Genuine concerns about the validity of applying 'adult' psychotic diagnoses in this young age group, together with the lack of diagnosis-specific interventions, have suggested a cautious approach to diagnosis

Results suggest that the tendency to see life events as the result of unstable or unpredictable causes is associated with social dysfunction independent of symptom level.

Before the recognition of childhood Autism, some patients who would now be classified as autistic were described as schizophrenic with attention to their unique symptoms.

Background. We measured psychopathic traits in boys with autism spectrum disorder (ASD) selected for difficult and aggressive behaviour. We asked (i) whether psychopathic tendencies can be measured in ASD independent of the severity of autistic behaviour; (ii) whether individuals with ASD with callous-unemotional (CU) traits differ in their cognitive profile from those without such traits; and (iii) how the cognitive data from this study compare with previous data of youngsters with psychopathic tendencies.Method. Twenty-eight ASD boys were rated on psychopathic tendencies, autistic traits and a range of cognitive measures assessing mentalizing ability, executive functions, emotion recognition and ability to make moral-conventional distinction.Results. Our results indicate that psychopathic tendencies are not related to severity of ASD. In addition, such tendencies do not seem to be related to core autistic cognitive deficits, specifically in 'mind-reading' or executive function. Boys with co-occurring ASD and CU tendencies share some behaviours and aspects of cognitive profile with boys who have psychopathic tendencies alone.Conclusions. Callous/psychopathic acts in a small number of individuals with ASD probably reflect a 'double hit' involving an additional impairment of empathic response to distress cues, which is not part and parcel of ASD itself.

The induction of Fos-like immunoreactivity (FLI) was used to determine the brain localization affected by b-casomorphin-7 (b-CM7). Peripheral administration of human b-CM7 at different doses (5, 10 and 30 \#956;g/kg, IV for 1 hour) to rats induced moderate to strong FLI in discrete brain regions including the nucleus accumbens, caudate putamen, ventral tegmental and median raphe nucleus, and orbitofrontal, prefrontal, parietal, temporal, occipital and entorhinal cortex. All of the above areas have been shown to be altered either functionally or anatomically in patients with schizophrenia, and most have been shown to be functionally abnormal in autism. Some of these brain areas are originators or components of dopaminergic, serotoninergic and GABA-ergic pathways, suggesting that b-CM7 can affect the function of all of these systems. The role of some other affected areas in emotional and motivated behavior, social adaptation, hallucinations and delusions suggests that b-CM7, which was found in high concentration in the CSF, blood and urine of patients with either schizophrenia or autism, may be relevant to schizophrenia and autism. Induction of FLI in the above brain areas by a moderate dose (10 \#956;g/kg) of b-CM7 was attenuated significantly, or blocked, by pretreatment with naloxone (2 mg/kg, IP). It is concluded that human b-CM7 can cross the blood-brain barrier, activate opioid receptors and affect brain regions similar to those affected by schizophrenia and autism.

The majority of COS patients meet one or more criteria for pervasive developmental disorder, such as lack of interest in peers, poor eye contact, motor stereotypes, and odd speech or echolalia; but children do not meet full criteria for PDD or autism.

Mental health clinical assessment is the process of gaining a better understanding of an individual's concerns, needs, and strengths. A thorough clinical assessment helps the consumer and his family make more informed decisions.

In summary, there are interesting parallels between autism and schizophrenia that may, as P&S suggest, be explicable in terms of a common underlying deficit in cognitive coordination. Nevertheless, there are clear differences between the two disorders, although the later age of onset of schizophrenia would appear to be crucial in explaining many of these differences.

The presented findings confirm that premorbid symptomatology (language and/or motor developmental disorders) as well as early and insidious onset are salient prognostical indicators.

Psychotic symptoms in adolescents can often lead to misdiagnosis and inappropriate treatment approaches. Diagnostic difficulties arise given the marked developmental and psychosocial changes of adolescence.

Seven men with autistic disorders developed mood disorders or psychotic illnesses during adult life. This association has also been described in several previous reports. Although no firm conclusions can be drawn on the basis of case reports alone, it appears that autistic disorders may increase vulnerability to such psychoses. Possible reasons for the association are discussed, as is treatment.

People with Autistic Spectrum Conditions don't hear 'voices' in their heads or have visual hallucinations. The thinking of an Autistic person isn't distorted or illogical like the thinking of a Schizophrenic when in a psychotic state.

