Immersing the foot in painfully-cold water evokes ipsilateral extracranial vasodilatation.

Temporal pulse amplitude was recorded bilaterally in 56 participants before, during and after three ice-water immersions of the foot. Half of the participants were told that prolonged exposure to freezing temperatures could cause frostbite. Increases in pulse amplitude were greater in the ipsilateral than contralateral temple during and after the three foot-immersions. Although pulse amplitude decreased after threatening instructions and repeated immersion of the foot, the vasodilator response persisted during all three immersions. These findings suggest that nociceptive stimulation of the foot evokes an ipsilateral supra-spinal extracranial vasodilator response, possibly as part of a broader defense response.

Anatomical study of the external carotid artery and its branches for administration of superselective intra-arterial chemotherapy via the superficial temporal artery.

BACKGROUND: The branching patterns of the external carotid artery vary among individuals, and consideration of the proximity of nerves is important during catheter insertion in superselective intra-arterial infusion via the superficial temporal artery. We aimed to evaluate the anatomy of the external carotid artery and its surrounding nerves for safe and accurate administration of superselective intra-arterial chemotherapy via the superficial temporal artery. METHODS: We analyzed the external carotid artery and its branches morphometrically in 28 Japanese cadavers (56 sides). RESULTS: Vascular tortuosity in the preauricular region of the catheter insertion site was observed in 42.9% of the sides; the main trunk of the external carotid artery was excessively tortuous in 25.0% of the sides, primarily in the preparotid region. Faciolingual and superior thyrolingual trunks were observed in 28.6 and 1.8% of the sides, respectively. The superior thyroid, lingual, facial, occipital, and maxillary arteries branched from the external carotid artery above the carotid bifurcation in 41.1% of the sides. The mean distance between the insertion site and maxillary artery was 39.5 mm, indicating the extent of catheter insertion. The auriculotemporal nerve was observed near the superficial temporal artery in the preauricular region in 44.6% of the sides; however, the clearly identifiable nerves in the exposed area were difficult to avoid. CONCLUSION: Because of the branching variations observed in individuals and sides, preoperative angiography is extremely important for avoiding complications.

Perivascular mantle cell lymphoma affecting a temporal artery--a highly unusual cause of temporal headache.

INTRODUCTION: Temporal artery biopsy is a widely performed procedure for clinically suspected temporal arteritis. We the report the case of a 79-year-old male with mantle cell non-Hodgkin's lymphoma previously treated with chemotherapy under follow-up with right-sided orbital recurrence, who developed right temporal headache, tenderness, and visual symptoms in the right eye. His symptoms were unresponsive to steroid treatment and he underwent a temporal artery biopsy. METHODS: The temporal artery was fixed in standard 10% buffered formalin, processed to paraffin wax, 4 micron sections cut through the entire artery and stained with standard haematoxylin and eosin. Some sections were exposed to CD20, CD5, and cyclin D1 immunohistochemistry. RESULTS: Histology showed a perivascular, nodular lymphoid infiltrate composed of small centrocyte-type lymphocytes around the main artery and identical lymphocytes within the wall of a main artery branch. Additionally, the lymphocytes were located around a peripheral nerve in the peri-artery connective soft tissues. These lymphocytes were positive for CD5, CD20, and cyclin D1 indicating a diagnosis of peri-neural, peri-vascular mantle cell non-Hodgkin's lymphoma of identical appearance to that in the index biopsy. CONCLUSIONS: This report describes a highly unusual histological and clinical scenario of peri-temporal artery Mantle cell lymphoma causing temporal headache from peripheral nerve and artery side branch involvement by the lymphoma immediately adjacent to the temporal artery. We propose that involvement of a temporal artery by lymphoma be considered in the differential diagnosis, in patients with an established diagnosis of lymphoma, if presenting with "temporal arteritis" type headache symptoms.

Immersion of the hand in ice water releases adrenergic vasoconstrictor tone in the ipsilateral temple.

