Schizophrenia spectrum disorders comprise so many divergent findings at the clinical behavioural, neuroanatomical, physiological, and genetic level that a unifying theory covering all facets of these disorders cannot be expected.
One of the hallmarks of schizophrenia is, however, that patients have profound difficulties in social interaction, which often precede the manifestation of the first psychotic episode.
Children who as adults develop schizophrenia not only present with neurological
soft signs, but also with increased prevalence of socially abnormal behaviour including extreme shyness, withdrawal or aggression towards peers.
These behavioural abnormalities may be paralleled by children's difficulties in understanding other people's behaviour in terms of their mental states.
Ethological research into non-verbal behaviour of schizophrenic patients has revealed that they are reduced in their ability to promote Social interaction
even in one-to-one interview situations.
Schizophrenic patients with pronounced negative symptoms more often display behavioural patterns suggestive of avoidance or 'cutting-off' social contact altogether, whereas others, particularly those with paranoid ideation may be more likely to show subtle cues signalling threat such as 'staring'.
Interestingly,the non-verbal behaviour of patients with schizophrenia may sometimes appear indistinguishable from behavioural patterns found in depression, which in a general vein can be interpreted as correlates of submissive behaviour.
Whether or not children who later develop psychosis are more frequently insecurely
attached to caregivers is a matter of debate; as adults,the majority of shizophrenia patients report early attachment bonds in a dismissive or unresolved style, which correspond to insecure-avoidant or disorganized attachment.
It is, however, conceivable, similar to the case of autism,that disruptive neurodevelopment in the child exerts negative effects on early social interaction including the formation of an affectional bond between infant and primary caregiver.If such gene-environment correlations play a role early in childhood development of individuals who later become psychotic, additional aversive events to the point of physical or emotional abuse may be more likely to occur in problematic familial environments, and,in turn, may increase vulnerability for psychosis via chronic activation of the hormonal stress axis.
Evolutionary hypotheses regarding schizophrenia have revolved around the apparent paradox why such devastating disorders exist at all, despite the marked reproductive disadvantage of affected individuals by 30 to 70 percent particularly males.
Similar to other disorders, it has been proposed that a selective advantage of traits
may exist, of which only the extremes of variation are disadvantageous.
The number and diversity of evolutionary hypotheses of schizophrenia, however, are unparalleled in other major psychiatric disorders. They span as divergent aspects as advantages of schizotypal traits in relation to group selection, schizophrenia as a trade-off of human language acquisition or creativity,reduced risk of cancer in relatives of schizophrenic patients, schizophrenia as extreme negative variation of sexually selected traits, and effects of maternally imprinted genes.
Many of these explanatory approaches are implausible because they implicitly assume that schizophrenia is a homogenous 'disease entity', or that the risk for schizophrenia is conveyed by a single gene or several genetic polymorphisms with large effect size.
Neither assumption is currently supported by empirical evidence.
For example, schizophrenia is probably not the result of a single balanced polymorphism where the risk for schizophrenia (and reduced fecundity of affected individuals) is compensated by advantageous effects within the brain (e.g. benefit for the social group conveyed by schizotypal personality traits in relalives of affected individuals), or outside the brain (e.g.reduced cancer risk, greater resistance against infectious diseases or increased survival rates in relatives of schizophrenia patients).
However,there is some evidence for a recent positive selection in the human lineage at several loci including those coding for DISCI, dysbind in and neuregulin, of which the exact functional significance is as yet unknown.
An intensely discussed evolutionary hypothesis of schizophrenia has linked the disorder to a failure to establish functional dominance and language in one or the other hemisphere of the brain.
It has been proposed that cerebral dominance is under control of only a few regulatory genes, and that polymorphisms at one or several of these loci would not only reduce cerebral dominance but also convey a risk for schizophrenia.
In support of this hypothesis it has been found that children who later develop psychotic disorders are more often ambidextrous and have more language disorders and behavioural disturbances than children who as adults do not become psychotic.
Moreover, some studies have revealed a reduced cerebral asymmetry in schizophrenic adults compared with healthy subjects, and sex differences in normal asymmetry have been found disrupted in schizophrenia.
With regards to the representation of language,it is assumed that under normal conditions the organization of language is segregated such that the spatial or 'logical' component is represented in the non-dominant hemisphere and the temporal or 'phonetic' aspect in the dominant hemisphere, both of which normally interact via the corpus callosum.
Accordingly,'firstrank' symptoms in schizophrenia could reflect a disruption of the
normal transcallosal connection of the two hemispheres.Imprecise coordination of the logical and the phonetic aspect of language could produce symptoms such that an individual perceives his or her own thoughts as alien.
