Traumatic Brain Injury

Causes of TBI

Traumatic Traumatic brain injury (TBI) occurs when an external force causes damage to the brain, leading to a disruption in its normal function. Common causes of TBI include:

• Falling and hitting head on object

• Car accidents

• Sport injuries

• Physical assault

• Explosive blasts

 The severity of TBI can range from mild, causing temporary dysfunction, to severe, resulting in long-term impairment or even death.

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Symptoms of TBI

Mild TBI, also known as a concussion, often presents with symptoms such as: 

• Headache

• Dizziness

• Confusion

• Nausea

•  Temporary loss of consciousness

Memory problems, mood swings, and sensitivity to light or noise may also occur. While these symptoms typically resolve within days to weeks, some individuals may experience persistent cognitive or emotional difficulties.

 

Moderate to severe TBI can lead to more profound symptoms, including:

• Prolonged loss of consciousness

• Persistent headache

• Seizures

• Vomiting

• Slurred speech

• Weakness or numbness in limbs

• Profound confusion

 Behavioral changes such as agitation, combativeness, or profound lethargy may also manifest. In severe cases, individuals may enter a coma or experience profound cognitive deficits, impacting memory, language, and executive functions.

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Complications of TBI can arise both acutely and chronically. Acutely, increased intracranial pressure, bleeding within the skull, or swelling of the brain can lead to further damage if not promptly addressed. Chronic complications may include cognitive impairment, mood disorders such as depression or anxiety, increased risk of neurodegenerative diseases like Alzheimer's or Parkinson's, and epilepsy.

 

How Hyperbaric Oxygen Therapy Can Help?

Hyperbaric oxygen therapy (HBOT) can be used to obtain 100% saturation of hemoglobin and to significantly elevate the volume of physically dissolved oxygen fraction in blood plasma. This increased blood oxygen level then can penetrate tissue more deeply than under normal conditions. It reduces neuronal degeneration and prevents apoptosis after brain injury by regulation of oxidant/antioxidant status and reduction of oxidative stress such as significantly increased glutathione-peroxidase activity in the injured cortex while HBOT returned superoxide dismutase activity to almost control levels. HBOT initiates a statistically significant reduction in Malondialdehyde levels, pointing to the preservation of membrane integrity. In cases of TBI, there may be areas of the brain with reduced blood flow but still viable tissue (penumbra). HBOT can help deliver oxygen to these regions, potentially salvaging tissue that might otherwise be at risk of damage or death.

 

HBOT applied after TBI improves neurological status including motor and cognitive function, as well as learning and memory abilities as reported in several studies. HBOT prevents the spreading of neuroinflammation in the injured tissue by reducing the expression of intracellular adhesion molecules(ICAM-1) and targeting the passage of immune cells through the blood-brain barrier via inhibition of cell adhesion molecules. It improves neurofunctional recovery of the injured brain by enhancing neuronal plasticity via growth-associated protein 43(GAP43) and synaptogenesis via synaptophysin. HBOT promotes neurogenesis and angiogenesis after TBI by promoting endogenous neural stem cells to migrate to the site of injury and differentiate into mature neurons, contributing to improved neurofunctional recovery of the injured brain. Moreover, HBOT alters the morphology of neuronal precursors to a more mature morphology. Furthermore, HBOT effectively attenuates reactive astrogliosis and microgliosis, prevents tissue-damaging effects of neutrophils, and suppresses the formation of glial scar. Accordingly, by alleviating glial-mediated inflammatory response and limiting the production of inflammatory mediators HBOT fosters the formation of a more permissive environment for tissue repair, allowing the recovery of impaired brain function.

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