Auditory Verbal Hallucinations: A Comprehensive Review Across Psychiatric and Neurological Disorders

Abstract

Auditory Verbal Hallucinations (AVHs) represent complex perceptual phenomena where individuals experience the perception of speech, voices, or other complex auditory stimuli in the absence of any external acoustic source. While most prominently recognized as a cardinal symptom of schizophrenia, the contemporary understanding of AVHs extends far beyond this singular diagnosis. This comprehensive report delves deeply into the multifaceted nature of AVHs, providing an exhaustive exploration of their epidemiological prevalence across a diverse range of clinical populations, their intricate phenomenological characteristics, the evolving understanding of their neurobiological underpinnings, and their historical conceptualization and management strategies from antiquity to modern therapeutic approaches. By integrating insights from psychiatry, neurology, cognitive neuroscience, and social sciences, this document aims to provide a holistic and in-depth understanding of this compelling and often distressing human experience.

Many thanks to our sponsor Esdebe who helped us prepare this research report.

1. Introduction

Auditory Verbal Hallucinations (AVHs), often colloquially referred to as ‘hearing voices,’ constitute a profound and often debilitating clinical phenomenon characterized by the perception of speech, distinct voices, or other complex sounds without any corresponding external acoustic stimulus. This experience can range from simple, fleeting perceptions to elaborate, persistent conversations or commentaries that significantly impact an individual’s reality and functioning. For centuries, AVHs were primarily, and often exclusively, associated with severe mental illnesses, most notably schizophrenia, frequently leading to profound stigma and misunderstanding. However, advancements in clinical research, neuroimaging, and psychological inquiry have fundamentally transformed this narrow perspective.

The current paradigm recognizes AVHs as a transdiagnostic symptom, meaning they can manifest across a broad spectrum of psychiatric disorders, including mood disorders, personality disorders, and trauma-related conditions. Furthermore, AVHs are increasingly understood to occur in various neurological disorders, such as epilepsy and neurodegenerative conditions, as well as in individuals experiencing specific substance-induced states or even in otherwise healthy individuals under particular circumstances, such as sleep deprivation, bereavement, or extreme stress (pubmed.ncbi.nlm.nih.gov, en.wikipedia.org). This broadened understanding underscores the complexity of brain function, perception, and cognition, highlighting that AVHs are not merely indicators of severe mental illness but rather represent a disruption in fundamental brain processes that can arise from diverse etiologies.

Understanding the diverse manifestations, intricate underlying mechanisms, and the historical evolution of perspectives on AVHs is paramount for several reasons. Clinically, it informs more accurate differential diagnosis, enables more targeted and effective therapeutic interventions, and facilitates a more nuanced approach to patient care that moves beyond symptom suppression towards holistic recovery. From a research standpoint, studying AVHs offers unique insights into the neural correlates of self-awareness, language processing, source monitoring, and consciousness itself. This report endeavors to provide a detailed, comprehensive, and up-to-date exploration of these critical aspects, thereby contributing to a more informed and empathetic approach to individuals who experience AVHs.

Many thanks to our sponsor Esdebe who helped us prepare this research report.

2. Prevalence and Manifestations of AVHs Across Clinical Populations

The manifestation of Auditory Verbal Hallucinations is not uniform; their prevalence, phenomenology, and clinical significance vary considerably across different diagnostic categories. This section provides an in-depth analysis of AVH prevalence and characteristics within psychiatric disorders, neurological conditions, and substance-induced states, highlighting the unique features associated with each context.

2.1 Psychiatric Disorders

Schizophrenia

Auditory Verbal Hallucinations are considered one of the most prominent and debilitating hallmark symptoms of schizophrenia, impacting a significant majority of patients, with prevalence rates consistently reported between 60% and 80% globally (pubmed.ncbi.nlm.nih.gov). In schizophrenia, AVHs are typically characterized by their complexity, persistence, and often negative or persecutory content. Patients commonly report hearing multiple voices conversing with each other, commenting on the individual’s actions, or issuing commands. These voices can be distinct, identifiable as male or female, familiar or unfamiliar, and often possess unique tonal qualities and emotional valences, ranging from critical and derogatory to overtly hostile or threatening. The voices are frequently perceived as external, distinct from the individual’s own thoughts, and can be highly intrusive, creating significant distress and interfering with daily functioning. The content of these voices often aligns with an individual’s delusional beliefs, such as voices accusing them of wrongdoing, conspiring against them, or controlling their thoughts. For many individuals with schizophrenia, AVHs are a persistent, chronic experience, resisting conventional treatment and requiring ongoing management.

Bipolar Disorder

While less frequent and typically less complex or persistent than in schizophrenia, AVHs can occur in individuals with bipolar disorder, particularly during severe manic or depressive episodes with psychotic features (pubmed.ncbi.nlm.nih.gov). In the context of bipolar disorder, AVHs are often mood-congruent, meaning their content reflects the prevailing affective state. During manic episodes, voices might be grandiose, proclaiming the individual’s special abilities, divine status, or unlimited power. Conversely, during severe depressive episodes, the voices are often self-deprecating, guilt-ridden, or condemnatory, echoing themes of worthlessness, despair, or impending doom. These hallucinations are generally episodic, resolving with the stabilization of the mood episode, and are less likely to be chronic or pervasively disruptive compared to those in schizophrenia. The perception of the source may also vary, sometimes feeling more internal or less distinct than in schizophrenia.

Major Depressive Disorder with Psychotic Features

Auditory Verbal Hallucinations occur in a subset of individuals with Major Depressive Disorder, specifically when the condition is accompanied by psychotic features. The prevalence is lower than in schizophrenia or bipolar disorder, but their presence signifies a more severe form of depression. Similar to bipolar depression, the content of these AVHs is almost invariably mood-congruent, reflecting themes of guilt, worthlessness, deserved punishment, or self-reproach. For instance, a patient might hear voices constantly telling them they are a failure, condemning them for past mistakes, or instructing them to harm themselves due to their perceived unworthiness. These voices can intensify the individual’s depressive symptoms, increasing the risk of self-harm or suicide. Treatment often requires a combination of antidepressants and antipsychotics to address both the mood and psychotic symptoms.

