Search

It is relatively unknown that some of the possible side effects of antibiotic treatment can be transient psychotic episodes and other encephalopathies such as seizure disorders. Since these are rare events, there have not been many studies about them, nor is there a clear understanding of the underlying basis for these symptoms. This phenomenon was recently brought to our attention by a patient whose case history is discussed here. For the past few years, he has been diagnosed at different times with schizophrenia, schizoaffective disorder, bipolar disorder with psychosis, temporal lobe epilepsy, and psychogenic nonepileptic seizures. He was seen by a neurologist and placed on carbamazepine, which by his admittance helped him tremendously. During this same time period, psychiatrists placed him on various antipsychotic medications as well. The patient researched many medical conditions and came to the conclusion that his symptoms are caused by a large dose of an "antibiotic" given to him on his first day of basic training for the military, the so called "peanut butter shot", although he has not been able to convince his physicians of this theory. Whether or not this patient has a chronic schizophrenia-like illness or an adverse reaction to antibiotics, this case is presented so that clinicians are aware that neurological and psychiatric side effects can occur as rare reactions to antibiotic therapy and that treatment with an anti-seizure drug concurrently used as a mood stabilizer may be warranted in such cases. [ABSTRACT FROM AUTHOR]

With a political debate about the potential risks and benefits of cannabis use as a backdrop, the wave of legalization and liberalization initiatives continues to spread. Four states (Colorado, Washington, Oregon, and Alaska) and the District of Columbia have passed laws that legalized cannabis for recreational use by adults, and 23 others plus the District of Columbia now regulate cannabis use for medical purposes. These policy changes could trigger a broad range of unintended consequences, with profound and lasting implications for the health and social systems in our country. Cannabis use is emerging as one among many interacting factors that can affect brain development and mental function. To inform the political discourse with scientific evidence, the literature was reviewed to identify what is known and not known about the effects of cannabis use on human behavior, including cognition, motivation, and psychosis. [ABSTRACT FROM AUTHOR]

Schizophrenia likely results from poorly understood genetic and environmental factors. We studied the gene encoding the synaptic protein SHANK3 in 285 controls and 185 schizophrenia patients with unaffected parents. Two de novo mutations (R1117X and R536W) were identified in two families, one being found in three affected brothers, suggesting germline mosaicism. Zebrafish and rat hippo- campal neuron assays revealed behavior and differentiation defects resulting from the R1117X mutant. As mutations in SHANK3 were previously reported in autism, the occurrence of SHANK3 mutations in subjects with a schizophrenia phenotype suggests a molecular genetic link between these two neurodevelopmental disorders. [ABSTRACT FROM AUTHOR]

Background: For diagnosis of neuropsychiatric disorders, a categorical classification system is often utilized as a simple way for conceptualizing an often complex clinical picture. This approach provides an unsatisfactory model of mental illness, since in practice patients do not conform to these prototypical diagnostic categories. Family studies show notable familial co-aggregation between schizophrenia and bipolar illness and between schizoaffective disorders and both bipolar disorder and schizophrenia, revealing that mental illness does not conform to such categorical models and is likely to follow a continuum encompassing a spectrum of behavioral symptoms. Results and Methodology: We introduce an analytic framework to dissect the phenotypic heterogeneity present in complex psychiatric disorders based on the conceptual paradigm of a continuum of psychosis. The approach identifies subgroups of behavioral symptoms that are likely to be phenotypically and genetically homogenous. We have evaluated this approach through analysis of simulated data with simulated behavioral traits and predisposing genetic factors. We also apply this approach to a psychiatric dataset of a genome scan for schizophrenia for which extensive behavioral information was collected for each individual patient and their families. With this approach, we identified significant evidence for linkage among depressed individuals with two distinct symptom profiles, that is individuals with sleep disturbance symptoms with linkage on chromosome 2q13 and also a mutually exclusive group of individuals with symptoms of concentration problems with linkage on chromosome 2q35. In addition we identified a subset of individuals with schizophrenia defined by language disturbances with linkage to chromosome 2p25.1 and a group of patients with a phenotype intermediate between those of schizophrenia and schizoaffective disorder with linkage to chromosome 2p21. Conclusions: The findings presented are novel and demonstrate the efficacy of this approach in detection of genes underlying such complex human disorders as schizophrenia and depression. [ABSTRACT FROM AUTHOR]

