Origin and distribution of cerebral vascular innervation from superior cervical, trigeminal and spinal ganglia investigated with retrograde and anterograde WGA-HRP tracing in the rat

Arbab, M. A.-R.; Wiklund, Leif; Svendgaard, Niels-Aage

doi:10.1016/0306-4522(86)90293-9

Cited by 182 publications

(90 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has been found that sympathetic nerve activity (SNA) originating from the superior cervical ganglion increases promptly after pharmacologically (including phenylephrine) induced rapid increase in arterial pressure. 15 Considering that the cerebral vasculature is largely innervated by the superior cervical ganglion, 16 we speculate that phenylephrine bolus treatment may constrict cerebral resistance vessels indirectly via reflexively increased SNA to the brain. This assertion is supported by the findings that cerebral arteries are abundantly innervated by sympathetic nerve fibres 17 and that both a-and b-adrenoceptors are demonstrated in the vascular walls in the brain.…”

Section: Discussionmentioning

confidence: 98%

Effect of Phenylephrine and Ephedrine Bolus Treatment on Cerebral Oxygenation in Anaesthetized Patients

Meng¹,

Alexander²,

Yu³

et al. 2012

Survey of Anesthesiology

View full text Add to dashboard Cite

Editor's key points † Effects of different vasopressor agents on cerebral oxygenation have been unclear. † Ephedrine and phenylephrine, used for intraoperative hypotension, were investigated in a cross-over design study. † Phenylephrine, but not ephedrine, decreased cardiac output (CO) and brain oxygenation. † This study highlights the importance of CO in preserving brain oxygenation during management of intraoperative hypotension.Background. How phenylephrine and ephedrine treatments affect global and regional haemodynamics is of major clinical relevance. Cerebral tissue oxygen saturation (Sct O 2 )-guided management may improve postoperative outcome. The physiological variables responsible for Sct O 2 changes induced by phenylephrine and ephedrine bolus treatment in anaesthetized patients need to be defined.

show abstract

Section: Discussionmentioning

confidence: 98%

Effect of Phenylephrine and Ephedrine Bolus Treatment on Cerebral Oxygenation in Anaesthetized Patients

Meng¹,

Alexander²,

Yu³

et al. 2012

Survey of Anesthesiology

View full text Add to dashboard Cite

show abstract

“…Specifically, a collection of cell bodies in the trigeminal ganglion regulates blood flow in the pain-sensitive large cranial vessels and dura mater (O'Conner and van der Kooy, 1986;May and Goadsby, 1999), the pia mater (Mayberg, Langer, Zervas and Moskowitz, 1981), forebrain and the rostral basilar artery (Arbab, Wiklund and Svendgaard, 1986). Nerve fibres that project from the peripheral and central arms of the trigeminovascular system provide pathways for the transmission of pain signals from cranial vessels to brain centres involved in pain 10 sensation (Borsook et al, 2006), thereby providing the framework for trigeminal nociceptive activity to dilate cranial vessels.…”

Section: The Trigeminovascular System In Migrainementioning

confidence: 99%

Migraine and motion sickness: What is the link?

Cuomo-Granston

Drummond

2010

Progress in Neurobiology

View full text Add to dashboard Cite

The brainstem is a structurally complex region, containing numerous ascending and descending fibres that converge on centres that regulate bodily functions essential to life. Afferent input from the cranial tissues and the special senses is processed, in part, in brainstem nuclei. In addition, brainstem centres modulate the flow of pain messages and other forms of sensory information to higher regions of the brain, and influence the general excitability of these cortical regions. Thus, disruptions in brainstem processing might evoke a complex range of unpleasant symptoms, vegetative changes and neurovascular disturbances and that, together, form attacks of migraine. Migraine is linked with various co-morbid conditions, the most prominent being motion sickness. Symptoms such as nausea, dizziness and headache are common to motion sickness and migraine; moreover, migraine sufferers have a heightened vulnerability to motion sickness. As both maladies involve reflexes that relay in the brainstem, symptoms may share the same neural circuitry. In consequence, subclinical interictal persistence of disturbances in these brainstem pathways could not only increase vulnerability to recurrent attacks of migraine but also increase susceptibility to motion sickness. Mechanisms that mediate symptoms of motion sickness and migraine are explored in this paper. The physiology of motion sickness and migraine is discussed, and neurotransmitters that may be involved in the manifestation of symptoms are reviewed. Recent findings have shed light on the relationship between migraine and motion sickness, and provide insights into the generation of migraine attacks.