Borderline Personality Disorder (BPD)

Some individuals diagnosed with Borderline Personality Disorder report experiencing AVHs, though these are typically transient, less structured, and directly linked to states of high emotional arousal, severe stress, or dissociative episodes (pubmed.ncbi.nlm.nlm.nih.gov). Unlike the persistent, complex voices in schizophrenia, AVHs in BPD are often experienced as fleeting whispers, indistinct noises, or fragmented verbalizations. They may represent internalized critical voices or be triggered by interpersonal stress, serving as a manifestation of profound emotional dysregulation, identity disturbance, or dissociation. The individual may maintain some insight into their non-reality, recognizing them as ‘not real’ or as ‘thoughts that sound like voices.’ Their occurrence is often tied to the severity of other BPD symptoms, particularly paranoia and dissociation, and they tend to resolve as the acute stress or dissociative state abates.

2.2 Neurological Disorders

Auditory hallucinations are not exclusive to psychiatric conditions; they can also arise from various neurological disorders, often indicating specific brain pathology or dysfunction.

Epilepsy

Temporal lobe epilepsy (TLE) is particularly associated with auditory hallucinations, due to seizure activity originating in or spreading to brain regions crucial for auditory processing, such as the superior temporal gyrus. AVHs in epilepsy can manifest as either elementary (simple sounds like buzzing, ringing, clicks) or complex (music, voices, speech fragments, familiar sounds). Musical hallucinations, where individuals hear music without an external source, are a distinct and relatively common form of complex auditory hallucination in TLE (en.wikipedia.org). These hallucinations can occur during the aura phase (pre-ictal), during the ictal event itself, or post-ictally. Their characteristics (e.g., loudness, clarity, duration) depend on the precise location and spread of the seizure activity. While often benign, they can be distressing, and their presence warrants thorough neurological evaluation.

Dementia

Neurodegenerative conditions, such as Alzheimer’s disease, Lewy Body Dementia (LBD), and Parkinson’s Disease Dementia (PDD), can lead to AVHs, particularly as the disease progresses and impacts brain regions involved in perception and cognition. In Alzheimer’s disease, AVHs are less common than visual hallucinations but can occur, often presenting as simple sounds or vague voices that may be difficult to interpret. In LBD and PDD, while visual hallucinations are more characteristic, auditory hallucinations, including verbal ones, can also manifest. These are thought to arise from a complex interplay of neurochemical changes (e.g., cholinergic deficits) and structural brain alterations. They can be disorienting and contribute to patient distress and caregiver burden, particularly when combined with cognitive decline and paranoid delusions.

Auditory Verbal Agnosia (Pure Word Deafness)

Auditory Verbal Agnosia, also known as pure word deafness, is a specific neurological condition characterized by the inability to comprehend spoken language despite intact hearing, normal production of speech, and preserved comprehension of non-verbal sounds. This condition results from damage to specific areas of the brain, most commonly bilateral lesions in the posterior superior temporal gyrus, which includes Heschl’s gyrus (primary auditory cortex) and Wernicke’s area (language comprehension area), or their connections (en.wikipedia.org). While auditory verbal agnosia is fundamentally a deficit in auditory verbal processing—a loss of the ability to comprehend speech—rather than a gain or perception of non-existent speech (a hallucination), its study provides crucial insights into the neural pathways essential for normal auditory verbal perception. Understanding the precise regions whose damage leads to agnosia helps researchers delineate the neural circuits that, when dysregulated, may paradoxically generate illusory speech perceptions characteristic of AVHs. It underscores the intricate and specialized nature of the brain’s language processing centers and how their disruption can lead to profound and varied alterations in auditory experience.

Brain Tumors and Lesions

Space-occupying lesions such as tumors, cysts, or abscesses, particularly those located in the temporal lobe or involving auditory pathways, can irritate neural tissue and induce AVHs. The characteristics of the hallucinations (e.g., simple or complex, duration, frequency) depend on the exact location, size, and growth rate of the lesion. These AVHs are often accompanied by other neurological symptoms, such as headaches, seizures, or focal neurological deficits, which can aid in their diagnosis. Surgical removal or other targeted treatments for the lesion may lead to resolution of the hallucinations.

2.3 Substance-Induced States

Substances can profoundly alter neurochemistry, leading to transient or persistent alterations in perception, including the induction of AVHs. This category includes both acute intoxication and withdrawal states.

Drug Use (Intoxication)

Various psychoactive substances can induce AVHs, often in a dose-dependent manner, meaning higher doses are more likely to elicit such experiences. These hallucinations are typically reversible upon cessation of the substance or metabolism from the body (en.wikipedia.org).

• Stimulants: Amphetamines (including methamphetamine) and cocaine are potent dopaminergic agents. Excessive dopamine release in the mesolimbic pathway, critical for reward and salience attribution, can lead to paranoid delusions and prominent AVHs. These voices are often persecutory or threatening, reflecting the heightened paranoia. Crystal methamphetamine psychosis is a well-documented phenomenon, closely mimicking paranoid schizophrenia.
• Hallucinogens: Substances like Lysergic Acid Diethylamide (LSD), psilocybin (magic mushrooms), and mescaline primarily affect serotonergic systems, particularly 5-HT2A receptors. While visual hallucinations are more typical, auditory distortions and complex AVHs can occur, often described as disembodied voices or echoes, which may be profound but generally lack the organized, malevolent content seen in primary psychotic disorders. The individual often retains some awareness that the perceptions are drug-induced.
• Cannabis: High doses of cannabis, especially in genetically predisposed individuals or those with existing vulnerabilities, can induce transient psychotic symptoms, including AVHs. The precise mechanism is complex but involves cannabinoid receptor activation influencing dopamine and glutamate systems.
• PCP and Ketamine: These dissociative anesthetics are NMDA receptor antagonists. Their use can lead to a psychotic state with delusions, disorganized thought, and vivid hallucinations, including AVHs, which are thought to result from glutamatergic dysregulation.

