Twenty schizophrenic patients with tardive dyskinesia and an equal number of matched controls were tested on a novel cognitive task. The task had two components: cued response and spatial memory. Relative to controls, the dyskinetic subjects showed a superior cued response performance but an equal spatial memory ability. We speculate that this selective facilitation may reflect dopaminergic hyperactivity in the dyskinetic group.
Abstract Visual hallucinations in individuals following sight loss (Charles Bonnet syndrome; CBS) have been posited to arise because of spontaneous, compensatory, neural activity in the visual cortex following sensory input loss from the eyes—known as deafferentation. However, neurophysiological investigations of CBS remain limited. We performed a multi-modal investigation comparing visual cortical activity in 19 people with eye disease who experience visual hallucinations (CBS) with 18 people with eye disease without hallucinations (ED-Controls; matched for age and visual acuity) utilising functional MRI, EEG, and transcranial magnetic stimulation (TMS). A pattern of altered visual cortical activity in people with CBS was noted across investigations. Reduced BOLD activation in ventral extrastriate and primary visual cortex, and reduced EEG alpha-reactivity in response to visual stimulation was observed in CBS compared to ED-Controls. The CBS group also demonstrated a shift towards lower frequency band oscillations in the EEG, indicative of cortical slowing, with significantly greater occipital theta power compared to ED-controls. Furthermore, a significant association between reduced activation in response to visual stimulation and increased excitability (in the form of reduced TMS phosphene thresholds) was observed in CBS, indicating persistent visual cortical activation consistent with hyperexcitability, which was found to be significantly associated with increased hallucination severity. These results provide converging lines of evidence to support the role of increased visual cortical excitability in the formation of visual hallucinations in some people following sight loss, consistent with the deafferentation hypothesis.
Background and HypothesisVisual hallucinations (VH) are a core symptom of both Lewy body diseases (LBDs; e.g., Parkinson’s disease and dementia with Lewy bodies) and serotonergic psychedelics (SPs; e.g., psilocybin and mescaline). While these classes of VH differ in etiology, shared pathways are suggested by overlapping phenomenology and neural mechanisms. This review explores similarities and differences in VH between LBDs and SPs, focusing on phenomenology, cortical function, and serotonergic modulation.Study DesignThis narrative review synthesizes findings from neurology, cognitive neuroscience, and systems neuroscience to compare VH in LBDs and SPs. The literature includes studies with both human subjects and animal models that examine cortical activity patterns, neuromodulatory mechanisms, and VH phenomenology.Study ResultsBoth LBDs and SPs exhibit distinct visual aberrations, ranging from minor metamorphopsias to complex hallucinations. Specific classes of VH in LBDs resemble those induced by SPs (e.g., illusory motion and entity encounters), suggesting shared neural mechanisms. Neuroimaging studies indicate a common pattern of hyperactive associative cortex and hypoactive sensory cortex. At the neuromodulator level, SP-induced VH involves serotonin 2A and 1A receptor (5-HT₂AR and 5-HT₁AR) modulation, while in LBDs, 5-HT₂AR upregulation correlates with increased VH, and its inhibition (e.g., with pimavanserin) reduces VH. Two shared cortical signatures are highlighted: reduced visual evoked responses and shifts toward visual excitation.ConclusionsExamining cortical and neuromodulatory similarities between LBD- and SP-induced VH may elucidate the link between visual degradation, excitation, and hallucinogenesis. Future research should employ real-time neuroimaging of discrete hallucinatory episodes to identify shared mechanisms and develop targeted interventions for LBD hallucinations.
Hallucinations and other unusual sensory experiences (USE) can occur in all modalities in the general population. Yet, the existing literature is dominated by investigations into auditory hallucinations ('voices'), while other modalities remain under-researched. Furthermore, there is a paucity of measures which can systematically assess different modalities, which limits our ability to detect individual and group differences across modalities. The current study explored such differences using a new scale, the Multi-Modality Unusual Sensory Experiences Questionnaire (MUSEQ). The MUSEQ is a 43-item self-report measure which assesses USE in six modalities: auditory, visual, olfactory, gustatory, bodily sensations, and sensed presence. Scale development and validation involved a total of 1300 participants, which included: 513 students and community members for initial development, 32 individuals with schizophrenia spectrum disorder or bipolar disorder for validation, 659 students for factor replication, and 96 students for test-retest reliability. Confirmatory factor analyses showed that a correlated-factors model and bifactor model yielded acceptable model fit, while a unidimensional model fitted poorly. These findings were confirmed in the replication sample. Results showed contributions from a general common factor, as well as modality-specific factors. The latter accounted for less variance than the general factor, but could still detect theoretically meaningful group differences. The MUSEQ showed good reliability, construct validity, and could discriminate non-clinical and clinical groups. The MUSEQ offers a reliable means of measuring hallucinations and other USE in six different modalities.
Cognitive impairment is common in Parkinson's disease (PD). However, the psychosocial impact of living and coping with PD and cognitive impairment in people with PD and their carers have not been explored. This paper draws on a qualitative study that explores the subjective impact of cognitive impairment on people with PD and their carers. Thirty-six one-to-one interviews were completed; people with PD were from three groups: normal cognition, mild cognitive impairment, and dementia. Data collection and analysis were iterative, and verbatim transcripts were analysed using thematic analysis. Themes were interpreted in consultation with coping and adaptation theory. The analysis revealed four main themes: threats to identity and role, predeath grief and feelings of loss in carers, success and challenges to coping in people with PD, and problem-focused coping and finding meaning in caring. Our data highlight how cognitive impairment can threaten an individual's self-perception; the ostensible effects of cognitive impairment depended on the impact individual's perceived cognitive impairment had on their daily lives. For carers, cognitive impairment had a greater emotional impact than the physical symptoms of PD. The discussion that developed around protective factors provides possible opportunities for future interventions, such as psychological therapies to improve successful adjustment.
Each year, some two million people in the United Kingdom experience visual hallucinations. Infrequent, fleeting visual hallucinations, often around sleep, are a usual feature of life. In contrast, consistent, frequent, persistent hallucinations during waking are strongly associated with clinical disorders; in particular delirium, eye disease, psychosis, and dementia. Research interest in these disorders has driven a rapid expansion in investigatory techniques, new evidence, and explanatory models. In parallel, a move to generative models of normal visual function has resolved the theoretical tension between veridical and hallucinatory perceptions. From initial fragmented areas of investigation, the field has become increasingly coherent over the last decade. Controversies
and gaps remain, but for the first time the shapes of possible unifying models are becoming clear, along with the techniques for testing these.
This book provides a comprehensive survey of the neuroscience of visual hallucinations and the clinical techniques for testing these. It brings together the very latest evidence from cognitive neuropsychology, neuroimaging, neuropathology, and neuropharmacology, placing this within current models of visual perception.
Leading researchers from a range of clinical and basic science areas describe visual hallucinations in their historical and scientific context, combining introductory information with up-to-date discoveries. They discuss results from the main investigatory techniques applied in a range of clinical disorders. The final section outlines future research directions investigating the potential for new understandings of veridical and hallucinatory perceptions, and for treatments of problematic hallucinations.
Fully comprehensive, this is an essential reference for clinicians in the fields of the psychology and psychiatry of hallucinations, as well as for researchers in departments, research institutes and libraries. It has strong foundations in neuroscience, cognitive science, optometry, psychiatry, psychology, clinical medicine, and philosophy. With its lucid explanation and many illustrations, it is a clear resource for educators and advanced undergraduate and graduate students.
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