Cranial Circulation Research Articles

Cranial arterial foramen diameter in turtles: a quantitative assessment of size-independent phylogenetic signal

AbstractThe study of turtle systematics has relied heavily on characters of the cranial circulation, particularly the internal carotid system, which is represented by canals and foramina in the bony skull. Comparison of cranial arteries and foramina has been qualitative; we undertake a quantitative reassessment of these features. We compare three methods of size removal from morphological data, and suggest methods by which size standardisation may be achieved in instances of incomplete preservation and statistically inadequate sample sizes. Further, we demonstrate that cranial arterial foramina provide a reliable estimate of vessel size, and conclude that the internal carotid system varies quantitatively, significantly and consistently among turtle clades, in a fashion which allows predictions to be made about phylogenetic relationships.

The trigeminovascular system in the human. Cerebral blood flow, functional imaging and primary headache

Primary headache syndromes, such as cluster and migraine, are widely described as vascular headaches, even though there is considerable clinical evidence to suggest that both conditions are primarily central, that is regulated by the brain. The shared anatomical and physiological substrate for both clinical syndromes is the neural innervation of the cranial circulation. Early functional imaging using PET has shed light on the genesis of both syndromes, documenting activation in the midbrain and pons in migraine and in the hypothalamic gray in cluster headache. These areas are involved in the pain process in a permissive or triggering manner rather than simply as a response to first-division nociceptive pain impulses. This article reviews findings in the physiology of the trigeminovascular system which demand renewed consideration of the neural influences in many primary headaches and the physiology of the neural innervation of cranial circulation. Primary headaches should thus be regarded as neurovascular headaches to emphasize the interaction between nerves and vessels which is their underlying characteristic.

Isolation of the arterial supply to the carotid and central chemoreceptors in the sheep.

The aim of our study was to develop and validate a simple surgical model in the sheep which allows control of the gas composition of the blood supplying the carotid and central chemosensitive area independently of the rest of the body. This approach was made possible due to the specific features of the cranial circulation in the sheep. An extracorporeal circuit, consisting of a pump and a gas exchanger, was placed at the level of the two common carotid arteries to create a pressure gradient between the carotid and the systemic systems and to reverse blood flow in the vertebral vessels via the occipital arteries. When a pressure gradient of about 40 Torr was created between the systemic and carotid circulation, we found that no blood could reach the carotid bodies and the medulla without passing though the extracorporeal circulation. This was established (1) by measuring vertebral blood flow; and (2) by injecting either a coloured suspension or particles labelled with (99m*)Tc into the systemic or the carotid circulation. The slope of the relationship between minute ventilation (V(E)) and systemic arterial P(CO2) (P(a,CO2)) during high CO(2) inhalation in seven hyperoxic vagotomised and anaesthetised sheep was dramatically reduced, but remained above zero, when P(a,CO2) was maintained constant in the cephalic circuit (0.11 +/- 0.15 vs. 0.70 +/- 0.35 l min(-1) Torr(-1) for the control tests). This residual V(E) response to CO(2) inhalation remains to be explained since it could not be accounted for by any of the chemical or circulatory changes occurring in the cephalic circulation. Nevertheless, this preparation provides an easy method of maintaining chemical and circulatory homeostasis at the chemoreceptor level.

Toward ambulatory arteriovenous CO2 removal: initial studies and prototype development.

