Explaining the Brain: White Matter & Gray Matter

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Andrea is about two seconds from injuring her brain, and she doesn't know it yet.

She's stopped at a red light, mentally rehearsing her grocery list, when a distracted driver slams into her car from behind. The airbags deploy. Her head whips backward, then forward. In those milliseconds, her brain, suspended inside her skull, does the same thing.

Now, this imagery isn't pretty, but it'll get my point across: Imagine a bowl of Jello. Pick it up. Shake it violently back and forth. What happens to the Jello inside the bowl? It jiggles. It distorts. It slams against the sides.

Andrea's brain is the Jello.

Yeah. Ouch.

Gray Matter and White Matter

Before we talk about what happens to Andrea's brain, we need to understand what her brain is made of. Two things (mostly*): Gray matter and white matter.

Think of gray matter as the brain's processor: The part that does the thinking, the deciding, the feeling. It's made of densely packed cell bodies, the command centers of brain cells[1]. Gray matter lives mostly on the outer surface of the brain, in a wrinkly layer called the cortex.

White matter is the wiring. It's made of axons, the long, cable-like extensions of brain cells. White matter connects different parts of the brain so they can talk to each other[2]. It's the reason your visual cortex can tell your motor cortex to slam on the brakes when you see a red light.

When Andrea's head whips back and forth, both gray matter and white matter take a beating. But poor white matter, white matter is where the real damage happens.

*More brain parts coming up in future lessons. Stick around.

What Happens Seconds After Impact

When Andrea's brain slams against the inside of her skull, two things happen almost immediately.

First, her brain gets hit twice, not just once[3]. Her brain hits the front of her skull, then bounces backward and hits the back of her skull. Imagine throwing a bouncy ball at a wall, bounces back at you, right? Neurons in those impact zones get crushed, bruised, and torn.

There is a hidden third injury: The shaking doesn't just bruise the surface (gray matter). It stretches and shears the white matter deep inside the brain[4]. Those long, delicate axons (the brain's communication wiring) get twisted and torn. This is called diffuse axonal injury, and it's one of the most common and devastating consequences of traumatic brain injury[5].

Within seconds, those torn axons start leaking. Potassium floods out. Calcium floods in. The neuron's internal chemistry goes haywire[6]. The cell tries desperately to restore balance, burning through energy reserves. Meanwhile, the insulation around axons is torn and begins to break down, further disrupting communication between brain regions[7].

And here's the kicker: Much of this damage is invisible on a standard CT scan. The brain looks fine. But functionally? Parts of Andrea's brain have just been disconnected in the worst possible way.

The Neurological Cascade: Minutes After the Crash

In the minutes after Andrea's car comes to a stop, her brain is waging a microscopic war. Damaged neurons release a flood of glutamate[8]. In normal amounts, glutamate is fine. In excess, it's toxic. It overexcites neighboring neurons, triggering a chain reaction of cellular stress. This is called excitotoxicity, and it can kill neurons that weren't even directly injured in the crash[9].

Meanwhile, inflammation kicks in. The brain's immune cells, microglia, swarm to the site of injury, trying to clean up the damage[10]. Normally, this is helpful. But in traumatic brain injury, inflammation can spiral out of control, causing more harm. It's like calling in a cleanup crew that accidentally bulldozes the whole neighborhood.

And Andrea? She's still sitting in her car, dazed, wondering why the world feels fuzzy and far away.

Explaining the Brain, White Matter, & Gray Matter, to Your Patients

Brain Bite Takeaway: Brain injury doesn't stop at impact. The initial neurological cascade continues for hours to days after the initial trauma[11]. This is why patients like Andrea might seem "fine" in the ER, then deteriorate days later. The brain is still injuring itself.

Because so much of the damage happens in white matter patients often struggle with things that don't fit neatly into a diagnosis. They're slow to process information. They can't multitask. They get overwhelmed in noisy environments. Their brain's communication network has been disrupted, even if the processors themselves are mostly intact.

Understanding this cascade is the first step in communicating why brain injury survivors need follow-up and targeted rehabilitation. We encourage you and your colleagues to avoid saying: "You'll be fine in a few weeks," and encourage you to consider: "I'd like to see you back in a few weeks to check on your progress. In the meantime, let's get you connected with brain injury resources."

Andrea's brain is trying to heal itself. Our job is to give it the best possible environment to do so.

Thank you for reading Explaining Brains: White Matter & Gray Matter edition. Please connect your clients to brain injury specialists who help with the next stages of rehabilitation. We are happy to build a local referral list for your specific clinic or practice. Contact our clinic director at Hollis@Braininjurytherapy.org to start the conversation.

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References:

[1] Herculano-Houzel, S. (2009). The human brain in numbers. Frontiers in Human Neuroscience, 3, 31.

[2] Fields, R. D. (2008). White matter in learning, cognition and psychiatric disorders. Trends in Neurosciences, 31(7), 361-370.

[3] Bayly, P. V., et al. (2005). Deformation of the human brain induced by mild acceleration. Journal of Neurotrauma, 22(8), 845-856.

[4] Smith, D. H., et al. (2013). Diffuse axonal injury in head trauma. Journal of Head Trauma Rehabilitation, 18(4), 307-316.

[5] Blumbergs, P. C., et al. (1994). Diffuse axonal injury in head trauma. Journal of Neurology, Neurosurgery & Psychiatry, 57(11), 1342-1345.

[6] Xiong, Y., et al. (2013). Animal models of traumatic brain injury. Nature Reviews Neuroscience, 14(2), 128-142.

[7] Büki, A., & Povlishock, J. T. (2006). All roads lead to disconnection? Traumatic axonal injury revisited. Acta Neurochirurgica, 148(2), 181-194.

[8] Faden, A. I., et al. (1989). The role of excitatory amino acids and NMDA receptors in traumatic brain injury. Science, 244(4906), 798-800.

[9] Choi, D. W. (1988). Glutamate neurotoxicity and diseases of the nervous system. Neuron, 1(8), 623-634.

[10] Simon, D. W., et al. (2017). The far-reaching scope of neuroinflammation after traumatic brain injury. Nature Reviews Neurology, 13(3), 171-191.

[11] Werner, C., & Engelhard, K. (2007). Pathophysiology of traumatic brain injury. British Journal of Anaesthesia, 99(1), 4-9.