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Hallucination

A hallucination is a sensory perception that occurs in the absence of an external stimulus, often accompanied by a vivid sense of reality as if the experience were genuinely occurring.^[1] These perceptions can manifest across various sensory modalities, including visual (seeing images or figures), auditory (hearing voices or sounds), tactile (feeling touches or sensations on the skin), olfactory (smelling odors), or gustatory (tasting flavors), and are generated internally by the brain rather than from real environmental input.^[2] Unlike illusions, which distort actual stimuli, hallucinations involve no corresponding external trigger, distinguishing them as a form of perceptual anomaly.^[3] Hallucinations occur in approximately 6–15% of the general population over their lifetime, with prevalence varying by type and frequency; for instance, auditory verbal hallucinations are reported by 5–15% of individuals without associated psychopathology, often transiently during stress, bereavement, or sleep transitions.^[4] In clinical contexts, they are a hallmark symptom of psychiatric disorders such as schizophrenia, affecting 60–70% of patients primarily through auditory forms like hearing critical or commanding voices,^[1] and occur in bipolar disorder during manic or depressive episodes.^[5] Neurological conditions also contribute, including Parkinson's disease (visual hallucinations in 20–50% of cases),^[6] epilepsy (often focal seizures triggering sensory experiences), and migraines, while substance use—such as hallucinogens like LSD or withdrawal from alcohol—can induce acute episodes.^[7] Other precipitants include sensory deprivation, extreme fatigue, fever, or brain injuries, highlighting hallucinations as a multifaceted phenomenon influenced by neurobiological, psychological, and environmental factors.^[8] Management of hallucinations depends on the underlying cause and severity, with treatment aimed at addressing the root condition. For schizophrenia-spectrum disorders, antipsychotic medications are first-line and effective in reducing symptoms in approximately 70–80% of cases,^[9] supplemented by cognitive behavioral therapy (CBT) to enhance coping strategies.^[10] In neurological etiologies, interventions may target the specific condition; non-pharmacological approaches like transcranial magnetic stimulation show promise for refractory cases.^[11] Prevalence may increase with age, with reports of up to 37% in older adults, often linked to dementia or sensory loss, underscoring the need for comprehensive assessment.^[12]

Introduction

Definition

A hallucination is defined as a perception of an object, event, or phenomenon in the absence of a corresponding external sensory stimulus, which nonetheless feels vividly real to the experiencing individual.^[1]^[13] These perceptions can involve any of the sensory modalities, including sight, sound, smell, touch, or taste, though they most commonly manifest as visual or auditory experiences.^[14]^[15] Key characteristics of hallucinations include their vividness, involuntariness, and the subjective conviction of reality held by the perceiver, distinguishing them from mere thoughts or imaginings.^[1] These experiences occur while the individual is awake and alert, without external provocation, and often carry a sense of authenticity that can be distressing or neutral depending on context.^[16] Unlike illusions, which distort actual external stimuli, hallucinations arise entirely from internal processes.^[11] The term "hallucination" derives from the Latin hallucinatio, rooted in the verb alucinari (or hallucinari), meaning "to wander in the mind" or "to be distraught."^[17] It entered the English language in the mid-17th century, with the earliest recorded medical usage appearing in 1646 in the writings of physician Sir Thomas Browne, though contemporaries like Thomas Willis contributed to its application in neurological and psychiatric contexts during this period.^[18] Hallucinations are broadly classified into elementary (or simple) forms, consisting of basic sensory elements such as flashes of light, geometric patterns, dots, lines, or unformed sounds, and organized (or complex) forms, which involve structured scenes, recognizable objects, people, animals, or coherent voices.^[11]^[19] This distinction highlights the spectrum of hallucinatory complexity, from abstract percepts to elaborate narratives, without implying specific underlying causes.^[20] Hallucinations are often distinguished from illusions, which involve the misinterpretation or distortion of actual external sensory stimuli, whereas hallucinations occur in the complete absence of such stimuli. For instance, an optical illusion, such as the Müller-Lyer illusion where parallel lines appear bent due to contextual arrows, relies on a real visual input that is perceptually altered, but the perceiver recognizes the distortion upon closer inspection or measurement. In contrast, a hallucination generates a sensory experience without any corresponding external object or event, leading to a perception that feels as vivid and real as veridical sensation but lacks an objective basis.^[21]^[22] Delusions, another related phenomenon, differ fundamentally from hallucinations as they represent fixed, false beliefs about reality rather than sensory perceptions. A delusion might involve the unshakeable conviction that one is being persecuted by unseen forces, despite contradictory evidence, whereas a hallucination entails experiencing sensory content, such as hearing voices or seeing images, that is not externally present. Although both can coexist in psychiatric conditions like schizophrenia, where auditory hallucinations may reinforce persecutory delusions, the distinction lies in delusions being cognitive misinterpretations of reality and hallucinations being perceptual ones.^[23]^[24] Pseudohallucinations further blur the boundary but are differentiated by the individual's insight that the experience originates internally and is not externally real, lacking the compelling sense of objective reality characteristic of true hallucinations. The concept of pseudohallucinations remains controversial, with some researchers questioning its validity and distinctiveness from true hallucinations due to inconsistent definitions and low construct validity.^[25]^[26] For example, a person might vividly "hear" an internal voice commenting on their thoughts and explicitly recognize it as a mental construct, stating, "I know this is just in my mind," which contrasts with the external projection and conviction in genuine hallucinations. This awareness prevents pseudohallucinations from fully mimicking the perceptual authenticity of hallucinations, though they can still cause distress, particularly in psychiatric contexts.^[25]^[26] Hypnagogic and hypnopompic hallucinations, while classified as true hallucinations due to their perceptual nature without external triggers, are specifically delimited by their timing in relation to sleep cycles. Hypnagogic hallucinations emerge during the transition to sleep (sleep onset), often involving fleeting visual or auditory imagery that feels dream-like yet awake, whereas hypnopompic hallucinations occur upon awakening, sometimes extending dream content into brief wakefulness, such as seeing shadowy figures in the bedroom. Both lack voluntary control and external stimuli but are typically benign and short-lived, distinguishing them from more persistent pathological hallucinations through their association with normal sleep boundaries.^[27]^[28] In certain cultural or spiritual contexts, experiences like visions during meditation or near-death encounters may resemble hallucinations but are often differentiated by elements of voluntary induction, positive emotional valence, and interpretive frameworks that emphasize insight or transcendence rather than pathology. For instance, meditative visions might arise under intentional focus and be regarded as internally generated wisdom, contrasting with the involuntary and distressing quality of clinical hallucinations, while near-death visions frequently report enhanced serenity and purpose, lacking the disorientation typical of hallucinatory episodes. These distinctions highlight how cultural attribution influences perception, though overlap can occur without implying equivalence.^[29]^[3]

