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Endarterectomy of the vertebral artery from C2 to posterior inferior cerebellar artery intracranially
Endarterectomy of the Vertebral Artery from C2 to Posterior Inferior Cerebellar Artery Intracranially James I. Ausman, M,D., Ph.D.,* Fernando G. Diaz, M.D., Ph.D.,* Jeffrey E. Pearce, M.D.,* R. A. de los Reyes, M.D.,* William Leuchter, M.D.,~ B. Mehta, M.D.,$ and Suresh Patel, M.D.$ A new technical approach to endarterectomy of the vertebral artery at the cranial cervical junction is discussed. A patient had symptoms of vertebrobasilar insufficiency on clinical examination. Angiography demonstrated a stenotic plaque in the vertebral artery at the level of C1,
and an additional tandem lesion at the origin of the posterior inferior cerebellar artery. He underwent vertebral endarterectomy and was symptomatically improved postoperatively. The surgical approach used and possible alternatives will be discussed in detail. Ausman J1, Diaz FG, PearceJE, de los Reyes RA, Leuchter W, Mehta B, Patel S: Endarterectomyof the vertebral artery from C2 to posterior inferior cerebellar artery intracranially. Surg Neurol 18:400-404, 1982
In the 1950s, the only therapy available for vertebrobasilar insufficiency was anticoagulation [ 12]. Endarterectomy and decompression of the proximal vertebral artery were introduced in the early 1960s [8], but were not commonly performed because of the technical difficulty of the operation and the risks associated with angiography [ 17]. Controversy over the value of surgery for these lesions and the indications for its use were widespread [16]. In the 1970s, various procedures, which have been recently reviewed [71, were developed for correcting lesions in the cervical vertebral arteries. With refinements in angiography [6] and the development of microsurgical techniques [18], attention was directed to the distal vertebral and basilar systems as well. Extracranial-intracranial bypass, with anastomosis of an occipital artery to the posterior inferior cerebellar artery, was
utilized for cases in which there was compromise of the distal vertebral artery [2, 3, 10, I I , 13, 141. Stenoses of the basilar artery were approached with an occipital-anterior inferior cerebellar artery [4] or a superficial temporal to superior cerebellar artery or posterior cerebral artery bypass procedure, or other variations [3, 5, 9, 15]. Until recently, symptomatic lesions in the vertebral artery at Cl extending intracranially were seen but treated only with anticoagulation or distal surgical bypass. In 1981 Allen [11 described a patient who underwent endarterectomy for removal of a plaque in the intracranial portion of the vertebral artery. Our report describes the technique for removal of a plaque extending from C2 to beyond the level of the posterior inferior cerebellar artery on the vertebral artery.
Case Report
A 62-year-old white man was referred to us because of symptoms of vertebrobasilar insufficiency. Six months prior to admission, he experienced an episode of lightheadedness, diplopia, perioral numbness, dysarthria, tinnitus, vertigo, and blurred vision in the left eye. Over the ensuing months, while taking aspirin and dipyridamole, he had persistent tinnitus and increasingly frequent episodes of the previous symptoms plus ataxia. An angiogram performed at another hospital and another done at Henry Ford Hospital revealed a 60% stenosis of the left vertebral artery at C1, and a second tandem lesion with an additional 40% stenosis as the artery entered the foramen magnum (Fig. 1). The right vertebral artery ended in the posterior inferior cerebella artery. The vertebral origins were normal, and only one posterior communicating artery could be demonstrated. There was a 50% stenosis of the left subclavian artery proximal to the origin of the left vertebral From the *Department of Neurosurgery, Henry Ford Hospital, the ?De- artery. partment of Neurology, Sinai Hospitalof Detroit, and the :~Departmentof The patient's past medical history was significant for carRadiology, Divisionof Neuroradiology,HenryFord Hospital, Detroit, MI. diac dysrhythmias. These were well controlled with Address reprint requests to Dr. James I. Ausman, Department of quinidine sulfate, however, and Holter monitoring did not Neurosurgery, Henry Ford Hospital, 2799 W. Grand Blvd., Detroit, indicate the symptoms were related. The general as well as MI 48202. Key words: vertebrobasilarinsufficiency;vertebral artery endarterectomy; neurological examination was entirely within normal vertebral artery. limits. 400
0090-3019/82/120400-05501.25 (~) 1982 by Little, Brown and Company (inc.)
Ausman et ~1: Endarterectomy of Vertebral Artery
401
Fig. 2. Operative positioning fi,r intracranial vertebral en&~rterectcmty.
Fig. 1. Selective left vertebral arteri~t,,ram revealing atheroscler~tic plaques (arrows).
