Endovascular strategies for vertebrobasilar dissecting aneurysms.

BACKGROUND AND PURPOSE: Dissecting vertebrobasilar aneurysms are challenging to treat, and standard treatment modalities remain controversial. We retrospectively evaluated our experience using endovascular techniques to treat these aneurysms. MATERIALS AND METHODS: From February 1997 to December 2007, 42 patients with intradural vertebrobasilar dissecting aneurysms underwent endovascular treatment. Twenty-nine patients had ruptured aneurysms, and 13 patients had unruptured dissecting aneurysms. The endovascular modalities for vertebrobasilar dissecting aneurysms were the following: 1) trapping (n = 30), 2) proximal occlusion (n = 3), 3) stent with coil (n = 6), and 4) stent alone (n = 3). RESULTS: Seventeen of the 29 patients with ruptured vertebrobasilar dissecting aneurysms had successful outcomes without procedural complications following endovascular treatment. Procedure-related complications were the following: 1) rebleeding (n = 3), 2) posterior inferior cerebellar artery (PICA) territory infarction (n = 6), 3) brain stem infarction (n = 2), and 4) thromboembolism-related multiple infarctions (n = 1). Clinical outcomes were favorable in 32 patients (76.1%). There were 3 (7.1%) procedure-related mortalities due to rebleeding, and 1 (2.4%) non-procedure-related mortality due to pneumonia sepsis. All 13 patients with unruptured vertebrobasilar dissecting aneurysms had favorable clinical and radiologic outcomes without procedure-related complications. CONCLUSIONS: Endovascular procedures for treatment of unruptured symptomatic dissecting aneurysms resulted in favorable outcomes. Ruptured vertebrobasilar dissecting aneurysms are associated with a high risk of periprocedural complications. Risks can be managed by using appropriate endovascular techniques according to aneurysm location, configuration, and relationship with the PICA.

Subdural hematoma in spontaneous CSF hypovolemia.

Of 67 consecutive patients with spontaneous CSF hypovolemia (SCH), 11 (16.4%) had subdural hematoma (SDH). Patients with SDH were older (p = 0.005), more likely to be male (p = 0.035), and displayed longer time to diagnosis of SCH (p = 0.019) than those without SDH. All patients with SDH showed the findings of pseudo-subarachnoid hemorrhage on CT and responded favorably to epidural blood patches and neurosurgical drainage.

Hypoglossal-facial crossover in facial-nerve palsy: pure end-to-sideanastomosis technique.

Hypoglossal-facial crossover is the most popular method of reconstructing the facial nerve in facial palsy resulting from proximal facial-nerve injury near the brainstem. Conventional hypoglossal-facial crossover involves performing a partial hypoglossal-nerve section or incision and an interpositional nerve graft to bridge the gap between the two nerves, which sometimes results in hemiglossal atrophy and its sequelae. Furthermore, the nerve graft may delay recovery and make facial reanimation weak. To solve these problems, we attempted to perform 'pure end-to-side anastomosis' (without section of the hypoglossal nerve) between the hypoglossal and facial nerves in four patients with facial palsy. In two patients (group I) a sural-nerve graft was used to bridge the gap between the two nerves. In the other two patients (group II) the intratemporal facial nerve was mobilised to the neck and one tension-free end-to-side anastomosis was performed. Facial symmetry and tone at rest were restored in all cases. Facial reanimation was achieved in group II after 8 months. Despite the small number of cases, we believe that the technique of hypoglossal-facial crossover with 'pure end-to-side anastomosis' and mobilisation of the intratemporal facial nerve can decrease donor-nerve morbidity in facial-nerve rehabilitation.

Analysis of the causes of treatment failure in gamma knife radiosurgery for intracranial arteriovenous malformations.

OBJECT: The authors sought to analyze causes for treatment failure following gamma knife radiosurgery (GKS) for intracranial arteriovenous malformations (AVMs), in cases in which the nidus could still be observed on angiography 3 years postsurgery. METHODS: Four hundred fifteen patients with AVMs were treated with GKS between April 1990 and March 2000. The mean margin dose was 23.6 Gy (range 10-25 Gy), and the mean nidus volume was 5.3 cm3 (range 0.4-41.7 cm3). The KULA treatment planning system and conventional subtraction angiography were used in treatment planning. One hundred twenty-three of these 415 patients underwent follow-up angiography after GKS. After 3 years the nidus was totally obliterated in 98 patients (80%) and partial obliteration was noted in the remaining 25. There were several reasons why complete obliteration was not achieved in all cases: inadequate nidus definition in four patients, changes in the size and location of the nidus in five patients due to recanalization after embolization or reexpansion after hematoma reabsorption, a large AVM volume in five patients, a suboptimal radiation dose to the thalamic and basal ganglia in eight patients, and radioresistance in three patients with an intranidal fistula. CONCLUSIONS: The causes of failed GKS for treatment of AVMs seen on 3-year follow-up angiograms include inadequate nidus definition, large nidus volume, suboptimal radiation dose, recanalization/reexpansion, and radioresistance associated with an intranidal fistula.