Classification

Auditory Hallucinations

Auditory hallucinations involve the perception of sounds, such as voices, music, or noises, in the absence of an external stimulus.^[30] These experiences are the most prevalent form of hallucination in schizophrenia, affecting approximately 70-75% of patients.^[31]^[30] Subtypes of auditory hallucinations include command hallucinations, where voices issue direct orders, such as instructions to harm oneself or others; third-person commentary, involving voices that discuss or argue about the individual as if observing them; and simpler forms like unformed noises or incoherent sounds.^[32]^[30] Command hallucinations often carry an imperative tone, while third-person variants may involve multiple voices debating the person's actions or thoughts.^[33] Simple noises, such as buzzing or murmuring, lack verbal content and are less complex.^[30] These hallucinations are frequently repetitive, featuring emotional tones that range from threatening and derogatory to neutral, and they commonly evoke significant distress, though levels of insight into their unreality can vary among individuals.^[34]^[35] The repetitive nature often amplifies emotional impact, with negative content leading to heightened anxiety or fear in many cases.^[36] Representative examples include hearing accusatory voices that criticize or condemn the person's behavior, or perceiving the voice of a deceased loved one offering comfort or guidance, particularly in contexts like bereavement where such experiences may occur in up to 50% of grievers.^[37]^[38] Clinically, command hallucinations are associated with elevated risks of self-harm or violence toward others due to potential compliance with the directives, necessitating careful risk assessment and intervention.^[39]^[40] Unlike tinnitus, which involves distorted perceptions of actual internal auditory signals like ringing or buzzing, auditory hallucinations generate entirely false sensory experiences without such physiological basis.^[41]

Visual Hallucinations

Visual hallucinations refer to the perception of visual stimuli, such as lights, patterns, or complex scenes, in the absence of corresponding external sensory input. These experiences occur while the individual is awake and alert, distinguishing them from dreams or hypnagogic imagery. They are broadly categorized into simple (or elementary) forms, which include unformed geometric shapes, flashes of light, or indistinct colors, and complex (or formed) forms, which involve recognizable objects like people, animals, or narrative scenes.^[11]^[42]^[43] The prevalence of visual hallucinations varies by population but is notable in clinical settings. In patients with psychotic disorders, such as schizophrenia, they occur in 25-50% of cases, with a weighted mean of about 27% across studies. Among elderly individuals with significant vision loss, the rate rises to 10-15%, particularly in conditions like Charles Bonnet syndrome.^[42]^[44]^[45] Characteristics of visual hallucinations often include vivid, colorful imagery that appears dynamic and projected into the external space, giving the impression of reality. In peduncular hallucinosis, associated with brainstem lesions, these perceptions frequently feature Lilliputian figures—tiny, detailed representations of people or objects—adding a distinctive, miniature quality to the experience.^[11]^[46]^[47] Representative examples illustrate their diversity. In Charles Bonnet syndrome, patients with visual impairment may see brief flashes of light or recurring patterns, typically without emotional distress. In delirium, more elaborate scenes, such as crowds or fantastical landscapes, can emerge, often accompanying cognitive fluctuations.^[11]^[48] Culturally, visual hallucinations manifest in bereavement as sightings of deceased loved ones, reported by up to 30% of grieving individuals in some studies; these are generally viewed as comforting and non-pathological, differing from clinical hallucinations or those induced by cultural rituals.^[42]^[3]

Other Sensory Modalities

Olfactory hallucinations, also known as phantosmia, involve the perception of smells in the absence of external stimuli, often described as unpleasant odors such as burning rubber, rot, or smoke.^[49] These experiences are relatively uncommon, occurring in approximately 3.9% of pediatric migraine cases and up to 6% of general migraine episodes.^[50]^[51] They are frequently associated with temporal lobe epilepsy, where they may manifest as brief auras known as uncinate fits.^[52] Gustatory hallucinations entail the sensation of tastes without any ingested substance, typically simple and unformed, such as a metallic or bitter flavor.^[53] These are rarer than olfactory hallucinations, with an incidence estimated at about half that of olfactory types in seizure disorders.^[52] They commonly arise during temporal lobe seizures, where a metallic taste serves as a characteristic aura.^[54] Tactile hallucinations produce perceptions of touch or skin sensations without physical contact, including formication—the feeling of insects crawling on or under the skin.^[55] This phenomenon is notably prevalent in substance-related contexts, such as cocaine intoxication, where it contributes to intense distress and compulsive behaviors like skin-picking.^[55] Similar tactile experiences, including sensations of bugs or vermin, can emerge during alcohol withdrawal as part of delirium tremens.^[56] Somatic hallucinations involve illusory internal bodily sensations, such as unexplained pain, pressure, movement, or organ dysfunction within the body.^[57] Examples include the perception of a lump in the throat, animals moving inside the body, or twisting sensations in limbs without objective cause.^[58] These are less frequent than auditory or visual types in schizophrenia, with past-month prevalence rates around 4-7% for related tactile-somatic experiences.^[59] Sexual hallucinations are rare and encompass erotic sensations, genital arousal, or visions of sexual acts without external triggers.^[60] They often present as orgasmic auras or bodily feelings of sexual pleasure, predominantly linked to temporal lobe epilepsy where limbic structures are involved.^[61] Such experiences occur in a minority of cases, with reports emphasizing their episodic and intense nature in neurological contexts.^[62] Multimodal hallucinations integrate perceptions across multiple sensory modalities, such as a voice accompanied by a visual figure or tactile presence, which may signal greater clinical severity.^[63] In schizophrenia, these are more prevalent than unimodal hallucinations, affecting approximately 53% of individuals with any hallucinatory experiences over their lifetime.^[63] Command hallucinations, typically auditory directives to perform actions, can extend multimodally, incorporating visual or somatic elements to heighten their imperative quality.^[64]