Withdrawal States

Withdrawal from certain substances, particularly those that depress the central nervous system, can precipitate severe neurochemical imbalances leading to AVHs and other psychotic symptoms.

• Alcohol Withdrawal (Delirium Tremens): Severe alcohol withdrawal can lead to Delirium Tremens (DTs), a medical emergency characterized by profound autonomic instability, delirium, and often vivid hallucinations. Auditory hallucinations are common, ranging from simple sounds to complex, often threatening voices, frequently accompanied by visual and tactile hallucinations. This is due to a rebound hyperexcitability of the central nervous system following chronic suppression by alcohol, primarily affecting GABAergic and glutamatergic systems.
• Sedative-Hypnotic Withdrawal (e.g., Benzodiazepines): Abrupt cessation or rapid dose reduction of benzodiazepines (e.g., alprazolam, diazepam) after prolonged use can similarly lead to a withdrawal syndrome that includes anxiety, seizures, and a range of perceptual disturbances, including AVHs. The mechanism involves a similar rebound hyperexcitability of GABAergic systems.

Many thanks to our sponsor Esdebe who helped us prepare this research report.

3. Phenomenology of AVHs: The Subjective Experience

The phenomenology of Auditory Verbal Hallucinations refers to the subjective qualities and characteristics of the experience as reported by the individual. Understanding these nuances is crucial for accurate diagnosis, treatment planning, and empathic engagement with those who hear voices. Key phenomenological dimensions include content, frequency, duration, perceived source, and associated emotional impact.

3.1 Content and Themes

The content of AVHs is highly variable and often provides crucial diagnostic clues, frequently reflecting the individual’s underlying psychological state, cultural background, and core belief systems.

• Schizophrenia: Voices commonly present as commenting on the individual’s actions, conversing with each other about the individual in the third person, or issuing direct commands. The content is frequently negative, critical, derogatory, or persecutory (‘You’re worthless,’ ‘They’re watching you,’ ‘Kill yourself’). Less commonly, voices can be benevolent or neutral. Commanding hallucinations can be particularly dangerous if the commands are violent or self-harmful, necessitating careful clinical assessment and risk management.
• Major Depressive Disorder with Psychotic Features: As noted previously, the themes are typically mood-congruent, encompassing self-criticism, guilt, worthlessness, condemnation, or nihilistic pronouncements (‘You deserve to die,’ ‘You’re evil’). These voices exacerbate feelings of despair and hopelessness.
• Bipolar Disorder: In manic phases, voices might be grandiose, confirming inflated self-worth or special powers. In depressive phases, they mirror the themes of MDD with psychotic features.
• Epilepsy: While some individuals report distinct words or musical passages, hallucinations in epilepsy are often more elemental (e.g., buzzing, ringing, hissing sounds) or repetitive musical loops. When verbal, they tend to be less organized or complex than those in schizophrenia, often fragments of speech or familiar voices without clear conversational patterns (en.wikipedia.org).
• Post-Traumatic Stress Disorder (PTSD): In this context, AVHs can be re-experiencing phenomena, such as hearing the sounds or voices from the traumatic event (e.g., gunshots, screams, the perpetrator’s voice). These are often vivid, intrusive, and directly linked to the traumatic memory.
• Bereavement/Grief: Healthy individuals experiencing profound grief may transiently hear the voice of the deceased loved one, which is often perceived as comforting and is typically recognized as a memory or a wish rather than an external reality. This usually dissipates over time.

3.2 Frequency and Duration

AVHs can be episodic, occurring intermittently, or chronic, being present for extended periods. Their frequency (how often they occur) and duration (how long each episode lasts) are significantly influenced by the underlying condition, severity of symptoms, and the efficacy of ongoing treatment.

• Chronic and Persistent: Common in chronic schizophrenia, where voices may be heard daily, sometimes continuously, for years.
• Episodic and Transient: Typical in mood disorders, substance-induced psychoses, and neurological conditions, often resolving with treatment of the primary condition or removal of the precipitating substance.
• Stress-Dependent: In conditions like BPD or PTSD, voices may emerge or intensify during periods of acute stress, emotional dysregulation, or dissociation.

3.3 Perceived Source

The perceived origin of the voices is a critical phenomenological distinction. Individuals may perceive the voices as originating externally (e.g., coming from outside their head, from a specific location in the room, or from within walls) or internally (e.g., coming from inside their head, or indistinguishable from their own thoughts, but with an alien quality) (en.wikipedia.org).

• External Perception: Often associated with more severe psychopathology, such as schizophrenia, where the voices are clearly experienced as separate from the self and originating from the external world. This externalization contributes to the sense of reality and intrusiveness of the voices.
• Internal Perception: More common in non-psychotic AVHs or those associated with mild psychotic symptoms. The individual may experience the voices as internal but distinct from their normal inner monologue, or as a commentary within their own mind. In conditions like BPD or trauma, the voices might be internalized persecutory figures, resembling critical inner speech but perceived with an alien quality.
• Source Monitoring Deficit: The inability to accurately distinguish between self-generated internal thoughts and externally perceived stimuli is a key cognitive theory for AVHs. When an internal thought is misattributed as external, it contributes to the ‘external’ perceived source.

