Appearance Of Psychotic Symptoms Research Articles

Structural abnormalities in language circuits in genetic high-risk subjects and schizophrenia patients

Schizophrenia is a severe psychiatric disorder with a strong genetic predisposition. Structural and functional brain deficits throughout the cerebral cortex, particularly in the language-processing associated brain regions, are consistently reported. Recently, increasing evidence from magnetic resonance imaging (MRI) studies suggests that healthy relatives of schizophrenia patients also show structural brain abnormalities in cortical gray matter (GM) volume and thickness, suggesting that this may be associated with an unexpressed genetic liability for the disorder. Unfortunately, the findings are not consistent, which may be caused by different age ranges of the cohorts studied. In the present study, we examined the voxel-based whole brain cortical thickness, area, GM volume densities, and regional cortical thickness-related laterality indices in 14 bilateral regions of interest (ROIs) from known language-processing circuits in 20 schizophrenia patients, 21 young non-psychotic subjects with heightened genetic risk for schizophrenia at the peak ages for development of the disorder, and 48 matched controls. The results showed widespread significant reductions in cortical thickness, cortical GM volume density, and scattered decreases in cortical surface area in the schizophrenia patients compared with those in the high-risk subjects and normal controls. Moreover, the genetic high-risk subjects showed significantly increased regional cortical thickness in 7 of the 14 ROIs in the language-processing pathway when compared with controls. They also had increased GM volume density in scattered regions associated with language-processing when compared with the normal controls. Laterality analyses showed that the spatial distribution of abnormal cortical thickness in the schizophrenia patients, as well as in the high-risk subjects, contributes to a decrease of the normal left-greater-than-right anatomical asymmetry in the inferior orbital frontal area, and a increased left-greater-than-right pattern in the inferior parietal and occipital regions. Together with the existing findings in the literature, the results of the present study suggest that developmental disruption of the anatomical differentiation of the hemispheres provides a basis for understanding the language impairment and symptoms of psychosis, and that these may arise because of abnormal left–right hemispherical communications that interrupt the normal flow of information processing. The early structural deficits in language-processing circuits may precede the appearance of psychotic symptoms and may be an indicator of an increased risk of developing schizophrenia.

Endocannabinoid system and psychiatry: in search of a neurobiological basis for detrimental and potential therapeutic effects.

Public concern on mental health has noticeably increased given the high prevalence of neuropsychiatric disorders. Cognition and emotionality are the most affected functions in neuropsychiatric disorders, i.e., anxiety disorders, depression, and schizophrenia. In this review, most relevant literature on the role of the endocannabinoid (eCB) system in neuropsychiatric disorders will be presented. Evidence from clinical and animal studies is provided for the participation of CB1 and CB2 receptors (CB1R and CB2R) in the above mentioned neuropsychiatric disorders. CBRs are crucial in some of the emotional and cognitive impairments reported, although more research is required to understand the specific role of the eCB system in neuropsychiatric disorders. Cannabidiol (CBD), the main non-psychotropic component of the Cannabis sativa plant, has shown therapeutic potential in several neuropsychiatric disorders. Although further studies are needed, recent studies indicate that CBD therapeutic effects may partially depend on facilitation of eCB-mediated neurotransmission. Last but not least, this review includes recent findings on the role of the eCB system in eating disorders. A deregulation of the eCB system has been proposed to be in the bases of several neuropsychiatric disorders, including eating disorders. Cannabis consumption has been related to the appearance of psychotic symptoms and schizophrenia. In contrast, the pharmacological manipulation of this eCB system has been proposed as a potential strategy for the treatment of anxiety disorders, depression, and anorexia nervosa. In conclusion, the eCB system plays a critical role in psychiatry; however, detrimental consequences of manipulating this endogenous system cannot be underestimated over the potential and promising perspectives of its therapeutic manipulation.

