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Hallucinations: Etiology and clinical implications

Article  in  Industrial Psychiatry Journal · July 2009

DOI: 10.4103/0972-6748.62273 · Source: PubMed

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SEMINAR

Hallucinations: Etiology and clinical implications

A B S T R A C T
Santosh Kumar, The literature on hallucinations is reviewed, including history; theoretical background
Subhash Soren, from physiological, biochemical and psychological points of view; classification;
causation; presentation in different psychiatric and neurological disorders and in
Suprakash Chaudhury normal persons. The available evidence suggests that hallucinations result from a
Department of Psychiatry, failure of the metacognitive skills involved in discriminating between self-generated
Ranchi Institute of and external sources of information. Management of hallucinations is briefly
Neuropsychiatry and Allied discussed.
Sciences, Kanke, Ranchi,
Jharkhand, India

Address for correspondence:

Dr. Col. Suprakash Chaudhury,
Prof. and Head, Department of
Psychiatry, Ranchi Institute of
Neuropsychiatry and
Allied Sciences, Kanke,
Ranchi - 834 006, Keywords: Etiology, Hallucinations, Psychopathology
Jharkhand, India.
E-mail: suprakashch@gmail.com DOI: 10.4103/0972-6748.62273

H allucinations are intriguing psychological phenomena

that have a number of important clinical, theoretical
and empirical implications; they are also among the most
severe and puzzling forms of psychopathology. Usually
regarded as characteristic of psychoses, they are found
in a wide range of medical and psychiatric conditions.
Moreover, a substantial minority of normal individuals
report hallucinatory experiences. Phenomenologically they
are the commonest and the most important disorder of
perception. Although the exact cause and pathogenesis
of hallucinations are not known, evidence points
toward multiple etiological factors for the hallucinatory
phenomenon.
PSYCHODYANMIC APPROACH
Freud (1953) felt that hallucinations are very similar to
dreams and that both conditions represent a psychotic
state in which there is a complete lack of time sense. In
this process, thoughts are transformed into visual images,
mainly of a visual sort, that is, word presentations are taken
back to corresponding “thing” presentations. According
to Kolb and Brodie (1982), hallucinations represent a
breakthrough of preconscious or unconscious material
into consciousness in response to certain psychological
situations and needs, e.g., wish fulfillment, enhancement of
self-esteem, guilt feelings. The contents of hallucinations
are thought to reflect their psychodynamic significance.
Hallucinations often occurring with delusions during
psychotic states may represent the concrete symbolic
expression of delusional ideas that are seeking other routes
of expression.
PSYCHOPHYSIOLOGIC APPROACH
Neurophysiologic hypothesis
Hughlings Jackson (1932) suggested that hallucinations
occur when the usual inhibitory influences of the uppermost
level are impeded, thus leading to release of middle-level
activity, which takes the form of hallucinations. This
model is known as disinhibition model. Penfield et  al.
(1950) demonstrated that electrical stimulation of certain
cortical or subcortical structures induced different types of
hallucinations. He proposed the theory of abnormal brain
excitation as a mechanism of production of hallucinations.
The neurophysiologic dissociation theory (Marrazzi, 1970)
proposes that hallucinations result from a dissociation
between primary sensory cortex and cortical association
areas which exert a regulatory influence on the former.
The perceptual release theory (West, 1975) postulated the
presence of a censorship mechanism in the brain which
actively excluded from the consciousness the majority of
sensory information that is received continually by the brain.
But the censorship mechanism can operate only when there
is constant flow of sensory inputs. If by any chance there
is stoppage or impairment of sensory input (e.g., in case of

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Kumar, et al.: Hallucinations
excessive affects during “functional psychosis,” prolonged
periods of sensory deprivations), then earlier perception or
memory traces emerge into the conscious, and the individual
experiences hallucinations. This explains the occurrence of
hallucinations following specific sensory modality deprivation.
Neurotransmitter hypothesis
Dopamine
In schizophrenia (SCZ), there is evidence that very high
levels of dopamine in the limbic system play a major
role in emergence of hallucinations and delusions.