However,there is no unequivocal link of handedness and language, nor has cerebral dominance been successfully linked to oligogenetic effects. Furthermore,this hypothesis does not explain symptoms other than formal thought disorder or delusional beliefs.
In any event,the hypothesis points to the interesting observation that sexual selection could be involved in the pathogenesis of schizophrenia, since age at onset and symptom severity differs between the sexes.
Age at onset is usually earlier, and symptom severity is greater in men, and both features may be associated with the normally greater asymmetry between the cerebral hemispheres in men, which fails to be established in schizophrenia.
Several studies have shown that developmental instability is pronounced in patients
with schizophrenia. Normally, genes involved in neurodevelopment help to 'buffer'
against negative effects of multiple mutations, pathogens and toxins. Variation at these loci may lead to increased 'fluctuating asymmetry' (FA),that is, a near-normally distributed asymmetry of bilateral characters that are on average symmetrical in the population.
In schizophrenia, FA is greater in twin pairs concordant for schizophrenia than in
discordant pairs, which suggests that greater FA may indicate an imprecise expression of the developmental design due to genetically or environmentally caused developmental disruption.
This could explain,for example, why patients with schizophrenia have a greater number of minor physical abnormalities such as hypertelorism that could be indicative of an incomplete early cell migration.
Other characteristics putatively associated with a developmental instability in schizophrenia are greater homozygosity of blood alleles,lower premorbid intelligence,reduced cortical volume, and a relative instability of functional and anatomical lateralization of brain functions in schizophrenia.
FA is under partial control of sexual selection, as small FA is usually perceived more attractive than large FA.
It could therefore be that,in a very general vein,the broad spectrum of schizophrenia represents the unattractive extreme of variation of sexually selected traits including FA,language,intelligence, and social cognitive capacities that may be important for successful courtship behaviour.
In fact, many behavioural signs and symptoms and epidemiological findings seem to support this assumption,including the onset of the disorder at the point when mating and courtship behaviour normally peaks.
Competition for potential mates is pronounced for males compared with females, and the peak of mating effort is at a younger age for males, which could explain the earlier onset of schizophrenia and the more severe course and outcome in men.
By contrast,the need to attract suitable mates reaches a second peak in women near the end of their reproductive cycle, which may account for the higher prevalence of erotomanic delusions in women .
If the schizophrenia phenotype represents the low-fitness extreme of sexually selected traits,it is also plausible why patients with schizophrenia have lower than average reproduction rates.
In line with this hypothesis,it has recently been discovered that age at onset of schizophrenia varies with proximity to the equator:the closer people live,the earlier the onset.
One possibility for this finding could be that factors such as increased exposure to pathogens and higher levels of polygyny create a pressure towards mating at a younger age.
This, in turn, may lead to earlier expression of schizophrenic signs and symptoms produced by a stress-induced dopamine overshoot in the ventral striatum, where the need for intensified (premature) courtship behaviour serves as non-specific stressor.
Such a scenario may also explain why the search for replicable allelic variation involved in the pathogenesis of schizophrenia has been unsuccessful.
Since stabilizing selection tends to reduce deleterious mutations,it could be that an individual's higher than average number of fitness-reducing alleles leads to the expression of the schizophrenia phenotype, but that many of these alleles are evolutionarily transient.
However,the emergence of new fitness-decreasing mutations may contribute to an
equilibrium through which the average prevalence of schizophrenia in a population is maintained.
Taken together,the polygenetic inheritance of schizophrenia and the heterogeneity of the disorder can be understood as the negative side of sexually selected fitness-enhancing additive genetic variance.
Consistent with,though not identical to the hypothesis of schizophrenia as the
maladaptive extreme variation of sexually selected traits, some physical and behavioural characteristics indicate that genomic imprinting may play a role in the expression of schizophrenia-associated features. Generally speaking, several characteristics seem to support the assumption that maternal imprinting leads to a pattern of general undergrowth and 'Femaleness' of the brain in schizophrenia.
This could include reduction of grey matter,reduced lateralization, and overactive mechanisms involved in social cognition— the opposite of what is found in autism.
These general evolutionary hypotheses of schizophrenia are,in part,flawed by the fact that they hardly cover all clinical aspects of schizophrenia. Thus, in addition to these broad approaches to understand the heterogeneous nature of the schizophrenia spectrum phenotype,it is useful to analyse individual symptoms based on evolutionary theory. Of note,it is explicitly assumed that signs and symptoms are pathological exaggerations of variation of adaptive mechanisms that arise from a disturbed interplay between one or more levels of the triune brain .