3.4 Loudness, Location, Clarity, and Emotional Impact

Beyond content and source, other subjective qualities contribute to the richness and distress associated with AVHs:

• Loudness: Voices can range from faint whispers to extremely loud, shouting voices, impacting the individual’s ability to concentrate or engage with external reality.
• Location: While often perceived as external, the precise perceived location can vary, e.g., ‘behind me,’ ‘from the ceiling,’ ‘from everywhere,’ or ‘inside my head.’
• Clarity and Distinctiveness: Voices can be clear and distinct, allowing for easy comprehension of their words, or they can be muffled, indistinct, and difficult to decipher, adding to frustration and confusion.
• Emotional Impact: The emotional valence evoked by AVHs is crucial. Voices can induce profound fear, terror, anger, sadness, shame, or even, rarely, comfort or guidance. The emotional response is highly correlated with the content and perceived power of the voices. Critical or commanding voices often lead to high levels of distress, anxiety, and despair, while benevolent voices may be less distressing or even provide a sense of companionship, though still indicating a perceptual disturbance.

Many thanks to our sponsor Esdebe who helped us prepare this research report.

4. Neurobiological Underpinnings: The Brain in Hallucinations

The neurobiological basis of Auditory Verbal Hallucinations is a complex and active area of research, involving a combination of structural, functional, and neurochemical abnormalities. Modern neuroscience employs advanced neuroimaging techniques (e.g., fMRI, DTI, PET) to investigate the neural correlates of these illusory perceptions.

4.1 Structural Abnormalities

Studies comparing individuals with and without AVHs, particularly in the context of schizophrenia, have identified consistent structural brain differences.

• Temporal Lobe: Reduced gray matter volume and cortical thinning in specific regions of the temporal lobe are frequently observed in individuals experiencing AVHs (en.wikipedia.org). Key areas include:
  • Superior Temporal Gyrus (STG): This region, particularly the anterior STG, is critically involved in auditory processing and language comprehension (including Wernicke’s area). Reduced volume or abnormal structure here is thought to contribute to altered auditory perception and misinterpretation of internal speech.
  • Heschl’s Gyrus (Primary Auditory Cortex): Abnormalities in the primary auditory cortex, sometimes including increased volume in specific sub-regions, have been linked to AVHs, suggesting a structural predisposition to abnormal auditory processing.
  • Parahippocampal Gyrus and Hippocampus: These limbic structures, involved in memory and emotional processing, also show structural alterations, which might contribute to the emotional salience or memory-like quality of some voices.
• Arcuate Fasciculus: This major white matter tract forms a crucial connection between the superior temporal gyrus (Wernicke’s area, language comprehension) and the inferior frontal gyrus (Broca’s area, speech production). Diffusion Tensor Imaging (DTI) studies have consistently shown alterations in the integrity of the arcuate fasciculus (e.g., reduced fractional anisotropy) in individuals with schizophrenia, particularly those with AVHs (arxiv.org). Impaired connectivity along this pathway is hypothesized to disrupt the efficient flow of information between speech production and comprehension areas, leading to a failure of self-monitoring and subsequent misattribution of inner speech.
• Frontal Lobes: The prefrontal cortex, particularly the dorsolateral prefrontal cortex (DLPFC) and anterior cingulate cortex (ACC), plays a critical role in executive functions, working memory, attention, and cognitive control, including distinguishing self-generated thoughts from external stimuli (source monitoring). Reduced gray matter volume or structural abnormalities in these regions are consistently found in schizophrenia and are hypothesized to impair the top-down cognitive control necessary to inhibit or correctly attribute internal verbalizations, thereby contributing to the emergence of AVHs.

4.2 Functional Abnormalities

Functional neuroimaging, such as fMRI, allows researchers to observe brain activity in real-time, providing insights into the dynamic neural processes underlying AVHs.

• Overactivity in Auditory Cortex: A consistent finding in individuals experiencing AVHs is increased functional activity, particularly in the primary auditory cortex (Heschl’s gyrus) and surrounding auditory association areas (e.g., superior temporal gyrus) during the experience of hallucinations (en.wikipedia.org). This suggests that the brain regions responsible for processing external sounds become active even in the absence of such sounds, creating a ‘perceptual reality’ for the voices. Furthermore, activation is often seen in speech production areas (e.g., Broca’s area, inferior frontal gyrus), even when the individual is not overtly speaking, lending support to inner speech models.
• Dysfunctional Connectivity: AVHs are increasingly understood as a disorder of brain connectivity, rather than isolated regional dysfunction. Impaired functional connectivity between key brain networks is implicated:
  • Auditory and Language Processing Regions with Frontal Lobes: Weakened connectivity between temporal lobe auditory/language areas and frontal lobe executive control regions (e.g., DLPFC, ACC) is thought to impair the brain’s ability to ‘tag’ internally generated thoughts as such, leading to their misattribution as external voices. This contributes to the source monitoring deficit theory.
  • Salience Network Dysregulation: The salience network, comprising the anterior insula and anterior cingulate cortex, is responsible for detecting and integrating relevant internal and external stimuli. Dysfunction in this network is hypothesized to lead to ‘aberrant salience attribution,’ where internal thoughts or non-salient stimuli are assigned undue significance, potentially manifesting as externally perceived voices (en.wikipedia.org).
  • Default Mode Network (DMN) Hyperactivity: The DMN is active during internally focused tasks, such as self-reflection or mind-wandering. Hyperactivity or altered connectivity within the DMN, or between the DMN and other networks, may contribute to the generation of internal verbal content that then becomes misattributed.

4.3 Neurochemical Factors

Neurotransmitters play a crucial role in modulating brain activity and are heavily implicated in the genesis of AVHs. Dysregulation of several key neurochemical systems has been identified.