Extracorporeal arteriovenous carbon dioxide removal (AVCO2R) using percutaneous cannulae and a low resistance gas exchanger achieves near total CO2 removal, allowing lung rest and potentially improving survival. AVCO2R, redesigned to allow ambulation, has potential as treatment for severe chronic obstructive pulmonary disease or rehabilitation before lung transplant. The purposes of this study were to 1) determine the optimal ambulatory access for AVCO2 removal and 2) develop a prototype Ambulatory-AVCO2R gas exchanger. Initially, reinforced Gore-Tex 6 mm (two) and 8 mm (four) grafts were anastomosed to sheep carotid arteries and jugular veins as a loop in parallel to the cranial circulation to determine blood flow capabilities. Blood flow was 100-150 ml/min with a 14 gauge dialysis needle, and transected 6 mm Gore-Tex grafts achieved 500-900 ml blood flow, whereas transected 8 mm grafts achieved up to 2000 ml/min flow. The polytetrafluoroethylene (PTFE) loops were then connected to our newly developed ultra low resistance pumpless gas exchanger for ambulatory AVCO2R. The average pressure gradient across the prototype Ambulatory-AVCO2R gas exchangers (n = 5) was 2.8 +/- 0.8 mm Hg, and mean CO2 removal was 104.8 +/- 14.0 ml/min, with an average blood flow of 900 ml/min. We conclude that an 8 mm Gore-Tex reinforced graft arteriovenous loop supplies ample blood flow for our new ultra low resistance Ambulatory-AVCO2R to achieve near total CO2 removal.

Magnetic resonance angiography in facial and other pain: neurovascular mechanisms of trigeminal sensation.

For much of the twentieth century migraine and cluster headache have been considered as vascular headaches whose pathophysiology was determined by changes in cranial vascular diameter. To examine nociceptive neural influences on the cranial circulation, the authors studied healthy volunteers' responses to injection of the pain-producing compound capsaicin in terms of the caliber of the internal carotid artery. The study was conducted using magnetic resonance angiographic techniques. Injection of capsaicin into the skin innervated by the ophthalmic (first) division of the trigeminal nerve elicited 40% +/- 27% (mean +/- SD) increase in vascular cross-sectional area in the right (ipsilateral) internal carotid artery when compared with the mean baseline ( P < 0.001). Injection of capsaicin into the skin of the chin to stimulate the mandibular (third) division of the trigeminal nerve and into the leg led to a similar pain perception and failed to produce any significant change in vessel caliber. The data suggest that there is a highly functionally organized, somatotopically congruent trigeminal innervation of the cranial vessels, with a potent vasodilator effect of the ophthalmic division on the large intracranial vessels. The data are consistent with the notion that pain drives changes in vessel caliber in migraine and cluster headache, not vice versa. These conditions therefore should be regarded as primary neurovascular headaches not as vascular headaches.

Thiopental directly depresses lumbar dorsal horn neuronal responses to noxious mechanical stimulation in goats.

Thiopental has hypnotic actions in the brain, but it also depresses nociceptive transmission. In this study we examined whether thiopental had direct (spinal) and/or indirect (supraspinal) effects on the responses of single lumbar dorsal horn neurons to noxious mechanical stimulation, using a method to deliver thiopental differentially to either the torso or cranial circulation in goats. Goats (n=10) were anesthetized with isoflurane and neck dissections performed to permit cranial bypass. A lumbar laminectomy was made to permit single-unit recording of lumbar dorsal horn neuronal activity (1-2 neurons/animal). Isoflurane was maintained at 0.8+/-0.1% to both head and torso throughout the study. During cranial bypass, thiopental was separately administered to the torso (low dose, 1.5+/-0.5 mg/kg; high dose, 3.7+/-0.5 mg/kg) or cranial (low dose, 0.12+/-0.03 mg/kg; high dose, 0.2 mg/kg) circulation. Thiopental administered to the torso significantly depressed dorsal horn neuronal responses to noxious stimulation at the high dose: 757+/-471 to 392+/-305 impulses/min at 1 min post-injection, P<0.006 (n=14); evoked responses recovered at 5 min post-injection. At the low dose, there was a similar numerical decrease, but this did not reach significance: 876+/-780 to 407+/-499 impulses/min at 1 min post-injection, P>0.05 (n=6). No significant change was observed when thiopental was administered to the cranial circulation: low dose, 1061+/-1167 to 965+/-874 impulses/min at 1 min post-injection, P>0.05 (n=10); high dose, 864+/-331 to 917+/-525 impulses/min at 1 min post-injection, P>0.05 (n=8). Thiopental has a direct (spinal) depressant effect on dorsal neuronal responses to noxious stimulus, but no significant supraspinal effect.

