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Neurocognitive Models of Positive
Symptoms
Positive symptoms, such as delusions, hallucinations, and ego disorders, appear
to be much more heterogeneous in terms of their neurocognitive genesis than the
individual symptoms assigned to the negative syndrome and are therefore treated
separately below.
Positive symptoms, such as delusions, hallucinations, and ego disorders,
appear to be significantly more heterogeneous in terms of their neurocognitive
genesis than the individual symptoms assigned to the negative syndrome, and
will therefore be treated separately below. However, it proves difficult to pinpoint
the exact neurobiological correlates of positive subsymptoms and imaging stud-
ies frequently only report correlations with positive symptoms in general. This
reduces the number of studies whose results allow a more precise differentiation
between the neuronal correlates of delusions, hallucinations, and ego disorders.
5.1 Delusions
By definition, delusions are objectively “inaccurate” beliefs that are not normally
shared by other people and which are stubbornly held by those affected despite
evidence to the contrary. For example, it should be relatively easy to objectively
disprove Ms. L.’s delusion that she is involved with a famous actor in the case
study presented above. A number of findings suggest that the central neurocog-
nitive deficit that may contribute to delusion formation is impaired processing
of contextual information (Barch & Ceaser, 2012). This means that patients with
schizophrenia are less able than healthy individuals to use information from their
environment to validly interpret current experiences concerning themselves. Fur-
thermore, they are less able to test the plausibility of inferences drawn in light of
5
© Springer Fachmedien Wiesbaden GmbH, part of Springer Nature 2022
P. Thoma, Neuropsychology of Schizophrenia, Springer essentials,
https://doi.org/10.1007/978-3-658-36400-7_5
16
5 Neurocognitive Models of Positive Symptoms
experience stored in their memories (e.g., “Given my past experiences with my
neighbor, is it really likely that he would want to do me harm?”). Further on, we
will address the question of which neuropathological changes may be responsi-
ble for this. At the cognitive level, various aspects of altered information process-
ing contribute to these difficulties. These factors will be presented in more detail
below.
5.1.1 Cognitive Foundations
5.1.1.1 Unfavorable Decision Heuristics
Patients who are more prone to develop delusional symptoms tend to make rash
decisions based on an inadequate or ambiguous information base. This cognitive
bias is referred to as jumping to conclusions. Alternative information or expla-
nations are not sought or considered. Jumping to conclusions has been shown to
promote the formation and systematization of delusions that are held despite evi-
dence to the contrary. Experimentally, this well-studied, dysfunctional, cognitive
processing tendency is often examined using a probabilistic decision task called
the “marble” paradigm. Subjects are typically shown two jars containing marbles
of different shades (e.g., red and blue). The two vessels differ with respect to the
proportions of marbles in the two colors. For example, while the first jar contains
85% red and 15% blue marbles, the second jar contains exactly the opposite. One
after the other, marbles are drawn from only one of the two jars, hidden from
the view of the test persons. The participants’ task is to make a decision at some
point about which of the two vessels the marbles were probably drawn from. Typ-
ically, patients with schizophrenia and delusional symptoms settle on one of the
two vessels much earlier, that is, after a smaller number of marbles have been
drawn. Jumping to conclusions is said to occur when, in this paradigm, a decision
is made after only one or two moves. To a milder extent, this tendency persists
in patients with schizophrenia even during periods of remission. It is not entirely
clear exactly which cognitive mechanism leads to jumping to conclusions. In any
case, impairments in working memory and increased anxiety appear to exacer-
bate this cognitive processing tendency (Freeman & Garety, 2014). Further-
more, deficits in cognitive processing speed and cognitive flexibility have been
related to jumping to conclusions (Ochoa et al., 2014). This again highlights why
the treatment of cognitive performance deficits may also have a crucial impact
on the characteristic psychopathology of a mental illness. Additionally, patients
suffering from schizophrenia seem to have a more liberal acceptance threshold
for interpretations that are quickly rejected as absurd by healthy individuals. This
17
may also be related to a relatively low tolerance for ambiguous situations. That
is, people would rather accept an absurd interpretation than be unable to clarify a
situation unambiguously. However, the empirical evidence on this is inconsistent.
