Neurological manifestations of intracranial dural arteriovenous malformations

1986 ◽  
Vol 64 (5) ◽  
pp. 724-730 ◽  
Author(s):  
Pierre Lasjaunias ◽  
Ming Chiu ◽  
Karel Ter Brugge ◽  
Atul Tolia ◽  
Michel Hurth ◽  
...  
Keyword(s):  
Nervous System ◽  
Sinus Thrombosis ◽  
Venous Drainage ◽  
Venous Hypertension ◽  
Clinical Aspects ◽  
Content Type ◽  
Sagittal Sinus ◽  
Cortical Venous Drainage ◽  
Base Of The Skull ◽  
Fine Print

✓ The authors describe their experience with four cases of dural arteriovenous malformation (AVM) which led them to analyze the clinical aspects of these lesions in an attempt to understand their pathophysiology. An additional 191 previously reported cases of dural AVM's were reviewed with special attention to the mechanism of intradural, central, and peripheral nervous system manifestations. Apart from the peripheral cranial nerve symptoms, which are most likely due to arterial steal, the central nervous system (CNS) symptoms appear to be related to passive venous hypertension and/or congestion. Generalized CNS symptoms can be related to cerebrospinal fluid malabsorption due either to increased pressure in the superior sagittal sinus, to venous sinus thrombosis, or to meningeal reaction resulting from minimal subarachnoid hemorrhages. These phenomena are not related to the anatomical type of venous drainage. On the other hand, focal CNS symptoms are specifically indicative of cortical venous drainage. Seizures, transient ischemic attacks, motor weakness, and brain-stem and cerebellar symptoms can be encountered depending on the territory of the draining vein or veins. Therefore, the localizing value of focal CNS symptomatology relates to the venous territory and not to the nidus or to the arterial supply characteristics of dural AVM's. Furthermore, the venous patterns of various dural AVM's at the base of the skull are expressed by differences in their clinical presentation. Dural AVM's of the floor of the anterior cranial fossa and of the tentorium are almost always drained by the cortical veins and, therefore, have a high risk of intradural bleeding. The remarkable similarities in the manifestations of dural and brain AVM's and the differences in the manifestations of dural and spinal dural AVM's are pointed out. High-quality angiograms and a multidisciplinary approach to the study of dural AVM's will provide the best understanding of their symptoms and, therefore, the most appropriate treatment strategy.

A variant of arteriovenous fistulas within the wall of dural sinuses. Results of combined surgical and endovascular therapy

1991 ◽  
Vol 74 (2) ◽  
pp. 199-204 ◽  
Author(s):  
Stanley L. Barnwell ◽  
Van V. Halbach ◽  
Christopher F. Dowd ◽  
Randall T. Higashida ◽  
Grant B. Hieshima ◽  
...  
Keyword(s):  
Venous Drainage ◽  
Venous Hypertension ◽  
Neurological Dysfunction ◽  
Dural Sinus ◽  
Unique Type ◽  
Content Type ◽  
Av Fistula ◽  
Arteriovenous Fistulas ◽  
Av Fistulas ◽  
Cortical Venous Drainage

✓ Dural arteriovenous (AV) fistulas are thought to be acquired lesions that form in an area of thrombosis within a sinus. If the sinus remains completely thrombosed, venous drainage from these lesions occurs through cortical veins, or, if the sinus is open, venous drainage is usually into the involved sinus. Among 105 patients with dural A V fistulas evaluated over the the past 5 years, seven had a unique type of dural AV fistula in the superior sagittal, transverse, or straight sinus in which only cortical venous drainage occurred despite a patent involved sinus; the fistula was located within the wall of a patent dural sinus, but outflow was not into the involved sinus. This variant of dural AV fistulas puts the patient at serious risk for hemorrhage or neurological dysfunction caused by venous hypertension. Three patients presented with hemorrhage, one with progressive neurological dysfunction, one with seizures, and two with bruit and headaches. A combination of surgical and endovascular techniques was used to close the fistula while preserving flow through the sinus.

