A biomathematical model of intracranial arteriovenous malformations based on electrical network analysis: theory and hemodynamics

Hemodynamics play a significant role in the propensity of intracranial arteriovenous malformations (AVMs) to hemorrhage and in influencing both therapeutic strategies and their complications. AVM hemodynamics are difficult to quantitate, particularly within or in close proximity to the nidus. Biomathematical models represent a theoretical method of investigating AVM hemodynamics but currently provide limited information because of the simplicity of simulated anatomic and physiological characteristics in available models. Our purpose was to develop a new detailed biomathematical model in which the morphological, biophysical, and hemodynamic characteristics of an intracranial AVM are replicated more faithfully. The technique of electrical network analysis was used to construct the biomathematical AVM model to provide an accurate rendering of transnidal and intranidal hemodynamics. The model represented a complex, noncompartmentalized AVM with 4 arterial feeders (with simulated pial and transdural supply), 2 draining veins, and a nidus consisting of 28 interconnecting plexiform and fistulous components. Simulated vessel radii were defined as observed in human AVMs. Common values were assigned for normal systemic arterial pressure, arterial feeder pressures, draining vein pressures, and central venous pressure. Using an electrical analogy of Ohm's law, flow was determined based on Poiseuille's law given the aforementioned pressures and resistances of each nidus vessel. Circuit analysis of the AVM vasculature based on the conservation of flow and voltage revealed the flow rate through each vessel in the AVM network. Once the flow rate was established, the velocity, the intravascular pressure gradient, and the wall shear stress were determined. Total volumetric flow through the AVM was 814 ml/min. Hemodynamic analysis of the AVM showed increased flow rate, flow velocity, and wall shear stress through the fistulous component. The intranidal flow rate varied from 5.5 to 57.0 ml/min with and average of 31.3 ml/min for the plexiform vessels and from 595.1 to 640.1 ml/min with an average of 617.6 ml/min for the fistulous component. The blood flow velocity through the AVM nidus ranged from 11.7 to 121.1 cm/s with an average of 66.4 cm/s for the plexiform vessels and from 446.9 to 480 dyne/cm2 with an average of 463.5 dyne/cm2 for the fistulous component. The wall shear stress ranged in magnitude from 33.2 to 342.1 dyne/cm2 with an average of 187.7 dyne/cm2 for the plexiform vessels and from 315.9 to 339.7 cm/s with an average of 327.8 cm/s for the fistulous component. The described novel biomathematical model characterizes the transnidal and intranidal hemodynamics of an intracranial AVM more accurately than was possible previously. This model should serve as a useful research tool for further theoretical investigations of intracranial AVMs and their hemodynamic sequelae.     

Spontaneous disappearance of arteriovenous malformation during staged treatment of multiple cerebral arteriovenous malformations--case report

A 36-year-old male presented with aphasia and right hemiparesis due to the rupture of the larger of two arteriovenous malformations (AVMs) coexisting in the left hemisphere. The two AVMs had completely separate locations and different feeding arteries and draining systems. Two months after resection of the larger AVM and evacuation of the hematoma, carotid angiography showed the residual AVM had spontaneously disappeared. He was discharged without deficits. Change of cerebral hemodynamics after removal of the larger AVM presumably caused the spontaneous regression of the smaller one. Cerebral angiograms should be carefully examined because cerebral hemodynamics may be altered after removal of an AVM.     

The effect of blood viscoelasticity on pulsatile flow in stationary and axially moving tubes

An analytical solution for pulsatile flow of a generalized Maxwell fluid in straight rigid tubes, with and without axial vessel motion, has been used to calculate the effect of blood viscoelasticity on velocity profiles and shear stress in flows representative of those in the large arteries. Measured bulk flow rate Q waveforms were used as starting points in the calculations for the aorta and femoral arteries, from which axial pressure gradient delta P waves were derived that would reproduce the starting Q waves for viscoelastic flow. The delta P waves were then used to calculate velocity profiles for both viscoelastic and purely viscous flow. For the coronary artery, published delta P and axial vessel acceleration waveforms were used in a similar procedure to determine the separate and combined influences of viscoelasticity and vessel motion. Differences in local velocities, comparing viscous flow to viscoelastic flow, were in all cases less than about 2% of the peak local velocity. Differences in peak wall shear stress were less than about 3%. In the coronary artery, wall shear stress differences between viscous and viscoelastic flow were small, regardless of whether axial vessel motion was included. The shape of the wall shear stress waveform and its difference, however, changed dramatically between the stationary and moving vessel cases. The peaks in wall shear stress difference corresponded with large temporal gradients in the combined driving force for the flow.     

