Basal Arteries Research Articles

Arteriovenous differences of oxygen and transcranial Doppler sonography in the management of aneurysmatic subarachnoid hemorrhage

After subarachnoid hemorrhage (SAH) the detection of hemodynamically significant vasospasm is frequently difficult, especially in comatose patients. Most clinicians use transcranial Doppler sonography (TCD) to detect increasing mean blood flow velocities in the basal arteries as markers of cerebral vasospasm, without accounting for the effects of sedation and variations in blood pressure or pCO 2. This study was conducted to test the hypothesis that the arteriovenous difference of oxygen (avDO 2; in terms of % volume) could also be useful for the evaluation of vasospasm. A total of 22 SAH patients (M : F = 1 : 1.75, age 58 ± 10 years, median Hunt and Hess grade 4) were prospectively enrolled. All patients were sedated with continuous doses of midazolam/fentanyl and/or propofol. TCD studies and avDO 2 measurements were conducted at the same time or in close succession. The blood flow velocity of the middle cerebral artery was recorded. A cranial CT scan was conducted if the avDO 2 increased by at least 0.8%. Overall, 82 measurements were recorded in 22 patients between days 1 and 13 after SAH. TCD mean flow velocities increased as expected. In contrast, avDO 2 decreased until post-hemorrhage day 4 before it increased again. Overall, after SAH, avDO 2 was significantly lower than in normal individuals. Cerebral infarction occurred primarily in patients with a maximal change of avDO 2 of more than 1%. TCD velocities alone are poor indicators of the severity of vasospasm. In contrast, daily avDO 2 seems to be a more robust parameter. However, collection of additional metabolic information is warranted.

Cerebral vasculitis: imaging signs revisited

Inflammatory stenoses of cerebral blood vessels, although rare in general, are an important cause of cerebral ischemia in younger patients. The diagnosis is often difficult. The first step in the diagnostic process is the identification of brain lesions consistent with cerebral vasculitis. Brain lesions are frequently found in this patient group, especially if modern imaging tools such as diffusion and perfusion-weighted imaging are employed. Although no specific pattern for this entity exists, multiple infarcts of various ages in more than one vascular territory should raise this suspicion. The next step in the imaging of patients with suspected vasculitis is the demonstration of the underlying vascular pathology. MR angiography is the mainstay of investigating patients for intracranial vascular stenoses. However, at 1.5 T it is only diagnostic for stenoses of large brain arteries. Hence, conventional angiography is still required to investigate stenoses of medium and small-sized brain arteries. Recent work suggests that MRI can directly demonstrate mural thickening and contrast enhancement in basal brain arteries, rendering biopsy obsolete in this patient group. A classification for cerebral vasculitis is proposed according to the size of the affected brain vessels, analogous to the pertinent nomenclature of primary systemic vasculitis.

Skull Base Disease: The Interventional Neuroradiologist's Contribution

Interventional neuroradiology plays an important role in the management of skull base disease in two aspects: endovascular and CT-guided techniques. Endovascular procedures comprise devascularizing as well as recanalizing interventions. Preoperative embolization of vascular tumors (e.g., paraganglioma, angiofibroma) using particles reduces intraoperative blood loss and can even turn inoperable tumors into operable ones. The treatment of dural arteriovenous fistulae is based mainly on endovascular techniques. Contrary to transarterial embolization as in tumors, most fistulae are tackled on the transvenous route using free or detachable coils. In many cases occlusion of the venous side eliminates the goal of the fistula and is the only chance of permanent cure. Treatment of skull base-related aneurysm requires close cooperation between the neurosurgeon and neuroradiologist. Contrary to open surgery, the skull base per se is not an obstacle to endovascular techniques. In the treatment of aneurysms, usually detachable platinum coils are employed with or without the help of stents. Occlusion of the carrier vessel using coils or detachable balloons is a therapeutic alternative in selected cases. Of recanalizing interventions, treatment of vasospasm with endovascular balloon catheters can be a life-saving procedure in the setting of acute subarachnoid hemorrhage. Arteriosclerotic stenoses of basal arteries can be dilated with stent-assisted angioplasty in patients suffering from cerebrovascular symptoms that cannot be managed with medical treatment alone. Of the CT-guided interventions, bioptic techniques of tumors adjacent to the skull base can in some cases substitute for open biopsy.