show abstract

“…It appears likely that SP remaining after capsaicin re sides in an unreIeasable pool (Burks et a!., 1985). An important feature of trigeminovascular neurons is that they send divergent axon collaterals to inner vate multiple branches of the ipsilateral circle of Willis (Arbab et a!., 1986;O'Connor and van der Kooy, 1986). Because capsaicin affects neuropep tide levels in all the collateral axons, hyperemia is reduced throughout the hemisphere after applica tion to a solitary cortical branch.…”

Section: Postischemic Hyperperfusionmentioning

confidence: 99%

Chronic Trigeminal Ganglionectomy or Topical Capsaicin Application to Pial Vessels Attenuates Postocclusive Cortical Hyperemia but Does Not Influence Postischemic Hypoperfusion

Macfarlane

Taşdemiroğlu

Moskowitz

et al. 1991

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

Summary: Marked hyperemia accompanies reperfusion after ischemia in the brain, and may account for the pro pensity of cerebral hemorrhage to follow embolic stroke or carotid endarterectomy, and for the morbidity that fol lows head injury or the ligation of large arteriovenous malformations. To evaluate the contribution of trigeminal sensory fibers to the hyperemic response, CBF was de termined in 12 symmetrical brain regions, using micro spheres with up to five different isotopic labels, in four groups of cats. Measurements were made at 15-min inter vals for up to 2 h of reperfusion after global cerebral ischemia induced by four-vessel occlusion combined with systemic hypotension of either 10-or 20-min duration. In normal animals, hyperemia in cortical gray matter 30 min after reperfusion was significantly greater after 20 min (n = 10) than after 10 min (n = 7) of ischemia (312 milIOO g/min versus 245 ml/100 g/min; p < 0.01). CBF returned to preischemic levels �45 min after reperfusion and was reduced to �65% of basal CBF for the remaining 75 min. In cats subjected to chronic trigeminal ganglionectomy (n 261tery (MCA) territory, and was confined to regions known to receive a trigeminal innervation. In these animals, sub stance P (SP) levels in the MCA were reduced by 64% (p < 0.01), and the density of nerve fibers containing calci tonin gene-related peptide (but not vasoactive intestinal polypeptide or neuropeptide Y) was decreased markedly on the lesioned side. Topical application of capsaicin (100 nM; 50 f.LI) to the middle or posterior temporal branch of the MCA 10-14 days before ischemia decreased SP levels by 36%. Postocclusive hyperemia in cortical gray matter was attenuated throughout the ipsilateral hemisphere by up to 58%, but the cerebral vascular response to hyper capnia (PaC02 = 60 mm Hg) was unimpaired. The dura tion of hyperemia and the severity of the delayed hypo perfusion were not influenced by trigeminalectomy, cap saicin application, or the intravenous administration of ATP. These data demonstrate the importance of neuro genic mechanisms in the development of postischemic hyperperfusion, and suggest the potential utility of strat egies aimed at blocking axon reflex-like mechanisms to reduce severe cortical hyperemia.

show abstract

Origin and distribution of cerebral vascular innervation from superior cervical, trigeminal and spinal ganglia investigated with retrograde and anterograde WGA-HRP tracing in the rat

Cited by 182 publications

References 48 publications

Effect of Phenylephrine and Ephedrine Bolus Treatment on Cerebral Oxygenation in Anaesthetized Patients

Effect of Phenylephrine and Ephedrine Bolus Treatment on Cerebral Oxygenation in Anaesthetized Patients

Migraine and motion sickness: What is the link?

Chronic Trigeminal Ganglionectomy or Topical Capsaicin Application to Pial Vessels Attenuates Postocclusive Cortical Hyperemia but Does Not Influence Postischemic Hypoperfusion

Contact Info

Product

Resources

About