Immersion of the hand in painfully cold water induces cutaneous vasodilatation in the temples, more so ipsilaterally than contralaterally. To investigate the mechanism of this response, guanethidine or saline was administered by transcutaneous iontophoresis to a recording site in the temple of ten participants before they immersed one of their hands in ice water. Guanethidine displaces noradrenaline from sympathetic nerve terminals and inhibits sympathetic noradrenergic neurotransmission. Therefore, it was hypothesized that guanethidine pre-treatment would block vasodilatation mediated by release of sympathetic vasoconstrictor tone in cutaneous vessels in the temple. During hand immersion, increases in the amplitude of the pulse waveform detected by laser Doppler flowmetry were greater in the ipsilateral than contralateral temple (86% vs. 34% above baseline, p<0.05), and pre-treatment with guanethidine prevented this asymmetric response (ipsilateral response 21% above baseline and contralateral response 32%, difference not significant). Guanethidine also inhibited ipsilateral increases in cutaneous blood flow during hand immersion in responsive participants. These findings suggest that limb pain inhibited ipsilateral adrenergic vasoconstrictor outflow in the temple. Thus, the findings challenge the concept of the sympathetic nervous system as a "mass action" system that discharges in unison to meet environmental demands. Instead, they suggest that the sympathetic nervous system is highly differentiated, with separate control of discrete reflex pathways on each side of the body.

Anatomía quirúrgica del nervio auriculotemporal en el acceso pre-auricular / Surgical anatomy of the auriculotemporal nerve in the pre-auricular acces

Con el objetivo de aportar datos anatómicos, que posibiliten el acceso a la región pre-auricular, con menor riesgo de lesión del nervio auriculotemporal en procedimientos quirúrgicos, fue realizada esta investigación, sobre las relaciones topográficas y biométricas de este nervio con la arteria y vena temporales superficiales y el trago. Fueron disecadas 24 hemicaras de cadáveres fijados con formaldehído al 10 por ciento, disponibles en el Laboratorio de Anatomía del Departamento de Morfología Humana de la Universidad Federal de Alagoas, Brasil. En siete casos (29,2 por ciento) el nervio subía posteriormente a los vasos temporales superficiales, y en otros siete (29,2 por ciento), subía junto a la vena. En tres casos (12,5 por ciento) el nervio emergía junto con la arteria. En dos casos (8,3 por ciento), el nervio estaba en posición intermedia. En cinco casos (20,8 por ciento), el nervio subía junto con ambos vasos. La menor distancia del nervio auriculotemporal a la línea pre-auricular fue de 0,3 mm, y la mayor fue de 11,5 mm, con media de 1,89 mm. La menor distancia del nervio con la arteria temporal superficial fue de 0,1 mm, y la mayor fue de 14,6 mm, con media de 8,66 mm, situándose la arteria anterior. Cuando la vena era anterior al nervio, la menor distancia entre sí, fue de 0,2 mm y la mayor, 10,9 mm, con media de 2,91 mm. Cuando la vena estaba en posición posterior, la distancia mínima fue de 0,1 mm, y la máxima de 9,4 mm, siendo la media de 2,54 mm. Concluimos que el nervio auriculotemporal presenta posición variable en la región pre-auricular y es la estructura más próxima a la línea pre-auricular.

Central projections of sensory innervation of the rat superficial temporal artery.