Endovascular treatment of intracranial dural arteriovenous fistulas with spinal perimedullary venous drainage

1992 ◽  
Vol 77 (5) ◽  
pp. 718-723 ◽  
Author(s):  
Y. Pierre Gobin ◽  
Andre Rogopoulos ◽  
Armand Aymard ◽  
Mazen Khayata ◽  
Daniel Reizine ◽  
...  
Keyword(s):  
Endovascular Treatment ◽  
Endovascular Therapy ◽  
Sinus Thrombosis ◽  
Venous Drainage ◽  
Transverse Sinus ◽  
Venous Hypertension ◽  
Arterial Phase ◽  
Content Type ◽  
Arteriovenous Fistulas ◽  
Av Fistulas

✓ Intracranial dural arteriovenous (AV) fistulas with spinal perimedullary venous drainage are rare lesions that have distinctive clinical, radiological, and therapeutic aspects. Five patients presented with an ascending myelopathy, which extended to involve the brain stem in three cases. Myelography and magnetic resonance imaging showed slightly dilated spinal perimedullary vessels. Spinal angiograms were normal in the arterial phase. Diagnosis was only possible after cerebral angiography, which demonstrated posterior fossa AV fistulas fed by meningeal arteries and draining into spinal perimedullary veins. Endovascular treatment alone resulted in angiographic obliteration of the lesion in three patients. Two patients required surgery in addition to endovascular therapy. One patient died postoperatively, and in one a transient complication of embolization was observed. Improvement after treatment was good in two cases and fair in two. Transverse sinus thrombosis was observed in three cases and was probably the cause of the aberrant venous drainage of the fistula into the spinal perimedullary veins. The pathophysiology is related to spinal cord venous hypertension. These lesions were classified as Type 5 in the Djindjian and Merland classification of dural intracranial AV fistulas. Endovascular therapy is a safe effective method in the treatment of these fistulas and should be tried first.

Fatal progression of posttraumatic dural arteriovenous fistulas refractory to multimodal therapy

2001 ◽  
Vol 94 (5) ◽  
pp. 831-835 ◽  
Author(s):  
Jonathan A. Friedman ◽  
Fredric B. Meyer ◽  
Douglas A. Nichols ◽  
Robert J. Coffey ◽  
L. Nelson Hopkins ◽  
...  
Keyword(s):  
Multimodal Therapy ◽  
Transarterial Embolization ◽  
Subsequent Treatment ◽  
Venous Hypertension ◽  
Content Type ◽  
Arteriovenous Fistulas ◽  
Sagittal Sinus ◽  
Pulsatile Mass ◽  
Dural Arteriovenous Fistulas ◽  
Fine Print

✓ The authors report the case of a man who suffered from progressive, disseminated posttraumatic dural arteriovenous fistulas (DAVFs) resulting in death, despite aggressive endovascular, surgical, and radiosurgical treatment. This 31-year-old man was struck on the head while playing basketball. Two weeks later a soft, pulsatile mass developed at his vertex, and the man began to experience pulsatile tinnitus and progressive headaches. Magnetic resonance imaging and subsequent angiography revealed multiple AVFs in the scalp, calvaria, and dura, with drainage into the superior sagittal sinus. The patient was treated initially with transarterial embolization in five stages, followed by vertex craniotomy and surgical resection of the AVFs. However, multiple additional DAVFs developed over the bilateral convexities, the falx, and the tentorium. Subsequent treatment entailed 15 stages of transarterial embolization; seven stages of transvenous embolization, including complete occlusion of the sagittal sinus and partial occlusion of the straight sinus; three stages of stereotactic radiosurgery; and a second craniotomy with aggressive disconnection of the DAVFs. Unfortunately, the fistulas continued to progress, resulting in diffuse venous hypertension, multiple intracerebral hemorrhages in both hemispheres, and, ultimately, death nearly 5 years after the initial trauma. Endovascular, surgical, and radiosurgical treatments are successful in curing most patients with DAVFs. The failure of multimodal therapy and the fulminant progression and disseminated nature of this patient's disease are unique.

Transcranial approach for venous embolization of dural arteriovenous fistulas

2002 ◽  
Vol 97 (2) ◽  
pp. 280-286 ◽  
Author(s):  
Emmanuel Houdart ◽  
Jean-Pierre Saint-maurice ◽  
René Chapot ◽  
Adam Ditchfield ◽  
Alexandre Blanquet ◽  
...  
Keyword(s):  
Operating Room ◽  
Sinus Thrombosis ◽  
Transverse Sinus ◽  
Dural Sinus ◽  
Content Type ◽  
Arteriovenous Fistulas ◽  
Sagittal Sinus ◽  
First Case ◽  
Transcranial Approach ◽  
Fine Print

