Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
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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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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 neuroimaging of experimental and clinical pain has revolutionised our understanding of the physiological responses to pain and paved the way for a better understanding of the pathophysiology of chronic pain syndromes. Extensive research on the central mechanisms regarding the sensory-discriminative dimensions of pain have revealed a complex network of cortical and subcortical brain structures involved in the transmission and integration of pain, the so-called pain matrix. Although brain imaging and pharmacological studies have generated some insight into the circuitry that may be involved in the generation of chronic pain symptoms, further research into brain imaging of chronic pain is clearly warranted. However, modern neuroimaging suggests that the chronification of pain (and headaches) involves functional and structural plasticity of both the central and peripheral nervous system.
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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.
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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.