ECT and ketamine: not the whole truth

In my last post I discussed an article in the Observer about the Manchester ECT and ketamine study. The article described how a number of mental health professionals had raised concerns about the study. On 30 June the Guardian gave Ian Anderson, professor of psychiatry at Manchester University and the lead investigator of the study, some space to respond to these concerns.

The response explains how ketamine is “an anaesthetic in daily use throughout the NHS” and has sometimes been used as an anaesthetic for ECT. The main objective of the study, it says, is to investigate whether “cognitive side effects, including memory problems” can “reduced or eliminated.” The response points to the fact that other similar studies have been done but are too small to provide conclusive evidence of ketamine’s ability to reduce the cognitive effects of ECT, hence the need for the Manchester researcher’s own larger study. Smaller studies have however, it says, provided “evidence that ketamine can be can be safely given as the anaesthetic”. Here, rather bizarrely, there is a link to a study which found that: “Ketamine inductions resulted in higher number of adverse effects, higher subject dropout rates, and a longer reorientation time with respect to methohexital inductions.” (In this study ketamine was used as an alternative to methohexital, rather than as an adjunct as in the Manchester study.)

There is also a link to a study published in the Journal of Affective Disorders in December 2012 (“Neuropsychological and mood effects of ketamine in electroconvulsive therapy: a randomised controlled trial” by CK Loo et al). This Australian study is very similar to the Manchester one, and is cited as evidence that “the short-lived psychological effects of ketamine such as confusion and hallucinations are rarely seen”. What Ian Anderson however omits to say is that this Australian study found that “the addition of ketamine did not result in reduced neuropsychological side effects”. It is possible that, with a larger number of patients, different patients or different electrical parameters, different tests or timing of tests, the Manchester group may be able to find an advantage for ketamine where the Australians didn’t, but it looks unlikely that the addition of ketamine to the anaesthetic for ECT is going to reduce the cognitive effects in any major way. What is striking about the Australian study is the number of patients (over one third of those still eligible to participate) who were dropped from follow-up because they “could not be contacted” one week after ECT.

I have been unable to find any evidence that Professor Anderson has ever been interested in reducing the effects of ECT on memory and cognition. In 2002 he co-edited a book with Ian Reid, Fundamentals of clinical psychopharmacology. Here is what the book, in a section written by Ian Reid, says about the cognitive effects of ECT, in a typically trivialising way:

“Acute confusional state… this lasts for about 20 minutes
Anterograde amnesia: Patients may experience difficulty in learning new material for a couple of months after treatment. This effect is transient, and may be less significant than the anterograde learning difficulties seen in untreated depressive disorder.
Retrograde amnesia: Many patients report difficulty in recalling memories that were intact prior to treatment. This is usually restricted to events just prior to each treatment but, less commonly, some patients complain of persistent deficits extending back decades. This impairment is difficult to demonstrate using objective neuropsychological tests.
It is difficult to disentangle the cognitive effects of depression from those induced by ECT. Often, overall cognitive function improves as depression lifts.”

These don’t sound like the words of psychiatrists who are particularly concerned about the damaging effects of ECT.

More recently, Ian Anderson co-authored (with Grace Ferguson) the chapter on “mechanism of action of ECT” in the 3rd edition of the Royal College of Psychiatrists’ handbook on ECT. This is a clue as to where his real interests lie – in theories about the mechanism of action of ECT. The ECT and ketamine study has provided an opportunity to use brain imaging techniques to explore his theories.

Ian Anderson’s response concludes:

“The truth about the study is that it seeks primarily to investigate whether or not it is possible to reduce one of the major problems associated with ECT. If successful, it will be immensely beneficial to those who need to have this treatment to alleviate their depression.”

The truth? If the researchers had truly wanted to see if ketamine can reduce the damaging effects of ECT they could have done so without the use of brain-imaging, which would have made the £million plus study a lot cheaper.