Concussion and traumatic brain injury

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Introduction0:00–0:37

When an external force strikes the head with enough energy to cause damage, it's called head trauma. However, if a head trauma temporarily or permanently disrupts brain function, it's known as a traumatic brain injury.
Now while riding a roller coaster, twisting, turning, and dropping at full speed, your brain is right there with you. But despite all that motion, the brain stays remarkably safe, thanks to multiple layers of protection.
First, the skull acts as a solid helmet, and beneath it we have three protective layers called the meninges. The outer layer is the dura mater.

Physiology0:37–2:29

The middle layer is the arachnoid mater, and the innermost layer is the pia mater. Between the arachnoid and pia mater lies the subarachnoid space filled with a clear, watery liquid called cerebrospinal fluid.
Think of this fluid as a built-in shock absorber that protects the brain and spinal cord from bumps and jolts. Beneath the meninges lies the brain.
The brain is made up of neurons, each dendrites look like tiny tree branches and receive signals from other neurons. The soma or cell body, contains the nucleus and organelles such as mitochondria.
The axon, which is a long single extension, carries signals away from the neuron to other cells. Inside the neuron, microtubules stabilized by tau protein provide structural support and serve as tracts that transport proteins and organelles throughout the cell and along the axon.
For example, when a neuron synthesizes neurotransmitters like glutamate, It packages them into vesicles and transports them to the axon terminals.
Upon activation, the neuron releases glutamate, which binds to ligandgated calcium channels called NMDA receptors on the dendrites of the next neuron.
Activated NMDA receptors allow calcium to enter the neuron, which triggers the opening of sodium channels, enabling sodium to rush in.
This influx of calcium and sodium ions depolarizes the neuron, causing it to fire in action potential. Traumatic brain injury occurs when an external force to the head temporarily or permanently disrupts brain function.

Causes2:29–3:56

This injury can come from blunt impacts like getting hit with a baseball bat, penetrating injuries like gunshots, or blast waves from explosions.
It can also occur from accelerating decelerating forces, which are common in motor vehicle crashes. Depending on whether the injury affects just one part or widespread areas of the brain.
These injuries are classified as focal or diffuse traumatic brain injuries. First, let's focus on focal traumatic brain injuries, such as brain contusions and intracranial bleeding.
Contusions are basically bruises on the brain, which occur when the head hits a solid object, causing the brain to be jolted inside the skull.
If the brain slams into the skull right where the head was struck, that's called a coup injury. If the impact is strong enough to make the brain bounce back and hit the opposite side of the skull, that's called a contracoup injury.
These injuries usually affect the temporal lobes in the inferior surface of the frontal lobes. When a contusion happens, small blood vessels break, allowing red blood cells and fluid to leak into the brain tissue, causing local bleeding and edema.

Pathology3:56–5:54

As the red blood cells start to breakdown, they release hemoglobin, creating a bit of a mess. That's when macrophages step in to clean things up, clearing out the leftover red blood cells and hemoglobin.
Inside the macrophages, hemoglobin gets broken down into a yellowish brown pigment called hemosiderin. Over time, hemosiderin can accumulate, leaving behind yellowish brown patches on the ridges of the gyri called plaque june.
Depending on the severity and location of the injury, contusions can cause symptoms ranging from headaches to complete loss of consciousness.
But head injuries don't always directly damage brain tissue. In some cases they can cause intracranial bleeding.
With epidural hematoma, a blow to the temporal region can cause a fracture near the teron that tears the middle meningeal artery, causing blood to pool between the skull and the dura mater.
Next, subdural hematomas occur when rapid head movements like in whiplash or violent shaking rupture small bridging veins, causing blood to accumulate between the dura mater and the arachnoid mater.
In subarachnoid hemorrhages, blood accumulates between the arachnoid and pia mater, often causing a sudden intense headache described as the worst headache of someone's life.
Finally, intracerebral hemorrhage occurs when trauma tears vessels deep in the brain parenchyma, causing blood to pool within the brain.
Moving on to diffuse brain injuries, which affect widespread areas of the brain and include concussions and diffuse axonal injury.

