl-D-aspartate) receptor antagonist MK-801 (dizocilpine maleate) is known to cause increased locomotion and various stereotypic behaviors in rodents. However, the MK-801 dose ranges commonly examined usually begin at tenth of mg/kg and going higher, with the implicit assumption of lower doses being ineffective. We report here that very low dose MK-801, well below the commonly studied doses, exert distinct effects on rodent behaviors. In C57BL/6 mice, very low dose MK-801 (0.02 mg/kg) has strikingly different effects than higher doses commonly reported in the literature. Locomotion, rearing, grooming, and other behaviors are strongly inhibited, replaced by periods of immobility. This is in contrast to the mobility-enhancing effect of MK-801 at commonly reported dose ranges. The effects of very low dose MK-801 are qualitatively similar to those observed with moderate doses (0.1-0.2 mg/kg) of the typical antipsychotic haloperidol. These results highlight the complexity of the dose-response relation for MK-801-induced behaviors.

Animals↗
PubMed2006

Neurotoxicity of Coscinium fenestratum stem, a medicinal plant used in traditional medicine.

Coscinium fenestratum is a common medicinal plant widely used in the Indochina region, but scientific data on its safety is very limited. This study aimed to observe the effect of this plant on neurotoxicity and neurobehavior. Oral administration of plant alcoholic extract at dosages of 5, 10 and 20 mg/kgBW for 14 days increased the rats body weight and decreased the neuron density in the cerebral cortex, hippocampus and striatum. The plant extract significantly increased stereotyped behavior in licking but did not cause anxiolytic activity, anti-depression, sensory motor co-ordination impairment and ataxia. It is concluded that the plant possesses neurotoxicity and is able to induce neurobehavioral changes in rats. Therefore, the application of this plant as either drug or supplementary food should be reconsidered.

Animals↗
PubMedDate not supplied

Developmental deficits in social perception in autism: the role of the amygdala and fusiform face area.

Autism is a severe developmental disorder marked by a triad of deficits, including impairments in reciprocal social interaction, delays in early language and communication, and the presence of restrictive, repetitive and stereotyped behaviors. In this review, it is argued that the search for the neurobiological bases of the autism spectrum disorders should focus on the social deficits, as they alone are specific to autism and they are likely to be most informative with respect to modeling the pathophysiology of the disorder. Many recent studies have documented the difficulties persons with an autism spectrum disorder have accurately perceiving facial identity and facial expressions. This behavioral literature on face perception abnormalities in autism is reviewed and integrated with the functional magnetic resonance imaging (fMRI) literature in this area, and a heuristic model of the pathophysiology of autism is presented. This model posits an early developmental failure in autism involving the amygdala, with a cascading influence on the development of cortical areas that mediate social perception in the visual domain, specifically the fusiform "face area" of the ventral temporal lobe. Moreover, there are now some provocative data to suggest that visual perceptual areas of the ventral temporal pathway are also involved in important ways in representations of the semantic attributes of people, social knowledge and social cognition. Social perception and social cognition are postulated as normally linked during development such that growth in social perceptual skills during childhood provides important scaffolding for social skill development. It is argued that the development of face perception and social cognitive skills are supported by the amygdala-fusiform system, and that deficits in this network are instrumental in causing autism.

Amygdala↗
PubMed2004

Chronic pain in individuals with previously undiagnosed autistic spectrum disorders.

UNLABELLED: The aim of this article is to heighten clinician awareness by describing 2 patients with signs and symptoms of a possible autistic disorder. Autistic spectrum disorders are neurodevelopmental disorders characterized by impairment in reciprocal social interaction skills or communication skills and/or by the presence of stereotyped behavior, interests, and activities. Pain can be the initial presenting symptom for individuals with a previously undiagnosed autistic spectrum disorder. Two case presentations show indicators, such as reported sensory abnormalities, impaired social behaviors, and unusual interests, that should lead the physician to consider a referral for further evaluation. An accurate diagnosis of autism or related disorder can lead to a greater understanding of the nature of the patient's pain, as well as to more appropriate and effective treatment strategies. In addition, such patients might benefit from therapeutic interventions to improve overall functioning and decrease distress and, consequently, to decrease pain and other symptoms. Finally, autism research might inform pain researchers on topics such as neurobiology, development, and treatment of chronic pain disorders. PERSPECTIVE: Pain experts might be underrecognizing signs and symptoms of autistic spectrum disorders (ASDs) in their patients. Clinical evaluation for ASDs should be considered in patients with specific unusual characteristics. Research on the topic of ASDs and pain is encouraged.

Adolescent↗
PubMedDate not supplied

Effects of fluoxetine on ethanol withdrawal syndrome in rats.

