Current pain and headache reports
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Curr Pain Headache Rep · Jun 2006
ReviewPregabalin for neuropathic pain based on recent clinical trials.
Pregabalin is a ligand for the alpha-2-delta subunit of voltage-gated calcium channels with anticonvulsant, analgesic, and anxiolytic properties. It has predictable absorption across the gastrointestinal tract, is neither metabolized nor protein-bound, and has minimal drug-drug interactions. It is effective with two or three-times daily dosing in a dose range of 150 to 600 mg daily. ⋯ The 50% responder rates for PHN and DPN compare favorably with other first-line agents for neuropathic pain. Pregabalin is well tolerated in most patients with infrequent severe adverse effects. Pregabalin is an important addition to the treatment armamentarium for neuropathic pain.
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Curr Pain Headache Rep · Jun 2006
ReviewNeuropathic pain: translational research and impact for patient care.
Neuropathic pain syndromes (ie, pain after a lesion or disease of the peripheral or central nervous system) are clinically characterized by spontaneous pain (ongoing, paroxysms) and evoked types of pain (hyperalgesia, allodynia). Different pathophysiologic mechanisms occur solitarily or combined at peripheral nociceptors, spinal cord, or in the brain, which cause a broad variety of signs and symptoms. ⋯ Therefore, a new concept was proposed in which pain is analyzed on the basis of underlying mechanisms. The increased knowledge of pain-generating mechanisms and their translation into signs and symptoms may allow for a dissection of the individual mechanisms, and it ultimately should be possible to design optimal treatments for each patient.
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The understanding of migraine pathophysiology has evolved from the belief that migraine is a vascular disorder, to evidence that better defines migraine as a neurogenic disorder associated with secondary changes in brain perfusion. There is evidence to suggest that the early phase of migraine pain results from neurogenic inflammation affecting cranial blood vessels and dura. Allodynia, hyperalgesia, and expansion of nociceptive fields occur during most well-established migraine attacks. ⋯ A hypothesis that defines migraine pain as a unique neuropathic pain disorder can imply the potential for neural plasticity and may provide insight into the mechanisms that underlie the transformation of episodic to chronic forms of migraine. The neuropathic pain model of migraine pathophysiology not only paves the way for mechanism-based treatment strategies that can improve the acute and preventive management of migraine attacks, but also opens the door for the discovery of novel therapeutic targets. It also lends momentum to an understanding of clinically intriguing topics such as opiate-induced hyperalgesia and medication-overuse headache (rebound headache), opioid resistance in the treatment of chronic headache, and disease modification in defending against the potential for migraine transformation.
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Although the influence of age on the prevalence of migraine is well known, the clinical characterization of migraine across the lifespan remains poorly studied. Limited evidence suggests that migraine attacks get shorter and less typical with advancing age. Similar results were found for transformed migraine at different ages. ⋯ We then discuss the epidemiology and profile of transformed migraine across the lifespan. Clarifying the influence of age on migraine is of importance for clinical diagnosis and treatment. It also may contain clues to evolving disease biology.
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Curr Pain Headache Rep · Jun 2006
ReviewCurrent views of the risk of stroke for migraine with and migraine without aura.
The association between migraine and stroke is complex and is a continued focus of attention. Several observational studies have identified migraine as an independent risk factor for ischemic stroke. However, a distinction should be made between migraine with and migraine without aura. ⋯ Most studies have not found an association between migraine without aura and ischemic stroke. Although there are several hypotheses about the biologic link between migraine with aura and ischemic stroke, the precise mechanisms remain unclear. However, because the absolute risk of stroke is low in patients with migraine with aura, and migraine without aura is likely not associated with ischemic stroke, most migraine patients will not experience a stroke event.