Secondary mechanisms of brain trauma

Mild brain trauma is not associated with major structural injuries affecting the brain.

A focal impact injury represents mechanical damage, which can result in contusions (bruising of brain tissue), lacerations (tears) and intracranial haemorrhage (bleeding). Such clinical findings are more likely to be associated with severe injuries.

Diffuse injuries are characterised by acceleration or deceleration forces, e.g., due to car accidents, which can cause stretching and tearing of fragile brain tissue. Concussion is a milder form of diffuse injury caused by mechanical stresses, but without the presence of overt morphological damage. Nevertheless, the stretching and shearing that originate from the impact can disrupt cell protein functions and lead to the destabilisation of the axons of the neuron almost immediately following the event.

Such tissue damage is related to the rotational acceleration-deceleration forces, which also act on the midbrain and thalamus. The resulting disruption of these systems may cause a dysregulation of the reticular activating system, which is related to a number of symptoms associated with concussion and longterm impairments of neuropsychological pathways, including pain processes.

Even very minor concussions (also called sub-concussive injuries) can - if there are repeated injuries, as in certain sports - lead to subtle changes to the neural axons, disrupt the blood-brain barrier and trigger neuro-inflammation.

Non-traumatic injuries, caused by aneurisms, haemorrhages, tumours or meningitis, may also cause headaches. This is because space-occupying processes and inflammation increase intra-cranial pressure and brain membranes or blood vessels may be subject to related micro-injuries.

The brain itself is not sensitive to pain and, therefore, cannot hurt. It is very useful to inform patients about parts of the head that can and cannot hurt. This is because patients often fear that their persistent headaches signal further injuries to the brain.

Secondary consequences of brain injury begin at the moment of impact, but may present clinically only after a delay. A brain that is undergoing changes following a mild brain injury is in a particularly vulnerable state. Further injuries during this time period exacerbate concussion symptoms, including headaches.

These secondary consequences include metabolic and pathophysiological changes. Understanding such changes is important to determine the extent of the damage and to plan clinical interventions.

The neurochemical alterations following mild traumatic brain injury involve a cascade of destructive events associated with cerebral blood flow changes and the disruption of cell metabolism. Micro-ischaemia leads to anaerobic glycolysis, which is an adaptive process involving the transformation of glucose and very quick production of ATP (adenosine-5'-triphosphate, important for cell energy metabolism and neural signalling) when limited oxygen is available. This process is only efficient as an emergency measure for periods between ten seconds and two minutes. The glycolysis byproducts - lactic acids - lead to membrane permeability and micro-oedema. If blood flow and oxygen provision cannot be restored after the very short burst of energy, then ATP resources become depleted. As a result, the ion pumps in axons and nerve cells fail to function, leading to membrane depolarisation and the excessive release of excitatory transmitters. The influx of positively charged ions activates further intracellular reactions. These lead to progressive structural changes of cell membranes and DNA fragmentation and dysfunction. Membrane degeneration of vascular and cellular structures results in the necrotic and programmed death of cells. Such neurochemical disturbances ultimately lead to neurologic deficits.

In a healthy brain, the cerebral blood flow is tightly coupled with the glucose metabolism and neuronal activity. Injuries to the central nervous system cause a deviation from the well-balanced metabolism. The neuron membrane pumps work in overdrive to restore the ionic balance. This causes an energy deficit and a surge of hyperglycolysis to satisfy the demand. This constitutes a period of hypermetabolism and an imbalance between blood flow and metabolism, leading to reduced cerebral blood flow. This increases the energy crisis, which can cause prolonged neuronal dysfunction.

Cerebral blood flow changes following traumatic brain injury can have a detrimental effect in relation to tissue damage, neurophysiological alterations and mechanical vessel distortion. They have been reported months, even years, after an injury and may be associated with chronic headache symptoms.

Immediately following the onset event, stretching and shearing forces act on the neuronal membranes, resulting in a biomechanical injury. This causes a cycle of cell and membrane depolarisation and subsequent excitation of the brain. This is followed by cortical depression. In contrast to the classic cortical depression mentioned in the migraine pathophysiology, the neuronal depression in brain trauma can occur in several diffuse areas of the brain simultaneously. The depletion of energy resources may further intensify this process. It is assumed that these mechanisms cause the cognitive difficulties associated with concussion.

There are a number of additional pathologies associated with concussion including oedema and inflammation. Oedema also develops as a consequence of cell membrane degeneration, leading to intracellular water accumulation associated with an osmotic imbalance. This can further lead to increased intracranial pressure (in more severe injuries) or secondary ischemia (e.g., mini-strokes).

The complex pathophysiological responses associated with brain injury also release cellular regulators that activate inflammatory processes. These are related to immune system activities that aim to eliminate injured neuronal tissue and synthesize scar tissue.

In summary, concussion and mild brain injury can lead to a cascade of alterations in brain tissue related to cerebral blood flow and metabolic disturbances, neuronal hyper-excitability, oedema formation, inflammation and changes to important cell proteins.

It is assumed that such changes are related to the neurological and neuropsychological symptoms reported by people with mild brain trauma. It is important to consider these processes in association with the secondary pain pathways and the complex emotional-cognitive evaluation of the experience.

People with mild brain trauma and posttraumatic headache benefit from the validation from their therapist that that they certainly have hurt themselves. They are keen to receive an appreciation of the fact that their symptoms are real and have a biological substrate, which confirms that they have not made up the whole story. The information about structural muscular-skeletal changes, nerve injuries as well as metabolic and molecular micro-physiological changes can help explain to patients the organic nature of their symptoms. They want reassurance that their condition is well understood, that nothing sinister is going on underneath and that they can make a good recovery.

The headache clinic, with its embedded formulation session, is an ideal setting in which to provide patients with such explanations, prepare them for the shift towards their health management during their recovery and enlist their engagement with a biopsychosocial approach.

 
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