Raised intracranial pressure and cerebral blood flow: 2. Supratentorial and infratentorial mass lesions in primates

Changes in cerebral blood flow with increasing intracranial pressure were studied in anaesthetized baboons during expansion of a subdural balloon in one of two different sites. With an infratentorial balloon, cerebral blood flow bore no clear relation to intracranial pressure, but was linearly related to cerebral perfusion pressure. Apart from an initial change in some animals, cerebrovascular resistance remained constant with increasing intracranial pressure, and autoregulation appeared to be lost from the outset. With a supratentorial balloon, cerebral blood flow remained constant as intracranial pressure was increased to levels around 60 mm Hg, corresponding to a cerebral perfusion pressure range of approximately 100 to 40 mmHg. Cerebrovascular resistance fell progressively, and autoregulation appeared to be effective during this phase. At higher intracranial pressure levels (lower cerebral perfusion pressure levels), autoregulation was lost and cerebral blood flow became directly dependent on cerebral perfusion pressure. The importance of the cause of the increase in intracranial pressure on the response of the cerebral circulation and the relevance of these findings to the clinical situation are discussed.     

Raised intracranial pressure and cerebral blood flow: I. Cisterna magna infusion in primates

Changes in cerebral blood flow during incremental increases of intracranial pressure produced by infusion of fluid into the cisterna magna were studied in anaesthetized baboons. Cerebral blood flow remained constant at intracranial pressure levels up to approximately 50 mm Hg. At intracranial pressure levels between 50-96 mm Hg a marked increase in cerebral blood flow occurred, associated with the development of systemic hypertension and changes in cerebrovascular resistance. Further increases of intracranial pressure led to a progressive fall in cerebral blood flow. Prior section of the cervical cord prevented both the increase in cerebral blood flow and the systemic hypertension. Alteration of cerebral perfusion pressure by bleeding during the hyperaemia in a further group of animals suggested that autoregulation was at least partially preserved during this phase. After maximum hyperaemia had occurred, however, autoregulation appeared to be lost. The clinical implications of these findings are discussed.     

Cerebral microcirculation during increased intracranial pressure--assessment with reflectance photometry

The cerebral microcirculation under increased intracranial pressure was evaluated by using reflectance photometric method. The values of tissue hemoglobin (IHb) and its oxygen saturation (ISO2) detected by this method were evaluated in cat brain tissue. The correlation between IHb and content of cortical hemoglobin subunits in vitro was high. High correlation between ISO2 and blood oxygen saturation in superior sagittal sinus was also noted in hypoxic hypoxia. Thus, the reflectance photometric method was revealed to be applicable for evaluation of regional hemoglobin content and oxygen saturation. Using this method the cerebral microcirculation was studied in an increased intracranial pressure model produced by injection of artificial CSF into the cisterna magna in cats. Regional cortical cerebral blood flow (CBF) was measured simultaneously by thermal diffusion method. During decrease of perfusion pressure down to 40 mmHg with preservation of CBF, compensatory increase of IHb was not observed, but IHb rather gradually decreased. The decrease of IHb would be due collapse of capacitance vessels by increased intracranial pressure. Cerebral ISO2 was stable as well as CBF. Less than 40 mmHg of perfusion pressure, ISO2 started to decrease in association with CBF and IHb. Since ISO2 seems to be closely related to the tissue oxygen extraction the change of ISO2 reflect the CBF and tissue cerebral oxygen metabolism. Present study suggest the evaluations of IHb and ISO2 were an useful monitoring indexes in various cerebral disorders.     

Superior sagittal sinus thrombosis as a rare complication of spontaneous intracranial hypotension syndrome: a case report and review of the literature

