This report discusses the case of a 54-year-old woman with a complex psychiatric history including schizophrenia, tardive dyskinesia, borderline intellectual function, and congenital deafness that reported auditory and visual hallucinations during an acute exacerbation of schizophrenia. After resuming a previous lithium regimen and introducing olanzapine, the patient improved and was discharged without hallucinations. In our report we explore some of the challenges we faced, discuss similar cases, and examine the unresolved debate about whether congenitally deaf patients can experience auditory hallucinations.

Hallucination is a sensory perception that occurs in the absence of external stimuli during abnormal neurological disturbances and various mental diseases. Hallucination is recognized as a core psychotic symptom and is particularly more prevalent in individuals with schizophrenia. Strikingly, a significant number of subjects with Alzheimer\'s disease (AD), Parkinson\'s disease (PD), Huntington\'s disease (HD), and other neurological diseases like cerebral stroke and epileptic seizure also experience hallucination. While aberrant neurotransmission has been linked to the neuropathogenic events of schizophrenia, the precise cellular mechanism accounting for hallucinations remains obscure. Neurogenesis is a cellular process of producing new neurons from the neural stem cells (NSC)-derived neuroblasts in the brain that contribute to the regulation of pattern separation, mood, olfaction, learning, and memory in adulthood. Impaired neurogenesis in the hippocampus of the adult brain has been linked to stress, anxiety, depression, and dementia. Notably, many neurodegenerative disorders are characterized by the mitotic and functional activation of neuroblasts and cell cycle re-entry of mature neurons leading to a drastic alteration in neurogenic process, known as reactive neuroblastosis. Considering their neurophysiological properties, the abnormal integration of neuroblasts into the existing neural network or withdrawal of their connections can lead to abnormal synaptogenesis, and neurotransmission. Eventually, this would be expected to result in altered perception accounting for hallucination. Thus, this article emphasizes a hypothesis that aberrant neurogenic processes at the level of reactive neuroblastosis could be an underlying mechanism of hallucination in schizophrenia and other neurological diseases.

BACKGROUND: In recent years, a growing body of evidence has demonstrated the efficacy of non-pharmacological interventions for schizophrenia spectrum disorders (SSD) including positive symptoms such as auditory hallucinations (AH). However, clinical trials predominantly examine general treatment effects for positive symptoms. Therefore, previous research is lacking in comprehensive and clear evidence about psychological and psychosocial approaches that are primarily tailored to treat AH. To overcome this knowledge gap in the current literature, we will conduct a systematic review and meta-analysis to assess the efficacy of clearly targeted psychological and psychosocial interventions for AH in persons with SSD.
METHODS: This study protocol has been developed according to the guidelines of the Preferred Reporting Items for Systematic Reviews and Meta-Analysis Protocols. We will include all randomized controlled trials analyzing the efficacy of targeted psychological and psychosocial interventions especially aimed at treating AH in SSD. We will include studies on adult patients with SSD experiencing AH. The primary outcome will be the change on a published rating scale measuring AH. Secondary outcomes will be delusions, overall symptoms, negative symptoms, depression, social functioning, quality of life, and acceptability (drop-out). We will search relevant databases and the reference lists of included literature. The study selection process will be conducted by two independent reviewers. We will conduct a random-effect meta-analysis to consider heterogeneity across studies. Analyses will be carried out by software packages in R. The risk of bias in each study will be evaluated using the Cochrane Risk of Bias tool. Assessment of heterogeneity and sensitivity analysis will be conducted.
CONCLUSIONS: The proposed study will augment the existing evidence by providing an overview of effective treatment approaches and their overall efficacy at treating AH in SSD. These findings will complement existing evidence that may impact future treatment implementations in clinical practice by addressing effective strategies to treat AH and therefore improve outcomes for the addressed population.
BACKGROUND: No ethical issues are foreseen. We will publish the results from this study in peer-reviewed journals and at relevant scientific conferences.
BACKGROUND: PROSPERO registration number: CRD42023475704.

We present a young woman with clozapine-resistant schizoaffective disorder who was treated with maintenance electroconvulsive therapy and multiple antipsychotics but continued to have auditory hallucinations. She had a haemorrhagic stroke secondary to a ruptured arteriovenous malformation at the right superior temporal gyrus, which was excised during emergency craniotomy. Despite having neurological deficits after the stroke, she reported cessation of auditory hallucinations. Magnetic resonance imaging of the brain showed Wallerian degeneration over the right temporal region. Personalised neuromodulation intervention may be a more effective treatment option for clozapine-resistant schizophrenia.

BACKGROUND: Auditory-verbal hallucinatory experiences (AVH) have a 12% prevalence in the general pediatric population. Literature reports a higher risk of developing AVH in post-traumatic stress disorder (PTSD). The persistence of AVHs during adolescence represents a risk of evolution into psychotic disorders. Social cognition and emotional markers could be considered prodromes markers of this evolution. The objectives of this prospective observational study are to observe social cognition and emotional markers correlation with the presence and persistence of AVH over two years and with the evolution of PTSD and psychotic diagnosis.
METHODS: This prospective case-control study, longitudinal over two years (with an interim reassessment at six months and one year), will include 40 participants aged 8 to 16 years old with a diagnosis of PTSD and without a diagnosis of psychosis according to the criteria of DSM-5 (K-SADS-PL). Subjects included are divided into two groups with AVH and without AVH matched by gender, age and diagnosis. The primary outcome measure will be the correlation between social cognition and emotional makers and the presence of AVH in the PTSD pediatric population without psychotic disorders. The social cognition marker is assessed with the NEPSY II test. The emotional marker is assessed with the Differential Emotion Scale IV and the Revised Beliefs About Voices Questionnaire. The secondary outcome measures are the correlation of these markers with the persistence of AVH and the evolution of the patient\'s initial diagnosis two years later.
CONCLUSIONS: The originality of our protocol is to explore the potential progression to psychosis from PTSD by cognitive biases. This study supports the hypothesis of connections between PTSD and AVH through sensory, emotional and cognitive biases. It proposes a continuum model from PTSD to psychotic disorder due to impaired perception like AVH.
BACKGROUND: Clinical trial registration: ClinicalTrials.gov Identifier: NCT03356028.