Causes

Hallucinations can arise from normal physiological processes, particularly during transitions between wakefulness and sleep, without indicating underlying pathology. These experiences, often linked to the intrusion of rapid eye movement (REM) sleep elements into conscious awareness, are common in the general population and typically benign.^[27] Hypnagogic hallucinations occur at the onset of sleep and involve vivid sensory perceptions, such as visual images of shapes or faces, auditory sounds like voices, or tactile sensations of falling. They affect up to 70% of individuals at some point, representing a frequent normal variant rather than a disorder. These phenomena are associated with REM sleep intrusion, where dream-like activity overlaps with wakefulness during the hypnagogic state.^[27]^[27] Hypnopompic hallucinations, analogous to hypnagogic ones, emerge upon awakening from sleep and feature similar multisensory content, though they are less prevalent, reported by approximately 12.5% of people. Like their counterparts, they stem from incomplete separation between REM sleep and wake states, often resolving spontaneously without intervention.^[65] Sleep paralysis frequently accompanies these hallucinations, characterized by temporary immobility during sleep-wake transitions, with an estimated lifetime prevalence of 7.6% in the general population. Up to 75% of episodes include hallucinatory elements, such as terrifying visions of shadowy figures or intruders, heightening distress but remaining non-pathological in isolation.^[66]^[67] In narcolepsy, a sleep disorder involving disrupted REM regulation, hypnagogic or hypnopompic hallucinations occur in about 50% of cases, often alongside cataplexy—sudden muscle weakness triggered by emotions. These hallucinations intensify the disorder's impact on daily functioning but are directly tied to the condition's core pathophysiology of REM instability.^[68] Brief hallucinations also manifest as normal variants in states of extreme fatigue or grief, where sensory perceptions like hearing a deceased loved one's voice provide temporary emotional relief without signifying mental illness. Such experiences, termed bereavement hallucinations, are reported by a significant portion of mourners and typically fade as adjustment progresses.^[69]

Neurological and Medical Conditions

Hallucinations can arise from various neurological and medical conditions, often linked to disruptions in brain structure, function, or systemic processes. These manifestations differ from those in other categories by their association with underlying diseases such as lesions, degenerative disorders, or immune-mediated responses, rather than transient physiological states or external triggers. Common features include visual, tactile, olfactory, or gustatory experiences that may accompany motor, cognitive, or sensory symptoms, providing diagnostic clues for the underlying pathology. Peduncular hallucinosis is a rare syndrome characterized by vivid, complex visual hallucinations, often featuring colorful, Lilliputian scenes of people, animals, or landscapes, resulting from lesions in the brainstem, particularly the midbrain or thalamus. These hallucinations typically emerge following vascular events, infections, or tumors compressing the peripeduncular region, and they are usually non-distressing, occurring in clear consciousness alongside sleep disturbances or oculomotor abnormalities. The condition was first described in 1922 and remains distinct due to its anatomical specificity in the rostral brainstem. Delirium tremens represents a severe form of alcohol withdrawal delirium, marked by tactile and visual hallucinations such as sensations of insects crawling on the skin or vivid scenes of threats, accompanied by tremors, autonomic hyperactivity, and potential seizures. It typically onset 48-72 hours after cessation of heavy alcohol use in dependent individuals, reflecting excitotoxic neuronal changes in the central nervous system. This medical emergency affects a subset of withdrawal cases, with hallucinations contributing to profound confusion and agitation. In Parkinson's disease, visual hallucinations occur in 20-40% of patients over the disease course, often depicting people, animals, or familiar figures in realistic but recurring scenarios, fluctuating in intensity alongside motor symptoms like bradykinesia and rigidity. These are linked to dopaminergic dysregulation and Lewy body pathology in visual processing areas. In Lewy body dementia, the prevalence rises to 60-80%, with similar complex visual content that may recur nightly and correlate with cognitive decline, distinguishing it from other dementias. Migraine-associated hallucinations include elementary visual auras like scintillating scotomas during attacks, as well as more complex perceptual distortions in syndromes such as Alice in Wonderland syndrome, where objects or body parts appear distorted in size, shape, or distance. These episodes, often lasting minutes to hours, stem from cortical spreading depression in the occipital and parietal lobes, and in rare cases, may persist in migrainous coma. Alice in Wonderland syndrome, first linked to migraine in 1955, exemplifies these transient, episodic phenomena without loss of reality testing. Charles Bonnet syndrome involves recurrent, elaborate visual hallucinations in elderly individuals with significant vision loss from conditions like macular degeneration or glaucoma, serving as a compensatory response to deafferentation in the visual cortex. Patients typically recognize these images—such as landscapes, figures, or patterns—as unreal and non-threatening, with episodes triggered by low light or fatigue. The syndrome, named after an 18th-century observer, affects up to 30% of those with profound visual impairment and lacks the delusions seen in psychiatric disorders. Focal epilepsy, particularly temporal lobe seizures, can produce brief, stereotyped olfactory or gustatory hallucinations, such as unpleasant burning smells or metallic tastes, arising from hyperexcitability in the uncus or insula. These auras last seconds to minutes, often preceding impaired awareness, and are ictal phenomena rather than interictal distortions. Such sensory seizures highlight the role of limbic structures in multisensory integration. Non-celiac gluten sensitivity rarely manifests with auditory or visual hallucinations as part of a broader neuropsychiatric syndrome, potentially driven by immune-mediated inflammation crossing the blood-brain barrier. Case reports describe resolution of such symptoms, including persecutory voices or fleeting images, upon gluten elimination in individuals without celiac disease or wheat allergy. This association, emerging in literature since the 2010s, underscores gluten's role in atypical immune responses affecting the central nervous system. Hallucinations have also been reported in association with COVID-19 infection and its long-term effects (long COVID), particularly in severe cases involving neuroinflammation, hypoxia, or delirium. These can include visual and auditory hallucinations, with prevalence of psychotic symptoms estimated at 1-3% in long COVID patients as of 2024, and up to 21.6% during inpatient rehabilitation following acute infection. Such episodes often resolve with treatment of the underlying condition but may persist in rare cases without prior psychiatric history.^[70]^[71]