In addition to an orthostatic headache, spontaneous intracranial hypotension syndrome can lead to subdural hematoma and diffusion, subarachnoid hemorrhage, and brain sag. However, cerebral venous sinus thrombosis is rarely reported in patients with spontaneous intracranial hypotension. We present the case of a 35-year-old male who developed an orthostatic headache, nausea, vomiting, and photophobia for 5 days. An enhanced brain magnetic resonance image showed extensive linear pachymeningeal enhancement in the bilateral cerebral hemispheres. Lumbar puncture showed that cerebrospinal fluid pressure was 80 mmH₂O. Subsequent magnetic resonance scans demonstrated subdural effusion of the bilateral frontoparietal lobes, hyperintense T1-weighted images, and T2WI lesions within the superior sagittal sinus in 17?days. The patient was given low molecular weight heparin and adverse events occurred. Head computed tomography showed cerebral external fluid accumulation in the bilateral frontoparietal lobes. Then, digital subtraction angiography was performed at 22?days, which confirmed superior sagittal sinus thrombosis, and the patient recovered fully after therapy. The evolution of the disease and radiological findings support the diagnosis of spontaneous intracranial hypotension with superior sagittal sinus thrombosis. To the best of our knowledge, there are very few case reports describing superior sagittal sinus thrombosis as a complication of spontaneous intracranial hypotension. When spontaneous intracranial hypotension and cerebral venous thrombosis occur together, difficult practical questions arise regarding the treatment of these two conditions.     

Blood flow velocities during experimental intracranial hypertension in pigs

Abstract

Objectives: A purely hydraulic mechanism consisting in the pulsatile cuff-compression effect, by the cerebrospinal fluid displacement induced by the arterial pulsation, on the final portion of the bridging veins, has recently been hypothesized. This mechanism is able to maintain the constancy of cerebral blood flow (CBF) within the autoregulatory range, thus implying an exact balance between arterial inflow and venous outflow. In this study, we correlated arterial inflow and venous outflow during an experimentally induced condition of intracranial hypertension in pigs.

Methods: Mock cerebrospinal fluid (CSF) was progressively infused until a condition of brain tamponade was reached. Blood flow velocities at middle cerebral artery and sagittal sinus sites were evaluated simultaneously.

Results: Mean intracranial arterial blood flow velocity (IABFV), mean sagittal sinus blood flow velocity (SSBFV), and pulsatile-IABFV remained almost constant until cerebral perfusion pressure (CPP) dropped below 60–70 mmHg; then, a progressive decrease in mean IABFV and SSBFV, together with an increase in pulsatile-IABFV, was evident.

Conclusion: The strict similarity between mean IABFV and SSBFV patterns suggests that CBF decrement is mainly due to a decrease in the venous outflow, which, in turn, produces an obstacle to the arterial inflow. The correspondent increase in pulsatile-IABFV confirms the presence of a distal outflow obstruction. All these findings point towards a purely hydraulic mechanism underlying the cerebral autoregulation which acts at the level of the so-called Starling resistor.     

Infratentorial intracranial pressure monitoring in neurosurgical intensive care unit

Abstract

Monitoring intracranial pressure (ICP) is an important element of neurosurgical critical care that is used primarily as an indicator of adequate cerebral perfusion. Such monitoring is usually done with intraparenchymal, subdural or intraventricular pressure sensor connected to a pressure transducer system. In the past, multiple studies have shown that there are certain pressure gradients between various intracranial compartments, especially if there is some focal intracranial pathological process. Several clinical and laboratory studies measured ICP inside the posterior fossa by placing the sensor into the cisterna magna or the cerebellopontine angle. None of them, however, monitored direct intraparenchymal pressure in the posterior fossa. Such measurement may be a more sensitive way to assess focal swelling, ischemia and tissue perfusion in the posterior fossa structures. We simultaneously monitored supratentorial ICP using an external ventricular drain placed in the lateral ventricle and infratentorial ICP with an intraparenchymal sensor inserted into the cerebellum. We subsequently analyzed data from five patents with different posterior fossa pathology each of which had simultaneous supra- and infratentorial ICP recordings for up to five days. We found difference in ICP between the infratentorial and supratentorial compartments and this difference changed over time. In this article, we discuss feasibility and safety of simultaneous infra- and supratentorial ICP monitoring in patients with the posterior fossa pathology.     

Arterial inflow and venous outflow in idiopathic intracranial hypertension associated with venous outflow stenoses.

A reduction in the proportion of the arterial inflow drained by the superior sagittal sinus in idiopathic intracranial hypertension (IIH) patients without stenoses has been noted and this has suggested elevated collateral flow. This study defines the interaction between arterial inflow and venous outflow in patients with outflow stenoses and IIH. Forty patients with clinical IIH underwent standard MRI, MR venography and MR flow quantification studies of the cerebral arteries and veins. There were 21/40 patients with venous stenoses. The arterial inflow was 21% higher than normal (p=0.01); however, the superior sagittal sinus outflow was normal, giving a reduced percentage of venous outflow compared to inflow. Seven patients were followed up after remission of their symptoms and the arterial inflows and percentage outflow returned to normal. There is a spectrum of findings in IIH; patients with stenoses have lower inflows than those with patent sinuses but still have evidence of collateral flow.     

