Samuel Guthrie, a U.S. physician from Sackets Harbor, New York, also appears to have produced chloroform in 1831 by reacting chlorinated lime with ethanol, as well as noting its anaesthetic properties; he also believed that he had prepared chloric ether, however. Justus von Liebig carried out the alkaline cleavage of chloral. Eugène Soubeiran obtained the compound by the action of chlorine bleach on both ethanol and acetone. In 1834, French chemist Jean-Baptiste Dumas determined chloroforms empirical formula and named it. In 1835, Dumas prepared the substance by the alkaline cleavage of trichloroacetic acid. Regnault prepared chloroform by chlorination of chloromethane. In 1842, Robert Mortimer Glover in London discovered the anaesthetic qualities of chloroform on laboratory animals. In 1847, Scottish obstetrician James Y. Simpson was the first to demonstrate the anaesthetic properties of chloroform on humans, provided by local pharmacist William Flockhart of Duncan, Flockhart and company, and helped to popularise the drug for use in medicine. By the 1850s, chloroform was being produced on a commercial basis, in Britain about 750,000 doses a week by 1895, by using the Liebig procedure, which retained its importance until the 1960s. Today, chloroform – along with dichloromethane – is prepared exclusively and on a massive scale by the chlorination of methane and chloromethane. Production
In industry production, chloroform is produced by heating a mixture of chlorine and either chloromethane (CH3Cl) or methane (CH4).
Diencephalic syndrome, or Russells syndrome, is a rare neurological disorder seen in infants and children and characterised by failure to thrive and severe emaciation despite normal or slightly decreased caloric intake. Classically there is also locomotor hyperactivity and euphoria. Less commonly diencephalic syndrome may involve skin pallor without anaemia, hypoglycaemia, and hypotension. The syndrome is a rare but potentially fatal cause of failure to thrive in children. Failure to thrive presents on average at seven months of age. Of note the syndrome is not associated with developmental delay. There may be associated hydrocephalus.Diencephalic syndrome was first described by Dr. A. Russell in 1951. It is usually caused by a brain tumor such as a low-grade glioma or astrocytoma located in the hypothalamic-optic chiasmatic region. It is not yet understood how diencephalic syndrome causes the effects on appetite and metabolism which are seen, though inappropriately high growth hormone release has been proposed, as has excessive β-lipotropin secretion and overall increased metabolic demand. It is treated with nutritional optimisation while the underlying lesion is treated with chemotherapy, surgery or radiotherapy. == References ==