Operative Procedure On September 11, 1981, the patient underwent a left intracranial vertebral endarterectomy. The posterior half of the patient's head and neck was shaved. An arterial line was placed for continuous monitoring of blood pressure. The patient was anesthetized and intubated with a coiled endotracheal tube to prevent kinking with flexion of the neck. The three-quarter prone position was used with the vertebral artery to be dissected on the inferior side of the exposure, so that a direct line of sight along the course of the artery intracranially could be maintained by the operating surgeon. A double mattress was placed on the operating table, with the upper pad offset by 15 cm to allow the patient's shoulder and downside arm to be cushioned in a more natural position on the underlying mattress. Pillows were placed between the patient's legs and beside the chest to support the upper arm. The head was flexed in the three-quarter prone position and held in three-point fixation (Fig. 2). The operating microscope was positioned so that the assistant was 120 degrees to the left of the operating surgeon. Straight binoculars with 12.5-power eyepieces and a
250-ram objective were used. A midline incision was made from 2 cm above the external occipital protuberance to the C6 vertebral level. The C2-C5 cervical spinous processes and laminae on the left side were exposed laterally to the articular facets, and the subocciput and arch of C1 were dissected free of soft tissues. The vertebral artery was then dissected free from the vertebral groove atop C1 to the point where it turned 90 degrees inferiorly to enter the transverse foramen. The C2 nerve root was isolated and divided lateral to the transverse process, to prevent injury to a possible radicular collateral. Using a small Kerrison rongeur, the transverse foramen of C1 was unroofed, freeing the vertebral artery to the foramen at C2. There was a kink at the inferior margin of C1 and a very hard, indurated plaque extending from the C1-2 interspace over C1 superiorly. A plastic loop, similar to umbilical tape, was passed around the vertebral artery as it left the C2 foramen to provide proximal control. The dissection was performed under the operating microscope because bleeding from the overlying vertebral venous plexus could then be controlled more carefully by coagulation with a bipolar coagulating forceps, separating the plexus from the artery and sectioning it in the midline. This maneuver prevented the extensive bleeding encountered in a previous operation. A small suboccipital craniectomy was performed in the area of the foramen magnum, where the artery penetrated the dura mater. At this point, the overlying venous plexus is quite extensive. Sharp dissection and bipolar coagulation are required to completely isolate the artery as it penetrates the dura mater. The dura mater immediately above the artery was then opened to allow exposure of the artery and structures in the posterior fossa. A fine dural band tethers the vertebral artery as it enters the intracranial space; it must be sectioned. The dentate ligament next to the eleventh cranial nerve must also be sectioned. Further coagulation and incision of the venous plexus surrounding the vertebral artery com-
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pleted the exposure of the entire vertebral artery, from the top of C2 to the basilar junction. A second atherosclerotic plaque was visualized, extending past the origin of the posterior inferior cerebellar artery. After the patient was given 5,000 units of heparin intravenously and 1 gm of additional sodium thiopental, a DeBakey clamp was used to occlude the vertebral artery at C2 while an angled thumb clamp was placed on the vertebral artery intracranially. A Heifetz clip was used to temporarily occlude the posterior inferior cerebellar artery. The vertebral artery was opened horizontally along the arch of C1 between the two atheromatous plaques. After the arteriotomy, the intracranial vertebral clip was momentarily relaxed, and profuse backflow was seen. The primary surgeon, who had a direct line of sight to the vertebral artery as it penetrated the intracranial space, then separated the distal plaque from the surrounding arterial wall. It was necessary to temporarily relax the intracranial clamp to allow removal of the entire plaque. The distal clamp was then repositioned proximal to the posterior inferior cerebellar artery, and the Heifetz clip removed from the posterior inferior cerebellar artery to allow resumption of retrograde flow after the artery had been occluded for 23 minutes. The proximal plaque that was located at the C1 level was then removed by the assistant. From his position, he was in a direct line of sight with the artery as it passed down through Cl. Removal of the proximal plaque and suturing of the vessel then took an additional 21 minutes, using running 7-0 Prolene (monofilament polypropylene) suture. The artery was allowed to bleed from each end before final closure, and it was irrigated with heparin. No thrill was palpated, and a good pulse was present in the intracranial vessel beyond the arteriotomy site. The incision was then closed in multiple layers. The following day, leakage of cerebrospinal fluid from the operative site was noted and the patient was placed on spinal drainage for five days, with resolution. The postoperative course was otherwise unremarkable. After the postoperative angiogram, the patient experienced an episode of unexplained decreased auditory acuity and tinnitus on the right side that gradually cleared. Angiograms taken after the operation showed the endarterectomized segment from C2 to the intracranial vertebral artery was patent and slightly larger in diameter than the nonendarterectomized, previously uninvolved segment (Fig. 3). The patient was discharged twelve days after the operation without neurological deficits, and was continued on dipyridamole and disopyramide phosphate. After discharge, he experienced two more episodes of diplopia but none of the other previous symptoms. He has had continued tinnitus. When last examined in April, 1982, the patient stated that he had begun to experience occasional episodes of dizziness. A repeat angiogram revealed the endarterectomized left ver-
Fig. 3 Postoperative left vertebral angiogram shou,ing patent endarterectomy site.