It is suggested that chromosome 18p11 is a susceptibility region for both bipolar disorder and schizophrenia. Aiming to identify susceptibility gene(s), we investigated a family whose members have either schizophrenia or schizophrenia-spectrum psychosis and carried a t(18;21)(p11.1;p11.1) translocation. Fluorescence in situ hybridization showed that the breakpoint on chromosome 21 was localized to a bacterial artificial chromosome (BAC) clone RP11-2503J9, which contained coding sequences for transmembrane phosphatase with tensin homology, although this gene was not disrupted. On chromosome 18p, the break point was narrowed to BAC clone RP11-527H14. In silico sequence analysis of this clone identified possible pseudo genes and gene fragments but no intact genes. RP11-527H14 also showed sites of cross hybridization, including 21p11.1. To test for a position effect on 18p11 sequences translocated to 21p11, we performed quantitative RT-PCR to measure the expression of the candidate gene C18orf1 in translocation carriers, but found no significant differences from controls in lymphoblastoid cells.Journal of Human Genetics (2009) 54, 386–391; doi:10.1038/jhg.2009.47; published online 22 May 2009 [ABSTRACT FROM AUTHOR]

Abstract: A novel magnetic resonance imaging method was used to determine whether it is feasible to detect early signs of cortical atrophy among individuals who are at high risk for developing schizophrenia. Fifteen individuals at high-risk for schizophrenia and 15 of their first degree relatives diagnosed with schizophrenia were compared with controls (n =25) who did not have a family history of psychiatric illness or psychiatric hospitalizations. On the basis of a voxelwise analysis of apparent diffusion coefficient (ADC) maps derived from diffusion weighted magnetic resonance imaging, these individuals showed evidence of deficits in four separate regions of the brain, all on the left side only: parahippocampal gyrus, lingual gyrus, superior frontal gyrus, and middle frontal gyrus. However, conventional volumetric quantification of ventricular space to detect atrophy failed to reveal differences between high-risk subjects and controls. It is concluded that ADC may be a more sensitive measure than ventricular volume assessments for use in future studies of early prediction of schizophrenia. [Copyright &y& Elsevier]

Abstract: The present study used magnetic resonance imaging to examine the volumes of the temporal lobe and the superior temporal gyrus in a 10-year follow-up study of 27 patients with schizophrenia and 10 controls. No change over time was observed in these structures when patients were compared with controls. These results do not support the notion that progressive temporal lobe deterioration occurs in schizophrenia. [Copyright &y& Elsevier]

Background: Since their introduction as diagnostic criteria by Schneider in 1937, nuclear symptoms have played a key role in concepts of schizophrenia, but their relationship to each other and to genetic predisposition has been unclear.Aims: To ascertain the factor structure and familiality of nuclear symptoms.Methods: Nuclear (Schneiderian) symptoms were extracted from case notes and interviews in a study of 103 sibling pairs with DSM-III-R schizophrenia or schizoaffective disorder.Results: Principal components analysis demonstrated two major factors: one, accounting for about 50% of the variance, groups thought withdrawal, insertion and broadcasting, with delusions of control; and the second, accounting for < 20% of the variance, groups together third-person voices, thought echo and running commentary. Factor I was significantly correlated within sibling pairs.Conclusions: The correlation within sibling pairs suggests that, contrary to the conclusion of some previous studies, some nuclear symptoms do show a degree of familiality and therefore perhaps heritability. [ABSTRACT FROM AUTHOR]

