Migraine

The clinical features of migraine after brain trauma appear almost identical to those of idiopathic migraine, either with or without aura.

According to the International Classification of Headache Disorders, migraine attacks include unilateral throbbing pain accompanied by nausea, vomiting and photophobia. As a result, individuals typically avoid routine activities, especially physical ones, but also cognitive tasks.

It is now agreed that migraine is a neurological disorder. Former vascular migraine hypotheses have been discarded. The activation of the trigemino-vascular pain pathways that innervate the dural vasculature is thought to be responsible for this type of headache. The disruption in sensory processing within the brain stem is understood to be the core neurophysiological disturbance.

A typical migraine attack consists of three stages: the aura, headache and postdrome phase. Neurological migraine mechanisms are highly complicated and there is an overlap of neurophysiological pattern in each of the migraine stages.

Migraine provides an example of shared mechanisms between mild brain trauma and pain processes. The experience of acute distress, either due to a trauma event or a migraine attack, triggers the subcortical alarm system. A cascade of neurocognitive disturbances is unleashed, which involves subcortical features such as the fear-processing amygdala and the memoryprocessing hippocampus. Both play crucial roles in pain and trauma pathways. The hippocampus registers and encodes the negative event and the amygdala amplifies this with a powerful fear response. This ensures such efficient communication with higher level cortical evaluations and memory that the individual is programmed to avoid such unpleasant stimuli in future, even though this process takes place outside conscious awareness.

As migraine attacks cannot be consciously self-regulated, they can lead to generalised anxiety, depression and concentration disturbances or shortterm memory problems. Such symptoms are also characteristic of mild brain trauma per se.

Persistent posttraumatic migraines are the combination of a perceived association with a trigger - e.g. traumatic injury event, cognitive difficulty - and secondary mood symptoms.

The hypothalamus, along with the brain stem, is not only a key organ for cognitive processing of pain and trauma. It plays a vital role in regulating the experience of eating and sleeping, as well as in the production of nausea and vomiting symptoms linked with migraines.

The brain stem plays a key role in migraine pathophysiology. Brain stem dysfunction can lead to disturbed eating and sleeping patterns due to dys- regulated dopamine pathways. The trigemino-vascular activation and sensitisation amplifies this process. Migraineurs report that food factors as well as sleep disturbances can trigger attacks. However, because brain stem disturbances are unbeknown to the individual, a mis-association and psychological conditioning may develop. Altered behaviours after a brain trauma might aggravate a migraine predisposition. A mildly traumatised person might feel disorganised, fall behind on tasks and become stressed or skip meals, thus setting off subcortical and brain stem pain mechanisms.

Migraineurs’ prefrontal and temporal cortical networks appear to differ slightly from those of healthy people. Genetic neurophysiological and also lifestyle factors play a substantial role in predisposing people to the condition. It appears to be that challenging life events - such as an injury to the head and potential brain trauma - may be processed inefficiently, hence making it more likely that a genetic predisposition to the condition is triggered.

Stress and negative emotions are commonly reported by migraine patients whether they have experienced mild brain trauma or not. In contrast, some patients in clinical settings may report that they do not experience elevated stress. Even if they do, they may rather encounter a migraine attack during rest periods, e.g., at weekends. A straightforward link between heightened cortisol levels and migraine attacks is indeed not proven. In fact, cortisol levels in migraineurs may be quite dysregulated and may not follow the typical circadian rhythm.

From a neurophysiological point of view, stress can be explained using the Allostatic model. It explains how a long-term maladaptive HPA-axis represents physical or bodily distress. This process results in dysregulated cortisol distribution, which can enhance migraine vulnerability.

It is assumed that posttraumatic migraine mechanisms are similar to idiopathic migraine. Such primary migraine involves activation and sensitisation of the pain matrix: the trigemino-vascular pathways, brain stem, cingulate cortex, prefrontal cortex, thalamus, nuclei within the diencephalon and other brain areas. It has been suggested that migraines are connected with altered cortical excitability and also with changes in energy metabolism of central pain-processing pathways. At the core of the migraine experience - which can begin many hours before an aura or before the attack is felt - lies a dysfunction of neural processing in the brain stem and hypothalamus, which sets off alterations in cellular and vascular processes in almost all parts of the brain. Dysregulation of neural traffic along the associated brain regions leads to altered sensory experiences and impaired function of pain-processing pathways.

The persistent nature of the migraine condition can lead to Central Sensitisation. This means that cortical vigilance during normal activity is heightened and that situations are sooner identified as challenging. This increases the likelihood of episodes occurring. Anxiety symptoms, particularly fear of pain and depression due to helplessness, are simultaneously primary and secondary emotional experiences. Ultimately, a complex phenomenon is created whereby the sufferer responds negatively to the environment, which in turn reinforces neurophysiological maladaptation.