Diagnoses That may Underpin Persistent Symptoms After Mild Traumatic Brain Injury
The foundation of our approach to persistent symptoms after mTBI is the recognition that the symptoms are non-specific. This means that, in different people, there might be a range of possible diagnoses within which such symptoms could cluster. Alternatively, numerous different underlying diagnoses might be present in another individual with the same persistent symptoms and those symptoms may have a high degree of overlap between diagnoses. The assessment therefore needs to tease apart (or indeed cluster together) symptoms to establish a reasonable diagnostic formulation shared with the patient, with the express purpose of developing a rational bio-psycho-socio-ecological treatment plan informed by that formulation. To illustrate this approach, we have used two of the most commonly described symptoms after mTBI; headache and dizziness (Figure 1).
Two distinct approaches to the same symptom complex post mTBI. (A) Panel demonstrates the consequence of the PCS label being applied, resulting in a single non-specific treatment. (B) Adopting an individualized diagnostic formulation to consider and identify the multiple potential causative factors potentially underlying identical symptom complexes. The consequence is the instigation of targeted evidence-based individualized treatment plans. Dotted arrows represent contributory processes to symptom persistence/amplification.
When compared to primary headache disorders, post-traumatic headache most commonly represents a migraine-type headache with associated migraine symptoms, including nausea, light and noise sensitivity, irritability and cognitive symptoms—symptoms that are also listed as typical symptoms of PCS itself. Furthermore, a pre-existing or family history of migraine are risk factors for prolonged post-traumatic headache.[56,57] However, although migraine and post-traumatic headache pathophysiology may overlap in some patients, there is likely to be a range of pathophysiological processes underpinning post-traumatic headache and treating all the same is unlikely to be successful. For example, persistent psychological factors and medication overuse are recognized to prolong post-traumatic headache. Therefore, treatment trials that fail to stratify patients and instead treat all post-traumatic headache as the same are at risk of failure. Despite these caveats, early treatment of post-traumatic headache, particularly in those at greatest risk, and a diagnostic explanation for the patient including the clustering of other 'postconcussional' symptoms are warranted.
Post-traumatic dizziness is another good example of symptom clustering. The commonest causes following mTBI are benign paroxysmal positional vertigo (40%) and vestibular migraine (34%). Vestibular migraine is associated with other migrainous symptoms as discussed above but, perhaps surprisingly, benign paroxysmal positional vertigo is also associated with cognitive impairments and heightened anxiety, especially if left untreated.
Relationship to Psychiatric Disorders
Mild TBI increases the risk of developing a subsequent psychiatric condition nearly threefold. However, trying to distinguish psychiatric conditions such as anxiety, depression or post-traumatic stress disorder from the effects of a mTBI can be challenging due to symptom overlap, yet has important implications for symptom persistence (Table 3).[54,63,64] It is important to remember that symptom overlap can obscure diagnostic clarity, 50% of people with depression who have not had a TBI meet the criteria for moderate to severe PCS. Alongside the psychosocial impact of head injury, it is of course also possible for depression and anxiety to be related to structural brain injury, either as a result of macroscopic damage or triggering of a secondary inflammatory process.[66–68]
There also remains stigma surrounding mental health diagnoses, which results in a higher likelihood of misattributing the cognitive changes to the injury, rather than potentially reversible psychological or psychiatric causes. The unfortunate consequence of this is that appropriate, evidence-based treatment may not be accessed in a timely way, subsequently worsening the treatment responsiveness and prognosis of the psychiatric condition.
Functional Neurological Disorder and Somatic Symptom Disorder
Functional neurological disorder is characterized by internal inconsistency, typically demonstrated by the complaint of abnormal function in a system that can be demonstrated (usually clinically, but sometimes by investigation) to be capable of normal function. Over 80% of people with functional neurological disorder report a health event near to the onset of functional symptoms. These events, which include accidental injuries, are typically minor and would be expected to improve and not produce lasting symptoms in their own right.
This preceding discussion clearly has relevance for the development of persistent symptoms after mTBI. The immediate and lasting physical and psychological consequences of accidents and injuries causing TBI could undoubtedly act as triggers to the onset of functional neurological disorder and/or somatic symptom disorder in some people, also interacting with pre-morbid risk factors and subsequent behaviours such as fear avoidance. Positive diagnosis of such symptoms is possible within normal clinical practice, and diagnostic explanation according to best practice is typically a positive and empowering experience for patients.
Medicolegal processes appear to be correlated with persistence of symptoms in some people, a finding that is often interpreted as evidence that mTBI is psychological in nature. The fact that there is often someone at fault or to blame, resulting in adversarial circumstances between involved parties, means that primary psychological reactions are naturally triggered by the litigation process, such as loss aversion, anger or revenge. The financial implications in this context are not necessarily the motivator for the feigning behaviour.[73,74] It is notable that often from the outset of the medicolegal process, the injury might not be acknowledged by the other party. This can result in anger from the injured individual, particularly if they are subject to independent assessments where the assumption is that they are not injured at all, or perhaps not as severely as thought, or even that they are malingering. These effects translate into an increased likelihood of feigning behaviour as a behavioural expression of the emotional sequelae of the mTBI or the need for revenge if trust is violated.
In addition to the above causes, it is important to consider the potential effect of non-brain injury factors. For example, extracranial injuries influence symptom persistence. This may be related to effects on sleep, pain and psychological impact. Finally, medications commonly prescribed after traumatic injuries, particularly opiate based analgesics, can impair cognitive functions, disrupt sleep and cause dizziness and nausea.
Brain. 2022;145(6):1906-1915. © 2022 Oxford University Press