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Jungfer, Patricia --- "Psychiatric aspects of mild traumatic brain injury: the obsolete diagnosis of post-concussion syndrome" [2017] PrecedentAULA 10; (2017) 138 Precedent 37



By Dr Patricia Jungfer

The definition of severity of traumatic brain injury (TBI) varies widely in scientific research, clinical practice and in the community. In the period 2002–2006, there were an estimated 576.8 per 100,000 TBIs of varying severities in the United States.[1] The incidence of TBI is similar in Australia, and the majority of these TBIs are considered mild (85 per cent). Motor vehicle accidents are a significant cause of TBI in Australian communities. The severity of injury is defined by clinical criteria, as a true pathological diagnosis of severity of brain injury can be achieved only by post-mortem. Mild TBI (MTBI) does not have a consistent definition across medical professionals, and the criteria for the diagnosis may not be accurately applied. In addition, the initial diagnosis of severity may not be an indicator of long-term symptomatic and functional recovery, especially in the MTBI populations. Further confounding the understanding of the consequences of MTBI is the variable manner in which long term consequences may be studied and reported in the medical literature.

Brain injury should be distinguished from head injury, as a head injury does not imply that a brain injury has occurred. Head injury is damage to any structures of the head through trauma, whereas brain injury is determined by evidence via clinical examination or medical investigation of injury to brain parenchyma.


The severity of brain injury is predominantly determined on the basis of the depth and duration of the loss of consciousness, the duration of the impairment in memory processing and the Glasgow Coma Score (GCS). There are a multitude of definitions of what constitutes a mild brain injury.[2] Consistent in the definition is the GCS at 30 minutes of 13-15, a duration of loss of consciousness of less than 30 minutes, alteration in mental state at the time of injury or shortly thereafter that suggests neurological compromise such as confusion and/or being dazed, and the duration of post-traumatic amnesia (PTA) of less than 24 hours. MTBI can also be described as complicated, and this indicates the presence of abnormality on neuroimaging consistent with acute cerebral trauma. The outcome of a complicated MTBI may be less optimal than predicted by other MTBI criteria.[3]


There is evidence in animal models of TBI that neuropathology occurs on a continuum from severe to mild injury.[4] Abnormalities of axon architecture[5] is a consistent experimental finding of TBI with the extent of this abnormality varying according to injury severity. There remains controversy as to whether the animal models reflect what occurs in the human brain and, due to limitations of modern medicine, measures in living subjects are indirect (such as neuroimaging). Standard neuroimaging, especially after the acute period has passed, is often unhelpful. There is emerging evidence of the value of diffusion tensor imaging[6] following MTBI, as it allows mapping of white matter pathways and brain connectivity. Functional imaging studies also show promise, but are currently still only at the research stage.


The sequelae of MTBI can be divided into acute or chronic. The acute features are commonly evident in the first few days and weeks after the injury. Chronic consequences may occur up to years after the injury. The common symptoms associated with MTBI are frequently divided in to the physical consequences, cognitive symptoms and behavioural complaints. There has been propensity tendency to describe the consequences of MBTI as a post-concussive syndrome. Clinically, this terminology is often applied to those people who have sustained a MTBI and remain symptomatic after three months post-injury, although the criteria of length of time after injury for which this term is used is not consistently applied.

The cognitive abnormalities which are reported after MTBI are the most frequently studied. Common abnormalities include problems in processing speed, concentration, attention, and memory. The physical consequences described include headache, dizziness and fatigue. The emotional or behavioural changes reported include anxiety, irritability, and depression. The abnormalities of cognition are often no longer able to be detected by psychometric testing days after injury, and return to baseline of cognitive skills frequently determines when elite athletes are able to return to active play after acute injury. By 1-3 months post-injury, most neuropsychology studies indicate a return to baseline or no detectable abnormalities.[7] While patient populations may not have detectible cognitive abnormalities on testing, a proportion of subjects continue to report concentration problems and other symptoms.