The lack of vasoconstrictor effect of the pineal hormone melatonin in an animal model predictive of antimigraine activity.

The pineal hormone, melatonin, has been implicated in the pathophysiology of migraine and several studies have demonstrated its vasoconstrictor properties. In the present study, systemic and carotid haemodynamic effects of melatonin, administered directly into the carotid artery, were investigated in anaesthetized pigs. Ten-minute intracarotid infusions of melatonin (1, 10 and 100 microg kg(-1) min(-1)) produced slight decreases in blood pressure and total carotid and arteriovenous anastomotic blood flows, but nutrient blood flow was not affected. The decrease in carotid blood flow was entirely caused by the hypotension, since no changes in vascular conductance values were observed. It is concluded that melatonin itself is not capable of producing vasoconstriction in the cranial circulation of anaesthetized pigs. Thus, it appears that melatonin has no anti-migraine potential via a vasoconstrictor mechanism.

Neuroimaging in headache.

Neuroimaging of primary headache syndromes, such as cluster headache and migraine, has begun to provide a glimpse of the neuroanatomical and physiological basis of the conditions. Although these headache types have been widely described as vascular, there is now considerable imaging and clinical evidence to suggest that they are primarily driven from the brain. The shared anatomical and physiological substrate for both of these clinical problems is the neural innervation of the cranial circulation. Functional imaging with positron emission tomography (PET) has shed light on the genesis of both syndromes, documenting activation in the midbrain and pons in migraine, and in the hypothalamic grey in cluster headache. These areas are involved not simply as a response to first division nociceptive pain impulses but specifically in each syndrome, probably in some permissive or dysfunctional role. In a recent PET study in cluster headache, as well as brain activation, tracer pooled in the region of the major basal arteries. This is likely to be due to vasodilatation of these vessels during the acute pain-attack and represents the first convincing activation of neural vasodilator mechanisms in humans. The author takes the view that the known physiology and pathophysiology of the systems involved dictate that these disorders should be collectively regarded as neurovascular headaches to place emphasis on the interaction between nerves and vessels, which is the underlying characteristic of these syndromes. Understanding this neurovascular relationship facilitates an understanding of the pain mechanisms, while characterising the CNS dysfunction will ultimately allow us to dissect out the basic pathogenesis of these disorders.

Propofol action in both spinal cord and brain blunts electroencephalographic responses to noxious stimulation in goats.

Anesthetics, including propofol, depress the electroencephalogram (EEG) and neuronal activity in the midbrain reticular formation (MRF). Because propofol has anesthetic effects in the spinal cord, we hypothesized that it would indirectly depress EEG and MRF neuronal responses to noxious stimulation in part by a spinal cord action. Six goats were anesthetized with isoflurane and the jugular veins and carotid arteries were isolated to permit cranial bypass and differential propofol delivery. A noxious mechanical stimulus was applied to the distal forelimb while recording bifrontal EEG and MRF single-unit activities. Propofol was separately administered to the cranial (0.08 +/- 0.06 mg/kg) and torso circulations (4 mg/kg) and the noxious stimulus applied at 1,5, 10, and 15 min after each injection. N/A. N/A. N/A. Noxious stimulation decreased total power (TP) from 96 +/- 33, microV2/Hz to 38 +/- 20microV2/Hz, (mean +/- SD) and increased spectral edge frequency (SEF) from 10 +/- 3 Hz to 19 +/- 5 Hz (p<0.01). Propofol administered to the torso prevented stimulus-evoked changes in TP (121+/- 80 microV2/Hz, 121 +/- 74 microV2/Hz, 114 +/- 74 microV2/Hz at 1,5, and 10 min respectively, p<0.01 compared to control evoked response) and SEF (11 +/- 6Hz, 9 +/- 2Hz, 10 +/- 6Hz, and 12 +/- 5Hz at 1, 5, 10 and 15 min, respectively, p<0.001 compared to control evoked response). Propofol administered to the cranial circulation significantly blunted the EEG and MRF response, while torso-administered propofol had slight effects on MRF responses. Propofol blunted the EEG response to noxious stimulation in part via a subcortical action.