• Dopamine Dysregulation: The ‘dopamine hypothesis of psychosis’ is one of the oldest and most enduring neurochemical theories. It posits that elevated dopamine levels, particularly in the mesolimbic pathway (connecting the ventral tegmental area to the nucleus accumbens, amygdala, and hippocampus), contribute to the positive symptoms of psychosis, including AVHs (en.wikipedia.org). This pathway is involved in assigning motivational salience to stimuli. Excess dopamine activity is thought to lead to the aberrant salience of internal thoughts or experiences, causing them to be perceived as external and meaningful. Antipsychotic medications, which primarily block dopamine D2 receptors, effectively reduce AVHs, lending strong support to this hypothesis.
• Serotonin Imbalance: Serotonin (5-HT) systems also play a significant role. Hallucinogenic drugs like LSD exert their effects primarily through agonism at 5-HT2A receptors, producing profound perceptual distortions including AVHs. This suggests that dysregulation of serotonergic pathways can influence the perception of reality. Furthermore, some atypical antipsychotics modulate both dopamine and serotonin receptors, contributing to their efficacy.
• Glutamate Hypofunction: The N-methyl-D-aspartate (NMDA) receptor hypofunction hypothesis of schizophrenia suggests that reduced activity of glutamatergic neurotransmission, particularly at NMDA receptors, plays a central role in the pathophysiology of psychosis. Glutamate is the primary excitatory neurotransmitter in the brain and is crucial for synaptic plasticity, learning, and cognitive processes. NMDA receptor antagonists (e.g., ketamine, PCP) can induce psychotic symptoms, including AVHs, in healthy individuals. Glutamate dysregulation can lead to downstream effects on dopamine and GABA systems, further contributing to abnormal neuronal firing and aberrant perceptions.
• GABAergic Dysfunction: Gamma-aminobutyric acid (GABA) is the brain’s primary inhibitory neurotransmitter. Deficits in GABAergic interneurons or dysfunctional GABA signaling can lead to disinhibition of neural circuits, particularly in the cortex. This imbalance between excitation and inhibition could result in spontaneous, uncontrolled neuronal firing in auditory areas, contributing to the experience of AVHs. Some theories suggest that reduced GABAergic inhibition might explain the hyperactivity observed in the auditory cortex during hallucinations.

Many thanks to our sponsor Esdebe who helped us prepare this research report.

5. Theories on the Origin of AVHs: From Cognition to Prediction

Beyond neurobiological correlates, several cognitive and psychological models attempt to explain how AVHs arise, focusing on specific cognitive deficits or biases. These theories often overlap and complement neurobiological findings, providing a more comprehensive understanding.

5.1 Inner Speech Models (Source Monitoring Deficit)

One of the most widely accepted cognitive theories for AVHs is the ‘inner speech’ or ‘source monitoring deficit’ model (en.wikipedia.org). This theory posits that AVHs originate from the misattribution of self-generated inner speech or thoughts as external voices.

Normally, when an individual engages in inner speech (e.g., silently talking to oneself, planning, or rehearsing), the brain generates a ‘corollary discharge’ or ‘efferent copy’ of the motor command for speech production. This internal signal is then sent to sensory areas, effectively ‘predicting’ the sensory consequences of the self-generated action. This prediction allows the brain to distinguish between sounds produced by oneself (which are attenuated or ‘canceled out’) and sounds originating from the external environment. This process is crucial for ‘source monitoring’ – the ability to correctly attribute the origin of a thought, memory, or perception.

In individuals prone to AVHs, particularly in schizophrenia, this corollary discharge mechanism is hypothesized to be impaired. The internal speech command is generated, but the corresponding efferent copy is either absent, attenuated, or incorrectly processed. Consequently, the brain fails to recognize the self-generated speech as originating from within. Instead, it misinterprets this internally generated verbal content as novel, external auditory input, leading to the perception of ‘voices.’ This model is supported by neuroimaging findings showing activation in both speech production (Broca’s area) and speech comprehension (Wernicke’s area) regions during AVHs, as if the person is both ‘speaking’ and ‘hearing’ their own misattributed internal vocalizations.

5.2 Salience Network Dysfunction

The salience network (SN), primarily composed of the anterior insula (AI) and the anterior cingulate cortex (ACC), plays a critical role in detecting novel, relevant, or emotionally significant stimuli and directing attention to them. It acts as a switch between the default mode network (DMN, active during introspection) and the central executive network (CEN, active during task-focused attention) (en.wikipedia.org).

Dysfunction within the salience network, particularly aberrant connectivity or reactivity, is proposed to contribute to AVHs by causing ‘aberrant salience attribution.’ In this scenario, internally generated thoughts, memories, or even random neural noise that would normally be ignored are incorrectly tagged as highly salient and meaningful. This aberrant salience then drives the perception of these internal events as external voices. For example, a fleeting thought might be assigned undue importance and perceived as a distinct, external voice, simply because the salience network is malfunctioning and inappropriately flagging it as significant. This theory integrates well with the dopamine hypothesis, as dopamine is known to modulate salience attribution.

5.3 Cognitive Models and Biases

Beyond specific neural mechanisms, several cognitive models highlight how thought processes, biases, and emotional factors contribute to the development and maintenance of AVHs.