Background: There have been many studies reporting reduced volume of the hippocampus or other limbic structures in patients with schizophrenia, but the literature is inconsistent.Aims: To compare patients with either first-episode or chronic schizophrenia with controls using high-resolution volumetric magnetic resonance imaging (MRI) scans.Method: Thirteen patients with first-episode schizophrenia, 27 with chronic schizophrenia and 31 controls had 1.5 mm coronal slices taken through the whole brain using a spoiled-grass MRI acquisition protocol.Results: The parahippocampal gyrus was reduced significantly on the left side in patients with chronic schizophrenia compared with controls for both male and female patients, whereas the hippocampus was reduced significantly on both sides only in female patients. There were no significant reductions in any structure between patients with first-episode schizophrenia and controls.Conclusions: Volumetric reduction seen in patients with chronic schizophrenia may be due to an active degenerative process occurring after the onset of illness. [ABSTRACT FROM AUTHOR]

We investigated linkage between schizophrenia and the loci DXYS14, DXYS17, and MIC2 within the pseudoautosomal region in 85 families with two or more siblings suffering from schizophrenia or schizoaffective disorder. A maximum lod score of 2.44 was reached at MIC2, with a dominant model of inheritance at a recombination fraction of 0.367 in females and 0.046 in males (a F:M sex ratio > 1, i.e. opposite to that expected with a pseudoautosomal locus). Evidence consistent with linkage (P = 0.01) was also obtained with a sibling pair analysis at the MIC2 locus. These data do not support (although they do not definitively exclude) a locus within the pseudoautosomal region; they are consistent with the presence of a gene that predisposes to schizophrenia in the sex-specific regions of the X and Y chromosomes. [ABSTRACT FROM AUTHOR]

The hypothesis that at least a subgroup of familial cases of schizophrenia could be due to a genetic defect on the X chromosome is supported by the observation of an excess of X-chromosome aneuploidies (XXX and XXY) among populations of patients with psychosis. The distal long arm, Xq27-q28, is a candidate region where linkage has been claimed to manic-depressive disorder and a fragile site has been associated with schizophrenia spectrum disorders. The present study excluded linkage to a large part of this region using four polymorphic probes and multipoint lod-score analysis in 10 families with multiple members with schizophrenia. [ABSTRACT FROM AUTHOR]

The hypothesis that the gene for schizophrenia is located in the pseudoautosomal region of the sex chromosomes predicts that same-sex concordance will occur in paternally rather than maternally derived pairs. In 120 families that included at least one sibling pair with schizophrenia, affected members were significantly more likely to be of the same sex when there was a history of illness on the paternal than on the maternal side, the difference remaining significant when parent of origin was assessed by three different methods. The finding is as predicted by the pseudoautosomal hypothesis: therefore a search for the gene should be focused on this small (three megabase) region of the genome. The ratio of same to mixed sex pairs in paternally-derived cases (approximately 3:1) suggests the gene is located in the centromeric one-third of the pseudoautosomal region. [ABSTRACT FROM AUTHOR]

Serum immunoglobulins were quantified in 85 consecutively admitted patients from an acute-care psychiatric in-patient unit. The patients were diagnosed as: major depressive disorder, 53; chronic schizophrenia, 12; schizophreniform psychosis, 4; substance abuse disorder, 12; and miscellaneous other diagnoses, 4. A small sub-group of these patients, which included six with major depression, one with chronic schizophrenia, and one with a personality disorder, were found to have low IgM concentrations. Immunoglobulin levels were not associated with use of medication or length of illness prior to this hospital admission. This study provides further evidence for suppression of humoral immunity in some psychiatric patients (approximately 10%). [ABSTRACT FROM AUTHOR]