Perivascular nerve damage in the cerebral circulation following traumatic brain injury

Traumatic brain injury (TBI) causes cerebral vascular dysfunction. Most have assumed that it was the result of endothelial and/or smooth muscle alteration. No consideration, however, has been given to the possibility that the forces of injury may also damage the perivascular nerve network, thereby contributing to the observed abnormalities. To test this premise, we subjected rats to impact acceleration. At 6 h, 24 h and 7 days post-TBI, cerebral basal arteries were removed and processed with antibody targeting protein gene product 9.5 (PGP-9.5), with parallel assessments of 5-hydroxytryptamine (5-HT) accumulation in the perivascular nerves. Additionally, Fluoro-Jade was also used as a marker of axonal degeneration. The perivascular nerve network revealed no abnormality in sham animals. However, by 6 h post injury, Fluoro-Jade reactivity appeared in the perivascular regions, with the number of fibers increasing with time. By 24 h post injury, a significant reduction in the perivascular 5-HT accumulation occurred, together with a reduction in PGP-9.5 fiber staining. At 7 days, a recovery of the PGP-9.5 immunoreactivity occurred, however, it did not reach a control-like distribution. These studies suggest that neurogenic damage occurs following TBI and may be a contributor to some of the associated vascular abnormalities.

Evaluation of Intrapulmonary Vascular Dilatations With High-Resolution Computed Thorax Tomography in Patients With Hepatopulmonary Syndrome

We aimed to determine the role of thorax high-resolution computed tomography (HRCT) in demonstrating the pulmonary vasodilatation in patients with hepatopulmonary syndrome (HPS). Traditionally, the presence of intrapulmonary vascular dilatations can be detected by using one of the three diagnostic modalities: contrast-enhanced echocardiography, technetium 99 m-labeled macroaggregated albumin scan, and pulmonary angiography. The study group included 10 patients with HPS (Group 1), 12 patients with normoxemic cirrhosis (Group 2), and 12 healthy controls (Group 3). All of the subjects underwent conventional and HRCT of thorax. The diameters of pulmonary trunk, main pulmonary arteries, and right lower lobe basal segmental arteries were measured. The ratios of right lower lobe basal segmental pulmonary artery to bronchus diameter were calculated. The mean diameters of the main pulmonary trunk, right and left main pulmonary arteries were not different between the groups. Mean diameters of right lower lobe basal segmental pulmonary arteries were significantly higher in Group 1 compared with Group 2 (P=0.01) and Group 3 (P=0.002). Mean right lower lobe basal segmental pulmonary artery to bronchus ratios were significantly higher in Group 1 compared with Group 2 (P=0.03) and Group 3 (P<0.001). Group 2 had significantly higher pulmonary artery to bronchus ratios than Group 3 (P<0.001). Thorax HRCT may be helpful in the diagnosis of HPS by demonstrating the dilated peripheral pulmonary vessels or increased pulmonary artery to bronchus ratios in patients with liver disease and hypoxemia.

Morphometry of the Basal Plate Superficial Uteroplacental Vasculature in Normal Midtrimester and at Term