tebral artery to be patent, but a progressing stenosis of the proximal left subclavian artery was seen. No otological or pharmacological cause of the patient's symptoms has been found. A surgical approach to the left subclavian stenosis is being considered. Discussion The patient was admitted because of increasingly frequent episodes of diplopia, vertigo, dysarthria, perioral numbness, and imbalance that were not alleviated by antiplatelet therapy. Angiography revealed stenosis of the left vertebral artery from the superior margin of C2 to the level of the posterior inferior cerebellar artery. The right vertebral artery ended in the posterior inferior cerebellar artery. The specimen removed from the left vertebral artery appeared to have considerable stenosis. The plaque was microscopically
Ausman et ah Endarterectomy of Vertebral Artery
ulcerated, but contained no grossly visible thrombus or debris. The patient has had persistent tinnitus and has experienced several episodes of diplopia since the operation. All other symptoms have been resolved. It would appear, in this case, that the patient's symptoms resulted from diminished perfusion in the distal vertebrobasilar territory. In contrast, a plaque removed in another patient who underwent an intracranial vertebral endarterectomy was grossly ulcerated, and local emboli were believed to account for the patient's symptoms. Details in three additional cases and the implications for the pathogenesis of vertebrobasilar insufficiency will be published later. In our experience, there is evidence that either emboli or diminished perfusion can be the source of symptoms in these cases. Of the three intracranial vertebral endarterectomies that we have performed, two were done with the patient in the three-quarter prone position, and one in the prone position. There are many advantages to the three-quarter prone position for this procedure. First, the patient is horizontal rather than seated, which eliminates the problems of an air embolus or hypotension during anesthesia. People with compromised cerebral circulation are extremely sensitive to changes in perfusion, and any factor that may produce hypotension should be avoided. Complications related to the sitting position during vertebrobasilar revascularization have been reported [11, 13, 14]. Second, if the patient is positioned with the involved artery on the inferior side in the three-quarter prone position, adequate exposure of the vertebral artery can be achieved intracranially, since the surgeon's line of sight follows the vessel toward the brain stem and basilar artery. Third, if an endarterectomy cannot be performed, the patient is already ideally positioned for an occipital artery-posterior inferior cerebellar artery bypass. To provide this option the course of the occipital artery should be identified with a Doppler flow meter and marked prior to draping. Fourth, the three-quarter prone position allows the surgeon to perform the operation with minimum fatigue because the surgeon's arms are comfortably at his side rather than raised to shoulder level. The operating field is also accessible from a wider area with the patient in this position, allowing more active participation by an assistant. Fifth, the three-quarter prone position is easier on the patient and avoids compression of the chest and abdomen, which may increase venous bleeding in the prone position. Bleeding from the vertebral venous plexus surrounding the artery can be a difficult problem. In addition to using optimal positioning, by finding a plane of dissection between the vertebral plexus and the vertebral artery, and by using a bipolar forceps to coagulate before cutting as the separation proceeds, bleeding can be well controlled. A long incision from above the inion to C5 or C6 allows retraction of the paraspinal musculature far enough laterally
403
to expose the transverse foramen of C1 and C2. The exposure also permits a minimal suboccipital craniectomy and dissection of the vertebral artery as it penetrates the dura mater. In Allen and associates' [1] first case, endarterectomy could not be performed, because after exposure of the vertebral artery intracranially, the plaque was found to extend too far beyond the posterior inferior cerebellar artery. If the incision in the vertebral artery is relatively short and the plaque is carefully dissected free until it tapers to a fine margin, manipulation of the brain stem and difficulty with closure of a long arteriotomy are circumvented. A short incision is made in the vertebral artery. Using Rhoton and Penfield dissectors, the plaque is separated circumferentially from the wall of the vertebral artery. After the plaque breaks free, the distal margin can be visualized intraluminally. In our experience, the plaque will generally taper to a fine margin and break off cleanly. If there are some intraluminal pieces of plaque that remain, these can be removed under direct vision with a microbiopsy forceps. W h e n the plaque extends beyond the clip on the distal portion of the vertebral artery, the clip can be removed and nontraumatic vascular forceps used to occlude the vertebral artery as close to the basilar artery as possible, while the rest of the plaque is removed with gentle traction. Our patients are given a bolus of sodium thiopental and are heparinized before occlusion of the vertebral artery. The heparin is not reversed. No problems occurred with either form of therapy.