This study aimed to identify risk factors for relapse (psychiatric emergency department visits or hospitalization) and lack of follow-up with outpatient psychiatric care in the 12 months after ending services in an urban safety net coordinated specialty care (CSC) program for first episode psychosis (FEP). The study population (n = 143) were individuals with FEP who had any CSC care between 2014 and 2021. To identify risk factors for relapse and follow up after exit, multivariable logistic regression was performed using data from electronic health records and linked insurance claims data. Individuals with any emergency department visit or hospitalization 12 months prior to ending CSC (aOR = 4.69, 95 % CI 1.78–12.34) and those who were using cannabis at last CSC contact (aOR = 4.06, 95 % CI 1.56–10.56) had a higher risk of relapse after ending CSC services. Cannabis use at last contact was also associated with lower rates of outpatient psychiatric follow-up (aOR = 0.32, 95 % CI 0.12–0.94), while CSC duration in months had a small positive association with post-CSC psychiatric follow-up. There were no differences in relapse or follow-up by race or ethnicity, primary diagnosis, or medication usage. Prior relapse during CSC predicted relapse in the 12 months after ending CSC services, but not outpatient follow up. Cannabis use predicted both a higher rate of relapse and a lower rate of follow up after ending services. There were no differences by race or ethnicity in our sample, suggesting that once individuals engaged in FEP care there were no evident disparities in the observed outcomes. [ABSTRACT FROM AUTHOR]

• Tobacco increases risk of psychosis, but the effect of nicotine vaping is unknown. • Use of nicotine vapes was associated with a twofold higher risk of first episode psychosis. • This finding was confined to only the heaviest users of nicotine vapes. • Trends in nicotine vape use and mental health sequelae should be closely monitored. Tobacco use has been established as a possible risk factor for psychosis, but the effect of electronic nicotine delivery systems (ex. nicotine vapes) has not been independently established. Using the Population Assessment of Tobacco and Health study, we found that use of electronic nicotine products was significantly associated with later first episode psychosis after controlling for substance use and other confounders, and that this relationship was only significant among the heaviest users (>20 puffs/day). Given the rapid rise in electronic nicotine products use, clinicians and public health professionals should consider potential impacts and closely monitor trends in the coming years. [ABSTRACT FROM AUTHOR]

Abstract: Background: Cannabis is one of the most highly abused illicit drugs in the world. Several studies suggest a link between adolescent cannabis use and schizophrenia. An understanding of this link would have significant implications for legalization of cannabis and its medicinal value. The present study aims to determine whether familial morbid risk for schizophrenia is the crucial factor that underlies the association of adolescent cannabis use with the development of schizophrenia. Methods: Consecutively obtained probands were recruited into four samples: sample 1: 87 non-psychotic controls with no drug use; sample 2: 84 non-psychotic controls with cannabis use; sample 3: 32 patients with a schizophrenia spectrum psychosis with no drug use; sample 4: 76 patients with schizophrenia spectrum psychosis with cannabis use. All cannabis using subjects used this drug during adolescence, and no other substance, with the exception of alcohol. Structured interviews of probands and family informants were used to obtain diagnostic information about probands and all their known relatives. Results: There was an increased morbid risk for schizophrenia in relatives of the cannabis using and non-using patient samples compared with their respective non-psychotic control samples (p=.002, p<.001 respectively). There was no significant difference in morbid risk for schizophrenia between relatives of the patients who use or do not use cannabis (p=.43). Conclusions: The results of the current study suggest that having an increased familial morbid risk for schizophrenia may be the underlying basis for schizophrenia in cannabis users and not cannabis use by itself. [Copyright &y& Elsevier]

Introduction Several studies have associated cannabis use with the development of schizophrenia. However, it has been difficult to disentangle the effects of cannabis from that of other illicit drugs, as previous studies have not evaluated pure cannabis users. To test whether the onset of cannabis use had an effect on the initiation of psychosis, we examined the time relationship between onset of use and onset of psychosis, restricting our analysis to a cohort of individuals who only used cannabis and no other street drugs. Methods Fifty‐seven subjects with non-affective psychoses who used cannabis prior to developing a psychosis were interviewed using the Diagnostic Interview for Genetic Studies (DIGS). The Family Interview for Genetic Studies (FIGS) was also used to interview a family informant about psychiatric illness in the patient and the entire family. Multiple linear regression techniques were used to estimate the association between variables. Results After adjusting for potential confounding factors such as sex, age, lifetime diagnosis of alcohol abuse or dependence, and family history of schizophrenia, the age at onset of cannabis was significantly associated with age at onset of psychosis ( β = 0.4, 95% CI = 0.1–0.7, p = 0.004) and age at first hospitalization ( β = 0.4, 95% CI = 0.1–0.8, p = 0.008). The mean time between beginning to use cannabis and onset of psychosis was 7.0 ± 4.3. Age at onset of alcohol use was not associated with age at onset of psychosis or age at first hospitalization. Conclusion Age at onset of cannabis is directly associated with age at onset of psychosis and age at first hospitalization. These associations remain significant after adjusting for potential confounding factors and are consistent with the hypothesis that cannabis could cause or precipitate the onset of psychosis after a prolonged period of time. [ABSTRACT FROM AUTHOR]