Object. Transvenous embolization is effective in the treatment of an intracranial dural arteriovenous fistula (DAVF). Access to the fistula via the internal jugular vein (IJV) may be limited by associated dural sinus thrombosis; a transcranial approach has been developed for venous embolization in such a situation. The authors report their experiences with the use of a transcranial approach for venous embolization of DAVFs. Methods. Ten patients with DAVFs underwent craniectomy and embolization procedures in which direct sinus puncture was performed. The DAVFs were located inside the dura mater that constituted the walls of the transverse sinus in five cases, the superior sagittal sinus in four cases, and the superior petrosal sinus in one case. All DAVFs drained directly into a sinus with secondary reflux into leptomeningeal veins. In all cases, the fistula could not be accessed from the IJVs. Craniectomy was performed in an operating room and, in seven cases, subsequent enlargement of the craniectomy was required. Sinus catheterization was performed after the patient had been transferred to the angiography room. The DAVFs were embolized using coils only in five patients, glue only in two patients, and both coils and glue in three patients. Angiographic confirmation that embolization of the fistula was successful was obtained in all cases. A transient complication occurred during the first case after sinus catheterization was attempted in the operating room. Conclusions. The transcranial approach allows straightforward access to DAVFs located on superficial dural sinuses that are inaccessible from the IJVs. The effectiveness of this approach is similar to that of the standard retrograde venous approach. The correct location and adequate extent of the craniectomy are essential for success to be achieved using this technique.

Expression of angiogenic growth factors in dural arteriovenous fistula

1999 ◽  
Vol 91 (5) ◽  
pp. 781-786 ◽  
Author(s):  
Ryunosuke Uranishi ◽  
Hiroyuki Nakase ◽  
Toshisuke Sakaki
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Growth Factors ◽  
Growth Factor ◽  
Dural Arteriovenous Fistula ◽  
Sinus Thrombosis ◽  
Angiogenic Growth Factors ◽  
Connective Tissues ◽  
Content Type ◽  
Fine Print

Object. Although various mechanisms of the development of dural arteriovenous fistula (AVF) have been described, the exact course of its pathogenesis, including molecular processes mediating its genesis, is still unknown. Recently, the importance of sinus thrombosis and venous hypertension has been reported in experimental and clinical studies. Additionally, a role of angiogenic growth factors in the pathogenesis of vascular malformations of the central nervous system has been reported. In this study, the authors investigated the existence of sinus thrombosis in dural AVF and the expression of angiogenic growth factors (basic fibroblast growth factor [bFGF] and vascular endothelial growth factor [VEGF]) in nine patients with dural AVFs that were surgically resected.Methods. The authors examined histological features of dural AVFs that involved the transverse/sigmoid sinus in seven patients and the superior sagittal sinus in two. Sinus thrombosis was verified angiographically in seven cases and histologically in all cases. In surgically resected specimens the angiogenic growth factors bFGF and VEGF were examined immunohistochemically in nine patients with dural AVFs, with five dural sinuses from cadavers with unrelated central nervous system diseases serving as a normal control group. The media and perivascular connective tissues of the arteries in the wall of the normal dural sinuses stained faintly for bFGF; on the other hand, the expression of VEGF was not detected. In all patients with dural AVFs, the thick wall of the dural sinus stained strongly for bFGF, mainly in the subendothelial layer and media of the strongly proliferative vessels in the sinus wall, in addition to the perivascular connective tissues. In all nine cases VEGF was expressed in the endothelium of the sinus and perivascular connective tissues. In two cases, VEGF was expressed in many capillaries proliferating in the granulation-like tissues in sinuses that were obliterated by organized thrombi.Conclusions. It is concluded that the pathogenesis of dural AVF is still unknown, but that angiogenic growth factors, which might be produced by the healing process due to sinus thrombosis, may participate in the genesis of dural AVF. Understanding the mechanism of molecular pathogenesis in the development of dural AVF might aid in the establishment of a new therapeutic strategy for this dynamic vascular disease.