EBV persistence in memory B cells in vivo

OBJECT: Successful therapeutic embolization of arteriovenous malformations (AVMs) of the brain with liquid polymers (glues) requires precise knowledge of highly variable AVM structure and flow velocities and transit times of blood through the AVM nidus. The goal of this study was to improve AVM flow measurement and visualization by the substitution of the insoluble Ethiodol (ethiodized oil) contrast agent for the soluble contrast media normally used in angiographic studies. METHODS: Before enbucrilate embolization of 24 AVM feeding pedicles in 13 patients, standard contrast medium was superselectively injected into each target pedicle, followed by infusion of 20 microl of Ethiodol microdroplets. Transport of contrast material was assessed using high-speed biplane pulsed digital subtraction angiography (DSA) operating at 15 frames per second. The mean blood flow transit times through AVMs after administration of Ethiodol were found to be approximately half as long as in those measured after injection of soluble contrast materials (0.22 +/- 0.10 seconds compared with 0.46 +/- 0.19 seconds [mean +/- standard deviation]; p < 0.0001). The discrete Ethiodol microdroplets travel with the core flow, more closely approximating the dynamic behavior of enbucrilate, allowing the AVM structure to be traced with high spatial and temporal resolution. There were no inadvertent vessel occlusions or pulmonary complications related to the use of Ethiodol for DSA. CONCLUSIONS: Because of diffusion and convection, forces that decrease concentration, visualization of the contrast front is reduced, often resulting in deceptively long transit times when soluble contrast materials are used. Overestimation may prove dangerous when planning embolizations. The Ethiodol droplet DSA method provides accurate transit time measurements and precise, detailed, and dynamic AVM visualization. Further development of this method will improve the safety and precision of AVM treatments.     

Alternative splicing of CYP2D mRNA in human breast tissue

Cerebrovascular arteriovenous malformations (AVMs) display abnormal vascular development and dysautoregulation of blood flow. Genetic mechanisms that contribute to the pathogenesis and phenotype of cerebral AVMs are unknown. As a first step in understanding the pathophysiology of AVMs, the authors investigated the hypothesis that endothelial dysfunction-specifically, deregulation of endothelin-1 (ET-1) secretion-contributes to the abnormal vascular phenotype and the lack of hemodynamic autoregulation elaborated by these lesions. Endothelin-1 peptide and preproendothelin-1 (ppET1) messenger RNA were not detected in the intranidal vasculature of all 17 patients with AVMs studied, but were prominently expressed in human control subjects with normal cerebrovasculature (p < 0.01). Although AVM vasculature lacked ET-1, its expression was prominent in vasculature distant from these lesions, suggesting local repression of the ppET-1 gene. Local repression of ET-1 was specific to AVMs; ET-1 in vascular malformations of patients with Sturge-Weber disease was actually elevated compared to normal controls (p < 0.01). Repression of the ppET-1 gene was an intrinsic phenotype of AVM endothelial cells and was not due to factors in the AVM microenvironment. The authors also showed that ETA receptor expression was low in AVM vasculature compared to normal controls. Together, these results demonstrate that the ppET-1 gene is locally repressed in AVM lesions and suggest a role for abnormal ppET-1 gene regulation in the pathogenesis and clinical sequelae of cerebral AVMs.     

Handling flammable liquids

Control of hemorrhage during AVM surgery is one of the key issues to prevent NPPB. Inadequate procedures for hemostasis of feeders and drainers, so-called dilated capillaries and arteries (moja moja blood vessels) that are located on the side facing the normal brain, and inappropriate surgical strategies for intraoperative hemorrhage from these blood vessels are frequently the main cause of the difficulty in achieving hemostatic control. We conclude that it is important to aggressively reduce the occurrence of intraoperative hemorrhage and prevent or minimize the dilatation of abnormal capillaries and arteries due to inappropriate surgical procedures on the basis of the fundamental surgical strategy, i.e., feeder-->nidus-->drainer. Adequately securing the length and adequate coagulation of hemorrhagic blood vessel, employing a skillful bipolar coagulator technique aimed at controlling intraluminal pressure and blood flow on the central side, are believed to be key factors in hemorrhage treatment.     