Substance-Induced Causes

Substance-induced hallucinations arise from the ingestion, intoxication, or withdrawal of various psychoactive substances, disrupting normal sensory processing and perception through alterations in neurotransmitter systems such as serotonin, dopamine, and glutamate. These hallucinations can manifest across sensory modalities, often resolving upon cessation of exposure but sometimes persisting or recurring. They are distinct from endogenous causes, as they are directly linked to exogenous chemical triggers, with clinical presentations varying by substance class and dosage.^[72] Classic hallucinogens like lysergic acid diethylamide (LSD) and psilocybin primarily induce vivid visual hallucinations, including geometric patterns, color distortions, and synesthetic experiences, mediated by agonism at 5-HT2A serotonin receptors. These effects typically onset within 30-90 minutes of ingestion and last 6-12 hours, with users reporting enhanced perceptual depth rather than full detachment from reality at moderate doses. Dissociative anesthetics such as ketamine, an NMDA receptor antagonist, produce out-of-body experiences, depersonalization, and immersive visual or auditory hallucinations, often accompanied by a sense of ego dissolution; these emerge at sub-anesthetic doses and contribute to dissociative states mimicking near-death phenomena.^[72]^[73]^[74] Stimulants including cocaine and amphetamines trigger hallucinations through excessive dopamine release, commonly featuring paranoid auditory perceptions (e.g., voices accusing the user) and tactile sensations known as formication, where individuals feel insects crawling under their skin—a hallmark of cocaine-induced psychosis. Visual hallucinations may also occur, with prevalence rates of psychotic symptoms reaching 60-86% among chronic cocaine users and 17-37% for amphetamines, often escalating with binge use. Alcohol withdrawal, particularly in severe cases of delirium tremens, leads to multimodal hallucinations (visual, auditory, and tactile) peaking 48-72 hours after cessation, involving terrifying imagery such as small animals or insects; these affect up to 12% of hospitalized alcohol-dependent individuals and are compounded by autonomic hyperactivity.^[72]^[75]^[76] Anticholinergic agents like atropine cause delirium with predominantly visual hallucinations, such as fragmented scenes or animate objects, due to muscarinic receptor blockade disrupting cholinergic signaling in the brain; these are common in toxicity from therapeutic or accidental overdose, presenting alongside confusion and agitation. Cannabis, via CB1 receptor partial agonism, occasionally induces mild auditory hallucinations or perceptual distortions, particularly in high-potency strains or vulnerable users, with psychotic symptoms reported in 0.8-10% of regular consumers. Opioid-related hallucinations are rare, occurring in less than 2% of users during intoxication or withdrawal, but when present, they are typically visual (e.g., vivid scenes) and may be precipitated by agents like morphine or during naloxone-induced withdrawal, often in palliative care contexts.^[77]^[72]^[78] Among hallucinogen users, 4.2% experience hallucinogen persisting perception disorder (HPPD), characterized by recurrent visual disturbances like trails or geometric patterns long after substance clearance, potentially lasting months to years and linked to prior LSD or psilocybin exposure.^[79]

Environmental and Experimental Causes

Sensory deprivation, often induced in controlled environments like isolation tanks filled with saltwater, can lead to hallucinations as the brain compensates for the lack of external stimuli by generating internal perceptual experiences. Studies have shown that visual and auditory hallucinations may emerge after prolonged exposure, typically within 24 to 48 hours, due to the brain's tendency to fill sensory gaps with spontaneous neural activity.^[80] For instance, early experiments demonstrated that participants in sensory isolation reported vivid imagery and auditory perceptions, highlighting the role of reduced input in triggering these phenomena. Extreme stress or trauma, such as bereavement, can also provoke hallucinations, particularly in the form of sensing the presence or voice of a deceased loved one. A meta-analysis of bereavement hallucinations indicates that approximately 56.6% (95% CI: 49.9–63.2%) of grievers experience such episodes, often visual or auditory encounters with the departed, which are typically short-term and non-pathological.^[81] These experiences are attributed to heightened emotional states disrupting normal perceptual processing, providing temporary comfort without indicating underlying disorder.^[69] In experimental settings, substances like mescaline and psilocybin have been used to induce hallucinations under controlled conditions, revealing dose-dependent effects on visual perceptions. The Harvard Psilocybin Project (1960–1963), led by Timothy Leary and Richard Alpert, administered these psychedelics to participants and documented progressive intensification of visual distortions and geometric patterns with increasing doses, contributing to early understandings of hallucinogenic mechanisms.^[82] Modern dose-response studies confirm that higher psilocybin levels correlate with stronger perceptual alterations, including vivid hallucinations, underscoring the reproducibility of these effects in research.^[83] High-altitude exposure and associated hypoxia can trigger auditory and visual hallucinations among mountaineers, stemming from oxygen deprivation affecting brain function. Research on extreme-altitude climbers above 8,500 meters without supplemental oxygen found that 88% reported hallucinatory experiences, such as seeing companions or hearing voices, often linked to cerebral hypoxia rather than altitude sickness alone.^[84] These episodes typically resolve upon descent and acclimatization, illustrating the environmental impact on sensory processing.^[85] Electrostimulation techniques, particularly transcranial magnetic stimulation (TMS) applied to the occipital cortex, can experimentally induce phosphenes—perceived flashes of light resembling simple visual hallucinations. Seminal studies have established that TMS pulses generate these phosphenes by directly exciting visual cortical neurons, with thresholds varying by coil type and intensity, providing a non-invasive model for probing hallucinatory pathways.^[86] This method has been instrumental in distinguishing phosphene induction from broader hallucinatory states, aiding neuroscientific investigations.^[87]

Pathophysiology

Neurochemical Mechanisms

Hallucinations arise from disruptions in neurotransmitter systems that regulate sensory processing, perception, and cognition. Key mechanisms involve imbalances in dopamine, serotonin, acetylcholine, glutamate, and endogenous opioids, each contributing to specific types of hallucinatory experiences across various conditions. The dopaminergic hypothesis posits that hyperactivity in the mesolimbic dopamine pathway, particularly excessive stimulation of D2 receptors, underlies positive symptoms of schizophrenia, including auditory hallucinations. This excess dopamine release in subcortical regions like the nucleus accumbens enhances salience attribution to internal stimuli, leading to perceptual distortions interpreted as external voices or sounds.^[88] Positron emission tomography studies confirm elevated dopamine synthesis and release in the striatum of individuals prone to psychotic symptoms, supporting this pathway's role in hallucination generation.^[89] Serotonergic pathways are critically involved in visual hallucinations, with agonism of 5-HT2A receptors by psychedelics such as psilocybin inducing profound perceptual alterations. Psilocybin reduces parieto-occipital alpha oscillations and N170 visual-evoked potentials, shifting cortical processing toward internal imagery and causing vivid visual distortions that correlate strongly with subjective hallucinatory intensity.^[90] These effects are selectively blocked by 5-HT2A antagonists like ketanserin, confirming receptor specificity. Inversely, serotonergic hypoactivity, as implicated in depression, may facilitate hallucinatory phenomena by diminishing inhibitory control over sensory networks, though such occurrences are less common and often tied to severe mood dysregulation.^[91] Cholinergic deficiency, characterized by reduced acetylcholine signaling in cortical areas, contributes to visual hallucinations in Alzheimer's disease, where degeneration of basal forebrain cholinergic neurons impairs attention and sensory gating. This hypoactivity disrupts the integration of visual information, leading to misperceptions of environmental stimuli as hallucinatory elements.^[92] The scopolamine model exemplifies this mechanism, as muscarinic receptor blockade induces delirium-like states with prominent visual and tactile hallucinations, mimicking cholinergic loss without neuronal damage and highlighting acetylcholine's role in maintaining perceptual stability.^[93] Glutamatergic dysfunction, particularly NMDA receptor hypofunction, produces hallucinations resembling those in schizophrenia when induced by ketamine. As an uncompetitive NMDA antagonist, ketamine disrupts excitatory-inhibitory balance in cortical circuits, increasing glutamate release in prefrontal and temporal regions while impairing gamma oscillations essential for sensory binding, resulting in dissociative and perceptual symptoms like vivid illusions and voices.^[94] This model demonstrates dose-dependent escalation from mild perceptual changes to full psychotic episodes, underscoring glutamate's modulatory influence on hallucinatory states.^[95]