Redefined role of angiogenesis in the pathogenesis of dural arteriovenous malformations

1997 ◽  
Vol 87 (2) ◽  
pp. 267-274 ◽  
Author(s):  
Michael T. Lawton ◽  
Ronald Jacobowitz ◽  
Robert F. Spetzler
Keyword(s):  
Arteriovenous Malformations ◽  
Sinus Thrombosis ◽  
Venous Hypertension ◽  
External Jugular Vein ◽  
Hypertensive Rats ◽  
Angiogenic Activity ◽  
Content Type ◽  
Sagittal Sinus ◽  
Dural Avm

✓ To investigate the role of angiogenesis in the pathogenesis of dural arteriovenous malformations (AVMs), 40 rats underwent common carotid artery—external jugular vein (CCA-EJV) anastomosis, bipolar coagulation of the vein draining the transverse sinus, and sagittal sinus thrombosis to induce venous hypertension. Fifteen rats underwent a similar surgical procedure, but venous hypertension was not induced. The 55 rats were divided into seven groups. Four groups, each containing 10 rats, underwent induced venous hypertension. The other three groups, each containing five rats, did not undergo induced venous hypertension. After 1, 2, or 3 weeks, dura mater was obtained from one group of hypertensive rats and from one group of nonhypertensive rats and was assayed for angiogenic activity (rabbit cornea bioassay). The remaining group of 10 hypertensive rats was not assayed to determine if sampling affected dural AVM formation. Unlike rats without CCA-EJV anastomosis, rats with CCA-EJV anastomosis had significantly increased postoperative sagittal sinus pressures (p < 0.0001). Mean angiogenesis indices were significantly greater in rats with venous hypertension than in rats without venous hypertension (p = 0.004). Dural AVMs formed in 42% of the 55 rats and facial AVMs formed in 51%. Angiogenic activity correlated positively with venous hypertension (ρ = 0.74). Development of dural AVMs correlated positively with both venous hypertension (p = 0.0009) and angiogenic activity (p = 0.04). These data indicate that venous hypertension may induce angiogenic activity either directly or indirectly by decreasing cerebral perfusion and increasing ischemia, and that dural AVM formation may be the result of aberrant angiogenesis.

Multiplicity of dural arteriovenous fistulas

2002 ◽  
Vol 96 (1) ◽  
pp. 76-78 ◽  
Author(s):  
J. Marc C. Van Dijk ◽  
Karel G. TerBrugge ◽  
Robert A. Willinsky ◽  
M. Christopher Wallace
Keyword(s):  
Venous Drainage ◽  
Entire Group ◽  
Additional Risk ◽  
Content Type ◽  
Arteriovenous Fistulas ◽  
Bilateral Involvement ◽  
Dural Arteriovenous Fistulas ◽  
Cortical Venous Drainage ◽  
Risk Of Hemorrhage ◽  
Fine Print

Object. Dural arteriovenous fistulas (AVFs) are a well-known pathoanatomical and clinical entity. Excluding bilateral involvement of the cavernous sinus, multiple dural AVFs are rare, with isolated reports in the literature. The additional risk associated with multiplicity is unknown, although it has been claimed that there is a greater risk of hemorrhage at presentation. In a group of 284 patients with dural AVFs consecutively treated at a single center, the occurrence of multiplicity is investigated and its risk factors for hemorrhage are identified. Methods. Among the 284 patients with both cranial and spinal dural AVFs, 20 patients with multiple fistulas were found. Nineteen (8.1%) of 235 patients with cranial AVFs had multiple cranial fistulas, and one (2%) of 49 patients with spinal AVFs harbored two spinal fistulas. Twelve patients were found to have a lesion at two separate sites, seven patients had them at three locations, and one patient had four fistulas, each at a different site. In the subgroup with multiple AVFs the percentage of hemorrhage at presentation was three times higher than in the entire group (p = 0.01). Cortical venous drainage in cranial fistulas was present in 84% of patients with multiple lesions compared with 46% of patients with solitary lesions (p < 0.005). Conclusions. Multiple dural AVFs are not rare. In this group of 284 patients it was found in 8.1% of all patients with cranial dural AVFs. Multiplicity was associated with a higher percentage of cortical venous drainage, a pattern of drainage reportedly yielding a higher risk for hemorrhage.

Lessons from a case of kleeblattschädel

1995 ◽  
Vol 82 (6) ◽  
pp. 1071-1074 ◽  
Author(s):  
Dominic N. P. Thompson ◽  
Richard D. Hayward ◽  
William J. Harkness ◽  
Robert M. Bingham ◽  
Barry M. Jones
Keyword(s):  
Skin Flap ◽  
Venous Drainage ◽  
Craniocervical Junction ◽  
Venous Hypertension ◽  
Content Type ◽  
Emissary Veins ◽  
Hindbrain Herniation ◽  
The Relationship ◽  
Fine Print ◽  
Anomalous Pattern