Doppler examination of cerebral arteries in uremic children

Transcranial Doppler ultrasonography is a useful method for the estimation and monitoring of cerebral circulation in dialyzed patients. The aim of this study was to evaluate the effect of disease and treatment on cerebral circulation in children on maintenance hemodialysis (HD) and children prior to renal replacement therapy. We demonstrated that in uremic children blood flow velocities of the internal carotid artery (ICA), anterior cerebral artery (ACA), middle cerebral artery (MCA), and posterior cerebral artery (PCA) 120 min and 240 min from the beginning of an HD session were significantly lower than values immediately before HD. Changes in blood flow velocities of MCA and ACA during HD correlated significantly with changes in mean arterial pressure during HD. There was no correlation between changes in blood flow velocities and intradialytic changes in hematocrit values, ultrafiltration, hemoglobin concentration, and blood urea nitrogen values. Mean blood flow velocities of ICA, MCA, and PCA in euvolemic children on conservative treatment were significantly higher than after a HD session in children on maintenance HD. The factors responsible for intradialytic velocity changes of cerebral arteries in uremic children require further examination.     

Relief of hemiballism from a basal ganglia arteriovenous malformation after radiosurgery

A patient with a 3-year history of progressive hemiballism presented with an unruptured arteriovenous malformation (AVM) in the contralateral caudate nucleus and putamen. PET demonstrated a matched reduction of cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) in the basal ganglia and adjacent frontal lobe. The patient underwent radiosurgery for the AVM. After a period of no clinical change for 6 months, the movement disorder resolved by month 7 post-treatment. The AVM was successfully obliterated 2 years after irradiation without any significant change in the regional CBF or CMRO2.     

Glucose 6-phosphate and fructose 1,6-bisphosphate can be used as ATP-regenerating systems by cerebellum Ca2+-transport ATPase

BACKGROUND AND PURPOSE: The use of flow velocity changes in the middle cerebral artery (MCA) measured by Doppler techniques as an index of corresponding cerebral blood flow (CBF) changes is based on the assumption that the insonated arterial diameter remains stable. The postulate of unchanging vessel calibers during CBF changes, however, is still under debate. We performed simultaneous measurements of arterial and venous blood flow velocities by transcranial Doppler ultrasound during various stages of hypercapnia to analyze diameter changes in the insonated vessels by comparing differences in the vasomotor reactivity. METHODS: Simultaneous Doppler recordings of 1 MCA and of a contralateral venous vessel thought to represent the sphenoparietal sinus (SPS) were carried out with a pair of 2-MHz range-gated transducers in 16 young healthy subjects during variations of end-tidal PaCO2. RESULTS: During hypercapnia the mean blood flow velocity of the MCA rose from 62. 5+/-10.2 to a maximum of 99+/-12.2 cm/s (vasomotor reactivity of 60. 1+/-17.3%). The corresponding values in the SPS were significantly higher (P<0.001), revealing a rise from 17.8+/-5.7 to 34.9+/-14.3 cm/s (vasomotor reactivity of 91.4+/-25.9%). Exponential and linear regression analyses revealed an identical high correlation (r2=0.97 and 0.98 for the MCA and SPS, respectively). Slopes were 0.034+/-0. 01 on the arterial and 0.048+/-0.01 on the venous side. The CO2 reactivity (percentage per mm Hg, EtCO2) was found to be 4.5+/-1%/mm Hg in the MCA and 6.8+/-1.5%/mm Hg in the SPS. This difference indicates a vasodilation of the MCA in comparison to the venous vessel. CONCLUSIONS: We have demonstrated a different reaction pattern between intracranial venous and arterial vessels related to end-tidal CO2. Relating the flow velocities to the square of the vessel diameter and assuming a global rise of CBF and not extensible sinus walls, our results indicate that the MCA undergoes a vasodilation of 9.5+/-7% in maximal hypercapnia.     

Transluminal angioplasty and intra-arterial papaverine for the treatment of cerebral vasospasm after ruptured arteriovenous malformations

BACKGROUND: This is the first report on the use of intra-arterial papaverine and percutaneous transluminal angioplasty in two patients with severe, symptomatic cerebral vasospasm who suffered ruptured arteriovenous malformations (AVMs). CASE DESCRIPTIONS: The source of hemorrhage was a venous aneurysm in the first case and a pedicular aneurysm of the distal posterior inferior cerebellar artery in the second case. In both cases, the AVMs were located in the superior vermis and there was minimal subarachnoid hemorrhage. The first patient underwent removal of the AVM before the period of cerebral vasospasm and the second patient underwent removal of the AVM after the cerebral vasospasm had resolved. The outcome was excellent in the first patient and poor in the second patient. CONCLUSION: Arteriovenous malformation with ruptured aneurysms may be at high risk for cerebral vasospasm even when there is minimal subarachnoid hemorrhage. We recommend early treatment of AVMs with ruptured pedicular, intranidal, or venous aneurysms to avoid rebleeding and to allow for aggressive treatment of cerebral vasospasm. The management of cerebral vasospasm after AVM rupture is discussed.     