Uteroplacental (UP) vascular arterial pathology has been associated with pregnancy complications. UP arterial structure has been characterized in placental bed biopsies, at the decidual-myometrial junction. Basal plate UP arteries, which are delivered with the placenta and thus routinely available, are not well characterized. We compared basal plate UP arterial segment morphometry in cases of elective termination of a clinically normal pregnancy at 11 to 24 weeks and of term birth. This study was done in a community-based obstetric service in New York City. UP arteries were identified in placentas of 20 midtrimester (MT) cases and 17 term (TERM) cases. We measured 336 UP artery cross-sections from 46 TERM and 290 MT cases. The basal plate UP artery path length was calculated as the distance between (x,y) coordinates of estimated centers of lumen cross-sections. Basal plate thickness near UP arteries, UP artery cross-sectional areas, vascular luminal eccentricity, and radial standard deviation were directly measured off digital images. Nonparametric and parametric methods compared groups, with P < 0.05 considered statistically significant. In TERM cases, the basal plate thickness near UP arteries was 1.8-fold thinner (P = 0.002) and mean basal plate path lengths were 2.13-fold shorter (P < 0.0001) than in MT cases. Mean TERM UP artery cross-sectional area was 3.15-fold larger, the major axis was 1.95-fold larger, and the minor axis was 1.75-fold larger than in MT arteries (P = 0.001 to 0.008). Our data demonstrate that basal plate UP arteries (delivered with the placenta) are less tortuous, with shorter path lengths and larger areas as gestation advances. Normative morphometric data may allow improved diagnostics of placentas from complicated pregnancies.

Uterine artery embolisation for massive uterine fibroids in the presence of submassive pulmonary emboli

A 46-year-old woman was admitted to our hospital with acute shortness of breath and pre-syncope. She had known massive uterine fibroids with a history of menorrhagia and dysmenorrhoea, and had been awaiting total abdominal hysterectomy and bilateral salpingo-oophorectomy. She had no past or family history of venous thromboembolism (VTE). She was an ex-smoker with a 16-pack/year smoking history. On examination, she looked unwell, was sweaty and clammy, but apyrexial. Her heart rate was 130 per minute and her blood pressure was 140/95 mmHg. She was tachypnoeic with a respiratory rate of 28 breaths per minute; however, her chest was clear. Abdominal examination revealed an enormous uterus, equivalent to the size of a 30-week pregnancy. There was no clinical evidence of deep vein thrombosis (DVT). She was hypoxic: oxygen saturation on air was 88%; arterial blood gas measurement on 100% oxygen—pH 7.4, PO2 29.0mmHg, PCO2 3.5mmHg, bicarbonate 18.5mmol/L, base excess of 7.5 mol/L. Her full blood count revealed a microcytic anaemia with a mean cellular volume of 67.9 fl (normal: 81–99 fl) and haemoglobin of 9.4 g/dL (normal: 12.0–15.0 g/L). Her D-dimer was significantly elevated at 1.7 Ag/mL (normal: <0.5 Ag/mL). Other blood tests including renal profile, liver function, thyroid function, C-reactive protein and clotting profile were all within normal limits. Her 12 lead electrocardiogram demonstrated sinus rhythm with right bundle branch block and T wave inversion in V1-3 with classic ‘S1QIIITIII’ changes. Her Chest X-ray showed blunting of the basal pulmonary arteries particularly on the right. Transthoracic echocardiography findings were consistent with submassive pulmonary embolism: the left ventricular size and function was normal; the right ventricle was dilated with moderately impaired systolic function; the right atrium was also dilated; the inferior vena cava was distended and failed to collapsewith inspiration; the estimated right ventricular systolic pressure was 50 mmHg. A contrast CT pulmonary angiogram revealed occlusive thrombus in the proximal basal left and mid and basal right pulmonary arteries. She was initially managed with aggressive fluid resuscitation and was commenced on intravenous unfractionated heparin (target APTT ratio of 2.0–3.0). On day 3 she began to heavily menstruate and required a total of nine units of blood over the ensuing 10 days. She was given subcutaneous Zoladex and 30 mg TDS provera to reduce her menstrual blood loss. On day 13 she underwent iliac venography and inferior cavography with insertion of a temporary IVC filter. No free intravascular thrombus was seen in either common iliac vein or within the IVC. There was however significant compression on all three of these veins. Immediately following this, she underwent uterine artery embolisation (UAE). At the time of UAE, her uterus and dominant fibroid measured 3800 and 3220 mL, respectively. Two weeks post-UAE her caval filter was removed, via a jugular route, without complication. A follow up pelvic MRI, one month later, confirmed complete fibroid degeneration with migration of the fibroid into the endometrial cavity (Fig. 1). The uterus measured 2200 mL and the fibroid 1000 mL, correlating with a 42% and 69% respective relative reduction in size. At six weeks she passed a large ‘steak-sized’ degenerate fibroid. At three months pelvic ultrasound showed that the uterus had reduced to 315 mL and the fibroid volume was 1.5 mL. The patient has made a complete recovery and has been given life-long warfarin.

