Mervyn J. Eadie

On November 8, 1923, William John Adie described an unusual disorder to the Section of Neurology of the Royal Society of Medicine. The condition comprised frequent momentary stereotyped impairments of consciousness that occurred in children, did not respond to antiseizure medications, and did not develop into epilepsy, as that term was then commonly understood, since no convulsive seizures occurred. After some time, the episodes terminated spontaneously, leaving the sufferer unhandicapped and neurologically intact. Almost certainly, Adie had described the present-day entity of childhood absence epilepsy. He termed it "pyknolepsy," knowing that the name "pyknolepsie" had been used for a similar disorder in Germany from 1916 onwards, though not reported elsewhere. Following Adie's account, published in 1924, reports of the disorder appeared in the English and French-language literature and continued to be published in German. It became increasingly accepted that pyknolepsy was a form of epilepsy that was part of Lennox's petit mal triad. The word pyknolepsy itself never became widely used and is now largely forgotten. Adie never took up the topic in print again. However, he had awakened English-language readers to one component in a broadening of the concept of what constituted epilepsy.

Despite the availability over the past decade of a number of new pharmaceutical agents with different mechanisms of action from those of the drugs used previously, the contemporary drug therapy of migraine attacks falls rather short of what would be desirable, while the pharmacological attempt to prevent further attacks appears to prove unsatisfactory about as often as it is successful. The present paper explores reasons for these shortcomings in both the earlier and the current drug therapy of the disorder. Significant major contributory factors appear to be an incomplete understanding of the underlying pathogenic mechanisms of the various stages of the migraine attack, less than optimal pharmacokinetic characteristics of many of the drugs used, and migraine sufferers failing to employ the available drugs to their best advantage. New drugs developed in the light of a more complete understanding of the molecular basis of migraine pathogenesis, together with awareness of pharmacokinetic desiderata in relation to treating and preventing migraine attacks, may go some way towards remedying the situation, but patient decision making may prove more difficult to modify.

Edward Henry Sieveking (1816–1904) was a professionally successful and well respected nineteenth-century London physician who, over the span of some half a century, continuously held appointment to British royalty, including Queen Victoria and King Edward VII. In 1858, he published a monograph On Epilepsy and Epileptiform Seizures, with a second edition in 1861. In both editions, he described an entity cephalalgia epileptica that comprised the occurrence of headache in association with phenomena that resembled the premonitory symptom of some epileptic seizures. However, the sufferers did not have epilepsy, in that they did not experience generalized convulsions. Sieveking, like most of his British contemporaries, had little awareness of the existence of the variety of migraine phenomena apart from headache itself. In retrospect, it seems likely that migraine with aura probably was the main basis of the disorder Sieveking designated, one that later may have been termed migralepsy.