Restless Leg Syndrome in the Setting of Patients With End-Stage Renal Disease on Hemodialysis: A Literature Review.

Restless Leg Syndrome (RLS), or Willis-Ekbom disease (WED), is an irresistible urge to move the legs, predominantly while resting, sitting, or sleeping, which disrupts sleep and impairs quality of life. RLS can occur secondary to uremia in chronic kidney disease (CKD) patients due to inadequate hemodialysis. Early diagnosis is essential to prevent muscular atrophy and to improve the quality of life of RLS patients, especially those with end-stage renal disease (ESRD). Cardiac mortality high in uremic RLS patients due to associated discomfort and lowering the duration of hemodialysis treatment. This review focuses on and discusses the diagnosis, treatment, and associated comorbid conditions of uremic RLS. Though the exact pathophysiology is unknown, altered transferrin expression in the choroid plexus, increased glutamate levels in the thalamus, decreased opioid receptors, dopamine system dysfunction, calcium/phosphate imbalance, and single nucleotide polymorphisms in the BTBD9 and MEIS1 genes are a few nonconfirmatory pathophysiological concepts for uremic RLS. Nonpharmacological options include lowering the temperature of dialysate by 1 degree C and home-based therapies like massages, warm/cold baths, and aerobic exercises. Pharmacological therapy like dopamine agonists ropinirole and pramipexole reduces the symptoms effectively. However, surgical options like parathyroidectomy and renal transplantation are stated as the best treatment options in patients suffering from uremic RLS.

Probability of COVID-19 Being the Culprit in Neurocognitive Deception: A Case Series of Incidental Strokes in ICU Patients With COVID-19.

The coronavirus disease 2019 (COVID-19) pandemic caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus, originated in Wuhan, China, and spread rapidly throughout the world, infecting millions and killing thousands. Although some patients have mild or even asymptomatic responses to this infection, hospitalized patients present with symptoms such as fever, cough, and difficulty breathing. Some patients have a severe response to the insult and experience rapid progression to acute respiratory distress and multiorgan failure. Furthermore, many patients developed complications due to this infection. Here, we present three patients who had strokes during their hospitalization for COVID-19 pneumonia.

Neuroprotective and Neurodegenerative Aspects of Coffee and Its Active Ingredients in View of Scientific Literature.

Coffee and its components have several neuroprotective properties that lower the risk of cognitive decline and other neurodegenerative diseases. This study reviews the mechanisms by which coffee and its respective compounds affect the brain and its pathologies. Many epidemiological studies in this literature review have shown coffee to reduce the risk of developing dementia, stroke, and Alzheimer's disease. It may also have a positive impact on the disease course of amyotrophic lateral sclerosis, Parkinson's disease, and depression. The optimal benefits achieved from coffee in these pathologies rely on higher daily doses. Most of its effects are attributed to caffeine by the antagonism of adenosine receptors in the central nervous system; however, other coffee constituents like chlorogenic acids have also shown much promise in therapeutic value. Existing research considers coffee to have great potential, but additional studies are still needed to clarify the mechanisms and actual causal relationships in certain neuropathologies.

Mechanisms of Beta-Blocker Induced Psoriasis, and Psoriasis De Novo at the Cellular Level.

Beta-blockers are a commonly prescribed medication, but the increase in use goes hand in hand with increasing side effects; one of particular interest lately has been its dermatological reactions. Although rare, beta-blockers can exacerbate pre-existing psoriasis and also cause de novo psoriasis in patients naïve to the disease. The mechanism by which this occurs is still unclear, although numerous articles have been published throughout the years as to how this unusual effect takes place. The most common mechanism suggests that beta-blockers cause intracellular changes in calcium, affecting both keratinocyte proliferation and granulocyte function via decreased cyclic adenosine monophosphate (cAMP) levels. Several inflammatory mediators are known to play a role, as well as reduced expression and desensitization of the beta-adrenergic receptor itself. We discuss these posed pathways in-depth and how each contributes to the worsening or formation of new psoriasis. With this knowledge, future physicians may be more mindful of this side effect should it occur, and why they occur, to better manage our patients on this widely used medication.