Understanding a Brain Injury

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concussions

The CDC estimates that 3.8 million people sustain a concussion annually while playing sports in the US. TBI symptoms vary and can be mild or severe, affecting memory, behavior, and mood. It is important to note that X-rays, MRIs, and CTs scans cannot diagnose a concussion. It will be essential to note the Signs and Symptoms for evaluation.

Signs:

  • Loss of consciousness

  • Difficulty maintaining balance

  • A vacant or distant expression in the eyes

  • Memory loss (amnesia)

  • Slower response to questions or commands

  • Difficulty retaining and recalling instructions, assignments, or game details, including the score or opponent

  • Random outbursts of emotions

  • Episodes of vomiting

Symptoms that often accompany a brain injury are

  1. Persistent head pain

  2. Feeling faint or dizzy

  3. Experiencing lightheadedness

  4. Feeling nauseous

  5. Heightened sensitivity to light

  6. Increased sensitivity to noise

  7. Struggling with concentration

  8. Experiencing difficulties with memory

  9. Finding it hard to maintain focus

  10. Facing challenges when multitasking

  11. Difficulty completing cognitive tasks

  12. Changes in sleep patterns, including increased or decreased sleep duration

  13. Sleep onset difficulties or trouble falling asleep

  14. Anxiety

  15. Depression

  16. Panic attacks

Note: This list isn't exhaustive; concussion symptoms may not show up immediately after the initial injury, sometimes taking a few days. 

Dr. Keifer Decodes the Complexity of Concussion:

A concussion sparks a chain reaction in your brain, set off by the powerful impact. Think of it as a series of events triggered by disrupting your brain's delicate balance. This disruption makes the protective membranes of your brain cells permeable, unleashing a cascade of changes. To break it down:

  • Mechanical Forces Unleash Chaos: The impact creates mechanical forces that disrupt the equilibrium of your brain cells.

  • Cell Membranes Turn Porous: The stretching and shearing forces induce porosity in cell membranes, leading to the outflow of intracellular potassium and widespread neuronal depolarization. This marks the beginning of the acute neurometabolic cascade.

  • Key Changes Unleashed: This cascade involves a dance of neurotransmitters, including glutamate and GABA, along with shifts in potassium, calcium, and glucose. These changes contribute to hyper- and hypometabolic phases lasting for about 10-14 days.

Now, let's delve into the aftermath and the subsequent energy crisis:

  • Brain Energy Crisis Unfolds: Following the initial impact, there's an increased demand for energy in the brain, triggering heightened neuronal glycolysis for several weeks.

  • Triphasic Response in Blood Flow: The blood flow in the brain responds in three phases, influenced by regulatory compromise, vasoreactivity disturbances, and structural vessel changes, especially in areas linked to autonomic regulation and emotion processing.

Moving on to the microstructural damage and its effects:

  • Axonal and Cytoskeletal Injury: The rapid deceleration of the head induces microstructural axonal damage, peaking within the first 1-2 days. This can disrupt the brain's electrical signaling and the regulation of the hypothalamic-pituitary-adrenal (HPA) axis and stress responses.

Now, the inflammatory response and its persistence:

  • Neuroinflammation Unleashed: Microglial activation, increased inflammatory cytokines, and immune cell infiltration correlate with persistent symptoms.

  • Blood-Brain Barrier Drama: Dysfunction in the blood-brain barrier, indicated by structural alterations and temporal variations in permeability, suggests a biphasic course, with "late" dysfunction observed months post-injury. Chronic neuroinflammation in brain-injured populations has been reported months to years later.

Though cell death is limited, neuroimaging reveals structural changes:

  • Limited Cell Death: In mild traumatic brain injury (mTBI), cell death is restricted, but neuroimaging shows diffuse volume loss, atrophy, and regional changes. However, these morphological alterations are subtle and require expensive and less accessible imaging techniques for detection.

Subclinical Traumatic BrAIn Injury

Subclinical TBIs, formerly known as “sub-concussive impacts,” are blows to the head that do not result in symptoms and have been found to have potentially harmful effects on the brain over time. Repeated sub-concussive impacts have been linked to decreased brain recovery resilience. Subclinical TBIs combined with TBIs can impact the development of CTE.

Chronic Traumatic Encephalopathy (CTE)

Chronic Traumatic Encephalopathy is a progressive degenerative brain disease caused by repeated blows or trauma to the head. It is commonly associated with contact sports like football, boxing, hockey, and military combat. CTE is characterized by the accumulation of a protein called tau in the brain, leading to brain cell death over time.

The symptoms of CTE can include memory loss, confusion, impaired judgment, aggression, depression, and dementia. However, it is essential to note that CTE can only be definitively diagnosed after death through a post-mortem examination of the brain. Nonetheless, advanced brain imaging techniques, such as SPECT scans, can provide indicators suggesting CTE in living individuals. Although there is no cure for CTE, lifestyle changes and treatments can significantly impact its lasting effects and lower the risk of developing it. For further information on CTE, we suggest The Concussion Legacy Foundation.

second impact syndrome (SIS)

A second brain injury while recovering from a first one can lead to a condition known as "second impact syndrome" or a termination injury. Second impact syndrome occurs when the brain sustains a second injury before fully recovering from the first and can result in severe brain swelling, rapid deterioration, and even death.

Several high-profile cases of SIS have been in recent years, particularly in sports-related injuries. One such case involved a high school football player named Damon Janes, who suffered a head injury during a game in 2013 and later died from SIS after returning to the field and experiencing a second blow to the head. Another notable case involved a professional ice hockey player named Don Sanderson, who died from SIS in 2009 after hitting his head on the ice during a fight and then being involved in a second fight just weeks later.

These tragic examples highlight the importance of allowing the brain sufficient time to heal after a TBI and avoiding activities that could lead to a second injury before the brain fully recovers.

Pathogenic Complications

Prolonged post-concussion syndrome (PCS) can occur when the symptoms of a concussion persist for an extended time, often months or even years after the initial injury. Recent research suggests that specific pathogens may contribute to the development of prolonged PCS. Please see our pathogenic infection page for more information.