Mechanism of Contraction of Rat Isolated Tail Arteries by Hyposmotic Solutions

Contraction induced by hyposmotic swelling was examined in rat tail arteries mounted on a myograph containing a modified Krebs physiological saline solution (PSS) containing 50 mM mannitol (300 mosm/l). Hyposmotic swelling was induced by removing mannitol. In arteries having basal tone or arteries precontracted with K⁺ or the thromboxane mimetic U-46619, removal of mannitol caused a concentration dependent contraction of rat tail arteries. Concurrent measurement of tension and intracellular calcium [Ca²⁺]_iin arteries loaded with fura-2 showed that both tension and [Ca²⁺]_i increased on exposure to a hyposmotic solution. Removal of endothelium or inhibition of nitric oxide and cyclooxygenase together did not affect contractile responses. Removal of extracellular Ca²⁺ abolished the contractile response to hyposmotic solution and NiCl₂, a nonspecific inhibitor of Ca²⁺ influx pathways, blocked the rise in [Ca²⁺]_i and tension in response to a hyposmotic solution. Verapamil and nisoldipine, inhibitors of Ca_v1.2 (L-type) calcium channels significantly reduced the contractile response to a hyposmotic solution. Addition of NiCl₂ to nisoldipine caused an additional inhibition of the response to a hyposmotic solution. Inhibition of calcium release from the sarcoplasmic reticulum by ryanodine or cyclopiazonic acid (CPA) did not cause any change in the tension response to a hyposmotic solution. CPA did not significantly inhibit the response to a hyposmotic solution in the presence of N^G-methyl-L-arginine, oxyhaemoglobin and indomethacin. We conclude that contraction induced by a hyposmotic solution is largely due to Ca_v1.2 calcium channels although other Ca²⁺ influx pathways also contribute.

Maternal vascular underperfusion: nosology and reproducibility of placental reaction patterns.

Placental examination can be a useful tool for specifying the etiology, prognosis, and recurrence risk of pregnancy disorders. The purpose of this study was to test the reliability of a predetermined set of placental reaction patterns seen with maternal vascular underperfusion in the hope that this might provide a useful diagnostic framework for practicing pathologists. Study cases (14 with clinical and pathologic evidence of maternal underperfusion plus 6 controls) were evaluated for the presence or absence of 11 lesions by eight perinatal pathologists. After analysis of initial results, diagnostic criteria were refined and a second, overlapping set of cases was reviewed. The collective sensitivity, specificity, and efficiency of individual assessments for the 11 lesions relative to the group consensus ranged from 74-93% (22/33 > 90%). Reproducibility was measured by unweighted kappa-values and interpreted as follows: < 0.2 poor, 0.2-0.6 fair/moderate, > 0.6 substantial. Kappa values for lesions affecting villi and the intervillous space were increased syncytial knots (any -0.42, severe -0.50), villous agglutination (0.42), increased intervillous fibrin (0.25), and distal villous hypoplasia (0.57). Individual estimates of percent involvement for syncytial knots, intervillous fibrin, and distal villous hypoplasia were correlated with placental and fetal weight for gestational age. Extent of increased intervillous fibrin showed the strongest correlation with both placental weight ( R = -0.64) and fetal weight ( R = -0.45). Kappa values for lesions affecting maternal vessels and the implantation site were acute atherosis (0.50), mural hypertrophy of membrane arterioles (0.43), muscularized basal plate arteries (0.48), increased placental site giant cells (0.54), and immature intermediate trophoblast (0.36). Correlation of maternal vessel and implantation site lesions with the clinical diagnosis of preeclampsia showed that excessive placental site giant cells and immature intermediate trophoblast were more sensitive and efficient predictors, whereas atherosis and muscularized basal plate arteries were more specific. Kappa value for a thin umbilical cord, a possible indicator of fetal volume depletion, was 0.61. Reproducibility for a global impression of maternal vascular underperfusion, taking into account all of the above lesions, was moderate (kappa 0.54) and improved after inclusion of additional pathologic and clinical data (kappa 0.68). Adoption of this clearly defined, clinically relevant, and pathologically reproducible terminology could enhance clinicopathologic correlation and provide a more objective framework for future clinical research.

