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ARTICLES: Eelco F.M. Wijdicks and Eric A. Pfeifer Neuropathology of brain death in the modern transplant era Neurology 2008; 0: 01.wnl.0000289762.50376.b6v1 [Abstract]

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Neuropathology of brain death in the modern transplant era

David W. Evans   (3 July 2008)

Neuropathology of brain death in the modern transplant era

Michael Potts   (3 July 2008)

Reply from the authors

Eelco .F.M. Wijdicks, Eric A. Pfeifer   (3 July 2008)

Neuropathology of brain death in the modern transplant era

Calixto Machado, Julius Korein   (26 June 2008)

Reply from the authors to Machado et al

Eelco F.M. Wijdicks, Eric A Pfeifer   (26 June 2008)

Neuropathology of brain death in the modern transplant era 3 July 2008
David W. Evans, Queens' College 27 Gough Way, Cambridge, CB3 9LN, UK Send Correspondence to journal: Re: Neuropathology of brain death in the modern transplant era dwevansmd{at}doctors.org.uk David W. Evans	I read the article by Wijdicks et al. with interest. [1] The proper scientific conclusion to be drawn from these neuropathological findings is that the clinical diagnosis should be called into question. The absence of even "moderate" ischemic changes in the thalamus and midbrain in 66% and 63% of patients respectively casts doubt on the presumption of irreversible cessation of function within and thus negates diagnoses of whole brain death on those clinical grounds. The absence of such changes in the medulla oblongata in 60% of cases should be particularly interesting to those who rely exclusively on brain stem testing for the diagnosis of death for transplant purposes as is done in the UK. This may explain the persistence of vasopressor and cardio-accelerator responses to the trauma of organ procurement. [2] References 1. Wijdicks EFM, Pfeifer EA. Neuropathology of brain death in the modern transplant era. Neurology 2005;70:1234-1237. 2. Wetzel RC, Setzer, N, Stiff JL, Rogers MC. Hemodynamic Responses in Brain Dead Organ Donor Patients Anaesthesia & Analgesia 1985;64:125-128. Disclosure: The author reports no disclosures.
Neuropathology of brain death in the modern transplant era 3 July 2008
Michael Potts, Professor of Philosophy, Methodist University 5400 Ramsey Street, Fayetteville, NC 28311-1498 Send Correspondence to journal: Re: Neuropathology of brain death in the modern transplant era gratiaetnatura{at}yahoo.com Michael Potts	The article by Wijdicks and Pfeifer begs the question concerning the value of autopsy studies for the diagnosis of brain death. [1] In his textbook on logic, Hurley states that “begging the question...creates the illusion that inadequate premises provide adequate support for the conclusion by leaving out a possibly false (shaky) premise, by restating a possibly false premise as the conclusion, or by reasoning in a circle.” [3] Wijdicks and Pfeifer are guilty of reasoning in a circle when they assume in advance that brain death “is a precisely defined clinical diagnosis.” [1] The autopsy evidence showed “no distinctive neuropathological features” characteristic of brain death yet the authors conclude that, “Neuropathological examination is therefore not diagnostic of brain death.” The authors should then question the validity of brain death criteria. Their argument is the equivalent of saying, “Brain death can be accurately diagnosed by clinical tests. But autopsy evidence does not reveal significant pathological findings associated with brain death. Thus, brain death can still be accurately diagnosed by clinical tests.” Such circular reasoning is unfortunate when the diagnosis of brain death is literally a matter of life and death for prospective organ donors. References 3. Hurley PJ. A Concise Introduction to Logic, Tenth Edition. Belmont, CA: Thompson-Wadsworth, 2008. Disclosure: The author reports no disclosures.
Reply from the authors 3 July 2008
Eelco .F.M. Wijdicks, Mayo Clinic 200 First Street SW, Rochester, MN 55905, Eric A. Pfeifer Send Correspondence to journal: Re: Reply from the authors wijde{at}mayo.edu Eelco .F.M. Wijdicks, et al.	Dr. Evans rejects the clinical diagnosis of brain death. His interpretation of our study findings—documenting a mosaic of ischemic changes throughout the brain and not total necrosis—is not unexpected. Evans has questioned whether spinal reflexes are indeed ‘spinal’ and believes that cardiac acceleration and hypertension during organ procurement in some patients could be implicitly explained by a functioning medulla. He feels that our study showing 60 percent mild ischemic changes in the medulla oblongata corroborates that. I disagree. These responses can be explained by intact cervical and thoracic sympathetic pathways. Cardiac acceleration does not occur with atropine due to absent output from the dorsal nucleus of the vagal nerve. The clinical findings in our apneic patients with an invariant heartrate and the need for aggressive hemodynamic support were indubitable. Similarly, Dr. Potts believes that our neuropathologic study questions the validity of brain death. There is no basis for that. Brain death is a distinct comatose state and patients have irrevocably lost all brain function. The diagnosis of brain death has never been based on neuropathologic or electrophysiological findings. Prior investigators have tried to equate brain death with ‘Respirator Brain’ or complete liquefaction but our study shows that such a finding should be interpreted as a result of prolonged support in a brain dead patient with increased intracranial pressure. Disclosure: The authors report no disclosures.
