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Impaired capillary perfusion and brain edema following experimental subarachnoid hemorrhage: a morphometric study

Hiroo Johshita, Neal F. Kassell, Tomio Sasaki, and Hisayuki Ogawa

✓ To evaluate microcirculatory disturbance and cerebral edema associated with subarachnoid hemorrhage (SAH), both stereological morphometry on the intraparenchymal capillary network and microgravimetry were performed on a rabbit SAH model. Autologous arterial blood (5 ml) was injected into the cisterna magna, and the animals were sacrificed at intervals of 6 hours, 1 day, 2 days, or 6 days after SAH. Capillaries in the piriform cortex, parasagittal cortex, and ventral brain stem of the midline-hemisectioned brain were injected with Evans blue dye 1 minute before sacrifice, and were planimetrically evaluated under a fluorescence microscope connected to an image analysis system. Stereological and morphological parameters including the volume density, surface density, numerical density, minimum intercapillary distance, and the diameter of Evans blue-perfused capillaries were also computed.

In the piriform cortex and ventral brain stem, the volume and surface densities were significantly reduced and the minimum intercapillary distance was significantly increased 1 to 2 days after SAH. In the parasagittal cortex far from the cisternal clot, changes in the parameters were minimal. Cerebral blood volume (CBV) in the normal condition and edema formation associated with SAH were studied by the microgravimetric technique. The mean CBV in the parasagittal cortex, piriform cortex, and brain stem was 6.9%, 6.8%, and 5.6%, respectively. Following SAH, specific gravity in the piriform cortex and the ventral brain stem of the other side of the hemisectioned brain was significantly decreased at 1 to 2 days, showing a change parallel to that of the stereological parameters. The results obtained from the morphometric technique indicated the occurrence of impaired capillary perfusion and reduced capillary blood volume following SAH, while microgravimetry suggested the formation of brain edema during this period. These changes in the intraparenchymal vessels may play an important role in the pathophysiology of SAH.

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Lenticulostriate aneurysm of infancy

Case illustration

George J. Kaptain, Jason P. Sheehan, and Neal F. Kassell

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Supraorbital craniotomy by fracture of the anterior orbital roof

Technical note

Johnny B. Delashaw Jr., John A. Jane, Neal F. Kassell, and Craig Luce

✓ The authors describe a new and rapid method to safely perform a supraorbital craniotomy. This technique can be used when tumor does not invade the orbital roof. Previous descriptions of the supraorbital craniotomy involved exposure of the frontal sinus by removing its anterior wall and using the Gigli saw to separate the orbital roof. This new approach avoids removal of the anterior frontal sinus wall and separates the supraorbital bone flap from the calvaria by fracturing the anterior orbital roof forward. In addition, a method for harvesting a laterally based pericranium and muscle pedicle that contains a section of contralateral temporalis muscle is described. This vascularized pedicle can be used for repair of cerebrospinal fluid leaks or bone defects along the anterior fossa floor and orbit.

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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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Glomus jugulare tumor presenting with increased intracranial pressure

Case report

David W. Beck, Neal F. Kassell, and Charles G. Drake

✓ The authors report a case of glomus jugulare tumor presenting with papilledema and visual loss. The tumor was extremely vascular with significant shunting of arterial blood into venous sinuses. There was no intracranial extension of tumor, and papilledema resolved after removal of the lesion.

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Transmission of Increased Intracranial Pressure

I. Within the Craniospinal Axis

Thomas W. Langfitt, James D. Weinstein, and Neal F. Kassell

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Transmission of Increased Intracranial Pressure: II. Within the Supratentorial Space

Thomas W. Langfitt, James D. Weinstein, Neal F. Kassell, and L. John Gagliardi

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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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Characteristics of relaxation induced by calcitonin gene—related peptide in contracted rabbit basilar artery

Bernhard Sutter, Satoshi Suzuki, Neal F. Kassell, and Kevin S. Lee

✓ Increasing evidence suggests that disturbances in the modulatory influence of the vasoactive peptide, calcitonin gene—related peptide (CGRP), contribute to the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage (SAH). However, only limited success has been achieved in trials attempting to ameliorate vasospasm by modifying CGRP function. To better understand the potential utility of targeting CGRP-mediated relaxation, it is important both to identify the interactions CGRP may have with other elements of the vasospastic response and to characterize the mechanisms through which CGRP elicits vasodilative effects. The present studies examined the effects of CGRP on vascular responsiveness using tension measurements of ring strips of rabbit basilar artery maintained in vitro. Pretreatment of vessels with CGRP (100 nM) inhibited vasoconstrictor responses to the potent protein kinase C (PKC) activator, phorbol 12,13-dibutyrate (PDB). This particular contractile response was selected because PKC-mediated vasoconstriction is a critical component of the vasospastic response after SAH. In a posttreatment paradigm, CGRP was also found to reverse established constriction responses to PDB (2 nM) and histamine (3 µM) in a dose-dependent manner.

When tested against the maximum effective dose of PDB (30 nM) in the posttreatment paradigm, CGRP (100 nM) did not elicit significant relaxation. However, after washing both of these drugs out of the test chamber, a persistent effect of CGRP was revealed: the decay of PDB-induced contraction was accelerated in vessels that had previously been treated with CGRP. These findings indicate that CGRP elicits both immediate and sustained influences on contractile responses mediated by PKC.

Finally, two potential mechanisms for the vascular response to CGRP were examined. Adenosine triphosphate (ATP)—sensitive K+ channels do not appear to participate in CGRP-mediated dilation; inhibitors of these channels, glibenclamide and tolbutamide, did not block CGRP-induced relaxation. In contrast, a possible role for the nucleotide cyclic adenosine monophosphate (cAMP) in the vascular response to CGRP was indicated by the dose-dependent elevation of cAMP levels by CGRP.

Together these studies indicate that CGRP can modulate the contractile response to PKC activation. These effects are associated with increases in the levels of cAMP, but occur independently of fluxes through ATP-sensitive K+ channels.