Recurrent Extratrigeminal Stabbing and Burning Sensation with Allodynia in A Migraine Patient

Piovesan, EJ; Young, BW; Lc, Werneck; Kowacs, PA; Oshinsky, Michael L.; Silberstein, SD

doi:10.1046/j.1468-2982.2003.00541.x

Cited by 10 publications

(19 citation statements)

References 20 publications

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“…There may also be a relationship between migraine transformation and increasing frequency, severity, and extended distributions of stabs in this patient. Maybe, we could derive the same speculation as Piovesan et al, 7 susceptibility to sensitization is present in both disorders. Positive response to both frequency of migraine attacks and stabs with propranolol therapy in Piovesan et al's case and response to sodium‐valproate therapy in our case seem to be supporting this view.…”

Section: Commentssupporting

confidence: 63%

“…Recently, Piovesan et al 7 have reported a patient with history of migraine, who developed cranial and extracranial (limbs and abdomen) stabbing and burning pain (ESBA) associated with allodynia, which was independent of migraine attacks; however, both migraine attacks and ESBA resolved with β‐blocker therapy. They suggested that ESBA should be included in the category of migraine‐related or migraine‐like disorders.…”

Section: Commentsmentioning

confidence: 99%

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Extracephalic Stabbing Pain Temporally Related to Cephalic Ones

Selekler

Komşuoğlu²

2004

Headache

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A 23-year-old woman consulted with the complaint of short-lasting, severe stabbing headaches and mild-to-moderate degree near-daily migrainous headaches. Further questioning revealed that she also had stabbing pain on both ipsilateral hand and calf. Stabs on the hand were time-locked to cephalic ones and stabs in the calf were alternating with the ones in the hand. Dizziness and scotomas were accompanying symptoms to cephalic ones and paresthesia was the accompanying symptom in the hand. Patient's cephalic and extracephalic stabbing pains responded to indomethacine and daily headaches responded to prophylactic sodium valproate therapy. The stabs were felt in the head; hand and calf are considered as the parts of a whole. Along with its accompanying symptoms, stabbing pain may be the result of complex interactions in central nervous system.

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Section: Commentssupporting

confidence: 63%

Section: Commentsmentioning

confidence: 99%

Extracephalic Stabbing Pain Temporally Related to Cephalic Ones

Selekler

Komşuoğlu²

2004

Headache

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“…This is the reason why some headaches are associated with limb pain [18]. The authors have described a patient with migraine who showed recurrent extratrigeminal stabbing and burning sensation with allodynia on different parts of the body [19]. These features support the view that the perception of cranial pain is caused by a functional continuum between trigeminal and cervical fibers that converge on neurons in the TNC and upper cervical segments [15].…”

Section: Introductionmentioning

confidence: 81%

Convergence of cervical and trigeminal sensory afferents

Piovesan¹,

Kowacs²,

Oshinsky³

2003

Current Science Inc

141

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Cranial nociceptive perception shows a distinct topographic distribution, with the trigeminal nerve receiving sensory information from the anterior portions of the head, the greater occipital nerve, and branches of the upper cervical roots in the posterior regions. However, this distribution is not respected during headache attacks, even if the etiology of the headache is specific for only one nerve. Nociceptive information from the trigeminal and cervical territories activates the neurons in the trigeminal nucleus caudalis that extend to the C2 spinal segment and lateral cervical nucleus in the dorsolateral cervical area. These neurons are classified as multimodal because they receive sensory information from more than one afferent type. Clinically, trigeminal activation produces symptoms in the trigeminal and cervical territory and cervical activation produces symptoms in the cervical and trigeminal territory. The overlap between the trigeminal nerve and cervical is known as a convergence mechanism. For some time, convergence mechanisms were thought to be secondary to clinical observations. However, animal studies and clinical evidence have expanded our knowledge of convergence mechanisms. In this paper, the role of convergence mechanisms in nociceptive physiology, physiopathology of the headaches, clinical diagnosis, and therapeutic conduct are reviewed.

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“…The headache phase of migraine, which typically follows aura, is characterized by moderate to severe unilateral throbbing head pain that persists for longer than 4 hours but can last up to 72 hours. Additional symptoms associated with the headache phase include nausea, vomiting, enhanced sensitivity to light, sound and smell, and cutaneous allodynia (Piovesan et al, 2003; Goadsby, 2009a; Levy, 2010; Giamberardino, 2003; Burstein et al, 2004). After the headache subsides, many patients report postdrome symptoms such as cognitive impairments, fatigue, and changes in mood that can persist for 18-24 hours post-headache (Goadsby, 2009a).…”

Section: 1 Introductionmentioning

confidence: 99%

Neurovascular contributions to migraine: Moving beyond vasodilation

2016

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Migraine is the third most common disease worldwide, the most common neurological disorder, and one of the most common pain conditions. Despite its prevalence, the basic physiology and underlying mechanisms contributing to the development of migraine is still poorly understood and development of new therapeutic targets is long overdue. Until recently, the major contributing pathophysiological event thought to initiate migraine was cerebral and meningeal arterial vasodilation. However, the role of vasodilation in migraine is unclear and recent findings challenge its necessity. While vasodilation itself may not contribute to migraine, it remains possible that vessels play a role in migraine pathophysiology in the absence of vasodilation. Blood vessels consist of a variety of cell types that both release and respond to numerous mediators including growth factors, cytokines, adenosine triphosphate (ATP), and nitric oxide (NO). Many of these mediators have actions on neurons that can contribute to migraine. Conversely, neurons release factors such as norepinephrine and calcitonin gene-related peptide (CGRP) that act on cells native to blood vessels. Both normal and pathological events occurring within and between vascular cells could thus mediate bi-directional communication between vessels and the nervous system, without the need for changes in vascular tone. This review will discuss the potential contribution of the vasculature, specifically endothelial cells, to current neuronal mechanisms hypothesized to play a role in migraine. Hypothalamic activity, cortical spreading depression (CSD), and dural afferent input from the cranial meninges will be reviewed with a focus on how these mechanisms can influence or be impacted by blood vessels. Together, the data discussed will provide a framework by which vessels can be viewed as important potential contributors to migraine pathophysiology, even in light of the current uncertainty over the role of vasodilation in this disorder.

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Recurrent Extratrigeminal Stabbing and Burning Sensation with Allodynia in A Migraine Patient

Cited by 10 publications

References 20 publications

Extracephalic Stabbing Pain Temporally Related to Cephalic Ones

Extracephalic Stabbing Pain Temporally Related to Cephalic Ones

Convergence of cervical and trigeminal sensory afferents

Neurovascular contributions to migraine: Moving beyond vasodilation

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