Plasma levels of calcitonin gene-related peptide in chronic tension-type headache.

Calcitonin gene-related peptide (CGRP) is involved in the pathophysiology of migraine and cluster headache. Whether CGRP has any role in chronic tension-type headache is unknown. To compare interictal plasma levels of CGRP between patients with chronic tension-type headache and healthy control subjects, to investigate plasma CGRP in relation to headache state, and to compare plasma CGRP between the peripheral and the cranial circulation. Blood from the antecubital vein was drawn from 30 patients with chronic tension-type headache and 34 healthy control subjects. In addition, blood samples from the consecutive first 15 patients and from the consecutive first 20 healthy control subjects were also collected from the external jugular vein. CGRP levels measured in the peripheral circulation in patients on days without headache, 63+/-5 pmol/L, tended to be higher than CGRP levels in control subjects, 53+/-3 pmol/L (p = 0.06). In patients, no differences were found between CGRP levels assessed ictally and interictally in either the cranial (p = 0.91) or the peripheral (p = 0.62) circulation. Plasma CGRP level was higher in the external jugular vein than in the antecubital vein on days without headache (p = 0.03) but not on days with headache (p = 0.82). In control subjects, CGRP levels in the cranial circulation did not differ from CGRP levels in the peripheral circulation (p = 0.92). Exploratory analyses showed that 8 patients whose usual headache quality was throbbing had a higher interictal plasma CGRP level than control subjects (p = 0.002), whereas plasma CGRP level was normal in 22 patients with pressing headaches (p = 0.36). Plasma levels of CGRP are normal in patients with chronic tension-type headache and are unrelated to headache state. Interictal plasma CGRP was increased in patients with a pulsating pain quality. Because the authors have previously shown a similar increase of interictal CGRP levels in migraine, this study suggests that headaches with symptoms that fulfill International Headache Society criteria for tension-type headache may be pathophysiologically related to migraine, if the headache has a pulsating quality.

Development and Clinical Application of Electroencephalographic Bispectrum Monitoring

Development and Clinical Application of Electroencephalographic Bispectrum Monitoring Jay Johansen;Peter Sebel; Anesthesiology

Propofol directly depresses lumbar dorsal horn neuronal responses to noxious stimulation in goats.

We tested the hypothesis that propofol, acting in the brain, would either enhance, or have no effect, on lumbar dorsal horn neuronal responses to a noxious mechanical stimulus applied to the hindlimb. We recorded the response of lumbar dorsal horn neurons during differential delivery of propofol to the brain and torso of goats. Goats were anesthetized with isoflurane and neck dissections performed which permitted cranial bypass. A laminectomy was made to allow microelectrode recording of lumbar dorsal horn neuronal activity. Isoflurane was maintained at 0.8+/-0.1% to both head and torso throughout the study. During cranial bypass propofol was separately administered to the torso (1 mg x kg(-1), n = 7; 3.75 mg x kg(-1), n = 8) or cranial (0.04 mg x kg(-1), n = 7; 0.14 mg kg(-1), n = 8) circulations. Propofol administered to the torso depressed dorsal horn neuronal responses to noxious stimulation: low dose: 500+/-243 to 174+/-240 impulses x min(-1) at one minute post-injection, P<0.001; high dose: 478+/-204 to 91+/-138 impulses x min(-1) at one minute post-injection, P<0.05). Propofol administered to the cranial circulation had no effect: low dose: 315+/-150 to 410+/-272 impulses x min(-1), P>0.05; high dose: 462+/-261 to 371+/-196 impulses x min(-1), P>0.05. These data indicate that propofol has a direct depressant effect on dorsal horn neuronal responses to noxious stimulation, with little or no indirect supraspinal effect.

