Abstract and Introduction
Persistent symptoms following a minor head injury can cause significant morbidity, yet the underlying mechanisms for this are poorly understood. The shortcomings of the current terminology that refer to non-specific symptom clusters is discussed. This update considers the need for a multi-dimensional approach for the heterogenous mechanisms driving persistent symptoms after mild traumatic brain injury. Relevant pathophysiology is discussed to make the case for mild traumatic brain injury to be conceptualized as an interface disorder spanning neurology, psychiatry and psychology. The relevance of pre-injury factors, psychological co-morbidities and their interaction with the injury to produce persistent symptoms are reviewed. The interplay with psychiatric diagnoses, functional and somatic symptom disorder presentations and the influence of the medicolegal process is considered. The judicious use and interpretation of investigations given the above complexity is discussed, with suggestions of how the explanation of the diagnostic formulation to the patient can be tailored, including insight into the above processes, to aid recovery. Moving beyond the one-dimensional concept of 'postconcussional syndrome' and reframing the cause of persistent symptoms following mild traumatic brain injury in a bio-psycho-socio-ecological model will hopefully improve understanding of the underlying contributory mechanistic interactions and facilitate treatment.
Traumatic brain injury (TBI) is common. Fortunately, the vast majority of injuries are mild, typically causing transient, self-limiting symptoms and no long-term sequelae. However, approximately 20% of people report persistent symptoms at 3 months post-injury following mild TBI (mTBI). For these people, the long-term outlook is poor, with many experiencing ongoing negative impact on work and social function.[1,2] Given how common mTBI is, this represents a huge number of affected individuals.
Persistent symptoms that occur after mTBI are likely to be due to a range of identifiable disorders, many of which have evidence-based treatments. However, we argue that clinical and research practice has been held back by the use of syndromic terms such as postconcussional syndrome (PCS) to categorize patients. Clinically, it produces bias away from considering treatable underlying causes of symptoms. From a research perspective, it fosters an assumption that people with such symptoms are a single group pathophysiologically. However, we would argue that the diagnostic heterogeneity here means that group data from, for example functional MRI studies, are unlikely to provide a valid source of information to make inferences about mechanisms of symptoms, nor to extrapolate from, in order to determine new avenues for treatment development.
Brain. 2022;145(6):1906-1915. © 2022 Oxford University Press