Antipsychotic medications, which block central dopamine
activity, alleviate the hallucinations of psychosis. Drugs
with strong dopaminergic effect, such as L-dopa,
methylphenidate, bromocriptine, pramipexole and
piribedil, may induce hallucinations. D-amphetamine, a
direct dopamine agonist, may also induce psychosis and
hallucinations. The fact that hallucinations were also
described in Parkinson’s disease before the introduction
of L-dopa indicates that not only hyperdopaminergic
states but also hypodopaminergic states, presumably due
to progressive loss of dopamine projections to the cortex,
can induce hallucinations.
Acetylcholine
A deranged cholinergic neurotransmission has also been
involved in the pathophysiology of hallucinations. For
example, alteration of consciousness and hallucinations
have been described widely since ancient times for
members of the Solanaceae family of plants (belladonna
and dhatura), which contain scopolamine, atropine and
other antimuscarinic agents. Hallucinations occur in about
30% of patients with Alzheimer’s disease and 60% of
patients with Lewy body dementia, which are characterized
by reduction in acetylcholine and abnormalities in nicotinic
and muscarinic receptor expression.
Serotonin
Serotonin has also been implicated in the causation
of hallucinations, based on the fact that a number of
hallucinogenic drugs, like lysergic acid diethylamide (LSD),
mescaline, psilocybin and ecstasy, appear to act, at least
in part, as serotonin 5 HT2A receptor agonist or partial
agonists. In addition, hallucinations have been reported
as side effects of Selective serotonin reuptake inhibitors
(SSRIs), which increase the availability of serotonin in the
synaptic cleft.
Glutamate
A possible role of glutamate in hallucinations is suggested
by the finding that glutamate antagonists like phencyclidine
and ketamine can induce hallucinations. This has led to
the hypothesis that psychotic symptoms may in part be
attributed to hypofunction of NMDA receptors.
Jul-Dec 2009 | Vol 18 | Issue 2 120
GABA-A
PET and SPECT studies using GABA-A receptor ligands
showed that the intensity of hallucinations was strongly
associated with diminished GABA-A binding, specifically
in the left medial temporal region.
Electroencephalographic studies
Using cognitive tasks involving speech production and
perception, Heinks-Maldonado et  al. (2007) suggested
that in healthy subjects, EEG synchrony preceding
speech reflects the action of a forward model system,
which dampens auditory responsiveness to self-generated
speech. However, the dampening was deficient in SCZ
patients with hallucinations. Hubl et al. (2007) investigated
the responsiveness of the auditory cortex during
hallucinations in SCZ patients using the N100 evoked
potential in response to auditory stimulation. During
hallucinations, the N100 amplitude was smaller, presumably
because of a reduced left temporal responsivity. They
concluded that the findings indicate competition between
auditory stimuli and hallucinations for physiological
resources in the primary auditory cortex. Abnormal
activation of the primary auditory cortex may thus be a
constituent of auditory hallucinations.
Neuro-imaging studies
Structural imaging
In a systematic review of 46 studies (including 1444 patients
with SCZ and 1327 controls) on superior temporal
gyrus  (STG), volumetry MRI studies in SCZ revealed
that left STG or subregions appear to be more involved
in the generation of hallucinations and thought disorder
than right sides. The majority of 5 follow-up studies
found evidence of progressive changes in volumes
(Sun  et  al.,  2009). Volume reductions in the prefrontal
and cerebellar cortices have also been reported and may
be associated with impairment in the monitoring or
awareness and volition of internal speech. MRI brain scans
of 66 patients of type I bipolar disorder and 66 controls
indicated that hallucinations and positive symptoms were
associated with gray matter reduction in the left middle
temporal gyrus (Stanfield et al., 2009).