Plasma levels of substance P, neuropeptide Y and vasoactive intestinal polypeptide in patients with chronic tension-type headache

Animal and human studies have shown that substance P (SP), neuropeptide Y (NPY) and vasoactive intestinal polypeptide (VIP) are involved in the pathophysiology of acute and chronic pain conditions. The primary aim of the present study was to compare plasma levels of SP, NPY and VIP in external jugular vein between patients with chronic tension-type headache and healthy controls. The secondary aim was to examine plasma levels of these neuropeptides in relation to headache state. In addition, we wanted to study the relation between cranial circulation (jugular vein) and peripheral circulation (antecubital vein). Blood from the external jugular and antecubital vein was drawn from 20 patients with chronic tension-type headache and 20 healthy controls. Plasma SP in patients, 2.0 (1.4–2.2) pmol/l, did not differ significantly from plasma SP in controls, 1.7 (1.1–2.1) pmol/l, (P=0.44). No significant differences were found between SP levels on days with headache, 1.5 (0.3–1.7) pmol/l, and SP levels on days without headache, 1.7 (1.1–1.9) pmol/l, (P=0.06). Plasma NPY in patients, 118±3 pmol/l, did not differ significantly from plasma NPY in controls, 113±5 pmol/l, (P=0.40). There was no difference between NPY levels on days with headache, 120±3 pmol/l, and on days without headache, 118±3 pmol/l, (P=0.73). VIP levels in patients, 6 (4–7) pmol/l, did not differ significantly from VIP levels in controls, 5 (5–7) pmol/l, (P=0.50). No significant differences were found between VIP levels measured on days with headache, 5 (4–6) pmol/l, and VIP levels measured on days without headache, 6 (4–7) pmol/l, (P=0.81). Plasma levels of SP, NPY and VIP did not significantly differ between the peripheral and the cranial circulation neither in patients nor in controls (P>0.05). In summary, the present study indicates that plasma levels of SP, NPY and VIP are normal in chronic tension-type headache patients and largely unrelated to headache state.

Headache in childhood.

1. Rob Forsyth, MD* 2. Kevin Farrell, MD* 1. 2. *Division of Neurology, Department of Pediatrics, University of British Columbia; British Columbia Children’s Hospital, Vancouver, British Columbia, Canada. After completing this article, readers should be able to: 1. Describe what most parents who want help for a child who has a headache are seeking. 2. List the most common cause of severe headache in children. 3. Describe what tests must be performed prior to lumbar puncture in any patient who has a headache. 4. Determine common causes of chronic daily headache. Chronic or recurrent headache is common in children, occurring in approximately 40% of children by 7 years of age and 75% of children by 15 years. Most parents who seek help for a child who has headaches are looking for reassurance that the headache is not due to a serious cause. Pain referred to the head can arise from the following structures: 1) intracranial or extracranial arteries, large intracranial veins, or venous sinuses; 2) cranial or spinal nerves; 3) basal meninges; 4) cranial and cervical muscles; and 5) extra-cranial structures such as the nasal cavity and sinuses, teeth, mucous membranes, skin, and subcutaneous tissues. The brain, most of the meninges overlying the convexity, and the bony skull are not sensitive to pain. Pain arising from the cranial circulation and supratentorial structures travels primarily via the trigeminal nerve and is referred to the anterior part of the head. Pain arising from posterior fossa structures travels mainly via the first three cervical nerves, resulting in pain in the back of the head and neck as well as the forehead. The glossopharyngeal and vagal nerves innervate part of the posterior fossa, and pain is referred to the ear and throat. There are two major hypotheses regarding the pathogenesis of migraine. The vascular hypothesis proposes that vasoconstriction results in aura or focal neurologic signs and is followed by painful vasodilatation. The neurogenic hypothesis proposes that afferent inputs to the brainstem result in a slowly spreading …

The trigeminovascular system in humans: pathophysiologic implications for primary headache syndromes of the neural influences on the cerebral circulation.

