One Last Goodbye- Understanding Death Rally

A miracle. A return to normalcy. A wonder without warning.

Death rally -also known as terminal lucidity- is the “boost” mentally ill patients have right before death, where they speak with joy and strength that makes them seem almost “cured.” Although it has been reported for a long time, scientists of today still find it hard to explain what exactly is going on.

There are two hypotheses that try to explain terminal lucidity.

1. One possible explanation is the existence of reversible neural mechanisms in the brain.

2. Another possible explanation is neural compensation: the event where certain parts of the brain “take over” for neighboring parts that are not doing so well.

1 - Reversible neural mechanisms

Patients who experience terminal lucidity just as they are about to die usually suffer from some sort of dementia, or forgetting. One of the most common forms is Alzheimer’s Disease, which is caused by too many proteins in important parts of the brain. This type of dementia, along with others, is called a neurodegenerative disorder, which means the symptoms will get worse over time and will cause irreversible damage. These diseases usually have no cure.

“Dementia causes irreversible brain damage.” Or so we thought.

After a lot of research has been done, scientists are now thinking maybe the “irreversible” word is a little too strict. There are so many case studies where dementia patients miraculously seem to recover right before dying; they can remember their lives in full even if their amnesia made them forget the last 10 or more years of their lives. Now, researchers are suggesting some neurodegenerative diseases like dementia may have a little caveat in them, where memories are not deleted, but just stored somewhere else in the brain where it’s harder to get at.

Here are some examples from research studies that have been done:

In mice whose genes have been changed so that they include the protein that causes Alzheimer’s Disease, injections of a certain kind of antibody (anti-Aβ) make it so dementia goes away.

Memory in this case is measured in spatial memory, or when a mouse runs around in a cage and remembers the way to the exit, because, well, mice can’t exactly talk and tell you what they remember from a few days ago. The same thing happens with another kind of dementia called frontotemporal dementia (FTD).

There are mice whose genes have been altered to include the protein that causes memory failures and brain changes like what a human with FTD would experience. When researchers made it so that gene in these mice was “switched off,” the mice were able to find their way out of the maze, showing their memory is still pretty good. With these examples in animals, researchers think “irreversible” is probably too strong a word to describe neurodegenerative diseases, and that “dysfunctional” is probably a better fit.

2 - Neural compensation / neuroplasticity

Neuronal plasticity is basically how our brains can change as we grow. This is heavily affected by environment. The process where this happens is called long-term potentiation, which is when synapses (the junctions where two brain cells meet and “talk” to each other) get stronger through repeated use or even when new brain cells form. Plasticity can let a human deal surprisingly well even when they are missing large parts of their brain.

So how is knowing that relevant to our discussion of terminal lucidity?

Well, the strongest argument for how plasticity can explain terminal lucidity comes from compensation. The compensation theory is the idea that different regions of the brain “assist” damaged or otherwise dysfunctional parts.

For example, a healthy patient’s brain has two areas that are important for language- one for understanding the words they hear and one for actually speaking words. In a patient with a neurodegenerative disease, the part of the brain that is responsible for understanding words may be turned “offline.” If this patient goes through plasticity the right way, the part of the brain for speaking the words will jump in and help out the “offline” area. Theoretically, this patient will be able to understand and speak words just fine, even though the “understanding language” part of the brain technically isn’t working. 

There are plenty of studies that test and support this hypothesis. In order to break down one of those influential studies, we should know the basics of the brain first. When we think of the brain, most people will think of a fleshy gray organ with empty space. The fleshy part is called “gray matter” and these are the actual physical structures of the brain; while the empty space is actually not empty at all and it is called “white matter,” which is made of the connections between brain cells (these connections let one brain cell “talk” to a neighboring brain cell). 

The smaller the volumes of brain “flesh” (so gray matter) in regions that were considered important for performance on a certain task, the stronger the activation of additional networks in regions that were not considered important (Ji et al, 2018). Simply put, when a part of the brain that is thought to be important for a certain task (for example the hippocampus for a memory task) is smaller, other parts of the brain (in our hypothetical example perhaps the amygdala) will activate to help the weaker region.

This is a measure of neural compensation since networks that were not usually important to a task “pitched in to help” when the brain structure that was originally supposed to be managing the task couldn’t handle its “job.” The researchers in this study found that the patients who had higher compensation measures had higher memory performance.

This finding implies compensation could help memory, so terminal lucidity patients who compensated for their failing brain regions might be able to suddenly remember correctly after the plasticity happened, just before passing on.

So…

The theories of reversible neural mechanisms and neural compensation help us better understand how a death rally happens. This knowledge can provide closure for patients’ families, and also serve as a “launching pad” for future research.

— Allie Yuxin Lin