Infratentorial intracranial pressure monitoring in neurosurgical intensive care unit

Monitoring intracranial pressure (ICP) is an important element of neurosurgical critical care that is used primarily as an indicator of adequate cerebral perfusion. Such monitoring is usually done with intraparenchymal, subdural or intraventricular pressure sensor connected to a pressure transducer system. In the past, multiple studies have shown that there are certain pressure gradients between various intracranial compartments, especially if there is some focal intracranial pathological process. Several clinical and laboratory studies measured ICP inside the posterior fossa by placing the sensor into the cisterna magna or the cerebellopontine angle. None of them, however, monitored direct intraparenchymal pressure in the posterior fossa. Such measurement may be a more sensitive way to assess focal swelling, ischemia and tissue perfusion in the posterior fossa structures. We simultaneously monitored supratentorial ICP using an external ventricular drain placed in the lateral ventricle and infratentorial ICP with an intraparenchymal sensor inserted into the cerebellum. We subsequently analyzed data from five patients with different posterior fossa pathology each of which had simultaneous supra- and infratentorial ICP recordings for up to five days. We found difference in ICP between the infratentorial and supratentorial compartments and this difference changed over time. In this article, we discuss feasibility and safety of simultaneous infra- and supratentorial ICP monitoring in patients with the posterior fossa pathology.     

Suppression of epileptiform activity by increased intracranial pressure in cat.

This study investigated the relationships between changes in intracranial pressure and the activity of cortical epileptogenic foci in cats. Epileptiform spiking was produced by focal freezing and/or topical application of penicillin. Increases in intracranial pressure were produced by infusion of mock cerebrospinal fluid into the cisterna magna. We found that increases in intracranial pressure always produced decreases in epileptiform spike discharge rate. Some preparations also showed an enhancement or “rebound” of spike discharge rate soon after the intracranial pressure was returned to normal. We concluded that it is unlikely that compression or distortion of cerebral tissue play any role in these results. Decreases in cerebral blood flow may be a factor but only for the higher values of intracranial pressure in the less sensitive preparations. We suggest that the most important mechanism responsible for these findings is the desynchronizing effect of afferent input related to increased intracranial pressure. The source of this sensory activity may be from receptors in the cerebrospinal meninges and blood vessels.     

Association between arterial inflow and venous outflow in idiopathic and secondary intracranial hypertension.

Twenty-four patients with a clinical diagnosis of idiopathic intracranial hypertension underwent standard magnetic resonance (MR) imaging. On the basis of MR venography, two groups of patients could be identified: (i) one group with an intrinsic venous outflow obstruction (intrinsic); and (ii) a non-intrinsically obstructed (extrinsic) group. MRI flow quantification studies of the cerebral arteries and veins, measuring arterial blood inflow as well as superior sagittal sinus (SSS) and straight sinus (ST) outflow, were performed. The MR venography confirmed that there were 12 intrinsic patients and 12 extrinsic patients. In the intrinsic group, total arterial inflow was normal; however, the SSS outflow was reduced by 35% (p=0.0001). Arterial inflow in extrinsic patients was 55% higher than normal (p=0.0001); however, the SSS flow was normal. In intrinsic venous outflow obstruction, total cerebral inflow is maintained despite a reduction in outflow. In the idiopathic cases, there was cerebral hyperaemia suggesting a derangement of autoregulation.     

Manometry combined with cervical puncture in idiopathic intracranial hypertension.

OBJECTIVE: To determine by cerebral venography and manometry in patients with idiopathic intracranial hypertension the cause of the previously demonstrated venous hypertension in the superior sagittal and proximal transverse sinuses. METHODS: Cerebral venous sinus pressure was measured before and immediately after C1-2 puncture with removal of 20 to 25 mL of CSF. RESULTS: Lowering the intracranial pressure by lateral C1-2 puncture during manometry has shown that the venous hypertension resolves immediately. CONCLUSION: These studies indicate that the venous hypertension is due to compression of the transverse sinuses by raised intracranial pressure and not due to a primary obstructive process in the cerebral venous sinuses.     

