Complete Recovery from Hemiplegia Following Excision of a Giant Basal Ganglia Arteriovenous Malformation Hoi Sang U, M.D.,* and Jay Rosenberg, M.D.t sensorium. Her neurological history dated back to 1967 when she developed the onset of simple partial seizures at the age of 18. This progressed to secondary tonic-clonic seizures two years later that responded adequately to phenobarbital. During the first trimester of her second pregnancy in 1976, she was examined because of an increasing number of simple partial seizures in the left upper extremity. A computerized tomographic (CT) scan done at that time disclosed a vascular lesion in the right basal ganglia. The diagnosis of an arteriovenous malformation of the right basal ganglia was confirmed by angiography but surgical treatment was declined. Her condition remained stable, The clinical presentation of cerebral arteriovenous malfor- and her seizures were well controlled on medications. In mation (AVM) is well recognized and the clinical course March, 1979, she experienced an episode of severe with or without therapy is amply documented in the litera- headache. Evaluation of subarachnoid hemorrhage with a ture [3-5, 7-9]. There is little doubt that proper treatment lumbar puncture was negative. Subsequently, she conentails total obliteration of the malformation. However, tinued to do well until November, 1979, when she noted there are some lesions that have been deemed inoperable the onset of subtle weakness in the left leg, that over two due to their location in relatively inaccessible areas of the days progressed to hemiparesis and finally hemiplegia. A brain. AVMs in the basal ganglia would fall into this cate- cerebral angiogram showed minimal interval enlargement gory [ 12]. Advances in neuroradiology have, however, led of the AVM with rapid arteriovenous (AV) shunting (Fig. to a clearer definition of the vascular pathology in these 1). Two main groups of arterial feeders supplied the lesions so that a more aggressive approach towards their ex- lesion--the lenticular striate branches and the distal middle cerebral branches entering the external capsule. The cision can be taken using microsurgical techniques. One pathophysiological feature of these lesions is the patient was treated with Decadron with no improvement. shunting of blood destined for the surrounding brain away Progressive somnolence associated with headache, nausea, from it, thus causing ischemia [10]. Neurological impair- and vomiting as well as loss of parietal lobe function enment secondary to vascular shunting may be reversed by sued. Neurological examination disclosed a somnolent but eliminating the malformation. In the following case report arousable patient who was oriented and cooperative. She cerebral ischemia was indicated as the most likely cause of was able to relate her history well and she demonstrated a the progressive neurological impairment in this patient; good fund of knowledge. Her attention span was short and complete recovery followed the total microsurgical excision she fell asleep during the examination. Examination of the cranial nerves was notable for the presence of bilateral of the malformation. papilledema and a left central facial weakness. Motor examination disclosed a dense left hemiplegia with mildly inCase Report creased tone. Left-sided hyperreflexia could be demonA 30-year-old white female was seen in December, 1979, strated, together with clonus of the left foot and a left-sided with a progressive left hemiparesis and slow decrease in Babinski response. Astereognosis and graphesthesia were From the *Departmentsof SurgeryfNeurosurgeryand Biology,University present. of California, San Diego, La Jolla, CA, and *Departmentof Neurology, Because of the rapidly progressive nature of the patient's Kaiser PermanenteMedical Center, San Diego. CA 92120. impairment, surgical excision of the AVM was undertaken. Address reprint requests to Dr. Hoi Sang U, 3350 La Jolla Village Drive, Excision of the lesion was performed in two stages through a San Diego, CA 92161. large frontotemporoparietal craniotomy. At the first stage Key words: arteriovenousmalformation;basal ganglia; microsurgicalexcision; hemiplegia. of the procedure, the entire hemisphere was seen to be A young female harbored a large arteriovenous malformation (AVM) in the basal ganglia associated with marked arteriovenous shunting. The complete recovery of her neurological deficit subsequent to excision of the AVM illustrates the reversibility of such severe cerebral impairment. Large lesions in the basal ganglia often have been deemed inoperable. However, modern advances in microsurgical techniques have provided the necessary illumination, magnification, and instrumentation that was needed for the exposure and gentle resection of the lesion in our patient. 328 0090.3019/81/050328-03501.25 © 1981 by Little, Brown and Company (Inc.) U and Rosenberg: Excision of Giant AVM ~f Basal Ganglia A 329 B Fig. 1. Anteroposterior (A) and lateral (B) views of a selective right internal carotid an~ogram in the late arterial phase. Note the immediate filling of large venous aneurysmal sacs in the AVM and rapid drainage superficially to the superi~rr sa~ttal sinus and centrally to the vein of Galen. There is a distinct paucity of filling of the arteries supplying the rest of the hemispheie. markedly swollen and edematous. The internal carotid and proximal middle cerebral arteries were exposed in an attempt to identify the lenticular striate feeders to the AVM. However, marked obliteration of the sylvian fissure by a dense adhesion made it impossible to separate the pathological from the normal vessels. The lesion was therefore approached by following the middle cerebral artery distally. At the site where the arterial feeders enter the lesion deep in the external capsule, an arterial aneurysm was found and obliterated. This aneurysm was directly lateral and adherent to two large venous aneurysms on the lateral aspect of the lesion. Partial excision of the superior anterior aspect of the lesion was then done through the development of a plane of cleavage in the