Primary headache syndromes, such as cluster headache and migraine, are widely described as vascular headaches, although considerable clinical evidence suggests that both are primarily driven from the brain. The shared anatomical and physiologic substrate for both of these clinical problems is the neural innervation of the cranial circulation. Functional imaging with positron emission tomography has shed light on the genesis of both syndromes, documenting activation in the midbrain and pons in migraine and in the hypothalamic gray in cluster headache. These areas are involved in the pain process in a permissive or triggering manner rather than as a response to first-division nociceptive pain impulses. In a positron emission tomography study in cluster headache, however, activation in the region of the major basal arteries was observed. This is likely to result from vasodilation of these vessels during the acute pain attack as opposed to the rest state in cluster headache, and represents the first convincing activation of neural vasodilator mechanisms in humans. The observation of vasodilation was also made in an experimental trigeminal pain study, which concluded that the observed dilation of these vessels in trigeminal pain is not inherent to a specific headache syndrome, but rather is a feature of the trigeminal neural innervation of the cranial circulation. Clinical and animal data suggest that the observed vasodilation is, in part, an effect of a trigeminoparasympathetic reflex. The data presented here review these developments in the physiology of the trigeminovascular system, which demand renewed consideration of the neural influences at work in many primary headaches and, thus, further consideration of the physiology of the neural innervation of the cranial circulation. We take the view that the known physiologic and pathophysiologic mechanisms of the systems involved dictate that these disorders should be collectively regarded as neurovascular headaches to emphasize the interaction between nerves and vessels, which is the underlying characteristic of these syndromes. Moreover, the syndromes can be understood only by a detailed study of the cerebrovascular physiologic mechanisms that underpin their expression.

Stimulation of an intracranial trigeminally-innervated structure selectively increases cerebral blood flow

The cranial circulation, both extracerebral and cerebral, is innervated by fibers from the trigeminal nerve. This system is known as the trigeminovascular system. The large venous sinuses and dura mater are pain-sensitive and are innervated primarily by branches of the ophthalmic division of the trigeminal nerve. Studies were conducted in the α-chloralose anaesthetised cat to examine bulk carotid and cerebral blood flow responses to electrical stimulation of the trigeminal ganglion and superior sagittal sinus. Bulk carotid blood flow was measured using an ultrasonic flow probe and meter applied to the common carotid artery while cerebral blood flow was measured using laser Doppler flowmetry. Vascular resistance was calculated using simultaneously collected blood pressure data. Stimulation of the trigeminal ganglion resulted in a frequency-dependent reduction in both bulk carotid and cerebral vascular resistance. The mean maximal reduction was 39±5% at 20/s for the carotid bed and 37±6% at 20/s for the cerebral circulation. Stimulation of the superior sagittal sinus resulted in a frequency-dependent reduction in resistance that involved the cerebral circulation with little effect on bulk carotid resistance. The mean maximum reduction was 37±6% at 20/s for the cerebral circulation and 11±3% at 2/s for bulk carotid resistance. The more focused effects of superior sagittal sinus suggest a highly organised somatotopic arrangement of the trigeminal innervation of the cranial circulation. Such a physiological schema fits the known anatomy as reflected by the differential peptidergic innervation from the trigeminovascular system to cranial vessels and may be important in understanding the pathophysiology of migraine, cluster headache and subarachnoid haemorrhage. ©1997 Elsevier Science B.V. All rights reserved.

CURRENT CONCEPTS OF THE PATHOPHYSIOLOGY OF MIGRAINE

An understanding of the basic anatomy and physiology of the cranial circulation facilitates the assessment and management of patients with headache, particularly vascular-type headaches, such as migraine. At the very least, all pain is perceived and processed in the brain. With migraine it is likely that the fundamental problem and its clinical expression are driven by the CNS; thus study of the brain regarding headache is warranted. As therapy evolves during the 1900s, such an understanding will be necessary, as new and highly specific receptor-targeted compounds allow treatment and improvement of headache in many patients. Since writing this article, the nomenclature for serotonin (5HT) receptors has changed so that any reference herein to 5HTID alpha is now 5HTID and 5HTID beta is now 5HTI beta. This change in nomenclature is discussed in Martig PR, Hoyer D, Humphrey PPA, et al: Alignment of receptor nomenclature with the human genome: Classification of 5HT-1 beta and 5HT-1D receptor subtypes. Trends in the Pharmacological Sciences 17:103, 1996.

