Scalp Arteriovenous Malformation Draining into the Superior Sagittal Sinus Associated with an Intracranial Arteriovenous Malformation: Just a Coincidence? Case Report

Neurosurgery ◽  
2003 ◽  
Vol 52 (2) ◽  
pp. 440-443 ◽  
Author(s):  
Giuseppe Lanzino ◽  
Emiliano Passacantilli ◽  
G. Michael Lemole ◽  
Cameron McDougall ◽  
Robert F. Spetzler

Abstract OBJECTIVE AND IMPORTANCE Recent experimental and clinical evidence suggests that hemodynamic changes in the venous system can induce the formation of new arteriovenous malformations (AVMs). In a rat model, increased venous pressure induces the formation of soft tissue and dural AVMs. We report a clinical observation that may support these data. CLINICAL PRESENTATION A 4-year-old boy with a midline scalp AVM draining into the superior sagittal sinus had an associated intracranial/parenchymal AVM. The cerebral AVM increased venous pressure in the superior sagittal sinus as revealed by angiography. INTERVENTION The scalp AVM was resected, and the intracranial AVM was treated by use of the gamma knife. CONCLUSION On the basis of reported experimental data and the morphological and hemodynamic characteristics in this patient's two lesions, we suggest that the scalp AVM might have been induced by hypertension in the superior sagittal sinus. This clinical observation supports the notion suggested by experimental studies that hemodynamic changes can induce the formation of associated AVMs.

2019 ◽  
Vol 10 (1) ◽  
pp. 79-83
Author(s):  
Yury G. Yakovlenko ◽  
Vladimir A. Moldovanov ◽  
Larisa V. Araslanova ◽  
Igor M. Blinov ◽  
Olga P. Suhanova

Clinical observation of the patient with parasagittal meningioma at the level of the middle third of the superior sagittal sinus and falx is presented. When such tumors are removed, the main task is to prevent damage to the parasagittal veins, the injury of which can cause a persistent neurological defi cit in the postoperative period. A feature of this case is the complex use of advanced minimally invasive methods of angiographic diagnosis when planning surgical treatment, which signifi cantly increases the chances of a successful outcome of the operation.


2017 ◽  
Vol 10 (1) ◽  
pp. 74-77 ◽  
Author(s):  
Daniel M S Raper ◽  
Thomas J Buell ◽  
Dale Ding ◽  
I Jonathan Pomeraniec ◽  
R Webster Crowley ◽  
...  

ObjectiveSafety and efficacy of superior sagittal sinus (SSS) stenting for non-thrombotic intracranial venous occlusive disease (VOD) is unknown. The aim of this retrospective cohort study is to evaluate outcomes after SSS stenting.MethodsWe evaluated an institutional database to identify patients who underwent SSS stenting. Radiographic and clinical outcomes were analyzed and a novel angiographic classification of the SSS was proposed.ResultsWe identified 19 patients; 42% developed SSS stenosis after transverse sinus stenting. Pre-stent maximum mean venous pressure (MVP) in the SSS of 16.2 mm Hg decreased to 13.1 mm Hg after stenting (p=0.037). Preoperative trans-stenosis pressure gradient of 4.2 mm Hg decreased to 1.5 mm Hg after stenting (p<0.001). No intraprocedural complication or junctional SSS stenosis distal to the stent construct was noted. Improvement in headache, tinnitus, and visual obscurations was reported by 66.7%, 63.6%, and 50% of affected patients, respectively, at mean follow-up of 5.2 months. We divided the SSS into four anatomically equal segments, numbered S1–S4, from the torcula to frontal pole. SSS stenosis typically occurs in the S1 segment, and the anterior extent of SSS stents was deployed at the S1–S2 junction in all but one case.ConclusionsSSS stenting is reasonably safe, may improve clinical symptoms, and significantly reduces maximum MVP and trans-stenosis pressure gradients in patients with VOD with SSS stenosis. The S1 segment is most commonly stenotic, and minimum pressure gradients for symptomatic SSS stenosis may be lower than for transverse or sigmoid stenosis. Additional studies and follow-up are necessary to better elucidate appropriate clinical indications and long-term efficacy of SSS stenting.


1997 ◽  
Vol 111 (8) ◽  
pp. 757-759 ◽  
Author(s):  
A. Tomkinson ◽  
R. G. S. Mills ◽  
P. J. Cantrell

AbstractThe pathophysiology of otitic hydrocephalus remains controversial. It has been argued that involvement of the superior sagittal sinus, by, at least, a mural thrombus is a necessary component of this disease.We present a case of otitic hydrocephalus where on magnetic resonance imaging (MRI) normal luminal and mural flow within the superior sagittal sinus is demonstrated. The presence of thrombus in the lateral venous sinus alone appears sufficient in this case to impede venous drainage of the intracranial contents into the neck and produce a rise in the cerebral venous pressure and a subsequent increase in the CSF pressure. The presence of a superior sagittal sinus mural thrombus is not required.