Elucidating the central sensory projection pathways of extra- and intracranial vessels appears to be of fundamental importance for understanding the pathogenetic mechanisms of primary headaches. In this paper, two kinds of tracers, choleragenoid (cholera toxin subunit b, CTb) and wheat germ agglutinin conjugated horseradish peroxidase (WGA-HRP), were used to transganglionically label the central sensory projections of the innervation of the superficial temporal artery (STA). Following either of the tracers applied on the adventitia of the STA, labelled terminations were found mainly in the ipsilateral C1-C3 spinal dorsal horns. Sparse labelling was also found in the interpolar and caudal parts of the spinal trigeminal nucleus. In the spinal cord, CTb labelled profiles were mainly located in laminae III and IV, whereas WGA-HRP labelled profiles were mainly located in laminae I and II. In the medulla, CTb but not WGA-HRP labelled terminals were found in a small dorsolateral extension of the cuneate nucleus. The present results indicate that the primary sensory nervous center of the STA is located in the rostral cervical spinal dorsal horn. The caudal parts of the spinal trigeminal nucleus, which has been demonstrated as a center of pain and temperature sensations of the head and face, transmits limited information from the STA to higher nervous centers.

Peptidergic innervation of human cerebral blood vessels and saccular aneurysms.

Peptidergic innervation of the human cerebral vasculature has not yet been described in detail and its role in the maintenance of cerebral autoregulation still needs to be established. Similarly, few data exist on the innervation of vascular malformations. The aim of this study was to clarify the peptidergic innervation patterns of human cerebral arteries of various sizes, and, for the first time, that of saccular aneurysms. Light microscopic study of whole-mount preparations of human cerebral arteries and aneurysm sacs resected either during tumor removal or after neck-clipping were carried out by means of silver-intensified light microscopic immunocytochemistry visualizing neuropeptide-Y, calcitonin gene-related peptide and substance P immunoreactivity. Systematic morphological investigations confirmed the presence of longitudinal fiber bundles on the adventitia and a network-like deeper peptidergic system at the adventitia-media border, while in smaller pial and intraparenchymal vessels, only sparse longitudinal immunopositive axons could be detected. The innervation pattern was totally absent in the wall of saccular aneurysms with the complete disappearance of peptidergic nerve fibers in some areas. To the best of our knowledge neither the disappearance of this network on small pial and intraparenchymal vessels, nor the absence of an innervation pattern in saccular aneurysms have been described before. Nonhomogeneous peptidergic innervation of the human cerebral vascular tree might be one of the factors responsible for the distinct autoregulatory properties of the capacitance and resistance vessels. Malfunction of this vasoregulatory system might lead to the impairment of autoregulation during pathological conditions such as subarachnoid hemorrhage.

Weakness of sympathetic neural control of human pial compared with superficial temporal arteries reflects low innervation density and poor sympathetic responsiveness.

BACKGROUND AND PURPOSE: The primary goal of these studies was to understand and investigate the capacity of perivascular nerves to influence the tone of human pial arteries and to compare them with other human cephalic arteries, the superficial temporal and middle meningeal. METHODS: Responses to electrical activation of intramural nerves and related features of fresh segments of human cephalic arteries-the pial (PA; 478+/-34 microm ID), middle meningeal (MMA; 540+/-41 microm ID), and superficial temporal (STA; 639+/-49 microm ID)-obtained from patients aged 15 to 82 years during surgical procedures were studied on a resistance artery myograph. RESULTS: The PA segment responses to electrical nerve activation and to norepinephrine (NE; 10[-5] mol/L) were 1% and 21% of tissue maximum, respectively, compared with 6% and 34% for the MMA and 14% and 90% for the STA. Tissue maximum was defined as the force increase to 127 mmol/L KCl plus arginine vasopressin (1 microm). All arteries dilated well to acetylcholine. Possible explanations for the PA marginal neurogenic responses were assessed. NE ED50 was 5.4+/-2.2 X 10(-7) mol/L and did not vary with age or diameter. NE responsiveness did not increase in vessels with spontaneous or raised potassium-induced tone. Relaxation to isoproterenol was variable and propranolol did not increase the neurogenic response. Neither N(G)-monomethyl-L-arginine, N(G)-nitro-L-arginine methyl ester, endothelium removal, nor indomethacin consistently influenced the contractions to NE or neurogenic reactivity. The weak PA neurogenic response is in keeping with its poor innervation. As determined by catecholamine histofluorescence, innervation in the PA is sparse, with density increasing in the order PA, MMA, and STA. The incidence of nerve structures in the PA adventitio-medial junction was only 3% of those in the STA, and these were situated more than 3 microm from the closest smooth muscle cell. CONCLUSIONS: We conclude that the weak neurogenic response of adult human pial artery reflects its poor innervation and responsiveness to NE, implying that these features are not important in the regulation of its diameter.