The affective symptoms that are typically reported include anxiety and depression. Post-traumatic stress symptoms and disorder are seen with all degrees of severity of injury and therefore the presence of such symptoms does not help in terms of determining whether an injury has been severe or mild or clarify why some patients remain symptomatic longer term and others recover.[8] There is controversy as to whether the symptoms of depression or anxiety are as a response to a biological change in the subject following MTBI, are due to the TBI, or whether the symptoms are a reaction to pain, and the nature of other physical symptoms. An extensive body of literature documents the increased incidence of mood and anxiety disorders after TBI. [9]

The physical changes reported by patients after MTBI include headache, dizziness and fatigue. Most frequently there is no evidence of underlying neurological abnormality to explain the presence of these symptoms but they can nevertheless be disabling. The pattern of recovery of these symptoms frequently mimics the cognitive and affective symptoms.


Up to 64 per cent of subjects who have sustained an MBTI continue to report symptoms three months after the initial injury. [10] The proportion that remain symptomatic after 12 months is lower, and usually in the area of 10 per cent. The longer-term consequences of the condition have most commonly been described in the literature as either post-concussive syndrome (PCS) or disorder, with there being little consistency in the literature. More recent research now refers to the patient complaints after MTBI that extend over time as post-concussion symptoms. While the distinction is subtle, a syndrome in medicine is a group of signs and symptoms that occur together and characterise a particular abnormality. More recent research in PCS has shown that the symptoms reported after MTBI are not specific to head or brain injury and may occur in carefully selected populations that have no evidence of TBI, such as pain populations.[11] Diagnostic and Statistical Manual of Mental Disorders IV (Text Revision) (DSM-IV-TR)[12] contained a section on post-concussion disorder in a section on areas that require further research. DSM V [13]does not include a diagnosis for post-concussive disorder, which has largely come about following research that has shown the non-specificity of the symptoms described in PCS.[14]

Factors Contributing to Outcome

Miller proposed that a major determinant for outcome following brain injury was the factor of compensation. His published works were based on subjects seen for medicolegal assessments and included no control groups.[15] It was his opinion that subjects would recover with the resolution of the litigation. While this opinion can still be found in some clinicians, good quality research which incorporates control groups of non-TBI subjects and normal controls has improved the understanding of the complex pattern of recovery for a proportion of the MTBI patients.

The majority of studies has now demonstrated the importance of the affective symptoms following MTBI as a possible factor contributing to poor outcomes. Borgaro et al,[16] when comparing complicated MTBI with uncomplicated MTBI and controls in a small sample of 14 in each group, found no differences in the uncomplicated MTBI subjects on cognition but an increase in the rate of affective symptoms. Losoi et al found that in a cohort of previously healthy subjects, those with a less than optimal recovery had at one month post-injury depression, possible post-traumatic stress disorder (PTSD) and low resilience.[17] Further evidence regarding the role of mental health in recovery has been repeatedly demonstrated in studies.[18]

Other studies have demonstrated that a past history of mental health problems will predict poor recovery from MTBI. The relevant mental health conditions included a previous affective or anxiety disorder or PTSD.[19] However, some studies have not found an association with pre-injury mental health conditions[20] except for a pre-injury history of traumatisation. In addition to the finding of pre-injury psychiatric illness possibly being a risk for poor outcome, other factors such as ineffective coping mechanisms and illness expectation have been shown to influence post-MTBI symptom reporting.[21]

One of the major problems with the published studies is often the method of obtaining patient samples for the study, selecting a biased sample or the absence of a control group. More recent studies have found that functional impairment from MTBI was only more likely in those subjects with an MTBI with psychiatric disorders. These findings suggest that it is not injury to the brain that contributes to the post-injury disability but the mental health problems post-trauma.[22]

As mentioned earlier, litigation has been considered a factor that contributes to poor outcome following MTBI.[23] Unfortunately, even in those studies showing a positive relationship to disability and litigation, the direction of the effect cannot be determined. It is recognised that the process of litigation may be stressful and therefore contribute to the disability.[24] The effect of litigation on outcome, however, appears to be small.