The distinct deficit in social competence in schizophrenia, which often precedes the
manifestation of the first psychotic episode,is paralleled by deficits in social cognition.
This deficit is perhaps triggered by a dopaminergic overstimulation of mesolimbic circuits, which one-sidedly influences the emotional positive symptoms of schizophrenia,for example, tend to be hypervigilant , in particular regarding
gaze monitoring of others, and to interpret social cues as threat.
They may also over-attribute mental states of others, often in a way that they falsely infer malicious intents of others, clinically expressed as persecutory delusion or delusion of reference.
Excessive mental state attribution may also contribute to some aspects of formal thought disorder.
For example, a patient who incorrectly assumes that his or her interlocutor shares his or her knowledge— perhaps due to the patient's fragile ego-boundaries associated with thought transference— may present with loose associations or derailment. Moreover,the tendency in some patients to form too many hypotheses about the mental states of others, while at the same time being unable to choose among these hypotheses the most plausible one, may lead to secondary negative symptoms, perhaps as self-protection from over-stimulation and arousal.
Consistent with this assumption, patients with schizophrenia fail to correctly attribute mental states 'on the spot' despite their tendency to over-infer mental states.
Over the course of the illness, negative symptoms often increase (whereas positive symptoms are still present, but less emotionally valent), accompanied by a decreased potential of the prefrontal cortex to be activated by dopamine.
Thus,in chronic schizophrenia, patients evaluate social situations less, and have even more difficulties in inferring mental states of self and others.It is at present unclear whether this 'mentalizing' deficit in schizophrenia is as selective as it seems to be in autism.
There is at least convincing evidence that patients with schizophrenia also have difficulties in integrating contextual and autobiographical information when judging mental states on the basis of observed behaviour.
Another frequent clinical finding in schizophrenia is the striking lack of awareness of
illness and insight.It would seem that impaired insight is related to patients' difficulties to reflect upon their own states of mind.
Patients also frequently experience so-called passivity symptoms,for example,that a patient's own action is perceived as being influenced by an external agent.
Thus,it is conceivable that disturbances in the neural network under
lying the representation of self and others may be central to many 'core' symptoms associated with schizophrenia.
The neural basis for the ability of mental state attribution or 'mentalizing' and self-
representation is now well known It comprises several interconnected regions of the frontal,temporal, and parietal lobes, among which adaptations, perhaps unique to primates, such as the mirror neuron system, play a crucial role in simulating actions and behavioural dispositions of significant others.
In addition,it has been speculated that the paracingulate sulcus, which separates the anterior cingulate cortex (ACC) from the medial wall of the prefrontal cortex and is inconsistently present in humans, represents an evolutionary novelty involved in social cognitive processes. Furthermore,the infraparietal lobule, which consists of the angular gyrus and the supramarginal gyrus, is probably involved in self-other distinction and representation of the self as acting agent.
Similar to prefrontal cortical midline structures,the infraparietal lobule myelinates late during ontogeny and is only rudimentary in great apes, suggesting that selection has operated on these particular brain areas involved in self-reflexivity and mental state attribution.
These brain regions have been found to be functionally and/or structurally damaged in patients with schizophrenia.
Apart from formal thought disorder, many aspects pertaining to the content of delusional beliefs appear to be tightly linked to scenarios that were selectively important in the human evolutionary past.
This does certainly not preclude influences on delusion formation from an individual's personal background, but the uniformity of delusional content across cultures suggests that universal patterns relating to survival and reproduction are mirrored in delusions.
For example,the content of persecutory delusions differs between men and women
regarding the number and sex of persecutors, as well as regarding the degree of familiarity with the perceived persecutor.
Whereas men usually feel more often threatened by groups of strange males, women more often feel persecuted by individuals from their personal environment. Both deluded men and women primarily report fears of being physically injured or assaulted. The rationale for these sex differences in persecutory delusional content could be that the main source of ancestral threats for men in the environment
of evolutionary adaptedness (EEA) were indeed strange males from other
tribes; by contrast, women, under ancestral conditions,formed the core of the kin-based highly cooperative social group, such that expulsion from the community was a real threat for women living in the EEA.
This assumption is further supported by data from chimpanzees, our closest living relatives,in which territorial competition and warfare between troops of rivalling males has been reported to be high, perhaps similar to what happened in ancestral human conditions. Moreover, until quite recently, similar scenarios were described in extant hunter-gatherer or horticultural societies, where a substantial number of men (up to 25 per cent) and women (up to 13 per cent) died premature violent deaths.
Similarly, delusions relating to mating effort and reproduction differ markedly
between men and women, and again,these patterns are highly uniform across cultures.
