British Journal of Neurosurgery, October 2013; 27(5): 698–700 © 2013 The Neurosurgical Foundation ISSN: 0268-8697 print / ISSN 1360-046X online DOI: 10.3109/02688697.2013.795524 SHORT REPORT Stenting venous outflow gives symptomatic improvement in a patient with an inoperable brainstem arteriovenous malformation J. Nicholas P. Higgins1 & Peter J. Kirkpatrick2 1Department of Radiology, Addenbrooke’s Hospital, Cambridge, UK, and 2Academic Neurosurgical Unit, Addenbrooke’s Br J Neurosurg Downloaded from informahealthcare.com by Michigan University on 03/03/15 For personal use only. Hospital, Cambridge, UK nant, the right being smaller with a prominent arachnoid granulation narrowing its anterior end (Fig. 1d). The pressure gradient from the torcula to the right atrium was 4 mm Hg. (Catheter venography, itself, was performed under local anaesthesia using a Rebar 27 microcatheter (EV3, Micro Therapeutics Inc) passed into the venous sinuses, supported by a 4F diagnostic catheter in the jugular vein from a right common femoral puncture. Pressures were transduced from the hub of the microcatheter on to a monitor.) He was admitted for stenting of the straight sinus, this procedure was carried out under general anaesthesia and full heparinisation using the left jugular vein for access. Two 5-mm-balloon-mounted stents (Pharos Vitesse; Codman) were used to dilate the whole of the straight sinus. He was given aspirin 150 mg and clopidogrel 150 mg in recovery and discharged taking aspirin 75mg daily for 6 weeks. His headache had resolved on the ward the next day. At 6 week follow up he was headache free and his speech was improved. He hadmild left-sided weakness and ataxia as before. Seven months following stenting he was reinvestigated because of increasing headache, although he remained substantially better than before treatment. CT and catheter venography revealed no problem with the stents (Fig. 2a and b). The pressure gradient along the straight sinus was reduced to 4 mm Hg. The pressure gradient along the rest of venous outflow was now 5 mm Hg, this is mainly along the transverse sinuses. He was admitted for a second procedure (also performed under general anaesthesia) in which the stents in the straight sinus were dilated with an angioplasty balloon to 6 mm. The right transverse sinus was then stented to 7 mm and the left to 10 mm (Omnilink Elite; Abbott) (Fig. 2c and d). He had some headache on the ward the next day but his walking was improved. At three-month follow-up, he was headache free and his speech was normal. He still had mild left-sided weakness but found it less debilitating than before. Abstract The extent to which arterial steal or venous hypertension contributes to symptoms in patients with high flow brain arteriovenous malformations (AVMs) is not always clear. We describe a patient with an inoperable AVM of the pons, presenting with headache and neurological deficit where improving venous outflow by stenting produced substantial clinical benefit. Keywords: arteriovenous malformation; vascular steal; venous hypertension; venous sinus stenting Introduction A 46-year-old man gave a 2-year history of progressive unsteadiness and falling to the left. He also complained of severe headaches, slurring of speech and occasional double vision. Clinical examination revealed dysarthria, gaze-induced nystagmus to the left and ataxic weakness in the left arm and leg. There was no papilloedema. Routine blood test reports and chest x-ray were found to be unremarkable. MRI showed an AVM occupying the whole of the right pons (Fig. 1a). The site and size of the AVM precluded surgery or radiotherapy. Angiography showed arterial supply from multiple small branches of the basilar artery with no safe vessel for injection of embolic material.(Fig. 1b) Primary venous drainage was to the straight sinus but there were numerous enlarged veins in the posterior fossa and some drainage to the cavernous and sagittal sinuses. (Fig. 1c) With the normal therapeutic options unavailable and the angiogram suggesting some compromise to venous outflow from the AVM, he was investigated to see whether there were any regions along the venous outflow tract that might have particular haemodynamic significance. He had CT venography and catheter venography which showed the straight sinus as a relatively narrow channel compared to the rest of venous sinus outflow and associated with an 8 mm Hg pressure gradient. The left transverse sinus was highly domi- Correspondence: Dr. Nicholas Higgins, Neuroradiology, Addenbrooke’s Hospital, Cambridge CB2 0QQ, UK. Tel: ⫹ 01223 216518. Fax: ⫹ 01223 217847. E-mail: nick.higgins@addenbrookes.nhs.uk Received for publication 18 October 2012; accepted 3 April 2013 698 Br J Neurosurg Downloaded from informahealthcare.com by Michigan University on 03/03/15 For personal use only. Stenting brainstem AVM 699 Fig. 1. (a) Parasagittal MRI showing the AVM as a mass of flow