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Reality-monitoring process enables to discriminate memories of internally generated information from memories of externally derived information. Studies have reported impaired reality-monitoring abilities in schizophrenia patients with auditory hallucinations (AHs), specifically with an exacerbated externalization bias, as well as alterations in neural activity within frontotemporoparietal areas. In healthy subjects, impaired reality-monitoring abilities have been associated with reduction of the paracingulate sulcus (PCS). The current study aimed to identify neuroanatomical correlates of reality monitoring in patients with schizophrenia.
Thirty-five patients with schizophrenia and AHs underwent a reality-monitoring task and a 3D anatomical MRI scan at 1.5 T. PCS lengths were measured separately for each hemisphere, and whole-brain voxel-based morphometry analyses were performed using the Computational Anatomy Toolbox (version 12.6) to evaluate the gray-matter volume (GMV). Partial correlation analyses were used to investigate the relationship between reality-monitoring and neuroanatomical outcomes (PCS length and GMV), with age and intracranial volume as covariates.
The right PCS length was positively correlated with reality-monitoring accuracy (Spearman’s ρ = 0.431, p = 0.012) and negatively with the externalization bias (Spearman’s ρ = −0.379, p = 0.029). Reality-monitoring accuracy was positively correlated with GMV in the right angular gyrus, whereas externalization bias was negatively correlated with GMV in the left supramarginal gyrus/superior temporal gyrus, in the right lingual gyrus and in the bilateral inferior temporal/fusiform gyri (voxel-level p < 0.001 and cluster-level p < 0.05, FDR-corrected).
Reduced reality-monitoring abilities were significantly associated with shorter right PCS and reduced GMV in temporal and parietal regions of the reality-monitoring network in schizophrenia patients with AHs.
Resistance to antipsychotic treatment affects up to 30% of patients with schizophrenia. Although the time course of development of treatment-resistant schizophrenia (TRS) varies from patient to patient, the reasons for these variations remain unknown. Growing evidence suggests brain dysconnectivity as a significant feature of schizophrenia. In this study, we compared fractional anisotropy (FA) of brain white matter between TRS and non–treatment-resistant schizophrenia (non-TRS) patients. Our central hypothesis was that TRS is associated with reduced FA values.
TRS was defined as the persistence of moderate to severe symptoms after adequate treatment with at least two antipsychotics from different classes. Diffusion-tensor brain MRI obtained images from 34 TRS participants and 51 non-TRS. Whole-brain analysis of FA and axial, radial, and mean diffusivity were performed using Tract-Based Spatial Statistics (TBSS) and FMRIB’s Software Library (FSL), yielding a contrast between TRS and non-TRS patients, corrected for multiple comparisons using family-wise error (FWE) < 0.05.
We found a significant reduction in FA in the splenium of corpus callosum (CC) in TRS when compared to non-TRS. The antipsychotic dose did not relate to the splenium CC.
Our results suggest that the focal abnormality of CC may be a potential biomarker of TRS.
This chapter focuses on advancements in the understanding of personality pathology gained from structural and functional neuroimaging studies. It draws from the literature on the most widely researched personality disorders including schizotypal, borderline, and antisocial personality disorder. Prominent findings in schizotypal personality disorder include abnormalities in temporal and frontal lobe volumes, decreased structural connectivity of temporal lobe regions, and inefficient recruitment of brain areas during task performance. In borderline personality disorder, neuroimaging findings are characterized by aberrant volume and activity of limbic and prefrontal brain areas that suggest diminished top-down control of affective responsivity. Studies in antisocial personality disorder reveal reduced volume in prefrontal and temporal lobe structures, white matter structure compromise, and altered brain network functional connectivity. Significant challenges in studying this complex population and limitations of current methodology are discussed. Suggestions for future directions of research in this field are provided.