gliotic tissue directly external to the AVM. All arterial feeders and draining veins were coagulated and divided in this plane. Any exposed areas of the AVM were also coagulated. These areas invariably shrank and the dissection plane was further developed. After this stage of the procedure, the patient noted immediate improvement in her mentation. She no longer had headache and there was no decrease in her sensorium whatsoever. However, left hemiplegia persisted. Repeat angiography disclosed marked improvement in the arterial filling of the hemisphere. The AVM was also slightly diminished in size. Ten days later she was returned to the operating room for complete excision of the lesion. At no Fig. 2. A lateral postoperative right internal carotid an~ogram demonstrating the absence of the A V M and marked improvement of arterial filling in the hemisphere. time during this or the previous procedure were signs of recent hemorrhage found. The procedure was monitored with serial angiograms until complete excision was effected. This was confirmed by a postoperative angiogram (Fig. 2). The patient's clinical recovery was much more rapid after the second procedure. By the sixth postoperative day the patient began to produce small movements of the left fingers and toes. By the second week the patient was able to take three steps while supporting herself on parallel bars. Over the ensuing month the patient recovered all neurological function with no hemiplegia whatsoever At present, 330 Surgical Neurology Vol 15 No 5 May 1981 she is intact neurologically and is resuming her normal home life one year after excision of the AVM. Discussion Cerebral AVMs continue to present difficult challenges, especially those AVMs that are large, located in deep areas, and involve substantial arteriovenous (AV) shunting. The case reported illustrates some aspects of these difficulties and one approach to them is described. Cerebral AVMs invariably involve shunting of arterial blood directly into venous channels due to the congenital absence of a capillary system. Depending on the degree of shunting, blood can be diverted from normal areas of the brain through the AV shunts, thus rendering these areas ischemic. The progressive nature of the present case, the significant amount of AV shunting seen on angiography, and the absence of recent bleeding observed during the surgical procedure is suggestive of either progressive enlargement of the AVM or the increased shunting of blood through the malformation leading to subsequent development of ischemia in the surrounding brain. The latter possibility seems more probable due to the minimal interval enlargement of the lesion seen between the two angiograms (1976 and 1979) and the marked edema suggestive of panhemispheric ischemia seen during surgery. Despite the rapidly progressive and grave nature of the patient's status, the occlusion of some of the major feeders into the lesion during the first operation appeared adequate to halt this process. Her clinical status improved and this was associated with improved filling of cerebral vessels as seen on angiography. Eventual complete recovery despite the severity of her clinical impairment demonstrates the degree of plasticity in the brain in some of these cases. Thus, prompt treatment in the face of a grave clinical status may lead to a very satisfying recovery. Advances in microsurgical techniques have led to a more aggressive attitude in the treatment of cerebral vascular lesions. With the illumination and magnification afforded by the surgical microscope, in addition to refined instrumentation, the neurosurgeon is armed with improved equipment for the gentle handling of delicate tissue and the exposure of deep-seated lesions. In the treatment of deep-seated AVMs in particular, the use of microsurgical techniques is invaluable. It allows the surgeon to develop his plane of dissection directly in apposition to the surface of the malformation. This is vital especially when the lesion is situated in a critical area where damage to the surrounding cerebral substance should be avoided at all cost. One technique that the senior author has found helpful is the coagulation of the surface of the AVM. This invariably leads to some shrinkage of the AVM that further helps in the development of a plane of dissection between the lesion and the surrounding brain. With progressive occlusion of feeders going into the AVM as well as shrinkage of the AVM through surface coagulation, the lesion becomes reduced in size and is therefore more manageable. Thus, extreme retraction of the surrounding brain for exposure can be avoided. The approach to AVMs associated with substantial AV shunting is still controversial. Total excisions of such lesions have been associated in some cases with catastrophic hyperemic or hemorrhagic intraoperative or postoperative complications [6, 13]. One mechanism responsible for such complications seems to be the breakthrough of a defective autoregulatory vascular system in the chronically ischemic brain as a result of recirculation after the excision of the AVM [11]. The devastating effects of such complications have led some authors to suggest a staged approach to the excision or the embolization of these lesions or both [2]. Whether such a rationale has a scientific basis is not proved at this time. In summary, the present report illustrates some of the challenges and discusses the ongoing controversy surrounding surgical treatment of AVMs. The latitude afforded by the operating microscope as well as microsurgical techniques has led to a more aggressive attitude in the treatment of large and deep-seated AVMs such as the one reported. The authors would like to thank R. Robbins for typing the manuscript. References I. Amacher AL, Allcock JM, Drake CG: Cerebral angiomas: the sequelae of surgical treatment. J Neurosurg 37:57l-575, 1972 2. Cromwell LD, Harris AB: Treatment of cerebral arteriovenous malformations. J Neurosurg 52:705-708, 1980 3. Forster DM, Steiner L, H~tkanson S: Arteriovenous malformations of the brain. 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