Abstract: Background: Structural and functional abnormalities have been found in language-related brain regions in patients with schizophrenia. We previously reported findings pointing to differences in word processing between people with schizophrenia and individuals who are at high-risk for schizophrenia using a voxel-based (whole brain) fMRI approach. We now extend this finding to specifically examine functional activity in three language related cortical regions using a larger cohort of individuals. Method: A visual lexical discrimination task was performed by 36 controls, 21 subjects at high genetic-risk for schizophrenia, and 20 patients with schizophrenia during blood oxygenation level dependent (BOLD) fMRI scanning. Activation in bilateral inferior frontal gyri (Brodmann''s area 44–45), bilateral inferior parietal lobe (Brodmann''s area 39–40), and bilateral superior temporal gyri (Brodmann''s area 22) was investigated. For all subjects, two-tailed Pearson correlations were calculated between the computed laterality index and a series of cognitive test scores determining language functioning. Results: Regional activation in Brodmann''s area 44–45 was left lateralized in normal controls, while high-risk subjects and patients with schizophrenia or schizoaffective disorder showed more bilateral activation. No significant differences among the three diagnostic groups in the other two regions of interest (Brodmann''s area 22 or areas 39–40) were found. Furthermore, the apparent reasons for loss of leftward language lateralization differed between groups. In high-risk subjects, the loss of lateralization was based on reduced left hemisphere activation, while in the patient group, it was due to increased right side activation. Language ability related cognitive scores were positively correlations with the laterality indices obtained from Brodmann''s areas 44–45 in the high-risk group, and with the laterality indices from Brodmann''s areas 22 and 44–45 in the patient group. Conclusions: This study reinforces previous language related imaging studies in high-risk subjects and patients with schizophrenia suggesting that reduced functional lateralization in language related frontal cortex may be a vulnerability marker for schizophrenia. Future studies will determine whether it is predictive of who develops illness. [Copyright &y& Elsevier]

We previously reported relative stability in neuropsychological functions over a 4- to 5-year period after the onset of a first episode of schizophrenia, with patients demonstrating less improvement than controls on some functions [Hoff, A.L., Sakuma, M., Wieneke, M., Horon, R., Kushner, M., DeLisi, L.E., 1999. A longitudinal follow-up study of neuropsychological functioning subsequent to a first-episode of schizophrenia. American Journal of Psychiatry 156, 1336-1341.]. The current study was conducted to extend follow-up evaluations through 10 years of illness to determine whether neuropsychological functions remain stable or deteriorate over a longer time period. Twenty-one first episode patients and 8 controls were re-evaluated 10 years after an initial evaluation on neuropsychological and clinical measures. Repeated measures analyses demonstrated no differences between patients and controls in degree of change over this time period nor was change in symptoms reliably associated with improvement or deterioration in cognitive abilities. However, baseline level of cognitive functioning was correlated with the degree of change. Thus, when the baseline level of functioning was controlled for in the analyses, less or lack of improvement was seen in the patients compared with controls in verbal intellectual functioning, delayed verbal and nonverbal recall, and cognitive inhibition (Stroop Color Word Test). In no test did patients deteriorate significantly more than controls. We conclude that most first episode patients have had considerable cognitive decline by the time of their first hospitalization and that it remains relatively stable through at least 10 years of illness. Most cognitive change takes place early in this illness, prior to the first hospitalization, but its exact timing still remains unknown. [ABSTRACT FROM AUTHOR]