This investigation reports the possible role of the endocannabinoid anandamide in modulating appetitive behaviour. Given that cannabinoids have been used clinically to stimulate appetite in HIV and cancer chemotherapy patients, there has been a renewed interest in the involvement of cannabinoids in appetite modulation. This is the ®rst report on the administration of anandamide into the ventromedial hypothalamus. Pre-satiated rats received an intrahypothalamic injection of anandamide (50 ng 0.5 ml 71 ) followed by measurement of food intake at 3 h post injection. Administration of anandamide induced signi®cant hyperphagia. Pretreatment with the selective CB 1 cannabinoid antagonist SR 141716 (30 mg 0.5 ml 71 ), 30 min prior to anandamide injection resulted in an attenuation of the anandamide-induced hyperphagia (P50.001). This study demonstrates that intrahypothalamic anandamide initiates appetite by stimulation of CB 1 receptors, thus providing evidence on the involvement of hypothalamic endocannabinoids in appetite initiation.

Screening and assessment (Chapter 2): screening techniques to identify patients with alcohol problems, and subsequent assessments for clinicians to undertake before providing specific treatments or interventions.• Interventions, treatments, relapse prevention and aftercare (Chapter 3): a range of varying interventions and treatments, including brief interventions, brief e-health interventions, psychosocial interventions, alcohol withdrawal management, pharmacotherapy options, and peer support programs. In the final section of this chapter, relapse prevention, aftercare, and long term follow-up strategies are discussed.• Considerations for specific populations (Chapter 4): the management of alcohol problems and treatment considerations for specific population groups of interest in Australia -genderspecific considerations, adolescents and young people, pregnant and breastfeeding women, Aboriginal and Torres Strait Islander peoples, culturally and linguistically diverse groups, sexually diverse and gender diverse populations, older people, and cognitively impaired people.• Understanding comorbidities (Chapter 5): the importance of considering a range of comorbidities when providing treatment for alcohol problems. Polydrug use, comorbid mental disorders, and physical-related comorbidities are discussed.The content of this supplement is based on the various chapters of the full Guidelines for the Treatment of Alcohol Problems, which were based on reviews of the evidence, including well designed meta-analyses and randomised controlled trials, wherever possible. Where this evidence was not available, recommendations were based on the best available research or clinical experience. Each recommendation in the guidelines is accompanied with a level of evidence based on National Health and Medical Research Council evidence recommendations (Box 2), 21 with "A" representing the most evidence and "GPP" (good practice point) indicating a recommendation with no evidence.For more on the Guidelines for the Treatment of Alcohol Problems, visit https://alcoh oltre atmen tguid elines.com.au/. Acknowledgements:The Guidelines for the Treatment of Alcohol Problems project was funded by the Australian Government, under the Drug and Alcohol Program. We would like to express our gratitude to members of the Guidelines Steering Committee for providing invaluable guidance and advice on this project. We thank Daniel Winter, Sophia Little, Brennan Geiger and James Pham for providing research and administrative support, and Joshua Watt for providing clinical support, across sections of this supplement. Finally, we thank Donna Ah Chee, Kylie Lee, Teagan Weatherall, Craig Holloway and Martin Nean for conversations and work which informed the Aboriginal and Torres Strait Islander peoples section in the guidelines and Chapter 4 of this supplement.Competing interests: Paul Haber has been funded by the Lambert Initiative for Cannabinoid Therapeutics at the University of Sydney to undertake clinical trials of cannabinoid treatment for alcohol withdra...

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Drugs can cause dysregulation of the hypothalamic-pituitary-adrenal axis which can result in a rise in core temperature. This type of hyperthermia is unresponsive to antipyretics and can be complicated by rhabdomyolysis, multi-organ failure and disseminated intravascular coagulation. Organic causes of fever such as infection must be ruled out. Syndromes associated with druginduced fever include neuroleptic malignant syndrome and anticholinergic, sympathomimetic and serotonin toxicity. The class of offending drugs, as well as the temporal relationship to starting or stopping them, assists in differentiating between neuroleptic malignant syndrome and serotonin toxicity. Immediate inpatient management is needed. The mainstay of management is stopping the drug, and supportive care often in the intensive care unit. The hot patient: acute drug-induced hyperthermia serotonergic drugs (especially when taken in combination), sympathomimetic drugs, anaesthetics and drugs with anticholinergic properties (Table 1). Non-drug-induced causes of hyperthermia There are numerous causes of complicated hyperthermia that are not due to drug exposure (Table 2). Non-drug causes should always be considered and excluded. Lethal catatonia (which can develop over weeks), central nervous system lesions or infections, and tetanus can all cause hyperthermia associated with muscle rigidity. The diagnosis is based on the history and clinical picture. Thyrotoxicosis and phaeochromocytoma should be considered in the differential diagnosis of hyperthermia. However, they are rarely associated with muscle rigidity.

Background: Accidental ingestion or consumption of supra-therapeutic doses of methadone can result in neurological sequelae in humans. We aimed to determine the neurological deficits of methadone-poisoned patients admitted to a referral poisoning hospital using brain magnetic resonance (MR) and diffusion weighted (DW) imaging. Methods: In this retrospective study, brain MRIs of the patients admitted to our referral center due to methadone intoxication were reviewed. Methadone intoxication was confirmed based on history, congruent clinical presentation, and confirmatory urine analysis. Each patient had an MRI with Echo planar T1, T2, FLAIR, and DWI and apparent deficient coefficient (ADC) sequences without contrast media. Abnormalities were recorded and categorized based on their anatomic location and sequence. Results: Ten patients with abnormal MRI findings were identified. Eight had acute-and two had delayed-onset encephalopathy. Imaging findings included bilateral confluent or patchy T2 and FLAIR high signal intensity in cerebral white matter, cerebellar involvement, and bilateral occipito-parietal cortex diffusion restriction in DWI. Internal capsule involvement was identified in two patients while abnormality in globus pallidus and head of caudate nuclei were reported in another. Bilateral cerebral symmetrical confluent white matter signal abnormality with sparing of subcortical U-fibers on T2 and FLAIR sequences were observed in both patients with delayed-onset encephalopathy. Conclusions: Acute-and delayed-onset encephalopathies are two rare adverse events detected in methadoneintoxicated patients. Brain MRI findings can be helpful in detection of methadone-induced encephalopathy.