References 1. Allen GS, Cohen RJ, Preziosi TJ: Microsurgical endarterectomy of the intracranial vertebral artery for vertebrobasilar transient ischemic attacks. Neurosurgery 8:56-69, 1981 2. Amman JI, Lee MC, Klassen AC, Seljeskog EL, Chou SN: Stroke: what's new ?Cerebral revascularization. Minn Med 59: 223- 227, 1976 3. Ausman J1, Lee MC, Chater N, Latchaw R: Superficial temporal artery to superior cerebellar artery anastomosisfor distal basilar stenosis. Surg Neurol 12:277-281, 1979 4. Ausman JI, Diaz FG, de los Reyes RA, Pak H, Patel S, Boulos R: Anastomosis of occipital artery to anterior inferior cerebellar artery for vertebrobasilar junction stenosis. Surg Neurol 16:99-102, 1981 5. Amman JI, Diaz FG, de los Reyes RA, Pak H, Patel S, Mehta B, Boulos R: Posterior circulation revascularization: superficial temporal artery to superior cerebellar artery anastomosis. J Neurosurg 56:766-776, 1982 6. Caplan L, Rosenbaum A: Role of cerebral angiography in vertebrobasilar occlusive disease. J Neurol Neurosurg Psychiatry 38:601612, 1975 7. Carney AL: Vertebral artery surgery: historical development, basic concepts of brain hemodynamics and clinical experience of 102 cases. Adv Neurol 30:249-282, 1981 8. DeBakeyME, Crawford ES, Morris GC, Cooley DA: Surgical consideration of occlusive disease of the innominate carotid subclavian and vertebral arteries. Ann Surg 154:698-725, 1961 9. Hopkins LN, Budny JL, Spetzler RF: Revascularization of the rostral brainstem. Neurosurgery 10:364-369, 1982 10. Khodadad G: Occipital artery-posterior inferior cerebellar artery anastomosis. Surg Neurol 5:225-227, 1976 11. Khodadad G: Short and long term results of microvascular anas-
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tomosis in the vertebrobasilar system. A critical analysis. Neurol Res 3:33-65, 1981 12. Millikan CH, Siekert RG, Shick RM: Studies in cerebrovascular disease. IlI. The use of anticoagulant drugs in the treatment of insufficiency or thrombosis within the basilar arterial system. Proc Staff Meet Mayo Clin 30:116-126, 1955 13. Roski RA, Spetzler RF, Hopkins LN: Occipital artery to posterior inferior cerebellar artery bypass fl~r vertebrobasilar ischemia. Neurosurgery 10:44-49, 1982 14. Sundt TM, Piepgras DG: Occipital to posterior inferior cerebellar bypass surgery. J Neurosurg 48:916-928, 1978
15. Sundt TM, Piepgras DG, Houser OW, Campbell JK: Interposition saphenous vein grafts for advanced occlusive disease and large aneurysms in the posterior circulation. J Neurosurg 56:205-215, 1982 16. Wesolowski SA, Gillie E, McMahon JD, Santos DS, Call JR, Uchida H: New arteriographic and surgical techniques for vertebral arteriopathies. Circulation 48(Suppl 3):21 l - 219, 1973 17. Williams D, Wilson G: The diagnosis of the major and minor syndromes of basilar insufficiency. Brain 85:741-774, 1962 18. Yasargil MG: Microsurgery Applied to Neumsurgery. New York: Academic, 1979
Book Review Chronic Low Back Pain
Edited by Michael Stanton-Hicks and Robert Boas New York, Raven Press Reviewed by Donlin M. Long, M.D., Baltimore, MD This is an interesting compilation of a number of short independent chapters on the general problem of low back pain. The book makes no attempt to be all inclusive or to be cohesive, but it provides a number of interesting chapters which would be useful to the individual interested in the ubiquitous problem of low back pain. The first three chapters on epidemiology, incidence, and prevalence are excellent and provide a very comprehensive summary of the public health aspects of this problem. The chapter on diagnosis emphasizes several important diseases that are not commonly discussed by neurosurgeons. This chapter provides an excellent review stressing nondiscogenic causes of low back pain. Dr. Nachemson has provided an excellent general review of back injury and the conservative management of low back pain. The chapter on assessment and management planning is less valuable. The nuances of patient history and physical examinations are summarized too briefly and the descriptions of the origins of back pain are similarly too short to be of real value. Differential nerve blocks are described in some detail, but there is no discussion to allow the nonbeliever to assess their real value. The psychological assessment is not described in enough detail to determine if the author's classifications have validity. The descriptions of the therapy of myofascial pain and various other kinds of low back pain are reviews of the author's methods and are not verified by supporting data. There is an extensive chapter on the radiological evaluation of back pain. Unfortunately, the reviews based upon computerized tomographic (CT) axial sections have been outdated by newer equipment, and the quality of currently available scans is much better than that of the scans the author had available for analysis, Epidural venography is described in some detail. The authors are enthusiastic about this tech-
nique, which does not correlate with the experience of many others. It is probable that the CT scan will make this relatively new technique obsolete before its value is proved or disproved. The chapter on psychological assessment and treatment by Dr. L. E. Peterson is excellent and will provide the neurosurgeon with insight into behavioral management techniques. The philosophical discussion of pain by Dr. John Loeser is equally valuable. There is an important chapter on strength testing and exercise to provide data for the workplace. This is an area which is virtually ignored in United States industry and one which is extremely important. The chapter on antiinflammatory drug therapy is brief, but very good. Very few neurosurgeons understand the use of the minor analgesics, and in general the appropriate use of analgesics is poorly understood. Physical therapy and exercise are covered well and these chapters should help the neurosurgeon who wishes to be involved in the total management of back pain. The book closes with a series of minor interventional procedures for back pain. Carron and Toomy have described epidural steroid therapy in detail. Again, the results appear to be interpreted purely subjectively and not substantiated by any data for the reader to assess. The chapter by Boas on facet joint injection is very useful and provides a simple description of the facet syndrome and its treatment by the neurosurgeon. Dr. Harold Wilkinson has written a chapter covering a potpourri of what he terms unconventional approaches. The most useful of these for the neurosurgeon is the excellent review of the surgical therapy of arachnoiditis, supplemented by a description of Dr. Wilkinson's extensive experience. I found this book enjoyable reading. It is not an exten-, sive treatise on low back pain and makes no pretense of being comprehensive. The individual chapters are uneven, but most are quite good and there is little misinformation. It certainly can be recommended to anyone with an interest in the low back problem who wishes to go beyond conventional orthopedic and neurosurgical approaches which focus upon discogenic pain and its surgical therapy.
