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Auditory verbal hallucinations (AVH) are a cardinal feature of schizophrenia, but they can also appear in otherwise healthy individuals. Imaging studies implicate language networks in the generation of AVH; however, it remains unclear if alterations reflect biologic substrates of AVH, irrespective of diagnostic status, age, or illness-related factors. We applied multimodal imaging to identify AVH-specific pathology, evidenced by overlapping gray or white matter deficits between schizophrenia patients and healthy voice-hearers.
Diffusion-weighted and T1-weighted magnetic resonance images were acquired in 35 schizophrenia patients with AVH (SCZ-AVH), 32 healthy voice-hearers (H-AVH), and 40 age- and sex-matched controls without AVH. White matter fractional anisotropy (FA) and gray matter thickness (GMT) were computed for each region comprising ICBM-DTI and Desikan–Killiany atlases, respectively. Regions were tested for significant alterations affecting both SCZ-AVH and H-AVH groups, relative to controls.
Compared with controls, the SCZ-AVH showed widespread FA and GMT reductions; but no significant differences emerged between H-AVH and control groups. While no overlapping pathology appeared in the overall study groups, younger (<40 years) H-AVH and SCZ-AVH subjects displayed overlapping FA deficits across four regions (p < 0.05): the genu and splenium of the corpus callosum, as well as the anterior limbs of the internal capsule. Analyzing these regions with free-water imaging ascribed overlapping FA abnormalities to tissue-specific anisotropy changes.
We identified white matter pathology associated with the presence of AVH, independent of diagnostic status. However, commonalities were constrained to younger and more homogenous groups, after reducing pathologic variance associated with advancing age and chronicity effects.
Decline in cognitive functioning precedes the first psychotic episode in the course of schizophrenia and is considered a hallmark symptom of the disorder. Given the low incidence of schizophrenia, it remains a challenge to investigate whether cognitive decline coincides with disease-related changes in brain structure, such as white matter abnormalities. The 22q11.2 deletion syndrome (22q11DS) is an appealing model in this context, as 25% of patients develop psychosis. Furthermore, we recently showed that cognitive decline also precedes the onset of psychosis in individuals with 22q11DS. Here, we investigate whether the early cognitive decline in patients with 22q11DS is associated with alterations in white matter microstructure.
We compared the fractional anisotropy (FA) of white matter in 22q11DS patients with cognitive decline [n = 16; −18.34 (15.8) VIQ percentile points over 6.80 (2.39) years] to 22q11DS patients without cognitive decline [n = 18; 17.71 (20.17) VIQ percentile points over 5.27 (2.03) years] by applying an atlas-based approach to diffusion-weighted imaging data.
FA was significantly increased (p < 0.05, FDR) in 22q11DS patients with a cognitive decline in the bilateral superior longitudinal fasciculus, the bilateral cingulum bundle, all subcomponents of the left internal capsule and the left superior frontal-occipital fasciculus as compared with 22q11DS patients without cognitive decline.
Within 22q11DS, the early cognitive decline is associated with microstructural differences in white matter. At the mean age of 17.8 years, these changes are reflected in increased FA in several tracts. We hypothesize that similar brain alterations associated with cognitive decline take place early in the trajectory of schizophrenia.
Hallucinations have consistently been associated with traumatic experiences during childhood. This association appears strongest between physical and sexual abuse and auditory verbal hallucinations (AVH). It remains unclear whether traumatic experiences mainly colour the content of AVH or whether childhood trauma triggers the vulnerability to experience hallucinations in general. In order to investigate the association between hallucinations, childhood trauma and the emotional content of hallucinations, experienced trauma and phenomenology of AVH were investigated in non-psychotic individuals and in patients with a psychotic disorder who hear voices.
A total of 127 non-psychotic individuals with frequent AVH, 124 healthy controls and 100 psychotic patients with AVH were assessed for childhood trauma. Prevalence of childhood trauma was compared between groups and the relation between characteristics of voices, especially emotional valence of content, and childhood trauma was investigated.
