Visual hallucinations are subjective perceptions of an object in the absence of an external stimulus and are caused by lesions or disturbances of the visual system 1. Visual hallucinations are comorbid with various neurological and psychiatric disorders, including schizophrenia, mood disorders, brain lesions and drug withdrawal syndromes 2. There isn’t one main underlying physiological mechanism to explain visual hallucinations, but there are several hypotheses to clarify the differences between the types of visual experiences. The etiology of visual hallucinations pertains to structural brain damage, neurochemical disturbances, prior experiences (top-down processing), and psychodynamic factors such as sleep1. Current findings show that injury to the parietal white-matter causes Anton’s syndrome, in which patients believe to see despite the lack of sight 3. Complex visual hallucinations have been implicated with the removal or disturbance of the brainstem, where serotonergic inhibitory raphe nucleus inputs are disrupted and thus lead to the over activation of the dorsal lateral geniculate nucleus 4. Functional magnetic resonance imaging and other techniques are proven to be useful in identifying the types and locations of visual hallucinations in the visual cortex 5. Pharmacotherapy, atypical antipsychotics, anticonvulant medications, surgical treatment and patient education have been effective in the treatment of visual hallucinations 5, 6.


Specialized visual cortex (Adapted from Ffytche, D.H. (2005))

Visual hallucinations can be classified into simple and complex subtypes. Simple hallucinations, also referred to as elementary or unformed, consist of dots, colors, flashes, or geometric patterns. Complex (or formed) hallucinations refer to well formed images of objects, animals and people 7. Simple hallucinations are more present in patients with sensory deprivation and eye disease; and complex hallucinations are frequent in Lewy body dementia, Alzheimer's disease and Parkinson's disease.
The type of hallucination one experiences directly relates to the location of activity increase within the visual cortex. Phasic increases in activity in the human colour centre (V4) produces a hallucinatory experience of a formless coloured blob (simple) while activity increases in the object specialized cortex results in the hallucination of a complex object 8.
There is a lack of validity in the objective assessment of classifying hallucinations. This occurs because many patients with visual hallucinations have communication or visual problems. Schizophrenic patients, for example, will attach meaning to simple hallucinations and thus reporting them as complex, such as reporting two lines as vicious snakes 8.

Underlying Mechanisms


Structure and regulation of perception systems. Gray areas indicate primary information flow, dotted arrows show cholinergic projections and black arrows the thalamic regulation. (Adapted from Collerton, D., Mosimann, U.P. (2010))

Structural lesions of the visual pathway, functional disturbances of the brain, sensory deprivation such as blindness and intoxication (drugs, alcohol and illicit drugs) are known to cause visual hallucinations in individuals.
There is no established model to explain the mechanisms underlying visual hallucinations. There are two commonly discussed hypothesizes: perceptual release theory and de-afferentiation theory. The former suggests visual hallucinations are due to a release of decreasing cortical inhibition that occurs when there is a loss of visual input. The latter states that a reduction in visual input increases visual cortical excitability 10. This reduction in visual input occurs when there is a disconnection between the cortical visual networks and subcortical inputs due to either structure lesions or functional disturbances 11, 12.


Examination of patients with Lewy body dementia reveals that the ascending brainstem cholinergic pathway is greatly implicated with visual hallucinatory experiences10. Lesioning of the brainstem causes cholinergic de-afferentiation of visual neurons, causing visual hallucinations to occur 10. The cholinergic pathway has a widespread of projections to areas associated with wakefulness, drowsiness and sleep. This involves intrusion of REM sleep fragments into phases of wakefulness. This occurrence of endogenous brain activity with consciousness makes patients with excessive day time sleepiness, narcolepsy or insomnia more prone to hallucinatory experiences 13. In addition, the cholinergic pathway is critical for cognitive functioning so individuals with reduced semantic fluency and impaired visuospatial abilities (cognitive impairment) are also at a higher risk for visual hallucinations 14.

Charles Bonnet Syndrome

Charles Bonnet Syndrome (CBS) is a disorder in which patients with normal cognition experience consistent or periodic complex visual hallucinations 6. Patients with CBS have no evidence of dementia, drug abuse, neurological or psychiatric abnormalities 5. Due to the lack of awareness regarding the syndrome, there is an underestimation of the prevalence of CBS. Some studies indicate that the prevalence of CBS ranges between 0.4% to 14% of patients, while other studies suggest the range is between 13% and 29% of patients with diminished visual acuity 13. It is difficult to interpret the prevalence due to the difference in diagnostic criteria. Visual Hallucinations in Charles Bonnet Syndrome tend to be clear, detailed and often incorporate people, animals or inanimate objects 1. On the onset of a hallucination, 80% of individuals with CBS are aware that the hallucinations are not real 5. Having realized that these hallucinations are not real, majority of patients have a neutral reaction 5. CBS often presents itself in elderly women between the ages of 74.9 to 83.3 years 5. Risk factors for CBS include any ocular pathology that occurs along the visual pathway, including bilateral visual impairment, cataracts, glaucoma, declining visual acuity, cerebral damage, optic neuritis, and macular holes 1,5.

