Treatment of aura: solving the puzzle

D’Andrea, Giovanni; Nordera, G. P.; Allais, Gianni

doi:10.1007/s10072-006-0579-x

Cited by 16 publications

(5 citation statements)

References 21 publications

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“…Lamotrigine is an antiepileptic drug acting by blocking voltage-sensitive channels leading to an inhibition of glutamate release [19]. A number of studies have confirmed the efficacy of lamotrigine in the prevention of the auras [20][21][22][23][24].…”

Section: Glutamate and Auramentioning

confidence: 99%

Biochemistry of primary headaches: role of tyrosine and tryptophan metabolism

D’Andrea¹,

Cevoli

Colavito³

et al. 2015

Neurol Sci

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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.

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Section: Glutamate and Auramentioning

confidence: 99%

Biochemistry of primary headaches: role of tyrosine and tryptophan metabolism

D’Andrea¹,

Cevoli

Colavito³

et al. 2015

Neurol Sci

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“…If we speculate that a similar alteration is present in migraine, we could hypothesize that an abnormal release of glutamate in the intersynaptic space, leading to an increased excitability of the cerebral cortex with development of the spreading depression, may induce an increase of plasma concentrations of the amino acid, and consequently of platelet re-uptake. Strong support for this hypothesis is provided by the fact that lamotrigine, which inhibits glutamate release, reduces the frequency of MA attacks (25). This evidence, coupled with our data, may allow one to hypothesize that glutamate released from platelets plays an important role in the pathophysiology of MA and, based on this assumption, that glutamate release from activated platelets is also blocked by lamotrigine.…”

Section: Discussionmentioning

confidence: 99%

Platelet Glutamate Uptake and Release in Migraine With and Without Aura

Vaccaro¹,

Riva

Tremolizzo

et al. 2007

Cephalalgia

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Glutamate may play an important role in the pathogenesis of migraine: glutamate release in the brain may be involved in the development of spreading depression and increased concentrations of this amino acid have been reported in plasma and platelets from migraine patients. Here we assessed platelet glutamate uptake and release in 25 patients affected by migraine with aura (MA) and 25 patients affected by migraine without aura (MoA), comparing the results with a group of 20 healthy matched controls. Both glutamate release from stimulated platelets and plasma concentrations of the amino acid were assessed by high-performance liquid chromatography, and were increased in both types of migraine, although more markedly in MA. Platelet glutamate uptake, assessed as 3H-glutamate intake, was increased in MA, while it was reduced in MoA with respect to the control group. These results support the view that MA might involve different pathophysiological mechanisms from MoA and, specifically, up-regulation of the glutamatergic metabolism. Understanding these dysfunctional pathways could lead to new, possibly more successful therapeutic approaches to the management of migraine.

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“…Stronger platelet aggregation with higher plasma serotonin levels provokes vasoconstriction [113]. In addition to platelet-released glutamate [54,114], a high serotonin concentration may induce gap-junctional slow calcium waves in astrocyte syncytium [115,116], thus being responsible for the slowly proceeding aura signs [117,118]. Platelet aggregation may be initiated by triggers that further enhance an already elevated platelet aggregability [119], such as emotional and physical stress, awakening in the morning, additives in food and beverages, oral contraceptives, and the monthly decrease of estrogen during the menstrual cycle [110].…”

Section: Arguments Against the Role Of Csd In Migraine Headachementioning

confidence: 99%

Arguments against the role of cortical spreading depression in migraine

Borgdorff

2018

Neurological Research

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Cortical spreading depression (CSD) is a wave of increased electrocortical activity and vasodilation, followed by sustained decreased activity and prolonged vasoconstriction. Although the discovery of CSD has been ascribed to Leão, rather than vasoconstriction, he only observed a depression of neural activity combined with vasodilation, with much weaker stimulation than used by his followers. There is a longstanding belief that CSD underlies migraine aura, with its positive symptoms such as mosaic patterns and its negative symptoms such as scotoma, and a similar propagation speed and vasoreaction pattern. However, there are many arguments against this theory. CSD is difficult to evoke in man, and electroencephalography (EEG) readings are not flattened during migraine (as opposed to EEG during CSD). Moreover, in contrast to CSD, migraine can occur bilaterally, and is not accompanied by a disrupted blood-brain barrier, increased cerebral metabolism, or cerebral cell swelling. Calcitonin gene-related peptide, which is thought to be characteristic of migraine pain, is increased in the blood from the external jugular vein during migraine in humans, but not during CSD in cats or rats. Moreover, CSD does not explain the appearance of premonitory symptoms or allodynia, long before the actual onset of aura. In addition, there is a variation in the pain mechanisms of migraine and CSD, and in their reaction to transcranial magnetic stimulation and several pharmacologic interventions. Finally, the origin of putative CSD in migraine is currently unknown.

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Treatment of aura: solving the puzzle

Cited by 16 publications

References 21 publications

Biochemistry of primary headaches: role of tyrosine and tryptophan metabolism

Biochemistry of primary headaches: role of tyrosine and tryptophan metabolism

Platelet Glutamate Uptake and Release in Migraine With and Without Aura

Arguments against the role of cortical spreading depression in migraine

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