Evidence for an altered dopamine-hydroxylase activity in migraine and tension-type headache

Gallai, Virgilio; Gaiti, Alberto; Sarchielli, Paola; Coata, Giuliana; Trequattrini, Alberto; Paciaroni, Maurizio

doi:10.1111/j.1600-0404.1992.tb05108.x

Cited by 26 publications

(23 citation statements)

References 32 publications

(14 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Neurol Sci (2015) 36 (Suppl 1):S17-S22 platelet DA levels are elevated in MwoA patients [31,39]; a polymorphism of the gene that code for DbH may be the cause of a reduction of this enzyme activity [40] and of the high levels of DA [41,42] since DbH transforms DA in NE.…”

Section: Glutamate and Auramentioning

confidence: 98%

Biochemistry of primary headaches: role of tyrosine and tryptophan metabolism

D’Andrea¹,

Cevoli

Colavito³

et al. 2015

Neurol Sci

View full text Add to dashboard Cite

The pathogenesis of migraine as well as cluster headache (CH) is yet a debated question. In this review, we discuss the possible role of the of tyrosine and tryptophan metabolism in the pathogenesis of these primary headaches. These include the abnormalities in the synthesis of neurotransmitters: high level of DA, low level of NE and very elevated levels of octopamine and synephrine (neuromodulators) in plasma of episodic migraine without aura and CH patients. We hypothesize that the imbalance between the levels of neurotransmitters and elusive amines synthesis is due to a metabolic shift directing tyrosine toward an increased decarboxylase and reduced hydroxylase enzyme activities. The metabolic shift of the tyrosine is favored by a state of neuronal hyperexcitability and a reduced mitochondrial activity present in migraine. In addition we present biochemical studies performed in chronic migraine and chronic tension-type headache patients to verify if the same anomalies of the tyrosine and tryptophan metabolism are present in these primary headaches and, if so, their possible role in the chronicity process of CM and CTTH. The results show that important abnormalities of tyrosine metabolism are present only in CM patients (very high plasma levels of DA, NE and tryptamine). Tryptamine plasma levels were found significantly lower in both CM and CTTH patients. In view of this, we propose that migraine and, possibly, CH attacks derive from neurotransmitter and neuromodulator metabolic abnormalities in a hyperexcitable and hypoenergetic brain that spread from the frontal lobe, downstream, resulting in abnormally activated nuclei of the pain matrix. The low tryptamine plasma levels found in CM and CTTH patients suggest that these two primary chronic headaches are characterized by a common insufficient serotoninergic control of the pain threshold.

show abstract

Section: Glutamate and Auramentioning

confidence: 98%

Biochemistry of primary headaches: role of tyrosine and tryptophan metabolism

D’Andrea¹,

Cevoli

Colavito³

et al. 2015

Neurol Sci

View full text Add to dashboard Cite

show abstract

“…More recently, in a separate study, the DBH insertion/deletion has been associated with migraine with aura [Fernandez et al, 2006]. As both genetic markers of DBH have been reported to be associated with differences in plasma and CSF levels of DBH [Cubells et al, 1998;Zabetian et al, 2003], and significant differences in serum DBH have been observed in migraine patients compared with control subjects [Gallai et al, 1992;Gotoh et al, 1976] and during a migraine attack [Anthony, 1981], DBH may play an important role in migraine and may prove to be a future target for specific migraine therapeutics. Anti-dopaminergic agents such as metoclopramide have been reported as effective treatments for migraine [Colman et al, 2004].…”

Section: Neurotransmitter-related Genesmentioning

confidence: 96%

Migraine genetics and prospects for pharmacotherapy

Colson

Fernandez

Griffiths

2007

Drug Development Research

View full text Add to dashboard Cite

Migraine is a common complex neurological disorder with a well-known but poorly characterized genetic liability. The search for migraine susceptibility genes has been the focus of intense research. It is now believed that common migraine is not a single gene disorder, but attributable to several potentially interacting genetic variants. These variants may differ in each sufferer and interact with environmental factors to set the individual migraine threshold. This genetic liability may play an important role in the clinical heterogeneity seen in migraine and also in the variability of treatment response. This review will look at genetic loci implicated in migraine to date and consider their current or prospective role in migraine therapy. To elucidate the complex nature of migraine genetic liability, approaches that consider detailed endophenotypic profiles that encompass treatment response may provide much more relevant information than simple end diagnosis. Drug Dev Res 68: 282-293, 2007. r 2007 Wiley-Liss, Inc.

show abstract

“…Actually, in some migraineurs, the level of plasma NE levels has been measured as being significantly lower in patients compared to controls [9], indicating a sympathetic dysfunction. In addition, significant differences of serum dopamine beta-hydroxylase activity (DBH) have been observed in migraine (MO and MA) patients compared with healthy control subjects [10].…”

Section: Introductionmentioning

confidence: 99%