Disease-Associated Prion Protein in Vessel Walls

Human prion diseases like Creutzfeldt-Jakob disease are infectious, inherited, or sporadic neurodegenerative disorders, characterized by the accumulation of an abnormal isoform of the host-encoded prion protein. This affects nervous tissue in sporadic Creutzfeldt-Jakob disease and, additionally, in lymphoid tissue in bovine spongiform encephalopathy-linked variant Creutzfeldt-Jakob disease. Experimental studies have established the involvement of cells of the lymphoid and peripheral nervous system in the transport of prions to their target central nervous system tissue. To evaluate the role of vessel wall-associated mobile cells, we obtained formalin-fixed tissue blocks from various brain regions and/or basal arteries from sporadic, variant and iatrogenic Creutzfeldt-Jakob disease, and unselected control cases. We demonstrate disease-associated prion protein deposits in intracranial vessel walls, in sporadic and variant Creutzfeldt-Jakob disease by performing immunohistochemical staining and paraffin-embedded tissue blotting. Using double immunofluorescence, these deposits co-localize with HLA-DR and S-100 immunoreactive cells in the intima, which are components of the vascular-associated dendritic cell network, as well as with HLA-DR and CD-68 immunopositive macrophages of the intima and media. We conclude that mobile cells in vessel walls like dendritic and monocyte/macrophage lineage cells may be involved in spread of disease-associated prion protein and possibly also of infectivity.

Cerebral Vasospasm Following Subarachnoid Hemorrhage.

Cerebral vasospasm and related ischemic stroke continue to be significant complicating factors in the course of many patients with subarachnoid hemorrhage from berry aneurysm rupture. The risk of this well-recognized but poorly understood complication can be estimated on the basis of patient medical history, neurologic examination, and head CT findings. Every patient with possible risk needs specialized neurologic intensive care unit care after aneurysm obliteration. Surgical and pharmacologic wash-out of subarachnoid blood around the basal arteries, proper management of intracranial pressure and fluid status, hyponatremia, hypomagnesemia, and fever, as well as use of calcium channel blockers, have been considered helpful in patient management prior to and with the symptomatic vasospasm development. Transcranial Doppler (TCD) ultrasound is important in detecting vasospasm before the patient suffers ischemic neurologic deficit or infarct. Elevated TCD velocities often initiate the use of triple-H (HHH: hypertension, hemodilution, and hypervolemia) therapy and subsequently guide it. Up to the end of the first 3 weeks after subarachnoid hemorrhage and aneurysm obliteration, development of any focal neurologic deficit or mental deterioration, unless convincingly proven otherwise, is assumed to be from cerebral vasospasm. When a hemodynamically significant vasospasm in the arterial segments of clinical concern is suggested, emergency cerebral angiography with balloon dilatation angioplasty or intra-arterial infusion of vasodilating agents may be helpful in relieving ischemic symptoms.

The Transsylvian Approach Is “Minimally Invasive” but Not “Atraumatic”