Since parental investment differs between men and women with women investing more than men in potential offspring,the former were selected to be choosier in terms of mate choice.In other words, women are, on average, more likely to seek socially high-ranking men as potential partners who are willing to invest in offspring.
In contrast,in established pair-bonds, paternity is less certain than maternity
such that strategies to ensure sexual fidelity were more strongly selected in males. These divergent selection pressures for males and females are strikingly mirrored in erotomania, the delusional conviction of being loved by another person, and delusional jealousy.
Erotomania is much more common in women, who usually choose socially high-standing men (politicians, physicians, actors, sportsmen, etc.) as 'love objects'.
Women with erotomania often try to 'convince' their love objects of their own mate value and tend to harass them. This form of following is, however, different from what is found in stalking behaviour. Stalkers are much more often men who pursue their victims sometimes using violent means.
Erotomania is uncommon among stalkers, however, jealousy (both delusional
and non-delusional)is frequently involved in stalking.
There is probably some
phenomenological overlap between stalking behaviour and delusional jealousy.
Delusional jealousy is much more frequently observed in men compared with women.
It can be seen as the counterpart to erotomania, aimed at partner retention and securing sexual fidelity.
Finally, many signs and symptoms commonly subsumed under the term catatonia can be interpreted as contextually abnormal and exaggerated fear response,fight-flight ambivalence, or behavioural patterns relating to submission or assertive behaviour.
Catatonic stupor,for example, strongly resembles a primitive fear reaction,
which markedly resembles tonic immobility seen in many animal species.In tonic
immobility, which is most likely elicited by impeding predatory threat where flight is
impossible,the animal stops moving to avoid detection. At the same time,it shows
heightened alertness,reduced vocalization, unfocused gaze, analgesia, and abrupt onset and offset of the behaviour,followed by a ferocious struggle to escape. Further similarities are found regarding autonomic instability.
In tonic immobility, heartrate initially rises and then drops below baseline, which can also be observed in catatonic stupor.
The parallels between catatonic stupor and tonic immobility as (primitive) fear responses—represented in the most ancient parts of the triune brain— are also supported by the fact that catatonia responds well to anxiolytic treatment with benzodiazepines and can be worsened by dopamine depleting drugs.
In addition, patients with catatonic stupor often report in retrospect extreme feelings of overwhelming anxiety during the catatonic state.
Catatonic stupor may be preceded or followed by states of extreme hyperactivity or
excitement, sometimes associated with assaultive behaviour. However, catatonic excitement is usually poorly coordinated, which may reflect a primitive behavioural escape response in situations in which the source of the perceived danger is hard to recognize.
Other behavioural symptoms labelled catatonic, such as waxy flexibility, abnormal
imitation and echoing movements including automatic obedience, can be interpreted as contextually abnormal submissive behaviours,the counterpart of which are represented by behaviours suggestive of exaggerated resistance to requests such as negativism.
The pathophysiological underpinnings of these inappropriate expressions of fear,
fight-flight ambivalence, and communicative behaviours are incompletely understood.
Dysfunction of the prefrontal cortex is probably involved, as bilateral lesions to the ACC produce akinetic mutism. Inhibition of imitative behaviour also implicates the distinction from self and other, such that it is conceivable that dysfunction of the infraparietal lobule contributes to catatonic behaviours. Moreover,there is possibly a lack of inhibitory control of the amygdala via the orbitofrontal cortex, which is reciprocally connected with the limbic system.
Little is currently known about the role of the amygdala in catatonia, but given its impact on fear and aggression related behaviour, and the response of catatonic symptoms to anxiolytic treatment,it can be presumed that this structure is central to the aetiology of catatonia.
In addition to the assumption of an inhibitory deficit it could also be that catatonic behaviours can be elicited in individuals Who are vulnerable to overstimulation of these brain areas.
In this context , it is important to note that many catatonic symptoms are indistinguishable from catatonic symptoms are phenomenologically dissociative symptoms, and that a terminological indistinguishable from dissociative symptoms, and that a terminological distinction is more due to convention rather than neurophysiological differences.
This notion is essential, because it throws light on the possibility that patients with early traumatization are perhaps more susceptible to develop dissociative/catatonic states if experiencing retial, because it throws light on the possibility that traumatization or other situations associated patients with early traumatization are perhaps more susceptible to develop dissociative/catatonic states if experiencing re-traumatization or other situations associated with unbearably intense fear.
Finally, catatonic behaviours (like all symptoms found in schizophrenia) can frequently be observed in other psychiatric disorders,foremost depression and bipolar affective disorder, which is,from an evolutionary point of view not surprising, given the importance of these behaviours for submission and appeasement strategies.
