✓ The clinical course, operative technique, and angiographic outcome are reported for a patient with a giant intracranial aneurysm of the proximal middle cerebral artery (MCA) who presented with symptoms of ischemia. Treatment of the aneurysm required bypassing the involved MCA bifurcation, but the patient lacked a suitable donor superficial temporal artery. The involved arterial segment was therefore bypassed with a side-to-side anastomosis of the anterior temporal artery to one of the secondary trunks of the MCA. This bypass eliminated the need to harvest a vein graft and re-established flow using in situ intracranial vessels of similar diameter, minimal arterial dissection, and only one suture line.
Joshua B. Bederson and Robert F. Spetzler
Joshua B. Bederson and Charles B. Wilson
✓ Outcome after 252 posterior fossa explorations for the treatment of trigeminal neuralgia was determined by a retrospective review. Patients with distortion of the fifth nerve root caused by extrinsic vascular compression underwent microvascular decompression, those with no compression underwent partial sensory rhizotomy, and those with vascular contact but no distortion of the nerve root underwent decompression and rhizotomy. The mean follow-up period was 5.1 years. An excellent (75%) or good (8%) clinical outcome was achieved in 208 patients; 13 patients (5%) experienced little or no pain relief. Thirty-one patients (12%) suffered recurrent trigeminal neuralgia an average of 1.9 pain-free years after operation; recurrence continued at a rate of approximately 2% per year thereafter. Reoperation for recurrent or persistent pain provided excellent or good results in 85% of reoperated patients, but partial sensory rhizotomy was required in most of these patients. Outcome was affected by previous surgical procedures. A previous percutaneous radiofrequency lesion was associated with a significantly greater incidence of fifth nerve complications and a worse outcome after posterior fossa exploration. Because of this finding, the authors recommend that percutaneous radiofrequency rhizolysis be reserved for patients who have failed posterior fossa exploration or who are not candidates for surgery. Patients with compressive nerve root distortion and a short duration of symptoms before surgery had a significantly better outcome than patients with a longer duration of symptoms. In contrast, there was no relationship between the duration of symptoms and outcome of patients without nerve root distortion. Vascular decompression may cause dysfunction of the trigeminal system in tic douloureux, but in patients who remain untreated for long periods an intrinsic abnormality develops that may perpetuate pain even after microvascular decompression. Posterior fossa exploration is recommended as the procedure of choice for patients with trigeminal neuralgia who are surgical candidates.
Joshua B. Bederson, Joseph M. Zabramski and Robert F. Spetzler
✓ The authors describe a new technique for treating unclippable aneurysms. The method involves a modification of the traditional wrapping technique, including a clip-reinforced cotton sling. The results of this method in four patients are presented.
Brian T. Andrews, Arthur Lutz, Joshua B. Bederson and Lawrence H. Pitts
✓ A new microclip for use on blood vessels 300 µ to 1 mm in diameter is described. This clip is suitable for either temporary or permanent occlusion and has been used in experimental applications. Potential clinical applications are described.
Joshua B. Bederson, Griffith R. Harsh IV, John A. Walker and Charles B. Wilson
✓ The authors report a case in which bilateral cystic temporal lobe necrosis developed after treatment of nasopharyngeal lymphoepithelioma with 7000 cGy of external beam radiation. The patient presented with an isolated memory deficit that was documented by neuropsychological testing. After fenestration and internal shunting of both cysts, there was striking resolution of the lesions and of the memory deficit.
Fatima A. Sehba, Victor Friedrich Jr., Girma Makonnen and Joshua B. Bederson
Structural changes in brain parenchymal vessels occur within minutes after subarachnoid hemorrhage (SAH). These changes include platelet aggregation, activation of vascular collagenases, and destruction of perivascular collagen IV. Because collagen IV is an important component of the basal lamina, the authors attempted to further define changes in vascular structure (length and luminal diameter) and their relationship to vascular permeability immediately after SAH. In addition, the authors explored whether such alterations were attenuated by administration of a nitric oxide (NO) donor.