Neuroimaging visualizes and quantifies age-related changes in brain structure, function, cerebral blood flow, and cerebral metabolic health. MRI studies show reductions in both overall and regional brain volumes, but to a lesser extent than in Alzheimer’s disease. Those aging non-pathologically tend to have relative preservation of mesial temporal and enthorhinal brain areas. White matter changes are also common as shown by hyperintensities on fluid attenuated inversion recovery and other T2 MRI images, presumably as a result of co-morbities that increasingly occur with age. Diffusion tensor imaging shows reductions in white matter integrity, including white matter fiber counts and overall white matter volume, beginning in mid- to late life. The neural response during both rest and task performance also shows reduced activation of core task-related networks but expansion to include other region activation. Reduced cerebral blood volume and flow also occur, likely reflecting alterations in hemodynamic function due to cerebrovascular and cardiovascular changes. Cerebral metabolic changes on MR spectroscopy occur with reduced concentrations of GABA and other neurotransmitters, as well as markers of neuronal integrity. Myoinositol, a marker of glial activation, may be elevated, indicating neuroinflammation, though this effect is likely not ubiquitous in successful aging.
Diagnostic testing for determining the sources of neuropathic pain has evolved over time. Good clinical practice requires that the clinician takes a good history and performs an appropriate clinical examination to establish the diagnosis of neuropathic pain as possible or probable. Quantitative sensory testing (QST) is helpful in the early diagnosis and follow-up of peripheral neuropathy affecting small-fiber function. Peripheral nerve biopsy was performed in certain circumstances, such as when vasculitis, amyloid, or an unspecified inflammatory condition could be the etiology of peripheral neuropathy. Computerized tomography (CT) and magnetic resonance imaging (MRI) scans can facilitate diagnoses by identifying causes of central and peripheral nervous tissue ischemia, demyelination, compression, or infiltration. Functional MRI works on the principle that regional cerebral blood flow (rCBF) is related to regional cerebral activity. Autonomic function testing relies on indirectly accessing the function of unmyelinated postganglionic fibers, which cannot be tested directly by conventional neurophysiological techniques.
This chapter describes the clinical phenomenology and pathophysiology of Gilles de la Tourette syndrome (GTS) and reviews current structural and functional neuroimaging data of this fascinating neuropsychiatric condition. Significant neuroimaging evidence exists for a primary cortical dysfunction in GTS. Structural changes were reported in the basal ganglia, including both the striatum and the globus pallidus. Diffusion tensor imaging (DTI) has pointed to the microstructural abnormalities in white matter in GTS patients, including the corpus callosum and anterior and posterior limb of the internal capsule. Defects in brain maturation could be one of the pathophysiological mechanisms that lead to emergence of the GTS symptoms in childhood and their persistence into adulthood. Evidence from pharmacological trials, especially the fact that dopamine receptor blockers are the most effective treatment for tics to date, and postmortem analyses suggested that abnormalities of dopaminergic neurotransmission play a key role in the pathogenesis of GTS.
This chapter focuses on classic congenital central hypoventilation syndrome (CCHS) cases in which symptoms appear early in life. The principal issues in CCHS are to determine what brain structures are damaged in CCHS to cause the loss of CO2 and O2 sensitivity, disturbances in autonomic function, and other affective and cognitive deficits. Among the processes affected in CCHS appears to be the integrity of multiple neurotransmitter systems. Structural and functional magnetic resonance imaging (MRI) procedures provide a valuable means to assess gray and white matter injury and impaired brain function in the syndrome, and, in the same fashion as numerous other disease processes, the descriptions have the potential to reveal normal mechanisms for serving breathing and autonomic functions. Injury in cognitive and memory regulatory areas has also been revealed. As MRI technology improves, further differentiation of the nature of injury, especially finer discrimination of fiber injury, will be possible.
This chapter focuses on the basic principles of computed tomography (CT) and magnetic resonance imaging (MRI) used for imaging the brain structure. Indications for brain imaging in Behavioral Neurology & Neuropsychiatry (BN&NP) patients include: poison or toxin exposures, dementia or cognitive decline of unknown etiology, delirium, brain injuries of any type with ongoing symptoms, new-onset psychiatric symptoms, abnormal neurological findings suggesting brain pathology, and new-onset atypical psychosis. Imaging of the brain with MRI depends on the polar characteristics of the water molecule and its unique behavior within a strong magnetic field. Factors important to consider when choosing an imaging modality include type of suspected pathology, acuity of the illness, and desired planes of section. Doppler ultrasound (US) evaluation has been used successfully in clinical neurology as a screening tool to evaluate internal carotid artery (ICA) disease.
Global brain abnormalities such as brain volume loss and grey- and white-matter deficits are consistently reported in first-episode schizophrenia patients and may already be detectable in the very early stages of the illness. Whether these changes are dependent on medication use or related to intelligence quotient (IQ) is still debated.