voids (arrows) in the right pons. (b) Early phase of left vertebral angiogram showing the AVM as multiple abnormal vessels posterior to the basilar artery. (c) Same injection in later phase shows numerous enlarged veins draining mainly to the straight sinus (SS) but some finding the cavernous sinus (CS) and sagittal sinus (SSS). (d) Axial CT angiogram showing the AVM in right pons. An arachnoid granulation narrows the anterior end of the right transverse sinus (curved arrow). (Straight sinus; straight arrow.). Fig. 2. (a) Sagittal reformatted CT angiogram showing the stents (arrows) widely patent in the straight sinus. (b) Subtracted, lateral view, catheter venogram: contrast injected through the microcatheter used for taking pressure measurements opacifies the stented straight sinus (arrows) and both transverse and sigmoid sinuses prior to stenting. (c) Unsubtracted oblique lateral view of the posterior fossa showing the stents in the straight sinus and both transverse sinuses. (d) Same view subtracted venogram shows good flow through the newly stented transverse sinuses. 700 J. N. P. Higgins & P. J. Kirkpatrick Br J Neurosurg Downloaded from informahealthcare.com by Michigan University on 03/03/15 For personal use only. Discussion Venous hypertension is well known as a cause of neurological dysfunction in spinal and cerebral dural fistulae, less so in symptomatic brain arteriovenous malformations (AVMs) brain where arterial steal might seem an equally valid mechanism.1 Either way, treatment is generally directed at occluding the arteriovenous shunt with a reduction in arterial steal or venous pressures, a by product of a successful occlusion. In the case we describe, treatment was focused purely on relieving venous hypertension with no attempt to reduce arteriovenous shunting. This means there is no attempt to reduce any arterial steal. In fact the reverse: the measures used to lower venous pressures would have been almost certain to increase arteriovenous shunting and, therefore, to increase any supposed arterial steal. The clinical result of this approach, in which there was a significant amelioration of symptoms, testifies to the relative importance of venous hypertension in this situation. Venous outflow compromise is a usual feature of cranial dural fistulae but can also be seen in brain AVMs.1,2 Uncertain in this case, however, is whether we are seeing abnormal venous outflow tracts coexisting with an AVM or normal venous outflow tracts being overwhelmed by AVM venous outflow. CT did not show any areas of exceptional venous narrowing but baseline catheter studies showed extensive filling of veins in the posterior fossa from the AVM suggesting venous hypertension and an 8 mm Hg pressure gradient along the straight sinus. This does not necessarily reflect an abnormally narrow sinus but it does show a sinus whose diameter is insufficient to cope with the additional outflow from an AVM without generating a substantial pressure gradient. The same concerns apply to the transverse sinuses. Their respective diameters may not have been an issue for normal cerebral venous outflow nor, as judged by the pressure recordings, were they a concern in this case while venous outflow was restricted by the straight sinus. However, once this restriction had been lifted, new pressure gradients developed further downstream suggesting that the calibre of the transverse sinuses had become haemodynamically significant. Hence they were included in the second stenting procedure. In general, partial treatment of an AVM confers no protection from haemorrhage, and may even increase the haemorrhage rate, but is justified when symptoms are disabling or distressing.1,3 Unknown, of course, is whether the particular approach we have taken (likely to increase arteriovenous shunting) could alter the risk of future haemorrhage. On the one hand flow aneurysms might be encouraged but on the other high pressure on the venous side of the nidus, a risk factor for haemorrhage,2 will be reduced. Nevertheless, these caveats accepted, looking at the venous outflow in patients with symptomatic inoperable AVMs may suggest alternative methods of palliation. Declaration of interests: The authors report no declarations of interest. The authors alone are responsible for the content and writing of the paper. References 1. Berenstein A , Lasjaunias P, ter Brugge KG. Surgical Neuroangiography, 2nd ed. Berlin, Heidelberg, New York: Springer-Verlag, 2004. 2. Miyasaka Y, Yada K, Ohwada T, et al. An analysis of the venous drainage system as a factor in hemorrhage from arteriovenous malformations. J Neurosurg 1992;76:239–43. 3. Ogilvy CS, Stieg PE, Awad I, et al. AHA Scientific Statement: Recommendations for the management of intracranial arteriovenous malformations: a statement for healthcare professionals from a special writing group of the Stroke Council, American Stroke Association. Stroke 2001;32:1458–71.