Psychopathology and personality traits in psychotic patients and their first-degree relatives

Personality dimensions have been associated with symptoms dimensions in schizophrenic patients (SP). In this paper we study the relationships between symptoms of functional psychoses and personality dimensions in SP and their first-degree relatives (SR), in other psychotic patients (PP) and their first-degree relatives (PR), and in healthy controls in order to evaluate the possible clinical dimensionality of these disorders. Twenty-nine SP, 29 SR, 18 PP, 18 PR and 188 controls were assessed using the temperament and character inventory (TCI-R). Current symptoms were evaluated with positive and negative syndrome scale (PANSS) using the five-factor model described previously (positive [PF], negative [NF], disorganized [DF], excitement [EF] and anxiety/depression [ADF]). Our TCI-R results showed that patients had different personality dimensions from the control group, but in relatives, these scores were not different from controls. With regard to symptomatology, we highlight the relations observed between harm avoidance (HA) and PANSS NF, and between self-transcendence (ST) and PANSS PF. From a personality traits-genetic factors point of view, schizophrenia and other psychosis may be initially differentiated by temperamental traits such as HA. The so-called characterial traits like ST would be associated with the appearance of psychotic symptoms.

Auditory P300 in individuals clinically at risk for psychosis

Background Alterations of the auditory evoked P300 potential are among the most reliable biological markers of schizophrenia. The aim of this study was to assess the amplitude, latency, and topography of the P300 in individuals at clinical high risk for psychosis. Methods P300 event-related potentials were acquired with an auditory oddball paradigm from 100 patients putatively in an early initial prodromal state (EIPS) for psychosis or in a late initial prodromal state (LIPS), according to the criteria of the German Research Network on Schizophrenia, and from 40 healthy controls comparable with respect to age, gender, and estimated verbal IQ. Results In the LIPS group, P300 amplitude was significantly smaller at midline and left hemispheric electrodes in comparison with controls. In the EIPS group, P300 amplitude was significantly reduced at a left temporoparietal site (TP7). A family history of schizophrenia was associated with smaller posterior P300 amplitudes in high-risk individuals. Midline P300 amplitudes were smaller in LIPS who had experienced already brief limited intermittent psychotic symptoms. Conclusion Smaller P300 amplitudes are present prior to a putative onset of psychosis in high-risk individuals. Selective left temporoparietal amplitude deficits may indicate a trait-like abnormality whereas deficits at sagittal midline electrodes may be partly determined by the changes that underlie the appearance of psychotic symptoms. P300 amplitude may be associated with left superior temporal lobe maturation abnormalities followed by further functional impairments later in life. Our follow-up study will reveal whether P300 amplitude alterations predict psychosis and help to targeting early intervention.

Cingulate gyral reductions are related to low executive functioning and psychotic symptoms in 22q11.2 deletion syndrome

A similar pattern of deficits in executive function and neuroanatomical abnormalities is shared between 22q11.2 deletion syndrome (22q11DS) and schizophrenia, suggesting that common cerebral alterations may lead to cognitive dysfunction and promote the appearance of psychotic symptoms in 22q11DS individuals. Specifically, there is increasing evidence for involvement of the cingulate gyrus (CG) in executive dysfunction and the expression of positive symptoms in schizophrenia. The aim of our study is to examine CG morphology in a 22q11DS population and its potential role as a cerebral marker of executive dysfunction and the manifestation of psychotic symptoms. Using region of interest (ROI)-based analysis, we compared CG volumes from 58 children and adults affected by 22q11DS with 64 healthy age- and gender-matched controls. After covarying for total cranium grey matter and age, a bilateral reduced CG grey matter volume, driven by a decrease in anterior CG cortex, was observed among 22q11DS patients. Further post hoc analyses suggest correlations between right CG cortical reductions, low-executive functioning and the occurrence of psychotic symptoms. The CG structural abnormalities observed in 22q11DS are consistent with previous reports in schizophrenic patients and are associated with pre-morbid cognitive impairments. The mechanisms by which these changes may modulate executive functioning and the expression of psychosis are discussed.

