How to Trip Rapid Review

Step 1: Select articles relevant to your search (remember the system is only optimised for single intervention studies)

Step 2: press

Step 3: review the result, and maybe amend the or if you know better! If we're unsure of the overall sentiment of the trial we will display the conclusion under the article title. We then require you to tell us what the correct sentiment is.

21,769 results for

Neurotransmitter Physiology

by
...
Latest & greatest
Alerts

Export results

Use check boxes to select individual results below

SmartSearch available

Trip's SmartSearch engine has discovered connected searches & results. Click to show

142. Male Sexual Dysfunction

of recommendations. Bmj, 2008. 336: 924. 23. Phillips, B. Oxford Centre for Evidence-based Medicine Levels of Evidence. Updated by Jeremy Howick March 2009. 1998. 24. Guyatt, G.H., et al. Going from evidence to recommendations. Bmj, 2008. 336: 1049. 25. Van den Broeck T, et al. What are the benefits and harms of testosterone treatment for male sexual dysfunction? PROSPERO: International prospective register of systematic reviews, 2015. 26. Gratzke, C., et al. Anatomy, physiology, and pathophysiology of erectile (...) -onset hypogonadism in males: ISA, ISSAM, EAU, EAA, and ASA recommendations. Eur Urol, 2009. 55: 121. 147. Khera, M., et al. A new era of testosterone and prostate cancer: from physiology to clinical implications. Eur Urol, 2014. 65: 115. 148. Corona, G., et al. Cardiovascular risk associated with testosterone-boosting medications: a systematic review and meta-analysis. Expert Opin Drug Saf, 2014. 13: 1327. 149. Baillargeon, J., et al. Risk of Myocardial Infarction in Older Men Receiving Testosterone

2019 European Association of Urology

146. Male Sexual Dysfunction

of recommendations. Bmj, 2008. 336: 924. 23. Phillips, B. Oxford Centre for Evidence-based Medicine Levels of Evidence. Updated by Jeremy Howick March 2009. 1998. 24. Guyatt, G.H., et al. Going from evidence to recommendations. Bmj, 2008. 336: 1049. 25. Van den Broeck T, et al. What are the benefits and harms of testosterone treatment for male sexual dysfunction? PROSPERO: International prospective register of systematic reviews, 2015. 26. Gratzke, C., et al. Anatomy, physiology, and pathophysiology of erectile (...) -onset hypogonadism in males: ISA, ISSAM, EAU, EAA, and ASA recommendations. Eur Urol, 2009. 55: 121. 147. Khera, M., et al. A new era of testosterone and prostate cancer: from physiology to clinical implications. Eur Urol, 2014. 65: 115. 148. Corona, G., et al. Cardiovascular risk associated with testosterone-boosting medications: a systematic review and meta-analysis. Expert Opin Drug Saf, 2014. 13: 1327. 149. Baillargeon, J., et al. Risk of Myocardial Infarction in Older Men Receiving Testosterone

2018 European Association of Urology

150. Antidepressant Withdrawal Syndrome

of several neurotransmitters that can lead to many downstream physiological consequences. When drug treatment stops, the body’s adaptive changes take time to recalibrate, resulting in a period of possible symptoms. 5 Clinical Features • Symptoms usually appear within a few days of stop- ping, or dose reduction. • Symptoms include anxiety, crying, dizziness, head- ache, increased dreaming, insomnia, irritability, myoc- lonus, nausea, electric shocks (zaps), tremor, flu-like symptoms, imbalance

2018 Therapeutics Letter

151. Consensus Guidelines on the Use of Intravenous Ketamine Infusions for Chronic Pain Full Text available with Trip Pro

pharmacological sources as an “anesthetic agent,” being able to induce general anesthesia and ablate protective airway reflexes. Consequently, most hospitals prohibit its use as a “bolus” by nonanesthesiologists, and many require an anesthetist to oversee its use in any context. Yet, similar to other drugs used in anesthesia, the physiological effects are dose related, which has led to variations in policies. The surge in use; lack of large-scale, methodologically sound studies to guide treatment; and absence (...) channel whose major endogenous agonist is glutamate, the predominant excitatory neurotransmitter in the CNS. When this receptor is inhibited, decreased neuronal activity ensues. Activation of the NMDA channel plays a major role in cognition, chronic pain, opioid tolerance, and mood regulation and is considered the principal receptor involved in phenomena of central sensitization and windup. Although some studies suggest a role for peripheral mechanisms in the analgesic effect of ketamine, reviews have