Magnetic resonance imaging scans were obtained for 20 medication-naive patients with first-episode schizophrenia and 26 matched healthy subjects. Volume measures of total brain grey and white matter, third and lateral ventricles and cortical thickness/surface were obtained. Differences between the groups were investigated, taking into account the effect of intelligence.
Medication-naive patients showed statistically significant reductions in whole-brain volume and cerebral grey- and white-matter volume together with lateral ventricle enlargement compared to healthy subjects. IQ was significantly lower in patients compared to controls and was positively associated with brain and white-matter volume in the whole group. No significant differences in cortical thickness were found between the groups but medication-naive patients had a significantly smaller surface in the left superior temporal pole, Heschl's gyrus and insula compared to controls.
Our findings suggest that brain volume loss is present at illness onset, and can be explained by the reduced surface of the temporal and insular cortex. These abnormalities are not related to medication, but IQ.
Paul E. Holtzheimer III, Department of Psychiatry and Behavioral Sciences Emory University School of Medicine Atlanta, GA, USA,
Helen S. Mayberg, Department of Psychiatry and Behavioral Sciences Emory University School of Medicine Atlanta, GA, USA
The field of mood disorders neuroimaging is vibrant, productive and at times chaotic. This chapter first addresses the clear variance between structural and functional neuroimaging study findings of depression and bipolar disorder. When reviewing the mood disorders neuroimaging literature to date, one can appreciate a consistent set of brain regions (including gray and white matter components) as critical to normal and abnormal mood regulation. The consistency across imaging studies in location of abnormality, if not always direction, provides a useful starting point for future investigation. The chapter suggests two primary goals for a mood disorders imaging research agenda: increasing the signal-to-noise ratio for structural and functional imaging studies through technological developments, large-scale multi-center trials and novel analytic methods; and shifting from hypothesis-free to hypothesis-guided investigations based within developing neural network models. It is expected that neuroimaging findings will be able to play a vital role in diagnosis, and treatment development.
Andrew R. Gilbert, Department of Psychiatry University of Pittsburgh School of Medicine Pittsburgh, PA, USA,
Alison M. Gilbert, Department of Psychiatry University of Pittsburgh School of Medicine Pittsburgh, PA, USA,
Jorge R. C. de Almeida, Department of Psychiatry University of Pittsburgh School of Medicine Pittsburgh, PA, USA,
Philip R. Szeszko, Department of Psychiatry The Zucker Hillside Hospital Glen Oaks, NY, USA and Albert Einstein College of Medicine Bronx, NY, USA
This chapter presents findings from structural neuroimaging studies of obsessive-compulsive disorder (OCD) in both pediatric and adult populations. It reviews the structural neuroimaging literature with a focus on regions strongly implicated in the pathophysiology of OCD, including the orbitofrontal cortex, anterior cingulate cortex, basal ganglia, and thalamus. Structural neuroimaging studies have identified abnormalities in CST neural systems, especially in the orbitofrontal cortex and have informed many of the dominant neurobiological models of OCD. The emergence of magnetic resonance (MR) imaging techniques advanced the field by providing higher-resolution images without the potential risk of ionizing radiation. Several structural neuroimaging studies reported less gray matter in the amygdala and hippocampus in adult patients with OCD compared to healthy controls, although Kwon et al. reported larger amygdala volume in patients. Recently, investigators have used diffusion tensor imaging (DTI) to investigate the potential role of white matter abnormalities in the pathogenesis of OCD.
This chapter briefly reviews the use of structural and functional neuroimaging in the assessment and management of parasomnias. The majority of the work in the area of neuroimaging and parasomnias and sleep-related movement disorders has been in the area of RLS and PLMD. The scope of the work performed to date has been driven by, and constrained by, clinical manifestations of the disorder and by the measurements currently available by using neuroimaging tools. The most extensive work has been performed in the area of central dopaminergic dysfunction in these disorders. Neuroimaging methods allow determination of brain volumetric changes in patient samples to see if structural cerebral abnormalities may play a role in the disorder. Low-dose opioid treatment has been used in the management of some RLS patients, and nuclear medicine study reveals regional brain function associated with sleepwalking.
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