In recent years, there have been significant advances in our understanding of the positive symptoms of schizophrenia, such as hallucinations and delusions. This progress has been significantly aided by the use of associative learning-based approaches in human subjects and preclinical animal models. Here, we first review experimental research focusing on the abnormal processing of absent stimuli using three different conditioning phenomena: conditioned hallucinations, mediated conditioning, and trace conditioning. We then review studies investigating the ability to reduce focal processing of physically present but informationally redundant stimuli using habituation, latent inhibition, and blocking. The results of these different lines of research are then summarized within the framework of Wagner\'s (1981) standard operating procedures model, an associative learning model with explicit reference to the internal representations of both present and absent stimuli. Within this framework, the central deficit associated with positive symptoms can be described as a failure to suppress the focal processing of both absent stimuli and present but irrelevant stimuli. This can explain the wide range of results obtained in different experimental settings. Finally, we briefly discuss the role of the hippocampus and its interaction with dopaminergic transmission in the emergence of such abnormal stimulus representations and learning. Overall, we hope that the theoretical framework and empirical findings offered by the associative learning approach will continue to facilitate and integrate analyses of schizophrenia conducted at the psychological and behavioral levels on the one hand, and at the neural and molecular levels on the other, by serving as a useful interface between them. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Musical hallucinations and musical obsessions are distinct phenomena. The first can be understood as a manifestation of the musical ear syndrome, which produces deafferentation auditory hallucinations, while the latter is an obsessive symptom of obsessive-compulsive disorders. Both symptoms are often poorly understood and mistaken for one another or for signs of psychotic disorders. We report two cases, one characterized by musical hallucinations and the other by musical obsessions, both with comorbid hearing impairment, which is the main confounding factor in their differential diagnosis. We critically compare the two cases and their key features, allowing diagnostic differentiation and a targeted therapeutic approach.
Alucinações musicais e obsessões musicais são fenômenos distintos. O primeiro é compreendido como uma manifestação da Síndrome do Ouvido Musical, a qual produz alucinações auditivas por desaferentação, enquanto o último é um sintoma obsessivo dos transtornos obsessivo-compulsivos. Ambos os sintomas são frequentemente pouco compreendidos e confundidos entre si ou com sinais de transtornos psicóticos. Nós relatamos dois casos, um caracterizado por alucinações musicais e o outro por obsessões musicais, ambos com deficiência auditiva comórbida, a qual é o principal fator confundidor no diagnóstico diferencial. Nós comparamos criticamente os dois casos e suas características-chave, permitindo um diagnóstico diferencial e um tratamento direcionado.

This report aims to present an elderly woman with persistent delirium after hospitalization for lethargy secondary to hyponatremia. The diagnosis of pontine myelinolysis was made and there were no characteristic neurological manifestations such as pupillary changes or spastic tetraparesis. Hallucinations and personality changes were the clues to the diagnosis and should be considered an atypical manifestation of pontine myelinolysis.
O objetivo deste relato é apresentar uma idosa que apresentou, após internação por letargia secundária à hiponatremia, delirium persistente depois da alta hospitalar. O diagnóstico de mielinólise pontina foi feito após a alta hospitalar e não houve manifestações neurológicas características, como alterações pupilares ou tetraparesia espástica. Alucinações e mudança de personalidade foram as pistas para o diagnóstico e devem ser consideradas como uma manifestação atípica de mielinólise pontina.

Visual hallucinations in Lewy body disease (LBD) can be differentiated based on phenomenology into minor phenomena (MVH) and complex hallucinations (CVH). MVH include a variety of phenomena, such as illusions, presence and passage hallucinations occurring at early stages of LBD. The neural mechanisms of visual hallucinations are largely unknown. The hodotopic model posits that the hallucination state is due to abnormal activity in specialized visual areas, that occurs in the context of wider network connectivity alterations and that phenomenology of VH, including content and temporal characteristics, may help identify brain regions underpinning these phenomena. Here we investigated both the topological and hodological neural basis of visual hallucinations integrating grey and white matter imaging analyses. We studied LBD patients with VH and age matched healthy controls (HC). VH were assessed using a North-East-Visual-Hallucinations-Interview that captures phenomenological detail. Then we applied voxel-based morphometry and tract based spatial statistics approaches to identify grey and white matter changes. First, we compared LBD patients and HC. We found a reduced grey matter volume and a widespread damage of white tracts in LBD compared to HC. Then we tested the association between CVH and MVH and grey and white matter indices. We found that CVH duration was associated with decreased grey matter volume in the fusiform gyrus suggesting that LBD neurodegeneration-related abnormal activity in this area is responsible for CVH. An unexpected finding was that MVH severity was associated with a greater integrity of white matter tracts, specifically those connecting dorsal, ventral attention networks and visual areas. Our results suggest that networks underlying MVH need to be partly intact and functional for MVH experiences to occur, while CVH occur when cortical areas are damaged. The findings support the hodotopic view and the hypothesis that MVH and CVH relate to different neural mechanisms, with wider implications for the treatment of these symptoms in a clinical context.

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