Thoracic outlet syndrome comprises a group of disorders that result in compression of the brachial plexus and subclavian vessels exiting the thoracic outlet. Symptoms include pain, paresthesia, pallor, and weakness depending upon the compromised structures. While consensus in diagnostic criteria has not yet been established, a thorough patient history, physical exam, and appropriate imaging studies are helpful in diagnosis. General first-line therapy for thoracic outlet syndrome is a conservative treatment, and may include physical therapy, lifestyle modifications, NSAIDs, and injection therapy of botulinum toxin A or steroids. Patients who have failed conservative therapy are considered for surgical decompression. This article aims to review the epidemiology, etiology, relevant anatomy, clinical presentations, diagnosis, and management of thoracic outlet syndrome.

Purpose of Review: This is a comprehensive review of the association between cannabis use and psychological disorders. It reviews the latest and seminal evidence that is available and attempts to conclude the strength of such association. Recent Findings: Cannabis is a flowering plant with psychoactive properties, attributed to cannabinoids that naturally occur within the plant. These act through the CB1 and CB2 receptors to inhibit GABA and glutamate release, as well through other forms of neuromodulation through the modulation of the endocannabinoid system (eCBs); a system that is otherwise involved in different pathways, including reward, memory, learning, and pain. Recent societal changes have increased the use of both medical and recreational cannabis. Patients with mental illness are considered more vulnerable and are prone to reward-seeking behavior. Cannabis use disorder (CUD) has been shown to have an increased prevalence in individuals with mental illness, creating an explosive cocktail. Approximately 1 in 4 patients with schizophrenia are also diagnosed with CUD. Cannabis use is associated with 2–4 times the likelihood of developing psychosis in healthy individuals. It has also been associated with multiple poor prognostic factors in schizophrenia, as well as in patients with a history of psychosis who do not meet diagnostic criteria for schizophrenia. Cannabis has been linked with anxiety; THC has been shown to elicit anxiety; however, anxiety is also a trigger for cannabis use. However, a recent large meta-analysis did not find a convincing link between cannabis and anxiety. This was reiterated in a recent epidemiological study that did not find such a correlation; however, it did identify a link between cannabis use, substance disorder, alcohol use disorder, drug use disorder, and nicotine dependence. Similarly, contradicting data exists regarding the link of depression and cannabis use. Summary: Cannabis use is increasing with recent societal shifts; however, its interaction with mental health is less well understood. CUD is highly prevalent in individuals with mental health disorders, especially those with other substance abuse disorders. There is evidence to support that cannabis use may trigger and worsen psychosis and schizophrenia. The link with depression and anxiety is less clear and needs further investigation. Personality disorder is linked with substance use disorder and shares similar risk factors with CUD.

Purpose of Review: This comprehensive review discusses the adverse effects known today about marijuana, for either medical or recreational use. It reviews the role of cannabis in the treatment of chronic pain, cognitive and neurological adverse effects, special cases and addiction. Recent Findings: Cannabinoids work through the endocannabinoids system and inhibit the release of GABA and glutamate in the brain, impact neuromodulation, as well as dopamine, acetylcholine and norepinephrine release. They affect reward, learning and pain. The use of cannabis is increasing nationally and world-wide for both recreational and medicinal purposes, however, there is relatively only low quality evidence to the efficacy and adverse effects of this. Cannabis and its derivatives may be used for treatment of chronic pain. They are via CB1 receptors that are thought to modulate nociceptive signals in the brain. CB2 receptors in the DRG likely affect pain integration in the afferent pathways, and peripherally CB2 also affects noradrenergic pathways influencing pain. A large proportion of users may see more than 50% of chronic pain alleviation compared with placebo. Cannabis affects cognition, most notably executive function, memory and attention, and may deteriorate the boundary between emotional and executive processing. Cannabis impairs memory in the short run, which become more significant with chronic use, and may also be accompanied by poorer effort, slower processing and impacted attention. It is generally believed that long-term use and earlier age are risk factor for neurocognitive deficits; neuroimaging studies have shown reduced hippocampal volume and density. Executive functions and memory are worse in adolescent users versus adults. Cannabis addiction is different and likely less common than other addictive substances, but up to 10% of users meet criteria for lifetime cannabis dependence. Addiction patterns may be linked to genetic and epigenetic differences. It is still unclear whether abstinence reverses patterns of addiction, and more research is required into this topic. Summary: Cannabis use has become more abundant for both medical and recreational use. It carries likely benefits in the form of analgesia, anti-emesis and improved appetite in chronic patients. The evidence reviewing adverse effects of this use are still limited, however, exiting data points to a clear link with neurocognitive deterioration, backed by loss of brain volume and density. Addiction is likely complex and variable, and no good data exists to support treatment at this point. It is becoming clear that use in earlier ages carries a higher risk for long-term deficits. As with any other drug, these risks should be considered alongside benefits prior to a decision on cannabis use.

Spondylolisthesis refers to the anterior, lateral, or posterior slippage of a superior vertebral disc over the adjacent inferior disc, and is often separated into categories based on the causative etiology. Spondylolisthesis is often asymptomatic but may present with low back pain and neurogenic claudication which is worsened with spinal extension and activity. A detailed history and physical exam, along with appropriate imaging tests are useful in making the diagnosis. Conservative therapy is first-line and includes pain management with physical therapy. Patients who fail conservative therapy may consider surgical decompression, stabilization, and fusion. This review aims to discuss the epidemiology, pathophysiology, presentation, and treatment options of spondylolisthesis.