Objective: To examine the evidence for the three kinds of aetiological model that dominate the current literature on poor insight in psychosis: clinical models, the neuropsychological model, and the psychological denial model.



Method:  Studies pertaining to one or more of these aetiological models were identified, reviewed and critically evaluated.



Results:  There is little support for clinical models, partly because they lack testable hypotheses. Several studies reveal a positive relationship between insight and executive function, which may be related to frontal lobe dysfunction. However, the extent to which this relationship is specific and independent of general cognitive impairment remains unclear. There is tentative evidence to support the psychological denial model. Recent data combining the latter two approaches suggest that multiple factors contribute to poor insight.



Conclusion:  Integration of different aetiological models is necessary for a fuller understanding of insight in psychosis. Future research should assess multiple aetiological mechanisms in single investigations.

Disease, deficit or denial? Models of poor insight in psychosis

braehial, lay immediately beneath the skin on the right side; one extending from below obliquely upwards; the other a little higher up, running inwards and downwards. On the left, a smaller artery could be felt; and on this side the carotid artery could be detected issuing from the upper border of the swelling. The consistence of the mass varied in different parts; it was generally soft and elastic, in some parts almost cartilaginous. The finger detected deep fissures, which seemed to separate the tumour into distinct lobes. There were two smaller detached masses on the left side; one of them, the higher of the two, was of about the size of a walnut, hard, extremely movable, and entirely unconnected with the chest. The other was softer, more elongated, and appeared to be connected with the main body of the tumour beneath the sterno-mastoid. On October 5th, the patient having been brought under the influence of chloroform, Mr. Erichsen proceeded to endeavour to isolate and tie the lower of the two large arteries on the right. It was, however (as had been anticipated), so incorporated with the tumour that it was not possible to isolate it. A pointed needle was accordingly thrust under it, and the vessel and parts in the neighbourhood were strangulated. At the same time, a solution of perchloride of iron was injected into the swelling. This was prepared according to the formula of the French code., of the specific gravity of 1-263; and was passed into the tumour by means of a small syringe used in injecting vascular tumours, which held about a drachm. of the solution. This was repeated in seven different parts of the tumour. The patient was very sick from the chloroform, and complained of great weakness afterwards; but the injection did not produce any local mischief, except that a drop or two of pus issued from some of the places where the perchloride had been injected. The pulsation in the swelling was much dimi. nished. The ligature came off the artery on the eighth day, and rather profuse bleeding occurred on that and the following day. This, however, was checked by a suture wound round two harelip pins. On October 14th, the injection was repeated, about one and a half drachm of the solution being injected in two different places. The point of the syringe then broke, and it was impossible to inject more. No chloroform was used. Three days afterwards, it is noted that the patient feels better and stronger; and that two of the spots, where the injection has been introduced, are decidedly harder; and the whole tumour feels much firmer. On October 22nd, four more parts were injected. This time the injection was followed by some rather alarming symptoms. On October 27th, the patient was complaining of great weakness; had had a very bad night, with rigors and fever. Her aspect was bad, complexion yellow, nind bowels relaxed. These symptoms, however, appeared to depend on the confinement of matter, as, after the discharge of some pus from one of the injected spots, they subsided; and the ease seemed progressing favourably, when, in consequence of sonmC quarrel with her nurse, she insisted on leaving the Hospital. REMIARKS. We have given publicity to this case, imperfect as it is, on account of its intrinsic interest, as being a form of disease very rarely met with, at any rate in England; and as an instance of the employment of a method of treatment which has not hitherto made much progress in London, though much recommended by various continental authorities. The action of perchloride of iron upon the tissue of vascular tumours, and the degree of riskwhich its injection involves, are subjects on which our experience in London is hardly sufficiently ex. tensive to enable us to speak positively. There exists in the Mliemnoires de la Sociiti de Chirurgie de Paris an elaborate memoir by M. Desgranges, in which he investigates the former point in the treatment of varices and hlemorrhoids. The ingenious author there comes to the conclusion, as the result of his experience, that the perchloride enters into a real combination. with the elements of the blood, when passed fairly into the cavity of a vessel; and that this new compound modifies the composition of the rest of the blood. Thus, as he conceives, the risks attending the introduction of foreign matter into the vessels are materially modified, since none of the perchloride passes in this state into the circulation, and the new product is inert for the purpose of exciting inflammation. This view does not derive any support from the case before us ; but it should be remembered that, in so large and complicated a tumour, it would not be possible, as in the simple form. treated by the French surgeon, to be sure of the precise position of the point of the syringe; and hence some of the solution might be extravasated into the cellular tissue-an accident to be avoided, according to him, with all possible care. As to the success of the treatment, all that can be said is, that the case was progressing favourably. The rather alarming symptoms noticed after the third injection appear to have depended on the presence of confined matter, and not on any inflammation of the linina membrane of the vessels; and the process of consolidation had certainly advanced. It is much to be regretted that the patient's waywardness prevented the complo. tion of a very interesting surgical case.

King's College Hospital.

