A Hit on the Head: Traumatic Brain Injury

Any hit to the head can be very serious. The head holds the brain, a powerful yet vulnerable organ. A high-speed or blunt-force impact on the head can irreparably damage the brain tissue and cause disability or even death. The primary injury to the brain can have serious consequences, but secondary effects and concussions can cause further damage to the brain and endanger the sufferer even more. As the brain cannot, as yet, be renewed or transplanted, it is imperative to treat traumatic brain injuries with the utmost care and monitor them to mitigate the risks of further injury and ensure the patient is safe. This can be done through monitoring the Intracranial Pressure or with imaging tests such as CT Scans, as well as making sure the patient withholds from being at risk of another brain injury until the first one has healed completely.

Traumatic Brain Injury

Traumatic brain injury (TBI) is defined as a physical injury that impairs brain function, either on a temporary or permanent basis. This is a common cause of death and disability throughout the world. TBI can occur in vehicle collisions, falls (particularly with young children and older adults), physical assault, and while playing sports. Although the initial injury can be extremely harmful, for those that survive, secondary injuries resulting from inadequate oxygen supply and perfusion (blood flow) to the brain can be equally damaging. Post-TBI care and monitoring are, therefore, of utmost importance to reduce the risk of death or disability in the days, weeks and months following a traumatic brain injury. When TBI is suspected, the diagnosis must be confirmed through imaging techniques. Computed Imaging (CT) scans are the most common diagnostic tool for TBI, though Magnetic Resonance Imaging (MRI) can also be used. Following diagnosis, the first treatment for TBI is to establish reliable airways for the patient and maintain their blood pressure (Parikh et al., 2007).

Primary traumatic brain injury is the initial damage caused by physical damage to brain tissue at the moment of injury. Blood vessels, axons, neurons and glia may be directly damaged in the primary TBI. Due to the highly interconnected nature of the brain, this primary TBI can cause a wide range of changes to the neurochemistry, metabolism and function of the brain. Primary TBI can cause diffuse axonal and vascular injury, intracerebral, subdural or extradural haemorrhage, as well as bruising (Finnie & Blumbergs, 2002). With severe TBI, the primary injury is followed by a secondary injury, including changes in cerebral blood flow, local and systemic inflammation, oxygenation, ischemic (caused by restricted blood flow) and apoptotic neuronal cell death. Intravascular clot formation is also common in severe TBI and contributes to brain ischemia (DeCuypere & Klimo, 2012). Secondary TBI evolves from complications of primary TBI. This includes ischemic damage (due to reduced blood flow), hypoxic damage (due to reduced oxygenation), brain swelling, effects of raised intracranial pressure, hydrocephalus (build-up of fluid in the brain), and infection. As primary damage to the brain results from mechanical forces at the moment of the impact, this type of injury is highly preventable (e.g. wearing safety equipment such as helmets while playing sports). However, secondary TBI happens as a result of primary TBI, and so may be reversible or preventable with adequate treatment. There is a therapeutic window between primary and secondary TBI where surgical and pharmacological interventions may prevent further brain damage, and preserve life and the quality of life of the patient (Finnie & Blumbergs, 2002).

Figure 1: Types of Traumatic Brain Injury (Javaid et al., 2021).

Traumatic brain injury can be mild, moderate or severe. This classification can be misleading, as even mild TBI can result in long-term disability (Yamamoto et al., 2018). The Glasgow Coma Scale (GCS) is a neurological scale used to describe the state of consciousness of a person and ranges from normal consciousness (score of 15) to unresponsive to all stimuli (score of 3) (Sternbach, 2000). Severe TBI is granted a GCS score of 3–8, moderate TBI is 9–12, and mild TBI has a score of 13–15 within 24 hours of impact. The GCS is a vital tool for the initial diagnosis of concussion and TBI, as well as for the continuing assessment of the patient's condition, and monitoring response to treatments. This scale can also be used to predict the outcome and the likelihood of recovery of a patient. However, there are some gaps in the abilities of this scale, such as not including brainstem reflexes and being skewed in favour of motor responses. Although new scales are being developed to include these indicators of consciousness, the Glasgow scale has been used in the bedside assessment of consciousness for nearly 50 years (Sternbach, 2000; Sussman et al., 2018; Teasdale et al., 2014).

