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Background: Sleep dysfunction commonly co-occurs with paranoia and is hypothesised to be a contributory causal mechanism in its development and maintenance., Objectives: To systematically review and quantitatively evaluate the evidence for the relationship between sleep dysfunction and paranoia across the spectrum of severity., Method: A systematic search was conducted to identify studies investigating the relationship between aspects of sleep and paranoia across clinical and non-clinical groups. A random effects model using a Fisher r-to-z transformed correlation coefficient was used for meta-analysis., Results: 45 studies were included in the review and 14 in the meta-analysis. The literature supports a small-to-moderate association (r = 0.30, 95 % CI: 0.16-0.40 for the seven studies using the most robust measures) with significant heterogeneity among studies but no evidence of publication bias. There is evidence that the relationship is to some extent causal, with sleep disruption leading to increased paranoia, though there is also some evidence of a bi-directional relationship. Negative affect is frequently seen as a mediator of this relationship., Conclusion: This review for the first time examines the significant relationship between sleep and paranoia individually. Studies are needed that further assess the potential for early intervention of sleep dysfunction in those experiencing paranoia., Competing Interests: Declaration of competing interest The authors declare no conflicts of interests., (Copyright © 2024 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Background: Sleep and mental health share a bidirectional relationship whereby problems in one exacerbate the other. Accordingly, sleep problems are frequent and severe in serious mental illness (SMI) populations, exacerbating SMI symptoms. This study examined the documentation and treatment of sleep problems within anonymised clinical records of SMI patients, and their association with attendance rates and number of appointments scheduled., Methods: Patient records between 01.09.2021 and 31.08.2022 were identified and relevant records (n = 229) extracted from an NHS Trust database. Content analysis was used to assess documentation and treatment of sleep problems and Chi-square tests were used to assess demographic differences. Mann-Whitney U tests were used to compare attendance rates and number of appointments scheduled between patients with/without sleep problems., Results: Most (n = 170; 84 %) patients with sleep problems had no or minimal assessment of the sleep problem within their records. Patients were primarily offered no (n = 115; 57 %) or non-recommended (n = 69; 34 %) sleep treatment. More outpatients were offered no sleep treatment (n = 89; 64 %) than inpatients (n = 26; 41 %) (p = .002) whilst more inpatients were offered non-recommended sleep treatments (n = 33; 52 %) than outpatients (n = 36; 26 %) (p < .001). No significant associations were found between sleep and attendance or appointments scheduled., Conclusions: There is a lack of routine clinical attention to sleep assessment and treatment in SMI groups. Where sleep is addressed, treatment often conflicts with guidelines. Improved sleep assessment and treatment could significantly enhance current SMI patient care., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.)

Background: Sleep dysfunction is extremely common in patients with schizophrenia. Recent research indicates that sleep dysfunction may contribute to psychotic experiences such as delusions and hallucinations., Objectives: The review aims to evaluate the evidence for a relationship between sleep dysfunction and individual psychotic experiences, make links between the theoretical understanding of each, and highlight areas for future research., Method: A systematic search was conducted to identify studies investigating sleep and psychotic experiences across clinical and non-clinical populations., Results: 66 papers were identified. This literature robustly supports the co-occurrence of sleep dysfunction and psychotic experiences, particularly insomnia with paranoia. Sleep dysfunction predicting subsequent psychotic experiences receives support from epidemiological surveys, research on the transition to psychosis, and relapse studies. There is also evidence that reducing sleep elicits psychotic experiences in non-clinical individuals, and that improving sleep in individuals with psychosis may lessen psychotic experiences. Anxiety and depression consistently arise as (partial) mediators of the sleep and psychosis relationship., Conclusion: Studies are needed that: determine the types of sleep dysfunction linked to individual psychotic experiences; establish a causal connection between sleep and psychotic experiences; and assess treatments for sleep dysfunction in patients with non-affective psychotic disorders such as schizophrenia., (Copyright © 2015 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Based on murine LD(50) values, the taipans (i.e. Oxyuranus microlepidotus, Oxyuranus scutellatus and Oxyuranus scutellatus canni) are the most venomous snake genus in the world. Despite this, little is known about the toxins contained in their venoms. The aim of the present study was to isolate and characterise post-synaptic neurotoxins from the venoms of the Papuan taipan (O. s. canni) and coastal taipan (O. scutellatus), and to compare their pharmacology. A 6770Da toxin (i.e. alpha-oxytoxin 1) and a 6781Da toxin (i.e. alpha-scutoxin 1) were isolated from the venoms of O. s. canni and O. scutellatus, respectively, using reverse-phase high performance liquid chromatography. Both alpha-oxytoxin 1 (0.3-1 microM) and alpha-scutoxin 1 (0.1-1 microM) caused concentration-dependent inhibition of indirect twitches in the chick biventer cervicis nerve-muscle preparation. Contractile responses to exogenous carbachol (CCh), but not potassium chloride (KCl), were inhibited by both toxins, suggesting a post-synaptic mode of action. The inhibitory effect of alpha-oxytoxin 1 was reversed by washing. Cumulative concentration-response curves to CCh were obtained in the presence and absence of the toxins with the subsequently determined pA(2) of alpha-scutoxin 1 being 44.7-fold higher than alpha-oxytoxin 1 (i.e. 8.38+/-0.59 versus 7.62+/-0.04). The current study shows that Papuan taipan and coastal taipan venom both contain potent post-synaptic neurotoxins which exhibit different pharmacological profiles. The effect of alpha-oxytoxin 1 is atypical of most snake venom post-synaptic neurotoxins displaying a 'competitive' mode of action, whereas alpha-scutoxin 1 possesses pseudo-irreversible or non-competitive activity., (Copyright (c) 2009 Elsevier Inc. All rights reserved.)