5.1.1.2 Overconfidence in One's Memories
Another cognitive distortion that contributes to the formation of delusions relates
to the recall of faulty memories in combination with an exaggerated tendency to
believe that these memories are real. It is not the memory impairment per se or,
for that matter, the tendency to produce false memories that is critical. Rather, it
is the diminished metacognitive awareness of one’s fallibility of memories that
predisposes both schizophrenic and healthy individuals to form false belief sys-
tems. The excessive certainty with which one's memories are believed to be real
may be related to the jumping to conclusions just described (overview in Moritz
& Woodward, 2006).
5.1.1.3 Affective Distortions, Low Self-Esteem,
and Unfavorable Attributional Styles
Those theories that place emotions at the forefront of their explanatory models
relate mainly to persecutory delusions. The central idea of approaches that see
persecutory ideation as a defense mechanism is that individuals who are prone
to delusion have low self-esteem. However, to protect themselves from the asso-
ciated negative emotions, they repress this and instead attribute negative events
to the hostility of others. In this respect, self-esteem-serving attribution pat-
terns may also play a role in the aetiology of delusions. However, this does not
always work, so that fluctuations in the self-esteem of affected individuals are
possible (Bentall et al., 2008), which would explain why corresponding studies
cannot consistently demonstrate better self-esteem in highly delusional patients.
Overall, the findings suggest that there is indeed a link between negative self-es-
teem and the formation of persecutory ideation but the extent to which repres-
sion and defense mechanisms play a role in this is unclear and also difficult to
prove empirically. Other approaches, however, see delusional thoughts as a direct
expression of a depressed mood and increased anxiety, without repression mecha-
nisms necessarily playing a role.
5.1.1.4 Changes in the Theory of Mind
Chris Frith, one of the leading schizophrenia researchers, was the first to suggest
in 1992 that an impaired ability to mentally empathize with others may contrib-
ute to the development of delusions. In particular, he said, this deficit predisposes
to persecutory delusions. However, reviews such as that by Freeman and Garety
5.1 Delusions
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5 Neurocognitive Models of Positive Symptoms
(2014) conclude that the majority of existing studies do not support an associa-
tion between positive symptoms and impaired theory of mind. Rather, they argue
that a link between negative symptoms and impairments in the ability to men-
talize is well established, putatively mediated by general impairments in neuro-
cognitive performance. It is also possible that positive symptoms, in particular,
are more likely to be due to “hypermentalizing,” which entails patients attribut-
ing mental states to others even when this may not be appropriate. For example,
some studies suggest that patients with schizophrenia show increased activation
in brain regions responsible for emotion processing even in response to neutral
faces (Lopez-Ibor et al., 2008; Mier et al., 2010). They also appear to impute
mental states and intentions to animated geometric figures significantly faster
than healthy subjects (Blakemore et al., 2003).
5.1.2 Neurobiological Foundations
The most important theories to explain the neurobiological basis of delusional
experiences assume the presence of a developmentally early occurring impaired
communication between frontal and limbic parts of the brain (Murray & Lewis,
1987; Weinberger, 1987). For example, a number of findings suggest altered
volumes and reduced functional connectivity of frontolimbic regions in patients
with schizophrenia (see review in Pankow et al., 2012). This is particularly overt
after puberty when the frontal brain should normally reach further developmental
milestones in healthy individuals. This means that in patients with schizophrenia,
those parts of the brain responsible for executive action control and plausibility
and reality checks (frontal brain) communicate inadequately with those mediating
memory functions (temporal lobe) (Thoresen et al., 2014). As a result, patients
with schizophrenia are less able to verify to what extent conclusions about cur-
rent experiences with their environment are at all plausible in light of past expe-
riences. In this context, one speaks of an impaired reality check or impaired
self-monitoring.
