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Eelco F. M. Wijdicks - One of the best experts on this subject based on the ideXlab platform.
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History of Brain Death
Oxford Medicine Online, 2017Co-Authors: Eelco F. M. WijdicksAbstract:The ability to diagnose brain death is linked to the ability to support catastrophic neurological injury and, thus, linked to the development of critical care. A new comatose state was noted with loss of all Brainstem Reflexes, absent respiratory drive, and loss of vascular tone leading to progressive hypotension and cardiac arrest. This chapter describes the evolution of thought and refinement of brain death criteria in the United States, from the Harvard criteria in 1968 to the American Academy of Neurology practice guidelines in 2010 and more recent pediatric guidelines.
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The Challenges with Brain Death Determination in Adult Patients on Extracorporeal Membrane Oxygenation
Neurocritical Care, 2011Co-Authors: Rajanandini Muralidharan, Farrah J. Mateen, Russell T. Shinohara, Gregory J. Schears, Eelco F. M. WijdicksAbstract:Background To identify a reliable method of performing apnea testing as part of brain death determination in adult patients who develop loss of Brainstem Reflexes while receiving extracorporeal membrane oxygenation (ECMO). ECMO provides extracirculatory support to patients in cardiorespiratory failure who would otherwise be expected to die. Many studies have reported brain death as a potential complication of adult ECMO, but none have cited how apnea testing was performed in these patients. Methods This retrospective review identified adults 15 years or older treated with ECMO at our institution (2002–2010) and the method of determination of brain death when complete loss of Brainstem Reflexes occurred. Results Loss of all Brainstem Reflexes was identified in three cases (3/87, 3.4%). The apnea test was not performed since it was deemed “difficult,” leading to withdrawal of ECMO and intensive care. Ancillary tests such as cerebral flow studies were not used because they may not document absent cerebral arterial flow due to the ischemic nature of the injury. We propose the use of an oxygenated apnea test on ECMO using continuous positive airway pressure (CPAP) through the ventilator or anesthesia bag, with an inline manometer and an end tidal CO_2 device. Conclusion Apnea testing is essential in the determination of brain death, but may not be employed in ECMO-treated adult patients. Apnea testing using the above protocol may assist in better decision making for adult ECMO patients at risk of brain death.
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the challenges with brain death determination in adult patients on extracorporeal membrane oxygenation
Neurocritical Care, 2011Co-Authors: Rajanandini Muralidharan, Farrah J. Mateen, Russell T. Shinohara, Gregory J. Schears, Eelco F. M. WijdicksAbstract:Background To identify a reliable method of performing apnea testing as part of brain death determination in adult patients who develop loss of Brainstem Reflexes while receiving extracorporeal membrane oxygenation (ECMO). ECMO provides extracirculatory support to patients in cardiorespiratory failure who would otherwise be expected to die. Many studies have reported brain death as a potential complication of adult ECMO, but none have cited how apnea testing was performed in these patients.
