This article is a clinical guide which discusses the “state-of-the-art” usage of the classic monoamine oxidase inhibitor (MAOI) antidepressants (phenelzine, tranylcypromine, and isocarboxazid) in modern psychiatric practice. The guide is for all clinicians, including those who may not be experienced MAOI prescribers. It discusses indications, drug-drug interactions, side-effect management, and the safety of various augmentation strategies. There is a clear and broad consensus (more than 70 international expert endorsers), based on 6 decades of experience, for the recommendations herein exposited. They are based on empirical evidence and expert opinion—this guide is presented as a new specialist-consensus standard. The guide provides practical clinical advice, and is the basis for the rational use of these drugs, particularly because it improves and updates knowledge, and corrects the various misconceptions that have hitherto been prominent in the literature, partly due to insufficient knowledge of pharmacology. The guide suggests that MAOIs should always be considered in cases of treatment-resistant depression (including those melancholic in nature), and prior to electroconvulsive therapy—while taking into account of patient preference. In selected cases, they may be considered earlier in the treatment algorithm than has previously been customary, and should not be regarded as drugs of last resort; they may prove decisively effective when many other treatments have failed. The guide clarifies key points on the concomitant use of incorrectly proscribed drugs such as methylphenidate and some tricyclic antidepressants. It also illustrates the straightforward “bridging” methods that may be used to transition simply and safely from other antidepressants to MAOIs.

Background. Verbal declarative memory is a core deficit in schizophrenia patients, seen to a lesser extent in unaffected biological relatives. Neuroimaging studies suggest volumetric differences and aberrant function in prefrontal and temporal regions in schizophrenia patients compared to controls. These deficits are also reflected in the small number of similar investigations in unaffected biological relatives. However, it is unclear the extent to which dysfunction is genetically mediated or a feature of the established illness.

Method. Event-related blood-oxygen-level-dependent (BOLD) functional magnetic resonance imaging (fMRI) was used to measure brain activation in 68 biological relatives of schizophrenia patients (of whom 27 experienced transient or isolated psychotic symptoms) and 21 controls during verbal classification and recognition.

Results. During word classification, the high-risk group showed a greater response relative to controls in the right inferior frontal gyrus. During correct recognition (relative to correct rejection), the high-risk group showed significantly greater response relative to controls in the right cerebellum. When the high-risk group was split into those with (HR+) and without (HR−) psychotic symptoms, the increased response in the right inferior frontal gyrus was only seen when the HR+ were compared to controls. The greater cerebellar response was seen when both HR groups were compared to controls.

Conclusions. Activation increases in the right inferior frontal gyrus and cerebellum in high-risk subjects compared to controls during a relatively low-load memory task are likely to represent compensation for genetically mediated abnormalities. This is consistent with a leftward shift of the inverted ‘U’ load–response model of cognitive function in schizophrenia.

Objective: To examine the demographic, prescription, ingestion, and psychiatric diagnostic factors that distinguished elderly from nonelderly patients treated for deliberate self-poisoning (DSP). Method: A prospective case series study of 2,667 patients presenting to a regional referral center for poisoning (Newcastle Mater Hospital, NSW, Australia), January 1991 to July 1998. The sample was stratified into two groups, 65 years or greater (n = 110) and 64 years or less (n = 2,557) at the time of index admission. The groups were compared using a forward stepwise logistic regression model. Uncontrolled comparisons were analyzed by chi-square statistic with Bonferroni-adjusted p values and controlled comparisons by odds ratio (OR) with 95% confidence interval (CI). Results: The elderly group represented 4.1% of the total. The logistic regression analysis found the elderly DSP group was more likely to have a longer length of stay (OR 5.90, CI 3.87–9.00), to have been prescribed “other” drugs (neither benzodiazepines, mood treatment drugs, nor paracetamol) before admission (OR 5.32, CI 3.34–8.48), to have been prescribed benzodiazepines (OR 3.15, CI 2.03–4.89), and to be diagnosed with major depression (OR 2.17, CI 1.41–3.36) than the younger group. The elderly group was less likely to have ingested paracetamol (OR 0.28, CI 0.14–0.54) or “other” drugs (neither benzodiazepines nor mood treatment drugs) in the DSP episode (OR 0.33, CI 0.20–0.54). Discussion: Elderly DSP patients differ in several important respects from younger patients. They have higher morbidity as a result of the DSP. Major depression plays a more important role. The strong relationship between benzodiazepine prescription and DSP in the elderly raises questions and possible prevention strategies.