Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
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Migraine is an episodic brain disorder that results in significant morbidity. Antiepileptic drugs (neuromodulators) are increasingly recommended for migraine prevention because of placebo-controlled double-blind trials that prove them effective. ⋯ Inhibition of trigeminocervical complex directly, or neurons that modulate sensory input, are also plausible mechanisms for the actions of neuromodulators in preventive therapy in migraine. Although it is unlikely that a single phenomenon serves as the only link between migraine and epilepsy, the neuronal hyperexcitability that may contribute to each condition may explain the effect of these drugs for both conditions.
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This paper reviews non-invasive behavioural approaches - broadly construed as cognitive, affective, behavioural and psychophysiological interventions - and examines whether they can impact central, peripheral or autonomic nervous system components responsive to pain in general and headache in particular. It focuses on two developing bodies of literature - neurophysiology of migraine and fMRI studies of pain networks. The available literature suggests behavioural interventions can affect neuromodulation, although further research is clearly warranted.
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Caffeine is the most widely consumed psychostimulant drug. It is a potent antagonist of adenosine receptors at dosages consistent with common dietary intake. ⋯ With chronic repetitive intake, caffeine is associated with an increased risk of development of analgesicoveruse headache, chronic daily headache and physical dependency. Cessation of caffeine use following chronic exposures leads to a withdrawal syndrome, with headache as a dominant symptom.
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Liability to spontaneous and experimental pain is genetically determined and there is considerable variability in the antinociceptive effects of drugs commonly used in treating pain conditions and migraine attacks. The causes for variability involve still unknown genetic aspects. Recently, a third gene, SCN1A, was discovered as a cause of familial hemiplegic migraine (FHM). ⋯ Catechol-O-methyltransferase (COMT) and the cytochrome P450 variant allele CYP3A5 modulate the genetic response to opioid medications in humans. Variability in drug pharmacokinetics and adverse drug reactions of pain medications are also very much related to genetic variation, especially in CYP genes. Pharmacogenomic studies of headache and pain are still in their infancy, but these recent advances in the genetics of migraine and pain arguably hold the promise of individualised treatments and prevention of adverse drug reactions.
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The studies of different antiepileptic drugs (AEDs) in the prophylaxis of episodic migraine, cluster headache (CH) and chronic headache forms (chronic daily headache, transformed or chronic migraine, chronic tension-type headache) are reviewed. The main results from published trials are summarised - focusing on responder rates as reported in placebo-controlled, double-blind studies. ⋯ Overall, evidence of efficacy of different AEDs in chronic headache forms and in CH is still lacking, most studies being open-label, small-sample trials. Nevertheless, encouraging data from controlled trials are emerging for TPM in the treatment of chronic headache forms.