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second brain death examination may negatively affect organ donation
Neurology, 2011Co-Authors: D Lustbader, Eelco F. M. Wijdicks, David Ohara, L Maclean, Waheed Tajik, A Ying, E Berg, Michael J GoldsteinAbstract:# {#article-title-2} To the Editors: Lustbader et al.1 concluded that one clinical examination—instead of two—is accurate for brain death (BD) determination. We wish to comment on the study's methodology and limitations. The time between two examinations may have been too short to detect reversible loss of Brainstem Reflexes. Rare cases of recovery of some Brainstem Reflexes have been reported in BD after observation periods greater than 24 hours.3 Cases of delayed recovery of Brainstem functions after profound Brainstem injury (short of BD) have also been reported.4,5 In addition, autopsy findings after BD do not often provide supporting histopathologic evidence of Brainstem injury and therefore cannot rule out that the loss of Brainstem Reflexes is reversible with time. The lead bias of the first BD examination can influence subsequent search for—and therapeutic correction of—confounding factors. For example, cervical spinal cord injury is usually present in BD and potentially recoverable over days. In addition, central hypothalamic-pituitary endocrine dysfunction of thyroid and adrenal axes is usually present in BD.6 This would preclude recovery of neurologic function on a second examination. The apnea test during the first examination causes elevated Paco2 and intracranial pressure which will worsen or precipitate brain herniation and Brainstem infarction.6 The second examination may simply confirm this self-fulfilling pathophysiologic process. The completeness of the clinical examination and the performance of confirmatory tests vary among institutions. This raises doubt whether BD determination among all 100 hospitals in the authors' report was consistent, complete, and accurate. It is possible that findings on an incomplete first BD examination may not change on a subsequent incomplete second BD examination. Claiming that BD determination …
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Teaching NeuroImages: Malignant cerebral venous thrombosis and pulmonary emboli
Neurology, 2010Co-Authors: Amandeep K. Dhillon, Alejandro A. Rabinstein, Eelco F. M. WijdicksAbstract:A 23-year-old woman on oral contraception developed headache and seizures. Hemorrhagic infarcts with early swelling resulted in coma with no response to osmotic diuretics (figure, A). On arrival, she had lost most Brainstem Reflexes and met the criteria of brain death within 3 days of onset. Factor V Leiden and prothrombin gene mutation …
Markus Kofler - One of the best experts on this subject based on the ideXlab platform.
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effect of spinal cord injury and of intrathecal baclofen on Brainstem Reflexes
Clinical Neurophysiology, 2012Co-Authors: Hatice Kumru, Markus KoflerAbstract:Reorganization of neural circuits within the central nervous system following injury appears to be a means of compensatory mechanism for loss of function. Reorganization following spinal cord injury is known to evoke changes at the cortical and spinal cord levels. Recent studies, however, provide evidence of enhanced Brainstem Reflexes and alterations in excitatory and inhibitory interneuronal Brainstem circuits, suggesting that reorganization following spinal cord injury occurs also at the Brainstem level. Reversal of these changes by continuous intrathecal baclofen infusion to normal levels or beyond indicates strong GABAergic involvement. Rapid changes in the blink reflex and its prepulse inhibition following intrathecal baclofen bolus application that parallel clinical changes in muscle hypertonia suggest a muscle tone regulating effect of baclofen at the Brainstem level. Enhanced Brainstem Reflexes in spinal cord injury patients may be the consequence of decreased GABA-mediated inhibition and/or strengthening of facilitatory connections due to either direct or indirect plastic changes occurring at the Brainstem level. Modulation of Brainstem Reflexes by baclofen may foster the understanding of pathophysiological mechanisms underlying diseases with increased Brainstem activity. Rehabilitation after central nervous system injury will always be a challenge, but understanding the mechanisms of reorganization of undamaged neural pathways may help to develop better strategies for enhancing neuronal plasticity and for implementing neuronal reorganization into carefully planned therapy.
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Brainstem Reflexes are enhanced following severe spinal cord injury and reduced by continuous intrathecal baclofen
Neurorehabilitation and Neural Repair, 2009Co-Authors: Hatice Kumru, Markus Kofler, Josep Vallssole, Enric Portell, Joan VidalAbstract:Objective. Plastic changes in the human central nervous system can occur at multiple levels, including circuits rostral to the lesion level in spinal cord injury (SCI). GABA is the most important inhibitory neurotransmitter in the brain. The authors hypothesized that one of the consequences of plasticity in SCI patients could be enhancement of Brainstem Reflexes, and they investigated the effect of continuous intrathecal baclofen (CITB) on such enhancement. Methods. The authors studied the early ipsilateral component R1 and the late component R2 of the blink reflex (BR), jaw jerk, masseter silent period (MSP), and auditory startle response (ASR) in 9 SCI patients without baclofen and in 8 with CITB. Nine healthy volunteers served as controls. Results. The amplitude of R1 of BR was significantly smaller in patients with CITB than in the other groups. The area of R2 of BR and of the ASR recorded in the orbicularis oculi, sternocleidomastoid, and biceps brachii muscles were significantly larger in SCI patien...
