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• Concussions involve violent jarring or shaking that disturbs brain function.
• They are a type of mild traumatic brain injury (mTBI) caused by a bump or blow to the head or body, leading to rapid brain movement within the skull.
• Bleeding can occur in some mTBI cases.
• They can result from brain movement within the skull, even without a direct physical blow to the head.

Epidemiology of Concussions

• Concussions can occur anywhere and anytime the head is impacted.
• The majority of concussions in children are due to sports accidents, with football being the most common, followed by hockey, soccer, and lacrosse.
• In adults or seniors, slips or falls are the main cause of concussions and TBIs.

Symptoms of a Concussion

• Physical symptoms include headache, ringing in the ears, nausea, vomiting, fatigue, drowsiness, and blurry vision.
• Cognitive symptoms involve confusion, amnesia, dizziness/seeing stars, forgetfulness, light sensitivity, and emotional disturbances.
• Amygdala-related symptoms include headache, feeling "slow" or "foggy," irritability, sadness, nervousness, increased emotionality, and loss of sleep.
• Anterior intra-parietal sulcus symptoms include light and noise sensitivity, motor control issues, and visual problems.
• Symptoms depend on the affected brain region and the location of the impact.

Causes of a Concussion

• Rapid changes in head velocity, such as acceleration/deceleration, cause the brain to hit the skull.

Coup-Contre Coup

• The brain can bounce off the skull, hitting the opposite side.
• Meninges and CSF help prevent brain damage but cannot stop this type of movement.
• Bruising and swelling can occur for up to 48 hours, increasing intracranial pressure and affecting neuron function.
• Contusion: brain bruise
• Edema: swelling
• The brain floats in CSF, creating a weightless environment, but abrupt velocity changes cause the brain to continue in its original direction.
• The direction of the hit affects severity, but the skull is generally not broken in a concussion.
• Coup refers to the side of the skull that receives the hit, creating pressure that produces a contrecoup on the opposite end.
• Contrecoup is the after-effect where the brain hits the opposite side of the skull.
• Brain movement can shear nerve fibers, causing microscopic lesions, particularly in the frontal and temporal lobes. Hematoma: blood trapped in the skull
• Epidermal hematoma: physical breaking of the skull

Impact of a Concussion

• Impact to the skull doesn't have to be direct to cause a concussion; it can occur indirectly, such as from a blast.
• 1 in 5 US military personnel have experienced a concussion.
• The type of the impact matters; angular, rotational, and linear.
• Typically a combination of these forces is involved, and the direction of force predicts the severity of the concussion.
• Concussions require 90-100 g-force (20mph).
• Severity is unrelated to force magnitude; a minimum force is needed, but increasing force beyond that point won't increase severity.
• The direction of force dictates symptom presentation and long-term consequences.
• This leads to individualized symptom presentation, making patient comparisons difficult.

Rotational Forces and the Brain

• The magnitude of rotation is directly related to severity and can cause Diffuse Axonal Injury (DAI).
• DAI involves shearing of the white matter; excessive glutamate release causes neurons to fire too much without adequate resources, leading to cell death.
• Tearing is more common and allows axons to repair over weeks.
• Excitatory induced lesions occur due to glutamate release 24-48 hours after a concussion.
• DAI in the midbrain and diencephalon results in loss of consciousness.
• Shearing of axons can lead to subdural hematoma, with clotted blood increasing pressure in the brain.
• Epidural hematoma is not typically found in concussions but from a skull fracture severing the middle meningeal artery.

Acute Metabolic Cascade

• This involves acute damage to neural and vascular brain tissue, including distortion of cell membranes.
• Increases neural activity via glutamate release, leading to an energy crisis due to increased resource use.
• Interrupts blood flow to the the brain.
• Metabolic cascade results in energy crisis.

What Happens in Acute Metabolic Cascade?

• Membrane stretching opens voltage-gated calcium and potassium channels, causing depolarization and glutamate release.
• Leads to a more transient increase in glucose metabolism and lactate production.
• Causes an immediate decrease in blood flow.
• Glucose goes up, but blood flow goes down.
• Depolarized cells massively increase, and sodium and potassium pumps must work overtime to restore ionic balance.
• The pump requires ATP, which is produced from metabolizing glucose.
• Blood flow reduction limits resources to affected areas.

Why Is a Glutamate Surge Bad?

• Glutamate, the main excitatory neurotransmitter, can become excitotoxic and damage surrounding neurons.
• Receptors like AMPA, NMDA, and Kainate are permeable to sodium, causing EPSPs.
• Necrosis involves rapid lysis due to osmotic swelling, where excessive ionic influx forces water into the cell, causing it to burst.
• Apoptosis: Programmed cell death and a delayed response to biochemical events cause DNA breakup and cell death.