There is evidence that Asperger syndrome is associated with delusional beliefs. Cognitive theories of delusions in psychosis literature propose a central role for impaired theory of mind ability in the development of delusions. The present study investigates the phenomenology of delusional ideation in Asperger syndrome. Fortysix individuals with Asperger syndrome participated and were found to have relatively high levels of delusional ideation, primarily grandiose or persecutory. Factors associated with delusional belief were anxiety, social anxiety and self-consciousness, but not theory of mind ability or autobiographical memory. The findings indicate that delusional belief is a prominent feature in Asperger syndrome, but do not support a mentalization based account. A preliminary cognitive model of delusions in Asperger syndrome is proposed and the theoretical and clinical implications of the findings are discussed.

Both autism and schizophrenia involve difficulties in comprehending mental states (mentalising), as measured by now-standard tests such as false-belief tests and story-sequencing.

I suggest that words are simply less lateralised in those genetically predisposed to suffer from schizophrenic symptoms.

Hallucinations can be regarded as underconstrained perceptions that arise when the impact of sensory input on activation of thalamocortical circuits and synchronisation of thalamocortical gamma activity is reduced. In conditions that are accompanied by hallucinations, factors such as cortical hyperexcitability, cortical attentional mechanisms, hyperarousal, increased noise in specific thalamic nuclei, and random sensory input to specific thalamic nuclei may, to a varying degree, contribute to underconstrained activation of thalamocortical circuits.

Civilizations have been struggling with understanding and treating psychotic disorders such as schizophrenia since ancient times. It was not until the advent of the Greek philosophical tradition, however, that the basis of our modern day theoretical structures began to form. Plato, Hippocrates, and other philosophers theorized about the physical basis of mental disorders, mind-body integration, and unconscious mental processes. Later thinkers such as Kraepelin and Bleuler refined our classificatory schemas, helping us to reliably identify and classify the various psychotic disorders. We are now encountering an explosion of scientific knowledge about the neurobiological underpinnings of schizophrenia that is helping us to unravel the mysteries of this disorder. Our intellectual understanding of the schizophrenic syndrome has not only resulted in better means of treatment but is also beginning to lessen the stigma that has accompanied this disorder. Deinstitutionalization, community care, and patient advocacy are just some of the movements that are helping both caregivers and patients to cope effectively with the many facets of this complex syndrome.

The autistic child will have prominent withdrawal, language retardation, and repetitive routines, while the child with schizophrenia will have delusions, hallucinations, and thinking disorders.

These data suggest that a continuum of schizophrenic-type traits affect the way a person processes information about the self and that mental state attribution and self-recognition are processed by similar neural substrates.

Clearly, I do not consider autism as an entity with an important organic basis, even if it has organic consequences, affecting mainly the muscular and neurological systems inasmuch as they themselves are dependant on family psychical activity.

Psychoses are manifested by pathology in all areas of mental function: behavior, cognition, and affect. They are relatively rare but pose significant problems for medical care.

This study has shown an increase in minor physical abnormalities in subjects with sporadic schizophrenia, especially males, but not in familial schizophrenic patients or first degree relatives of either group. This work therefore supports the notion that abnormality of prenatal development is particularly implicated in sporadic schizophrenia.

There are some children who display the severe, early-appearing social and communicative deficits characteristic of autism who ALSO display some of the emotional instability and disordered thought processes that resemble schizophrenic symptoms.

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Eight sane people gained secret admission to 12 different hospitals. Their diagnostic experiences constitute the data of the first part of this article; the remainder is devoted to a description of their experiences in psychiatric institutions.

In a previous study we showed that b-casomorphin-7 (b-CM7) is taken up by brain regions relevant to schizophrenia and autism. The present experiment was designed to find whether b-CM7 has any behavioral or analgesic effects in rats. About 65 seconds after treatment with different doses of b-CM7, rats became restless and ran violently, with teeth chattering and with rapid respiration. Seven minutes later, the rats became inactive with less walking, distancing themselves from the other rat in the same cage, and sitting in, or putting their head against, the corner of the cage. The sound response was reduced and social interaction was absent. One hour later, the rats showed hyperdefensiveness. The above behavioral effects of b-CM7 did not occur when rats were pretreated with naloxone (2 mg/kg, IP). The rats receiving saline did not show any behavioral changes throughout the 2 hour period of observation. b-CM7 also demonstrated analgesic effects, which could be blocked by naloxone. The results suggest that b-CM7 may play a role in behavioral disorders such as autism and schizophrenia.