Concussion

The most common type of mild TBI is a concussion. However, this terminology can cause confusion as mild TBI has a range of 13 to 15 on the GCS, while concussion is an actual clinical syndrome and can be seen in some cases of moderate and severe TBI. Concussion occurs when neurological, behavioural or cognitional processes are disrupted by an external force such as direct impact, rapid acceleration, deceleration or rotation. There is a variety of symptoms of concussion, and not all are exhibited in every case. The most common symptom is headache, while dizziness, vision changes, drowsiness, nausea or amnesia may also indicate a concussion. Only 4.6% of patients will actually lose consciousness. This makes it very difficult to recognise a concussion as 90% of concussions are mild. As a result, all head injuries should be monitored for signs of these symptoms (Cantu, 1998; Kamins & Giza, 2016). There has been an overall decrease in the number of sport-related concussions, due to an increase in safety procedures (e.g. helmets, guard rails, walking frames for the elderly), better on-field medical care and changes in the rules of many sports, for example, banning certain tackling moves that present a risk of head injury (Cantu, 1998).

The pathophysiology of concussion involves a dramatic increase in ions and excitatory neurotransmitters, causing a metabolic crisis in neurons. Following a TBI, the transmembrane potential of neurons is thrown into imbalance as ion channels and ATP-controlled ion pumps open and neurotransmitters, glutamate in particular, are released. This causes further ion influx. As the ion pumps are depleting the ATP supply, this results in hyperglycolysis. The TBI also decreases brain perfusion which, coupled with the hyperglycolysis, causes a metabolic crisis—a high demand for glucose, but the delivery of glucose is impaired. Following a concussion, metabolism in the brains of athletes has been shown to significantly decrease but returns to normal levels after 30 days (Kamins & Giza, 2016).

Figure 2: Signs and Symptoms of a Concussion (Unknown, n.d).

More than 13% of concussions are recurrent. Following a concussion, there is a period where the brain is metabolically vulnerable. While one TBI can decrease brain glucose levels, a second TBI further lowers glucose and prolongs this period of low glucose supply. Furthermore, a second TBI within a few days or weeks of the first can result in Second Impact Syndrome (SIS), where a second TBI occurs before the symptoms of an initial TBI are gone. As the brain is already vulnerable, a second injury can have devastating consequences and can result in cerebral oedema (brain swelling) and even death. Even a mild TBI where the patient remains conscious can still be followed by SIS. The best way to stop SIS is prevention. It is strongly advised that any patient who experienced symptoms following a head injury should avoid any situation where a second injury could occur until all symptoms have cleared. For example, an athlete who suffered a concussion should not practice the sport, or even train, until the symptoms have fully cleared. Incidents of SIS that were not prevented have been associated with the development of epilepsy, early dementia and paralysis (Cantu, 1998; Kamins & Giza, 2016).

Intracranial Pressure

One of the greatest risk factors following severe TBI is an increase in intracranial pressure (ICP) (Sahuquillo, 2006). ICP is the pressure exerted by cerebrospinal fluid (CSF), blood and neural tissue within the closed system of the intracranial compartment. As the bone of the skull surrounding the brain is not expandable, the pressure inside the skull must be kept within a certain level to ensure adequate blood flow and oxygenation of the brain. ICP is determined by the ratio of the contents of the intracranial compartment. In normal circumstances, the intracranial compartment contains approximately 83% brain tissue, 11% CSF, and 6% blood (Smith, 2008). ICP can be affected by a variety of everyday factors, such as standing vs. laying down, and age. In a healthy adult who is lying down, ICP is about 7-15mmHg, while in a child ICP is about 3-7mmHg. Baseline ICP is determined by the circulation of CSF. When the flow of CSF is disturbed due to TBI, ICP increases (Smith, 2008). An increase in ICP following TBI can seriously impede brain oxygenation and lead to disability, a vegetative state or death (Sahuquillo, 2006). Following a TBI, an ICP monitor is used as the standard to measure ICP after moderate or severe TBI. Further scans are recommended if an abnormal reading or change in ICP is found from the ICP monitor (Chesnut, 2013).

Figure 3: Increased Intracranial Pressure (Unknown, n.d).

Post-TBI Monitoring and Treatment

Considering that high ICP is the leading cause of death or disability from a severe TBI, frequently checking ICP is an essential part of post-TBI monitoring (Sahuquillo, 2006). Although increased ICP can cause severe harm, tracking ICP may also be used to monitor changes in the intracranial compartment and alert doctors if the patient is at further risk. Accurate measurements of ICP cannot be reliably taken from CT scans or testing lumbar CSF pressure. Furthermore, lumbar CSF extraction may be dangerous if ICP is high. ICP monitoring devices, such as intraventricular catheters or microtransducer sensors, are more accurate and reliable, though they must be surgically inserted into the patient. For example, the intraventricular catheter is the ‘gold standard’ in ICP monitoring but must be inserted into the patient’s lateral ventricle through a small hole made in the skull. Less invasive ICP monitoring techniques are being developed, such as transcranial Doppler ultrasonography and tympanic membrane displacement. These new techniques have been shown to estimate ICP within 10-15mmHg accuracy and may provide a reliable method of measuring ICP following TBI without the added risk of surgery (Smith, 2008).