Diagnostic criteria in psychiatry have been designed to improve the quality of cohorts of research groups. The diagnostic criteria generally do not imply causation, except for the diagnosis of post-traumatic stress disorder (PTSD). DSM IV-TR proposed research and diagnostic criteria for PCS, but studies based on these criteria have failed to demonstrate specificity, with the criteria often being fulfilled by patients with non-cranial trauma.[25] Research has shown that normal subjects and those with fibromyalgia[26] can have similar rates of PCS without having sustained a brain injury.[27] Patients with chronic pain, experiencing a traumatic injury with no evidence of TBI or psychiatric illness, will report symptoms consistent with PCS. The emotional distress and symptoms reported after MTBI have been shown by Meares et al to be unrelated to brain injury, but to pre-injury factors and non-neurological trauma factors.[28] Essentially, the use of the diagnosis of PCS after brain injury does not contribute to an understanding of the client and the relationship of the injury to the accident circumstances.


MTBI remains a common injury in the trauma patient group. While experimental studies in animals have demonstrated neuropathology, it is not clear whether this can be extrapolated to humans. While research utilising structural and functional imaging is able to document in some subjects abnormalities of neural connectivity, the significance of this to the post-MTBI clinical presentation is unclear. Subjects reporting symptoms following MBTI are more likely to have a pre-morbid history of mental health symptoms and may be less resilient to stress.

Research now suggests that brain injury factors may contribute little to the longitudinal presentation of MTBI subjects. It is accepted that criteria proposed for the clinical presentation after MTBI, the PCS, have been found to have little specificity for MTBI and therefore should be abandoned. More probably than not, the tendency to cluster the diverse symptoms that are reported after MTBI into one syndrome is an over-simplification of a complex clinical state. There is reasonable evidence that MTBI initially results in disruption of neuronal circuits. Personality variables, accident characteristics, pre-morbid psychological vulnerabilities including past psychiatric illness will all influence the reported symptoms post-MTBI. Subsequent health service and legal service contact will also contribute to symptom reporting. While MTBI and its reporting remains a challenge for the community, it is important to recognise that the label ‘mild’ implies good outcome but for a small proportion of subjects (10 per cent) there is long-term functional impairment, symptom reporting and disability.

Dr Patricia Jungfer is a consultant neuropsychiatrist specialising in the management of patients with white matter disorders. Dr Jungfer is a Disputes Assessor with Icare, and the State Insurance regulatory authority. Belvedere Consulting Rooms EMAIL

[1] JA Langlios Orman, JF Kraus, E Zaloshnja, T Miller; Chapter 1, Epidemiology: in JM Silver, TW McAllister, SC Yudofsky: Textbook of Traumatic Brain Injury, 2011, American Psychiatric Press, pp3-22.

[2] T Kay, DE Harrington, R Adams et al, ‘Definition of mild traumatic brain injury’, Journal of Head Trauma Rehabilitation, 8, 1993, pp86-87; LJ Carroll, JD Cassidy, PM Peloso et al, ‘Prognosis for mild traumatic brain injury: results of the WHO collaborating centre task force on mild traumatic brain injury’, Journal of Rehabilitation Medicine, (suppl 43), 2004, pp84-105;

M McCrea, Mild traumatic brain injury and postconcussion syndrome: the new evidence base on diagnosis and treatment, Oxford University Press, New York, 2008.

[3] S Kashluba, RA Hanks, JE Casey, SR Millis, ‘Neuropsychologic and functional outcome after complicated mild traumatic brain injury’, Archives of Physical Medicine and Rehabilitation, 89(5), 2008, pp 904-11.

[4] JT Povlishock, TH Coburn, ‘Morphopathological change associated with mild traumatic brain injury’, in H Levin, H Eisenberg and A Benton (eds), Mild Head Injury (Oxford University Press, 1989) pp37-53.

[5] An axon is a long, slender projection of a nerve cell, or neuron, that typically conducts electrical impulses away from the neuron's cell body. The function of the axon is to transmit information to different neurons, muscles and glands.