• Attributional Biases: Individuals experiencing AVHs often exhibit biases in how they attribute the causes of events. Specifically, they may externalize negative experiences or self-referential thoughts, attributing them to external entities (the voices) rather than to themselves. For instance, negative self-criticism might be experienced as an external voice condemning them, rather than their own internal self-doubt. This externalization can serve a protective function, distancing the individual from distressing thoughts, but it perpetuates the belief in external voices.
• Jumping to Conclusions (JTC): This cognitive bias refers to the tendency to make rapid decisions or form firm conclusions based on minimal evidence. In the context of AVHs, individuals might quickly conclude that an ambiguous internal experience is an external voice, and then rigidly adhere to this belief despite contradictory evidence. This bias can contribute to the development and maintenance of delusional beliefs surrounding the voices, making them more resistant to challenge.
• Anomalous Experiences and Cognitive Appraisal: This model suggests that AVHs begin as subtle, anomalous internal experiences (e.g., fleeting thoughts, unusual sensations, indistinct sounds). How an individual appraises or interprets these initial experiences determines whether they escalate into distressing, full-blown hallucinations. If these anomalous experiences are interpreted as threatening, supernatural, or external, they are more likely to develop into persistent and distressing AVHs. Past trauma, negative schemas, and emotional states can heavily influence this appraisal process.
• Emotional Factors and Trauma: A significant proportion of individuals who experience AVHs, particularly those with complex or persistent voices, report a history of childhood trauma (e.g., abuse, neglect). Psychological trauma can lead to dissociative states, altered self-perception, and difficulties with emotion regulation, all of which can contribute to the emergence of voices. The voices may represent internalized persecutors, victims, or aspects of the self that were disowned due to trauma, embodying distressing memories or unresolved conflicts.

5.4 Predictive Coding Models

More advanced theoretical frameworks, such as predictive coding, offer a unifying perspective that integrates neurobiological and cognitive insights. Predictive coding posits that the brain is essentially a ‘prediction machine,’ constantly generating internal models and predictions about incoming sensory information. It then compares these predictions with actual sensory input, and any discrepancy (‘prediction error’) is used to update the internal models.

In the context of AVHs, two main scenarios are proposed:

• Over-reliance on Top-Down Predictions: The brain might place too much weight on its own internal predictions or models, making them resistant to revision by incoming sensory data. This could lead to internally generated speech being so strongly ‘predicted’ that it is perceived as real, overriding the absence of external auditory input.
• Dysfunctional Prediction Error Processing: Alternatively, the brain might generate inaccurate prediction errors or fail to properly ‘attenuate’ self-generated predictions. This could mean that internal speech is incorrectly perceived as a ‘prediction error’ (i.e., something unexpected from the environment), leading to its misattribution as an external voice. This model elegantly integrates the concept of corollary discharge (as a form of prediction) with the idea of abnormal salience and misattribution, offering a sophisticated framework for understanding how internal representations can become externalized perceptions.

Many thanks to our sponsor Esdebe who helped us prepare this research report.

6. Historical Evolution of Understanding and Management of AVHs

The perception and treatment of Auditory Verbal Hallucinations have undergone a profound transformation throughout history, mirroring broader societal and scientific shifts in understanding the human mind and illness. From ancient spiritual interpretations to modern neuroscientific models, the journey reflects humanity’s evolving attempts to make sense of these enigmatic experiences.

6.1 Ancient Perspectives (Pre-18th Century)

In ancient civilizations and throughout the medieval period, AVHs were predominantly interpreted through spiritual, religious, or supernatural lenses. They were often seen as messages from deities, spirits, ancestors, or, conversely, as manifestations of demonic possession or divine punishment. This led to varied responses:

• Divine Revelation: In some cultures, hearing voices could signify a sacred connection, prophetic ability, or a shamanic calling. Oracles, prophets, and religious figures across many traditions (e.g., biblical prophets, Greek oracles) often reported hearing divine voices guiding their actions or revealing truths. These individuals were often revered and their experiences integrated into the societal fabric.
• Demonic Possession/Evil Spirits: Conversely, in many other contexts, particularly within Abrahamic traditions during periods of religious zeal, voices were attributed to malevolent entities, demons, or curses. This interpretation often led to fear, ostracization, and harsh ‘treatments’ aimed at expelling the perceived evil, such as exorcisms, rituals, prayers, purifications, and even physical torture or execution (e.g., during witch hunts).
• Early Medical Theories: While supernatural explanations predominated, some ancient medical traditions offered rudimentary physiological explanations. For instance, Hippocratic medicine occasionally linked mental disturbances to imbalances in bodily humors, though specific attention to hallucinations was limited. Trepanation (drilling holes into the skull) was an ancient practice, sometimes used to release evil spirits or to alleviate pressure thought to cause mental illness, though its direct link to AVH treatment is speculative.

6.2 19th and Early 20th Century: The Dawn of Psychiatry

The Enlightenment brought a shift towards more rational and scientific inquiry, gradually paving the way for the emergence of modern psychiatry. AVHs began to be conceptualized as symptoms of underlying mental illness rather than spiritual phenomena.

• Moral Treatment and Asylums: The late 18th and 19th centuries saw the rise of ‘moral treatment’ and the establishment of asylums. While these institutions aimed to provide more humane care, they often became overcrowded and custodial, with limited effective treatments for complex symptoms like AVHs. Patients with persistent voices were typically confined for long periods.
• Early Classification and Pathologization: Pioneers like Philippe Pinel in France and Benjamin Rush in America began to observe, categorize, and medically describe mental disorders. In the late 19th and early 20th centuries, Emil Kraepelin rigorously classified ‘dementia praecox’ (later schizophrenia), firmly establishing AVHs as a cardinal symptom of this severe mental illness. Eugen Bleuler later coined the term ‘schizophrenia’ and further refined the understanding of its symptoms, including hallucinations.
• Psychoanalytic Interpretations: Sigmund Freud’s psychoanalytic theories interpreted hallucinations as symbolic manifestations of repressed unconscious conflicts or wishes, often linked to early childhood experiences. Treatment focused on exploring these unconscious dynamics through talk therapy, though its direct efficacy for severe AVHs was limited.
• Early Somatic Treatments: Without effective psychopharmacology, clinicians resorted to various somatic treatments, often with little scientific basis and significant side effects, including hydrotherapy, insulin coma therapy, and the infamous lobotomy, which aimed to surgically alter brain connections to alleviate severe symptoms, including hallucinations.

