Lysergic acid diethylamide (LSD) was synthesized in 1938 and its psychoactive effects discovered in 1943. It was used during the 1950s and 1960s as an experimental drug in psychiatric research for producing so-called "experimental psychosis" by altering neurotransmitter system and in psychotherapeutic procedures ("psycholytic" and "psychedelic" therapy). From the mid 1960s, it became an illegal drug of abuse with widespread use that continues today. With the entry of new methods of research and better study oversight, scientific interest in LSD has resumed for brain research and experimental treatments. Due to the lack of any comprehensive review since the 1950s and the widely dispersed experimental literature, the present review focuses on all aspects of the pharmacology and psychopharmacology of LSD. A thorough search of the experimental literature regarding the pharmacology of LSD was performed and the extracted results are given in this review. (Psycho-) pharmacological research on LSD was extensive and produced nearly 10,000 scientific papers. The pharmacology of LSD is complex and its mechanisms of action are still not completely understood. LSD is physiologically well tolerated and psychological reactions can be controlled in a medically supervised setting, but complications may easily result from uncontrolled use by layman. Actually there is new interest in LSD as an experimental tool for elucidating neural mechanisms of (states of) consciousness and there are recently discovered treatment options with LSD in cluster headache and with the terminally ill.

No abstract

Alcohol withdrawal seizures are one major complication during detoxification treatment of alcohol dependent patients. Anticonvulsive pharmaceutical treatment can be administered but is associated with side-effects like nausea or hyponatriemia. Recent studies have identified different biomarkers that have been associated with the risk of alcohol withdrawal seizures. The aminoacid homocysteine as well as prolactin have been described to be associated with this individual seizure risk. Furthermore, markers of alcohol dependence like carbohydrate deficient transferrin (CDT) have been studied in this context. Also, genetic variants like the apolipoprotein E genotype have been found to be related to the history of withdrawal seizures. Knowledge and critical valuation of these recent findings on biomarkers may help to establish an assessment of the individual risk for withdrawal seizures and therefore may have important clinical implications.

No abstract

No abstract