✓ The authors describe the clinical, radiological, and postmortem findings of a case of cloverleaf skull syndrome. The presence of hindbrain herniation, abnormal cervical segmentation, and atlantoaxial subluxation illustrate the anatomical complexity of the skull base and the craniocervical junction that may coexist in this condition. Unavoidable division of occipital emissary veins during elevation of the skin flap at the time of vault remodeling surgery led to an acute and, ultimately, fatal rise in intracranial pressure. Postmortem examination and review of magnetic resonance imaging revealed an anomalous pattern of venous drainage of the intracranial structures that appeared to have developed in response to venous obstruction, secondary to intraosseous venous sinuses and stenosis of the jugular foramina. The relationship between venous hypertension, hindbrain herniation, and hydrocephalus in this situation is reviewed, and the implications for evaluation and management of this vexing disorder are discussed.

Sagittal sinus thrombosis related to oral contraceptives

1970 ◽  
Vol 33 (6) ◽  
pp. 714-717 ◽  
Author(s):  
Michael C. Shende ◽  
Herbert Lourie
Keyword(s):  
Oral Contraceptives ◽  
Superior Sagittal Sinus ◽  
Sinus Thrombosis ◽  
Obstructive Hydrocephalus ◽  
Pathological Findings ◽  
Content Type ◽  
Sagittal Sinus ◽  
Contraceptive Pills ◽  
Sagittal Sinus Thrombosis ◽  
Fine Print

✓ A case of thrombosis of the cortical veins and superior sagittal sinus occurred in a young woman with no obvious predisposing factors other than the possible implication of contraceptive pills. Angiographic, surgical, and pathological findings are presented. Survival in this case resulted from a large cranial decompression, and later a ventriculojugular shunt to control extraventricular obstructive hydrocephalus.

Enigma of raised intracranial pressure in patients with complex craniosynostosis: the role of abnormal intracranial venous drainage

2001 ◽  
Vol 94 (3) ◽  
pp. 377-385 ◽  
Author(s):  
Wendy J. Taylor ◽  
Richard D. Hayward ◽  
Pierre Lasjaunias ◽  
Jonathan A. Britto ◽  
Dominic N. P. Thompson ◽  
...  
Keyword(s):  
Intracranial Pressure ◽  
Venous Drainage ◽  
Venous Hypertension ◽  
Apert Syndrome ◽  
Raised Intracranial Pressure ◽  
Icp Monitoring ◽  
Venous Anatomy ◽  
Content Type ◽  
Complex Forms ◽  
Fine Print

Object. In this study the authors investigated whether patterns of intracranial venous drainage in children with complex craniosynostosis associated with raised intracranial pressure (ICP) were abnormal and, thus, could support the theory that venous hypertension is a major contributor to raised ICP that can lead to impaired visual function or even blindness in these patients. Methods. The authors analyzed the anatomy of intracranial venous drainage as demonstrated in the results of 24 angiography studies obtained in 23 patients, all of whom had either a craniosynostosis-related syndrome (18 patients) or a nonsyndromic multisutural synostosis (five patients). Twenty-one patients had experienced raised ICP (in 19 patients diagnosis was based on invasive ICP monitoring and in two patients on clinical grounds alone) 1 to 6 weeks before undergoing angiography. Of the two remaining patients (both with Apert syndrome) whose ICP monitoring was normal immediately before angiography, each had undergone two previous cranial vault expansion procedures. On results of 18 angiography studies a 51 to 99% stenosis or no flow at all could be observed in the sigmoid—jugular sinus complex either bilaterally (11 patients) or unilaterally (seven patients). In 11 of these patients a florid collateral circulation through the stylomastoid emissary venous plexus was also seen. Two angiography studies were performed in one patient with Crouzon syndrome. A comparison of the two studies demonstrated a progression of the abnormal venous anatomy in that case. The authors found no obvious correlation between each patient's baseline ICP and the degree of abnormality of their venous anatomy, as judged on the basis of a venous-phase angiography severity score. Conclusions. Based on their findings, the authors assert that in children with complex forms of craniosynostosis in whom other factors, such as hydrocephalus, are absent, abnormalities of venous drainage that particularly affect the sigmoid—jugular sinus complex produce a state of venous hypertension that, in turn, is responsible for the majority of cases of raised ICP. The incidence of these changes is unknown, but an analysis of the ages of the children in this study indicated that the period of particular vulnerability to the effects of venous hypertension lasts until the affected child is approximately 6 years old. After that age the collateral venous drainage through the stylomastoid plexus will likely become sufficient to allow ICP to normalize.

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