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Introduction

Focused ultrasound surgery

W. Jeffrey Elias and Neal F. Kassell

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Endovascular treatment for symptomatic cerebral vasospasm after subarachnoid hemorrhage: transluminal balloon angioplasty compared with intraarterial papaverine

Volker A. Coenen, Carolyn Apperson Hansen, Mstat, Neal F. Kassell, and Richard S. Polin

The authors retrospectively evaluated the short-term neurological improvement of 69 patients undergoing endovascular treatment for symptomatic cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH). The patient group observed here is a subset of patients enrolled in the multicenter North American Trial of Tirilazad in SAH. Thirty-one patients were treated with intraarterial administration of papaverine (IAP). Fourteen patients were only treated with transluminal balloon angioplasty (TBA), and 24 patients received a combination of angioplasty and papaverine.

The purpose of this study was to compare the effects of IAP and TBA on short-term clinical improvement of patients. Daily clinical staging with the modified Glasgow Coma Scale and every-other-day transcranial Doppler (TCD) measurements allowed for a close investigation of the clinical course. Furthermore, this study was designed to investigate the effects of treatment timing on short-term outcome.

Although TCD studies demonstrated a decrease in flow velocities in the middle cerebral artery in both treatment groups, indicating a vasodilating effect of both treatment modalities (dv = -18.4 cm/second for papaverine, dv = -26.04 cm/second for angioplasty; p = 0.5509), there was no significant difference in clinical improvement at Days 1 and 4 postprocedure (p = 0.1996). Neither of the two treatment forms showed an effect of therapy timing on neurological outcome.

Neither IAP nor TBA was correlated with a high percentage of short-term neurological improvement. The authors discuss reasons why those procedures may result in limited clinical change.

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Transcranial MR-guided focused ultrasound sonothrombolysis in the treatment of intracerebral hemorrhage

Stephen J. Monteith, Neal F. Kassell, Oded Goren, and Sagi Harnof

Intracerebral hemorrhage remains a significant cause of morbidity and mortality. Current surgical therapies aim to use a minimally invasive approach to remove as much of the clot as possible without causing undue disruption to surrounding neural structures. Transcranial MR-guided focused ultrasound (MRgFUS) surgery is an emerging technology that permits a highly concentrated focal point of ultrasound energy to be deposited to a target deep within the brain without an incision or craniotomy. With appropriate ultrasound parameters it has been shown that MRgFUS can effectively liquefy large-volume blood clots through the human calvaria. In this review the authors discuss the rationale for using MRgFUS to noninvasively liquefy intracerebral hemorrhage (ICH), thereby permitting minimally invasive aspiration of the liquefied clot via a small drainage tube. The mechanism of action of MRgFUS sonothrombolysis; current investigational work with in vitro, in vivo, and cadaveric models of ICH; and the potential clinical application of this disruptive technology for the treatment of ICH are discussed.

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Update on management of intracerebral hemorrhage

Nader Pouratian, Neal F. Kassell, and Aaron S. Dumont

Intracerebral hemorrhage (ICH) is a lingering cause of significant mortality and morbidity rates in contemporary society. Despite its established burden, considerably less investigative attention has been devoted to the study of ICH than other forms of stroke. Only a limited number of clinical studies have been performed to examine the surgical (both craniotomy and minimally invasive) and medical management of patients with ICH. No consistently efficacious strategies have been identified through such investigations. Limitations in study design and execution have universally impaired the interpretation and impact of available data. Management of ICH unfortunately remains heterogeneous across institutions, and it continues to suffer from the lack of proven medical and surgical effectiveness. Urgently needed are further prospective randomized controlled trials in which investigators consider the shortcomings of previous endeavors in the management of ICH. In the present article the authors review the current management practices of ICH, discuss the controlled trials, and highlight recent trials and future avenues of further study.

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Surgical management of unruptured basilar artery bifurcation aneurysms

Technical note

Aaron S. Dumont, Rod J. Oskouian Jr., Michael M. Chow, and Neal F. Kassell

The basilar artery (BA) bifurcation is the most common site for aneurysms arising from the posterior circulation. Their inhospitable location, nested within the narrow confines of the interpeduncular fossa anterior to the brainstem, coupled with the rich network of adjacent critical thalamoperforating arteries irrigating the midbrain and thalamus, pose difficult anatomical obstacles for the surgeon.

The age old adage that the only cure for intracranial aneurysms remains exclusion from circulation before rupture still holds true. Although management of unruptured aneurysms in general is still controversial, unruptured aneurysms of the BA bifurcation can be treated surgically with acceptable rates of morbidity. The clinician must gather and weigh all clinical, pathological, and radiological data when formulating recommendations for the individual patient.

