Covid Hallucinations: Mechanisms and Psychiatric Impact

Hallucinations have been reported in some individuals with COVID-19, raising concerns about the virus’s impact on the brain. While respiratory symptoms dominate public awareness, neurological and psychiatric effects are increasingly recognized. Understanding how COVID-19 contributes to hallucinations is crucial for clinical management and long-term patient care.

Neuropathological Mechanisms

SARS-CoV-2, the virus responsible for COVID-19, can affect the central nervous system (CNS) through multiple pathways, potentially leading to hallucinations. One proposed mechanism involves direct viral invasion of neural tissue. Studies using post-mortem brain samples and cerebrospinal fluid (CSF) analysis have detected viral RNA and proteins in neural structures, suggesting the virus may breach the blood-brain barrier (BBB) or enter through the olfactory nerve. This raises concerns about disruptions in neurotransmission, particularly in regions associated with sensory processing.

Disruptions in neurotransmitter systems further contribute to hallucinations. Dopaminergic dysregulation, a well-documented factor in psychotic disorders, has been implicated in COVID-19-related neuropsychiatric symptoms. Elevated dopamine levels, possibly triggered by viral interactions with basal ganglia circuits, may lead to sensory distortions. Additionally, altered glutamatergic signaling, fundamental to cognitive function, has been observed in patients with neurological manifestations of COVID-19. Reduced glutamate transmission in cortical and subcortical regions could impair sensory gating, making individuals more susceptible to perceptual distortions.

Brain imaging studies provide further insights. Functional MRI (fMRI) and positron emission tomography (PET) scans have revealed hypometabolism in the frontal and temporal lobes, areas integral to reality monitoring and sensory integration. These findings align with reports of delirium and acute confusional states, reinforcing the notion that COVID-19 can induce transient or persistent brain function alterations. White matter abnormalities, including microstructural damage detected via diffusion tensor imaging (DTI), suggest that even without direct viral invasion, secondary effects such as hypoxia or vascular injury may contribute to neural dysfunction.

Immune Response And Brain Inflammation

The immune response to SARS-CoV-2 plays a significant role in the neurological complications observed in some COVID-19 patients, including hallucinations. A hyperinflammatory state, often referred to as a cytokine storm, has been implicated in brain dysfunction. Elevated levels of pro-inflammatory cytokines like interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and interleukin-1β (IL-1β) have been detected in cerebrospinal fluid and blood samples from patients experiencing neuropsychiatric symptoms. While essential for immune defense, excessive production of these molecules can compromise the blood-brain barrier and trigger widespread neuroinflammation.

Once inflammatory mediators infiltrate the CNS, they disrupt neuronal signaling and induce structural damage. Microglial cells, the brain’s resident immune cells, become activated in response to systemic inflammation, releasing additional cytokines and reactive oxygen species. Excessive microglial activation has been linked to synaptic pruning and neuronal loss, particularly in sensory processing regions like the thalamus and temporal cortex. PET imaging studies have identified increased microglial activity in COVID-19 patients with neurological symptoms, suggesting a direct link between immune dysregulation and altered perception.

Endothelial dysfunction within cerebral vasculature further amplifies inflammatory damage. SARS-CoV-2 can infect endothelial cells lining blood vessels, leading to vascular leakage and microthrombi formation. These abnormalities reduce oxygen and nutrient delivery to neurons, exacerbating neuroinflammation and increasing the likelihood of cognitive disturbances. Autopsy reports have documented perivascular immune cell infiltration in deceased COVID-19 patients, reinforcing the role of inflammation-driven vascular injury in neurological manifestations, including hallucinations.

Types Of Hallucinations

Hallucinations in COVID-19 patients can manifest in various sensory modalities, with visual, auditory, and tactile experiences being the most frequently reported. These disturbances may arise during acute infection, particularly in severe cases or delirium, but can also persist as post-acute sequelae. The nature and intensity of these hallucinations vary based on neuroinflammation, neurotransmitter imbalances, and preexisting psychiatric conditions.

Visual

Visual hallucinations often involve shapes, flashes of light, or fully formed figures that are not present. These experiences have been documented in hospitalized individuals, particularly those in intensive care units (ICUs) who develop delirium. A study in The Lancet Psychiatry (2021) reported that ICU patients with COVID-19 frequently described seeing people, animals, or shadowy figures, often accompanied by fear or confusion. The underlying mechanisms may involve disruptions in the occipital and temporal lobes, which process visual input. Hypoxia, a common complication in severe cases, can further impair these areas, leading to distorted perception. Neuroinflammation affecting the thalamus, a key sensory relay center, may also contribute by altering the brain’s ability to filter and interpret visual stimuli accurately.