颅高压对兔静脉窦血栓后脑梗死的影响

目的利用兔静脉窦血栓的动物模型,观察兔静脉窦血栓后颅内压对脑组织的影响。方法成年健康日本大耳白兔95只,随机分为5组,其中建模成功90只:A、B、C、D组为处理组,均为结扎上矢状窦后1/3及其回流静脉,其中B、C、D组为在结扎基础上分别放置0.2 ml、0.4 ml、0.6 ml的硬膜外球囊,E组为假手术组(6只)。各组均在术后8 h、24 h、48 h观察脑含水量、脑梗死范围及病理变化。结果与E组相比,A、B、C、D组在相应时间点的脑含水量、脑梗死范围均明显增加,且随着颅内压增高呈增高趋势。结论在兔静脉窦血栓模型中,颅内压增高可加重脑水肿的程度和增加脑梗死的范围,解除颅内高压则可减轻脑水肿和脑梗死范围。     

脑桥静脉对颅内压增高的调节反应

目的 研究正常和过度换气时脑桥静脉对颅内压增高的血流动力学改变。方法 选择７头丹麦白约克猪通过向枕大池灌注人工脑脊液,逐步增加颅内压,从基础值（大约１．３ｋＰａ）到２．７ｋＰａ和４．０ｋＰａ,用彩色超声多谱勒测量正常和过度换气状态下,颅内压增高对于脑桥静脉的血流速度、直径和脉冲指数的影响。结果 随着颅内压增高,脑桥静脉的血流速度减慢,直径和脉冲指数增加,而颅内压增高对中心静脉压、动脉ＣＯ２分压、平     

Cerebral blood flow in experimental intracranial mass lesions. Part II: The postdecompression phase

Cerebral haemodynamics were evaluated after a period of cerebral compression produced by subarachnoid fluid infusion or inflation of an epidural balloon. Release of the compression resulted in a marked cerebral hyperperfusion which was generalized in the case of hydrostatically raised pressure but restricted to supratentorial structures after balloon compression. A rebound of intracranial pressure (ICP) occurred only after balloon compression, indicating that loss of vasomotor tone per se was not the primary reason for the rebound of ICP. In the balloon compression experiments the hyperaemia passed into a stage of hypoperfusion attributable in part to a reduction in cerebral perfusion pressure due to the rebound of ICP and in part to an increase in flow resistance probably related to external compression of the vascular bed by the accumulation of brain oedema. The observed flow changes, i.e. delayed hypoperfusion preceded by hyperaemia, were similar to those after temporary ischaemia, indicating that the rebound response is a non-specific postischaemic phenomenon.     

Contribution of mathematical modelling to the interpretation of bedside tests of cerebrovascular autoregulation

OBJECTIVES—Cerebral haemodynamic responses toshort and longlasting episodes of decreased cerebral perfusion pressurecontain information about the state of autoregulation of cerebral bloodflow. Mathematical simulation may help to elucidate which of theindices, that can be derived using transcranial Doppler ultrasonographyand trends of intracranial pressure and blood pressure, are useful inclinical tests of autoregulatory reserve.
METHODS—Time dependent interactions betweenpressure, flow, and volume of cerebral blood and CSF were modelledusing a set of non-linear differential equations. The model simulateschanges in arterial blood inflow and storage, arteriolar and capillaryblood flow controlled by cerebral autoregulation, venous blood storageand venous outflow modulated by changes in ICP, and CSF storage and reabsorption. The model was used to simulate patterns of blood flowduring either short or longlasting decreases in cerebral perfusionpressure. These simulations can be considered as clinically equivalentto a short compression of the common carotid artery, systemichypotension, and intracranial hypertension. Simulations were performedin autoregulating and non-autoregulating systems and compared withrecordings obtained in patients.
RESULTS—After brief compression of the commoncarotid artery, a subsequent transient hyperaemia can be interpreted asevidence of intact autoregulation. During longlasting sustainedhypoperfusion, a gradual increase in the systolic value of the bloodflow velocity waveform along with a decrease in the diastolic value isspecific for an autoregulating cerebrovascular system.
CONCLUSION—Modelling studies help to interpretboth clinical and experimental cerebral haemodynamic phenomena andtheir dependence on the state of autoregulation.