Both non-psychotic individuals with AVH and patients with a psychotic disorder and AVH experienced more sexual and emotional abuse compared with the healthy controls. No difference in the prevalence of traumatic experiences could be observed between the two groups experiencing AVH. In addition, no type of childhood trauma could distinguish between positive or negative emotional valence of the voices and associated distress. No correlations were found between sexual abuse and emotional abuse and other AVH characteristics.
These results suggest that sexual and emotional trauma during childhood render a person more vulnerable to experience AVH in general, which can be either positive voices without associated distress or negative voices as part of a psychotic disorder.
The field of left-right (LR) asymmetry is currently at an exciting point, with considerable body of genetic and cell-biological data elucidating dozens of mechanisms in a range of vertebrate and invertebrate model species. The patterning of the LR axis can conceptually be broken down into several distinct steps that have served as a working model for the field. The embryo orients the LR axis with respect to the dorsal-ventral and the anterior-posterior axes, hence being able to "tell its left from its right". Next, the embryo must set up a stable biophysical or molecular difference between the left and right sides, which can be imposed upon multicellular fields as the embryo divides. Third, cell fields on the left and right sides execute transcriptional cascades that set up differential gene expression patterns impinging on organ primordia. Fourth, the various organs make use of this asymmetric information as they undergo asymmetric morphogenesis.
This chapter summarizes literature on handedness, language, and cerebral asymmetry as evidenced by lesion and neuroimaging studies. The development of non-invasive techniques has allowed us to determine functional brain asymmetries even in healthy subjects. The chapter comments on the possible origin of dexterity and language lateralization, the individual differences in laterality, as well as the distribution of laterality at the population level. Human brain imaging studies indicate that Broca's area, which is located in the pars opercularis of the inferior frontal gyrus, may be part of the human mirror neuron system as well as the superior temporal sulcus and the inferior parietal lobule. The relation between handedness and language lateralization invites speculation on the underlying neural causes. Lateralization of language functions should aid the processing demands required for a full exhaustion of linguistic capacities.
In 1861 Paul Broca discovered that, in most individuals, the left hemisphere of the brain is dominant for language. Taking language as an example, the first part of this book explains the normal development of bodily asymmetry and lateralization, its association with hand preference, genetic aspects, geographical differences and the influence of gender. The coverage then moves on to review the association between language lateralization and psychosis, describing findings in patients with schizophrenia to suggest the dominant hemisphere may fail to completely inhibit the language areas in the non-dominant half. The language allowed to 'release' from the right hemisphere can lead to psychotic symptoms including auditory verbal hallucinations and formal thought disorder. This book should be read by psychiatrists, neurologists and neuroscientists working in the field of psychosis and other brain scientists interested in laterality.
In previous functional magnetic resonance imaging (fMRI) studies, participants with schizophrenia showed decreased language lateralisation, resulting from increased activation of the right hemisphere compared with controls.
To determine whether decreased lateralisation and increased right cerebral language activation constitute genetic predispositions for schizophrenia.
Language activation was measured using fMRI in 12 right-handed monozygotic twin pairs discordant for schizophrenia and 12 healthy right-handed monozygotic twin pairs who were matched for gender, age and education.
Language lateralisation was decreased in discordant twin pairs compared with the healthy twin pairs. The groups did not differ in activation of the language-related areas of the left hemisphere, but language-related activation in the right hemisphere was significantly higher in the discordant twin pairs than in the healthy pairs. Within the discordant twin pairs, language lateralisation was not significantly different between patients with schizophrenia and their co-twins.
Decreased language lateralisation may constitute a genetic predisposition for schizophrenia.
In this commentary we argue that evolution of the human brain to host the language system was accomplished by the selective development of frontal and temporal areas in the left hemisphere. The unilateral development of Broca's and Wernicke's areas could have resulted from one or more transcription factors that have an expression pattern restricted to the left hemisphere.
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