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Rapid and Sustained Relief of Migraine Attacks With Intranasal Lidocaine: Preliminary Findings
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In a noncontrolled study, 23 migraine headache patients were treated with intranasal instillation of 0.4 mL of a 4% lidocaine solution during attacks of varying intensities. Evaluated were pretreatment and posttreatment changes in pain intensity, nausea, and side effects. Posttreatment intensity ratings significantly improved over pretreatment ratings, as determined by a Sandler A analysis (0.077;
P
<.0005). Migraine attacks were aborted in 12 of 23 patients, of which 8 were completely relieved within 5 minutes. In no case did an aborted attack return to more than a dull level within 24 hours, as determined by follow‐up telephone calls.
A successful response of migraine attacks to lidocaine treatment was more apt to occur in patients having migraine solely, when compared to migraine patients who also had daily dull headaches; the difference was not significant. Unilateral attacks, however, were significantly more treatment‐responsive when compared to bilateral attacks (
X
2
=3.85;
P
=.05). Nausea, associated with migraine attacks in 6 of 12 responders, was similarly aborted by lidocaine in 5 of 6 patients. Other side effects included mild nasal and eye burning of short duration (seconds), and oropharyngeal numbness of approximately 20 minutes' duration. Despite the abrupt and absolute relief of migraine attacks afforded by lidocaine in most of our study patients, its level of efficacy awaits results of double‐blind, placebo‐controlled studies.
Our findings raise new questions regarding the differential pathogenesis of migraine and cluster headache attacks. It is suggested here that the rapid effect of lidocaine in aborting migraine attacks, as shown by others in cluster headache, may be due to a conduction‐blocking action on pterygopalatine, internal carotid, and cavernous sinus ganglia. This implies that pain‐evoking mechanisms in migraine and cluster headache may similarly involve parasympathetic activity and calls into question the primacy of the trigeminovascular system to that of vaso‐parasympathetic efferents.
Title: Rapid and Sustained Relief of Migraine Attacks With Intranasal Lidocaine: Preliminary Findings
Description:
In a noncontrolled study, 23 migraine headache patients were treated with intranasal instillation of 0.
4 mL of a 4% lidocaine solution during attacks of varying intensities.
Evaluated were pretreatment and posttreatment changes in pain intensity, nausea, and side effects.
Posttreatment intensity ratings significantly improved over pretreatment ratings, as determined by a Sandler A analysis (0.
077;
P
<.
0005).
Migraine attacks were aborted in 12 of 23 patients, of which 8 were completely relieved within 5 minutes.
In no case did an aborted attack return to more than a dull level within 24 hours, as determined by follow‐up telephone calls.
A successful response of migraine attacks to lidocaine treatment was more apt to occur in patients having migraine solely, when compared to migraine patients who also had daily dull headaches; the difference was not significant.
Unilateral attacks, however, were significantly more treatment‐responsive when compared to bilateral attacks (
X
2
=3.
85;
P
=.
05).
Nausea, associated with migraine attacks in 6 of 12 responders, was similarly aborted by lidocaine in 5 of 6 patients.
Other side effects included mild nasal and eye burning of short duration (seconds), and oropharyngeal numbness of approximately 20 minutes' duration.
Despite the abrupt and absolute relief of migraine attacks afforded by lidocaine in most of our study patients, its level of efficacy awaits results of double‐blind, placebo‐controlled studies.
Our findings raise new questions regarding the differential pathogenesis of migraine and cluster headache attacks.
It is suggested here that the rapid effect of lidocaine in aborting migraine attacks, as shown by others in cluster headache, may be due to a conduction‐blocking action on pterygopalatine, internal carotid, and cavernous sinus ganglia.
This implies that pain‐evoking mechanisms in migraine and cluster headache may similarly involve parasympathetic activity and calls into question the primacy of the trigeminovascular system to that of vaso‐parasympathetic efferents.
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