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Objectives Comorbidities that are less well known than substance use disorders may occur in individuals experiencing a first-episode psychosis (FEP). This article reviews the importance of these comorbidities through a synthesis of the literature, informed by the authors' clinical experience. Methods Five main groups of comorbidities are discussed: anxiety and obsessive-compulsive disorders, depression, borderline personality disorder, gambling disorder and attention deficit disorder. For each of these disorders, data on their frequency, their impact on the outcome of affected individuals, their detection and treatment will be discussed and interpreted in light of the authors' clinical experience. Results These comorbidities have been relatively neglected by research, even more so in the specific context of FEP. Nevertheless, the data that are available suggest that they are very common in this population. For example, it is estimated that the prevalence of social anxiety disorder may be as high as 50% and obsessive-compulsive disorder 13.6%. The manifestations of these comorbid disorders are sometimes difficult to dissociate from those of the illness; several manifestations of the psychoses can be encountered in these comorbid disorders and vice versa. For example, the social withdrawal sometimes encountered in anxiety disorders or depression may be confused with negative symptoms; behavioural disturbances resulting from delusional beliefs or behavioural disorganization occurring in psychosis may lead to a misdiagnosis of a personality disorder; psychotic symptoms occurring in a personality disorder share characteristics with those occurring in psychotic disorders; cognitive difficulties associated with an attention deficit disorder may give the impression of being directly related to the psychotic disorder. In some cases, antipsychotic treatment may contribute to the emergence of manifestations of these comorbid disorders, for example, obsessive-compulsive disorder occurring on clozapine, or gambling disorder occurring during treatment with a dopamine agonist. While treatments for these comorbidities have been poorly evaluated in the FEP setting, available data and clinical experience suggest that treatments used in other populations, when adapted to the FEP setting, may be effective. Conclusion Overall, there is little literature addressing these comorbid disorders in FEP. Yet, the available evidence suggests that they are common, and that their detection and treatment can support recovery in individuals coping with FEP. Thus, it is essential to consider them from a recovery-oriented early intervention practice perspective.

A special reactor coupled to a high-temperature mass spectrometer was specifically designed for the study of vaporization and thermal cracking of organometallic precursors. This reactor has two kinds of settings. One is a single Knudsen effusion cell which enables the analysis of the composition of saturated vapors and the determination of the partial pressure of each gaseous molecule in equilibrium with its condensed phase. This cell is an evaporation/sublimation cell (operating from 243 to 473 K), which can be tightly closed--like a vacuum chamber--in order to protect organometallic compounds against moisture and atmospheric components. This cell can be independently weighed usefully to evaluate the equilibrium vapor pressures of the sample using the mass-loss method. During experiments, the effusion aperture is externally opened for direct mass spectrometric measurements. The other setting dedicated to the study of thermal decomposition of gaseous molecules consists of a set of tandem cells: the previously described Knudsen cell and a cracking cell (operating from 293 to 973 K)., (Copyright (c) 2009 John Wiley & Sons, Ltd.)

3-Bromobenzyloxy phenyloxy hydroxymethyl propanol was labelled with iodine-125. Labeling yield was approximately 92%. Using HPLC and an RP18 column, Iodo*MD (MW = 412) was obtained at no-carrier-added conditions (specific activity 125 Ci/mmole). Biochemical experiments were carried out in vitro and showed a Ki for MAO-B of 5.4 nM and of 5000 for MAO-A (RA/B = 926). Using ex vivo kinetic inhibition in rat (dose: 5 mg/kg p.o.), the results demonstrated a strong similarity of action with BromoMD and IodoMD, with an inhibition percentage that decreased with time (91% at 1 hour, 48% at 8 hours, 2% at 24 hours). The rat brain Iodo*MD concentration was maximal after the first pass and inhibition decreased slowly with time (T1/2 = 1.8 hours). Uptake and wash-out of Iodo*MD was studied on two-day-old rat astrocytes in culture. Half-times of uptake and efflux were respectively 2.5 minutes and 7.5 minutes. The use of metabolic inhibitors (KCN and Digoxin) suggested the absence of any active transport. Binding studies with various concentration of cold MD 360194 showed that at 10(-8) M the uptake decreased significantly. Rats were dissected at different times post i.v. injection (0-2 hours), and the principal organs and brain were obtained (the brain was separated into 7 pieces). Radioactivity was concentrated mainly in the liver (24.6 +/- 4%), fat (12.4 +/- 3.4%) and muscles (18.4 +/- 3%). In the brain the concentration was approximately 1.2 +/- 0.3% within 30 minutes post i.v. injection and 0.84 +/- 0.15% thereafter. The hypothalamus and striatum were two-fold more active than the cortex.(ABSTRACT TRUNCATED AT 250 WORDS)