Stimulation of cranial vessels excites nociceptive neurones in several thalamic nuclei of the cat

Zagami, Alessandro S; Lambert, Geoffrey

doi:10.1007/bf02423504

Cited by 79 publications

(41 citation statements)

References 59 publications

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“…Using anatomical, physiological, histological and pharmaceutical techniques, such animal studies have demonstrated the presence of dura-sensitive neurons in brain and spinal cord structures, such as the medullary dorsal horn, thalamus, hypothalamus, periaqueductal gray (PAG) 15,17-24. In the medullary dorsal horn25,26 and thalamus27,28 the majority of these trigeminovascular neurons respond to noxious skin stimuli either preferentially (wide-dynamic range neurons) or exclusively (high-threshold neurons). Administration of anti-migraine drugs such as ergotamines, triptans, or CGRP antagonists have been shown to inhibit responses to electrical stimulation of the dura in dura-sensitive neurons in the medullary dorsal horn 19,29-31…”

Section: Experimental Activation Of Trigeminovascular Pathwaysmentioning

confidence: 99%

Sensitization of the Trigeminovascular Pathway: Perspective and Implications to Migraine Pathophysiology

2012

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Migraine headache is commonly associated with signs of exaggerated intracranial and extracranial mechanical sensitivities. Patients exhibiting signs of intracranial hypersensitivity testify that their headache throbs and that mundane physical activities that increase intracranial pressure (such as bending over or coughing) intensify the pain. Patients exhibiting signs of extracranial hypersensitivity testify that during migraine their facial skin hurts in response to otherwise innocuous activities such as combing, shaving, letting water run over their face in the shower, or wearing glasses or earrings (termed here cephalic cutaneous allodynia). Such patients often testify that during migraine their bodily skin is hypersensitive and that wearing tight cloth, bracelets, rings, necklaces and socks or using a heavy blanket can be uncomfortable and/or painful (termed her extracephalic cutaneous allodynia). This review summarizes the evidence that support the view that activation of the trigeminovascular pathway contribute to the headache phase of a migraine attack, that the development of throbbing in the initial phase of migraine is mediated by sensitization of peripheral trigeminovascular neurons that innervate the meninges, that the development of cephalic allodynia is propelled by sensitization of second-order trigeminovascular neurons in the spinal trigeminal nucleus which receive converging sensory input from the meninges as well as from the scalp and facial skin, and that the development of extracephalic allodynia is mediated by sensitization of third-order trigeminovascular neurons in the posterior thalamic nuclei which receive converging sensory input from the meninges, facial and body skin.

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Section: Experimental Activation Of Trigeminovascular Pathwaysmentioning

confidence: 99%

Sensitization of the Trigeminovascular Pathway: Perspective and Implications to Migraine Pathophysiology

2012

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“…Such studies have recorded neuronal responses to dural stimulation in the trigeminal nerve (Bove and Moskowitz, 1997) or ganglion (Dostrovsky, 1991;Strassman et al, 1996), medullary and upper cervical dorsal horn Dostrovsky, 1986, 1988a;Strassman et al, 1986;Lambert et al, 1991;Kaube et al, 1992;Burstein et al, 1998), and the ventrobasal thalamus (Davis and Dostrovsky, 1988b;Zagami and Lambert, 1990). Studies in our laboratory have examined response properties of dural afferent neurons in the trigeminal ganglion that can be activated by electrical stimulation of dural sites over the transverse sinus (Strassman et al, 1996;Strassman and Raymond, 1999;Levy and Strassman, 2002a, b).…”

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confidence: 95%

Axon diameters and intradural trajectories of the dural innervation in the rat

Strassman

Weissner

Williams

et al. 2004

J of Comparative Neurology

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Neurophysiological studies have characterized the sensory responses of primary afferent nociceptors that innervate the intracranial dura. The present study used anatomical methods to examine in greater detail the axonal trajectories within the dura, as well as the axonal size distribution of the dural innervation. Immunostaining for CGRP in dural wholemounts revealed a network of fibers extending across the entire dura, with an especially dense plexus running along the borders of the transverse and superior sagittal sinuses. The plexus along the caudal border of the transverse sinus partially overlapped the dural area that shows the greatest density of mast cells. Visualization of axon bundles by DiI application in formalin-fixed tissue revealed two separate systems of fibers in the dura that could be distinguished by the orientation of their trajectories: one that runs parallel to the middle meningeal artery (MMA), and another with a more or less orthogonal orientation that runs rostromedially from the transverse sinus across the MMA. Axons traversed large distances across the dura, but the majority of the branching and arborization was usually concentrated in the distal part of the trajectory. In separate animals, measurement of myelinated axon diameters with electron microscopy showed that approximately one-third of the myelinated axons in the nerves supplying the dura (nervus spinosus and tentorial nerves) could be classified as A-beta, since they were comparable in size to the majority of axons in the trochlear nerve and the upper end of the size range in the trigeminal nerve (i.e., > 5 microm).

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“…Wind-up ( fi g. 1 ) very specifi cally refers to an increase in neuronal responses with subsequent stimuli to A ␦ or C fi bre afferents that has a hyperbolic function with a typical plateau after approximately twenty stimuli. Interestingly we have recently been able to record typical wind-up in trigeminal 12 neurons with responses to electrical stimulation of facial receptive fi elds but not in any trigeminal neurons we studied with electrical stimulation to the dura mater, either for A ␦ or C fi bre inputs [35] . One must be cautious in a negative study but it is curious that intracranial nociceptive afferents do not easily exhibit wind-up.…”

Section: Central Sensitisationmentioning

confidence: 99%

Migraine, Allodynia, Sensitisation and All of That ...

Goadsby¹

2005

Eur Neurol

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Migraine is the most common form of disabling primary headache. One common and often troublesome feature of the disorder is an abnormal sensory state where normally innocuous stimuli are felt as painful: allodynia. This occurs in about two-thirds of patients and manifests as common complaints, such as pain when touching the hair. The neurophysiological correlate of allodynia is sensitisation, an increased afferent barrage for an unchanged peripheral stimulus. Sensitisation may be peripheral, central or disinhibitory. The potential mechanisms of each of these and their possible manipulation by treatments of the acute attack are considered.

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Stimulation of cranial vessels excites nociceptive neurones in several thalamic nuclei of the cat

Cited by 79 publications

References 59 publications

Sensitization of the Trigeminovascular Pathway: Perspective and Implications to Migraine Pathophysiology

Sensitization of the Trigeminovascular Pathway: Perspective and Implications to Migraine Pathophysiology

Axon diameters and intradural trajectories of the dural innervation in the rat

Migraine, Allodynia, Sensitisation and All of That ...

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