Death adder (genus Acanthophis) venoms display neurotoxic activity but were thought to be devoid of myotoxic components. Studies from our laboratory have shown that some species (i.e. Acanthophis rugosus and Acanthophis sp. Seram) possess venom with myotoxic activity [Wickramaratna JC, Fry BG, Aguilar M, Kini RM, Hodgson WC. Isolation and pharmacological characterisation of a phospholipase A2 myotoxin from the venom of the Irian Jayan death adder (A. rugosus). Br J Pharmacol 2003;138:333-342; Wickramaratna JC, Fry BG, Hodgson WC. Species-dependent variations in the in vitro myotoxicity of death adder (Acanthophis) venoms. Toxicol Sci 2003;74:352-360]. The present study describes the isolation and characterisation of two myotoxins (acanmyotoxin-2 and acanmyotoxin-3) from A. sp. Seram venom. Venom was fractionated into approximately 12 major peaks using reverse phase high performance liquid chromatography. Two components caused concentration (0.1-1 microM) dependent inhibition of direct (2 ms, 0.1 Hz, supramaximal V) twitches and an increase in baseline tension in the chick biventer cervicis nerve-muscle. Histological examination of the muscle confirmed damage. PLA2 activity was detected in both acanmyotoxin-2 (390.2+/-19.7 micromol/(min mg); n=4) and acanmyotoxin-3 (14.2+/-7.7 micromol/(min mg); n=4). In comparison, A. sp. Seram whole venom had a specific activity of 461.3+/-90.4 micromol/(min mg) (n=3). Mass spectrometry analysis indicated acanmyotoxin-2 had a mass of 13,082 Da and acanmyotoxin-2 13,896 Da. Acanmyotoxin-2 and acanmyotoxin-3 accounted for approximately 7 and 4% of total venom composition, respectively. N-terminal sequencing of the first 30 amino acids of each toxin indicated they shared some sequence homology with known myotoxins. In conclusion, clinicians should be aware that symptoms of envenoming by some species of death adder may include signs of myotoxicity as well as neurotoxicity. Future studies will investigate the efficacy of the current antivenom treatment against the myotoxic components of A. sp. Seram venom.

The Papuan black snake (Pseudechis papuanus) is found throughout the southern coastal regions of Papua New Guinea and is thought to occur in the adjacent region of Iriyan Jaya. Neurotoxicity is a major symptom of envenomation by this species. This study describes the isolation of the first neurotoxin papuantoxin-1 from the venom of P. papuanus. Papuantoxin-1 (6738Da), which accounts for approximately 5% of the whole venom, was purified to homogeneity using successive steps of RP-HPLC. The toxin (0.3-1.0 microM) caused concentration dependent inhibition of indirect twitches (0.1 Hz, 0.2 ms and supramaximal V) and inhibited the responses to nicotinic agonists in the chick biventer cervicis nerve-muscle preparation, indicating a postsynaptic mode of action. However, papuantoxin-1 displayed no signs of myotoxicity. Papuantoxin-1 displayed pseudo-irreversible antagonism of cumulative concentration-response curves to carbachol at the skeletal muscle nicotinic receptors with an estimated pA2 value of 6.9+/-0.3. CSL black snake antivenom, which is raised against the venom of the Australian black snake Pseudechis australis, appears to be effective in reversing the effects of papuantoxin-1. Thus, black snake antivenom should be considered for the treatment of the neurotoxic effects following envenomation by the Papaun black snake.