2018 American Society of Regional Anesthesia and Pain Medicine

152. Position Paper for the Treatment of Nightmare Disorder in Adults

the neurotransmitters norepinephrine, serotonin, and dopamine can produce nightmares. The withdrawal of REM-suppressing agents and drugs which affect gamma-aminobutyric acid (GABA) and acetylcholine may also be associated with nightmares. It is not known if there is any long-term impact on nightmares after removal of the offending drug. Finally, it is unclear if a common pathophysiology underlies the different types of nightmares. A practical review of various treatments requires an ability to assess outcomes (...) . No side effects were mentioned but there was a 26% dropout rate which the authors assert is within the typical range for trauma-related therapies. A second 6-month RCT from the same author assessed the use of ERRT in 47 civilian subjects diagnosed with nightmare disorder. Nightmares were assessed with the Trauma Related Nightmare Survey. The study also evaluated additional measures of mental and physical health, quality of life, and measures of nightmare-related physiological reactivity. Subjects were

2018 American Academy of Sleep Medicine

153. CRACKCast E151 – Antidepressants

discontinuation of the offending agent, and benzodiazepines. Rosens in Perspective I like the little trip down memory lane here! Fun medical history tidbit – the class of antidepressants we know as monoamine oxidase inhibitors (MAOI) came from the anecdotal findings that patients treated for TB with isoniazid and iproniazid (which inhibit MAO) had improved mood symptoms. Therefore, there was the formation of the >60 year old theory that depression stems from an imbalance of monoamine neurotransmitters (eg (...) is located on the outer mitochondrial membrane Responsible for breakdown of cytoplasmic catecholamines and other neurotransmitters (epinephrine, norepinephrine, dopamine, serotonin and tyramine) Monoamine oxidase type A (MAO-A) breaks down serotonin and norepinephrine Monoamine oxidase type B (MAO-B) breaks down phenylethylamine. Tyramine and dopamine are metabolized equally by both MAO A & B Most tissues contain both isozymes MAO-A = primarily placenta / sympathetic nerve terminals / intestinal mucosa

2018 CandiEM

154. Methamphetamine (Canadian Drug Summary)

and more rapid physiological response. Some amphetamines are prescribed in Canada for attention-deficit hyperactivity disorder (ADHD) and narcolepsy (e.g., Adderall and Vyvanse®), but methamphetamine use is currently illegal. Methamphetamine is often made in illegal, clandestine laboratories with commonly available, inexpensive chemicals, such as ephedrine and pseudoephedrine, found in medications, among other sources. The use of these medications as precursor chemicals for methamphetamine led (...) or injected, methamphetamine use also produces a state of euphoria accompanied by higher energy and less fatigue, called a “rush” or “flash.” The high associated with methamphetamine use is mediated by increased levels of dopamine in the brain, a neurotransmitter associated with pleasure, movement and attention. 1 In contrast with cocaine, methamphetamine has a larger effect on dopamine levels in the brain, which results in stronger, more prolonged effects. Whereas 50% of cocaine is removed from the body

2018 Canadian Centre on Substance Abuse

155. Evidence-based Clinical Practice Guideline for Deprescribing Cholinesterase Inhibitors and Memantine

inhibitors (ChEIs: donepezil, rivastigmine and galantamine) and the N-methyl-D-aspartate (NMDA) receptor antagonist, memantine [3]. ChEIs work by inhibiting the breakdown of acetylcholine—an important neurotransmitter that is reduced in people with dementia (the so-called ‘cholinergic hypothesis’) [13]. Memantine is thought to act through prevention of excitatory amino acid neurotoxicity, which is implicated in the pathogenesis of AD [14]. On average, people with dementia have four to six comorbidities