Biochemically, patients with delusional symptoms primarily show an over-
activity of the neurotransmitter dopamine in the mesolimbic dopamine system.
Dopamine is a neurotransmitter that is responsible, among other things, for signa-
ling which stimuli in our environment are particularly “salient”, i.e. which should
immediately attract attention. Against the background of a long-lasting, tonic
basic activity of the dopamine system, phasic increases in activity occur, which
mark which environmental events have a priority meaning and/or do not corre-
spond to the expectations of the individual. In the latter case, this is referred to
19
as a prediction error. The increased phasic activity to such unanticipated salient
events decreases again when it becomes clear that the unanticipated is becom-
ing normal (e.g., when the initial praise by the newly in love partner for each
new outfit eventually becomes permanently absent…). But this also means that
chronic over-activation of this system, especially in the areas of the brain respon-
sible for processing emotions and memory formation, can contribute to us clas-
sifying stimuli as significant to us, even though they are not. In this case, it is
no longer possible to distinguish between relevant and irrelevant stimuli. This
assumption has become known as the “salience-attribution hypothesis”. This is
in accordance with the tendency of patients with schizophrenia to regard all infor-
mation in their environment as personally important to them (e.g. Ms. L.: “My
lover sends me messages over the radio”).
In an EEG study by Debruille et al. (2007), it was demonstrated that patients
with more pronounced delusional symptoms generally have difficulty verify-
ing the extent to which information is coherent in a given context. The N400
component is a negative event-related potential in the electroencephalogram, the
amplitude of which increases the more information deviates from an expected
context of meaning. The component is usually elicited by presenting subjects
with sentences at the end of which unexpected information is presented. Thus,
the last word of the sentence “The pizza was too hot to cry” would elicit a higher
N400 amplitude than the last word of the sentence “The pizza was too hot to eat.”
In highly delusional patients with schizophrenia compared to patients with low-
level delusional symptomatology, this modulation of the N400 component by
non-expectancy-conforming sentence parts is significantly lower. This is also true
for sentences whose meaning is not at all related to the delusion topic and thus
argues for a general processing bias. This could be interpreted as further evidence
that a reduced ability to check environmental information for contextual fit may
contribute to the formation of delusional content.
Interim Summary
At the cognitive level, the development of delusions is mainly favored by
jumping to conclusions and a fundamental impairment in the processing of
contextual information. Neurobiologically, this is due to dopaminergic hyper-
activity in the mesolimbic dopamine system and impaired frontotemporal
communication. Thus, relevant stimuli can no longer be reliably distinguished
from irrelevant stimuli and current experiences cannot be checked for plausi-
bility in light of past experiences.
◄
5.1 Delusions
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5 Neurocognitive Models of Positive Symptoms
5.2 Hallucinations
Hallucinations describe sensory perceptions that are subjectively experienced as
real, although they are not based on any external stimulus. Auditory-verbal hallu-
cinations (AVH) are the most common, which is one of the reasons why they are
the best studied. Studying hallucinating patients using functional imaging poses
particular challenges to researchers, as patients must hallucinate reliably and
preferably repeatedly in the scanner. As a result, relatively few studies exist that
examine this phenomenon using functional magnetic resonance imaging. AVH
occurring in the context of schizophrenia characteristically often encompasses
dialogic, commentary, or imperative voices. In Ms. L.’s case, the voices talk about
her and instruct her to kill herself.
Bentall (1990, 2006) has identified several factors that may predispose to the
development of hallucinations. These include genetic vulnerability, psychological
stress, and certain environmental factors (e.g. sensory deprivation). In addition,
specific cognitive processing mechanisms play a role. On a conceptual-theoretical
level, a neuroscientific explanatory model dominates, which conceives of AVH as
a misattributed inner language. This approach emphasizes the role of top-down
processes, such as self/source monitoring, which help us to distinguish whether
our current internal processing refers to experiences generated by ourselves (such
as inner speech, linguistically encoded memories, or verbally encoded imagina-
tive content) or to events coming from outside (such as spoken language). The
second approach, which is less well supported empirically, refers to increased
neural spontaneous activations associated with AVH. In the following, the two
approaches will be presented in more detail.