It is helpful to know that catatonia can complicate autistic spectrum disorders and that individuals who present with catatonia may have an undiagnosed autistic spectrum disorder.

I would very definitely feel that the service provision for individuals suffering from autistic spectrum disorders and psychopathic disorders should be quite different from provision for antisocial or dissocial personality disorders.

Although schizophrenia is rare in younger adolescents and even rarer in prepubertal children, research over the past 2 decades has shown that schizophrenia does develop in some children and adolescents. This article reviews the symptoms of schizophrenia in children and adolescents and provides guidelines for distinguishing these symptoms from those of more common childhood disorders. Strategies for providing treatment to children who have schizophrenia and their families, including the use of medications, are reviewed.

Although schizophrenia is often thought of as an adolescent- or adult-onset disorder, there has been an increasing awareness over 90 years that schizophrenia can present in 6-12 year olds. There has been less focus on schizophrenia in children under the age of 6. We report here on two children diagnosed, at 4.25 and 5.92 years, with schizophrenia. Retrospectively, both children had psychotic symptoms documented during mental health evaluations prior to their fourth birthday. Both children had at least partial symptom reduction on antipsychotic medication, but both children were also highly sensitive to the side effects of treatment. Discussion focuses primarily on diagnostic issues, and provides some observations about treatment responsiveness.

The number of published studies investigating schizophrenia spectrum disorders in people with intellectual disabilities continues to increase slowly. The evidence base, however, needs to be strengthened, particularly by randomized controlled trials in pharmacotherapy, psychosocial interventions and service delivery.

In order to challenge our assumptions that there are clear lines between madness and sanity, abnormality and normality, try the following quiz!

Unemployment and early separation from both parents may be key factors behind the higher rates of schizophrenia in British African-Caribbeans, research suggests.

A vascular-inflammatory theory of schizophrenia brings together environmental and genetic factors in a way that can explain the diversity of symptoms and outcomes observed. If these ideas are confirmed, they would lead in new directions for treatments or preventions by avoiding inducers of inflammation or by way of inflammatory modulating agents, thus preventing exaggerated inflammation and consequent triggering of a psychotic episode in genetically predisposed persons.

The term theory of mind (ToM) refers to the capacity to infer one's own and other persons' mental states. A substantial body of research has highlighted the evolution of ToM in nonhuman primates, its emergence during human ontogeny, and impaired ToM in a variety of neuropsychiatric disorders, including schizophrenia. There is good empirical evidence that ToM is specifically impaired in schizophrenia and that many psychotic symptoms—for instance, delusions of alien control and persecution, the presence of thought and language disorganization, and other behavioral symptoms—may best be understood in light of a disturbed capacity in patients to relate their own intentions to executing behavior, and to monitor others' intentions. However, it is still under debate how an impaired ToM in schizophrenia is associated with other aspects of cognition, how the impairment fluctuates with acuity or chronicity of the schizophrenic disorder, and how this affects the patients' use of language and social behavior. In addition to these potential research areas, future studies may also address whether patients could benefit from cognitive training in this domain.

There is evidence that groups of people with schizophrenia have deficits in Theory of Mind (ToM) capabilities. Previous studies have found these to be linked to psychotic symptoms (or psychotic symptom severity) particularly the presence of delusions and hallucinations. A visual joke ToM paradigm was employed where subjects were asked to describe two types of cartoon images, those of a purely Physical nature and those requiring inferences of mental states for interpretation, and to grade them for humour and difficulty. Twenty individuals with a DSM-lV diagnosis of schizophrenia and 20 healthy matched controls were studied. Severity of current psychopathology was measured using the Krawiecka standardized scale of psychotic symptoms. IQ was estimated using the Ammons and Ammons quick test. Individuals with schizophrenia performed significantly worse than controls in both conditions, this difference being most marked in the ToM condition. No relationship was found for poor ToM performance and psychotic positive symptomatology, specifically delusions and hallucinations. There was evidence for a compromised ToM capability in the schizophrenia group on this visual joke task. In this instance this could not be linked to particular symptomatology.