and an additional tandem lesion at the origin of the posterior inferior cerebellar artery. He underwent vertebral endarterectomy and was symptomatically improved postoperatively. The surgical approach used and possible alternatives will be discussed in detail. Ausman J1, Diaz FG, PearceJE, de los Reyes RA, Leuchter W, Mehta B, Patel S: Endarterectomyof the vertebral artery from C2 to posterior inferior cerebellar artery intracranially. Surg Neurol 18:400-404, 1982
In the 1950s, the only therapy available for vertebrobasilar insufficiency was anticoagulation [ 12]. Endarterectomy and decompression of the proximal vertebral artery were introduced in the early 1960s [8], but were not commonly performed because of the technical difficulty of the operation and the risks associated with angiography [ 17]. Controversy over the value of surgery for these lesions and the indications for its use were widespread [16]. In the 1970s, various procedures, which have been recently reviewed [71, were developed for correcting lesions in the cervical vertebral arteries. With refinements in angiography [6] and the development of microsurgical techniques [18], attention was directed to the distal vertebral and basilar systems as well. Extracranial-intracranial bypass, with anastomosis of an occipital artery to the posterior inferior cerebellar artery, was
utilized for cases in which there was compromise of the distal vertebral artery [2, 3, 10, I I , 13, 141. Stenoses of the basilar artery were approached with an occipital-anterior inferior cerebellar artery [4] or a superficial temporal to superior cerebellar artery or posterior cerebral artery bypass procedure, or other variations [3, 5, 9, 15]. Until recently, symptomatic lesions in the vertebral artery at Cl extending intracranially were seen but treated only with anticoagulation or distal surgical bypass. In 1981 Allen [11 described a patient who underwent endarterectomy for removal of a plaque in the intracranial portion of the vertebral artery. Our report describes the technique for removal of a plaque extending from C2 to beyond the level of the posterior inferior cerebellar artery on the vertebral artery.
Case Report
A 62-year-old white man was referred to us because of symptoms of vertebrobasilar insufficiency. Six months prior to admission, he experienced an episode of lightheadedness, diplopia, perioral numbness, dysarthria, tinnitus, vertigo, and blurred vision in the left eye. Over the ensuing months, while taking aspirin and dipyridamole, he had persistent tinnitus and increasingly frequent episodes of the previous symptoms plus ataxia. An angiogram performed at another hospital and another done at Henry Ford Hospital revealed a 60% stenosis of the left vertebral artery at C1, and a second tandem lesion with an additional 40% stenosis as the artery entered the foramen magnum (Fig. 1). The right vertebral artery ended in the posterior inferior cerebella artery. The vertebral origins were normal, and only one posterior communicating artery could be demonstrated. There was a 50% stenosis of the left subclavian artery proximal to the origin of the left vertebral From the *Department of Neurosurgery, Henry Ford Hospital, the ?De- artery. partment of Neurology, Sinai Hospitalof Detroit, and the :~Departmentof The patient's past medical history was significant for carRadiology, Divisionof Neuroradiology,HenryFord Hospital, Detroit, MI. diac dysrhythmias. These were well controlled with Address reprint requests to Dr. James I. Ausman, Department of quinidine sulfate, however, and Holter monitoring did not Neurosurgery, Henry Ford Hospital, 2799 W. Grand Blvd., Detroit, indicate the symptoms were related. The general as well as MI 48202. Key words: vertebrobasilarinsufficiency;vertebral artery endarterectomy; neurological examination was entirely within normal vertebral artery. limits. 400
0090-3019/82/120400-05501.25 (~) 1982 by Little, Brown and Company (inc.)
Ausman et ~1: Endarterectomy of Vertebral Artery
401
Fig. 2. Operative positioning fi,r intracranial vertebral en&~rterectcmty.
Fig. 1. Selective left vertebral arteri~t,,ram revealing atheroscler~tic plaques (arrows).
