Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
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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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Over the last 100 years, the discovery of new analgesics has been a complex and difficult task. However, remarkable progress in the identification of novel molecular targets relevant for pain medicines has been reported. ⋯ Recent preclinical and clinical data on the localisation, regulation and plasma levels of CGRP and on the function of CGRP-R will be summarised. The reviewed findings highlight the major function of CGRP in migraine and the use of CGRP-R antagonists as a novel approach for the treatment of migraine attack and, perhaps, as migraine prophylactic medicines.
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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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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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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.