Comparisons can be odious

When I first started working in the field of epilepsy, over 25 years ago, therapeutic options were much more limited than they are today. Surgery had not yet reached an established place in the management of intractable epilepsy and the pharmaceutical industry seemed little interested in producing better drugs for treating the condition with fewer side-effects. By comparison, with the pressure today to use new drugs, the manufacturers who had just introduced carbamazepine and sodium valproate for the treatment of epilepsy seemed almost apologetic about their products. Extensive double blind clinical trials and evidence based medicine were very far away. The almost daily visits of keen drug representatives extolling the virtues of his or her anticonvulsant which we experience nowadays did not occur. We were left much more to our own endeavours and gradually learned to use the new anticonvulsants, discovering for ourselves both their virtues and their drawbacks, developing a clinical practice with them based largely on our own experience and the experience of colleagues that we trusted. My mentor, for instance, was Peter Jeavons who taught me to use valproate in his own unique way (using weight related doses, monitoring EEG responses as a guide to sufficient dosage and totally .ignoring blood levels). Likewise I learned the value from him of low, slow dose escalations of carbamazepine (so low and slow in fact that I have never personally caused a carbamazepine rash). I was learning my epilepsy skills in the seventies. Part of my research at that time was to study the effect of various prescribed drugs on cerebral function--particularly their effects on mood and psychomotor performance (especially as related to their possible detrimental influence on driving skills). As a result, for some time, I rubbed shoulders with physicians in the hypertension field at a time when there was a sudden surge in interest in the management of hypertension with somewhat less poisonous compounds than we had used previously; particularly the beta blocking drugs which were competing actively with each other to be the best antihypertensive with fewest side-effects. Debate raged as to whether lipid solubility was better than water solubility. Was some ISA activity necessary in your beta blocker? Was it better to have a beta blocker that penetrated the central nervous system or one that did not? Was Beta 2 activity a good thing or not? Debate, claims and counterclaims, were endless. As what seemed like dozens of compounds, all with slightly different properties, hit the market, polite young men and women in suits tried to persuade us of the outstanding virtues of their own particular product. At cardiological meetings endless Satellites were held in which men in slightly more expensive suits (the opinion leaders so beloved of the pharmaceutical industry) held forth about the virtues of different types of beta blocker. A plethora of pens, notepads and other little gifts suddenly appeared on doctors' desks all discretely labelled with the trade name of a particular beta blocker. Perhaps the competition of these heady days was a waste of money and resources but it did lead in its own insidious way to a great deal of basic research into the mechanisms of hypertension itself, which eventually led to better drugs with fewer side-effects and better understanding of the whole process of hypertension and some insight into the quality of life of people taking drugs for very long periods of time to control blood pressure. For the first time physicians did not treat hypertension as though they were just treating a column of mercury but began to think about the person with the raised blood pressure. Epileptologists are now, fairly suddenly, being exposed to a similar kind of pressure. In the last five years Several new compounds have emerged, (one or two to disappear almost as quickly as they had arrived) but some clearly becoming