Increased ICP is linked to intracranial mass lesions (including tumours), contusion injuries (e.g. bruising), vascular and blood pressure increases, and brain oedema (Smith, 2008). One way to help slow ICP increase or stop it is to reduce CSF. When the brain swelling causes ICP to increase, removing another component of the intracranial compartment can compensate for this increase. The body does this for minor brain swelling through spatial compensation, where CSF is moved out of the intracranial compartment to the spinal theca (Smith, 2008). For more significant swelling, Manet et al. (2017) showed that CSF can be removed through external lumbar drainage to reduce overall ICP. Removing CSF leaves more space in the intracranial compartment for the injured brain to swell without increasing ICP and causing further damage (Smith, 2008). High ICP can also be treated by sedating the patient or through medications. If ICP does not return to normal levels, surgery to remove part of the skull, known as a decompressive craniectomy, may be required. This is a neurosurgical procedure where part of the skull is removed to allow room for the injured brain tissue to swell without causing further damage to the brain as it presses against the skull bone. However, decompressive craniectomy surgeries have a risk ratio of 0.54 for death and 0.54 for an unfavourable outcome, such as the patient entering a vegetative state or obtaining a severe disability (Parikh et al., 2007; Sahuquillo, 2006). In cases of severe TBI intracranial hematomas may occur. This is an accumulation of blood in the brain, caused by blood vessels bursting. Surgery may be required to remove an intracranial hematoma (Parikh et al., 2007).

Figure 4: Ventricular Catheter (Unknown, n.d).

Conclusion

Traumatic brain injuries are a common cause of death and disability in otherwise healthy, young individuals. TBIs can cause a drastic change in the ICP of an affected individual, which can cause displacement of blood, cerebrospinal fluid and even the brain tissue itself. When it comes to traumatic brain injury, prevention is the best cure. Mild, moderate or severe TBIs can all have devastating, irreversible consequences, so protecting the head from injury is vital when participating in activities where head injury is a risk factor. Measures such as protective equipment (e.g. wearing a helmet when playing sports) can significantly decrease this risk. However, full recovery is possible. When a TBI does occur, it must be cared for properly to reduce the risk of further complications and secondary TBI. Careful treatment may also prevent the patient from becoming disabled or paralysed. Monitoring the progression of symptoms through ICP monitoring and CT scans, and taking precautions to avoid further injury, gives a patient the best chance of recovery from a TBI.

Bibliographical References

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Manet, R., Payen, J., Guerin, R., Martinez, O., Hautefeuille, S., Francony, G., & Gergelé, L. (2017). Using external lumbar CSF drainage to treat communicating external hydrocephalus in adult patients after acute traumatic or non-traumatic brain injury. Acta Neurochirurgica, 159(10), 2003–2009. https://doi.org/10.1007/s00701-017-3290-1

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Visual Sources

Cover image: Moyle, S. (n.d). Understanding Brain Damage Locations [Image]. Ausmed. https://www.ausmed.com/cpd/articles/understanding-brain-damage-locations

Figure 1: Javaid, S., Farooq, T. B., Rehman, Z., Afzal, A., Ashraf, W., Rasool, M. F., Alqahtani, F., Alsanea, S., Alasmari, F., Alanazi, M. M., Alharbi, M., & Imran, I. (2021). Dynamics of Choline-Containing phospholipids in traumatic brain injury and associated comorbidities. [Image]. International Journal of Molecular Sciences, 22(21), 11313. https://www.researchgate.net/figure/Pathological-events-happening-during-primary-and-secondary-phases-of-traumatic-brain_fig1_355464843

Figure 2: Unknown. (n.d). Signs and symptoms of concussion [Image]. Queensland Brain Institute. https://qbi.uq.edu.au/concussion/signs-and-symptoms-concussion

Figure 3: Unknown. (n.d). Raised intracranial pressure: What it is and how to recognise it. [Image]. Continuing Medical Education. http://www.cmej.org.za/index.php/cmej/article/view/2698/2840

Figure 4: Unknown. (n.d). Surgery to remove fluid in the brain. [Image]. Cancer Research UK. https://www.cancerresearchuk.org/about-cancer/brain-tumours/treatment/surgery/remove-fluid