Volume 26, Issue 8 pp. 968-972

Abnormal platelet trace amine profiles in migraine with and without aura

G D’Andrea

G D’Andrea

Headache Centre, Villa Margherita Hospital, Arcugnano (VI),

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F Granella

Corresponding Author

F Granella

Department of Neurosciences, University of Parma, Parma,

Dr Franco Granella, Dipartimento di Neuroscienze, Sezione di Neurologia, Università di Parma, Via Gramsci, 14, 43100 Parma, Italy. Tel. + 39 05 2170 2695, fax + 39 05 2170 4115, e-mail [email protected] Received 7 October 2005, accepted 23 January 2006 Search for more papers by this author
M Leone

M Leone

Neurological Institute ‘C. Besta’, Milan,

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F Perini

F Perini

Department of Neurology, Este-Monselice Hospital, Monselice (PD), and

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A Farruggio

A Farruggio

Department of Pathology, Este-Monselice Hospital, Este (PD), Italy

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G Bussone

G Bussone

Neurological Institute ‘C. Besta’, Milan,

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First published: 17 July 2006
Citations: 3

Abstract

Trace amines, including tyramine, octopamine and synephrine, are closely related to classic biogenic amines. In one study, where these substances were found elevated in plasma of migraineurs, it was hypothesized that trace amine metabolism is deranged in migraine. To confirm these findings, we studied, using a multichannel electrochemical high-performance liquid chromatography system, the concentrations of trace amines in platelets of migraine without aura (MoA) and migraine with aura (MA) patients in headache-free period, compared with controls. Platelet concentrations of trace amines, although elevated in both migraine types, showed a different profile in MoA and MA. Octopamine was significantly higher in MoA sufferers (0.69 ± 0.43 ng/108 platelets) compared with both control subjects (0.22 ± 0.16 ng/108 platelets) and MA patients (0.39 ± 0.37 ng/108 platelets). Synephrine was significantly higher in MA patients (0.72 ± 0.44 ng/108 platelets) with respect to both controls (0.33 ± 0.25 ng/108 platelets) and MoA sufferers (0.37 ± 0.29 ng/108 platelets). These results strengthen the hypothesis that tyrosine metabolism is deranged in migraine and may participate in its pathophysiology.

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