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Depression is the most prevalent psychiatric disorder in the world, affecting 4.4% of the global population. Despite an array of treatment modalities, depressive disorders remain difficult to manage due to many factors. Beginning with the introduction of fluoxetine to the United States in 1988, selective serotonin reuptake inhibitors (SSRIs) quickly became a mainstay of treatment for a variety of psychiatric disorders. The primary mechanism of action of SSRIs is to inhibit presynaptic reuptake of serotonin at the serotonin transporter, subsequently increasing serotonin at the postsynaptic membrane in the serotonergic synapse. The six major SSRIs that are marketed in the USA today, fluoxetine, citalopram, escitalopram, paroxetine, sertraline, and fluvoxamine, are a group of structurally unrelated molecules that share a similar mechanism of action. While their primary mechanism of action is similar, each SSRI has unique pharmacokinetics, pharmacodynamics, and side effect profile. One of the more controversial adverse effects of SSRIs is the black box warning for increased risk of suicidality in children and young adults aged 18–24. There is a lack of understanding of the complexities and interactions between SSRIs in the developing brain of a young person with depression. Adults, who do not have certain risk factors, which could be confounding factors, do not seem to carry this increased risk of suicidality. Ultimately, when prescribing SSRIs to any patient, a risk–benefit analysis must factor in the potential treatment effects, adverse effects, and dangers of the illness to be treated. The aim of this review is to educate clinicians on potential adverse effects of SSRIs.

Benzodiazepines (BZDs) are among one of the most widely prescribed drug classes in the United States. BZDs are a class of psychoactive drugs known for their depressant effect on the central nervous system (CNS). They quickly diffuse through the blood–brain barrier to affect the inhibitory neurotransmitter GABA and exert sedative effects. Related to their rapid onset and immediate symptom relief, BZDs are used for those struggling with sleep, anxiety, spasticity due to CNS pathology, muscle relaxation, and epilepsy. One of the debilitating side effects of BZDs is their addictive potential. The dependence on BZDs generally leads to withdrawal symptoms, requiring careful tapering of the medication when prescribed. Regular use of BZDs has been shown to cause severe, harmful psychological and physical dependence, leading to withdrawal symptoms similar to that of alcohol withdrawal. Some of these withdrawal symptoms can be life threatening. The current treatment for withdrawal is through tapering with clonazepam. Many drugs have been tested as a treatment for withdrawal, with few proving efficacious in randomized control trials. Future research is warranted for further exploration into alternative methods of treating BZD withdrawal. This call to action proves especially relevant, as those seeking treatment for BZD dependence and withdrawal are on the rise in the United States.

Thoracic outlet syndrome, a group of diverse disorders, is a collection of symptoms in the shoulder and upper extremity area that results in pain, numbness, and tingling. Identification of thoracic outlet syndrome is complex and a thorough clinical examination in addition to appropriate clinical testing can aide in diagnosis. Practitioners must consider the pathology of thoracic outlet syndrome in their differential diagnosis for shoulder and upper extremity pain symptoms so that patients are directed appropriately to timely therapeutic interventions. Patients with a definitive etiology who have failed conservative management are ideal candidates for surgical correction. This manuscript will discuss thoracic outlet syndrome, occurrence, physical presentation, clinical implications, diagnosis, and management.

Catatonia is a syndrome that has been associated with several mental illness disorders but that has also presented as a result of other medical conditions. Schizophrenia and other psychiatric disorders such as mania and depression are known to be associated with catatonia; however, several case reports have been published of certain medical conditions inducing catatonia, including hyponatremia, cerebral venous sinus thrombosis, and liver transplantation. Neuroleptic Malignant Syndrome and anti-NMDA receptor encephalitis are also prominent causes of catatonia. Patients taking benzodiazepines or clozapine are also at risk of developing catatonia following the withdrawal of these medications—it is speculated that the prolonged use of these medications increases gamma-aminobutyric acid (GABA) activity and that discontinuation may increase excitatory neurotransmission, leading to catatonia. The treatment of catatonia often involves the use of benzodiazepines, such as lorazepam, that can be used in combination therapy with antipsychotics. Definitive treatment may be found with electroconvulsive therapy (ECT). Aberrant neuronal activity in different motor pathways, defective neurotransmitter regulation, and impaired oligodendrocyte function have all been proposed as the pathophysiology behind catatonia. There are many clinical challenges that come with catatonia and, as early treatment is associated with better outcomes, it becomes imperative to understand these challenges. The purpose of this manuscript is to provide an overview of these challenges and to look at clinical studies regarding the pathophysiology, diagnosis, and treatment of as well as the complications and risk factors associated with catatonia.

