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BRIEF COMMUNICATIONS: J. A. Frontera, T. Rundek, J. M. Schmidt, J. Claassen, A. Parra, K. E. Wartenberg, R. E. Temes, S. A. Mayer, J. P. Mohr, and R. S. Marshall Cerebrovascular reactivity and vasospasm after subarachnoid hemorrhage: A pilot study Neurology 2006; 66: 727-729 [Abstract] [Full text] [PDF]

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Cerebrovascular reactivity and vasospasm after subarachnoid hemorrhage

George KC Wong, Stephanie CP Ng, Wayne WS Poon   (8 March 2006)

Reply from the authors

Jennifer A. Frontera, Randolph S. Marshall   (8 March 2006)

Cerebrovascular reactivity and vasospasm after subarachnoid hemorrhage 8 March 2006
George KC Wong, Department of Surgery, Chinese University of Hong Kong Department of Surgery, Prince of Wales Hospital, Shatin, NT, Hong Kong SAR., Stephanie CP Ng, Wayne WS Poon Send Correspondence to journal: Re: Cerebrovascular reactivity and vasospasm after subarachnoid hemorrhage georgewong{at}surgery.cuhk.edu.hk George KC Wong, et al.	We read with interest the article by Frontera et al. [1] The authors demonstrated that bedside transcranial Doppler (TCD) carbon dioxide reactivity (CO2R) testing could predict symptomatic vasospasm after aneurysmal subarachnoid hemorrhage (SAH) with 57 CO2R studies in 20 patients. A similar conclusion using transient hyperemic response test of cerebral autoregulation was previously published. [2] In that article, twenty aneurysmal subarachnoid hemorrhage patients with no immediate post- operative deficits were studied. Bedside transient hyperemic response test was done with 5-9 seconds of carotid artery compression and TCD criteria. Primary impairment (at day one after surgical clipping) was noted in six patients and five of them went on to develop delayed ischemic neurological deficits (DIDs, equivalent to symptomatic vasospasm). The other fourteen patients did not develop DID. It would be interesting to have the data of primary impairment of cerebrovascular reactivity of the study by Frontera et al to see whether a similar primary impairment would have similar predictive values. At the time of significant vasospasm, cerebrovascular reserve as predicted by CO2R should always be decreased. Another option to perform the CO2R, as in our hospital, would be through Acetazolamide injection. The pathophysiological implication of primary impairment of autoregulation predictive of symptomatic vasospasm might also be interesting. It might be hypothesized that a primary brain injury (initial hemorrhage or surgery) was a pre-requisite for DID caused by delayed vasospasm. This double injury model for DID might be worthwhile to explore for improvement in management for patients with aneurysmal subarachnoid hemorrhage. References 1.Frontera JA, Rundek T, Schmidt JM, et al. Cerebrovascular reactivity and vasospasm after subarachnoid hemorrhage: A pilot study. Neurology Epub January 25,2006. 2.Lam JM, Smielewski P, Marek C, Pickard JD, Kirkpatrick PJ. Predicting delayed ischemic deficits after aneurysmal subarachnoid hemorrhage using a transient hyperemic response test of cerebral autoregulation. Neurosurgery 2000;47:819-826.
Reply from the authors 8 March 2006
Jennifer A. Frontera, Columbia University College of Physicians and Surgeons 710 W 168th St. Neurological Institute 6th floor, Ny, NY 10032, Randolph S. Marshall Send Correspondence to journal: Re: Reply from the authors jfrontera{at}neuro.columbia.edu Jennifer A. Frontera, et al.	We appreciate the interest in our article [1] and the observations offered. The transient hyperemic response test (THRT) used by Lam et al found a significant association between abnormal THRT and delayed ischemic deficits after SAH. [2] This method of assessing autoregulation, in which transient decreases in carotid blood flow stimulate a compensatory arteriolar vasodiliation, simulates rapid blood pressure cuff deflation or pressure challenge techniques. Some limitations of this technique include the risk of emboli from carotid compression and there is evidence of limitations in accuracy. [3] Mechanoregulatory responses to changes in blood pressure may be mechanistically different than chemoregulatory CO2 challenges. Another option is dynamic cerebral autoregulation (dCA), which evaluates changes in middle cerebral artery mean flow velocity (MFV) in response to naturally occurring fluctuations in blood pressure. A direct correlation of MFV and blood pressure suggests a loss of autoregulation. This technique has been applied in SAH and does predict vasospasm diagnosed by transcranial Doppler parameters. [4,5] It is unclear whether dCA predicts symptomatic vasospasm or delayed ischemic deficits after SAH, though this technique seems promising since it is non-invasive and does not require a blood pressure challenge or carotid compression. Dynamic cerebral autoregulation testing and CO2 reactivity testing (or alternately acetazolamide challenge) may be complementary in determining the risk of vasospasm after SAH. Future studies comparing dCA, CO2 reactivity and other modalities of assessing autoregulation in SAH are warranted. References 3. Smielewski P, Czosnyka M, Kirkpatrick P, Pickard JD. Evaluation of the transient hyperemic response test in head-injured patients. J Neurosurg 1997;86:773-778. 4. Lang EW, Diehl RR, Mehdorn HM. Cerebral autoregulation testing after aneurysmal subarachnoid hemorrhage: the phase relationship between arterial blood pressure and cerebral blood flow velocity. Crit Care Med 2001;29:158-163. 5. Soehle M, Czosnyka M, Pickard JD, Kirkpatrick PJ. Continuous assessment of cerebral autoregulation in subarachnoid hemorrhage. Anesth Analg 2004;98:1133-1139, table of contents. Disclosure: The authors report no conflicts of interest.