Functional imaging
Stephane et  al. (2000) found increased rCBF in the left
temporal region in hallucinating patients. McGuire
et al. (1993) reported that hallucinatory state was associated
with greater blood flow in language-related areas, significantly
so in a region corresponding to Broca’s area and anterior
cingulate and left temporal cortices. Nonpsychotic visual
hallucinations in Parkinson’s disease (PD) were associated
with hypoperfusion in the right fusiform gyrus and
hyperperfusion in the right superior and middle temporal
gyri. These temporal regions are important for visual
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Kumar, et al.: Hallucinations
object recognition, and these rCBF changes are associated
with inappropriate visual processing and are responsible
for nonpsychotic visual hallucinations in PD (Oishi et al.,
2005). Using PET during auditory verbal hallucinations
(AVH), patients demonstrated a significant activation of
the supplementary motor area, anterior cingulum, medial
superior frontal area and cerebellum. Activation was also
observed in the left superior frontal area, right superior
temporal pole and right orbitofrontal region (Parellada
et al., 2008). Stephane et al. (2006) suggest that the abnormal
laterality of the supplementary motor area activity accounts
for the failure to attribute speech generated by one’s own
brain to one’s self and that the activation of Wernicke’s
area accounts for the perceptual nature (hearing) of
the patient’s experience. Lahti et  al. (2006) using PET
reported a positive correlation between hallucinations and
activation of anterior cortex and a negative correlation
with hippocampus-parahippocampus. Functional MRI
revealed that AVHs were associated with activation in the
right STG and posterior insula, the right middle temporal
gyrus, and hippocampus/parahippocampal gyrus. Somatic
hallucinations were associated with activation in the
thalamus, insula and posterior cingulate gyrus bilaterally.
Further activation was evident in the left middle frontal
gyrus, the precentral gyrus, twin foci in the postcentral
gyrus, inferior parietal lobule, the middle and superior
temporal gyri with right-sided inferior frontal gyrus,
and precuneus (Hoffman et  al., 2008; Ford et  al., 2009).
Functional imaging studies have consistently shown the
involvement of associative sensory areas. Moreover, the
hallucinating brain may be characterized by stronger inputs
from subcortical centers (especially the thalamus); reduced
control by the dorsolateral prefrontal cortex; and aberrant
activation of dorsal anterior cingulate, which is involved
in source monitoring.
Anatomical correlates
Hallucinations cause sensory modality-specific activation in
cerebral areas involved in normal sensation. A disturbance
in perception of speech seems to have a central role in
occurrence of auditory hallucinations. Anatomically,
auditory hallucinations appear to involve primary and
association cortices; Broca’s and Wernicke’s areas;
subcortical, paralimbic, limbic regions; ventral striatum; and
thalamus. Furthermore, they are suggested to be associated
with the dysmodulation of the information flow from
ventral striatum to thalamus and cortex caused by increased
dopaminergic activity in mesolimbic pathway. Hugdahl
et  al. (2008) proposed that auditory hallucinations are
internally generated speech perceptions that are localized
in the left temporal lobe, in the left peri-Sylvian region. If
hallucinations are misidentified perceptions originating in
the speech perception area of the left temporal lobe, then
hallucinating patients should have problems identifying
Industrial Psychiatry Journal 
a simultaneously presented external speech sound,
especially when the sound is presented lateralized to the
left hemisphere. Using a dichotic listening paradigm with
pair-wise presentations of consonant-vowel syllables, they
showed that patients with schizophrenia who experience
frequent and/or intense auditory hallucinations fail to
show an expected right ear advantage (REA), which may
be indicative of a functional deficit in this brain region.
Patients who experience frequent hallucinations are
impaired in their ability to use top-down cognitive strategies
to overcome a ‘bottom-up stimulus’-driven right ear effect
when instructed to focus attention on the left or right
ear stimulus. The behavioral data are supported by MR
brain imaging data looking for pathology of gray matter
density in patients with schizophrenia, particularly in the
left hemisphere. The reviewed studies revealed significant
reductions in gray matter density in the left peri-Sylvian
region, including thinning of the cortical mantle, also
supported by altered neuronal activation as seen in the
fMRI results.
Cognitive perceptual theories
Hallucinations can be seen as erroneous perception  or
“sensory deception.” Hence researchers have been
investigating the integrity of perceptual functions
in persons with hallucinations. Basically, 2 approaches can
be distinguished. The first is concerned with bottom-up,
or data-driven, perceptual processing, such as deficits in
the processing of incoming visual stimuli in primary visual
cortex; hearing impairment and auditory hallucinations
associated with sensory impairment in older people; or
the emergence of hallucinations in sensory deprivation.
The second approach is concerned with top-down, or
conceptual, processing in perception. This refers to
processes that contribute to perception that do not originate
in the external world but in the brain of the perceiver.