2018 Clinical Practice Guidelines Portal

156. CRACKCast Episode 185 – Alcohol Related Disease

physiologic effects of different levels are UNPREDICTABLE, some people are intolerant of levels as low as 5 mmol/L; a level of 32 mmol/L is where 50% of the adult population will be obviously intoxicated. Chronic alcoholics are tolerant of much higher levels. Excretion Excreted through the lungs, urine, and sweat [2] Define substance dependence. What are the signs of dependence? This is a misleading question, because some of the current terminology has shifted based on the DSM-V. Replacing the two DSM-IV (...) enhances inhibitory tone (via modulation of gamma-aminobutyric acid activity) and inhibits excitatory tone (via modulation of excitatory amino acid activity). Only the constant presence of ethanol preserves homeostasis. Abrupt cessation unmasks the adaptive responses to chronic ethanol use resulting in overactivity of the central nervous system. Gamma-aminobutyric acid — Gamma-aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the brain. Highly specific binding sites for ethanol

2018 CandiEM

157. Non-medical Prescription Stimulant Use among Post-secondary Students

alcohol and prescription stimulants together go beyond the potential for negative physiological side effects. Students who report co-use also report lower grade point averages, greater levels of illicit substance use and greater experience of severe alcohol-related consequences (e.g., driving while impaired, motor vehicle accidents, physical violence, being a victim of a crime, negative sexual encounters), even when controlling for sensation seeking (Egan et al., 2013). This increase in alcohol (...) , 2011). A large number of the studies conducted on the cognitive enhancing effects of drugs, such as methylphenidate, were completed in otherwise healthy adult humans or animals (Urban & Gao, 2014). This raises concerns about the effects of non-medical stimulant use among youth whose brains are not fully developed until approximately their mid-20s. Ingesting stimulants, which are known to alter dopamine and other neurotransmitters systems that are still maturing in areas of the brain (e.g

2018 Canadian Centre on Substance Abuse

158. Improving Quality of Life: Substance Use and Aging

with substance use (both licit and illicit substances) and problematic substance use. In that sense, there are interesting parallels between this topic and the one featured in our previous report in this series, which explored cannabis use during adolescence. Much like youth, older adults experience significant physiological, psychological and social change. It’s a period of rapid, dynamic and difficult transitions. Taking a closer look at the unique elements of later life and how they relate to substance (...) the aging process changes the brain will be critical to better understanding the impact of substance use on older adults’ health. After discussing how the brain’s function, structure and compensatory processes change with age, this chapter presents a detailed examination of the impact of aging on pharmacodynamics: the actions drugs have on the body. It explores the age-related changes that affect several neurotransmitter systems as well as the neuroendocrine and homeostatic systems. It also reviews

2018 Canadian Centre on Substance Abuse

159. British Association for Psychopharmacology consensus statement on evidence-based treatment of insomnia, parasomnias and circadian rhythm disorders: An update

balance between arousing and sleep-inducing physiological systems. Current research suggests that arousal and wakefulness are promoted by parallel neurotransmitter systems whose cell bodies are located in brainstem or midbrain centres, with projections to the thalamus and forebrain. These activating neurotransmittersarenoradrenaline,serotonin,acetylcholine, dopamine and histamine. In addition the newly discovered orexin system with cell bodies in the hypothalamus promotes wakefulness through (...) (Raskind et al., 2007). Trazodone is commonly used to promote sleep and has blocking actions at noradrenaline, 5HT and histamine receptors; this multiple action probably explains why it is widely used, although there are few controlled clinical trials. Other drugs such as sedating antidepressants and antipsy- chotics probably promote sleep in a similar fashion. The promotion of sleep is regulated by a number of other neurotransmitters (see Table 2); primary amongst these is gamma-aminobutyric acid

2019 British Association for Psychopharmacology

To help you find the content you need quickly, you can filter your results via the categories on the right-hand side >>>>