Schizophrenia seems to be a heterogeneous disorder. Emerging evidence indicates that low level neuroinflammation (LLNI) may not occur infrequently. Many infectious agents with low overall pathogenicity are risk factors for psychoses including schizophrenia and for autoimmune disorders. According to the mild encephalitis (ME) hypothesis, LLNI represents the core pathogenetic mechanism in a schizophrenia subgroup that has syndromal overlap with other psychiatric disorders. ME may be triggered by infections, autoimmunity, toxicity, or trauma. A ‘late hit’ and gene–environment interaction are required to explain major findings about schizophrenia, and both aspects would be consistent with the ME hypothesis. Schizophrenia risk genes stay rather constant within populations despite a resulting low number of progeny; this may result from advantages associated with risk genes, e.g., an improved immune response, which may act protectively within changing environments, although they are associated with the disadvantage of increased susceptibility to psychotic disorders. Specific schizophrenic symptoms may arise with instances of LLNI when certain brain functional systems are involved, in addition to being shaped by pre-existing liability factors. Prodrome phase and the transition to a diseased status may be related to LLNI processes emerging and varying over time. The variability in the course of schizophrenia resembles the varying courses of autoimmune disorders, which result from three required factors: genes, the environment, and the immune system. Preliminary criteria for subgrouping neurodevelopmental, genetic, ME, and other types of schizophrenias are provided. A rare example of ME schizophrenia may be observed in Borna disease virus infection. Neurodevelopmental schizophrenia due to early infections has been estimated by others to explain approximately 30% of cases, but the underlying pathomechanisms of transition to disease remain in question. LLNI (e.g. from reactivation related to persistent infection) may be involved and other pathomechanisms including dysfunction of the blood–brain barrier or the blood–CSF barrier, CNS-endogenous immunity and the volume transmission mode balancing wiring transmission (the latter represented mainly by synaptic transmission, which is often described as being disturbed in schizophrenia). Volume transmission is linked to CSF signaling; and together could represent a common pathogenetic link for the distributed brain dysfunction, dysconnectivity, and brain structural abnormalities observed in schizophrenia. In addition, CSF signaling may extend into peripheral tissues via the CSF outflow pathway along brain nerves and peripheral nerves, and it may explain the peripheral topology of neuronal dysfunctions found, like in olfactory dysfunction, dysautonomia, and even in peripheral tissues, i.e., the muscle lesions that were found in 50% of cases. Modulating factors in schizophrenia, such as stress, hormones, and diet, are also modulating factors in the immune response. Considering recent investigations of CSF, the ME schizophrenia subgroup may constitute approximately 40% of cases.

Updating the mild encephalitis hypothesis of schizophrenia.

Although neurological evidence is used with increasing frequency in criminal trials, there is limited research examining the effects that this evidence has on juror decision-making in insanity trials. Participants (396) were presented with a case summary and psychological testimony and asked to render either a verdict of guilty or not guilty by reason of insanity in a 2 (psychosis or psychopathy) x (presence or absence of an MRI indicating a brain lesion) x (presence or absence of testimony describing a car accident that caused injury to the brain) factorial design. Defendants diagnosed with a psychotic disorder, defendants who could demonstrate the existence of a brain lesion via MRI, and defendants who had a history of brain injury were more likely to be found not guilty by reason of insanity than those defendants who did not present any neurological testimony. Participants who reported they were more influenced by the psychological and neurological testimony were almost six times more likely to render a verdict of NGRI than those participants who reported that the psychological and neurological testimony and evidence did not influence their decision regarding verdict. Language: en

The effects of neuroimaging and brain injury on insanity defenses

BACKGROUND: Several studies have suggested that neuropsychological and structural brain deficits are implicated in poor insight. Few insight studies however have combined neurocognitive and structural neuroanatomical measures.

AIMS: Focusing on the ability to relabel psychotic symptoms as pathological, we examined insight, brain structure and neurocognition in first-onset psychosis.

METHOD: Voxel-based magnetic resonance imaging data were acquired from 82 individuals with psychosis and 91 controls assessed with a brief neuropsychological test battery. Insight was measured using the Schedule for the Assessment of Insight.

RESULTS: The principal analysis showed reduced general neuropsychological function was linked to poor symptom relabelling ability. A subsequent between-psychosis group analysis found those with no symptom relabelling ability had significant global and regional grey matter deficits primarily located at the posterior cingulate gyrus and right precuneus/cuneus.

CONCLUSIONS: The cingulate gyrus (as part of a midline cortical system) along with right hemisphere regions may be involved in illness and symptom self-appraisal in first-onset psychosis.

https://www.cambridge.org/core/services/aop-cambridge-core/content/view/B498113F7ACE651355ABA369E3C5727C/S0007125000252872a.pdf/div-class-title-insight-grey-matter-and-cognitive-function-in-first-onset-psychosis-div.pdf

Insight, grey matter and cognitive function in first-onset psychosis.

Background Minor physical anomalies are more prevalent among people with psychosis. This supports a neurodevelopmental aetiology for psychotic disorders, since these anomalies and the brain are both ectodermally derived. However, little is understood about the brain regions implicated in this association.

Aims To examine the relationship between minor physical anomalies and grey matter structure in a sample of patients with first-episode psychosis.

Method Sixty patients underwent assessment of minor physical anomalies with the Lane scale. High-resolution magnetic resonance images and voxel-based methods of image analysis were used to investigate brain structure in these patients.

Results The total anomalies score was associated with a grey matter reduction in the prefrontal cortex and precuneus and with a grey matter excess in the basal ganglia, thalamus and lingual gyrus.

Conclusions Minor physical anomalies in a sample of patients with first-episode psychosis are associated with regionalgrey matter changes. These regional changes may be important in the pathogenesis of psychotic disorder.

R Mallet

Papers

Grey matter correlates of minor physical anomalies in the AeSOP first-episode psychosis study.

Insight: Unitary or multi-dimensional phenomenon?

Neuroanatomical correlates of poor insight: The AESOP first-onset psychosis study

Effects of psychological therapy on brain activation in patients with a diagnosis of schizophrenia

Duration of untreated psychosis in first episode affective and nonaffective psychosis