A co-operative study: clinical characteristics of 334 Korean patients with moyamoya disease treated at neurosurgical institutes (1976-1994). The Korean Society for Cerebrovascular Disease.

A co-operative study was conducted to determine the clinical characteristics of patients with moyamoya disease who were diagnosed and treated at neurosurgical institutes in Korea before 1995. Twenty-six hospitals contributed 505 cases and among them, the clinical characteristics of 334 patients with definite moyamoya disease were evaluated. The number of patients began to increase from the late 1980s, and after that approximately 20 patients were treated each year. There were two age peaks: from six to 15 and from 31 to 40 years of age. Haemorrhagic manifestations occurred in approximately 43% of the patients. The major clinical manifestations were haemorrhage in adults (62.4%) and ischaemia in children (61.2%). Overall 54.5% of the patients experienced decreased consciousness levels, mainly due to intracranial haemorrhage or cerebral infarction. In the patients with ischemic manifestations, the adult patients were more likely to have cerebral infarction than the pediatric patients (80% vs. 39%) and the pediatric patients were more likely to have TIA (61% vs. 25%). Thirty eight percent of the patients underwent bypass surgery and 53% of these procedures were performed bilaterally. Treatment policies, including indications for bypass surgery and commonly used drugs, were somewhat different according to the institution. Overall favorable outcome was 73%, and the most significant factor affecting poor outcome was haemorrhagic manifestation. This article describes the characteristics of 334 patients with moyamoya disease, who were diagnosed and treated at neurosurgical institutes in Korea before 1995.

Radiologic and histopathologic changes after Gamma Knife radiosurgery for acoustic schwannoma.

Gamma knife radiosurgery (GKRS) is a widely used treatment option for acoustic schwannomas, 3 cm in diameter or less. Between May 1990 and February 1998, 102 acoustic tumors in 101 patients were treated with GKRS. There are 77 patients with a follow-up period of more than six months (mean 55, range 7 to 90 months). Seventy (91%) of these tumors have remained unchanged or reduced in volume. After GKRS there was an increase in volume in seven cases. In four the volume increase affected solid tumour. Among these, three patients were in stable condition and are being observed. One of these patients developed brain stem compression symptoms and was operated. In another three cases, cysts with multiple septa developed medial to the tumor and compressed the brain stem and fourth ventricle, thus necessitating post-GKRS surgery. In these three patients, MRI had shown loss of central contrast enhancement followed by its return. Histological findings at surgery before and after GKRS were compared for these four tumours. In spite of the MRI changes, there were no definite histological findings after GKRS which could be attributed to radiation induced changes. The development of cysts occurred after the treatment of larger tumors.

Gamma knife treatment of acoustic neurinoma.

The results of treatment of acoustic neurinomas using Gamma Knife radiosurgery (GKR) during a 6-year period in our center were reviewed. Since May 7, 1990, we treated 88 cases of acoustic neurinoma with GKR. During a 52-month mean follow-up period, MRI was obtained in 63 patients. Reduction in tumor size occurred in 34 (54%) cases, and another 27 (42.8%) tumors showed no change. The tumor control rate was thus 95%. Tumor size increased in 3 (4.8%) cases, but one case is still in early follow-up. Two cases were operated after GKR. Histological examination of the tumors removed at surgery 8 months after GKR were obtained. The examinations showed enlargement of nucleoli and cytoplasm and proliferation of endothelial cells due to delayed radiation changes. Post-GKR facial neuropathy was noted in 7 (8.8%) patients, of which 4 recovered during the follow-up period. The tumor volume, margin dose, number of isocenters and marginal isodose did not have any statistically significant relationship with the development of facial neuropathy. Transient trigeminal neuropathy were noted in 3 patients. Hearing was preserved in 2 of 3 hearing patients. In conclusion, our GKR results for acoustic neurinomas were very similar to the previously reported series, which makes GKR for acoustic tumors an excellent treatment modality for small- to medium-sized tumors with or without microsurgical tumor removal.

Vascular occlusion produced over 24 hours increases spinal cord tolerance to occlusion.

Occlusion over a 24-hr period of vessels which supply the spinal cord was tolerated better than occlusion of the same vessels acutely. Spinal cord ischemia was produced in 12 New Zealand White rabbits by transection of four or five pairs of lumbar segmental arteries arising from the abdominal aorta plus 30-min occlusion of the remaining segmental artery pair either acutely or 24 hr later. Of these 12 rabbits, 6 were occluded acutely and served as controls. Recovery, or failure to recover, as assessed by examining the rabbits for permanent loss of sensory and motor function in the hindlimbs, was compared in the two groups. The duration of the temporary occlusion was sufficient to lead to a total or near total loss of sensory and motor function in all control rabbits but resulted in no deficit in all but 1 of the rabbits which had the occlusion produced in two stages. These results have implications for the care of patients subjected to spinal cord ischemia during and after operations on the thoracic aorta.

