conclusions and discussion summary

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Conclusions and discussion summary Jean Schoenen, Peter Kropp Contrary to studies of temporalis muscle suppressions (see above), those of CNV need special equipment and expertise, which are not available in every laboratory. Whatever the protocol used, all CNV studies performed in migraine without aura between attacks concordantly show an increased amplitude compared to tension-type headache or controls. However, as a diagnostic tool CNV has only moderate sensitivity and specificity (see Schoenen and Timsit-Berthier, this issue). Possible reasons for this are that CNV is influenced by a number of internal as well as external factors and that it can be modified in other neurological and psychiatric disorders. Interes tingly, CNV findings in migrainous children are very similar to those in adult migraineurs (see Besken et al., this issue). Moreover, in children CNV clearly differs between controls and tension-type headache patients, which is not the case in adults . For future studies a quantified analysis of CNV habituation would be worthwhile (see Kropp and Gerber, this issue). During discussion it clearly arose that the methodology for recording CNV may depend on the objectives of the study. Longer interstimulus intervals (3 to 4 sec) allow a separate analysis of early and late CNV components, which have a pathophysiologic al interest and may also increase the diagnostic yield (see Kropp and Gerber, this issue). Pathophysiological deductions from CNV studies in migraine can only remain speculative as long as the precise neurobiological phenomena behind this brain activity are not fully understood. Increased CNV amplitude might be due to hyperactivity or hype rreactivity of central catecholaminergic, especially noradrenergic, systems. This could explain why CNV normalizes in migraineurs after treatment with beta-blockers. However, this is probably a simplistic view. Kropp and Gerber (this issue) in discus sing their results on CNV habituation raise the interesting possibility that CNV abnormalities in migraine might be related, behaviorally, to disturbed learning or conditioning processes and, biochemically, to reduced activity of certain serotonergic neurons. Finally, it is still puzzling-. why CNV is normal in migraine with aura. Clearly, CNV research in headache has not yet grown to maturity. Many problems remain to be solved, for which comparative studies with behavioral and biochemical investigations are required.

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Page 1: Conclusions and discussion summary

Conclusions and discussion summary

Jean Schoenen, Peter Kropp

Contrary to studies of temporalis muscle suppressions (see above), those of CNV need special equipmentand expertise, which are not available in every laboratory.

Whatever the protocol used, all CNV studies performed in migraine without aura between attacksconcordantly show an increased amplitude compared to tension-type headache or controls. However, as adiagnostic tool CNV has only moderate sensitivity and specificity (see Schoenen and Timsit-Berthier, thisissue). Possible reasons for this are that CNV is influenced by a number of internal as well as external factorsand that it can be modified in other neurological and psychiatric disorders. Interestingly, CNV findings inmigrainous children are very similar to those in adult migraineurs (see Besken et al., this issue). Moreover, inchildren CNV clearly differs between controls and tension-type headache patients, which is not the case inadults. For future studies a quantified analysis of CNV habituation would be worthwhile (see Kropp andGerber, this issue).

During discussion it clearly arose that the methodology for recording CNV may depend on the objectivesof the study. Longer interstimulus intervals (3 to 4 sec) allow a separate analysis of early and late CNVcomponents, which have a pathophysiological interest and may also increase the diagnostic yield (see Kroppand Gerber, this issue).

Pathophysiological deductions from CNV studies in migraine can only remain speculative as long as theprecise neurobiological phenomena behind this brain activity are not fully understood. Increased CNVamplitude might be due to hyperactivity or hyperreactivity of central catecholaminergic, especiallynoradrenergic, systems. This could explain why CNV normalizes in migraineurs after treatment withbeta-blockers. However, this is probably a simplistic view. Kropp and Gerber (this issue) in discussing theirresults on CNV habituation raise the interesting possibility that CNV abnormalities in migraine might berelated, behaviorally, to disturbed learning or conditioning processes and, biochemically, to reduced activity ofcertain serotonergic neurons. Finally, it is still puzzling-. why CNV is normal in migraine with aura.

Clearly, CNV research in headache has not yet grown to maturity. Many problems remain to be solved,for which comparative studies with behavioral and biochemical investigations are required.