One of the hallmarks of schizophrenia is, however, that patients have profound difficulties in social interaction, which often precede the manifestation of the first psychotic episode.
Children who as adults develop schizophrenia not only present with neurological
soft signs, but also with increased prevalence of socially abnormal behaviour including extreme shyness, withdrawal or aggression towards peers.
These behavioural abnormalities may be paralleled by children's difficulties in understanding other people's behaviour in terms of their mental states.
Ethological research into non-verbal behaviour of schizophrenic patients has revealed that they are reduced in their ability to promote Social interaction
even in one-to-one interview situations.
Schizophrenic patients with pronounced negative symptoms more often display behavioural patterns suggestive of avoidance or 'cutting-off' social contact altogether, whereas others, particularly those with paranoid ideation may be more likely to show subtle cues signalling threat such as 'staring'.
Interestingly,the non-verbal behaviour of patients with schizophrenia may sometimes appear indistinguishable from behavioural patterns found in depression, which in a general vein can be interpreted as correlates of submissive behaviour.
Whether or not children who later develop psychosis are more frequently insecurely
attached to caregivers is a matter of debate; as adults,the majority of shizophrenia patients report early attachment bonds in a dismissive or unresolved style, which correspond to insecure-avoidant or disorganized attachment.
It is, however, conceivable, similar to the case of autism,that disruptive neurodevelopment in the child exerts negative effects on early social interaction including the formation of an affectional bond between infant and primary caregiver.If such gene-environment correlations play a role early in childhood development of individuals who later become psychotic, additional aversive events to the point of physical or emotional abuse may be more likely to occur in problematic familial environments, and,in turn, may increase vulnerability for psychosis via chronic activation of the hormonal stress axis.
Evolutionary hypotheses regarding schizophrenia have revolved around the apparent paradox why such devastating disorders exist at all, despite the marked reproductive disadvantage of affected individuals by 30 to 70 percent particularly males.
Similar to other disorders, it has been proposed that a selective advantage of traits
may exist, of which only the extremes of variation are disadvantageous.
The number and diversity of evolutionary hypotheses of schizophrenia, however, are unparalleled in other major psychiatric disorders. They span as divergent aspects as advantages of schizotypal traits in relation to group selection, schizophrenia as a trade-off of human language acquisition or creativity,reduced risk of cancer in relatives of schizophrenic patients, schizophrenia as extreme negative variation of sexually selected traits, and effects of maternally imprinted genes.
Many of these explanatory approaches are implausible because they implicitly assume that schizophrenia is a homogenous 'disease entity', or that the risk for schizophrenia is conveyed by a single gene or several genetic polymorphisms with large effect size.
Neither assumption is currently supported by empirical evidence.
For example, schizophrenia is probably not the result of a single balanced polymorphism where the risk for schizophrenia (and reduced fecundity of affected individuals) is compensated by advantageous effects within the brain (e.g. benefit for the social group conveyed by schizotypal personality traits in relalives of affected individuals), or outside the brain (e.g.reduced cancer risk, greater resistance against infectious diseases or increased survival rates in relatives of schizophrenia patients).
However,there is some evidence for a recent positive selection in the human lineage at several loci including those coding for DISCI, dysbind in and neuregulin, of which the exact functional significance is as yet unknown.
An intensely discussed evolutionary hypothesis of schizophrenia has linked the disorder to a failure to establish functional dominance and language in one or the other hemisphere of the brain.
It has been proposed that cerebral dominance is under control of only a few regulatory genes, and that polymorphisms at one or several of these loci would not only reduce cerebral dominance but also convey a risk for schizophrenia.
In support of this hypothesis it has been found that children who later develop psychotic disorders are more often ambidextrous and have more language disorders and behavioural disturbances than children who as adults do not become psychotic.
Moreover, some studies have revealed a reduced cerebral asymmetry in schizophrenic adults compared with healthy subjects, and sex differences in normal asymmetry have been found disrupted in schizophrenia.
With regards to the representation of language,it is assumed that under normal conditions the organization of language is segregated such that the spatial or 'logical' component is represented in the non-dominant hemisphere and the temporal or 'phonetic' aspect in the dominant hemisphere, both of which normally interact via the corpus callosum.
Accordingly,'firstrank' symptoms in schizophrenia could reflect a disruption of the
normal transcallosal connection of the two hemispheres.Imprecise coordination of the logical and the phonetic aspect of language could produce symptoms such that an individual perceives his or her own thoughts as alien.