Examples of such top-down factors are prior knowledge,
perceptual expectations, attentional modulation and mental
imagery. Bentall (1990) proposed that discrimination
between internal and external sources of information is a
metacognitive skill called source monitoring. Hallucinations
result from failure of this skill. Hoffman et  al. (1994)
using psycholinguistic approach postulated that auditory
hallucinations stem from disruption in language production
caused by parasitic memory. David (1994) linked verbal
hallucinations to inner speech. He argued that inner speech
is produced and controlled by an inner-voice-inner-ear
system, and the disruption of the system may lead to
verbal hallucinations. Hamsley postulated that normal
perception is dependant on an interaction between current
sensory input and regularities that have been detected in
previous sensory input. Memory of previous regularities
and the current context result in ‘expectancies’ or ‘response
biases’ towards the current sensory input. The central
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Kumar, et al.: Hallucinations
defect in hallucinations is the reduction of the influence
of regularities of past experiences on current perception.
This weakened influence would result in ambiguous and
unstructured sensory input. Thus the unstructured sensory
input would fail to inhibit the emergence of material from
long-term memory into awareness; its emergence would be
experienced as hallucinations (David, 1994).
Perception and attention deficit model
Collerton et al. (2005) proposed a PAD model of complex
visual hallucination, in which the hallucinatory images
generally occur in the focus of the visual field and are
seen against the background of the existing visual scene.
According to the PAD model, both sensory impairment
and attentional abnormalities are needed for hallucinations
to arise. More specifically, a combination of impaired
attentional binding and poor sensory activation of a correct
proto-object, in conjunction with a relatively intact scene
representation, biases perception to allow the intrusion
of a hallucinatory proto-object into a scene perception.
Proto-objects refer to holistic or part-based abstracted
object representations that are segmented from visual
information and act as candidates for further processing
but are at such an early processing stage that they have
not yet entered conscious awareness. Such proto-objects
are in multiple competitions for further processing. The
interplay of top-down and bottom-up biasing information
will eventually determine which proto-object will “win” and
enter conscious awareness. Cholinergic dysfunction may
result in a failure to properly integrate sensory information
(bottom-up) and prior expectation (top-down). The PAD
model proposes that impaired attentional binding is due
to abnormal lateral frontal activity; poor sensory activation
of a correct proto-object is due to abnormal ventral
visual stream activity; and intrusion of a hallucinatory
proto-object is mediated by increased temporal versus
frontal activity. Diederich et al. (2005) suggested that visual
hallucinations should be considered a dysregulation of the
gating and filtering of external perception and internal
image production. Contributive factors for their model
include poor primary vision, reduced activation of primary
visual cortex, aberrant activation of associative visual
and frontal cortex, lack of suppression or spontaneous
emergence of internally generated imagery through the
ponto-geniculo-occipital system, intrusion of rapid eye
movement dreaming imagery into wakefulness, erratic
changes of the brainstem filtering capacities through
fluctuating vigilance and medication-related overactivation
of mesolimbic system. Not all of these have to be present,
and different combinations will lead to differences in
phenomenology. Llinas and Pare (1991) suggested that
conscious perception is subserved by intrinsic activity in
thalamocortical circuits that is constrained or modulated
by sensory input. They considered the primary difference
Jul-Dec 2009 | Vol 18 | Issue 2 122
between conscious perception and dream imagery to be
found in the weight given to sensory input, which is a
large weight in conscious perception, and hence sensory
factors largely determine the final percept, whereas this
weight is negligible in dream imagery. Integrating the
sensory impairment approach with the top-down approach,
Behrendt and Young (2004) viewed hallucinations as
“underconstrained perceptions” that arise when the impact
of sensory input on thalamocortical circuits is reduced. If
sensory constraints (i.e., bottom-up processing of incoming
information) are weak, e.g., due to sensory impairment,
attentional mechanisms (i.e. top‑down  influences) may
become the dominant modulatory influence on thala
mocortical oscillatory activity that gives rise to conscious
percepts — in this case, hallucinations.