In light of the competition between microneurosurgery and alternative methods such as stereotactic radiosurgery, we tested the hypothesis that changes in the cerebral circulation after microneurosurgery are common among patients without evidence of cerebrovascular or neoplastic disease. Blood flow velocities (BFVs) were recorded with transcranial Doppler ultrasonography, before surgery and every other day after surgery, for a group of 50 patients who underwent transsylvian selective amygdalohippocampectomies for treatment of hippocampal sclerosis. Hexamethylpropylene amine oxime-single-photon emission computed tomographic testing, including acetazolamide testing of cerebrovascular reactivity, was performed during the second postoperative week for 20 of the 50 patients. BFVs in basal arteries ipsilateral to the surgical approach increased significantly (P < 0.001) from preoperative baseline values of approximately 52 +/- 13 cm/s (mean +/- standard deviation) to values of approximately 86 +/- 27 cm/s on postoperative Day 3 and reached their maximal values of approximately 115 +/- 37 cm/s after a median of 7 days. BFVs in contralateral vessels exhibited a similar but somewhat attenuated pattern. Hexamethylpropylene amine oxime-single-photon emission computed tomography demonstrated ipsilateral regions of hypoperfusion in 100.0% of the cases and contralateral hypoperfusion in 80.0%. Cerebrovascular reactivity was impaired in 83.3% of the cases ipsilaterally and in 33.3% contralaterally. A significant proportion of patients who undergo microneurosurgical procedures develop bilateral alterations of their cerebral circulation. The elevations in mean BFV values represent cerebral vasospasm. Because these changes remain asymptomatic for the majority of patients, the transsylvian approach can be considered "minimally invasive" but not "atraumatic." Alternative surgical routes and alternative treatment modalities should be investigated in a similar manner.

Post-partum cerebral angiopathy: Repetitive TCD, MRI, MRA, and EEG examinations

We report of a woman with post-partum cerebral angiopathy (PCA), in whom we repetitively performed transcranial Doppler sonography (TCD), MR imaging (MRI), and MR angiography (MRA) to evaluate the underlying pathophysiology. A 31-year-old woman, Gemini pregnant, complained of severe throbbing frontal headache four days after an uneventful delivery by Cesarean section. Blurred vision occurred eight days after delivery, followed by three generalized tonic-clonic seizures. Neurological examination revealed a somnolent woman without focal neurological deficits. At the day of the seizures increased flow velocities and disturbed flow were observed in the right posterior and anterior cerebral artery on transcranial Doppler (TCD). MRI showed infra- and supratentorial patchy hyperintensities in T2-weighted images and in the FLAIR sequence. Diffusion-weighted imaging revealed corresponding multi-focal hyperintense areas indicating increased diffusion and MRA showed a diffuse multisegmental narrowing of all pial arteries. MRI at day 10 was completely normal, but MRA still revealed vascular narrowing in the right posterior cerebral artery. General slight flow accelerations in all basal arteries occurred after 10 days and lasted for three weeks. PCA is apparently associated with a vascular narrowing causing cerebral ischemia with increased diffusion. Later reactive cerebral hyperperfusion is observed. Vascular narrowing and cerebral hyperperfusion still persist after MRI has normalized. [Neurol Res 2002; 24: 570-572]

Congenital arteriovenous fistula of the brain with an atrial septal defect: case report

Introduction: Aneurysmal malformation of the vein of Galen (AVG) is caused by an arteriovenous fistula (AVF) between the basal arteries and deep venous sinuses of the brain. Congenital forms of AVG are potentially fatal, leading to a left-to-right shunt and cardiomegaly, and the death is most commonly as a result of cardiac failure. We present a case with an AVF of brain with an ASD. Material and methods: A mature male baby born at gestational week 38 was admitted to PICU with tachydyspnoe 4 h after birth. Ultrasound (US) and computed tomography scans of the brain detected a large bilateral AVF with dilated basal arteries and venous sinuses (sinus petrosus, sinus confluens, sinus transvs. and sagittal inferior sinus), hydrocephalus and brain atrophy. Cardiac US showed right ventricular hypertrophy, persistent ductus Botall and ASD. The patient died of cardiac failure 6 days after birth. Results: Autopsy examination of the brain showed dilatation of the vein of Galen and venous sinuses, a large conglomerate of dilated blood vessels in the midline and left occipital lobe, oedema and hydrocephalus. Examination of the heart confirmed Us findings and showed an ostium secundum ASD. Histologically, the occipital mass revealed features of an AVF, consistent with AVG. Chronic ischaemic lesions with ferruginated neurons were also present. Conclusions: The presence of chronic hypoxic changes in the brain suggests intrauterine damage as a result of a congenital AVF. The left-to-right shunt, in addition to causing cardiomegaly, may also have interfered with the development of the atrial septum, leading to an ostium secundum ASD, aggravating the clinical course.

