A concussion happens when a force to your head, neck, or body causes your brain to move rapidly inside your skull, stretching and straining brain cells. The injury isn’t about bruising the brain itself. It’s about the sudden acceleration and deceleration that distorts brain tissue at a cellular level. Roughly 21 million traumatic brain injuries occur worldwide each year, and concussions make up the majority of them.
What Happens Inside Your Skull
Your brain floats in cerebrospinal fluid, a clear liquid that acts as a cushion, absorbing everyday bumps and keeping the brain from bouncing against bone. This system works well under normal conditions. But when a hit delivers enough force, the fluid can’t absorb the energy fast enough, and your brain shifts inside the skull.
Two types of movement matter most. The first is linear acceleration: a straight-line jolt, like your head hitting a car headrest in a rear-end collision. This can cause your brain to slam against the front of the skull, then rebound against the back, a pattern sometimes called coup-contrecoup. The second, and more damaging, type is rotational acceleration: a twisting or spinning motion of the head. Rotational forces create shearing strain deep inside the brain, pulling apart tissue that was never designed to twist. Research consistently shows that rotational acceleration is the dominant contributor to concussion, more so than a simple straight-line hit.
These forces don’t need to come from a direct blow to the head. A hard tackle that whips your neck, a fall that snaps your head forward, or an explosion’s shockwave can all transmit enough rotational energy to injure the brain without anything ever touching your skull.
How Impact Duration Changes the Equation
The speed of the impact matters, but so does how long the force lasts. In very short impacts (around 10 to 15 milliseconds, roughly the duration of a helmet-to-helmet collision in football), the brain and skull move at different speeds. That relative motion stretches blood vessels and bumps brain tissue against bone. In longer-duration impacts, the brain starts moving with the skull, and the damage shifts inward, creating stress and strain in deeper, central brain structures that then spread outward through the cortex.
This is why concussions can look so different from one person to the next. The same overall force can injure different parts of the brain depending on the direction, speed, and duration of the hit.
The Chemical Chain Reaction After Impact
The moment brain cells are stretched, a rapid chemical cascade begins. Strained nerve fibers release a flood of glutamate, one of the brain’s primary signaling chemicals. That glutamate triggers a massive shift of charged particles across cell membranes: potassium rushes out of cells while sodium and calcium rush in. This ionic imbalance essentially short-circuits normal brain communication, which is why symptoms like confusion, slowed thinking, and dizziness appear so quickly.
To fix this imbalance, your brain cells burn through enormous amounts of energy. The brain enters a state of hyperglycolysis, devouring glucose at a far higher rate than normal. But here’s the problem: blood flow to the brain drops by as much as 50% after a concussion (demonstrated in animal studies), choking off the oxygen and fuel supply right when the brain needs it most. When the glucose demand can’t be met, the brain shifts into an energy-depleted state. This mismatch between energy demand and energy supply is a core reason concussion symptoms can linger for days or weeks.
Damage to the Brain’s Wiring
The brain’s white matter, the long cable-like fibers that connect different regions, is especially vulnerable. These fibers (called axons) carry signals across the brain the way wires carry electricity. Rotational forces stretch and twist them, disrupting the internal transport system that keeps each fiber alive and functioning. The protective insulation around these fibers can break down, and the junctions where signals hop from one segment to the next can be damaged.
Critically, most of this damage doesn’t happen at the moment of impact. Secondary injury processes unfold over hours and days afterward, driven by inflammation, calcium buildup inside cells, and ongoing energy failure. This is why concussion symptoms sometimes appear or worsen well after the initial hit. Some symptoms show up immediately, while others emerge hours or even days later.
Hits That Don’t Cause Symptoms Still Matter
Not every concerning head impact produces noticeable symptoms. Repeated hits below the concussion threshold, sometimes called subconcussive impacts, can cause measurable changes in the brain. Studies have found that these impacts raise markers of neuroinflammation in the blood, suggesting some degree of neurological injury even when the person feels fine.
Imaging studies show that repeated exposure to these lower-level hits is associated with thinning of the brain’s outer layer, loss of brain volume, and structural damage to white matter. Over the long term, cumulative exposure to these impacts may increase the risk of neurodegenerative diseases, including chronic traumatic encephalopathy (CTE) and ALS. In professional football players, the total duration of exposure to these non-concussive hits has been a stronger predictor of CTE status and severity than the number of diagnosed concussions. This finding has shifted how researchers think about brain injury in contact sports: it may not be the big, dramatic hits that do the most long-term damage, but rather the thousands of smaller ones accumulated over a career.
How Concussions Are Identified
Concussion is a clinical diagnosis, meaning no single scan or test can confirm it. A healthcare professional evaluates the situation based on symptoms, cognitive testing, balance, eye tracking, and the circumstances of the injury. The most widely used standardized tool in sports is the SCAT6 (Sport Concussion Assessment Tool, 6th edition), which takes at least 10 to 15 minutes to administer and is designed for use within the first 72 hours after injury. Even so, a normal score on the SCAT6 does not rule out a concussion.
The assessment typically includes checking the Glasgow Coma Scale (a measure of consciousness), asking memory questions about the game or event, examining the neck for spinal injury, and testing coordination and eye movement. Certain red flags require urgent medical attention: neck pain or tenderness, seizures, double vision, loss of consciousness, vomiting, weakness or tingling in the arms or legs, a severe or worsening headache, or increasing agitation.
Why Some People Are More Vulnerable
The force needed to cause a concussion varies significantly between individuals. Research on college football players estimated a 50% probability of concussion at a peak rotational velocity of about 28 radians per second, but that’s a population average, not a universal threshold. Factors like neck strength, head size, the angle of impact, and whether the person braced for the hit all shift that number. Previous concussions also lower the threshold, making each subsequent injury easier to sustain. Children and adolescents are generally more vulnerable because their brains are still developing and their neck muscles are weaker relative to head size.
This variability is why two players can take what looks like the same hit and have completely different outcomes. The physics of concussion are consistent, but the biology of each brain is not.