Neural network model
To test different hypotheses regarding neurocognitive
basis of hallucination, Hoffman and McGlasher (2006)
developed a neural network simulation. Their model
specifically concerns auditory hallucinations as typically
reported in people with schizophrenia and is based on
2 popular hypotheses regarding neurobiological basis
of schizophrenia: (a) overzealous pruning of synapses
that are an extension of normal developmental pruning
during adolescence and (b) alterations in the dopaminergic
neuromodulatory system in schizophrenia. To assess
and compare these 2 hypotheses, a computer simulation
of some aspects of speech perception was developed.
This system was found to produce spontaneous percepts
simulating hallucinated speech when the working memory
component was excessively pruned or when neuronal
responses were modulated to simulate a hyperdopaminergic
system. Comparing the performance of the network
with that of actual hallucinating patients and normal
controls while tracking (repeating while simultaneously
listening to) speech that was phonetically degraded,
revealed that the neural network simulation producing
the best match to speech-tracking performance of human
hallucinators was an overpruned system with compensatory
hypodopaminergic adjustments.
Metacognitive process: Reality monitoring and
metacognitive beliefs
Metacognition refers to “thinking about thinking” or to
beliefs and attitudes held about cognition. Most recent
models of hallucinations assume that hallucinations are
related to misattribution of private events. These private
events may include a number of types and modalities,
such as inner images, inner speech, voices, intrusive
thoughts, vivid daydreams and bodily sensations. Different
approaches have attempted to explain this misattribution,
with the most prominent of these relating hallucinations
to a misattribution of inner speech, problems in source
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Kumar, et al.: Hallucinations
monitoring, and relations between hallucinations and
beliefs. Recent cognitive models of hallucination have
attributed these misattributions to cognitive bias or
cognitive deficit. Cognitive biases are present when some
forms of information are processed preferentially in
comparison to others. Examples of cognitive bias include
the preferential recall of negative information in patients
with depression. Cognitive deficits occur when there are
disruptions of specific cognitive functions, including, for
example, problems with working memory, inhibition or
attention. It is probable that disturbances in cognitive
processes as a result of cognitive deficits (i.e., bottom-up
factors) and cognitive bias factors (top-down factors) are
both responsible for hallucinations.
Reality monitoring and hallucinations — Bentall’s
(1990) hallucination model
Some studies provide evidence for Bentall’s notion that
hallucinators are impaired in their ability to discriminate
between real and imagined events and reveal a specific bias
towards attributing their thoughts to an external source.
This externalizing bias seems related, at least in part, to the
effects of both an inadequate use of cognitive effort cues
and the emotional salience of stimuli (Laroi et al., 2004)
on source-monitoring tasks.
Hallucinations and beliefs — Morrison’ hallucination
model
Morrison is in agreement with the theory that hallucinations
are internal cognitive events that are misattributed to an
external source. His explanation for this misattribution
is based on the fact that hallucinations are in some way
linked to normal intrusive thoughts and that because of
motivational factors these intrusive thoughts become
externalized by the individual (Morrison et  al., 1995).
An  important aspect of this theory concerns research
showing similarities between intrusive thoughts and
hallucinations, because the genesis of hallucinations is seen
as a reaction to intrusive experiences. Like hallucinations,
intrusions are also often experienced as ego dystonic
and uncontrollable; share similarities in terms of form,
content and triggers (e.g., stressful events); and are usually
accompanied by subjective discomfort. The theory also
states that the need to attribute intrusive thoughts to an
external source is due to motivational factors. The presence
of certain intrusive thoughts may lead to negative affect in
the subject in the form of anxiety or cognitive dissonance.
According to cognitive dissonance theory, dissonance
occurs when 2 cognitions (e.g., thoughts, beliefs and feelings
the person is aware of) contradict each other, resulting in an
uncomfortable state from which an individual is motivated
to escape. Morrison et al. (1995) argued that to reduce the
levels of negative affect, the subject chooses to externalize
the intrusive thought, resulting in hallucinations. Morrison
Industrial Psychiatry Journal 
also posited the important role that metacognitive beliefs
may play in this misattribution process. Metacognitive
beliefs are beliefs concerning one’s own mental process.
