Roy G.Beran, Suite 5, 6th Floor, 12 Thomas Street, Chatswood, NSW 2067, Australiroy.beran@unsw.edu.au
P.J. Spira
Submitted May 05, 2004
Dr Silberstein [1] raised three issues in relation to our paper. [2]
Firstly he questioned "What were they treating with gabapentin?"
indicating his belief that we did not attempt to sub-classify the headache
form/s leading to CDH. This was discussed and demonstrated that confident
sub-classification was impracticable in most cases as almost 2/3 of
subjects had a history of both tension-type headache and migraine. The
phenomenology of CDH is such that the predominant headache type often has
a poor fit with IHS criteria for both migraine and tension-type headache.
The exercise of sub-classifying CDH is often guesswork rather than high
science.
Secondly, Dr Silberstein commented that failure to exclude "analgesic
over-use" from our trial could have been a confounding factor. We assert
the contrary. Had we excluded subjects who treated all or most of their
headaches with simple or compound analgesics we would have obtained data
in a highly atypical group of CDH patients. Instead we chose to use
change in analgesic intake as a secondary outcome measure and performed
subgroup analysis to see if high analgesic intake modified responses to
the trial agent.
Finally, Dr Silberstein expressed doubt regarding the clinical
importance of a 9.1% reduction in headache-free days. This point was also
canvassed in the paper emphasizing this was a mean response rather than
response in the individual. CDH is a highly recalcitrant headache form
and more than half of our patients retained absolute daily headaches on
the trial drug. The 9.1% mean response was achieved because among the
responders more than 1/3 reduced their headache frequency to less than 50%
of baseline. This is clinically important, even disregarding the
significant improvements in the secondary outcome measures.
The management of CDH involves the often-disappointing exercise of
serial trials of headache prophylactics. Our study indicates that
gabapentin, like all other medications employed in headache prevention,
will not succeed in all, or even most, cases but that the agent can
achieve a sufficient response in a significant proportion of the CDH
population to render it a worthwhile therapeutic option.
1. Silberstein, SD. December 23 Highlight and Commentary: Gabpentin
in the treatment of chronic daily headache. Neurology 2003; 61: 1637.
2. Spira PJ, Beran RG. Gabapentin in the prophylaxis of chronic daily
headache. Neurology; 61: 1753-1759.
Dr Silberstein [1] raised three issues in relation to our paper. [2] Firstly he questioned "What were they treating with gabapentin?" indicating his belief that we did not attempt to sub-classify the headache form/s leading to CDH. This was discussed and demonstrated that confident sub-classification was impracticable in most cases as almost 2/3 of subjects had a history of both tension-type headache and migraine. The phenomenology of CDH is such that the predominant headache type often has a poor fit with IHS criteria for both migraine and tension-type headache. The exercise of sub-classifying CDH is often guesswork rather than high science.
Secondly, Dr Silberstein commented that failure to exclude "analgesic over-use" from our trial could have been a confounding factor. We assert the contrary. Had we excluded subjects who treated all or most of their headaches with simple or compound analgesics we would have obtained data in a highly atypical group of CDH patients. Instead we chose to use change in analgesic intake as a secondary outcome measure and performed subgroup analysis to see if high analgesic intake modified responses to the trial agent.
Finally, Dr Silberstein expressed doubt regarding the clinical importance of a 9.1% reduction in headache-free days. This point was also canvassed in the paper emphasizing this was a mean response rather than response in the individual. CDH is a highly recalcitrant headache form and more than half of our patients retained absolute daily headaches on the trial drug. The 9.1% mean response was achieved because among the responders more than 1/3 reduced their headache frequency to less than 50% of baseline. This is clinically important, even disregarding the significant improvements in the secondary outcome measures.
The management of CDH involves the often-disappointing exercise of serial trials of headache prophylactics. Our study indicates that gabapentin, like all other medications employed in headache prevention, will not succeed in all, or even most, cases but that the agent can achieve a sufficient response in a significant proportion of the CDH population to render it a worthwhile therapeutic option.
1. Silberstein, SD. December 23 Highlight and Commentary: Gabpentin in the treatment of chronic daily headache. Neurology 2003; 61: 1637.
2. Spira PJ, Beran RG. Gabapentin in the prophylaxis of chronic daily headache. Neurology; 61: 1753-1759.