Operative Procedure On September 11, 1981, the patient underwent a left intracranial vertebral endarterectomy. The posterior half of the patient's head and neck was shaved. An arterial line was placed for continuous monitoring of blood pressure. The patient was anesthetized and intubated with a coiled endotracheal tube to prevent kinking with flexion of the neck. The three-quarter prone position was used with the vertebral artery to be dissected on the inferior side of the exposure, so that a direct line of sight along the course of the artery intracranially could be maintained by the operating surgeon. A double mattress was placed on the operating table, with the upper pad offset by 15 cm to allow the patient's shoulder and downside arm to be cushioned in a more natural position on the underlying mattress. Pillows were placed between the patient's legs and beside the chest to support the upper arm. The head was flexed in the three-quarter prone position and held in three-point fixation (Fig. 2). The operating microscope was positioned so that the assistant was 120 degrees to the left of the operating surgeon. Straight binoculars with 12.5-power eyepieces and a
250-ram objective were used. A midline incision was made from 2 cm above the external occipital protuberance to the C6 vertebral level. The C2-C5 cervical spinous processes and laminae on the left side were exposed laterally to the articular facets, and the subocciput and arch of C1 were dissected free of soft tissues. The vertebral artery was then dissected free from the vertebral groove atop C1 to the point where it turned 90 degrees inferiorly to enter the transverse foramen. The C2 nerve root was isolated and divided lateral to the transverse process, to prevent injury to a possible radicular collateral. Using a small Kerrison rongeur, the transverse foramen of C1 was unroofed, freeing the vertebral artery to the foramen at C2. There was a kink at the inferior margin of C1 and a very hard, indurated plaque extending from the C1-2 interspace over C1 superiorly. A plastic loop, similar to umbilical tape, was passed around the vertebral artery as it left the C2 foramen to provide proximal control. The dissection was performed under the operating microscope because bleeding from the overlying vertebral venous plexus could then be controlled more carefully by coagulation with a bipolar coagulating forceps, separating the plexus from the artery and sectioning it in the midline. This maneuver prevented the extensive bleeding encountered in a previous operation. A small suboccipital craniectomy was performed in the area of the foramen magnum, where the artery penetrated the dura mater. At this point, the overlying venous plexus is quite extensive. Sharp dissection and bipolar coagulation are required to completely isolate the artery as it penetrates the dura mater. The dura mater immediately above the artery was then opened to allow exposure of the artery and structures in the posterior fossa. A fine dural band tethers the vertebral artery as it enters the intracranial space; it must be sectioned. The dentate ligament next to the eleventh cranial nerve must also be sectioned. Further coagulation and incision of the venous plexus surrounding the vertebral artery com-
402
SurgicalNeurology Vol 18 No 6 December 1982
pleted the exposure of the entire vertebral artery, from the top of C2 to the basilar junction. A second atherosclerotic plaque was visualized, extending past the origin of the posterior inferior cerebellar artery. After the patient was given 5,000 units of heparin intravenously and 1 gm of additional sodium thiopental, a DeBakey clamp was used to occlude the vertebral artery at C2 while an angled thumb clamp was placed on the vertebral artery intracranially. A Heifetz clip was used to temporarily occlude the posterior inferior cerebellar artery. The vertebral artery was opened horizontally along the arch of C1 between the two atheromatous plaques. After the arteriotomy, the intracranial vertebral clip was momentarily relaxed, and profuse backflow was seen. The primary surgeon, who had a direct line of sight to the vertebral artery as it penetrated the intracranial space, then separated the distal plaque from the surrounding arterial wall. It was necessary to temporarily relax the intracranial clamp to allow removal of the entire plaque. The distal clamp was then repositioned proximal to the posterior inferior cerebellar artery, and the Heifetz clip removed from the posterior inferior cerebellar artery to allow resumption of retrograde flow after the artery had been occluded for 23 minutes. The proximal plaque that was located at the C1 level was then removed by the assistant. From his position, he was in a direct line of sight with the artery as it passed down through Cl. Removal of the proximal plaque and suturing of the vessel then took an additional 21 minutes, using running 7-0 Prolene (monofilament polypropylene) suture. The artery was allowed to bleed from each end before final closure, and it was irrigated with heparin. No thrill was palpated, and a good pulse was present in the intracranial vessel beyond the arteriotomy site. The incision was then closed in multiple layers. The following day, leakage of cerebrospinal fluid from the operative site was noted and the patient was placed on spinal drainage for five days, with resolution. The postoperative course was otherwise unremarkable. After the postoperative angiogram, the patient experienced an episode of unexplained decreased auditory acuity and tinnitus on the right side that gradually cleared. Angiograms taken after the operation showed the endarterectomized segment from C2 to the intracranial vertebral artery was patent and slightly larger in diameter than the nonendarterectomized, previously uninvolved segment (Fig. 3). The patient was discharged twelve days after the operation without neurological deficits, and was continued on dipyridamole and disopyramide phosphate. After discharge, he experienced two more episodes of diplopia but none of the other previous symptoms. He has had continued tinnitus. When last examined in April, 1982, the patient stated that he had begun to experience occasional episodes of dizziness. A repeat angiogram revealed the endarterectomized left ver-
Fig. 3 Postoperative left vertebral angiogram shou,ing patent endarterectomy site.