This may include beliefs that mental events should be
controllable, that thoughts are dangerous or harmful or that
intrusive thoughts are acceptable and beneficial. When the
occurrence of intrusive thoughts does not comply with the
subject’s metacognitive beliefs, an aversive state of arousal
results (cognitive dissonance), which the subject tries to
escape by externalizing the intrusive thoughts (resulting in
hallucinations), thus maintaining consistency in his belief
system. A number of studies have found evidence for an
association between metacognitive beliefs and the presence
of hallucinations.
A comprehensive cognitive model of hallucinations
Alemon and Laroi (2008) presumed that an integrated
network of cognitive processes may contribute to
perceptual experience, and proposed that 4 different routes
may result in a hallucination: (a) release phenomena due to
lesions in sensory pathways/the arousal system (brainstem,
thalamus); (b) irritative processes acting on cortical centers
that integrate perceptual information; (c) unconstrained
activation of the attentional spotlight; and (d) a cognitive
route with key roles for affective state, top-down factors
and source-/self-monitoring.
Release phenomena: Disturbed visual input may cause
hallucinations by means of an abnormal release of
central processing, though the level at which the release
occurs is unclear. The implication of primary and sensory
cortices seems straightforward, but changes have also been
observed in subcortical brain areas (e.g., lateral geniculate
nucleus) in patients with optic nerve lesions. The capacity
for generating complex visual hallucinations may be located
in the association cortex, which is released by restricted
lesions, a loss of cortico-cortical inputs, and alteration of
activity via the reticular activating system. In this model,
release hallucinations would arise from damage to the
component sensory input or its connecting pathway to
sensory experience.
Irritative processes: Hallucinations caused by spontaneous
activation of sensory cortical areas have been primarily
described in epilepsy. The fact that focal cortical resection
can result in complete remission of epileptic hallucinations
indicates that these hallucinations cannot be attributed to
a release phenomenon. According to this model, irritative
processes would be confined to aberrant activation of the
module sensory experience.
Attentional spotligh: The thalamic reticular nucleus (TRN)
acts as a searchlight to guide attention to certain features
of the environment and thereby intensifies processing of
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Kumar, et al.: Hallucinations
these features. The thalamus is acknowledged as one of
the three important nodes in a network underlying selective
attention that comprises the prefrontal cortex, parietal
cortex and the thalamus. The TRN facilitates sensory
processing by facilitating detection and discrimination
through the initiation of burst-firing (when a population
of neurons fires with a high-frequency burst in contrast to
a continuous low-frequency baseline firing) in the lateral
geniculate nucleus (LGN). Although the encoding of an
externally presented stimulus becomes distorted during
burst-firing, the background noise decreases significantly,
thereby enhancing signal detectability. This model
proposes that activation of the TRN in the absence of
sensory input could explain the involuntary character of
hallucinations. Such activation is possible via connections
from the prefrontal cortex to the TRN, via feedback from
sensory association cortex and via neurotransmitters such
as dopamine and acetylcholine.
Cognitive route: The model assumes that hallucinations may
arise from a cognitive route, in which emotion, top-down
perceptual mechanisms and metacognitive functions (e.g.,
source- or self-monitoring) play a decisive role. The idea
here is that an affective state (stress and anxiety) negatively
influences monitoring systems, resulting in external
misattribution of internally generated events, but can also
influence top-down factors such as perceptual expectations.
There is evidence that emotional factors can modulate
verbal self-monitoring and source-monitoring. Neuro-
imaging studies show that amygdala activation in response
to emotional stimuli can boost activation of perceptual
areas, which indicates that the affective state can influence
perception and imagery.
