by Thomas A. Ban

Potassium bromide was the first widely used sedative in medicine. It is the potassium salt of bromine, the element that was named for its “stench” (“bromos”).

Bromine was first isolated in 1826 from the ashes of seaweed by A.J Balard, an apothecary in Montpelier, France. He found bromine in its natural form too corrosive for ingestion and prepared for clinical use the potassium and sodium salts of the substance (Shorter, 1997).

Bromine was introduced into medical practice by François Magendie in Bordeaux (France) and subsequently, in the 1830s and ‘40s, bromide was extensively used as a substitute for iodine in a variety of disorders (Garrison, 1960). It was only in the mid-1850s that Charles Lockock, a London internist, discovered the anticonvulsant property and sedative action of the drug. It was one of the many quaint examples of serendipity in which a false theory led to correct empirical results. Lockock, like many physicians in his time, believed that convulsions and epilepsy were caused by masturbation and since bromides were known to curb sex drive, he administered potassium bromide with the rationale that by reducing the frequency of masturbation he will be able to control epileptic seizures (convulsions) in his patient (Lehmann and Ban, 1970). The treatment was a success insofar as control of convulsions was concerned. It also focused attention on the sedating properties of the drug (Ban, 2006).  

During the second half of the 19th century, potassium bromide was widely used for sedation and for the control of anxiety and convulsions (Balme, 1976). In 1900, Neil Macleod, a Scottish physician, reported on “bromide sleep” in the treatment of acute mania.  Yet, the bromides were difficult drugs to use. Since they act by replacing chlorides, their activity depends not only on the amount of bromide given, but also on the chloride intake, fluid consumption and renal function of the patient. The problem is compounded by its slow excretion and rapid accumulation in the blood. The earliest manifestations of bromide intoxication are sleepiness and fatigue; and as blood-concentrations increase appetite is lost, weight decreases and a characteristic mental dullness appears. A toxic delirium is triggered when bromide levels pass a critical threshold (Ban, 1969).

In one particular aspect the bromides differ from all other sedatives: they don’t induce drowsiness and sleep when given in a large single dose. Nevertheless, because of their relatively low efficacy coupled with high toxicity the use of bromides were virtually restricted for controlling seizures in pediatrics by the late 1960s (Ban, 2006).


Balme RH. Early medicinal use of bromides. J Roy Coll Physicians 1976; 10 205 - 8.

Ban TA. The role of serendipity in drug discovery. Dialogues in Clinical Neuroscience 2006; 8: 335-44.

Ban TA. Psychopharmacology. Baltimore: The Williams & Wilkins Company; 1969, p. 167.

Garrison FH. History of Medicine. Fourth Edition. Philadelphia: Saunders; 1960, p.466.

Lehmann HE, Ban TA. Pharmacotherapy of Tension and Anxiety. Springfield: Charles C. Thomas; 1970, p. 12-3.

Macleod N.  The bromide sleep. A new departure in the treatment of acute mania. BMJ 1900; 1: 134-6.

Shorter E. A History of Psychiatry. New York: John Wiley and Sons; 1997, 202-3.


Thomas A. Ban
October 24, 2013

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