Determining the chronology and components of psychosis onset: The Nottingham Onset Schedule (NOS)

The Nottingham Onset Schedule (NOS) is a short, guided interview and rating schedule to measure onset in psychosis. Onset is defined as the time between the first reported/observed change in mental state/behaviour to the development of psychotic symptoms. Onset is conceptualised as comprising of (i) a prodrome of two parts: a period of ‘unease’ followed by ‘non-diagnostic’ symptoms; (ii) appearance of psychotic symptoms; and (iii) a build-up of diagnostic symptoms leading to a definite diagnosis. Twenty consecutive cases of first-episode psychosis were administered the NOS schedule to determine its psychometric properties including inter-rater and test–retest reliability. Its clinical and research potential as a reliable measure of duration of untreated psychosis (DUP) was assessed in a cohort of 99 cases of first-episode psychosis (56 schizophrenia, 43 affective psychoses). NOS identified all prodromal symptoms previously reported in other studies. There was high degree of inter-rater and test–retest reliability for all components of NOS. Duration of untreated psychosis was significantly longer ( p < 0.05) in schizophrenia (mean 179 days, S.D. 344; median 52 days) than in affective psychosis (mean 15 days, S.D. 116; median 12 days) but there were no gender differences between lengths of prodrome or treatment delays. The NOS provides a standardised and reliable way of recording early changes in psychosis and identifying relatively precise time points for measuring several durations in emerging psychosis. The scale is easy to use and is not time-consuming or labour intensive. Onset, as measured by NOS, is significantly longer in schizophrenic disorders than in affective psychosis. A small proportion of schizophrenia cases have very long DUP. Some cases with schizophrenia receive anti-psychotics in the prodromal phase, prior to the emergence of frank psychotic symptoms.

Estilo atribucional en el espectro esquizofrénico

In this article we present a review of empirical studies into the attributional style in patients with schizophrenic disorders which have been published in the last fifteen years. Some of these investigations, irrespective of their diagnosis, have focused on the study of attributions in persons experiencing persecutory delusions. Others have centred on the attributional style of specific diagnostic categories, such as delusional disorder or schizophrenia. Because of the diversity of the samples studied, we have found contradictory results. On the other hand, all these investigations are transversal, which does not permit us to study the causal relationship between the attributional style and the appearance of psychotic symptoms. With future research in this area these limitations may be overcome.

Manifestaciones psiquiátricas de la enfermedad de Parkinson tras la cirugía de estimulación cerebral profunda del núcleo subtalámico

To review the increasing number of papers that report diverse neuropsychiatric disorders that happen in patients diagnosed of Parkinson's disease submitted to brain deep stimulation of subthalamic nuclei with high frequency current. It is a fact the need to evaluate carefully all the patients who have to submit to this surgical procedure analyzing previous psychiatric history, and the possible appearance of psychiatric sphere symptoms after surgery. The acute depression and the euphoric moods (than can occur immediately after surgery) and major depression, obsession, widespread anxiety and substance abuse (among those of more delayed appearance) constitute examples of this pathology. The treatment of previous psychiatric disorders is forced in all cases and specially relevant in the major depression when suicide ideas coexist. Information that allow to predict the risk of developing depressive disorders in the postoperative period does not exist at present time, though it is more predictable that it happens in those patients with previous severe depressive history. In general, euphoric moods, apathy and depression, usually are transient and of multifactorial origin that includes the existence of endogenous predisposition, the change to an independence pattern after surgery, the psychotropic effect of levodopa, and the high frequency current stimulation effect on the non motor structures target and in the adjacent regions. It must be outlined that it is possible the appearance of psychotic symptoms after brain deep stimulation of subthalamic nuclei in patients with ideal results on motor disability.

Evidence of a cohort effect for age at onset of schizophrenia.

The authors address whether a possible age-at-onset cohort effect may have introduced a bias into anticipation studies of schizophrenia. A retrospective review of the medical records of all admissions for psychotic disorders (N=877) was conducted. All subjects with a confirmed DSM-IV diagnosis of schizophrenia and age-at-onset data were included (N=419). For analyses, subjects were placed into one of three successive birth cohorts: 1905-1944 (N=96), 1945-1964 (N=200), and 1965-1984 (N=123). The mean age at first appearance of psychotic symptoms and, similarly, the mean age at first hospitalization significantly decreased over time in successive birth cohorts (25.3, 23.3, and 20.4 years, respectively, for age at first appearance of psychotic symptoms). This potential birth cohort effect for age at onset of schizophrenia needs to be incorporated into genetic models.

