It can also be used as an antidote for dimenhydrinate poisoning.It has been shown to improve long-term memory, and was once explored as a therapy for Alzheimers disease, but in clinical trials it was not shown to confer convincing benefits, and it led to very common moderate to severe side-effects such as nausea, vomiting, diarrhea, loss of appetite, abdominal pain, and tremors, resulting in a high rate of withdrawal. Physostigmines poor tolerability led to it being abandoned in favor of later acetylcholinesterase inhibitors, three of which are currently in use: donepezil, galantamine, and rivastigmine. Recently, it has begun to be used in the treatment of orthostatic hypotension. Recently, physostigmine has been proposed as an antidote for intoxication with gamma hydroxybutyrate (GHB, a potent sedative-hypnotic agent that can cause loss of consciousness, loss of muscle control, and death). Physostigmine may counteract GHB by producing a nonspecific state of arousal. However, not enough scientific evidence shows physostigmine properly treats GHB toxicity. Furthermore, lower doses of GHB produce a stronger action at the GHB receptor than at the GABAB-receptor, resulting in a stimulating effect which would act synergistically with physostigmine and produce hyperstimulation when the GHB blood levels begin to drop. Physostigmine also has other proposed uses: it could reverse undesired side effects of benzodiazepines such as diazepam, alleviating anxiety and tension. Another proposed use of physostigmine is to reverse the effects of barbiturates (any of a group of barbituric acids derived for use as sedatives or hypnotics). Pharmacology
Physostigmine acts by interfering with the metabolism of acetylcholine.
Eponym
This condition is named after the German translation for "snail-pelvis" (Schneckenbecken), this name was first used by Borochowitz et al. when they described a Californian fetus with the symptoms of the disorder and referred to said symptoms as "Schneckenbecken dysplasia". Mouse knockout model
In 2007, Hiraoka et al. created an SLC35D1-knockout mouse model, said experiment revealed that while mice heterozygous for the genetic mutation were born normally without any associated complications, mice homozygous for said mutation died during their neo-natal life. The latter mice had micromelia, craniofacial bone hypoplasia, vertebrae flattening, severely short long bones and iliac bones, Hiraoka noted these symptoms to be similar to those experienced by human fetuses with Schenckenbecken dysplasia, and concluded that this gene must be important for normal ante-natal skeletal formation in mice. See also
Achondroplasia


== References ==