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Archived Comments for: Movements after the clinical diagnosis of brain death: supraspinal motor responses or spinal reflexes

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  1. Assumptions and Facts in the discussion of Brain Death

    Noam Stadlan, NorthShore University Medical Group

    27 February 2015

    This comment reflects a number of commonly mentioned assumptions that are not necessarily true. The authors state that "on histopathological examination, about 60% of heart-beating donors have normal or minimal ischemic injury to the brainstem", quoting the seminal study by Wijdicks et al. However, they fail to mention the accompanying editorial comment(1) which states "The assessment method used by the authors(neuronal eosinophilia) is a fairly late development in the course of neuronal necrosis. More advanced techniques (DNA fragmentation, immunohistochemistry,in situ hybridization methods to explore caspase-mediated/independent mechanisms of cell death) could provide earlier indications of irreversible neuronal damage." In other words, not-dead by H and E staining criteria at 36 hours under conditions of brain death does not imply that the cells have the capacity to function or that they indeed are alive.(2)
    THe authors also make assumptions regarding the mechanism of cessation of CBF- stating that "Compression of the vertebral-basilar arteries (causing intracranial circulatory arrest) and the spinal nerve roots by cerebellar tonsillar herniation at the foramen magnum would abolish the spinal accessory nerve reflex as well as cause cervicomedullary infarction."
    They assume that cessation of vertebro-basilar blood flow is due to direct compression of the arteries themselves, and that this amount of compression at the foramen magnum should be adequate to inactivate the spinal acessory nerve. However, direct compression of the vertebral and basilar arteries is not thought to be the mechanism of cessation of flow. An in depth summary of research in 1989 stated: "Conclusive evidence of a vascular collapse on one particular level of the 'vascular waterfall' is lacking. Instead, circulatory standstill may be due to ICP-induced reduction of the pressure drop along the still patent vascular bed. With decreasing driving force, it seems conclusive that flow arrest commences in the vesels with the slowest flow(that is the capillaries).(3). Furthermore, at least regarding the internal carotid artery, "Intracranial compression of the ICA at its entrance into the subdural space...was considered unlikely..because the ICP usually did not exceed the intraluminal pressure of the vessel and because progressive reduction of the luminal area would increase the wall resistance to further compression in the think-walled ICA. The lumina of the intracranial ICA's were patent on postmortem examination....."(3). Therefore cessation of CBF in the posterior circulation does not have to automatically mean high pressures at the foramen magnum. 
    Patients who lose all brain mediated neurological exam(become brain dead) due to hypoxia may not geerate high ICP's. Hypoxia is more likely to damage the neurons than the glia, and the glia generate the edema that leads to high ICP. This may explain why some brain dead patients do not also exhibit cerebral circulatory arrest. The patient described did indeed exhibit cerebral circulatory arrest(CCA). However, the case may illustrate a combination of brain damage and ICP high enough to cause CCA but not high enough to destroy the spinal accesory nerve at the foramen magnum. Obviously the authors may be correct in their assumptions, but they should be labelled assumptions, and not stated as facts.
    1. Saposnik, Gustavo, and David Munoz. "Dissecting brain death: Time for a new look" Neurology 2008 70:1230-1231
    2. This common misconception(and others) are discussed in the appendix to a book review published in the Journal Meorot avaliable here: http://www.yctorah.org/images/stories/about_us/%235%20-%20stadlan.pdf see appendix page 15.
    3. Hassler, Werner, Steinmetz, Helmuth, and Jurgen Pirschel "Transcranial Doppler study of the intracranial circulatory arrest". Journal of Neurosurgery 1989 71:195-201.

    Competing interests

    none

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