The temporal branch of the facial nerve: how reliably can we predict its path?

A thorough examination of the temporal branch of the facial nerve was performed to characterize precisely the number of rami crossing the zygomatic arch and their location with respect to bone and soft-tissue landmarks. Fresh cadaver dissection was performed in 12 facial halves, dissecting the facial nerve superiorly from the stylomastoid foramen to identify all branches crossing the zygomatic arch. There were a median of three (range two to four) rami of the temporal branch crossing the lower aspect of the zygomatic arch, with distinct anterior and posterior divisions identified in each dissection. In 8 of the 12 dissections, one or more separate middle divisions of the nerve also were seen at the inferior aspect of the zygomatic arch. Superior to the zygomatic arch, frequent interconnections were noted between all divisions of the temporal branch, but no connections were noted to other branches of the facial nerve. Previous descriptions of the course of the temporal branch based on soft-tissue landmarks most closely correlated with nerve rami that were found in the present study to be located within the anterior division of the nerve. On crossing the inferior aspect of the zygomatic arch, the anterior and middle divisions of the temporal branch were located a median of 12 and 4 mm anterior to the articular eminence, respectively; the posterior division ranged in location from 10 mm posterior to 7 mm anterior to the articular eminence. The range over which rami of the temporal branch crossed the inferior aspect of the zygomatic arch was equally divided anterior and posterior to the articular eminence and covered up to 50 percent of the total length of the zygomatic arch. The present study confirms that the temporal branch is not a single nerve branch but consists of multiple rami that cross the zygomatic arch anywhere for over half the length of its inferior border. Techniques for localizing the nerve based on reference points from two soft-tissue landmarks are therefore unreliable.

An anatomic study of the temporoparietal fascial flap.

OBJECTIVE: To clarify the neurovascular relationships in the temporoparietal fascial flap and to access its possible use as a sensate free of a pedicled flap. DESIGN: Anatomic dissections (gross) and examinations (histologic) were performed on 10 fresh cadaver heads. SETTING: Academic tertiary care facility, Boston, Mass. MAIN OUTCOME MEASURES: To determine the relationship of the sensory innervation (the auriculotemporal nerve) to the vascular supply (the superficial temporal artery) of the temporoparietal fascial flap, in addition to determining safe incisions and the level of flap elevation that will preserve the sensory supply to the flap. RESULTS: There is a consistent relationship of the auriculotemporal nerve to the superficial temporal artery allowing for auriculotemporal nerve preservation with standard flap elevation techniques and easy nerve identification in this cadaveric study. CONCLUSION: A clear understanding of the anatomic pattern allows for the potential creation of a sensate fascial flap or vascularized nerve graft that would add a potential additional dimension to this fascial flap.

The peptidergic innervation of the human superficial temporal artery: immunohistochemistry, ultrastructure, and vasomotility.