MONITORING
Prefrontal cortex, Dorsal anterior cortex,
Parietal cortex
Images
TOP-DOWN
FACTORS
EMOTION & DLPFC,
MOTIVATION Secondary
sensory cortex,
Amygdala,
STS, PPC or
Ventral striatum,
FFG
Ventral anterior
cortex
Figure 1: The role of emotion and motivation in cognitive processes. DLPFC - Dorsolateral prefrontal cortex; STS - Superior temporal sulcus;
PPS - Posterior parietal sulcus; FFG - Fusiform gyrus
Jul-Dec 2009 | Vol 18 | Issue 2 124
The top-down factors’ subsystem in the model refers to
the influence of prior knowledge, perceptual expectations
and attention on perception. Excessive activation of such
top-down factors can “push” images to the right within
the sensory experience box [Figure 1]. As a result, images
will acquire stronger sensory and reality characteristics due
to excessive top-down modulation and will therefore be
more easily confused with bottom-up percepts. Activation
of the thalamus in top-down attention has also been
reported. Connections from the lateral prefrontal cortex
to the thalamus may also mediate top-down influences
in normal circumstances, in which bottom-up influences
constrain the LGN activation by inputs to the reticular
nucleus. Hyperactivation in the lateral prefrontal cortex or
from emotion regulation areas in the orbitofrontal cortex
to the reticular nucleus could lead to diminished control
of the LGN and hence result in spontaneous burst activity,
affecting projections to the sensory association cortex. These
frontal regions target sensory tiers of the TRN to select
relevant and motivationally significant signals. Alternatively,
increased input into perceptual areas (e.g.,  Wernicke’s
area) from frontal areas (e.g., Broca’s area) may affect the
reticular nucleus via corticothalamic projections originating
in the sensory association cortex. This mechanism of
top-down influences largely overlaps with the attentional
spotlight. In fact, it concerns a final common pathway
(involving the TRN and the sensory association cortex)
with different causative agents: Top‑down factors such as
expectations generated in prefrontal regions versus direct
influences (e.g., through acetylcholine) in the third route
(i.e., activation of the attentional spotlight) described above.
It is also possible that top-down influences act without any
intervention from the thalamus.
Percepts
SENSORY EXPERIENCE
Primary and secondary
sensory cortex
SENSORY INPUT
Sensory organs and
afferents
SPOTLIGHT
Reticular thalamic
nucleus
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Kumar, et al.: Hallucinations
The monitoring subsystem in the model [Figure 1] refers to
the metacognitive processes in which the cognitive system
makes a decision regarding the source of perceptual events,
that is, whether they are internally generated or externally
presented. These 2 types of perceptual representations
(images vs. bottom-up percepts) are shown in the sensory
experience box [Figure 1]. The vertical line between
images and percepts denotes the criterion for classifying
a perceptual event as internally generated imagery versus
externally presented sensory information. The gradient by
which some experience is likely to be classified as an image
or as a bottom-up percept is strongly affected by 2 factors:
Vividness and sense of reality. Vividness refers to sensory,
semantic and contextual details: A bottom-up percept is
generally clear and rich in such details, whereas images are
much fainter. The same holds for a sense of reality, which is
of course influenced by vividness but is also influenced by
expectations and metacognitive factors. Faulty monitoring
of one’s mental processes could shift the criterion line to
the left, thereby resulting in a misclassification of certain
imagery experiences as being percepts originating from
the outside. It is doubtful whether monitoring errors alone
can cause hallucinations, as it is unclear how thought, inner
speech or retrieved memories can be transformed into
experiences with perceptual qualities just by virtue of their
misattribution to an external origin. However, when they
interact with overactive top-down systems, such biases
could contribute to erroneous perceptual decision making.
With regard to the neural basis of monitoring, the anterior
cingulate cortex has a pivotal role. The premotor cortex
and superior temporal gyrus (in the case of verbal material)
are also involved in self-monitoring.
CONCLUSION
Hallucination is a fundamental symptom in psychiatry. Two
hundred years of research into this phenomenon has not
yet answered the following questions: (1) Are hallucinations
pathognomic of psychosis? (2) Can the presence of
hallucinations as such or in different modalities and forms
include or exclude certain diagnoses? (3) What is the neural
substrate of hallucination? These questions are very basic to
the understanding of mental diseases, and more research in
both phenomenological and theoretical areas is necessary to
fathom the secret. Conventionally, hallucinations are treated
as psychotic features. However, there is ample evidence
to support the fact that hallucination could be present in
nonpsychotic conditions. Mechanism and nosological status
of these conditions are yet not clear. Assessing cultural
background in the evaluation of hallucination is important
as the concept of reality varies across cultures and there
is a possibility of culturally sanctioned hallucination.
A  part from effective pharmacological treatment, more
Industrial Psychiatry Journal 
awareness is needed regarding psychological treatment
of hallucination, which can help us deal with refractory
hallucinations.
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Source of Support: Nil, Conflict of Interest: None declared.
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