Symptoms5:54–6:12

Concussions, also known as mild traumatic brain injuries, usually occur when a sudden hit or jolt to the head causes the brain to move rapidly inside the skull, such as during football tackles.

Diagnosis6:12–6:25

This mechanical force stretches axons, causing diffuse axonal injury and disrupting their membranes. As a result, potassium leaks out, while sodium and calcium rush in, causing neuronal depolarization.

Treatment6:25–6:33

This triggers a massive wave of action potentials. And widespread release of glutamate, which binds to NMDA receptors, allowing even more calcium to enter neurons.

Review6:33–12:11

High intracellular calcium activates enzymes that damage cell membranes and mitochondria, which is a process known as excitotoxicity.
This widespread neuronal firing increases the brain's metabolic demand for glucose and energy. However, in concussion, there is a paradoxical drop in cerebral blood flow, which starves neurons of energy and worsens the injury.
This results in temporary disruption of brain function and symptoms such as confusion, memory loss, and in some cases, loss of consciousness.
Most people recover within about 2 weeks. However, in some cases, headaches, dizziness, Cognitive difficulties and sleep disturbances can persist for weeks or months after a concussion.
These findings are suggestive of post-concussion syndrome. Chronic traumatic encephalopathy can occur with repeated head trauma, with recurrent concussions and axonal injuries, such as that seen in boxers.
A key feature of chronic traumatic encephalopathy is abnormal hyperphosphorylation of tau protein, which causes it to detach from microtubules and aggregate into neurofibrillary tangles.
These tangles typically accumulate in the depths of the cortical sulci and around blood vessels in the frontal and temporal lobes.
This disrupts neuronal communication, leading to brain atrophy, ventricular enlargement, and progressive dementia. Next, diffuse axonal injury or DAI results from severe acceleration deceleration forces, or rotational injuries that cause widespread shearing of axons throughout the brain's white matter.
This shearing damages the axonal cytoskeleton, disrupting axonal transport and causing the axon to swell. If the injury is severe enough, the axon snaps into two pieces.
Once the axon breaks down, the part of the axon attached to the soma retracts, forming a round, swollen end called an axonal retraction ball.
The widespread axonal disruption primarily affects the corpus callosum, internal capsule, and brain stem. And results in severe neurological manifestations such as loss of consciousness and even coma.
All focal and diffuse brain injuries fall under the primary phase of injury, meaning they occur at the moment of trauma.
However, in some cases, a secondary phase of injury sets in, where damage continues to unfold over days, weeks, or even months.
First, mitochondrial dysfunction causes impaired cellular energy metabolism and oxidative stress, which can ultimately trigger programmed cell death or apoptosis.
Next, axonal damage leads to swelling and demyelination, disrupting communication between neurons. Meanwhile, the body activates glial cells called astrocytes to contain injury and clear debris, however, these cells form glial scars that act like roadblocks, impairing signaling long after the injury.
Secondary injury can also cause cerebral edema and increased intracranial pressure, further damaging brain tissue. Together, these processes contribute to long-term neurological deficits such as seizures, cognitive decline, and motor impairment, as well as behavioral changes, including agitation, emotional lability, and impulsivity.
Diagnosis of traumatic brain injury involves a thorough neurological exam to assess consciousness and neurological function, as well as imaging such as CT or MRI to detect structural brain damage, swelling, and intracranial bleeding.
Finally, treatment focuses on preventing further brain injury. And stabilizing vital functions by managing intracranial pressure and ensuring adequate oxygen and blood flow.
All right, as a quick recap, Traumatic brain injury occurs when an external force to the head temporarily or permanently disrupts brain function.
These injuries are classified as focal, such as contusions and intracranial bleeding, and diffuse like concussions and diffuse axonal injury.
While the primary injury happens at the moment of impact, a secondary phase can unfold over days to months, leading to long-term complications such as seizures, cognitive decline, motor impairment, and behavioral changes.