Neuropathology of brain death in the modern transplant era 26 June 2008
Calixto Machado, Institute of Neurology and Neurosurgery 29 y D, Vedado, La Habana 10400, Julius Korein Send Correspondence to journal: Re: Neuropathology of brain death in the modern transplant era braind{at}infomed.sld.cu Calixto Machado, et al.	In this interesting article, Wijdicks and Pfeifer again review the neuropathologic findings in brain dead patients. They also acknowledge that improved organ transplant processes have shortened the required time to brain fixation in autopsies. [1] It is true that the classic description of the “respirator brain” occurred when organ transplant protocols were not fully developed. [2] We would like to add some remarks about the neuropathologic findings in the spine in brain death (BD). By the use of short latency somatosensory evoked potential (SEPs) in brain dead patients stimulating the median nerve, we found in one case no somatosensory components after P9 N9 –Erb potential in any of the cephalic and non-cephalic derivations. This patient suffered an intracerebral hemorrhage and had been diagnosed brain dead 26 hours before the SEPs study. Based on the SEPs assessment, we concluded that the somatosensory electrical conduction was blocked at the level of the brachial plexus, and that no impulse transmission passed through the cervical spine segments. Cardiac arrest occurred within 38 hours after withdrawal of support when organ harvesting was completed. Brain and spine were fixated in this case about 45 hours after BD diagnosis. The neuropathologic study confirmed that severe necrosis affected all cervical spine segments. [3,4] Wijdicks and Pfeifer reported that moderate to severe neuronal ischemic changes involved midbrain in 37%, pons in 41%, and medulla in 40% of cases. [1] Walker et al. reported that the cervicomedullary junction was necrotic in about half of their brain dead patients. [3] Moreover, Chiappa emphasized that the region of the cervicomedullary junction is considered an interphase be-tween extracranial and intracranial blood supply, which might explain functional activity in this region for some time after the onset of BD syndrome. [4] In the future, it would be interesting to perform neuropathologic studies of the spine in brain dead patients and correlate autopsy findings with time on the ventilator until cardiac arrest occurs after BD diagnosis. This may also help to explain the presence of spontaneous and reflex movements in brain dead patients. [5] References 1. Wijdicks EFM, Pfeifer EA. Neuropathology of brain death in the modern transplant era. Neurology 2008; 70:1234-1237. 2. Walker AE, Diamond,EL, Moseley J. The neu¬ropathological findings in irreversible coma. A critique of the "respirator". J Neuropathol Exp Neurol 1975;34:295-393. 3. Machado C, Valdés P, García O, et al. Short latency somatosensory evoked potentials in brain dead patients using restricted low cut filter setting. J. Neurosurgical Sciences 1993;37:133-140. 4. Chiappa KH. Evoked potentials in clinical medicine. Second Edition. New York: Raven Press, 1990: 424-426. 5. Saposnik G, Maurino J, Saizar R, et al. Spontaneous and reflex movements in 107 patients with brain death. Am J Med 2005;118:311-314. Disclosure: The authors report no disclosures.
Reply from the authors to Machado et al 26 June 2008
Eelco F.M. Wijdicks, Mayo Clinic Mayo Clinic, Rochester, MN, Eric A Pfeifer Send Correspondence to journal: Re: Reply from the authors to Machado et al Wijde{at}mayo.edu Eelco F.M. Wijdicks, et al.	We appreciate Drs. Machado and Korein's comments. It is expected that the lower medulla oblongata and upper cervical spinal cord can be affected in brain death. This is largely a result of tonsillar compression or severe anoxic-ischemic injury in patients with prolonged arrested blood flow before resumption of circulation. In our study, most medulla oblongata sections were taken at the nuclei levels and we do not have detailed information about the pathology of the cervical spine. This would have required retrieval of wet tissue and—as suggested—a separate study. We are uncertain if that information would be illuminating. We are also uncertain whether a reliable correlation with spinal cord reflexes can be obtained. Movements originated from spinal neurons are spontaneous but commonly uncovered when provoked with unusual stimuli (e.g. the undulating toe sign after forceful flexion of the big toe). If not studied prospectively, they can be missed. Disclosure: The authors report no disclosures.