Neuroanatomical Basis

Hallucinations arise from disruptions in specific brain regions and networks that process sensory information and internal representations, often involving aberrant activation or connectivity in cortical and subcortical structures. Functional neuroimaging studies have identified key areas implicated in the generation of hallucinatory experiences across modalities, highlighting the role of both localized hyperactivity and distributed network dysfunction.^[96] Auditory hallucinations, particularly auditory verbal hallucinations in schizophrenia, are associated with hyperactivity in the superior temporal gyrus, including Heschl's gyrus, which processes auditory stimuli. This region shows increased blood oxygen level-dependent signals during hallucination episodes, as captured by functional magnetic resonance imaging (fMRI). Additionally, Broca's area in the inferior frontal gyrus is involved in the language-related aspects of perceived voices, with decoding studies demonstrating predictive activity in this area prior to hallucination onset.^[97]^[98]^[99] Visual hallucinations engage the occipital and temporal lobes, where the ventral visual stream processes complex object recognition and scene formation. In Charles Bonnet syndrome, which occurs in individuals with visual impairment, lesions or deafferentation in the occipital cortex lead to vivid, formed visual percepts, often involving activation of visual association areas in the temporal lobe. These findings indicate that reduced sensory input can trigger spontaneous activity in the "what" pathway of visual processing.^[100]^[101] Multimodal hallucinations, involving combined sensory modalities, implicate the thalamus as a critical relay for integrating sensory inputs and the parietal lobe for cross-modal synthesis. Thalamic nuclei facilitate the gating of sensory signals to cortical areas, and disruptions here contribute to the blending of sensory experiences in psychotic states. The parietal lobe, particularly the inferior parietal lobule, supports spatial and attentional integration, with aberrant activity linked to hallucinatory perceptions across senses.^[102]^[103] Subcortical structures, such as the brainstem, play a role in peduncular hallucinosis, where lesions in the midbrain or pons disrupt ascending reticular activating pathways that modulate arousal and sensory filtering. These lesions, often vascular or compressive, lead to vivid, Lilliputian visual hallucinations without insight impairment, underscoring the brainstem's influence on thalamocortical transmission.^[104]^[105] Network-level models emphasize dysregulation of the default mode network (DMN), which includes the medial prefrontal cortex, posterior cingulate, and angular gyrus, as a mechanism for generating involuntary sensory imagery. In conditions like schizophrenia and Parkinson's disease, hyperconnectivity or reduced anticorrelations within the DMN allow internal mentation to intrude into perceptual awareness, bypassing external sensory checks. This triple-network imbalance, involving the DMN, salience network, and executive network, further propagates hallucinatory states.^[106]^[96]^[107]

Diagnosis

Clinical Assessment

Clinical assessment of hallucinations begins with a thorough history-taking to characterize the experience. Clinicians inquire about the sensory modality of the hallucinations, which may include auditory, visual, tactile, olfactory, or gustatory perceptions, as well as their frequency, duration, content, and associated distress levels.^[108] For auditory hallucinations, a semi-structured interview such as the Psychotic Symptom Rating Scales (PSYRATS) auditory hallucinations subscale is commonly used; this tool rates dimensions including frequency (e.g., daily occurrence), duration (e.g., lasting minutes to hours), intensity, emotional impact, and degree of control over the experience, providing a multidimensional profile to gauge severity and impact.^[109] The mental status examination (MSE) further evaluates the patient's perceptual disturbances and related cognitive features. Key components include assessing insight—whether the patient recognizes the hallucinations as unreal or believes them to be veridical—and observing the patient's affect during recall of the experiences, such as anxiety, fear, or indifference, which can indicate emotional burden.^[110] This examination helps distinguish hallucinations from other perceptual anomalies and informs the functional implications. Screening questionnaires aid in quantifying hallucination proneness, particularly in non-acute settings or for research purposes. The Launay-Slade Hallucination Scale (LSHS), a 12-item self-report measure, assesses predisposition to hallucinatory experiences across modalities by rating the frequency of phenomena like intrusive thoughts or vivid imagery on a Likert scale, with higher scores indicating greater proneness; it is validated for use in both clinical and general populations.^[111] Collateral information from family members or caregivers is essential to contextualize the patient's report, providing details on the onset, progression, and situational triggers of hallucinations, as well as any observable behavioral changes.^[108] Basic laboratory investigations are performed to exclude metabolic or toxic etiologies. These typically include a complete blood count, comprehensive metabolic panel (to assess electrolyte imbalances, glucose levels, and renal/hepatic function), thyroid function tests, urinalysis, and toxicology screening for substances.^[13]

