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Transcranial Doppler Ultrasonographic Features During Drug Withdrawal From Drug‐Induced Headache. A Transcranial Doppler Follow‐up Study
Author(s) -
Haase Claus G.,
Diener HansChristoph
Publication year - 1998
Publication title -
headache: the journal of head and face pain
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.14
H-Index - 119
eISSN - 1526-4610
pISSN - 0017-8748
DOI - 10.1046/j.1526-4610.1998.3809679.x
Subject(s) - ergotamine , medicine , transcranial doppler , anesthesia , migraine , cerebral blood flow , blood pressure , hemodynamics , heart rate , cardiology
Background.—A vascular component in ergotamine‐induced headache has been proposed. No study has been carried out to evaluate cerebral hemodynamic changes by means of transcranial Doppler during withdrawal from migraine medication; in particular, ergotamine‐containing drugs. Method.—We examined 21 patients suffering from drug‐induced headache during their in‐hospital withdrawal from ergotamine (n=8) and compared them with patients during withdrawal from analgesics (n=13) and with healthy controls (n=14). Cerebral blood flow velocities were measured with transcranial Doppler, and pulsatility indices were calculated. Blood pressure, heart rate, and end‐tidal carbon dioxide were documented. A subjective analog headache rating scaling was used for day‐to‐day evaluation of headache severity. Results.—Mean cerebral blood flow velocities dropped significantly after discontinuation of ergotamine‐containing drugs but not after stopping common analgesics. Pulsatility indices remained unchanged. Cerebral blood flow velocities were higher in drug‐ingesting patients compared to the control group and showed significant changes in patients with headache using ergotamine and in those using analgesics. Carbon dioxide, heart rate, and blood pressure remained unchanged. The headache rating scale did not show a constant trend. Comments.—Our results indicate that ergotamine and, to a lesser extent, common analgesics including caffeine might influence cerebral blood flow velocities and pulsatility indices causing transient and reversible disturbance of cerebral autoregulation.