However,there is no unequivocal link of handedness and language, nor has cerebral dominance been successfully linked to oligogenetic effects. Furthermore,this hypothesis does not explain symptoms other than formal thought disorder or delusional beliefs.
In any event,the hypothesis points to the interesting observation that sexual selection could be involved in the pathogenesis of schizophrenia, since age at onset and symptom severity differs between the sexes.
Age at onset is usually earlier, and symptom severity is greater in men, and both features may be associated with the normally greater asymmetry between the cerebral hemispheres in men, which fails to be established in schizophrenia.
Several studies have shown that developmental instability is pronounced in patients
with schizophrenia. Normally, genes involved in neurodevelopment help to 'buffer'
against negative effects of multiple mutations, pathogens and toxins. Variation at these loci may lead to increased 'fluctuating asymmetry' (FA),that is, a near-normally distributed asymmetry of bilateral characters that are on average symmetrical in the population.
In schizophrenia, FA is greater in twin pairs concordant for schizophrenia than in
discordant pairs, which suggests that greater FA may indicate an imprecise expression of the developmental design due to genetically or environmentally caused developmental disruption.
This could explain,for example, why patients with schizophrenia have a greater number of minor physical abnormalities such as hypertelorism that could be indicative of an incomplete early cell migration.
Other characteristics putatively associated with a developmental instability in schizophrenia are greater homozygosity of blood alleles,lower premorbid intelligence,reduced cortical volume, and a relative instability of functional and anatomical lateralization of brain functions in schizophrenia.
FA is under partial control of sexual selection, as small FA is usually perceived more attractive than large FA.
It could therefore be that,in a very general vein,the broad spectrum of schizophrenia represents the unattractive extreme of variation of sexually selected traits including FA,language,intelligence, and social cognitive capacities that may be important for successful courtship behaviour.
In fact, many behavioural signs and symptoms and epidemiological findings seem to support this assumption,including the onset of the disorder at the point when mating and courtship behaviour normally peaks.
Competition for potential mates is pronounced for males compared with females, and the peak of mating effort is at a younger age for males, which could explain the earlier onset of schizophrenia and the more severe course and outcome in men.
By contrast,the need to attract suitable mates reaches a second peak in women near the end of their reproductive cycle, which may account for the higher prevalence of erotomanic delusions in women .
If the schizophrenia phenotype represents the low-fitness extreme of sexually selected traits,it is also plausible why patients with schizophrenia have lower than average reproduction rates.
In line with this hypothesis,it has recently been discovered that age at onset of schizophrenia varies with proximity to the equator:the closer people live,the earlier the onset.
One possibility for this finding could be that factors such as increased exposure to pathogens and higher levels of polygyny create a pressure towards mating at a younger age.
This, in turn, may lead to earlier expression of schizophrenic signs and symptoms produced by a stress-induced dopamine overshoot in the ventral striatum, where the need for intensified (premature) courtship behaviour serves as non-specific stressor.
Such a scenario may also explain why the search for replicable allelic variation involved in the pathogenesis of schizophrenia has been unsuccessful.
Since stabilizing selection tends to reduce deleterious mutations,it could be that an individual's higher than average number of fitness-reducing alleles leads to the expression of the schizophrenia phenotype, but that many of these alleles are evolutionarily transient.
However,the emergence of new fitness-decreasing mutations may contribute to an
equilibrium through which the average prevalence of schizophrenia in a population is maintained.
Taken together,the polygenetic inheritance of schizophrenia and the heterogeneity of the disorder can be understood as the negative side of sexually selected fitness-enhancing additive genetic variance.
Consistent with,though not identical to the hypothesis of schizophrenia as the
maladaptive extreme variation of sexually selected traits, some physical and behavioural characteristics indicate that genomic imprinting may play a role in the expression of schizophrenia-associated features. Generally speaking, several characteristics seem to support the assumption that maternal imprinting leads to a pattern of general undergrowth and 'Femaleness' of the brain in schizophrenia.
This could include reduction of grey matter,reduced lateralization, and overactive mechanisms involved in social cognition— the opposite of what is found in autism.
These general evolutionary hypotheses of schizophrenia are,in part,flawed by the fact that they hardly cover all clinical aspects of schizophrenia. Thus, in addition to these broad approaches to understand the heterogeneous nature of the schizophrenia spectrum phenotype,it is useful to analyse individual symptoms based on evolutionary theory. Of note,it is explicitly assumed that signs and symptoms are pathological exaggerations of variation of adaptive mechanisms that arise from a disturbed interplay between one or more levels of the triune brain .
The distinct deficit in social competence in schizophrenia, which often precedes the
manifestation of the first psychotic episode,is paralleled by deficits in social cognition.