Purpose of Review Enhanced recovery pathways are a multimodal, multidisciplinary approach to patient care that aims to reduce the surgical stress response and maintain organ function resulting in faster recovery and improved outcomes. Recent Findings A PubMed literature search was performed for articles that included the terms of metabolic surgical stress response considerations to improve postoperative recovery. The surgical stress response occurs due to direct and indirect injuries during surgery. Direct surgical injury can result from the dissection, retraction, resection, and/or manipulation of tissues, while indirect injury is secondary to events including hypotension, blood loss, and microvascular changes. Greater degrees of tissue injury will lead to higher levels of inflammatory mediator and cytokine release, which ultimately drives immunologic, metabolic, and hormonal processes in the body resulting in the stress response. These processes lead to altered glucose metabolism, protein catabolism, and hormonal dysregulation among other things, all which can impede recovery and increase morbidity. Fluid therapy has a direct effect on intravascular volume and cardiac output with a resultant effect on oxygen and nutrient delivery, so a balance must be maintained without excessively loading the patient with water and salt. All in all, attenuation of the surgical stress response and maintaining organ and thus whole-body homeostasis through enhanced recovery protocols can speed recovery and reduce complications. Summary The present investigation summarizes the clinical application of enhanced recovery pathways, and we will highlight the key elements that characterize the metabolic surgical stress response and improved postoperative recovery.

Introduction: Attention Deficit Hyperactivity Disorder (ADHD) is one of the most common neurodevelopmental disorders, characterized by the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), which is marked by symptoms such as inappropriate levels of inattention, hyperactivity, and impulsivity that can affect academic, social, and personal functioning in children and adolescents. This review summarizes clinical trials demonstrating the effectiveness of Alpha-2 agonists in reducing symptoms of inattention, hyperactivity, and impulsivity in children with ADHD. Studies were identified through a systematic search of PubMed and Cochrane databases. However, these medications’ long-term safety and efficacy remain uncertain, with a lack of data on their effects on growth, cardiovascular function, and other adverse events. Further studies are required to determine these medications’ optimal dose and treatment duration. Methods: Medications that target the noradrenergic system, such as Alpha-2 agonists, have been increasingly used as a treatment option for ADHD, with guanfacine and clonidine being two of the most commonly used medications. They function by selectively targeting Alpha-2 adrenergic receptors in the brain leading to improved attention and reduced hyperactivity and impulsivity symptoms in children with ADHD. Results: Clinical trials have demonstrated the effectiveness of Alpha-2 agonists in treating ADHD in children by reducing symptoms of inattention, hyperactivity, and impulsivity. However, these medications’ long-term safety and efficacy still need to be completely understood. Due to a lack of information on the effects of Alpha-2 agonists on growth, cardiovascular function, and other long-term adverse events, more studies must investigate the optimal dose and treatment duration for these medications. Conclusions: Despite these concerns, Alpha-2 agonists remain a valuable treatment option for ADHD in children, especially those unable to tolerate stimulant medications or who have coexisting conditions such as tic disorders. Future research should continue to explore the safety and efficacy of Alpha-2 agonists in the long term. In conclusion, Alpha-2 agonists show promise as a treatment for ADHD in children; however, the safety and efficacy of these drugs in the long term are not yet completely understood. Additional studies are required to investigate the optimal dose and treatment duration for these medications in their use as a treatment for this debilitating disease.

Depression is a leading cause of disability globally, with a prevalence of 3.8% among the whole population, 5% of the adult population, and 5.7% of the elderly population over 60 years of age. There is evidence that depression is linked to certain neurodegenerative diseases, one being Alzheimer’s disease (AD). The efficacy of conventional antidepressants to treat depression in AD is conflicting, especially regarding selective serotonin reuptake inhibitors (SSRIs). A recent systemic review and meta-analysis of 25 randomized controlled trials including fourteen antidepressant medications showed no high efficacy in treating AD patients’ symptoms. However, ketamine, a nonselective N-methyl-D-aspartate (NMDA) receptor antagonist, can mediate a wide range of pharmacological effects, including neuroprotection, anti-inflammatory and anticancer properties, multimodal analgesia, and treatment of depression, suicidal attempts, and status epilepticus. Esketamine, which is ketamine formulated as a nasal spray, was approved by the Federal Drug Administration (FDA) in March 2019 as an adjuvant drug to treat treatment-resistant depression. NMDA receptor antagonists treat AD through offsetting AD-related pathological stimulation of subtypes of glutamate receptors in the central nervous system. Recent clinical findings suggest that ketamine may provide neuroprotection and reduce neuropsychiatric symptoms associated with AD. In the present investigation, we evaluate the potential role of ketamine and its postulated mechanism in AD management.