The present study was designed to investigate the effects of fluoxetine, a selective serotonin reuptake inhibitor, on ethanol withdrawal syndrome in rats. Adult male Wistar rats (218-255 g) were subjects. Ethanol (7.2%, v/v) was given to rats by a liquid diet for 21 days. Control rats were pair fed an isocaloric liquid diet containing sucrose as a caloric substitute to ethanol. Fluoxetine (2.5, 5 and 10 mg/kg) and saline were injected to rats intraperitoneally just before ethanol withdrawal. After 2nd, 4th and 6th hour of ethanol withdrawal, rats were observed for 5 min, and withdrawal signs that included locomotor hyperactivity, agitation, stereotyped behavior, wet dog shakes and tremor were recorded or rated. A second series of injections was given at 6 h after the first one, and subjects were then tested for audiogenic seizures. Fluoxetine produced some dose-dependent and significant inhibitory effects on all the signs of ethanol withdrawal during ethanol withdrawal period. Our results suggest that acute fluoxetine treatment has some beneficial effects on ethanol withdrawal in rats. Thus, this drug may be useful for treatment of ethanol withdrawal syndrome.

Administration, Oral↗
PubMed2006

Hyperbaric oxygen therapy may improve symptoms in autistic children.

Autism is a neurodevelopmental disorder that currently affects as many as 1 out of 166 children in the United States. Recent research has discovered that some autistic individuals have decreased cerebral perfusion, evidence of neuroinflammation, and increased markers of oxidative stress. Multiple independent single photon emission computed tomography (SPECT) and positron emission tomography (PET) research studies have revealed hypoperfusion to several areas of the autistic brain, most notably the temporal regions and areas specifically related to language comprehension and auditory processing. Several studies show that diminished blood flow to these areas correlates with many of the clinical features associated with autism including repetitive, self-stimulatory and stereotypical behaviors, and impairments in communication, sensory perception, and social interaction. Hyperbaric oxygen therapy (HBOT) has been used with clinical success in several cerebral hypoperfusion syndromes including cerebral palsy, fetal alcohol syndrome, closed head injury, and stroke. HBOT can compensate for decreased blood flow by increasing the oxygen content of plasma and body tissues and can even normalize oxygen levels in ischemic tissue. In addition, animal studies have shown that HBOT has potent anti-inflammatory effects and reduces oxidative stress. Furthermore, recent evidence demonstrates that HBOT mobilizes stem cells from human bone marrow, which may aid recovery in neurodegenerative diseases. Based upon these findings, it is hypothesized that HBOT will improve symptoms in autistic individuals. A retrospective case series is presented that supports this hypothesis.

Autistic Disorder↗
PubMed2006

Hyperbaric oxygen therapy might improve certain pathophysiological findings in autism.

Autism is a neurodevelopmental disorder currently affecting as many as 1 out of 166 children in the United States. Numerous studies of autistic individuals have revealed evidence of cerebral hypoperfusion, neuroinflammation and gastrointestinal inflammation, immune dysregulation, oxidative stress, relative mitochondrial dysfunction, neurotransmitter abnormalities, impaired detoxification of toxins, dysbiosis, and impaired production of porphyrins. Many of these findings have been correlated with core autistic symptoms. For example, cerebral hypoperfusion in autistic children has been correlated with repetitive, self-stimulatory and stereotypical behaviors, and impairments in communication, sensory perception, and social interaction. Hyperbaric oxygen therapy (HBOT) might be able to improve each of these problems in autistic individuals. Specifically, HBOT has been used with clinical success in several cerebral hypoperfusion conditions and can compensate for decreased blood flow by increasing the oxygen content of plasma and body tissues. HBOT has been reported to possess strong anti-inflammatory properties and has been shown to improve immune function. There is evidence that oxidative stress can be reduced with HBOT through the upregulation of antioxidant enzymes. HBOT can also increase the function and production of mitochondria and improve neurotransmitter abnormalities. In addition, HBOT upregulates enzymes that can help with detoxification problems specifically found in autistic children. Dysbiosis is common in autistic children and HBOT can improve this. Impaired production of porphyrins in autistic children might affect the production of heme, and HBOT might help overcome the effects of this problem. Finally, HBOT has been shown to mobilize stem cells from the bone marrow to the systemic circulation. Recent studies in humans have shown that stem cells can enter the brain and form new neurons, astrocytes, and microglia. It is expected that amelioration of these underlying pathophysiological problems through the use of HBOT will lead to improvements in autistic symptoms. Several studies on the use of HBOT in autistic children are currently underway and early results are promising.

Autistic Disorder↗