5.2.1 Theories of Deficient Self-Monitoring
and Disturbing Action Prediction
A variant of theories of impaired self-monitoring postulates that verbally hal-
lucinating patients falsely experience inner speech as coming from the outside.
Inner speech is an everyday phenomenon that occurs when our thoughts become
internally verbalized and conscious. A variety of findings suggest that this inner
speech is also accompanied by subvocal articulations, i.e., use of the motor
speech apparatus without true vocalizations. For example, it has been shown that
similar motor activity occurs in subvocal speech and AVH. Moreover, the major-
21
ity of AVH appears to be interrupted when subjects open their mouths wide, thus,
disrupting subvocal articulations.
Based on the assumption that inner speech is a motor act, feed-forward models
of motor control have been invoked to explain the occurrence of verbal halluci-
nations (e.g., Frith et al., 2000). There is evidence that patients with schizophre-
nia show impairments in the mechanism that predicts intentional movements and
recognizes them as self-planned after execution. In essence, we use the match
between actions we plan and the sensory consequences of actions we actually
perform to attribute events in our environment to ourselves or, in the absence of a
corresponding pre-generated movement plan, to recognize that they are externally
directed movements. The model assumes that the intention to perform a particular
motor action is first generated in the frontal brain. In the premotor areas of the
frontal brain, this movement plan is translated into specific motor action instruc-
tions (e.g., the control of certain muscle groups). This movement plan is sent to
the parietal lobe as a so-called efference copy. When the planned movements are
executed, this generates a specific pattern of sensorimotor feedback (e.g. certain
sensations in the muscles and joints). The feedback generated by the execution
of the movement is compared with the efference copy stored in the parietal lobe
(reafference). This mechanism is useful to enable a quick correction of the exe-
cuted actions. At the same time, the perception of sensory sensations associated
with self-directed actions is down-regulated. In this way, one can also explain
why it is hardly possible to tickle oneself. Following this logic, the disturbing
prediction of planned actions seems to play a role not only in the development of
hallucinations but also in the genesis of ego disorders (Sect. 5.3), especially in
the relatively characteristic feeling of being remotely controlled from outside in
schizophrenia.
5.2.2 Increased Spontaneous Activations
Studies show that during hallucinations those primary sensory areas are active
that are also responsible during the processing of the corresponding sensory
modality. One theoretical explanation assumes that intrusive cognitions form
the basis of hallucinations. At the neural level, increased spontaneous activation
in brain areas responsible for auditory representations of voices and/or for their
memory representations could contribute to the occurrence of AVH. This basi-
cally means that spontaneous discharges in these brain areas favor the occurrence
of AVH (Cho & Wu, 2013). Indeed, it has been demonstrated that patients with
schizophrenia activate voice-sensitive regions along the superior temporal sul-
5.2 Hallucinations
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5 Neurocognitive Models of Positive Symptoms
cus and superior temporal gyrus in the auditory cortex while experiencing AVH.
Increased activation of these brain regions compared to healthy controls was
recorded even during episodes of silence. At the same time, these patients showed
decreased signals in such regions that predicted the activity of these brain areas
(Horga et al., 2014), which fits with the previously presented theories of impaired
action prediction. Evidence for the theory that AVH is based on increased neu-
ronal spontaneous activation is derived, for example, from the finding that hal-
lucinating patients show an increased tendency to identify voices in white noise
compared to healthy controls.