     

Vascular responses to acute intracranial hypertension

In 27 rhesus monkeys the cerebrospinal fluid pressure (CSFP) was raised by injections into the cisterna magna to about 40 to 50 mm Hg in steps of 5 mm Hg every five minutes. During the initial phase of the rise of the CSFP to about 15 mm Hg normal animals showed a significant fall in the systolic arterial blood pressure. With a further elevation of the CSFP the BP rose till the CSFP reached 30 to 40 mm Hg. If the CSFP were raised higher than that, a large number of the animals showed a significant fall in the BP. In animals which were shocked before the CSFP was raised there was no drop in the systolic BP during the initial phase. This study indicates that vascular decompensation occurs in the majority of animals when the CSFP goes higher than 30 to 40 mm Hg; there is a significant rise in the pulse rate, superior sagittal sinus pressure (SSP), and internal jugular vein pressure (JVP). The JVP was related to the SSP, indicating that the JVP most probably reflected the pressure changes in the intracranial venous sinuses. Four animals suddenly collapsed at the highest CSFP. In the remaining 23 animals, on a sudden lowering of the CSFP to zero from the highest level, 13 monkeys died in less than half an hour and four in about an hour, while six animals stood this elevation of the CSFP well, with a good recovery. This indicates that, once the vascular decompensation has set in, the prognosis is generally poor even after lowering the CSFP to normal. The drop of the CSFP to zero produced no significant change in the pulse rate but a significant fall in the BP. The SSP rose when its pre-lowering level was less than 7·5 mm Hg and fell when the level was at or above 7·5 mm Hg level. The JVP showed a significant correlation with the variations in the SSP. The fundus examination at the end of the experiment revealed no abnormality.     

Alterations in the intracranial venous sinuses in spontaneous nontraumatic chronic subdural hematomas

Occlusion of the cerebral venous system is frequently associated with intraparenchymal or subarachnoid hemorrhage. There are few reports of cerebral venous thrombosis associated with nontraumatic chronic subdural hematoma (CSH). We aimed to evaluate the intracranial venous system in patients with spontaneous nontraumatic CSH and to identify alterations in their venous sinuses. In this study, eight patients with spontaneous, nontraumatic CSH were followed for a 7-year period (mean: 2.2 years, range: 1–7 years). Neuroradiological images were taken at the onset of symptoms and during follow-up. Venous angiography or magnetic resonance venography was used to evaluate the cerebral venous system of patients. In all patients, medical or surgical treatments were based on clinical symptoms. In seven of the eight patients, the CSH was in the left hemisphere, whereas one patient had bilateral CSH. In one of the eight patients, thrombosis of the transverse sinus and sigmoid sinus was found, but recanalization was observed at follow-up. In a further three patients, the superior sagittal sinus, the straight sinus, and the vein of Galen were markedly reduced in diameter compared to normal or were not visible at presentation, but normal flow was observed at follow-up. In the remaining four patients, the transverse sinus was not observed at symptom onset or during long-term follow-up. A nontraumatic CSH can occur secondary to a venous thrombosis or it can be associated with the inability to image some of the venous sinuses. Venous flow was restored at long-term follow-up. Increased intravenous pressure is thought to be the pathogenic factor that causes a nontraumatic CSH.     

Cerebral circulatory and metabolic effects of hypotension produced by deep halothane anaesthesia

Hypotension to a mean blood pressure of 33 mmHg for periods of 70 to 187 minutes was induced by increasing the inspired halothane concentration in 11 baboons which were already anaesthetized with 0·5% halothane, nitrous oxide, and oxygen. During hypotension, cerebral blood flow, measured by Xenon clearance and by a carotid electromagnetic flowmeter, decreased by more than half, and sagittal sinus oxygen saturation was 46%. Cerebral oxygen uptake fell from 5·15 to 3·56 ml./100 g/min at this deeper level of halothane anaesthesia. Cerebral hyperaemia developed after hypotension in those animals which regained a mean blood pressure greater than 70 mmHg. Acidbase measurements on CSF from the cisterna magna revealed no metabolic acidosis during or after hypotension. In all four animals with intact autoregulation before hypotension, this was absent or impaired afterwards.     