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Effect of the inhibitory phenomenon following magnetic stimulation of cortex on Brainstem motor neuron excitability and on the cortical control of Brainstem Reflexes
Muscle & nerve, 1993Co-Authors: A. Arturo Leis, Markus Kofler, Dobrivoje S. Stokic, Gert J. GrubwieserAbstract:We studied the effect of the inhibitory phenomenon following transcranial magnetic stimulation (TMS) on Brainstem motor neuron excitability and on the cortical control of Brainstem Reflexes in 5 normal subjects. The R1 component of the blink reflex assessed excitability of the facial nucleus during the period of post-TMS inhibition (experiment 1). TMS effect on the cortical control of Brainstem Reflexes was assessed by delivery of a stimulus that was less than or equal to the threshold for the R1 with the subject relaxed, yet elicited a potentiated reflex during maneuvers requiring cortical input (i.e., voluntary eye-closure and anticipation, experiment 2). In experiment 1, a suprathreshold electric stimulus applied during post-TMS inhibition elicited an R1 response that was preserved in amplitude (mean 476 ± 44 μV; 123%) compared to control responses not preceded by TMS (mean 386 ± 31 μV). Conversely, in experiment 2, when the R1 was dependent on cortical drive, the mean R1 amplitude during post-TMS inhibition was only 15% (P < 0.01) and 8% (P < 0.01) of control values obtained during eye-closure and anticipation, respectively. These findings imply that the inhibition following TMS originates rostral to the facial nucleus, at a cortical level. © 1993 John Wiley & Sons, Inc.
Hatice Kumru - One of the best experts on this subject based on the ideXlab platform.
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jendrassik maneuver effect on spinal and Brainstem Reflexes
Experimental Brain Research, 2019Co-Authors: Lale A Ertuglu, Hatice Kumru, Josep Vallssole, Asli Aydin, Eloy Opisso, Serpil Cecen, Kemal S TurkerAbstract:The effect of Jendrassik Maneuver (JM) has been extensively studied on monosynaptic Reflexes in numerous muscles below the level at which the maneuver was performed. Here we hypothesize that the effect of JM could be observed also on other Reflexes, indicating a widespread influence of performing a motor act such as the JM. We examined polysynaptic Reflexes caudal (i.e., the withdrawal reflex of the lower extremities) and rostral (i.e., the blink reflex to supraorbital nerve stimulation) to the level of JM contraction. We have assessed soleus tendon (T) reflex; withdrawal reflex in tibialis anterior and soleus muscle; blink reflex (BR), blink reflex excitability recovery curve (BR-ER) and prepulse inhibition of the blink reflex. Our results showed that (1) T-reflex amplitude increased during JM and decreased just after and 15 min after JM; (2) no change in the withdrawal reflex; (3) R2 area of BR reduced significantly just after or 15 min after JM; (4) Prepulse inhibition in BR reduced significantly during JM; (5) no change in BR-ER. Our results indicate that JM leads to generalized effects on neural excitability at both caudal and rostral levels. Furthermore, JM has a selective effect on excitability of reflex circuitries.
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effect of spinal cord injury and of intrathecal baclofen on Brainstem Reflexes
Clinical Neurophysiology, 2012Co-Authors: Hatice Kumru, Markus KoflerAbstract:Reorganization of neural circuits within the central nervous system following injury appears to be a means of compensatory mechanism for loss of function. Reorganization following spinal cord injury is known to evoke changes at the cortical and spinal cord levels. Recent studies, however, provide evidence of enhanced Brainstem Reflexes and alterations in excitatory and inhibitory interneuronal Brainstem circuits, suggesting that reorganization following spinal cord injury occurs also at the Brainstem level. Reversal of these changes by continuous intrathecal baclofen infusion to normal levels or beyond indicates strong GABAergic involvement. Rapid changes in the blink reflex and its prepulse inhibition following intrathecal baclofen bolus application that parallel clinical changes in muscle hypertonia suggest a muscle tone regulating effect of baclofen at the Brainstem level. Enhanced Brainstem Reflexes in spinal cord injury patients may be the consequence of decreased GABA-mediated inhibition and/or strengthening of facilitatory connections due to either direct or indirect plastic changes occurring at the Brainstem level. Modulation of Brainstem Reflexes by baclofen may foster the understanding of pathophysiological mechanisms underlying diseases with increased Brainstem activity. Rehabilitation after central nervous system injury will always be a challenge, but understanding the mechanisms of reorganization of undamaged neural pathways may help to develop better strategies for enhancing neuronal plasticity and for implementing neuronal reorganization into carefully planned therapy.
