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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Multicenter Study Comparative Study
Headache and anxiety-depressive disorder comorbidity: the HADAS study.
Psychiatric comorbidity (prevalence and types) was tested in a naturalistic sample of adult patients with pure migraine without aura, and in two control groups of patients, one experiencing pure tension-type headache and the other combined migraine and tension-type headaches. The study population included 374 patients (158, 110 and 106) from nine Italian secondary and tertiary centres. Psychiatric comorbidity was recorded through structured interview and also screened with the Mini International Neuropsychiatry Interview (MINI). ⋯ Anxiety (mostly generalised) was reported by 18.4% of patients with migraine, 19.3% of patients with tension-type headache, and 18.4% of patients with combined migraine and tension-type headaches. The values for panic disturbance were 12.7, 5.5 and 14.2, and those for obsessive-compulsive disorders were 2.3, 1.1 and 9.4% (p=0.009). Based on these results, psychopathology of primary headache can be a reflection of the burden of the disease rather than a hallmark of a specific headache category.
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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.