31 research outputs found

    Cannabis-based medicinal products (CBMPs) for the treatment of Long COVID symptoms: current and potential applications

    Get PDF
    Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection can result in a range of persistent symptoms impacting everyday functioning for a considerable proportion of patients, a condition termed Long coronavirus disease (COVID) or post COVID-19 syndrome. The severity and set of symptoms vary between patients, and include fatigue, cognitive dysfunction, sleep disturbances, palpitations, tachycardia, pain, depression, and anxiety. The high prevalence of Long COVID combined with the lack of treatment approaches has resulted in considerable unmet clinical needs. There is a growing body of evidence that cannabis-based medicinal products (CBMPs) can be used to treat symptoms including pain, anxiety, depression, fatigue, sleep, headaches, and cognitive dysfunction, which are commonly reported in Long COVID. This article provides an overview of the pathophysiology of Long COVID and discusses preliminary pre-clinical, clinical trials, and real-world evidence (RWE) for CBMPs in the context of Long COVID. This review summarises current clinical trials and studies exploring CBMPs in Long COVID. The current evidence provides a rationale to further explore CBMPs as a treatment for Long COVID symptoms. In addition to further randomised controlled trials (RCTs), the increasing availability of CBMPs globally, coupled with the continued prevalence of Long COVID in the population, also highlights the value of real-world data in the research of CBMPs in Long COVID. Critically, there is an evident need for multidisciplinary approaches of CBMPs and Long COVID in real-world clinical practice settings

    The anticonvulsant actions of novel ’broad-spectrum’ Ca2+ channel blockers and low affinity, uncompetitive NMDA receptor antagonists

    No full text
    Epilepsy is a prominent neurological disorder. Presently available anticonvulsant drugs however fail to alleviate seizures in approximately 25% of individuals, and are often accompanied by serious side effects. More efficacious and less toxic agents are required. In this study, the effects of a range of structurally dissimilar a site ligands were examined against evoked and spontaneous epileptiform activity induced in rat hippocampal slices by perfusion with Mg2+-free medium. Extracellular recordings were made in the CA1 hippocampal region of epileptiform activity evoked by stimulation of the Schaffer collateral (SC) pathway, and of spontaneous epileptiform activity originating from the CA3 hippocampal region. Evoked and spontaneous epileptiform activity was inhibited by all compounds tested with the rank order (IC5 0 values against evoked epileptiform activity in uM): dextrorphan (2) > ifenprodil (6) > dextromethorphan (10) > l,3-di(2-tolyl)guanidine (15) > loperamide (28) > carbetapentane (38) > caramiphen (46) > opipramol (52). Ifenprodil, loperamide, caramiphen and dextrorphan were also examined for their effects on the input/output (I/O) functions along the SC pathway and on the paired pulse facilitation (PPF) ratio. An effect was observed only in the presence of caramiphen, which showed a decrease in the synaptic transmission I/O function and reduced markedly the PPF ratio. The (micromolar) concentrations required for the anticonvulsant activity of the CT ligands tested suggests that their anticonvulsant actions are not mediated by high affinity (nanomolar) binding to rj binding sites, but rather to blockade of high voltage activated Ca2 + channels and/or NMD A receptors, actions which occur at micromolar concentrations.Medicine, Faculty ofGraduat
    corecore