Diagnostic Tests: Transcranial ultrasound - clinical applications in cerebral ischaemia

SYNOPSIS Transcranial ultrasound can rapidly and non-invasively image blood flow in the major basal intracranial arteries. Its accuracy makes it acceptable for use in screening for haemodynamically significant intracranial stenoses or vessel occlusions. Although it has a relatively limited field of view and is not technically feasible in approximately 10% of cases, the information obtained is becoming increasingly relevant to therapeutic decision-making in the prevention and management of stroke. Transcranial Doppler ultrasound or transcranial colour-coded duplex have the advantages of relatively low cost, ease of repeatability, and excellent safety and tolerability, but they provide inferior spatial and anatomical detail in comparison to angiographic techniques. Index words: stroke, magnetic resonance angiography, angiography. (Aust Prescr 2001;24:137–40)

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.

PET and MRA findings in cluster headache and MRA in experimental pain.

Cluster headache (CH), like migraine, is still regarded as a vascular headache although in both conditions a CNS cause has been suggested. To examine neurovascular mechanisms in CH. The authors used functional imaging with PET to investigate 18 CH patients (25 to 62 years old). Ten were in the active period (nine patients with induced attacks and one with spontaneous attack) and eight were out of their bout. In addition, the authors studied spontaneous CH and experimental pain in volunteers using MR angiography. When an acute CH attack was triggered with nitroglycerin (NTG), activation occurred in the ipsilateral posterior inferior hypothalamic gray, the contralateral ventroposterior thalamus, the anterior cingulate cortex, the ipsilateral basal ganglia, the right anterior frontal lobe, and both insulae. In patients out of the bout who experienced only a mild NTG headache, activation was seen bilaterally in the insulae and frontal cortices, the anterior cingulate cortex, the right thalamus, and the left basal ganglia, but not in the hypothalamic gray area. In addition, the authors found a significant activation (vasodilatation) in the region of the major basal arteries that was caused in part by NTG but was also observed in the spontaneous case and could be induced by capsaicin injection into the forehead. Therefore, the vasodilatation is likely to be mediated by neural mechanisms involved in the acute CH attacks that are present in every human being. Dilatation of cranial vessels is not specific to any particular headache syndrome but generic to cranial neurovascular activation, probably mediated by the trigeminoparasympathetic reflex. These data confirm that CH is a CNS disorder best considered as a form of neurovascular headache.

F04Prognostic value of Dopplerometry during antirecurrent hormonal therapy in patients with hyperplastic process of the endometrium

BackgroundThe purpose of study was to find out changes of Doppler parameters in all uterine arteries during antirecurrent hormonal courses and to define their role in prediction of outcomes.Method53 patients receiving hormonal therapy (Norcolut, Provera, Danazol) after D &amp; C were undergone 6 months monitoring by transvaginal ultrasound with Color Flow Mapping and Doppler assessment of the main uterine, arcuate, radial and basal arteries. The mean values of resistance indices (RI) were calculated after retrospective division into groups with effective (n = 41) and effectless (n = 12) treatment. Investigated RI data were used for statistical creation of prognostic upper and lower cut‐off levels (for P &lt; 0.05).ResultsThe resistance indices were: Healthy Effective treatment Effectless treatment Cut‐off intervals for P &lt; 0.05 Uterine arteries 0.88 0.86 0.83 0.83–0.87 Arcuate arteries 0.78 0.74 0.72 0.65–0.80 Radial arteries 0.71 0.73* 0.65* 0.60–0.75 Basal arteries 0.57 0.62 0.57 0.48–0.68 – p &lt; 0.10 ConclusionFor predicting effectiveness of hormonal treatment after two months from its beginning Doppler measurements should be carried out in Radial Arteries and RI must exceed 0.75.

Reduced vasomotor reactivity in cerebral microangiopathy : a study with near-infrared spectroscopy and transcranial Doppler sonography.