1974 ◽  
Vol 41 (4) ◽  
pp. 427-434 ◽  
Author(s):  
Yoku Nakagawa ◽  
Mitsuo Tsuru ◽  
Kenzoh Yada

✓ The pressure gradient of the venous pathway between the cortical vein and superior sagittal sinus was measured in adult mongrel dogs by recording the pressures of the bridging vein, lateral lacuna (proximal portion), and superior sagittal sinus, together with the systemic blood pressure while gradually increasing the intracranial pressure up to the level of mean systemic blood pressure. The pressure gradient between the lateral lacuna and the superior sagittal sinus was also measured under increased intracranial pressure. Pressures of the bridging vein and lateral lacuna were constantly 50 to 250 mm H2O higher than the intracranial pressure, regardless of the level of intracranial pressure. An abrupt drop in the intraluminal pressure was observed at a point 1 to 2 mm proximal to the junction of the lateral lacuna and the superior sagittal sinus, regardless of the level of intracranial pressure. It is concluded that gradual stenosis of the parasagittal venous pathways took place 1 to 2 mm proximal to the junction between the lacuna and the superior sagittal sinus, and thus cortical venous pressure was maintained 50 to 250 mm H2O higher than intracranial pressure. The authors believe that an “intracranial venous pressure regulation mechanism” exists at the junction of the lateral lacuna and the superior sagittal sinus.


1984 ◽  
Vol 60 (4) ◽  
pp. 727-736 ◽  
Author(s):  
Christian Sainte-Rose ◽  
Jacques LaCombe ◽  
Alain Pierre-Kahn ◽  
Dominique Renier ◽  
Jean-François Hirsch

✓ From a previous study of achondroplasia as well as from the observation of patients with hydrocephalus associated with craniostenosis, the authors have concluded that an increased superior sagittal sinus venous pressure (SSVP) could be the cause of the enlarged ventricles. However, other workers have demonstrated that an increased SSVP could be the consequence of increased intracranial pressure (ICP). Therefore, the authors undertook a study to determine if there was a physiological test that could distinguish between rare instances of increased SSVP caused by structural and irreversible narrowing of the sinus and those caused by increased ICP. In 20 hydrocephalic infants and children, pressure was simultaneously measured in the lateral ventricle, the superior sagittal sinus, and the jugular vein. Stable baseline pressures were recorded, as well as the variations observed after the withdrawal of an amount of cerebrospinal fluid (CSF) sufficient to lower ICP to zero. Similar recordings were taken after reinjection of an equal quantity of CSF. In all of the patients, SSVP was increased, but not as much as the ICP. In the cases of hydrocephalus without any associated cranial malformation, and therefore without any likely anatomical interruption of the sinus, CSF withdrawal induced a simultaneous decrease of ICP and SSVP. However, whereas ICP could be lowered to zero, SSVP never fell below the jugular venous pressure, which remained stable (around 5 mm Hg) throughout the recording session. Results were different when sinography demonstrated an anatomical interruption of the sinus, as in cases of hydrocephalus associated with achondroplasia or craniostenosis. In these cases, although ICP was normally lowered by CSF withdrawal, SSVP remained nearly unchanged, usually greater than the jugular venous pressure. The present study demonstrated that SSVP recording during ICP variations induced by CSF withdrawal permits differentiation between a reversible collapse of the sigmoid sinus due to increased ICP and a fixed obstructive lesion of the sinuses. Based upon this test and the results of sinography, the authors inserted a venous bypass between the lateral sinus and a jugular vein in three patients.


1986 ◽  
Vol 65 (2) ◽  
pp. 199-202 ◽  
Author(s):  
M. Sean Grady ◽  
Robert F. Bedford ◽  
T. S. Park

✓ Air embolism is a potential hazard during craniotomy whenever intracranial venous pressure is subatmospheric. In order to better understand both the risk of air embolism and its treatment in neurosurgical patients, the authors have investigated the relationship of superior sagittal sinus pressure (SSP) to head position in 15 children and examined the effects of both jugular venous compression and positive end-expiratory airway pressure (PEEP) on SSP. Progressive head elevation significantly decreased mean SSP and, in five patients, SSP was less than 0 mm Hg at 90° torso elevation. A PEEP of 10 cm H2O was ineffective in significantly increasing SSP at any degree of head elevation, whereas bilateral internal jugular compression always caused a significant increase in SSP. The authors conclude that children are at risk for venous air embolism when undergoing suboccipital craniectomy in the sitting position because intracranial venous pressure is often subatmospheric when the head is elevated. Furthermore, maintaining PEEP does not appear to be a reliable treatment for increasing SSP, whereas bilateral internal jugular compression is effective.


1970 ◽  
Vol 33 (4) ◽  
pp. 407-414 ◽  
Author(s):  
Thomas C. Guthrie ◽  
Howard S. Dunbar ◽  
Barbara Karpell

✓ Intracranial venous pressure was increased by blocking the torcular Herophili in 10 dogs. At intervals of 1 to 29 weeks, pressure in the superior sagittal sinus and cerebrospinal fluid (CSF) were recorded and the size of the ventricles determined at autopsy. Changes in venous pathways were documented by sinograms. Significant increase in both sagittal sinus and CSF pressures occurred after torcular block. CSF pressures remained elevated for as long as 29 weeks at an average of 100 mm above preblock levels. Neurological deficits after torcular block were minimal. Autopsies showed normal-sized ventricles without any stigmata of hydrocephalus.


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