When a blow to the head is more than "a moment of dizziness"

A fall down the stairs. A car or bicycle accident. Two heads colliding hard during a football match. A knee to the head (see the incident with Dutch player Summerville during the 2026 World Cup), a hard tackle, or a kick to the skull. Often, the person gets up again afterwards. Sometimes, nothing unusual appears to be visible on a CT scan or MRI. And yet, at that very moment, deep within the brain, a complex neurophysiological reaction may have developed that is not visible to the naked eye.

That is precisely where a major problem lies. Concussions or mild traumatic brain injury (mTBI) are still frequently underestimated or trivialized. The message is often: "Just rest for a few days, and it will go away on its own." Fortunately, for many people, that is true. But for a significant group of patients, recovery proceeds very differently. They continue to struggle for weeks, months, or even years with concentration problems, dizziness, hypersensitivity to light and sound, memory impairments, fatigue, headaches, balance problems, and severely reduced physical capacity.

When someone returns to work too soon, engages in intensive sports, or receives insufficient recovery time, there is a risk that the vulnerable brain will be stressed again while the underlying neurobiological processes are still in full swing. As a result, symptoms may persist or even worsen. Not infrequently, this leads to long-term absence from work, loss of sports careers, or severe limitations in daily life. The societal and personal consequences are often enormous, while the original impact was sometimes labeled as "mild."

Modern neuroscience shows that a brain trauma is much more than just a "blow to the head." Within milliseconds, mechanical changes occur in nerve cells, followed by disruptions in energy supply, metabolism, communication between brain cells, and ultimately, inflammatory processes. This sequence of events—the so-called neurometabolic cascade—explains why someone may feel relatively well immediately after a trauma, while the brain is actually in an extremely vulnerable biological state.

In the explanation below, we take you step by step through what actually happens from the very first millisecond following a direct impact on the brain. Not to create anxiety, but to provide insight into why adequate recovery, proper guidance, and a careful assessment are so important. Understanding what happens in the brain is the first step towards responsible recovery and preventing long-term symptoms.

Direct impact on the brain

At the moment of a direct impact on the front of the brain, the first event is not "inflammation," but mechanical deformation of the nerve tissue.

0-10 milliseconds: biomechanical phase

The impact on the forehead causes rapid acceleration-deceleration and rotational shear force. The frontal cortex, orbitofrontal areas, the corpus callosum, and the subcortical white matter experience tension. Axons stretch, membranes deform, and mechanosensitive ion channels open.

Seconds: membrane and ion phase

Neuronal membranes become temporarily unstable. There is potassium outflow, sodium and calcium inflow, and excessive release of glutamate. This causes acute neuronal depolarization and excitotoxic pressure. The Na⁺/K⁺-ATPase subsequently requires a high ATP concentration to restore ion balance, causing an immediate energy crisis. This is crucial for the "neurometabolic cascade" of a concussion.

Minutes: mitochondrial redox phase

Calcium enters the mitochondria, reducing the efficiency of oxidative phosphorylation. ATP production drops, while the amount of reactive oxygen species increases. This links impact biomechanics to mitochondrial dysfunction, oxidative stress, lipid peroxidation, and impaired cell repair.

Minutes-hours: axonal/cytoskeletal phase

Axonal stretching disrupts microtubules and neurofilaments. Transport along the axon becomes disrupted. This can lead to the release of markers such as NfL, GFAP, S100B, or tau-related proteins, especially with repeated impacts. Recent data on headers in football suggest that even a subconcussive header can temporarily alter blood markers associated with brain injury, although the clinical significance depends on the dose, the repetition, and the recovery time.

Hours: neurovascular and inflammatory phase

Astrocytes, microglia, and endothelial cells respond. Blood-brain barrier permeability may increase, neurovascular coupling may be disrupted, and cytokine signaling may be initiated. In frontal impacts, the orbitofrontal and juxtacortical white matter regions may be particularly vulnerable to repeated head movements.

In short: a frontal impact first causes mechanical deformation of the membrane and axons, which immediately leads to ion imbalance, glutamate release, ATP crisis, mitochondrial calcium overload, oxidative stress, cytoskeletal disruption, and early neuroinflammatory signaling.