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Objective: Olfactory identification deficits and their relationship to negative symptoms in patients with schizophrenia were examined in patients with recent-onset psychosis, the majority of whom were neuroleptic naive. Method: Seventy-four inpatients with a first episode of psychosis (27 with schizophrenia or schizophreniform disorder, nine with schizoaffective disorder, 17 with affective psychoses, and 21 with other psychoses), 49 of whom had not received antipsychotic medication, were compared to 38 age- and gender-matched normal subjects. Olfactory identification ability was assessed with the University of Pennsylvania Smell Identification Test. Forty patients and 13 comparison subjects were reassessed at 6 months to examine whether olfactory deficits were specific to schizophrenia or schizophreniform disorder and were stable over time. Results: At baseline, the patients had significant impairment in olfactory identification ability compared to the normal subjects. This difference persisted after controlling for gender, premorbid or current IQ, smoking history, cannabis use, or the effects of medication. Diagnostic subgroups did not differ in olfactory identification ability. The deficits remained stable at 6-month follow-up and were associated with negative symptoms at both time points. No relationship was found between olfactory identification ability and length of either untreated psychosis or illness prodrome. Conclusions: Impairment in olfactory identification ability was apparent from the outset of psychotic illness and was not specific to schizophrenia or schizophreniform disorder. No change in the degree of this deficit was found after patients were stabilized and had responded to medication. The deficit could not be explained by peripheral factors that might contribute to olfactory identification ability, suggesting that it reflects central mechanisms. [ABSTRACT FROM AUTHOR]

Objectives Mental health triage services are the first contact for people wanting support for their mental health and provide access to public mental health services in Victoria, Australia. People living with young-onset dementia and their families may contact triage services seeking assistance for behaviour changes and pathways to care as there are few alternative services available. Methods The authors reviewed the minimum triage dataset from one of the largest mental health services in Victoria, Australia from 2018 to 2021 investigating reasons for referral for people with young-onset dementia. Results Of the 1766 referrals for 'dementia', 145 were for young-onset dementia. Of these, 69% were referred for behaviour changes. About half of the referrals for behaviour changes were triaged as 'advice only'. One-third of referrals were from general practitioners. Conclusions The availability of dementia-specific support services that could provide advice on dementia as well as advice for behaviour changes related to the disease could potentially ease the burden of phone calls received by mental health triage services.

Objectives: This narrative paper describes the influences behind the development of, and key components of a specialist younger-onset dementia service located in metropolitan Victoria, Australia., Conclusion: The Melbourne Young-Onset Dementia Service was established in 2013 and provides diagnosis and ongoing care for people with younger-onset dementia and their families, through collaboration with other medical units, allied health and community services. It is potentially a model for other younger-onset dementia services nationally and internationally.

Objective: To investigate the hypothesis that patients diagnosed with psychogenic nonepileptic seizures (PNES) on video-EEG monitoring (VEM) have increased mortality by comparison to the general population., Methods: This retrospective cohort study included patients evaluated in VEM units of 3 tertiary hospitals in Melbourne, Australia, between January 1, 1995, and December 31, 2015. Diagnosis was based on consensus opinion of experienced epileptologists and neuropsychiatrists at each hospital. Mortality was determined in patients diagnosed with PNES, epilepsy, or both conditions by linkage to the Australian National Death Index. Lifetime history of psychiatric disorders in PNES was determined from formal neuropsychiatric reports., Results: A total of 5,508 patients underwent VEM. A total of 674 (12.2%) were diagnosed with PNES, 3064 (55.6%) with epilepsy, 175 (3.2%) with both conditions, and 1,595 (29.0%) received other diagnoses or had no diagnosis made. The standardized mortality ratio (SMR) of patients diagnosed with PNES was 2.5 (95% confidence interval [CI] 2.0-3.3). Those younger than 30 had an 8-fold higher risk of death (95% CI 3.4-19.8). Direct comparison revealed no significant difference in mortality rate between diagnostic groups. Among deaths in patients diagnosed with PNES (n = 55), external causes contributed 18%, with 20% of deaths in those younger than 50 years attributed to suicide, and "epilepsy" was recorded as the cause of death in 24%., Conclusions: Patients diagnosed with PNES have a SMR 2.5 times above the general population, dying at a rate comparable to those with drug-resistant epilepsy. This emphasizes the importance of prompt diagnosis, identification of risk factors, and implementation of appropriate strategies to prevent potential avoidable deaths., (© 2020 American Academy of Neurology.)

It is thought that hypothalamic-pituitary-adrenal (HPA) axis functioning mediates between the experience of stress and development of psychotic symptoms. This study aimed to evaluate this model in a cohort of young people at ultra high risk (UHR) of psychosis. Information about the experience of psychological symptoms and recent stressful experiences was obtained from 23 young people who met UHR criteria. Plasma samples were taken to assess cortisol and glucocorticoid receptor numbers, and an MRI scan was also performed. Plasma cortisol levels were significantly and positively correlated with the experience of 'hassles' but not with the experience of stressful life events. Significant positive associations were also found between plasma cortisol levels and level of depression and anxiety. No significant relationships were found between plasma cortisol level and global psychopathology, psychotic symptomatology, functioning or pituitary and hippocampal volumes. These results suggest that the number of hassles experienced by young people at UHR of psychosis could be an important factor in raising their cortisol levels, which might, in turn, affect the severity of depressive and anxiety symptoms. No other relationships were found between plasma cortisol levels and the experience of psychotic symptoms, functioning or hippocampal and pituitary volumes. These results indicate possible impairment in HPA-axis functioning in the early stages of psychotic illness, but further investigation of the relationships between these parameters is required.

Although the underlying neurobiology of emerging psychotic disorders is not well understood, evidence from structural imaging and other studies support the notion that schizophrenia arises as a consequence of both an 'early neurodevelopmental' disturbance, as well as 'late neurodevelopmental' changes occurring during the initial stages of a psychotic illness, including around the time of transition to illness. In line with this, our longitudinal MRI findings in individuals at ultra-high risk for developing a psychotic illness show that there are excessive neuroanatomical changes in those who convert to psychosis. These aberrant changes are observed most prominently in medial temporal and prefrontal lobe regions. In a further series of longitudinal studies in first-episode psychosis, we have identified changes in prefrontal regions that indicate an accelerated loss of grey matter in patients compared to healthy control subjects. We suggest that the available evidence is consistent with the presence of subtle regionally and temporally specific neurobiological changes through the course of psychosis (Pantelis et al., 2005), including: (1) evidence for early (pre- and peri-natal) neurodevelopmental anomalies, (2) evidence for progressive grey matter loss involving medial temporal and orbital prefrontal regions around the time of transition to illness, and (3) evidence of late (post-pubertal) neurodevelopmental changes soon after the onset of psychosis, involving an acceleration of normal brain maturational processes, associated with significant loss of grey matter in dorsal prefrontal regions. The pathological processes underlying such changes remain unclear and may reflect anomalies in genetic and/or other endogenous mechanisms responsible for brain maturation, the adverse effects of intense or prolonged stress, or other environmental factors. These findings suggest that early markers of impending illness may prove difficult to define, and that brain changes in psychosis may better be conceptualized as anomalous trajectories of brain development. Further, active changes during transition to illness may present the potential to intervene and ameliorate these changes with potential benefit clinically.