Bilateral chronic subdural haematomas in a patient with meningioma of the superior sagittal sinus - case report and pathophysiological study

Bilateral chronic subdural haemorrhage accompanying meningioma is a very rare clinical condition. We present a case of a 69-year-old female patient with large meningioma completely obliterating the posterior third part of the superior sagittal sinus with accompanying bilateral chronic subdural haematomas. Three anatomical zones of venous collateral circulation were revealed by the preoperative digital subtraction angiography. The tumour and haematomas were removed completely with no major complications. The most likely pathomechanism of the development of bilateral chronic subdural haematomas was venous hypertension caused by an occlusion of major cerebral venous trunks. As a result of a minor thrombotic incident or insignificant head injury, the distended veins of collateral circulation that were volumetrically burdened could have been damaged. Patients with large tumours occluding the superior sagittal sinus, who did not qualify for or refused surgery, should be carefully monitored clinically and neuroradiologically because of possibly increased risk of an intracranial haemorrhage.     

Evolution of angiographic signs of venous hypertension and clinical signs of intracranial hypertension in intracranial dural arteriovenous fistulas]

Dural arteriovenous fistulas (dAVFs) can cause cerebral venous hypertension (VHT). The most common mechanism is due to the fact that some dAVFs can drain retrogradelly in cortical (better defined as leptomeningeal) veins (directly or after drainage in a dural sinus) causing venous engorgement and consequently an impairment of the cerebral venous drainage. However, more rarely, dAVFs without a cortical venous drainage can also be responsible for VHT probably due to dAVF shunts causing insufficient antegrade cerebral venous drainage. In addition, dAVFs are often associated with stenosis and/or thrombosis of dural sinus(es) which can worsen the VHT. Raised pressure within the superior sagittal sinus causes impeded cerebrospinal reabsorption in the arachnoid villi allowing increased intracranial pressure. The venous engorgement in the cortical veins can cause a venous congestive encephalopathy analogous to the venous congestive myelopathy of the spinal dural AVFs. Clinically VHT can cause not only symptoms related to increased intracranial pressure but also seizures, neurological deficits, impairment of the cognitive functions and dementia. An important aspect is the risk of hemorrhage in dAVFs with a leptomeningeal venous drainage leading to VHT. Although the term VHT sensu strictu should be used if venous pressure measurements are performed, angiographic criteria for VHT such as delayed circulation time, venous engorgement and abnormal visualization of the cerebral veins are well established. The purpose of our study was to evaluate the angiographic signs of VHT in patients with dAVF and to study the course of the VHT and of the clinical signs of increased intracranial pressure before and after dAVF endovascular treatment. A retrospective chart analysis of 22 patients (13 males, 9 females) ranging in age from 20 to 87 years (mean: 53 ys.) with a dAVF associated with angiographic signs of VHT was performed. Ten dAVFs were located on the transverse/sigmoid sinus(es), 6 on the superior sagittal sinus, 3 on the petro-tentorial incisura, 1 on the inferior petrosal sinus, 1 on the anterior ethmoidal region and 1 on the Galen vein region. All dAVFs had a retrograde leptomeningeal venous drainage. Stenosis or thrombosis of the dural AVF sinus was observed in 17 cases and stenosis or thrombosis of another sinus(es) and/or of the jugular vein in 8 cases. In 11 patients, the angiographic signs of VHT were global affecting the entire cerebral venous drainage and, in the other 11 patients, the VHT was focal. The VHT caused clinical symptoms of increased intracranial pressure in 18 patients. Other clinical findings included: bruit (11 cases), seizures (3 cases), vertigo (3 cases), visual deficits (2 cases) and impairment of cognitive functions (4 cases). Three patients presented hemorrhage (one parenchymal hematoma, one hemorrhagic infarction and one subarachnoid hemorrhage). The 4 patients without clinical symptoms of increased intracranial pressure presented only bruit in 2 cases, bruit and vertigo in 1 case, bruit and hemorrhagic infarction in another one. The dAVFs were treated by endovascular therapy (arterial approach: 3 cases, venous approach: 6 cases and both arterial and venous approach: 13 cases). Endovascular sessions ranged from 1 to 7 (mean: 2.8) for each patient. After the endovascular treatment, in 12 patients with complete occlusion of the dAVF, the disappearance of angiographic signs of VHT and clinical cure were observed. In 8 patients with partial occlusion of the dAVF, the disappearance of angiographic signs of VHT and clinical cure were observed in 4 cases (almost complete dAVF occlusion in 2 cases); in the other 4 cases, only reduction the angiographic signs of VHT and clinical improvement were obtained. In all 16 patients who were clinically cured angiographic signs of VHT disappeared despite the persistence of dAVF shunts as observed in 4 cases. (ABSTRACT TRUNCATED)