Rotational state populations in 16O+154Sm near-barrier fusion

Spaceflight induces a cephalad redistribution of fluid volume and blood flow within the human body, and space motion sickness, which is a problem during the first few days of spaceflight, could be related to these changes in fluid status and in blood flow of the cerebrum and vestibular system. To evaluate possible changes in cerebral blood flow during simulated weightlessness, we measured blood velocity in the middle cerebral artery (MCA) along with retinal vascular diameters, intraocular pressure, impedance cardiography, and sphygmomanometry on nine men (26.2 +/- 6.6 yr) morning and evening for 2 days during continuous 10 degrees head-down tilt (HDT). When subjects went from seated to head-down bed rest, their heart rate and retinal diameters decreased, and intraocular pressures increased. After 48 h of HDT, blood flow velocity in the MCA was decreased and thoracic impedance was increased, indicating less fluid in the thorax. Percent changes in blood flow velocities in the MCA after 48 h of HDT were inversely correlated with percent changes in retinal vascular diameters. Blood flow velocities in the MCA were inversely correlated (intersubject) with arterial pressures and retinal vascular diameters. Heart rate, stroke volume, cardiac output, systolic arterial pressure, and at times pulse pressure and blood flow velocities in the MCA were greater in the evening. Total peripheral resistance was higher in the morning. Although cerebral blood velocity is reduced after subjects are head down for 2 days, the inverse relationship with retinal vessel diameters, which have control analogous to that of cerebral vessels, indicates cerebral blood flow is not reduced.     

Alterations in pulmonary artery flow patterns and shear stress determined with three-dimensional phase-contrast magnetic resonance imaging in Fontan patients

OBJECTIVE: This study compares in vivo pulmonary blood flow patterns and shear stresses in patients with either the direct atrium-pulmonary artery connection or the bicaval tunnel connection of the Fontan procedure to those in normal volunteers. Comparisons were made with the use of three-dimensional phase contrast magnetic resonance imaging. METHODS: Three-dimensional velocities, flows, and pulmonary artery cross-sectional areas were measured in both pulmonary arteries of each subject. Axial, circumferential, and radial shear stresses were calculated with the use of velocities and estimates of viscosity. RESULTS: The axial velocities were not significantly different between subject groups. However, the flows and cross-sectional areas were higher in the normal group than in the two patient groups in both pulmonary arteries. The group with the bicaval connection had circular swirling in the cross section of both pulmonary arteries, causing higher shear stresses than in the controls. The disorder caused by the connection of the atrium to the pulmonary artery caused an increase in some shear stresses over the controls, but not higher than those found in the group having a bicaval tunnel. CONCLUSIONS: We found that pulmonary flow was equally reduced compared with normal flow in both patient groups. This reduction in flow can be attributed in part to the reduced size of the pulmonary arteries in both patient groups without change in axial velocity. We also found higher shear stress acting on the wall of the vessels in the patients having a bicaval tunnel, which may alter endothelial function and affect the longevity of the repair.     

Preoperative assessment and prediction of postoperative results in an artificial arterial network using computer simulation

A computer model has been developed that can be used to describe the human arterial system mathematically. It simulates the complex relationship of morphology and hydraulics in the vessel network. After entering patient data into a standard vessel model, the mean flow velocity, the flow direction, and the blood pressure at each specified point of the flow network can be calculated. The vessel picture can be altered and modified with the help of a graphic editor. Localized or diffuse stenoses, bypasses with simple or multiple anastomoses, end-to-end anastomoses, end-to-side anastomoses, etc., can be studied in terms of the hydraulic effects on the local situation or on the entire vessel system. Experimental results of ultrasonic mean flow data in vessel systems of leg and cerebral arteries of patients are compared with calculated values. The predicted and measured flow velocities show a mean difference of about 10% indicating that such a computer model may be successfully used in the optimal planning of bypass operations.     

