Why We Hallucinate: Neuroscience, Drugs, and Mental Health

Hallucinate: Understanding the Causes and TreatmentsHallucinations—perceptions experienced without an external stimulus—can be vivid, disorienting, and distressing. They affect people across age groups and clinical conditions, and can involve any sensory modality: visual, auditory, tactile, olfactory, or gustatory. This article explains what hallucinations are, the mechanisms behind them, common causes, how clinicians evaluate them, available treatments, and practical coping strategies for patients and caregivers.

What is a hallucination?

A hallucination is a sensory experience that appears real but is created by the mind. Unlike illusions, which are distorted perceptions of actual stimuli, hallucinations occur in the absence of an appropriate external input. Hallucinations may be simple (e.g., flashes of light or buzzing) or complex (e.g., fully formed voices, people, or scenes). They can be transient or persistent, benign or a sign of a serious medical or psychiatric condition.

Key distinctions:

• Hallucination: Perception without external stimulus.
• Illusion: Misperception of an actual external stimulus.
• Pseudohallucination: Recognized by the person as unreal (less common term in modern clinical practice).

Types of hallucinations

• Visual: Seeing objects, people, or lights that aren’t present. Common in neurological conditions, substance use, and Charles Bonnet syndrome (visual loss-related).
• Auditory: Hearing sounds or voices. Most commonly reported in psychotic disorders like schizophrenia but also in hearing impairment and in bereavement.
• Tactile: Sensations on or under the skin (e.g., insects crawling). Often linked to substance withdrawal (amphetamine, cocaine), alcohol withdrawal, or peripheral neuropathy.
• Olfactory: Smelling odors that aren’t present. Can be caused by temporal lobe epilepsy, head trauma, or neurodegenerative disorders.
• Gustatory: Tastes without a source. Less common, may occur with seizure disorders or brain lesions.

Neurobiology: how hallucinations arise

Hallucinations arise from abnormal activation or misinterpretation within sensory pathways and higher-order cognitive networks. Key mechanisms include:

• Sensory cortex hyperactivity: Spontaneous firing in modality-specific cortex (e.g., visual cortex) can produce percepts without input.
• Predictive coding errors: The brain constantly predicts sensory input; when predictions are weighted more heavily than actual input, internally generated patterns can be mistaken for external stimuli.
• Dysconnectivity: Abnormal communication between sensory regions and frontal or attentional networks impairs reality-monitoring (the ability to distinguish internal from external sources).
• Neurochemical imbalances: Dopamine, serotonin, glutamate, and acetylcholine systems influence perceptual processing; imbalances can predispose to hallucinations.
• Deafferentation: Loss of sensory input (e.g., vision or hearing loss) can lead the brain to generate its own percepts—Charles Bonnet syndrome is one example.

Causes and associated conditions

Hallucinations are a symptom, not a diagnosis. They occur in many contexts:

1. Psychiatric disorders

   • Schizophrenia spectrum disorders (auditory hallucinations are common).
   • Bipolar disorder with psychotic features.
   • Severe depression with psychosis.
   • Delirium and acute psychosis.

2. Neurological disorders

   • Parkinson’s disease and Lewy body dementia (visual hallucinations are common).
   • Alzheimer’s disease and other dementias.
   • Epilepsy (especially temporal lobe seizures).
   • Head trauma, brain tumors, and stroke.

3. Sensory impairment

   • Charles Bonnet syndrome (visual hallucinations following significant vision loss).
   • Auditory hallucinations in hearing impairment.

4. Substance-related

   • Intoxication: psychedelics (LSD, psilocybin), stimulants (amphetamine, cocaine), cannabis (in some), alcohol (less commonly).
   • Withdrawal states: alcohol withdrawal (delirium tremens), benzodiazepine withdrawal, stimulant withdrawal.

5. Medical and metabolic causes

   • Infections (e.g., encephalitis, sepsis).
   • Metabolic disturbances (e.g., hepatic or renal failure, electrolyte imbalances).
   • Medication side effects (anticholinergics, corticosteroids, dopaminergic agents).

6. Sleep-related

   • Hypnagogic (falling asleep) and hypnopompic (waking) hallucinations—common and often benign.
   • Sleep paralysis can be accompanied by vivid hallucinations.

7. Bereavement and cultural phenomena

   • Grief-related visual or auditory experiences of deceased loved ones—often transient and not pathological.
   • Culturally sanctioned experiences may not indicate illness.