The peptidergic innervation of the human superficial temporal artery was investigated by means of immunohistochemical, ultrastructural, and in vitro pharmacological techniques. A dense network of nerve fibers was found in the adventitia. The majority of the nerve fibers displayed immunoreactivity for tyrosine hydroxylase and neuropeptide Y (NPY). A moderate supply of perivascular nerve fibers displayed either acetylcholinesterase activity or immunoreactivity for vasoactive intestinal peptide (VIP), peptide histidine methionine-27 (PHM), and calcitonin gene-related peptide (CGRP). Only a few nerve fibers displayed substance P (SP), neurokinin A (NKA), and neuropeptide K (NPK) immunoreactivity. In double immunostained preparations, SP immunoreactivity was co-localized with NPK and CGRP in the same nerve fibers. Ultrastructural studies revealed the presence of numerous axon variocosities at the adventitial--medial border. NPY, VIP, and CGRP immunoreactivities occurred in the same type of large granular vesicles, but in morphological distinct nerve profiles. NPY had, in general, no direct vasoconstrictor effect. However, at a low concentration of NPY contractile response induced by NA (10(-7)-10(-6)M) was 9-15 times enhanced. The NPY-induced potentiation of the NA-induced contraction was not dependent on the presence of an intact endothelium. No significant difference was found between acetylcholine, VIP, and PHM in either potency or degree of relaxation. SP, NKA, and CGRP also acted as vasodilatory agents, with CGRP being more potent than the tachykinins. The response to SP, but not CGRP, was dependent on an intact endothelium. Pretreatment of the vessels with a low concentration of NPY did not change the responses to ACh, VIP, SP, or CGRP.

Histological and functional studies on the nitroxidergic nerve innervating monkey cerebral, mesenteric and temporal arteries.

Nitroxidergic nerves and their functional role were determined in a variety of monkey arteries. Nitric oxide synthase-immunoreactive nerve fibers innervating the monkey arterial wall were histochemically determined by the use of nitric oxide synthase antiserum. Thin nitric oxide synthase-immunoreactive fibers were consistently found in the outer media of monkey cerebral, mesenteric and temporal arteries, in addition to many thicker fibers and nerve bundles in the adventitia. In the monkey pterygopalatine ganglion, the immunoreactivity was clearly seen in nerve cells, bundles and fibers. Helical strips of monkey arteries were exposed to the bathing media for tension recordings and were stimulated by electrical square pulses. In helical strips of the cerebral artery denuded of the endothelium, transmural electrical stimulation produced relaxations that were abolished by tetrodotoxin or NG-nitro-L-arginine, a nitric oxide synthase inhibitor. In the monkey mesenteric and temporal arterial strips treated with alpha-adrenoceptor antagonists, the relaxation caused by electrical stimulation was also abolished by the nitric oxide synthase inhibitor, and it was restored by L-arginine. Nitroxidergic perivascular nerves, histologically demonstrated, appear to play an important role in dilating the monkey cerebral artery and in counteracting a vasoconstriction associated with noradrenergic nerve activation in the mesenteric and temporal arteries.

Responses to perivascular nerve stimulation of distal temporal arteries from dogs and monkeys.

In helical strips of dog distal superficial temporal artery denuded of endothelium and partially contracted with prostaglandin F2 alpha (PGF2 alpha), nicotine produced a moderate relaxation preceded by no contraction or a slight contraction. The contraction was less than that observed in proximal arterial strips obtained from the same dogs and was abolished by alpha-adrenoceptor antagonists. Relaxations under alpha-receptor blockade were greater in the distal than in the proximal arteries. Treatment with NG-nitro-L-arginine (L-NA), a nitric oxide (NO) synthase inhibitor, abolished the relaxation caused by nicotine and transmural electrical stimulation (5 Hz for 40 s), the response being reversed by L- but not by D-arginine. In monkey temporal arteries of the distal and proximal portions treated with alpha-antagonists, nicotine produced similar magnitudes of relaxation, which were abolished by treatment with the NO synthase inhibitor. Vasodilator nerves appear to play an important role in regulation of small arterial tone; noradrenergic vasoconstrictor function is less and vasodilator nerve function is more evident in dog distal arteries than in dog proximal arteries. The neurally induced relaxation in dog and monkey distal temporal arteries is postulated to be mediated by NO derived from nerves.

Nitric oxide synthase-immunoreactive nerve fibers in dog cerebral and peripheral arteries.