6.3 Mid-20th Century to Present: The Biopsychosocial Revolution

The mid-20th century marked a revolutionary turning point with the accidental discovery of antipsychotic medications, fundamentally changing the landscape of mental health care.

• The Pharmacological Revolution (Mid-20th Century): The introduction of chlorpromazine in the 1950s was a watershed moment. As the first effective antipsychotic, it demonstrated the potential to reduce the severity and frequency of AVHs and other psychotic symptoms, leading to significant de-institutionalization and a greater focus on community-based care. Subsequent development of first-generation (typical) antipsychotics, which primarily blocked dopamine D2 receptors, further solidified the pharmacological approach to AVHs.
• Neuroscientific Advances (Late 20th Century): The development of neuroimaging techniques (CT, MRI, PET, fMRI) allowed researchers to study the living brain, revealing structural and functional abnormalities associated with AVHs, leading to more refined neurobiological models (e.g., dopamine hypothesis, connectivity theories). The development of second-generation (atypical) antipsychotics in the 1990s, with broader receptor profiles (e.g., serotonin-dopamine antagonism) and fewer motor side effects, provided more treatment options.
• Cognitive-Behavioral Therapy (CBT) for Psychosis (Late 20th Century): As understanding evolved, it became clear that medication alone was often insufficient. Cognitive-Behavioral Therapy (CBT) was adapted for psychosis (CBTp), providing non-pharmacological strategies to help individuals cope with and reduce the distress caused by AVHs. CBTp focuses on challenging beliefs about voices, developing coping strategies, and normalizing the experience (en.wikipedia.org).
• The Biopsychosocial Model (21st Century): Contemporary psychiatry embraces a comprehensive biopsychosocial model, recognizing that AVHs arise from a complex interplay of biological vulnerabilities (genetics, neurobiology), psychological factors (cognitive biases, trauma, coping styles), and social influences (stress, stigma, support systems). Treatment today emphasizes an integrated approach combining pharmacological interventions, evidence-based psychotherapies, social support, rehabilitation, and psychoeducation.
• The Hearing Voices Movement (HVM): Originating in the Netherlands in the late 1980s, the HVM represents a significant paradigm shift, offering an alternative perspective on voice-hearing. It advocates that hearing voices is a meaningful human experience that, while sometimes distressing, does not necessarily indicate severe mental illness. The HVM emphasizes acceptance, understanding, and finding meaning in voices, empowering individuals to cope and live fulfilling lives with their experiences rather than solely focusing on symptom eradication. This movement has profoundly influenced recovery-oriented approaches and peer support networks globally.

Many thanks to our sponsor Esdebe who helped us prepare this research report.

7. Treatment Strategies for Auditory Verbal Hallucinations

Effective management of Auditory Verbal Hallucinations typically involves a multifaceted approach that integrates pharmacological, psychotherapeutic, and, in some cases, neuromodulation techniques. The choice of treatment is individualized, considering the underlying cause, the severity and distress associated with the AVHs, and the individual’s preferences.

7.1 Pharmacological Interventions

Pharmacotherapy remains the cornerstone of treatment for many individuals experiencing AVHs, particularly when associated with psychotic disorders.

• Antipsychotics: These medications are the primary pharmacological treatment for AVHs in schizophrenia and other psychotic disorders. Their main mechanism of action involves blocking dopamine D2 receptors in the mesolimbic pathway, which is thought to reduce the aberrant salience and intensity of hallucinations.
  • First-Generation (Typical) Antipsychotics: Examples include haloperidol, chlorpromazine, and fluphenazine. While effective in reducing positive symptoms like AVHs, they are often associated with significant motor side effects (extrapyramidal symptoms like Parkinsonism, dystonia, tardive dyskinesia) due to their potent D2 blockade in the nigrostriatal pathway.
  • Second-Generation (Atypical) Antipsychotics: Examples include olanzapine, risperidone, quetiapine, aripiprazole, and clozapine. These generally have a broader receptor profile, including serotonin 5-HT2A antagonism in addition to D2 blockade. They are often preferred due to a lower propensity for motor side effects and potential benefits for negative and cognitive symptoms. Clozapine is particularly noteworthy for its superior efficacy in treatment-resistant schizophrenia, including refractory AVHs, though its use requires regular blood monitoring due to the risk of agranulocytosis.
• Antidepressants and Mood Stabilizers: In mood disorders with psychotic features (e.g., major depressive disorder with psychotic features, bipolar disorder), antidepressants (e.g., SSRIs, SNRIs) and mood stabilizers (e.g., lithium, valproate, lamotrigine) are used in conjunction with antipsychotics to address the underlying mood dysregulation. The antipsychotic component directly targets the AVHs, while the mood medications stabilize affective symptoms that might trigger or worsen the hallucinations.
• Adjunctive Medications: In some cases, other medications might be used adjunctively to manage associated symptoms. Anxiolytics (e.g., benzodiazepines) may be used short-term for severe agitation or anxiety related to voices, and hypnotics for sleep disturbances.

7.2 Psychotherapeutic Interventions

Psychotherapeutic approaches empower individuals to understand, cope with, and reduce the distress caused by AVHs, often complementing pharmacological treatments.