Clinical evaluation

A careful assessment determines cause and guides treatment. Key steps:

• History: onset, duration, frequency, sensory modalities, content, level of distress, insight (does the person recognize the experience as unreal?), triggers (sleep, substances), medical history, medications.
• Mental status exam: assess thought disorder, mood, cognition, suicidality.
• Neurological exam: focal deficits, signs of neurodegenerative disease.
• Laboratory tests: CBC, electrolytes, kidney and liver function, thyroid studies, B12, glucose; toxicology screen if substance use suspected.
• Imaging: brain MRI or CT if focal neurological signs, new-onset persistent hallucinations, or head trauma.
• EEG: when seizures or encephalopathy suspected.
• Sensory assessments: vision and hearing tests.
• Collateral history: family/caregiver reports can clarify frequency and impact.

Treatment principles

Treatment targets the underlying cause and reduces distress/functional impairment. Approaches often combine pharmacologic and nonpharmacologic strategies.

1. Treat underlying medical causes

   • Correct metabolic disturbances, treat infections, manage withdrawal syndromes, optimize sensory impairments (e.g., hearing aids, cataract surgery).

2. Medication

   • Antipsychotics: dopamine D2 antagonists or atypical agents (e.g., risperidone, olanzapine, quetiapine) are the mainstay for persistent psychotic hallucinations, especially in schizophrenia, bipolar disorder, or severe psychosis.
   • For Parkinson’s disease and Lewy body dementia: low-risk antipsychotics (quetiapine, clozapine) or cholinesterase inhibitors (e.g., rivastigmine) are preferred; many antipsychotics worsen motor symptoms.
   • Antiepileptics: if seizures are the cause, optimized anti-seizure therapy is primary.
   • Cholinesterase inhibitors: sometimes helpful for visual hallucinations in Lewy body dementia.
   • Medications for substance-related states: benzodiazepines for alcohol withdrawal, antipsychotics for stimulant-induced psychosis when needed.
   • Novel and adjunctive options: NMDA modulators, serotonin receptor agents, or pimavanserin (for Parkinson’s psychosis) in specific contexts.

3. Psychosocial and nonpharmacologic interventions

   • Cognitive-behavioral therapy for psychosis (CBTp) helps patients reframe beliefs about hallucinations, reduce distress, and develop coping strategies.
   • Reality-testing and grounding techniques: checking external sources, sensory reorientation, focusing on tactile stimuli.
   • Sensory rehabilitation: hearing aids, vision correction; reducing isolation and offering structured daily routines.
   • Family education and support: teaching caregivers how to respond calmly, avoid confrontation, and prioritize safety.
   • Environmental modifications: improve lighting, reduce clutter and shadows (for visual hallucinations), ensure sleep hygiene.
   • Neuromodulation: transcranial magnetic stimulation (TMS) shows promise for auditory hallucinations in research settings; evidence is evolving.

Practical coping strategies for patients and caregivers

• Maintain routines and regular sleep—sleep disruption often worsens hallucinations.
• Use sensory aids (glasses, hearing aids) and ensure proper fit and function.
• Reduce substances that can provoke hallucinations (alcohol, recreational drugs, certain medications); consult a clinician before stopping prescribed drugs.
• Distraction and grounding: listen to music, hold an ice cube, count objects in the room, describe the environment aloud.
• Reality testing: ask trusted people whether others perceive the same thing; keep a journal documenting episodes (time, triggers, duration).
• Safety planning: if hallucinations command harmful acts or increase suicide risk, seek immediate medical help; remove dangerous items and involve caregivers.
• Psychoeducation: understanding that hallucinations are symptoms—not moral failings—reduces stigma and promotes help-seeking.

Prognosis

Prognosis depends on cause, duration, severity, and treatment response. Acute, substance-induced, or medically driven hallucinations often resolve with treatment of the underlying condition. Chronic hallucinations associated with schizophrenia or neurodegenerative disorders may persist but can often be reduced in intensity and distress with combined pharmacological and psychosocial interventions.

Research directions

Active research areas include:

• Refining neural circuit models (predictive coding, network dysconnectivity).
• Developing targeted neuromodulation (TMS protocols, transcranial direct current stimulation).
• Novel pharmacotherapies that modulate glutamate, serotonin, or cholinergic systems without heavy dopamine blockade.
• Digital therapeutics and virtual-reality–based interventions for coping skills training.

When to seek urgent help

Seek immediate medical or psychiatric evaluation if hallucinations:

• Are accompanied by suicidal ideation or commands to harm self/others.
• Impair the ability to care for oneself.
• Appear suddenly with confusion, fever, headache, or focal neurological deficits.
• Follow head trauma or suspected overdose.

Hallucinations are a heterogeneous symptom with many causes. A careful, stepwise evaluation identifies reversible medical contributors, while tailored pharmacologic and psychosocial treatments reduce distress and improve functioning.