Occurrence of severe vasospasm following intraventricular hemorrhage from an arteriovenous malformation. Report of two cases

The authors present two rare cases of severe cerebral vasospasm following the rupture of arteriovenous malformations (AVMs). Computerized tomography revealed intracerebral hemorrhage in the thalamus in one case and in the putamen in the other, both accompanied by cast formation of intraventricular clots without radiological evidence of subarachnoid hemorrhage. Initial angiograms showed arterial narrowing of the bilateral internal carotid arteries in the supraclinoid portion but failed to demonstrate an arteriovenous shunt. Subsequent angiograms clearly demonstrated the existence of an AVM. Radiological features and possible mechanisms are discussed.     

Effect of coat on rate of temperature increase in muscle during ultrasound treatment of dogs

BACKGROUND AND PURPOSE: The vasomotor response can be tested by means of transcranial Doppler sonography. If a constant vessel diameter is assumed, the flow velocity changes will reflect blood flow volume changes. This hypothesis is difficult to verify. Simultaneous assessment of intracranial flow velocity and extracranial flow volume changes may solve this problem. METHODS: We tested vasomotor response in 32 volunteers (age, 42+/-18 years) with 5% CO2. Acetazolamide (1 g) was tested in 15 volunteers (age, 28+/-8 years). To evaluate drug-dependent flow changes in the external carotid artery territory, acetazolamide was administered in 7 patients with unilateral occlusion of the internal carotid artery without evidence of collateralization through the ophthalmic artery (age, 67+/-12 years). Simultaneous recording included measurements of flow volume in the common carotid arteries (M-mode color duplex system) and flow velocity in the middle cerebral arteries. RESULTS: With CO2 and acetazolamide, intracranial flow velocity increased by 31% and 39%, respectively, with a simultaneous increase of common carotid artery flow volume of 47% and 50%, respectively. No change in extracranial flow volume was observed in patients with an occluded internal carotid artery. CONCLUSIONS: These data show not only the expected increase of flow velocity in the middle cerebral artery but also suggest an increase in cross-sectional vessel diameter of 6% and 4% with CO2 and acetazolamide, respectively. It remains unresolved whether this observation is due to a direct effect of the drug on the vessel walls or is simply pressure dependent.     

Monitoring of cerebrospinal fluid pressure during embolization of AVM

We experienced that therapeutic embolization of a large cerebral arteriovenous malformation (AVM) led to venous outflow obstruction resulting in intracranial hypertension in a patient who had undergone external decompression. To evaluate hemodynamic changes after embolization, we monitored the cerebrospinal fluid pressure in the next four patients who underwent endovascular treatment. The embolization of a medium AVM resulted in a slight increase in the cerebrospinal fluid pressure. In two medium AVMs, embolization produced slight decreases in the cerebrospinal fluid pressure. In a small AVM, we did not observe any changes in the cerebrospinal fluid pressure during the endovascular treatment. We discuss the mechanism of changes in the intracranial pressure after embolization and conclude that monitoring of the cerebrospinal fluid pressure immediately yields useful information for hemodynamic changes during endovascular treatment.     

A case of large neonatal arteriovenous malformation with heart failure. Color Doppler sonography, MRI and MR angiography as early non-invasive diagnostic procedures

We report a case of a large arteriovenous malformation (AVM) of neonatal onset with heart failure. Transfontanel color Doppler sonography revealed abnormal vessels in the early stage of the investigation. Magnetic resonance imaging (MRI) revealed numerous flow voids suggesting abnormal vessels, and magnetic resonance angiography (MRA) disclosed numerous bizarre abnormal vessels. Color Doppler sonography is a convenient and appropriate procedure for the early bedside diagnosis of neonatal AVMs. MRI and MRA can replace cerebral angiography for the diagnosis of neonatal AVMs.     