An “Accidental” Acute Psychosis with Ecstasy Use

Over the last 10 years, Europe has witnessed the development of the ecstasy phenomenon; this term is used to describe several products sharing more or less the same effects. The most widely used and hence the most well known is 3,4 MDMA, but MDA, MDEA, MBDB and even 2CB or nexus are available. The psychopathological consequences of MDMA use in man are relatively poorly understood. The case reported here involves an acute psychotic episode with residual symptoms after six months, with a sudden onset at least 12 hours after taking alcohol and ecstasy without realising it, in an individual with no previous psychopathology other than a moderate anxiety disorder. Twelve cases of acute psychotic episodes after taking ecstasy have been reported in the literature; two after taking the drug on two occasions and one after a single use. No authors have examined the previous mental state or possible previous psychopathology with any precision. The present subject had not displayed any previous psychotic behavior when tested with a proven standardized interview technique; this was confirmed by his peers and his family. He did, however, show signs of social phobia. Although the personality of an individual is a factor in taking a drug, and probably in the quality of the psychotropic effects experienced, a host of arguments favor the appearance of psychotic symptoms de novo, which were probably related to direct toxicity by MDMA and/or its metabolites on the serotoninergic neurons.

Early brain screening may predict schizophrenia

Screening for early brain changes may predict schizophrenia, scientists have claimed. A new brain imaging study published in the American Journal of Psychiatry (2000;157(111);1829-34) shows that there are substantial brain changes in schizophrenia at the earliest stages of the illness, implying that these changes pre- cede the appearance of psychotic symptoms. PET scans also show changes in the schizophrenic human brain (DR MONTY BUSCHBAUM, PETER ARNOLD INC/ SCIENCE PHOTO LIBRARY) The findings from the Institute of Psychiatry indicate that brain …

Earlier puberty as a predictor of later onset of schizophrenia in women.

The aim of this study was to determine whether puberty plays a mediating role in onset of schizophrenia. The hypothesis was that there is an inverse relation between age at puberty (menarche) and age at onset in women. Competent and consenting individuals with DSM-IV-defined schizophrenia or schizoaffective disorder and their mothers underwent a 45-minute interview to ascertain age at first odd behavior, age at first psychotic symptoms, age at first hospitalization, and ages at various indices of puberty. Information about substance use, head injury, perinatal trauma, and first-degree family history of schizophrenia was also obtained. In the women (N = 35), the earlier the age at menarche, the later the ages at both the first psychotic symptoms and the first hospitalization. There was no significant association between puberty and onset in the men (N = 45). Other than gender, none of the examined variables played a role in the interaction of puberty and onset of illness. In women, early puberty (whether through hormonal or social influence) was associated with later onset of schizophrenia. This effect was not found in men; in fact, the trend was in the opposite direction.

Establishing the onset of psychotic illness.

To date, the literature has provided no standardized, replicable method for establishing illness onset. The authors describe a method for dating the first appearance of prodromal signs of psychotic illness, the emergence of an acute episode, and the initiation of treatment seeking. Using reports by family and friends about a sample of 141 subjects with first-episode psychosis, the investigators derived a checklist of behaviors describing the evolution of various phases of illness. Supplied with the checklist, clinician pairs independently rated the critical phases in the evolution of illness: first appearance of noticeable symptoms, first appearance of prominent psychotic symptoms, and initiation of treatment seeking. The judges achieved good reliability in assigning age at the first appearance of psychotic symptoms and at initiation of treatment seeking. Judging the beginning of the prodrome proved more difficult. Insidious onset proved as characteristic of affective psychosis as of schizophrenia, while treatment lag--the interval between emergence of acute psychotic symptoms and initiation of treatment seeking--was longer for schizophrenia than for affective psychosis. Onset of schizophrenia occurred earlier in women than in men. Depression with psychotic features appeared earlier in men than women. Although dating the onset of illness phases is probably feasible, efforts to improve reliability must continue. The study results challenge beliefs about gender differences in age at onset.