Deafferentation Theory

Positron emission tomography (PET)-CT scan conducted in a patient with CBS. Hypermetabolism of the right temporal area and the left thalamus is no longer present after being treated with valproic acid for 8 months. (Adapted from Jang, J., Youn, YC., Seok, J., Ha, S., Shin, H., Ahan, S., Park, K., Kwon, OS. (2011))

The deafferentation theory is the most accepted hypothesis for visual hallucinations present in Charles Bonnet Syndrome. It is understood that these hallucinations arise due to a deafferentation of the visual association cortex associated with lesions in the visual pathway 6. Deafferentation refers to the destruction or injury of sensory nerve fibers causing the elimination of sensory nerve impulses 5. Biochemical and molecular changes, such as the increase of neurotransmitters released in the presynaptic neuron or an increase in the amount of receptors in the post synaptic membrane due to prolonged inactivity increases the excitability of the deafferentated neurons 5,6. Plasticity of the visual system also allows the sprouting of new axons in the damaged area and reorganization of receptive fields thus making the brain area more sensitive to elicit visual hallucinations 5. This theory of hyperexcitability after impairment is similar to ‘phantom limb’ and ‘phantom pain’ concepts. There is evidence to show that this hyperexcitability in the thalamocortical circuit is responsible for visual hallucinations. Studies have been conducted in which hallucinations of colours, motion and geometric patterns were induced in individuals. The brain activity underlying hallucination, determined by electroencephalography and functional MRI, was found to be consistent with a shift in the activity in the thalamocortical circuitry from tonic firing to burst firing 15. In 2011, Jang and his colleagues observed hypermetabolic activity in the left thalamus of a patient who had been suffering from complex hallucinations for 5 years 6. After treatment of valproic acid for 8 months, this hypermetabolic region was no longer present in PET-CT scans (Figure). This supports the hypothesis of hyperexcitability to be cause of visual hallucinations after deafferentation.

Perceptual Release Theory

The perceptual release theory states that visual hallucinations are due to nerve impulses that were initially inhibited being disinhibited 5. After some damage to cortical or retinal areas, neurons increase their release of neurotransmitters by increasing the sensitivity of postsynaptic receptors 16. Missing input to the primary visual system causes the disinhibition of other visual association areas. As neurons attempt to adapt to the reduced visual input, they increase their sensitivity to incoming visual stimuli. It is hypothesized that this unmasking of other neuron activity leads to the formation of visual hallucinations by way of top down processing 17. The brain allows previously registered subconscious images to emerge into the consciousness.

Peduncular Hallucinosis

Peduncular Hallucinois is used to describe the complex hallucinations that result following an injury to thalamic, midbrain, hypothalamic and third ventral regions of the brain; they may be temporary and are often accompanied by sleep and wake disturbances 1,7,13. Common hallucinations defined by peduncular hallucinosis include animals, people or children, grotesque and deforming faces or heads, landscapes and patterns 4.They start within a few days of the initial injury and resolve within a few weeks during the evening, lasting from minutes to hours 1.
Lesions in the visual pathway cause loss of corticocortical or thalamocortical inputs, and via the perceptual release phenomenon they result in visual hallucinations. Lesions of mesencephalic regions interrupt serotonergic inhibitory afferents projecting into the dorsal lateral geniculate nucleus (LGN) of the thalamus. This results in a dysregulated LGN which then projects into the visual cortical regions, and produces hallucinations 4. The auditory form of peduncular hallucinosis is also associated with the loss of serotonergic raphe nuclei ascending inhibition.

Anton’s Syndrome

CT scan of the brain reveals infarction of both occipital lobes and of the subcortical white matter of the left parietal lobe (Adapted from Kondziella, D., Frahm-Falkenberg, S. (2011))

Anton’s syndrome is a type of cortical blindness in which patients are unaware of their blindness and behave as if they can see 18. In this form of anosognosia, patients experience a vivid hallucinatory visual world. Patients report seeing non-existent cars, animals and people. Computed tomography scans of patient brains have revealed the infraction of both the occipital lobes and subcortical white matter of the left parietal lobe 3. This parietal white-matter injury causes a disconnection between the area of the parietal cortex that integrates visual with other sensory information and intrahemispheric association pathways of the brain 3. Cerebral thrombosis or embolism usually precede cortical blinding, and leads up to the occlusion of both posterior cerebral arteries 18. The underlying mechanism of this syndrome for the most part remains unclear because it is not clear whether the experiences patients report are hallucinations or mere confabulations.

Treatment methods

The type of treatment entirely depends on the underlying cause of diagnosis of the patient. In terms of medication, second generation antipsychotics are used widely. Clozapine, known for interacting with the mesolimbic system, has shown efficient response rates of over 80% 14. Quetiapine, clozapine and cholinesterase inhibitors, used prevalently in patients with Lewy body dementia and Parkinson’s disease, have shown to be effective in reducing or abolishing visual hallucinations 14. Patients with frontal temporal dementia use selective serotonin reuptake inhibitors (SSRIs) to treat their declining levels of serotonin14. Cataract surgery, laser photocoagulation of the retina, and the use of optical correcting devices can be used to correct predisposing factor4. Patient education and therapy help improve the living conditions of a patient5.


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