Auditory

Auditory hallucinations, though less common than visual ones, have been reported in COVID-19 patients, particularly those with preexisting psychiatric conditions or prolonged hospitalization. These hallucinations typically involve hearing voices, music, or indistinct sounds with no external source. A case series in Schizophrenia Research (2022) described multiple patients who experienced auditory hallucinations during and after infection, with some reporting distressing voices commenting on their actions. The pathophysiology may involve dysregulation of the auditory cortex and limbic system, which process sound and emotional responses. Elevated dopamine activity in the mesolimbic pathway may also play a role, similar to psychotic disorders. Additionally, prolonged isolation, mechanical ventilation, and ICU delirium can contribute, as sensory deprivation and stress are known risk factors for hallucinatory experiences.

Tactile

Tactile hallucinations, or false sensations of touch, have been observed in some COVID-19 patients, often described as crawling, tingling, or pressure on the skin. A report in Frontiers in Neurology (2021) highlighted cases where patients experienced sensations of insects crawling on their skin or sudden temperature changes without an external cause. The mechanisms likely involve peripheral nerve dysfunction and central sensory processing abnormalities. COVID-19 has been associated with neuropathic symptoms, including paresthesia and dysesthesia, which may contribute to these false perceptions. Neuroinflammation affecting the somatosensory cortex, responsible for processing touch, may lead to misinterpretation of normal bodily sensations, resulting in hallucinatory experiences.

Psychiatric Comorbidities

Individuals experiencing hallucinations during or after COVID-19 often exhibit overlapping psychiatric conditions, complicating diagnosis and management. Anxiety and depression are widely documented in post-COVID patients, with some studies estimating that up to 30% develop significant mood disturbances. These conditions can heighten susceptibility to hallucinations by altering cognitive processing and emotional regulation. Patients with preexisting psychiatric disorders, such as schizophrenia or bipolar disorder, may also experience exacerbations of their symptoms.

Sleep disturbances have emerged as another contributing factor, with insomnia and fragmented sleep patterns frequently reported. Sleep deprivation is known to precipitate hallucinations by impairing the brain’s ability to differentiate internal thoughts from external reality. A study in Sleep Medicine (2022) found that individuals with persistent post-COVID insomnia were more likely to report sensory distortions, particularly auditory and tactile hallucinations. Disruptions in sleep architecture, including reduced slow-wave and REM sleep, may interfere with neural pathways responsible for reality monitoring.

Genetic And Environmental Contributors

The likelihood of experiencing hallucinations during or after COVID-19 may be influenced by genetic predisposition and environmental factors. Genetic studies on neuropsychiatric disorders have identified several genes associated with hallucinations, particularly those involved in dopamine and glutamate signaling. Variants in genes such as COMT (catechol-O-methyltransferase), which regulates dopamine metabolism, and GRIN2A, which affects glutamatergic neurotransmission, have been linked to increased susceptibility to psychotic symptoms. Individuals carrying these variations may be more vulnerable to COVID-19-related neurotransmitter disruptions.

Environmental factors further shape risk. Patients with a history of chronic stress, trauma, or substance use disorders may experience heightened neurological sensitivity, making them more prone to perceptual disturbances. Social isolation, common during post-COVID recovery, has been linked to sensory misperceptions, particularly auditory hallucinations. Prolonged hospitalization, especially in ICUs, has also been associated with delirium-related hallucinations, with studies indicating up to 80% of ICU patients experience temporary psychotic symptoms.

Neurocognitive Sequelae

Beyond transient hallucinations, some COVID-19 patients experience lasting neurocognitive impairments affecting memory, attention, and executive function. These deficits, often referred to as “brain fog,” have been reported in both mild and severe cases. Neuropsychological assessments show post-COVID patients perform worse on cognitive tasks, particularly in working memory and processing speed. Functional MRI data indicate reduced connectivity in the prefrontal cortex and hippocampus, contributing to disorganized thinking and difficulties distinguishing reality from hallucinations.

Persistent cognitive dysfunction may be linked to structural changes in the brain, with imaging studies revealing cortical thinning and white matter abnormalities. These changes may increase vulnerability to future neurodegenerative conditions. Some researchers have drawn parallels between post-COVID neurocognitive symptoms and early markers of dementia, raising concerns about long-term neurological consequences.