Psychosis Associated with Untreated Hypothyroidism in a Young Adolescent: A Review of Neuropsychiatrie Findings in Children and Adolescents with Thyroid Disorders

Four cases of psychosis coexisting with hypothyroidism have been reported in children and adolescents, but the psychosis was attributed to thyroid replacement therapy in three cases and hypothyroidism was thought to be etiological in only one case. This article describes a possible second case of psychosis due to hypothyroidism in an adolescent who, at age 13 years, is the youngest reported case of myxedema psychosis. Treatment of the psychosis with L-T4 produced a rapid improvement in symptoms, but obsessional symptoms persisted and responded to fluoxetine. Speculatively, the patient's comorbid obsessive–compulsive disorder may have contributed to an aggravation of anxiety symptoms or operated as a predisposing factor that led to the appearance of psychotic symptoms during the hypothyroid episode. As in many presentations of "myxedema madness" in adults, a coincidental therapeutic response to thyroid treatment cannot be ruled out, so the link between hypothyroidism and psychosis cannot be considered definitive. A discussion of the diagnostic dilemmas presented by cases of hypothyroidism and psychosis is presented, and possible biochemical interrelationships are considered. In both reported adolescent cases, psychosis was the first sign of hypothyroidism and (in contrast to most adult cases) the onset of psychosis was rapid. It is premature to offer specific guidelines about when thyroid workup would be useful or cost effective, but thyroid testing may be considered if psychosis in a child or adolescent is associated with a family history of thyroid disease, goiter, or acute onset of symptoms.

Neuropsychology of Late-Life Psychoses

The number of published neuropsychological studies of older psychiatric patients have been few. Moreover, almost nothing is known about the neuropsychological status of older individuals who develop psychotic symptoms for the first time later in life. Because of the spectrum of possible diagnostic considerations, careful diagnostic evaluations are of critical importance. Such evaluations should include comprehensive history-taking (using several sources), in addition to medical, psychiatric, neurologic, neuroimaging, and neuropsychological assessments. As the number of older individuals in our population grows, we will be increasingly faced with neuropsychiatric disorders that may arise de novo in the elderly. Multimodal and longitudinal investigations of older patients who develop psychotic or depressive symptoms are needed.

Exogenous psychoses in Parkinson syndrome. Frequency and causal conditions

Exogenous psychotic symptoms of a wide variety have been reported to appear more and more frequently since the introduction of levodopa in the therapy of Parkinson's disease. They were considered to be caused by treatment related imbalance of cerebral neurotransmitters and hypersensitivity of the dopaminergic receptors, respectively. In the present investigation an analysis was done concerning the relevance of different antiparkinsonian drugs and other factors such as severity of neurological and cerebroorganic symptomatology, age, duration of treatment, EEG and brain atrophic changes and additional physical diseases for the appearance of psychotic symptoms. The questions were posed to 152 patients (54 men, 88 women) aged 34-76 years, which received a treatment with levodopa alone, in combination with a decarboxylase inhibitor, amantadines and/or anticholinergics for a period of 1-9 years. An exogenous psychotic symptomatology was observed in 42 patients (27,6%), explicitly under all antiparkinsonistic drugs, but not when amantadines were given as the initial treatment. In patients receiving levodopa/decarboxylase inhibitor psychotic symptoms could be observed most frequently but at the same time the duration of treatment was the longest. In 15 patients psychotic symptoms appeared under different antiparkinsonian drugs. In 28 patients this symptomatology was followed by a constant severe dementia. Predisposing factors for exogenous psychosis proved to be: a higher age at the beginning of the treatment and the initiation of treatment, a pronounced neurological symptomatology and signs of dementia as well as additional physical diseases. Because of the very complex conditions under which exogenous psychosis can be observed and the additional fact that they can appear under each antiparkinsonian substance, levodopa cannot be considered as the sole cause.(ABSTRACT TRUNCATED AT 250 WORDS)

Responsibility of extrastriatal areas for the appearance of psychotic symptoms (clinical and biochemical human post-mortem findings).

1. A Dopa-medication leads sometimes in Parkinsonian patients to a psychosis. 2. The diminished capacity of striatal dopaminergic neurons to store DA leads to a storage of DA in serotoninergic or noradrenergic neurons. 3. Extrastriatal noradrenergic and/or serotoninergic neurons are involved. 4. Dopaminergic receptors of the striatium are not involved because of a lack of kinetic response after L-Dopa application in Parkinsonian patients with akinetic crises. 5. Extrastriatal dopaminergic receptors of DA as "false transmitter" at serotoninergic receptors seem to be responsible for the production of psychotic symptoms, whereas noradrenaline is not responsible. Psychotic symptoms can be imagined to be triggered by a contact of a transmitter to a nonspecific receptor.