Differential Diagnosis

Differential diagnosis of hallucinations involves distinguishing them from other perceptual disturbances, perceptual misinterpretations, and related psychiatric or neurological phenomena to guide appropriate clinical management. Hallucinations are defined as sensory perceptions occurring in the absence of corresponding external stimuli, and they can arise from diverse etiologies including psychiatric, neurological, and substance-related causes. Accurate differentiation requires careful history-taking, assessment of insight, sensory modality, content, duration, and associated symptoms, often necessitating neuroimaging, laboratory tests, or psychiatric evaluation to rule out underlying organic pathology.^[11]^[30] A primary distinction lies between hallucinations, illusions, and delusions. Illusions represent misperceptions of actual external stimuli, such as mistaking a shadow for a person, and typically resolve upon increased attention, lighting adjustment, or sensory correction, whereas hallucinations occur without any real stimulus and persist independently. Delusions, in contrast, are fixed false beliefs without a sensory perceptual component, such as a conviction of being persecuted, lacking the vivid sensory quality of hallucinations; for instance, a patient may hold a delusional belief about external threats but not experience auditory voices unless true hallucinations are also present. These differences are crucial in psychiatric evaluation, as illusions often signal environmental or sensory deficits, while delusions and hallucinations indicate more profound disruptions in reality testing.^[112]^[113] Organic causes of hallucinations must be differentiated from functional psychiatric origins through clinical features and ancillary investigations. Organic hallucinations, often linked to delirium, are typically acute, fluctuating in intensity, multimodal (involving multiple senses), and accompanied by altered consciousness, confusion, or identifiable medical triggers like infections, metabolic derangements, or medication side effects; for example, delirium in hospitalized elderly patients may present with vivid, fragmented visual hallucinations that wax and wane over hours. In contrast, functional hallucinations in conditions like schizophrenia are chronic, organized, and modality-specific (e.g., complex auditory voices with commentary), occurring with preserved consciousness and often featuring impaired insight; ruling out organic factors involves excluding delirium via tools like the Confusion Assessment Method and conducting targeted labs or imaging.^[11]^[30]^[114] Pseudohallucinations, particularly in borderline personality disorder (BPD), differ from true hallucinations by their internal origin, reduced vividness, and preserved insight, where individuals recognize the experiences as unreal or self-generated. In BPD, auditory verbal hallucinations are often described as originating "inside the head," transient, stress-related, and less distressing or commanding than those in psychotic disorders, with prevalence estimates of approximately 25-27% in clinical samples; these may reflect dissociative processes rather than primary psychosis, and differential diagnosis emphasizes evaluating for comorbid trauma or affective symptoms over antipsychotic trials.^[115]^[116] Cultural syndromes can mimic hallucinations through interpretive frameworks, requiring culturally sensitive assessment to avoid misdiagnosis. For instance, in Yoruba communities of Nigeria, experiences labeled as "Ode-Ori" (head carrier or madness) may involve spirit possession attributed to supernatural causes, presenting as auditory or visual perceptions interpreted as ancestral communications rather than pathological hallucinations; these differ from clinical hallucinations by their contextual acceptance within cultural rituals and lack of distress or functional impairment outside spiritual beliefs. Similarly, in Santería practiced by Afro-Caribbean communities, beliefs in spirit possession can complicate the diagnosis of mental illness, presenting as trance states that are not equated with psychotic hallucinations when insight into their cultural meaning is retained. Clinicians must collaborate with cultural experts to discern whether such experiences align with normative practices or indicate underlying psychopathology.^[117]^[118] Key differentials include hallucinations in dementia, which are often simple, recurrent visual phenomena (e.g., seeing deceased relatives or animals) without complex narratives, predominantly in dementia with Lewy bodies (affecting up to 80% of cases) and associated with visuospatial deficits, contrasting with the novel, elaborate content of primary psychotic hallucinations. In post-traumatic stress disorder (PTSD), flashbacks represent intrusive re-experiencing of past trauma—vivid but memory-based sensory reliving (e.g., reliving a combat scene)—rather than novel hallucinations, lacking the external attribution and persistence of true perceptual distortions; differentiation hinges on trauma history, episodic triggers, and absence of reality testing impairment beyond the event. Other mimics, such as Charles Bonnet syndrome in visual impairment, feature preserved insight and non-threatening visuals, underscoring the need for modality-specific evaluation.^[11]^[119]^[120]

Treatment

Pharmacological Treatments

Pharmacological treatments for hallucinations primarily target the underlying neurochemical imbalances, such as excessive dopaminergic activity in conditions like schizophrenia. Antipsychotic medications are the first-line intervention for hallucinations in schizophrenia spectrum disorders, rapidly reducing symptom severity through blockade of dopamine D2 receptors in the mesolimbic pathway.^[10] Typical antipsychotics, exemplified by haloperidol, exert potent dopamine antagonism, effectively suppressing positive symptoms including auditory and visual hallucinations.^[121] These agents are particularly useful in acute settings where rapid control is needed, though their use is tempered by a higher risk of extrapyramidal side effects (EPS), such as acute dystonia, parkinsonism, and akathisia, which require careful monitoring and potential adjunctive treatments like anticholinergics.^[122] Atypical antipsychotics, such as risperidone, olanzapine, and clozapine, provide broader efficacy by modulating both dopamine and serotonin receptors, often leading to better tolerability and sustained symptom control. These medications have demonstrated efficacy in alleviating auditory verbal hallucinations, with clozapine showing particular benefit in treatment-resistant cases.^[10] Compared to typical agents, atypicals are associated with a lower incidence of EPS but may carry risks of metabolic disturbances like weight gain and sedation, underscoring the need for individualized selection based on patient profile.^[121] For hallucinations arising in the context of mood disorders, such as psychotic depression, selective serotonin reuptake inhibitors (SSRIs) like fluoxetine address potential serotonergic dysregulation, though they are most effective when combined with antipsychotics for comprehensive symptom relief.^[123] In substance-induced cases, particularly alcohol withdrawal delirium featuring tremors and perceptual disturbances, benzodiazepines such as diazepam or lorazepam are standard to mitigate autonomic hyperactivity and prevent progression to severe hallucinations.^[124] Migraine-associated visual auras, considered a form of hallucination, respond acutely to triptans like sumatriptan for aborting attacks, while prophylactic agents such as topiramate reduce aura frequency by stabilizing neuronal excitability.^[125] For neurological conditions, visual hallucinations in Parkinson's disease are often managed by reducing dopaminergic medications when possible, or using pimavanserin (approved specifically for Parkinson's disease psychosis), quetiapine, or clozapine, which have lower risk of worsening motor symptoms. In epilepsy, anticonvulsants such as carbamazepine or levetiracetam address seizure-related hallucinations by controlling underlying epileptiform activity.^[126]^[7] In September 2024, the FDA approved Cobenfy (xanomeline and trospium chloride), a muscarinic receptor agonist, for the treatment of schizophrenia in adults, demonstrating efficacy in reducing positive symptoms such as hallucinations through a novel non-dopaminergic mechanism.^[127] Across these treatments, ongoing clinical monitoring is essential to balance efficacy against adverse effects, including the EPS linked to dopaminergic blockade in antipsychotics.^[122]