• Cognitive-Behavioral Therapy for Psychosis (CBTp): CBTp is an evidence-based therapy specifically adapted for individuals with psychotic experiences like AVHs (en.wikipedia.org). Key components include:
  • Psychoeducation and Normalization: Helping individuals understand that voice-hearing is a relatively common human experience that exists on a continuum, reducing shame and stigma.
  • Voice Formulation: Collaboratively developing a personalized understanding of the voices, including their content, triggers, perceived power, and meaning to the individual.
  • Challenging Unhelpful Beliefs: Addressing maladaptive beliefs about the voices (e.g., that they are all-powerful, omniscient, malevolent, or control the individual). Techniques include reality testing and logical disputation.
  • Coping Strategy Enhancement: Teaching and rehearsing practical strategies to manage the voices, such as distraction (engaging in activities, listening to music), selective attention, relaxation techniques, and reality testing.
  • Behavioral Experiments: Designing and conducting experiments to test the validity of beliefs about voices (e.g., ‘If the voice says I will fail, I will try this task and see what happens’).
  • Relapse Prevention: Developing strategies to recognize early warning signs of escalating voices and implementing coping plans.
• Metacognitive Training (MCT): MCT is a group-based cognitive therapy that focuses on addressing specific cognitive biases frequently observed in psychosis, such as jumping to conclusions, attributional biases, and deficits in theory of mind (en.wikipedia.org). By raising awareness of these biases and practicing alternative thinking styles, MCT aims to improve self-awareness and cognitive control, potentially leading to reduced hallucination severity and distress.
• Acceptance and Commitment Therapy (ACT): ACT focuses on psychological flexibility, encouraging individuals to accept their internal experiences (including voices) without judgment, while committing to actions aligned with their values. Rather than directly trying to eliminate voices, ACT helps individuals reduce distress by changing their relationship with the voices and engaging in meaningful life activities despite their presence.
• Voice Dialogue and Relational Approaches: Influenced by the Hearing Voices Movement, these approaches encourage individuals to develop a different, often more collaborative or confrontational, relationship with their voices, exploring the meaning and function of each voice. This can help individuals regain a sense of agency and reduce the voices’ power over them.
• Family Psychoeducation and Support: Involving family members in the treatment process through psychoeducation helps them understand AVHs, reduces familial stress, and provides a supportive environment for the individual, which can significantly improve outcomes.

7.3 Neuromodulation Techniques

For individuals with severe, treatment-resistant AVHs, neuromodulation techniques offer alternative or adjunctive strategies by directly influencing brain activity.

• Transcranial Magnetic Stimulation (TMS): rTMS is a non-invasive brain stimulation technique that uses magnetic pulses to generate electrical currents in specific brain regions. For AVHs, low-frequency (inhibitory) rTMS is often applied to the left temporoparietal junction (including the superior temporal gyrus and Wernicke’s area), which shows hyperactivity during hallucinations (en.wikipedia.org). The aim is to reduce the excitability of these overactive auditory processing regions. Research indicates promise in reducing the frequency and severity of AVHs in a subset of patients, particularly those resistant to pharmacological treatments.
• Transcranial Direct Current Stimulation (tDCS): tDCS is another non-invasive brain stimulation technique that delivers a weak direct electrical current to the scalp, modulating cortical excitability. It is less precise and less powerful than TMS but is also being explored as a potential treatment for AVHs, often targeting similar brain regions.
• Electroconvulsive Therapy (ECT): ECT involves inducing a brief therapeutic seizure under general anesthesia. It is typically reserved for severe, treatment-resistant forms of psychosis, particularly when accompanied by severe mood symptoms (e.g., catatonia, severe depression with psychotic features), where other treatments have failed to alleviate distressing AVHs. Its mechanism of action is complex but involves widespread neurochemical and neurophysiological changes.
• Deep Brain Stimulation (DBS): DBS is an invasive surgical procedure that involves implanting electrodes into specific brain regions to deliver continuous electrical impulses. While primarily used for movement disorders like Parkinson’s disease, it is being investigated as an experimental treatment for extremely refractory psychiatric conditions, including severe AVHs, in very select cases. Research is still in its early stages.

Many thanks to our sponsor Esdebe who helped us prepare this research report.

8. Conclusion

Auditory Verbal Hallucinations are complex and multifaceted perceptual phenomena that transcend the boundaries of a single diagnosis. From their historical interpretations as divine messages or demonic possession to modern conceptualizations rooted in neurobiology and cognitive science, our understanding of AVHs has evolved dramatically. They manifest with diverse phenomenological characteristics across a spectrum of psychiatric disorders (such as schizophrenia, bipolar disorder, and borderline personality disorder), neurological conditions (like epilepsy and dementia), and substance-induced states, highlighting their transdiagnostic nature.

The neurobiological underpinnings of AVHs involve intricate interplay of structural abnormalities (e.g., reduced gray matter in the temporal lobe, white matter integrity deficits in the arcuate fasciculus), functional dysregulations (including overactivity in the auditory cortex and dysfunctional connectivity within key neural networks like the salience network), and imbalances in critical neurotransmitter systems (dopamine, serotonin, glutamate, and GABA). Cognitive models, particularly the inner speech/source monitoring deficit theory, and the role of cognitive biases and traumatic experiences, provide crucial frameworks for understanding the subjective experience and maintenance of these voices.

Effective management of AVHs necessitates a personalized, integrated approach. Pharmacological interventions, primarily antipsychotics, remain central for symptom reduction, while evidence-based psychotherapies like Cognitive-Behavioral Therapy for Psychosis (CBTp) and Metacognitive Training empower individuals to cope with and reduce the distress caused by their voices. Emerging neuromodulation techniques such as Transcranial Magnetic Stimulation (TMS) offer promising avenues for treatment-resistant cases. Furthermore, the rise of the Hearing Voices Movement underscores the importance of a recovery-oriented approach that fosters acceptance, understanding, and personal agency.

Ongoing research into the precise neurobiological mechanisms, the influence of genetic and environmental factors, and the development of novel therapeutic modalities holds immense promise for further enhancing our ability to diagnose, treat, and support individuals affected by AVHs. A holistic and compassionate approach, informed by the latest scientific insights, is crucial to improving the quality of life for those who experience these profound and challenging perceptions.

Many thanks to our sponsor Esdebe who helped us prepare this research report.

References

• pubmed.ncbi.nlm.nih.gov
• en.wikipedia.org
• en.wikipedia.org
• en.wikipedia.org
• en.wikipedia.org
• arxiv.org