Neurosurgery Surgical Research Laboratory
Treatment of Post-Surgical Vasoconstriction
Dr Zervas | Recent
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Research in Cerbral Vasospasm Dr Zervas's Lab - PET Imaging of CBF, CBV, O2M, OEF and GluMetab
Images courtesy of Anna-Liisa Brownell, PhD in collaboration on a study of CNS tissue metabolism (rGMR, rCMRO2, rOEF, rCBF, rCBV) during cerebral vasospasm. (For more info.)
Images courtesy of CIPR (Center for Imaging and Pharmaceutical Research) as part of a collaboration with the CNS project group. The images are the work of George Hunter, MD and Leena Hamberg, PhD as part of a study on peripheral tissue perfusion (CBV, TTT, CBFi) during cerebral vasospasm. (For more info.)
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Despite intensive laboratory and clinical research efforts over the past l5 years, delayed chronic cerebral vasospasm remains a major source of morbidity and mortality following subarachnoid hemorrhage (SAH). Research efforts in my laboratory have taken two related paths: (1) In vitro efforts to define the basic mechanisms which underlie the pathogenesis of cerebral vasospasm, and (2) In vivo studies to identify pharmacological methods of prophylactic and/or therapeutic relief of cerebral vasospasm. In the course of this project, we developed and characterized the animal model of post-SAH cerebral vasospasm which has become the worldwide standard in vasospasm research. Over 40 laboratories internationally use the "doubleSAH canine model" routinely.
Most recently, innovations in the clinical management of subarachnoid hemorrhage patients has led to marked improvement in their general clinical outcome, except for those patients with a demonstrable severe focal constriction in some particular cerebral arterial perfusion zone. A new collaborative effort with the Wellman Laser Applications Group holds great promise for the treatment of these patients.
Using both in vitro systems and our well-established animal model, we have recently
shown that very brief pulses of low energy laser energy applied intraluminally to
constricted cerebral arteries can create a localized expansive fluid wave capable of
forcibly dilating the artery. While the method is, in principle, similar then to balloon
angioplasty: it has several features which represent distinct improvements. Since the
pulsed fluid wave can be made to propagate over a significant distance intraluminally, it
is not necessary to directly catheterize the injured vessels. That is, approach to within
a few centimeters distally is adequate, thus reducing possible injury to already "at
risk" arteries. Secondly, and perhaps most importantly, the pulsed-fluid wave will
propagate from the lumen of major conducting vessels to smaller branch vessels and perhaps
deep into the zones of reduced cerebral perfusion. We are currently working
collaboratively with several imaging groups (PET and CIPR) to establish the parameters of
laser-induced pulsed-fluid wave treatment which successfully reestablished normal levels
of cerebral perfusion in our animal model. The diffuse spread of vasodilation into
constricted microcirculatory beds by pulsed-wave application is in result unobtainable by
balloon angioplasty. Our research in this new methodology holds great promise for
developing a new and successful treatment modality for cerebral vasospasm.
Disclaimer: The information and reference materials contained herein is intended solely for the information of the reader. It should not be used for treatment purposes, but rather for discussion with the patient's own physician.© Copyright
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All Rights Reserved MGH Neurosurgical Service 1999 .
Revised: 02/17/05 PageServant or e-mail C. Owen