Glutamate & Calcium

• Activation of NMDA receptors also leads to calcium entry.
• Increased calcium causes negative effects on the mitochondria, impairing energy production.
• Increases demand for ATP and reduces blood flow, bringing fewer molecules to the brain, and reduces energy metabolism due to impaired mitochondria..

Steps of Acute Metabolic Cascade

• Rotational force shears neurons and vasculature, leading to glutamate release.
• Membranes stretch, potassium exits, and calcium enters the cell.
• Further glutamate release occurs.
• Glutamate further causes more polarizations of and calcium.
• Increased glucose metabolism occurs for ATP production.
• Decreased blood flow and impairment to mitochondria cause an energy crisis, reducing blood sugar in specific areas.
• Energy crisis leads to secondary injuries.

Secondary Injuries

• Due to increased energy needs, the brain shifts to anaerobic glucose metabolism (glycolysis), producing lactic acid.
• Lactic acid overproduction can lead to acidosis, damaging the blood-brain barrier (BBB).
• Damage to the BBB increases permeability and the risk of toxins entering the brain.
• If you are in a situation where energy is needed fast, you produce lactic acid, but too much creates a less strong BBB.

BBB & Inflammations

• The brain is normally resistant to inflammation due to the BBB, which prevents cytokines from entering.
• Disruption allows cytokines to enter, leading to patient deterioration; cytokines don't degrade quickly.
• Primary injuries: axonal damage, membrane disruption, and inflammation.
• Secondary injuries: cellular damage, apoptosis, and oxidative stress.

Symptoms and Signs of a Concussion

• Signs observed include:
  • Inability to recall events before the hit or fall
  • Appearing dazed or stunned
  • Forgetting instructions
  • Moving clumsily
  • Answering questions slowly
  • Brief loss of consciousness
  • Showing changes in mood, behavior, or personality
• Symptoms include:
  • Headache or pressure in the head
  • Nausea or vomiting
  • Balance problems or dizziness
  • Double or blurry vision
  • Sensitivity to light or noise
  • Feeling sluggish, lazy, or not feeling right

Concussion Detection

• Concussion Recognition Tool 5 (CRT5): Used by non-medical professionals to make an immediate call to remove a player and seek medical attention after injury.
• Immediate Post-Concussion & Cognitive Testing (IMPACT): A computer-based program with pre-screening evaluation following concussion screening.
• SCATS involves medical personnel using a tool to do the following:
  • Identify red flags, i.e. blurry vision or dizziness
  • Look for observable signs such as visible disorientation
  • Memory assessment
  • Glasgow Coma Score assessment
    • Light in the eye, etc
  • Cervical spine assessment
  • Follow-up office assessment

Second Impact Syndrome

• A condition in which a concussed individual sustains a second impact before fully recovering from the first blow.
• Prior concussions greatly increase the likelihood of another concussion.
• Repeated concussions have a cumulative effect on the brain, where the more you have negatively affects brain health even more.
• An energy crisis leaves the brain susceptible to further injury for up to 10 days.

Chronic Traumatic Encephalopathy (CTE)

• Animal models show a 50% mortality rate and a 100% morbidity rate.
• Results from repeated head trauma, including repeated sub-concussive blows, not necessarily concussions.
• Repeated concussions are a high risk factor for developing CTE.
• A progressive degenerative disease similar to Alzheimer's, characterized by neurofibrillary tangles, amyloid-beta plaques, and neuronal cell death.

Symptoms of CTE

• Typically appears years or decades after the last brain trauma or end of sports participation.
• Memory loss, confusion, impaired judgment, impulse control problems, aggression, anxiety, suicidality, Parkinsonism, and dementia.

Pathophysiology of CTE

• Neurofibrillary tangles (NFT) and increased Tau protein begin in the cortex.
• Mild enlargement of lateral and third ventricles.
• Amyloid beta plaques if older than 50.
• Frontal and temporal atrophy.
• Hippocampus NFT degeneration.
• Atrophy in white matter tracts, widespread myelin loss, and dense tau.

Case Study: Dave Duerson

• He endured 10 recorded concussions during his football career.
• After his career, he experienced problems with decision-making and temper control, with symptoms worsening over time.
• At age 50, he shot himself and was diagnosed with CTE post-mortem.
• His brain showed tau proteins and degenerating tissue in the frontal cortex and MTL.

Case Study: Aaron Hernandez

• Committed suicide while in jail after being found not guilty of murder. Post-mortem showed he had extremely advanced CTE (Stage IV), the brain is typically only seen in people over 46 years old.