This deficit is perhaps triggered by a dopaminergic overstimulation of mesolimbic circuits, which one-sidedly influences the emotional positive symptoms of schizophrenia,for example, tend to be hypervigilant , in particular regarding
gaze monitoring of others, and to interpret social cues as threat.
They may also over-attribute mental states of others, often in a way that they falsely infer malicious intents of others, clinically expressed as persecutory delusion or delusion of reference.
Excessive mental state attribution may also contribute to some aspects of formal thought disorder.
For example, a patient who incorrectly assumes that his or her interlocutor shares his or her knowledge— perhaps due to the patient's fragile ego-boundaries associated with thought transference— may present with loose associations or derailment. Moreover,the tendency in some patients to form too many hypotheses about the mental states of others, while at the same time being unable to choose among these hypotheses the most plausible one, may lead to secondary negative symptoms, perhaps as self-protection from over-stimulation and arousal.
Consistent with this assumption, patients with schizophrenia fail to correctly attribute mental states 'on the spot' despite their tendency to over-infer mental states.
Over the course of the illness, negative symptoms often increase (whereas positive symptoms are still present, but less emotionally valent), accompanied by a decreased potential of the prefrontal cortex to be activated by dopamine.
Thus,in chronic schizophrenia, patients evaluate social situations less, and have even more difficulties in inferring mental states of self and others.It is at present unclear whether this 'mentalizing' deficit in schizophrenia is as selective as it seems to be in autism.
There is at least convincing evidence that patients with schizophrenia also have difficulties in integrating contextual and autobiographical information when judging mental states on the basis of observed behaviour.
Another frequent clinical finding in schizophrenia is the striking lack of awareness of
illness and insight.It would seem that impaired insight is related to patients' difficulties to reflect upon their own states of mind.
Patients also frequently experience so-called passivity symptoms,for example,that a patient's own action is perceived as being influenced by an external agent.
Thus,it is conceivable that disturbances in the neural network under
lying the representation of self and others may be central to many 'core' symptoms associated with schizophrenia.
The neural basis for the ability of mental state attribution or 'mentalizing' and self-
representation is now well known It comprises several interconnected regions of the frontal,temporal, and parietal lobes, among which adaptations, perhaps unique to primates, such as the mirror neuron system, play a crucial role in simulating actions and behavioural dispositions of significant others.
In addition,it has been speculated that the paracingulate sulcus, which separates the anterior cingulate cortex (ACC) from the medial wall of the prefrontal cortex and is inconsistently present in humans, represents an evolutionary novelty involved in social cognitive processes. Furthermore,the infraparietal lobule, which consists of the angular gyrus and the supramarginal gyrus, is probably involved in self-other distinction and representation of the self as acting agent.
Similar to prefrontal cortical midline structures,the infraparietal lobule myelinates late during ontogeny and is only rudimentary in great apes, suggesting that selection has operated on these particular brain areas involved in self-reflexivity and mental state attribution.
These brain regions have been found to be functionally and/or structurally damaged in patients with schizophrenia.
Apart from formal thought disorder, many aspects pertaining to the content of delusional beliefs appear to be tightly linked to scenarios that were selectively important in the human evolutionary past.
This does certainly not preclude influences on delusion formation from an individual's personal background, but the uniformity of delusional content across cultures suggests that universal patterns relating to survival and reproduction are mirrored in delusions.
For example,the content of persecutory delusions differs between men and women
regarding the number and sex of persecutors, as well as regarding the degree of familiarity with the perceived persecutor.
Whereas men usually feel more often threatened by groups of strange males, women more often feel persecuted by individuals from their personal environment. Both deluded men and women primarily report fears of being physically injured or assaulted. The rationale for these sex differences in persecutory delusional content could be that the main source of ancestral threats for men in the environment
of evolutionary adaptedness (EEA) were indeed strange males from other
tribes; by contrast, women, under ancestral conditions,formed the core of the kin-based highly cooperative social group, such that expulsion from the community was a real threat for women living in the EEA.
This assumption is further supported by data from chimpanzees, our closest living relatives,in which territorial competition and warfare between troops of rivalling males has been reported to be high, perhaps similar to what happened in ancestral human conditions. Moreover, until quite recently, similar scenarios were described in extant hunter-gatherer or horticultural societies, where a substantial number of men (up to 25 per cent) and women (up to 13 per cent) died premature violent deaths.
Similarly, delusions relating to mating effort and reproduction differ markedly
between men and women, and again,these patterns are highly uniform across cultures.