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Brainstem Reflexes are enhanced following severe spinal cord injury and reduced by continuous intrathecal baclofen
Neurorehabilitation and Neural Repair, 2009Co-Authors: Hatice Kumru, Markus Kofler, Josep Vallssole, Enric Portell, Joan VidalAbstract:Objective. Plastic changes in the human central nervous system can occur at multiple levels, including circuits rostral to the lesion level in spinal cord injury (SCI). GABA is the most important inhibitory neurotransmitter in the brain. The authors hypothesized that one of the consequences of plasticity in SCI patients could be enhancement of Brainstem Reflexes, and they investigated the effect of continuous intrathecal baclofen (CITB) on such enhancement. Methods. The authors studied the early ipsilateral component R1 and the late component R2 of the blink reflex (BR), jaw jerk, masseter silent period (MSP), and auditory startle response (ASR) in 9 SCI patients without baclofen and in 8 with CITB. Nine healthy volunteers served as controls. Results. The amplitude of R1 of BR was significantly smaller in patients with CITB than in the other groups. The area of R2 of BR and of the ASR recorded in the orbicularis oculi, sternocleidomastoid, and biceps brachii muscles were significantly larger in SCI patien...
J. P. Cardinaud - One of the best experts on this subject based on the ideXlab platform.
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Fulminant Guillain-Barré syndrome mimicking cerebral death: case report and literature review.
Intensive care medicine, 2000Co-Authors: Frédéric Vargas, Gilles Hilbert, Didier Gruson, Ruddy Valentino, G Gbikpi-benissan, J. P. CardinaudAbstract:A 45-year-old woman was admitted to the intensive care unit (ICU) for respiratory arrest. One day prior to admission, she had been nauseated and in a state of total exhaustion. On the night of admission she was unresponsive and developed gasping respiration. The patient was comatose with absent Brainstem Reflexes and appeared brain dead. Blood chemistry findings and brain magnetic resonance imaging were normal. Electroencephalogram revealed an alpha rhythmical activity unresponsive to painful or visual stimuli. The cerebrospinal fluid showed an albuminocytological dissociation. Guillain-Barre syndrome (GBS) was suspected. The electrophysiological evaluation revealed an inexcitability of all nerves. The pathological findings of the sural nerve biopsy indicated an axonal degeneration secondary to severe demyelination. GBS can very rarely present with coma and absent Brainstem Reflexes. This case illustrates the importance of electrophysiological tests and laboratory and imaging studies in patients with suspected brain death where a cause is not clearly determined.
Joan Vidal - One of the best experts on this subject based on the ideXlab platform.
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Brainstem Reflexes are enhanced following severe spinal cord injury and reduced by continuous intrathecal baclofen
Neurorehabilitation and Neural Repair, 2009Co-Authors: Hatice Kumru, Markus Kofler, Josep Vallssole, Enric Portell, Joan VidalAbstract:Objective. Plastic changes in the human central nervous system can occur at multiple levels, including circuits rostral to the lesion level in spinal cord injury (SCI). GABA is the most important inhibitory neurotransmitter in the brain. The authors hypothesized that one of the consequences of plasticity in SCI patients could be enhancement of Brainstem Reflexes, and they investigated the effect of continuous intrathecal baclofen (CITB) on such enhancement. Methods. The authors studied the early ipsilateral component R1 and the late component R2 of the blink reflex (BR), jaw jerk, masseter silent period (MSP), and auditory startle response (ASR) in 9 SCI patients without baclofen and in 8 with CITB. Nine healthy volunteers served as controls. Results. The amplitude of R1 of BR was significantly smaller in patients with CITB than in the other groups. The area of R2 of BR and of the ASR recorded in the orbicularis oculi, sternocleidomastoid, and biceps brachii muscles were significantly larger in SCI patien...