Endovascular perforation was used to induce SAH in rats. Two sets of experiments were performed. The first established changes in vascular structure and permeability (collagen IV and endothelial barrier antigen [EBA] dual immunofluorescence) during the first 24 hours after SAH. In the second, the investigators examined the effects of an NO donor on vascular structure, permeability, and collagenase activity (in situ zymography). In this second study, animals received intravenous infusion of the NO donor S-nitrosoglutathione (GSNO, 1 μM/8 μl/min) 15 minutes after induction of SAH and were killed 3 hours after SAH onset. Controls were naive unoperated animals for the first study and saline-infused SAH animals for the second.
The authors found a time-dependent decrease in area fraction, length, and luminal diameter of collagen IV– and EBA-immunofluorescent vessels after SAH. The greatest change occurred at 3 hours after onset of SAH. Administration of GSNO was associated with striking preservation of collagen IV and EBA immunofluorescence compared with saline treatment. Zymography indicated decreased collagenase activity in GSNO-treated SAH animals compared with saline-treated SAH animals.
These results demonstrate changes in the structure and permeability of brain parenchymal microvessels after SAH and their reversal by treatment with an NO donor.
Fatima A. Sehba, Gulam Mostafa, Jared Knopman, Victor Friedrich Jr. and Joshua B. Bederson
Object. Aneurysmal subarachnoid hemorrhage (SAH) causes acute and delayed ischemic brain injuries. The mechanisms of acute ischemic injury following SAH are poorly understood, although an acute increase in microvascular permeability has been noted. The integrity of cerebral microvessels is maintained in part by components of basal lamina: collagen IV, elastin, lamina, and so forth. Destruction of basal lamina components by collagenases and matrix metalloproteinases (MMPs), especially MMP-9, has been known to occur in other ischemic models. The authors assessed the integrity of cerebral microvasculature after acute SAH by examining collagen IV and MMP-9 levels and collagenase activity in the microvessels.
Methods. Subarachnoid hemorrhage was induced in rats through endovascular perforation of the intracranial bifurcation of the internal carotid artery. Animals were killed 10 minutes to 48 hours after SAH or sham operation (time-matched controls). Levels of collagen IV and MMP-9 were studied in the microvasculature by performing immunoperoxidase and immunofluorescence staining, and collagenase activity was assessed by in situ zymography.
Little change occurred in collagen IV and MMP-9 immunostaining or collagenase activity at 10 minutes or 1 hour after SAH. Starting 3 hours after SAH, collagen IV immunostaining was reduced or eliminated along segments of microvessels whereas MMP-9 staining was segmentally increased. These effects reached a maximum at 6 hours and returned toward those values in sham-operated controls at 48 hours.
Conclusions. Results of this study demonstrated an acute loss of collagen IV from the cerebral microvasculature after SAH and indicated that MMP-9 contributes to this event. The loss of collagen IV might contribute to the known failure of the blood—brain barrier after SAH.
James M. Herman, Robert F. Spetzler, Joshua B. Bederson, James M. Kurbat and Joseph M. Zabramski
✓ A rat model was developed to determine the role of sinus thrombosis and elevated sinus pressures in the pathogenesis of dural arteriovenous malformations (AVMs) Five protocols were tested to compare various sinus pressures and thrombosis of a sinus: 1) Control I, sham operation (five animals); 2) Control II, occlusion of the right common carotid artery, the right external jugular vein, and the vein draining the left transverse sinus, as well as thrombosis of the sagittal sinus (10 animals); 3) arteriovenous fistula (AVF) I, anastomosis of the right common carotid artery to the external jugular vein causing retrograde flow through the transverse sinus (10 animals); 4) AVF II, anastomosis (as described in AVF I) and thrombosis of the sagittal sinus (12 animals); 5) AVF III, anastomosis (as described in AVF I) as well as thrombosis of the sagittal sinus and occlusion of the vein draining the transverse sinus on the left (12 animals). Mean arterial and sagittal sinus pressures were monitored and cerebral angiograms were obtained intraoperatively and again 90 days later. Afterward, the animals were sacrificed and their brains and dura were examined histologically.
Formation of a fistula resulted in a significant (p < 0.05) threefold increase in sagittal sinus pressure in the AVF II group and a significant (p < 0.05) sixfold increase in the AVF III group. Seven dural AVMs (three in the AVF II group and four in the AVF III group) were demonstrated angiographically and histologically. The seven malformations were located adjacent to a thrombosed sagittal sinus. All lesions were within the dura and sinus wall with direct thrombus—sinus wall connections demonstrated in four of the malformations. The other three lesions displayed arteriovenous connections within the sinus wall and dura. These data suggest the importance of not only sinus thrombosis but also sinus hypertension in the development of a dural AVM.