Reduction of cerebral blood flow and vasomotor reactivity (VMR) are thought to play an important role in the pathogenesis of cerebral microangiopathy. The aim of our study was to determine whether near-infrared spectroscopy (NIRS) can detect a reduced VMR in patients with microangiopathy, whether NIRS reactivities correlate with VMR assessed by transcranial Doppler sonography (TCD), and whether the differing extents of patients' microangiopathy demonstrated on MRI or CT can be distinguished by both noninvasive techniques. We compared the VMR of 46 patients with cerebral microangiopathy with 13 age-matched control subjects. Patients were classified with the Erkinjuntti scale. We monitored cerebral blood flow velocity (CBFV) in both middle cerebral arteries by TCD, changes in concentration of oxyhemoglobin (HbO(2)), deoxyhemoglobin (Hb) and blood volume (HbT) by NIRS, mean arterial blood pressure, and end-tidal CO(2) (EtCO(2)) during normocapnia and hypercapnia. VMRs were calculated as percent change of CBFV (NCR) and as absolute change in concentration of HbO(2), Hb, and HbT per 1% increase in EtCO(2) (CR-HbO(2), CR-Hb, CR-HbT). NCR and NIRS reactivities were significantly reduced in patients with cerebral microangiopathy. CR-HbO(2) and CR-Hb showed a close correlation with NCR, and NCR and NIRS reactivities were related to the severity of cerebral microangiopathy according to the Erkinjuntti scale. Validity of NCR and NIRS reactivities were similar. VMR is reduced in patients with cerebral microangiopathy and can be noninvasively assessed in basal arteries (with TCD) and brain parenchyma (with NIRS). Reduction of CO(2)-induced VMR, as measured by NIRS and TCD, may indicate the severity of microangiopathy.

Ultraschalldiagnostik der intra-kraniellen Hirnarterien und Monitoring-Techniken

There have been significant further developments in ultrasound diagnostics of the intracranial brain arteries in recent years. Besides the traditional transcranial Doppler sonography (TCD) the two-dimensional colour duplex technique (TCCS) has become a well-established method. This enables a safe differentiation of the basal brain arteries even without compression tests, as well as a clear definition against surrounding parenchymal structures. It is now possible to obtain safe and rapid information on the vascular status for immediate diagnosis in brain infarction patients. Since information on vascular malformations and aneurysms can be obtained only if the vascular pathology is sufficiently large, TCCS cannot replace other methods of identification as far as this aspect is concerned. The ultrasound contrast media for whom the lungs are patent greatly improve the signal-to-noise ratio of the Doppler signal. After enhancement by the ultrasound contrast media, Doppler signals may be analysed even under unfavourable conditions (for example: insufficient penetration of sound through the temporal bone). By means of haemodynamic TCD monitoring it is now possible to determine significant characteristics of brain blood supply with relatively little effort, such as changes in the median speed of flow, cerebrovascular resistance and autoregulation. The clinical application of this kind of monitoring is demonstrated by three examples. During the interventional neuroradiological experimental occlusion of the internal carotid artery the TCD data can be used to assess haemodynamic and possible clinical effects of such an occlusion. In the tilting-table test ICD can supply valuable insights into the cerebral effects of systemic dysregulations. In a subgroup of patients with orthostatic intolerance it was only TCD that showed clear pathological changes. For practical reasons it has not yet been possible to establish TCD monitoring in continuous control checking in stroke units. However, first experiences seem to point out that possibly TCD monitoring may reveal the development for critical cerebral circulatory disturbances in patients with space-occupying media infarctions and may thus supply a significant contribution to the indication for cranial decompression. By means of repeat examinations of the course, using the TCD and TTCS technique, it is possible to identify in patients with acute cerebral infarction the time of rechannelling and to estimate the space-occupying effect of an infarction by measuring the displacement of the third ventricle. Monitoring patients after thrombendarterectomy of the internal syndrome, whereas monitoring of an embolism helps to estimate the risk of a post-operative ischaemic event.