In the present report the authors describe their current technique for the surgical management of unruptured BA bifurcation aneurysms; this represents the culmination of the senior author's (N.K.) experience in the management of both ruptured and unruptured BA bifurcation aneurysms. A modified, right-sided subtemporal transtentorial approach has been adopted in all cases of isolated unruptured BA bifurcation aneurysms. Technical nuances are described.

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Attenuation of vasospasm and hemoglobin-induced constriction in the rabbit basilar artery by a novel protease inhibitor

Barbara Cappelletto, Hakan H. Caner, Frank Schottler, Aij-Lie Kwan, David Eveleth, Patricia L. Foley, Neal F. Kassell, and Kevin S. Lee

Calcium-activated proteolysis mediated by the protease inhibitor, calpain, has recently been implicated in the pathogenesis of cerebral vasospasm. The effect of one inhibitor of calcium-activated proteolysis, z-Leu-Phe-CONH-morpholene (zLF), on cerebrovascular constriction was examined in two experimental paradigms. In the first paradigm, the rabbit basilar artery (BA) was visualized via a transclival exposure, and its diameter was monitored using videomicroscopy. In the second experimental paradigm two intracisternal injections of autologous blood were administered to mimic a subarachnoid hemorrhage (SAH). The BA was visualized via the transclival exposure, and its luminal diameter was measured. Topical application of oxyhemoglobin (OxyHb), a known pathogenic agent in cerebral vasospasm, elicited vasoconstriction in normal animals, reducing arterial diameter to approximately 75% of resting levels. Pretreatment with zLF (100, 200, or 300 μM) attenuated vasoconstriction induced by OxyHb. In an experimental model of SAH, the diameter of the BA was reduced after the first injection of blood to approximately 67% of normal resting levels when measured 3 to 4 days later. This vasospastic response was reversed significantly by topical application of zLF (100 μM); vascular diameter was increased to approximately 84% of normal resting levels.

These findings demonstrate that both acute OxyHb-induced constriction and blood-induced vasospasm are sensitive to an inhibitor of the proteolytic enzyme, calpain. Together, these observations indicate an important role for calcium-activated proteolysis in the development and maintenance of vasospasm after SAH. In addition, it may be inferred from the data that inhibitors of calcium-activated proteolysis may be useful therapeutic agents for treating this form of cerebrovascular disease.

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Attenuation of cerebral vasospasm by systemic administration of an endothelin-A receptor antagonist, TBC 11251, in a rabbit model of subarachnoid hemorrhage

John E. Wanebo, Hunter G. Louis, Adam S. Arthur, Jie Zhou, Neal F. Kassell, Kevin S. Lee, and Gregory A. Helm

Cerebral vasospasm is a major complication of subarachnoid hemorrhage (SAH) after the rupture of an intracranial aneurysm. Although the cause of cerebral vasospasm has not been fully established, several lines of evidence suggest that the vasoconstrictor peptide endothelin (ET) may play a crucial role. In the present study the potential of TBC 11251 (TBC), a newly developed ETA receptor antagonist, to prevent and/or reverse cerebral vasospasm was examined in a well-established rabbit model of SAH.

Sixty-five New Zealand White rabbits were assigned to one of six groups. Experimental SAH was induced in rabbits comprising five of the groups by injecting autologous arterial blood into the cisterna magna. The treatment groups were as follows: 1) control (no SAH); 2) SAH only; 3) SAH + placebo at 24 and 36 hours (24/36); 4) SAH + TBC (24/36); 5) SAH + placebo twice daily (BID); and 6) SAH + TBC BID. All drug-treated animals received an intravenous dosage of 5 mg/kg TBC. After 48 hours, the animals were killed by intracardiac perfusion with fixative. The brainstems were removed and the basilar arteries (BAs) were prepared for histological examination. The cross-sectional area of each BA was measured using computer-assisted videomicroscopy by an investigator blind to the group from which it came. A one-way analysis of variance and paired group mean comparisons with the post-hoc Fisher least significant difference test were used for analysis of BA diameters and physiological parameters.

The model provided reliable vasospasm, with the mean BA cross-sectional area constricting from 0.388 mm2 in the control group to 0.106 mm2 (27.4% of control) in the SAH only group. Treatment with TBC (24/36) after SAH (reversal protocol) produced a mean BA area of 0.175 mm2 (44.2% of control) which, although larger than the placebo group value of 0.135 mm2 (39.9% of control), was not statistically significant. However, treatment with TBC BID (prevention protocol) produced a mean BA area of 0.303 mm2 (78.1% of control) compared with the placebo BID value of 0.134 mm2 (34.6% of control); this effect was statistically significant (p < 0.01). There were no side effects noted and no differences in the mean arterial pressures between drug and placebo groups.

These findings demonstrate that systemic administration of the ETA receptor antagonist TBC significantly attenuates cerebral vasospasm after SAH when given as a preventative therapy, and they provide additional support for the role of ET in the establishment of vasospasm.