Migraine headache pathophysiology

Various pain states (e.g. headache, toothache and migraine), primarily pathophysiological inflammatory pain, e.g. rheumatic pain and pain caused by bone metastases... 

The goal is to suppress or reduce the intensity of the clinical signs and stop their progression. The various mechanisms of action are related to the complexity of the pathophysiology of migraine headache. Schematically two mechanisms of action are proposed ... 

All the drugs used for migraine headache are aimed at symptom relief and not against the yet unrecognized cause. Two observations are however most striking first the impact on the concept of pain (for example see analgesics in the chapter on the treatment of pain) and secondly the fact that the pathophysiological principles are poorly defined. 

Figure 1 Diagrammatic representation of the putative pathophysiological mechanisms involved in the development of migraine headache and the potential sites of action of NKi receptor antagonists (adapted from Longmore et al., 1997).

Headaches are classified into three major categories primary, psychogenic, and secondary (Table 30.1). This section focuses on the characteristics, pathophysiology, management, and prevention of only migraine headache. 

The etiology of migraine headaches is currently attributed to the neurovascular hypothesis, with the release of vasoactive neuropeptides and subsequent vasodilation of blood vessels. Serotonin plays an important role in migraine pathophysiology, and serotonin agonists have an important role in migraine treatment. 

Edvinsson L. On migraine pathophysiology. In Edvinsson L, ed. Migraine and Headache Pathophysiology. London, Martin Dunitz, 1999 3-15. 

The therapy of migraine headaches is complicated by the variable responses among and within individual patients and by the lack of a firm understanding of the pathophysiology of the syndrome. The efficacy of antimigraine drugs varies with the absence or presence of aura, duration of the... 

The triptans are considered specific therapies in that they target the pathophysiology underlying migraine.33 They abort headache through beneficial effects on neuronal imbalances.11 Triptans inhibit neurotransmission in the trigeminal complex and activate serotonin lb/Id pathways that modulate nociception in the brain stem. They also decrease the release of vasoactive peptides leading to vascular reactivity and pain.34 Triptans are a welcome addition to the therapeutic armamentarium in that they are available in intranasal, subcutaneous, and oral... 

Q7 The mechanisms which trigger migraine remain controversial. The underlying pathophysiology could be due to vasoconstriction of the cerebral arteries, causing transient ischaemia. This would be followed by compensatory vasodilation of the cerebral blood vessels to protect the ischaemic areas. This vasodilation may lead to an increase in intracranial pressure, which causes a severe headache. These events may be followed by changes in nerve activity and neurotransmitter levels. Inflammatory components are also likely to be involved in the pathology of this condition. 

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