Nitric oxide synthase (NOS)-immunoreactive fibers innervating the dog arterial wall were histochemically determined by the use of NOS antiserum. NOS-immunoreactive fibers were consistently found in every arterial wall examined. In a whole-mount preparation, NOS-positive fibers were detectable in the small pial artery having a diameter of about 100 microns as well as the proximal middle cerebral artery. Further detailed analyses in thin cryostat sections indicated that in middle cerebral, basilar, temporal, mesenteric and femoral arteries, fine NOS-positive fibers were detected in outer zones of the media in addition to many thicker fibers in the adventitia. However, in the coronary artery, many thick fibers were situated in the adventitia, and fine NOS-positive fibers were not found in the media. Injection of ethanol to the pterygopalatine ganglion markedly decreased or abolished the NOS immunoreactivity in nerve cells and fibers and abolished the innervation of NOS-positive fibers in the wall of middle cerebral artery of the ipsilateral side. Together with findings in our previous publications concerning the functional role of nitroxidergic nerve in the control of arterial tone, we conclude that perivascular nerves containing NOS are crucial in eliciting the neurally induced, NO-mediated arterial relaxation.

Neurogenic and non-neurogenic relaxations caused by nicotine in isolated dog superficial temporal artery.

Nicotine produced a transient contraction followed by biphasic (rapid and slow) relaxations in dog superficial temporal arterial strips denuded of the endothelium. The responses to nicotine were abolished by treatment with hexamethonium. The nicotine-induced contraction was abolished by phentolamine and potentiated by NG-nitro-L-arginine (L-NA), a nitric oxide synthase inhibitor. The slowly developing relaxation was markedly suppressed by indomethacin and tranylcypromine, a prostaglandin I2 synthetase inhibitor, whereas the rapid relaxation was abolished by L-NA. The inhibitory effect of L-NA was reversed by L-, but not D-, arginine. NG-nitro-D-arginine had no effect. Transmural electrical stimulation elicited a transient relaxation in phentolamine-treated arteries. The relaxation was not influenced by indomethacin but was abolished by L-NA and tetrodotoxin. Nicotine increased intracellular cyclic AMP and cyclic GMP in the endothelium-denuded arteries. The increment of cyclic AMP was inhibited by indomethacin but not by L-NA, whereas that of cyclic GMP was not influenced by indomethacin but was abolished by L-NA. It may be concluded that nicotine stimulates the adrenergic and nitroxidergic nerves innervating the temporal arterial wall, resulting in a contraction and a rapidly developing relaxation, respectively; the latter is mediated by cyclic GMP. Potentiation by the nitric oxide synthase inhibitor of the contractile response to nicotine is expected to be a suppression of the relaxation mediated by the nerve-derived nitric oxide. Slow relaxations caused by nicotine appear to be associated with the elevation of cyclic AMP produced possibly by prostaglandin I2, which is released from subendothelial, non-neuronal tissues.

Reciprocal regulation by putatively nitroxidergic and adrenergic nerves of monkey and dog temporal arterial tone.

In monkey and dog superficial temporal artery strips denuded of the endothelium, transmural electrical stimulation and nicotine produced a contraction that was abolished by phentolamine and potentiated by NG-nitro-L-arginine (L-NNA), a nitric oxide (NO) synthesis inhibitor. The potentiation was reversed by L-arginine but not by its D-enantiomer. The arteries treated with phentolamine and contracted with prostaglandin F2 alpha responded to the electrical stimulation and nicotine with relaxations that were abolished by tetrodotoxin and hexamethonium, respectively, and were markedly inhibited by L-NNA but not by D-NNA, atropine, and timolol. The L-NNA-induced inhibition was reversed by L-arginine. Nicotine increased the level of guanosine 3',5'-cyclic monophosphate in the monkey arteries; the increment was prevented by L-NNA. It is concluded that the monkey and dog temporal arterial tone appears to be reciprocally regulated by adrenergic vasoconstrictor and nonadrenergic noncholinergic vasodilator nerves. The neurogenic relaxation would be mediated by NO that is possibly released from the vasodilator nerve and transmits information to smooth muscle; therefore the nerve may be called "nitroxidergic."