tebral artery to be patent, but a progressing stenosis of the proximal left subclavian artery was seen. No otological or pharmacological cause of the patient's symptoms has been found. A surgical approach to the left subclavian stenosis is being considered. Discussion The patient was admitted because of increasingly frequent episodes of diplopia, vertigo, dysarthria, perioral numbness, and imbalance that were not alleviated by antiplatelet therapy. Angiography revealed stenosis of the left vertebral artery from the superior margin of C2 to the level of the posterior inferior cerebellar artery. The right vertebral artery ended in the posterior inferior cerebellar artery. The specimen removed from the left vertebral artery appeared to have considerable stenosis. The plaque was microscopically
Ausman et ah Endarterectomy of Vertebral Artery
ulcerated, but contained no grossly visible thrombus or debris. The patient has had persistent tinnitus and has experienced several episodes of diplopia since the operation. All other symptoms have been resolved. It would appear, in this case, that the patient's symptoms resulted from diminished perfusion in the distal vertebrobasilar territory. In contrast, a plaque removed in another patient who underwent an intracranial vertebral endarterectomy was grossly ulcerated, and local emboli were believed to account for the patient's symptoms. Details in three additional cases and the implications for the pathogenesis of vertebrobasilar insufficiency will be published later. In our experience, there is evidence that either emboli or diminished perfusion can be the source of symptoms in these cases. Of the three intracranial vertebral endarterectomies that we have performed, two were done with the patient in the three-quarter prone position, and one in the prone position. There are many advantages to the three-quarter prone position for this procedure. First, the patient is horizontal rather than seated, which eliminates the problems of an air embolus or hypotension during anesthesia. People with compromised cerebral circulation are extremely sensitive to changes in perfusion, and any factor that may produce hypotension should be avoided. Complications related to the sitting position during vertebrobasilar revascularization have been reported [11, 13, 14]. Second, if the patient is positioned with the involved artery on the inferior side in the three-quarter prone position, adequate exposure of the vertebral artery can be achieved intracranially, since the surgeon's line of sight follows the vessel toward the brain stem and basilar artery. Third, if an endarterectomy cannot be performed, the patient is already ideally positioned for an occipital artery-posterior inferior cerebellar artery bypass. To provide this option the course of the occipital artery should be identified with a Doppler flow meter and marked prior to draping. Fourth, the three-quarter prone position allows the surgeon to perform the operation with minimum fatigue because the surgeon's arms are comfortably at his side rather than raised to shoulder level. The operating field is also accessible from a wider area with the patient in this position, allowing more active participation by an assistant. Fifth, the three-quarter prone position is easier on the patient and avoids compression of the chest and abdomen, which may increase venous bleeding in the prone position. Bleeding from the vertebral venous plexus surrounding the artery can be a difficult problem. In addition to using optimal positioning, by finding a plane of dissection between the vertebral plexus and the vertebral artery, and by using a bipolar forceps to coagulate before cutting as the separation proceeds, bleeding can be well controlled. A long incision from above the inion to C5 or C6 allows retraction of the paraspinal musculature far enough laterally
403
to expose the transverse foramen of C1 and C2. The exposure also permits a minimal suboccipital craniectomy and dissection of the vertebral artery as it penetrates the dura mater. In Allen and associates' [1] first case, endarterectomy could not be performed, because after exposure of the vertebral artery intracranially, the plaque was found to extend too far beyond the posterior inferior cerebellar artery. If the incision in the vertebral artery is relatively short and the plaque is carefully dissected free until it tapers to a fine margin, manipulation of the brain stem and difficulty with closure of a long arteriotomy are circumvented. A short incision is made in the vertebral artery. Using Rhoton and Penfield dissectors, the plaque is separated circumferentially from the wall of the vertebral artery. After the plaque breaks free, the distal margin can be visualized intraluminally. In our experience, the plaque will generally taper to a fine margin and break off cleanly. If there are some intraluminal pieces of plaque that remain, these can be removed under direct vision with a microbiopsy forceps. W h e n the plaque extends beyond the clip on the distal portion of the vertebral artery, the clip can be removed and nontraumatic vascular forceps used to occlude the vertebral artery as close to the basilar artery as possible, while the rest of the plaque is removed with gentle traction. Our patients are given a bolus of sodium thiopental and are heparinized before occlusion of the vertebral artery. The heparin is not reversed. No problems occurred with either form of therapy.