Spontaneous angiographic obliteration of cerebral arteriovenous malformations

OBJECTIVE: The factors associated with spontaneous angiographic obliteration of cerebral arteriovenous malformations (AVMs) are not well understood. We present a review of the literature and a report of our experience with six cases (four with no previous treatment intervention and two postoperative residual malformations) that were identified as having occurred during a 20-year period and describe the clinical and lesion features associated with this rare phenomenon. We present the first detailed histological study of a spontaneously thrombosed AVM specimen, including immunohistochemical analysis of angiogenesis factor expression. METHODS: A combined experience in the management of approximately 700 AVMs during 20 years identified six cases of spontaneous angiographic obliteration of cerebral AVMs. A literature review revealed another 24 cases with angiographic documentation of the initial AVMs and follow-up data showing nonfilling of the lesions. Histological analysis of a recently excised lesion included immunostaining with monoclonal antibodies to the antigens of Factor VIII, Tie, vascular endothelial growth factor, and its receptors, Flt-1 and Flk. RESULTS: A single draining vein was a feature in each of our 6 cases and in 12 of 14 (86%) cases from the literature. Hemorrhage as the presenting symptom was identified in 5 of our 6 (83%) cases and in 17 of 24 (71%) of the literature cases. The size of the AVM was less than 6 cm in each of our 6 cases and in 22 of 24 (92%) of the literature cases. A histological examination of a thrombosed AVM surgical specimen revealed persistent patent vascular channels within the lesion. Immunohistochemical analysis with angiogenesis and endothelia-specific factors showed expression of these factors within the lumen of the thrombosed nidus vessels. CONCLUSION: We propose that the occlusion of a single draining vein may lead to total venous outflow obstruction and lesion thrombosis. Hemorrhagic presentation and small nidus may also predispose to this phenomenon. Immunohistochemical analysis of a thrombosed AVM revealed possible ongoing angiogenic changes within the AVM vessels 1 month after angiographically documented thrombosis. It is possible that neovascularization within a thrombosed AVM may lead to lesion recanalization; however, this phenomenon seems to be clinically exceedingly rare.     

HLA and alveolar echinococcosis

OBJECTIVE: Haemodynamic changes as a consequence of application and release of aortic clamps for surgical repair of aortic coarctation are compensated by cerebrovascular autoregulation. Transcranial Doppler was used to study the effect of these haemodynamic changes upon brain circulation in children during aortic coarctation repair. METHOD: A 2-MHz transcranial Doppler system continuously recorded mean cerebral blood flow velocities from the left middle cerebral artery in 13 children (aged from 5 days to 14 years) during repair of their coarctation. Measurements were performed: prior to aortic clamping (baseline); during the first 5 min after clamp application; 1 min before declamping; at 1, 2, 4 and 6 min after the release of both proximal and distal aortic clamps; and at initial chest closure. A contralateral upper-limb non-invasive blood pressure cuff measured systemic blood pressures. Haemodynamic and anaesthetic parameters were monitored. Patients were stratified by age into two groups: age < 6 months (group A) and age > 6 months (group B). RESULTS: With aortic clamping, systemic blood pressures (range from: -16 to +54%) and cerebral blood flow velocities (range from -40 to +19%) changed slightly (P > 0.05) from initiation to end of aortic clamping. In group A, release of aortic clamps resulted in moderate fluctuations in systemic blood pressures (range from -34 to +15%) (P > 0.05) and a marked reduction in cerebral blood flow velocities (range from -63 to -33%) (P < 0.01). At the time of surgical closure, flow velocities had improved in all infants except one. Group B did not show major reductions in either cerebral blood flow velocity or systemic blood pressures throughout all measurements (P > 0.05). During aortic clamp release, young infants responded with lower brain blood flow velocities as compared to older children (r = 0.68; P < 0.05). CONCLUSION: Transient central nervous system hypotension results as a consequence of flow redistribution during aortic declamping in young infants. Older children usually show a faster autoregulatory compensation to these haemodynamic changes. The observed age-related physiologic differences, suggest that young infants may require higher systemic blood pressures during declamping to prevent the cerebral blood flow reduction. Transcranial Doppler appears to be a valuable monitor of these cerebral haemodynamic changes.     

The clinical assessment of attachment in children under five

Dural arteriovenous malformations (AVMs) are considered to be acquired lesions that develop secondary to venous obstruction, which sometimes happens in head trauma. However, there has been a report of an anterior cranial fossa dural AVM that occurred independently of a history of head trauma, and there has been speculation that these malformations are congenital. The authors recount their experience with a patient who had an anterior cranial fossa dural AVM that was discovered incidentally. The lesion was fed by the bilateral anterior ethmoidal arteries and drained into the superior sagittal sinus via frontal cortical veins. The patient had a history of severe head trauma that had occurred 30 years earlier. This is the first case report in which a previous head trauma is strongly believed to be the cause of an anterior cranial fossa dural AVM. The authors postulate that anterior cranial fossa dural AVMs can develop secondary to a head trauma.