Researchers at the Paris Brain Institute have conducted a groundbreaking study of the processes that occur in the brain during the transition from life to death, focusing particularly on a phenomenon called the “death wave.” The study, published in the journal Neurobiology of diseasesreveals that permanent cessation of brain activity involves a dramatic wave of neuronal depolarization, which could potentially inform interventions for acute brain injury and cardiorespiratory arrest.
Understanding the brain’s response to severe oxygen deprivation has long been the subject of intense research, primarily because of its implications in treating diseases such as stroke, cardiac arrest, and other forms of injury. cerebral. Previous research has found that as the brain approaches death, it not only shuts down but undergoes a series of complex biochemical and electrical changes.
This process includes an abrupt cessation of oxygen supply, leading to rapid depletion of adenosine triphosphate (ATP), the cell’s primary energy source. This energy crisis triggers a cascade of neurological events, starting with a breakdown in the brain’s electrical balance and a massive release of glutamate, a neurotransmitter that exacerbates neuronal damage.
Previous studies have also observed a mysterious increase in brain activity after the initial shutdown, including an increase in specific brain wave frequencies such as gamma and beta waves, which are typically associated with consciousness. This increase could possibly be linked to near-death experiences reported by cardiac arrest survivors. These intriguing observations highlighted the complexity of defining brain death and managing recovery after brain injury.
However, despite this progress, critical gaps remain. In particular, the precise origins and propagation patterns of the terminal wave of neuronal depolarization – called the “death wave” – remain unclear. While previous research indicated that this wave could potentially be reversed if intervention took place quickly, the specific areas of the brain most likely to suffer lasting damage during this process were not well defined.
In their new study, the researchers conducted experiments on rats in a highly controlled setup to simulate the conditions of anoxia and subsequent reoxygenation. This was achieved by adjusting the rats’ oxygen levels and monitoring several physiological parameters such as heart rate and brain electrical activity.
The researchers found that initially, when the brain enters a state of anoxia, there is a homogeneous level of neuronal activity in different cortical layers. However, a critical transition occurs with the emergence of the “death wave,” beginning primarily with pyramidal neurons in layer 5 of the neocortex, one of six layers that make up the cerebral cortex of the brain.
“This critical event, called anoxic depolarization, induces neuronal death throughout the cortex. Like a swan song, it is the real marker of transition towards the cessation of all brain activity,” explains Antoine Carton-Leclercq, doctoral student and first author of the study.
This wave propagates bidirectionally: upwards towards the surface of the brain and downwards into deeper areas of the white matter. This discovery is crucial because it identifies the origin of the wave in a specific type of neuron in a specific location in the brain, which was not previously understood.
“We noticed that neuronal activity was relatively homogeneous at the beginning of cerebral anoxia. Then, the death wave appeared in the pyramidal neurons located in layer 5 of the neocortex and propagated in two directions: upward, i.e. the surface of the brain, and downward, i.e. i.e. white matter,” said co-author Séverine Mahon, a neuroscience researcher. “We observed this same dynamic in different experimental conditions and think it could exist in humans.”
This pattern of spread suggests a structured vulnerability within cortical layers, with deeper layers showing greater susceptibility to oxygen deprivation. This vulnerability is likely related to the high metabolic demands of layer 5 pyramidal neurons, which require more energy to function and are therefore more susceptible to damage when energy stores (ATP) are low.
The researchers also noted that this neuronal activity ultimately led to a state of perfect electrical silence, indicating a cessation of all detectable brain activity, which was briefly interrupted by the death wave – a critical marker of an irreversible cessation of functions cerebral.
In addition, research has highlighted the potential reversibility of this catastrophic wave under specific conditions. When the researchers reintroduced oxygen to the brain shortly after detecting the wave of anoxic depolarization, they observed a replenishment of ATP levels, leading to repolarization of neurons and restoration of synaptic activity. .
This finding is particularly crucial because it suggests that rapid medical intervention could potentially restore brain function in humans following similar episodes of oxygen deprivation, such as during cardiac or respiratory arrest.
However, in a few cases (3 out of 49), the resuscitation process did not result in the restoration of normal brain activity. In these cases, the lack of recovery of brain activity quickly led to cardiac arrest. This suggests that there is a critical window during which oxygen must be restored to ensure recovery; If resuscitation occurs too late or is ineffective, the electrical disturbances in the brain caused by the initial lack of oxygen can become irreversible, leading to the failure of other vital systems, such as the heart.
“This new study advances our understanding of the neural mechanisms underlying changes in brain activity as death approaches. It is now established that, from a physiological point of view, death is a process that takes its time… and that it is currently impossible to rigorously dissociate it from life. We also know that a flat EEG does not necessarily mean the definitive cessation of brain functions,” concluded Stéphane Charpier, head of the research team. “We now need to establish the exact conditions under which these functions can be restored and develop neuroprotective drugs to support resuscitation in heart and lung failure. »
The study entitled “Laminar organization of neocortical activities during systemic anoxia” was written by Antoine Carton-Leclercq, Sofia Carrion-Falgarona, Paul Baudin, Pierre Lemaire, Sarah Lecas, Thomas Topilko, Stéphane Charpier and Séverine Mahon.
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