[6] Diffusion tensor imaging (DTI) is a MRI-based neuroimaging technique which makes it possible to visualise the location, orientation, and anisotropy of the brain's white matter tracts.

[7] J Ponsford, C Willmott, A Rothwell et al, ‘Factors influencing outcome following mild traumatic brain injury in adults’, Journal of the International Neuropsychological Society, 6, 2000, pp568-79.

[8] RA Bryant, JE Marosszeky, J Crooks, JA Gurka, ‘Post-traumatic stress disorder after severe traumatic brain injury’, American Journal of Psychiatry, 157:4, 2000, pp629-31.

[9] RE Jorge, RG Robinson, ‘Mood disorders’, in JM Silver, TW McAllister and SC Yudofsky (eds), Textbook of traumatic brain injury (American Psychiatric Press, 2011).

[10] C Blake, SR McCauley, HS Levin et al, ‘Limited agreement between criteria-based diagnoses of post-concussional syndrome’, Journal of Neuropsychiatry, Clinical Neuroscience, 14, 2004, pp493-99.

[11] GL Iverson, ND Zasler, RT Lange, ‘Post Concussive Disorders’, in ND Zasler, D Katz and RD Zafonte (eds), Brain Injury Medicine Principles and Practices (Demos Publishing, 2006) pp373-405.

[12] American Psychiatric Association, Diagnostic and Statistical Manual of Mental Disorders, American Psychiatric Publishing, Arlington VA, 2000.

[13] American Psychiatric Association, Diagnostic and Statistical Manual of Mental Disorders, American Psychiatric Publishing, Arlington VA, 2013.

[14] D Friedland, ‘Post-Concussion Syndrome/Disorder or MTBI: diagnostic issues and treatment’, Advances in Clinical Neuroscience and Rehabilitation 15(1), 2015, pp24-5.

[15] H Miller, ‘Accident Neurosis’, British Medical Journal, 1, 1961, pp911-12.

[16] SR Borgaro, GP Prigatano, C Kwasnica and JL Rexer, ‘Cognitive and Affective sequelae in complicated and uncomplicated MBTI’, Brain Injury, 17(3), 2003, pp189-98.

[17] H Losoi, ND Silverberg, Wallasey M et al, ‘Recovery from mild traumatic brain injury in previously healthy adults’, Journal of Neurotrauma, 33, 2016, pp1-11.

[18] G Mooney and J Speed, ‘The association between mild traumatic brain injury and psychiatric conditions’, Brain Injury, 15(10), 2001, pp865-77.

[19] S Meares, EA Shores, AJ Taylor et al, ‘Mild traumatic brain injury does not predict acute post-concussion syndrome’, Journal of Neurology, Neurosurgery, and Psychiatry 79(3), 2007, pp300-6.

[20] G Mooney, J Speed and S Shepherd, ‘Factors related to recovery after mild traumatic brain injury’, Brain Injury, 19(12), 2005, pp975-87.

[21] A Panayiotou, M Jackson and SF Crowe, ‘A meta-analytic review of the emotional symptoms associated with MTBI’, Journal of Clinical and Experimental Neuropsychology, 32(5), 2010, pp463-73.

[22] R Bryant, ML O’Donnell, M Creamer et al, ‘The psychiatric sequelae of Traumatic injury’, American Journal of Psychiatry, 167, 2010, pp312-20.

[23] See above note 5.

[24] WH Rutherford, ‘Post-Concussion symptoms: relationship to acute neurological indices, individual differences, and circumstances of the injury’ in HS Levin, HM Eisenberg and AL Benton (eds), Mild Head Injury (Oxford University Press, 1989) pp217-29.

[25] C Boake, SR McCauley, HS Levin et al, ‘Diagnostic criteria for post-concussional syndrome after mild to moderate brain injury’, The Journal of Neuropsychiatry and Clinical Neurosciences, 17(3), 2005, pp350-6.

[26] Fibromyalgia is a chronic medical condition characterised by widespread pain and tenderness. It is frequently associated with depression, anxiety, and posttraumatic stress disorder.

[27] See above note 11.

[28] See above note 19.

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