Non-Pharmacological Interventions

Non-pharmacological interventions for hallucinations emphasize psychological therapies, supportive strategies, and lifestyle modifications to alleviate distress and enhance coping without relying on medications. These approaches target the emotional impact and functional impairment of hallucinations, fostering insight and resilience. Among the most established methods is Cognitive Behavioral Therapy (CBT), particularly tailored for voice-hearing experiences, which involves normalizing the phenomenon, challenging distressing content, and building adaptive responses. A systematic review of randomized and non-randomized trials indicates that CBT significantly reduces the frequency, severity, and distress of auditory hallucinations, with notable improvements in standardized measures like the Psychotic Symptom Rating Scales (PSYRATS).^[128] Reality testing, a core component of CBT protocols, equips individuals with techniques to evaluate the validity of hallucinatory experiences and differentiate them from reality. Common practices include journaling episodes to log sensory details, emotional triggers, and contradictory evidence, which promotes metacognitive awareness and diminishes the perceived power of hallucinations. This approach has been integrated into evidence-based manuals for psychosis treatment, showing benefits in reducing preoccupation and conviction in delusional or hallucinatory beliefs.^[129] For visual hallucinations in Charles Bonnet syndrome, arising from sensory deprivation due to vision loss, low-vision rehabilitation plays a key role by providing optical aids such as magnifiers and enhancing environmental stimulation to counteract deprivation. Clinical evaluations demonstrate that these interventions improve visual acuity and functional outcomes, thereby decreasing the occurrence and intensity of hallucinations in affected patients.^[130] Peer support through organizations like the Hearing Voices Network offers practical coping strategies, including selective attention to positive voices, distraction via engaging activities, and narrative reframing to empower voice-hearers. These groups emphasize community validation and skill-sharing, which help mitigate isolation and emotional burden associated with hallucinations.^[131] Lifestyle adjustments further support management, such as implementing sleep hygiene for hypnagogic hallucinations—characterized by vivid imagery at sleep onset—through consistent schedules, dark environments, and avoidance of stimulants to stabilize sleep-wake transitions and reduce episode frequency.^[132] Similarly, mindfulness-based stress reduction techniques cultivate non-reactive observation of experiences, leading to gradual declines in hallucination severity and related delusions, as evidenced in intervention studies tracking symptom trajectories over weeks.^[133]

Epidemiology

Prevalence and Incidence

In the general population, the lifetime prevalence of hallucinations is estimated to be between 5% and 15%, based on large-scale epidemiological studies.^[134] This figure encompasses various sensory modalities, with auditory verbal hallucinations being among the most commonly reported, occurring in approximately 5-28% of individuals over their lifetime.^[135] Rates are notably higher in specific non-pathological contexts, such as bereavement, where meta-analyses indicate that 50-60% of grieving individuals experience sensory perceptions of the deceased, often visual or auditory in nature.^[81] Among psychiatric populations, hallucinations are substantially more prevalent. In schizophrenia spectrum disorders, 60-80% of patients report hallucinations, predominantly auditory, though visual and multimodal experiences also occur frequently.^[136] In bipolar disorder, lifetime prevalence of psychotic symptoms including hallucinations ranges from 50% to 70%, typically emerging during manic or mixed episodes and often involving auditory or visual content.^[137] These rates underscore the role of hallucinations as core symptoms in psychotic disorders, contributing to diagnostic criteria in frameworks like the DSM-5. Prevalence patterns vary by age and gender. Auditory hallucinations peak in young adults, with past-year rates reaching 7% among those aged 16-19 years and declining steadily across the lifespan to about 3% in individuals over 70.^[138] In contrast, visual hallucinations are more common in the elderly, affecting around 10% of older psychiatric outpatients and often linked to age-related sensory decline or neurological conditions.^[139] Overall, there is a slight female predominance in hallucination reporting across populations, potentially influenced by gender differences in symptom expression and help-seeking behaviors.^[134] Global variations in reported prevalence reflect cultural influences on disclosure and interpretation. Rates appear higher in some developing countries, such as West African nations like Ghana (90% auditory hallucinations in clinical samples) and Nigeria (85%), compared to European countries like Austria (66%), attributed to greater cultural acceptance of spiritual or supernatural explanations for such experiences.^[140] Recent surveys from the World Mental Health Initiative in the 2010s have highlighted increasing recognition of hallucinations in non-clinical samples worldwide, with median lifetime prevalence of psychotic experiences around 7%, emphasizing their continuum from normative to pathological.^[141]

Associated Risk Factors

Hallucinations exhibit a significant genetic component, particularly in the context of schizophrenia-spectrum disorders where they are a core symptom. Twin and family studies estimate the heritability of schizophrenia at approximately 80%, with genetic factors accounting for 30-60% of the variance in psychotic experiences including hallucinations among affected and non-clinical individuals. Polygenic risk scores (PRS) derived from genome-wide association studies further support this, as elevated PRS for schizophrenia predict increased severity and frequency of auditory and visual hallucinations in both clinical and non-clinical populations.^[142]^[143] Childhood trauma represents a key environmental risk factor for developing hallucinations in adulthood, especially auditory forms. Experiences of physical, sexual, or emotional abuse during childhood approximately double the odds of auditory hallucinations later in life, with odds ratios ranging from 1.2 to 2.5 across trauma categories.^[144] This association is thought to arise from altered stress response systems and neurodevelopmental disruptions, though the precise mechanisms remain under investigation.^[145] Substance use, particularly lifetime exposure to cannabis and other drugs, substantially elevates the risk of hallucinations. Individuals with heavy lifetime cannabis use (more than 50 occasions) face odds ratios of around 3.1 for psychotic experiences including hallucinations, while dependence on substances like methamphetamine can yield odds ratios as high as 3-5 times greater compared to non-users.^[146] These effects are dose-dependent and interact with genetic vulnerability, amplifying risk in those with high schizophrenia PRS.^[147] Sensory deprivation due to vision or hearing impairment also heightens hallucination susceptibility, often through deafferentation mechanisms where reduced input leads to spontaneous neural activity. Visual impairment increases the risk of visual hallucinations by approximately 20%, as seen in conditions like Charles Bonnet syndrome affecting 11-15% of those with significant vision loss.^[148] Similarly, hearing impairment raises the likelihood of auditory hallucinations by about 20%, with prevalence climbing to 16-24% in severe cases, correlating linearly with impairment degree.^[149] Comorbid conditions such as sleep disorders and migraines serve as additional predictors of hallucinations. Chronic insomnia quadruples the odds of hallucinatory experiences compared to normal sleep patterns, likely due to disrupted REM sleep and heightened perceptual sensitivity.^[150] Migraines, especially those with aura, are linked to transient hallucinations, with affected individuals showing elevated risk for visual and auditory perceptual distortions during attacks.^[151]