Jack J. Haslett, Lindsey A. LaBelle, Xiangnan Zhang, J Mocco, Joshua Bederson and Christopher P. Kellner
Carotid artery disease is a common illness that can pose a significant risk if left untreated. Treatment via carotid endarterectomy (CEA) or carotid artery stenting (CAS) can also lead to complications. Given the risk of adverse events related to treating, or failing to treat, carotid artery disease, this is a possible area for litigation. The aim of this review is to provide an overview of the medicolegal factors involved in treating patients suffering carotid artery disease and to compare litigation related to CEA and CAS.
Three large legal databases were used to search for jury verdicts and settlements in cases related to untreated carotid artery disease, CEA, and CAS. Search terms included “endarterectomy,” “medical malpractice,” “carotid,” “stenosis,” “stenting,” “stent,” and combinations of those words. Three types of cases were considered relevant: 1) cases in which the primary allegation was negligence performing a CEA or perioperative care (CEA-related cases); 2) cases in which the primary allegation was negligence performing a CAS or perioperative care (CAS-related cases); and 3) cases in which the plaintiff alleged that a CEA or CAS should have been performed (failure-to-treat [FTT] cases).
One hundred fifty-four CEA-related cases, 3 CAS-related cases, and 67 FTT cases were identified. Cases resulted in 133 verdicts for the defense (59%), 64 settlements (29%), and 27 plaintiff verdicts (12%). The average payout in cases that were settled outside of court was $1,097,430 and the average payout in cases that went to trial and resulted in a plaintiff verdict was $2,438,253. Common allegations included a failure to diagnose and treat carotid artery disease in a timely manner, treating with inappropriate indications, procedural error, negligent postprocedural management, and lack of informed consent. Allegations of a failure to timely treat known carotid artery disease were likely to lead to a payout (60% of cases involved a payout). Allegations of procedural error, specifically where the resultant injury was nerve injury, were relatively less likely to lead to a payout (28% of cases involved a payout).
Both diagnosing and treating carotid artery disease has serious medicolegal implications and risks. In cases resulting in a plaintiff verdict, the payouts were significantly higher than cases resolved outside the courtroom. Knowledge of common allegations in diagnosing and treating carotid artery disease as well as performing CEA and CAS may benefit neurosurgeons. The lack of CAS-related litigation suggests these procedures may entail a lower risk of litigation compared to CEA, even accounting for the difference in the frequency of both procedures.
Fatima A. Sehba, Gulam Mostafa, Victor Friedrich Jr. and Joshua B. Bederson
Object. The mechanisms underlying acute cerebral ischemia after subarachnoid hemorrhage (SAH) are not well established. Platelets aggregate within major cerebral vessels hours after SAH, but this has not been studied in the microvasculature. Platelet aggregates within the microvasculature could mechanically obstruct the lumen and initiate events that injure vessel structure. In the present study the authors examined the hypothesis that platelets aggregate within the cerebral microvasculature acutely after SAH.
Methods. Subarachnoid hemorrhage was induced in the rat by using the endovascular perforation model. The animals were killed between 10 minutes and 48 hours after SAH. Immunostaining for the platelet surface receptor glycoprotein (GP)IIb/IIIa, which mediates platelet aggregation, was used to detect platelet aggregation. Sham-operated animals were used as controls.
The GPIIb/IIIa immunoreactive platelet aggregates were abundant in the microvasculature of the basal and frontal cortex, striatum, and hippocampus 10 minutes after SAH. These aggregates decreased in number from 1 to 6 hours post-SAH and then increased to a peak at 24 hours. No immunoreactive aggregates were observed 48 hours after SAH.
Conclusions. The data indicate that widespread platelet aggregation occurs very rapidly in response to SAH followed by a decrease within 6 hours and a subsequent increase 24 hours after SAH. Microvascular platelet aggregates may contribute to decreased cerebral blood flow and ischemic injury after SAH via a number of mechanisms.