References 1. Allen GS, Cohen RJ, Preziosi TJ: Microsurgical endarterectomy of the intracranial vertebral artery for vertebrobasilar transient ischemic attacks. Neurosurgery 8:56-69, 1981 2. Amman JI, Lee MC, Klassen AC, Seljeskog EL, Chou SN: Stroke: what's new ?Cerebral revascularization. Minn Med 59: 223- 227, 1976 3. Ausman J1, Lee MC, Chater N, Latchaw R: Superficial temporal artery to superior cerebellar artery anastomosisfor distal basilar stenosis. Surg Neurol 12:277-281, 1979 4. Ausman JI, Diaz FG, de los Reyes RA, Pak H, Patel S, Boulos R: Anastomosis of occipital artery to anterior inferior cerebellar artery for vertebrobasilar junction stenosis. Surg Neurol 16:99-102, 1981 5. Amman JI, Diaz FG, de los Reyes RA, Pak H, Patel S, Mehta B, Boulos R: Posterior circulation revascularization: superficial temporal artery to superior cerebellar artery anastomosis. J Neurosurg 56:766-776, 1982 6. Caplan L, Rosenbaum A: Role of cerebral angiography in vertebrobasilar occlusive disease. J Neurol Neurosurg Psychiatry 38:601612, 1975 7. Carney AL: Vertebral artery surgery: historical development, basic concepts of brain hemodynamics and clinical experience of 102 cases. Adv Neurol 30:249-282, 1981 8. DeBakeyME, Crawford ES, Morris GC, Cooley DA: Surgical consideration of occlusive disease of the innominate carotid subclavian and vertebral arteries. Ann Surg 154:698-725, 1961 9. Hopkins LN, Budny JL, Spetzler RF: Revascularization of the rostral brainstem. Neurosurgery 10:364-369, 1982 10. Khodadad G: Occipital artery-posterior inferior cerebellar artery anastomosis. Surg Neurol 5:225-227, 1976 11. Khodadad G: Short and long term results of microvascular anas-
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tomosis in the vertebrobasilar system. A critical analysis. Neurol Res 3:33-65, 1981 12. Millikan CH, Siekert RG, Shick RM: Studies in cerebrovascular disease. IlI. The use of anticoagulant drugs in the treatment of insufficiency or thrombosis within the basilar arterial system. Proc Staff Meet Mayo Clin 30:116-126, 1955 13. Roski RA, Spetzler RF, Hopkins LN: Occipital artery to posterior inferior cerebellar artery bypass fl~r vertebrobasilar ischemia. Neurosurgery 10:44-49, 1982 14. Sundt TM, Piepgras DG: Occipital to posterior inferior cerebellar bypass surgery. J Neurosurg 48:916-928, 1978
15. Sundt TM, Piepgras DG, Houser OW, Campbell JK: Interposition saphenous vein grafts for advanced occlusive disease and large aneurysms in the posterior circulation. J Neurosurg 56:205-215, 1982 16. Wesolowski SA, Gillie E, McMahon JD, Santos DS, Call JR, Uchida H: New arteriographic and surgical techniques for vertebral arteriopathies. Circulation 48(Suppl 3):21 l - 219, 1973 17. Williams D, Wilson G: The diagnosis of the major and minor syndromes of basilar insufficiency. Brain 85:741-774, 1962 18. Yasargil MG: Microsurgery Applied to Neumsurgery. New York: Academic, 1979
Book Review Chronic Low Back Pain
Edited by Michael Stanton-Hicks and Robert Boas New York, Raven Press Reviewed by Donlin M. Long, M.D., Baltimore, MD This is an interesting compilation of a number of short independent chapters on the general problem of low back pain. The book makes no attempt to be all inclusive or to be cohesive, but it provides a number of interesting chapters which would be useful to the individual interested in the ubiquitous problem of low back pain. The first three chapters on epidemiology, incidence, and prevalence are excellent and provide a very comprehensive summary of the public health aspects of this problem. The chapter on diagnosis emphasizes several important diseases that are not commonly discussed by neurosurgeons. This chapter provides an excellent review stressing nondiscogenic causes of low back pain. Dr. Nachemson has provided an excellent general review of back injury and the conservative management of low back pain. The chapter on assessment and management planning is less valuable. The nuances of patient history and physical examinations are summarized too briefly and the descriptions of the origins of back pain are similarly too short to be of real value. Differential nerve blocks are described in some detail, but there is no discussion to allow the nonbeliever to assess their real value. The psychological assessment is not described in enough detail to determine if the author's classifications have validity. The descriptions of the therapy of myofascial pain and various other kinds of low back pain are reviews of the author's methods and are not verified by supporting data. There is an extensive chapter on the radiological evaluation of back pain. Unfortunately, the reviews based upon computerized tomographic (CT) axial sections have been outdated by newer equipment, and the quality of currently available scans is much better than that of the scans the author had available for analysis, Epidural venography is described in some detail. The authors are enthusiastic about this tech-
nique, which does not correlate with the experience of many others. It is probable that the CT scan will make this relatively new technique obsolete before its value is proved or disproved. The chapter on psychological assessment and treatment by Dr. L. E. Peterson is excellent and will provide the neurosurgeon with insight into behavioral management techniques. The philosophical discussion of pain by Dr. John Loeser is equally valuable. There is an important chapter on strength testing and exercise to provide data for the workplace. This is an area which is virtually ignored in United States industry and one which is extremely important. The chapter on antiinflammatory drug therapy is brief, but very good. Very few neurosurgeons understand the use of the minor analgesics, and in general the appropriate use of analgesics is poorly understood. Physical therapy and exercise are covered well and these chapters should help the neurosurgeon who wishes to be involved in the total management of back pain. The book closes with a series of minor interventional procedures for back pain. Carron and Toomy have described epidural steroid therapy in detail. Again, the results appear to be interpreted purely subjectively and not substantiated by any data for the reader to assess. The chapter by Boas on facet joint injection is very useful and provides a simple description of the facet syndrome and its treatment by the neurosurgeon. Dr. Harold Wilkinson has written a chapter covering a potpourri of what he terms unconventional approaches. The most useful of these for the neurosurgeon is the excellent review of the surgical therapy of arachnoiditis, supplemented by a description of Dr. Wilkinson's extensive experience. I found this book enjoyable reading. It is not an exten-, sive treatise on low back pain and makes no pretense of being comprehensive. The individual chapters are uneven, but most are quite good and there is little misinformation. It certainly can be recommended to anyone with an interest in the low back problem who wishes to go beyond conventional orthopedic and neurosurgical approaches which focus upon discogenic pain and its surgical therapy.