Carbon dioxide at anesthetic levels protects against irreversible damage during spinal cord ischemia.

Carbon dioxide inspired as a 40% mixture in oxygen and halothane protected the spinal cords of 5 rabbits subjected to 30 min of surgically created spinal cord ischemia. Spinal cord ischemia was produced in 20 New Zealand White rabbits by transection of four of the five pairs of segmental arteries arising from the abdominal aorta below the renal arteries plus temporary occlusion of the remaining pair. The artery was occluded for 15 min in 9 control rabbits, for 30 min in 6 control rabbits, and for 30 min in 5 treated rabbits after inhalation of 40% carbon dioxide. The extent of spinal cord injury was assessed by examining the rabbits for permanent loss of sensory and motor function in the hindlimbs and was compared in the treated and control groups. These results have implications for the management of patients subjected to aortic occlusion.

Mild hypothermia protects against irreversible damage during prolonged spinal cord ischemia.

Mild hypothermia to 32 degrees C protected the spinal cords of 5 rabbits subjected to 90 min of surgically created spinal cord ischemia. Spinal cord ischemia was produced in 10 New Zealand White rabbits by transection of four out of the five segmental arteries arising from the abdominal aorta below the renal arteries plus 90-min occlusion of the remaining segmental artery 24 hr later. Of these 10 rabbits, 5 served as controls. Recovery, or failure to recover, as assessed by examining the rabbits for permanent loss of sensory and motor function in the hind limbs, was compared in the two groups. The duration of the ischemia was sufficient to lead to a total or near total loss of sensory and motor function in all control rabbits. These results may have implications for the care of patients subjected to spinal cord ischemia.

Evidence of the role of hemolysis in experimental cerebral vasospasm.

The short-term (less than or equal to 72-hour) reaction to subarachnoid injections of various blood components was determined in a canine model of cerebral vasospasm. Platelet-rich plasma (PRP) formed durable clots in the basal cistern surrounding the basilar artery and provoked no vascular reaction in 72 hours or more. Freshly isolated autologous erythrocytes resuspended in PRP likewise provoked no vasoconstriction in 72 hours although a second injection of fresh erythrocytes in PRP induced significant reaction, as in the conventional "double subarachnoid hemorrhage (SAH)" canine model. Hemolysate of fresh erythrocytes led to a severe immediate vascular reaction after introduction into the basal cistern using PRP as the carrier/clotting medium, as did the injection of intact erythrocytes incubated ex vivo for 72 hours. Resolution of the initial reaction was rapid for hemolysate, but slow and (depending on hematocrit) incomplete for intact "aged" erythrocytes. In vitro measurements of erythrocyte lysis in these media and histological examination indicate that the production of erythrocyte lysate was responsible for the vascular reaction observed, suggesting that the rate of lysis of erythrocytes in the subarachnoid clot is a major factor in the genesis of vasospasm after SAH.

The role of inflammation in experimental cerebral vasospasm.

The short-term (less than or equal to 72-hour) cerebral vascular reaction to subarachnoid injectates of various specific blood components was determined by angiography in a canine model of cerebral vasospasm. Cell-free subarachnoid clots of autologous plasma in the basal cistern were found to produce no significant reaction of the basilar artery, while whole-blood clots induced a small (15%) chronic constriction after 24 hours. Because the plasma clots were not well retained in the basal cistern, however, small beads (dextran or latex) were added to stabilize them. Injection of beads and plasma led to moderate-to-severe chronic vasoconstriction (35% to 40%) with rapid onset. Control experiments demonstrated that these foreign bodies (beads) alone induced this vascular reaction. Histological examination showed that severe inflammation followed the introduction of subarachnoid beads. The experiments demonstrate that inflammation alone, in the absence of other processes associated with subarachnoid hemorrhage, may induce persistent and severe cerebroarterial constriction and raises the possibility that inflammation in response to subarachnoid blood may play a role in clinical vasospasm.

Immunological reaction against the aging human subarachnoid erythrocyte. A model for the onset of cerebral vasospasm after subarachnoid hemorrhage.

The role of the aging human erythrocyte in the mechanisms leading to cerebral vasospasm after subarachnoid hemorrhage was investigated using an in vitro model for the environment of the erythrocyte in a subarachnoid blood clot. It has long been suspected that, due to its potent vasoactivity, erythrocyte lysate provides the major vasoconstrictive input to cerebral arteries during vasospasm. Under the model conditions (incubation at 37 degrees C in an artificial cerebrospinal fluid), however, the rate of spontaneous hemolysis was quite slow (about 1%/day), becoming only somewhat more rapid after 4 days' incubation. The rate of hemolysis of aging erythrocytes was dramatically increased (500- to 1000-fold) by the addition of plasma proteins, but only after the erythrocytes had aged 2 to 3 days, or more. The mechanism of age-dependent, plasma-induced hemolysis of originally autologous erythrocytes is shown to involve activation of the plasma complement protein pathway, analogous to the mechanisms of innate immunity which lead to lysis of nonautologous cell types and activate the inflammatory response.