Oxygenation in fetal lambs supported by extrauterine right atrium to artery extracorporeal membrane oxygenation

OBJECTIVE: Our purpose was to determine the adequacy of oxygenation, particularly cranial and cardiac oxygenation, in exteriorized fetal lambs on right atrium to artery extracorporeal membrane oxygenation. STUDY DESIGN: Thirteen fetal lambs were placed on right atrium to artery extracorporeal membrane oxygenation between the gestational ages of 113 and 133 days. Various P O 2 and oxygen saturation (S O 2) values were obtained by varying the oxygen concentrations at the oxygenator membrane. Blood gases, pH, and S O 2 were observed on samples taken before and after membrane oxygenation from the left ventricle and through the cranial carotid arterial catheter. These were compared with control values obtained before the cessation of umbilical circulation. Fetal coronary oxygenation was represented by left ventricle P O 2 and S O 2 and cranial oxygenation by carotid artery P O 2 and S O 2. RESULTS: We classified oxygen saturation as low, medium, and high on the basis of the level of postmembrane S O 2. Carotid artery cranial oxygenation in the low S O 2 group was equivalent to control values, but that in the medium and high S O 2 groups was significantly higher than in the control group. Left ventricle oxygenation was consistently lower than cranial oxygenation in any S O 2 group. In the low group left ventricle oxygenation was significantly lower than the control values. CONCLUSIONS: Right atrium to artery extracorporeal membrane oxygenation appears sufficient to oxygenate the fetal cranial circulation but may be inadequate for the efficient distribution of oxygenated blood into the left ventricle and thus the coronary circulation. (A M J O BSTET G YNECOL 1996;174:535-9.)

Body magnetic resonance angiography and its effect on the use of alternative imaging--experience in 1026 patients.

Time-of-flight magnetic resonance (MR) angiography has been described for numerous applications but the number of patients described in published reports is usually relatively small. There is little information concerning the general utility of MR angiography in the body, outside the cranial circulation, or its effect on use of other imaging studies. Utilization of two-dimensional (2D) time-of-flight MR angiography over a 3 year period was reviewed to determine its accuracy and impact on other imaging modalities. Cranial and cardiac studies were excluded. Correlation was made with alternative imaging and surgical findings. Between January 1990 and December 1992 2D time-of-flight MR angiography was used to examine 1026 patients. MR angiography was used most frequently to examine the venous system. There was a slight reduction in the use of alternative imaging with two exceptions. When chest MR venography was performed, alternative imaging was completely abolished. Also, contrast portal venography was virtually eliminated. Five errors (0.2% of total MR angiography examinations) were recorded. Time-of-flight MR angiography, especially MR venography, is accurate and can replace contrast venography for abdominal and thoracic applications. Cost and limited availability means that other imaging, usually ultrasound, often precedes MR angiography.

Recent developments in tachykinin NK1 receptor antagonists: prospects for the treatment of migraine headache.

The role of substance P and the influence of neurokinin 1 (NK1) receptor antagonists in the cranial circulation are described in the present review, particularly with respect to the mechanisms involved in the etiology of migraine headache. Substance P is distributed throughout the cranial vasculature, in the trigeminal sensory afferent nerve fibres, and its release can be demonstrated following activation of the trigeminovascular system in animals and humans. Following its release and NK1 receptor activation, dilatation and edema result, two events that are implicated in the pathogenesis of migraine headache. The recently developed selective NK1 receptor antagonists inhibit substance P mediated dilatation and plasma protein extravasation in the cranial circulation, suggesting that they may provide an effective and novel acute treatment for migraine.