The neurometabolic cascade of an injured brain explains why rest after concussion is critical for recovery

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Mild traumatic brain injury (mTBI), more commonly known as concussion, initiates a series of events that occur on the cellular level. These cellular events, referred to in the literature as the neurometabolic cascade of concussion, are responsible for immediate symptoms following concussion. Understanding the neurometabolic cascade is key to shaping recommendations for treatment and recovery.

What happens during a concussion?

The term “concussion” refers to traumatic head injuries that cause no obvious changes to the structure of the brain. We typically think of a direct head impact as a requirement for, or even the definition of a concussion. However, the high-energy head and neck movements that occur during a head injury are thought to be more damaging to the brain than focal impact. Such motion of the head and neck causes the brain to move back and forth and side-to-side within the skull, which results in shearing, or tearing, of the neurons and connective fibers that make up brain tissue.

The energy crisis

Neurons, or brain cells, must maintain a balance of charged particles, or ions, in order to function properly. The outer layer of the cell, the cell membrane, must be physically intact to maintain the right balance of ions inside the cell. Shearing of brain tissue, which can occur as a result of concussion, compromises the structure of cell membrane, allowing ions to diffuse in and out in an unregulated manner. Because neurons use ions to communicate with their neighbors, the change in ionic equilibrium of a single cell spreads to neighboring cells. In response, the cells use a massive amount of energy to try to reestablish ionic equilibrium, resulting in an energy deficit in the brain. This energy deficit typically causes the feeling of fatigue and fogginess that many people report after a concussion.

Like other cells in the body, neurons break down glucose to generate energy, a process which requires oxygen. The oxygen that is required for glucose metabolism is supplied by blood. Under normal circumstances, blood is supplied to the brain in proportion to its need: blood flow to the brain is greater when the brain is working hard. During a concussion, the blood vessels that supply blood to the brain become more narrow, which decreases blood flow. As a result, though the brain is working in overdrive to restore its ionic equilibrium, it does not receive the resources it needs to do so. Damage to parts of the brain that are responsible for generating cellular energy can also contribute to brain energy deficits in the aftermath of a concussion.

Why is rest so important?

Research suggests that recovery from a concussion requires a period of physical rest, as well as a period of cognitive rest. Studies indicate that a recently concussed brain is at a higher risk of subsequent concussion, due in part to the energy crisis as well as to the physical damage that the neurons have sustained. Researchers who used brain imaging techniques to measure changes in brain function and structure for 10 days after a concussion found that brain structure is compromised and function is diminished during this time period. Physical rest is important to reduce the chance of repeatedly injuring the brain while it is in a heightened state of vulnerability.

Equally important is allowing the brain a period of cognitive rest. The energy crisis is not short-lived: blood flow to the brain is reduced for about 7-10 days following concussion. During this time, all of the brain’s limited resources are required to repair the damage caused by the injury that was sustained. As we noted earlier, a healthy brain receives a greater blood supply when it is working hard, but increased need is not supported by increased supply after concussion. Therefore, a period of cognitive rest allows the brain to channel all of its resources into healing itself.


Churchill NW et al. The first week after concussion: blood flow, brain function and white matter microstructure. Neuroimage: Clinical. (2017).

Giza CC & Hovda DA. The neurometabolic cascade of concussion. Journal of Athletic Training. (2001).

Giza CC & Hovda DA. The new neurometabolic cascade of concussion. Neurosurgery. (2014).

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