Telemedicine, telehealth, and E-health all offer significant benefits for pain management and healthcare services by fostering the physician–patient relationship in otherwise challenging circumstances. A critical component of these artificial-intelligence-based health systems is the “agent-based system”, which is rapidly evolving as a means of resolving complicated or straightforward problems. Multi-Agent Systems (MAS) are well-established modeling and problem-solving modalities that model and solve real-world problems. MAS’s core concept is to foster communication and cooperation among agents, which are broadly considered intelligent autonomous factors, to address diverse challenges. MAS are used in various telecommunications applications, including the internet, robotics, healthcare, and medicine. Furthermore, MAS and information technology are utilized to enhance patient-centered palliative care. While telemedicine, E-health, and MAS all play critical roles in managing chronic pain, the published research on their use in treating chronic pain is currently limited. This paper discusses why telemedicine, E-health, and MAS are the most critical novel technologies for providing healthcare and managing chronic pain. This review also provides context for identifying the advantages and disadvantages of each application’s features, which may serve as a useful tool for researchers.

Purpose of Review Regenerative medicine through interventional pain procedures is evolving with data demonstrating efficacy for a number of pain states in recent years. Platelet-rich plasma (PRP), defined as a sample of plasma with a platelet concentration 3 to 5 times greater than the physiologic platelet concentration found in healthy whole blood, releases bioactive proteins which can restore anatomical function in degenerative states. PRP is dense in growth factors, such as platelet-derived growth factor, transforming growth factor-beta1, basic fibroblastic growth factor, vascular endothelial growth factor, and epidermal growth factors. Recent Findings To date, well-designed case–control or cohort studies for the use of PRP have demonstrated efficacy in lumbar facet joint, lumbar epidural, and sacroiliac joint injections. At present, there is only level IV evidence indicating the need for larger and more carefully controlled prospective studies. PRP is utilized autogenously in order to facilitate healing and injection and has been studied in the long-term management of discogenic low back pain. In this regard, numerous studies have evaluated PRP to steroid injections in chronic pain states with favorable results. Summary PRP represents an opportunity for a new strategy in the therapeutic treatment of degenerative states of spines, joints, and other locations throughout the body with evolving data demonstrating both safety and long-term efficacy.

Warfarin administration poses a notable challenge in clinical practice due to the increased susceptibility of patients to major bleeding, particularly when co-administered with other medications capable of modulating its metabolic pathways. Among these medications, antibiotics have been recognized as potential agents that can either induce or inhibit cytochrome P450-2C9, thereby impacting the effects of warfarin. A wealth of evidence from numerous studies consistently supports an elevated risk of serious bleeding in patients concurrently receiving antibiotics and warfarin therapy. This narrative review elucidates the intricate interactions between warfarin and various antibiotic classes. Notably, significant increases in the International Normalized Ratio (INR) were observed among warfarin-treated patients receiving penicillin derivatives, fluoroquinolones, TMP-SMX, and macrolides. Conversely, investigations have also demonstrated a reduction in INR levels in patients on warfarin when exposed to rifampin, a potent inducer of cytochrome P-450. Intriguingly, cephalosporin antibiotics and amoxicillin/clavulanate, despite not interfering with the cytochrome P450 system, exhibited a positive association with increased INR values. The findings of this narrative review underscore the importance of diligent monitoring in patients on warfarin requiring concomitant antibiotic therapy, as this surveillance strategy proves pivotal in mitigating the risk of major bleeding complications. Additionally, for patients necessitating cytochrome P450 inhibitors such as penicillin derivatives, fluoroquinolones, TMP-SMX, and macrolides, the consideration of dose reduction in warfarin therapy may confer substantial benefits in reducing the occurrence of major bleeding events. Similarly, patients who are co-administered rifampin alongside warfarin necessitate vigilant monitoring, with a potential need for escalating warfarin doses to counteract the risk of a hypercoagulable state.