5.2.3 An Integrative Cognitive Model of AVH
Waters and colleagues (2012) have proposed a cognitive model of AVH in
patients with schizophrenia based on related theoretical approaches and the most
recent findings on this topic. This includes, on a first level, bottom-up processes
resulting in aberrant activations of functional networks around the auditory cor-
tex. These can be triggered by both environmental and internal (e.g., psycholog-
ical stress) factors. When they cross the perceptual threshold, they are likely to
be perceived as unexpectedly intense (hypersalient) sensory stimulation, which
may partly explain why these signals are misattributed as coming from the out-
side. Certain auditory signals (e.g., verbal memories, inner speech) may have a
higher probability of being perceived as AVH in this context, which may explain
the verbal nature of most AVH. In addition, top-down processes determine the
form, content, and meaning of AVH. Different modes of attention, executive
control processes, past experiences and memory representations, and emotional
states determine the form and content. In this context, patients might first have an
increased tendency to perceive auditory stimuli in the environment and to believe
them to be real due to impaired processes of signal detection. Second, impaired
cognitive inhibition could contribute to the failure to adequately suppress such
aberrant signals. After some time, appropriate expectations and anxious hyper-
vigilance could ensure that such experiences are repeated and even more read-
ily accepted as real. According to the authors, the precise content of the AVH is
shaped by factors such as prior experience/knowledge, perceptual expectations,
and pictorial imaginative content. Finally, the meaning that the particular AVH
has for the individual should be determined by state-dependent (e.g., momen-
tary arousal) and dispositional (e.g., general temperament) characteristics of the
individual. In patients with schizophrenia, factors such as a negative mood and
reduced self-esteem, unfavorable assumptions about the world, and a reduced
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capacity for insight come into play here in particular. The difference between ver-
bal and non-verbal hallucinations is explained in the model by different activa-
tions within the ventral “what” processing pathway, which determines the identity
of a sound in the inferior frontal cortex and temporal auditory cortices. In con-
trast, the localization of AVH as coming from inside or outside may be explained
by activations at different locations of the dorsal “where” pathway. Neuronal
activity in the planum temporale with projection to the inferior parietal cortex is
likely to result in external sound localization. A recent review by Hughdahl and
Sommer (2018) additionally addresses the role of genetic, molecular, and trans-
mitter-dependent factors in the genesis of AVHs. Fig. 5.1 illustrates the model.
Interim Summary
A combination of factors is currently implicated in the genesis of AVH. These
include bottom-up processes, such as aberrant spontaneous activations in
sensory cortices, as well as top-down processes, such as impaired executive
control mechanisms, memory content, emotional processes, and patients’ char-
acteristics that determine the form, content, and meaning of AVH.
◄
5.3 Ego Disorders
Among the ego disorders that typically occur in the context of schizophrenic psy-
choses is the feeling that one’s thoughts and movements are remotely controlled
from outside. Schneider (1938) spoke here of the particular characteristic first
rank symptoms. For example, patients have the impression that they are being fed
“alien” thoughts that are not their own. Some describe this experience as if their
mind were merely a projection screen for the thought processes of others, some
of which they can name. Other patients feel as if they are no longer in control
of their movements and as if these are controlled by, for example, aliens. This
section focuses on the neuropsychological approaches that might explain this par-
ticular form of ego disorder.
5.3.1 Models of Disturbing Prediction of Intended
Movements
The most widespread explanation for ego disorders refers to the disturbances in
the prediction of intended movement sequences already described in connection
5.3 Ego Disorders
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5 Neurocognitive Models of Positive Symptoms
with AVHs. These models assume that, in particular, a faulty production of effer-
ence copies in the (inferior) parietal lobe plays a role in the genesis of the experi-
ence of alien control. As a result, the programmed movement sequences are
not stored in the parietal lobe by the motor areas in the prefrontal cortex before
they are executed and thus are not available for comparison with the movements
already executed. In addition, there is no downregulation of sensory perceptions
Fig. 5.1 Cognitive model of auditory-verbal hallucinations according to Waters et al.
(2012)