Other Contexts

Hallucinations in Artificial Intelligence

In artificial intelligence, hallucinations refer to instances where models generate false, fabricated, or unsubstantiated information presented as factual, often due to the probabilistic nature of their outputs. This phenomenon is particularly prevalent in large language models (LLMs) and generative systems, where the AI produces responses that appear plausible but lack grounding in reality or training data. Unlike perceptual distortions in human cognition, AI hallucinations are output errors arising from the model's inability to verify facts internally, leading to inventions such as non-existent references or events.^[152]^[153] The primary causes of AI hallucinations include limitations in training data, such as biases, inaccuracies, or incomplete coverage, which lead the model to overfit or extrapolate erroneously. Additionally, the autoregressive generation process in LLMs—predicting tokens sequentially based on statistical patterns without inherent fact-checking—amplifies the issue, especially under ambiguous prompts or when handling out-of-distribution queries. Model architecture constraints, like limited context windows, further contribute by forcing reliance on compressed representations that may introduce distortions. In early models like GPT-3.5, benchmarks revealed hallucination rates as high as 39.6% in tasks involving factual recall or citation generation.^[154]^[155]^[156]^[157] Notable examples illustrate the impact: ChatGPT has been observed fabricating bibliographic citations, such as inventing scholarly articles or legal cases that do not exist, which can mislead users in research or professional contexts. In image generation, tools like DALL-E or Stable Diffusion often produce anatomically impossible scenes, such as humans with extra limbs or objects defying physics, due to training on vast but noisy datasets that prioritize visual coherence over realism. These errors highlight the risks in applications like journalism, healthcare, or creative design, where unverified outputs can propagate misinformation. As of 2025, hallucination rates in leading LLMs have declined by approximately 3% per year but remain significant in high-stakes domains like legal analysis, averaging 6.4–18.7%.^[158]^[159]^[160]^[161]^[162] To mitigate hallucinations, techniques such as retrieval-augmented generation (RAG) integrate external knowledge bases to ground responses in verifiable sources, reducing fabrication rates by up to 50% in controlled evaluations. Fine-tuning on domain-specific data and implementing confidence scoring—where models abstain from low-certainty outputs—further enhance reliability. By 2025, advancements in neurosymbolic AI, which combines neural pattern recognition with symbolic logic for verifiable reasoning, have shown promise in reducing hallucinations in targeted domains like legal analysis.^[163]^[164]^[165] Unlike human hallucinations, which involve subjective perceptual experiences rooted in neurology and often tied to altered states of consciousness, AI versions lack any internal sensory or experiential component; they are purely computational confabulations driven by optimization for fluency over accuracy. This distinction underscores that AI hallucinations stem from design choices in probabilistic modeling, not cognitive phenomenology.^[166]

Cultural and Historical Perspectives

In ancient civilizations, hallucinations were frequently interpreted as divine communications rather than pathological phenomena. For instance, in 5th-century BCE Greece, oracles at sites like Delphi are speculated to have employed hallucinogenic substances such as henbane or inhaled ethylene gas from geological fissures to induce visions believed to convey messages from gods like Apollo, influencing political and military decisions across the Hellenic world.^[167]^[168] This perspective framed altered sensory experiences as sacred intermediaries between humans and the divine, a view echoed in various prophetic traditions where visions were seen as infallible due to their inspirational origin.^[169] By the 19th century, Western psychiatry shifted toward medicalizing hallucinations, classifying them as symptoms of mental disorder. French psychiatrist Jean-Étienne-Dominique Esquirol played a pivotal role in this transition, providing the first modern definition of hallucinations as perceptions without external stimuli and integrating them into a semiology of mental illnesses, often linking them to monomania or schizophrenia precursors.^[170] Esquirol's work, detailed in his 1838 Des Maladies Mentales, emphasized clinical observation and statistical analysis, marking hallucinations as indicators of "wandering mind" rather than supernatural events, which entrenched stigma in European medical discourse.^[171] Culturally, interpretations of hallucinations vary widely, with non-Western traditions often viewing them as spiritually significant. In Native American shamanic practices, such as peyote rituals within the Native American Church, induced visions from the cactus Lophophora williamsii are regarded as pathways to healing, spiritual insight, and communal bonding, legally protected as religious sacraments since the 1978 American Indian Religious Freedom Act.^[172] In contrast, Western medicine has historically stigmatized such experiences as deviant, while some African traditions, like those among the Xhosa in South Africa, interpret auditory hallucinations as ancestral communications or benevolent entities, fostering acceptance and integration rather than pathologization.^[173] This cultural shaping influences phenomenology, with voices in non-Western contexts often reported as more dialogic or supportive compared to the distressing, commanding tones prevalent in Western reports.^[174] Notable historical cases highlight these interpretive tensions. In the 15th century, Joan of Arc's visions of saints and divine missions, which guided her military campaigns during the Hundred Years' War, have been retrospectively debated as potential auditory hallucinations, possibly linked to temporal lobe epilepsy or cultural religious fervor, though contemporary accounts framed them as holy inspirations leading to her canonization in 1920.^[175] Similarly, in 1943, Swiss chemist Albert Hofmann's accidental ingestion of lysergic acid diethylamide (LSD-25) induced profound hallucinations, sparking 20th-century research into psychedelics as tools for exploring consciousness, though initially pursued for psychiatric applications before cultural backlash in the 1960s.^[176] The 21st century has seen efforts to destigmatize hallucinations through movements recognizing their non-pathological forms. The Hearing Voices Network, founded in 1987 and expanding globally, promotes peer support groups that reframe voice-hearing as a meaningful human experience influenced by trauma or culture, challenging biomedical dominance and advocating for lived-experience perspectives in mental health policy.^[177] This shift aligns with broader philosophical debates on reality, as in René Descartes' 1641 Meditations on First Philosophy, where the "evil demon" hypothesis posits a deceptive entity capable of fabricating illusory perceptions indistinguishable from reality, underscoring skepticism about sensory reliability and paralleling modern discussions of hallucinatory epistemology.^[178]

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