Analysis of the potentiating action of N(G)-nitro-L-arginine on the contraction of the dog temporal artery elicited by transmural stimulation of noradrenergic nerves.

Dog temporal artery strips without endothelium responded to transmural electrical stimulation with a contraction which was potentiated by NG-nitro-L-arginine (L-NNA). The noradrenaline-induced contraction and the release of 3H-noradrenaline were not affected. The stimulation-induced contraction was reversed to a relaxation by phentolamine. The relaxation was not influenced by timolol and atropine but inhibited by L-NNA; L-arginine abolished the inhibition. Transmural stimulation released NOx from the arteries, the release being abolished by L-NNA. Potentiation by L-NNA of the neurally-induced contraction appears to be due to elimination of NO produced by non-adrenergic, non-cholinergic vasodilator nerve activation.

[Morphologic changes in the skin and superficial temporal arteries in Sneddon's syndrome]. / Morfologicheskie izmeneniia v kozhe i poverkhnostnykh visochnykh arteriiakh pri sindrome Sneddona.

Skin biopsies from livedo's areas of 25 patients and fragments of superficial temporal arteries of 10 patients with Sneddon's syndrome were examined. Pathological changes in the dermis arteries of small and medium calibers were found in the form of the intima hyperplasia, proliferation of vascular wall cell elements (80%), arterial thrombosis (with diameter of 60-200 microns). These changes were found in 68% of observations when clinical and morphological signs of vasculitis were lacking. "Arteriopathy" is the most appropriate term for such lesions. Focal and diffuse fibro-muscular elastic hyperplasia of the intima and muscular layer fibrosis in the wall of superficial temporal arteries may be considered as age-associated lesions. Ultrastructurally, a selective damage of the non-adrenergic part of the nervous apparatus of the dermal arteries and superficial temporal arteries were observed; this suggests the participation of the damaged vascular neurogenic regulation in the formation of organic vascular changes.

Density of sympathetic nerve terminals in human superficial temporal arteries: potassium permanganate fixation and monoamine oxidase histochemistry.

The density of sympathetic nerve terminals in human superficial temporal arteries from 5 cases at intra- and extracranial bypass surgery was examined with two histochemical methods, one with potassium permanganate fixation and the other with the new monoamine oxidase staining technique. By potassium permanganate fixation, small cored vesicles containing fibers of noradrenergic nerve terminals made up 29.2% of all nerve fibers in the adventitia. The monoamine oxidase-containing nerves in the adventitia made up 31.4%. According to this study, sympathetic nerve terminal density in human superficial temporal arteries was assumed to consist of approximately 30% of all adventitial nerve terminals. In periadventitial nerve bundles, some unmyelinated axons contained monoamine oxidase activity. Thus, staining is considered to be useful in demonstrating the periadventitial and intervaricose fibers as well as the nerve terminals of sympathetic nerves in human cerebral arteries.

Peptide-containing nerve fibres in human extracranial tissue: a morphological basis for neuropeptide involvement in extracranial pain?

It has been suggested that a number of peptides may be involved in the transmission of pain. In order to evaluate the possible role of peptides in the development of headache, we have, in the present study, examined the presence of nerve fibres containing neuropeptide Y (NPY), vasoactive intestinal peptide (VIP), substance P (SP) and calcitonin gene-related peptide (CGRP) in human temporal and occipital tissues. In the skin, delicate VIP, SP and CGRP fibres occur beneath the epidermis, sometimes running into the folds of the dermal ridges. In deeper layers of the dermis, small blood vessels are occasionally surrounded by single nerve fibres containing NPY, VIP, SP and CGRP. Large temporal and occipital arteries are surrounded by a meshwork of such fibres. In addition, NPY and VIP fibres are seen around sweat glands and hair follicles. Smooth muscle bundles in the dermis are surrounded by VIP fibres, whereas the temporal muscle per se is devoid of such fibres.