Since parental investment differs between men and women with women investing more than men in potential offspring,the former were selected to be choosier in terms of mate choice.In other words, women are, on average, more likely to seek socially high-ranking men as potential partners who are willing to invest in offspring.
In contrast,in established pair-bonds, paternity is less certain than maternity
such that strategies to ensure sexual fidelity were more strongly selected in males. These divergent selection pressures for males and females are strikingly mirrored in erotomania, the delusional conviction of being loved by another person, and delusional jealousy.
Erotomania is much more common in women, who usually choose socially high-standing men (politicians, physicians, actors, sportsmen, etc.) as 'love objects'.
Women with erotomania often try to 'convince' their love objects of their own mate value and tend to harass them. This form of following is, however, different from what is found in stalking behaviour. Stalkers are much more often men who pursue their victims sometimes using violent means.
Erotomania is uncommon among stalkers, however, jealousy (both delusional
and non-delusional)is frequently involved in stalking.
There is probably some
phenomenological overlap between stalking behaviour and delusional jealousy.
Delusional jealousy is much more frequently observed in men compared with women.
It can be seen as the counterpart to erotomania, aimed at partner retention and securing sexual fidelity.
Finally, many signs and symptoms commonly subsumed under the term catatonia can be interpreted as contextually abnormal and exaggerated fear response,fight-flight ambivalence, or behavioural patterns relating to submission or assertive behaviour.
Catatonic stupor,for example, strongly resembles a primitive fear reaction,
which markedly resembles tonic immobility seen in many animal species.In tonic
immobility, which is most likely elicited by impeding predatory threat where flight is
impossible,the animal stops moving to avoid detection. At the same time,it shows
heightened alertness,reduced vocalization, unfocused gaze, analgesia, and abrupt onset and offset of the behaviour,followed by a ferocious struggle to escape. Further similarities are found regarding autonomic instability.
In tonic immobility, heartrate initially rises and then drops below baseline, which can also be observed in catatonic stupor.
The parallels between catatonic stupor and tonic immobility as (primitive) fear responses—represented in the most ancient parts of the triune brain— are also supported by the fact that catatonia responds well to anxiolytic treatment with benzodiazepines and can be worsened by dopamine depleting drugs.
In addition, patients with catatonic stupor often report in retrospect extreme feelings of overwhelming anxiety during the catatonic state.
Catatonic stupor may be preceded or followed by states of extreme hyperactivity or
excitement, sometimes associated with assaultive behaviour. However, catatonic excitement is usually poorly coordinated, which may reflect a primitive behavioural escape response in situations in which the source of the perceived danger is hard to recognize.
Other behavioural symptoms labelled catatonic, such as waxy flexibility, abnormal
imitation and echoing movements including automatic obedience, can be interpreted as contextually abnormal submissive behaviours,the counterpart of which are represented by behaviours suggestive of exaggerated resistance to requests such as negativism.
The pathophysiological underpinnings of these inappropriate expressions of fear,
fight-flight ambivalence, and communicative behaviours are incompletely understood.
Dysfunction of the prefrontal cortex is probably involved, as bilateral lesions to the ACC produce akinetic mutism. Inhibition of imitative behaviour also implicates the distinction from self and other, such that it is conceivable that dysfunction of the infraparietal lobule contributes to catatonic behaviours. Moreover,there is possibly a lack of inhibitory control of the amygdala via the orbitofrontal cortex, which is reciprocally connected with the limbic system.
Little is currently known about the role of the amygdala in catatonia, but given its impact on fear and aggression related behaviour, and the response of catatonic symptoms to anxiolytic treatment,it can be presumed that this structure is central to the aetiology of catatonia.
In addition to the assumption of an inhibitory deficit it could also be that catatonic behaviours can be elicited in individuals Who are vulnerable to overstimulation of these brain areas.
In this context , it is important to note that many catatonic symptoms are indistinguishable from catatonic symptoms are phenomenologically dissociative symptoms, and that a terminological indistinguishable from dissociative symptoms, and that a terminological distinction is more due to convention rather than neurophysiological differences.
This notion is essential, because it throws light on the possibility that patients with early traumatization are perhaps more susceptible to develop dissociative/catatonic states if experiencing retial, because it throws light on the possibility that traumatization or other situations associated patients with early traumatization are perhaps more susceptible to develop dissociative/catatonic states if experiencing re-traumatization or other situations associated with unbearably intense fear.
Finally, catatonic behaviours (like all symptoms found in schizophrenia) can frequently be observed in other psychiatric disorders,foremost depression and bipolar affective disorder, which is,from an evolutionary point of view not surprising, given the importance of these behaviours for submission and appeasement strategies.