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Understanding MTBI: incidence, classification, evidence & implications
- Dec 12, 2023
- Latest Journal
by Dr Tracey Ryan-Morgan
Consultant Clinical Neuropsychologist, Talis Consulting Limited
How common is MTBI?
It is an established fact that “more than 90% of all TBI cases are classified as mild, based on a GCS of 13-15” (Maas et al, The Lancet, 2022 p.1033). It is important to understand how injuries to the head and brain are categorized. The following indicators are commonly referred to in order to classify whether a head injury constitutes a TBI with the caveat that not all head injuries result in a brain injury.
How do we classify brain injuries?
• Level of awareness / consciousness (Glasgow Coma Scale Score: GCS)
GCS comprises three separate measures (Eye, Verbal, Motor) all of which can be confounded by the presence of substances ingested prior to the injury or by the administration of medications at scene or on arrival at the ED. Research indicates that GCS on arrival at A&E is the more reliable prognostic indicator than GCS at scene (Lesko et al, 2013). Allen et al (2013) highlight clearly that a GCS of 8 can mean different outcomes due to the heterogeneity of TBI injuries (Extra Dural Haematoma vs Diffuse Axonal Injury vs Sub Dural Haematoma vs Contusion, for example). For that reason, GCS is not considered to be a particularly robust prognostic indicator.
• Loss of Consciousness
Similar measurement difficulties apply to assessing length of loss of consciousness, particularly in cases where the individual may have been under the influence of substances immediately prior to injury. In my clinical experience, patients with MTBI often grossly over-estimate the amount of time that they lose consciousness for, if at all. The best sources of corroborative evidence are from witnesses at scene and the contemporaneous ambulance records. It is possible to sustain a mild traumatic brain injury without a loss of consciousness.
• Post Traumatic Amnesia (PTA)
PTA is notoriously difficult to assess retrospectively as many patients who receive pre-hospital care can have orthopaedic injuries for which they are administered opiate analgesia. This confounds measurement of PTA (McCarter et al, 2007). Ruff et al (2009) discuss the difficulties of extrapolating genuine memories from information the person has been told or has surmised. Unless formally measured using a recognised measure such as the Westmead PTA scale, subjective measurement tends to be unreliable. PTA is explored in more detail below.
It is important to be aware that, "the GCS remains the main instrument for classifying the severity of TBI...(but)….the duration of PTA is widely used as an indicator of injury severity and reported to be a strong predictor of outcome" (Lancet, 2022, p.1024)
• Evidence of brain injury from neuroradiological investigations
Most “milder” brain injuries tend to be routinely investigated by CT scan which may not sufficiently sensitive to detect axonal or vascular injuries which can then be (erroneously) excluded (Sharp & Jenkins, 2015). In addition, there is an imperfect correlation between neuropathology and functional and/or cognitive impairment which needs to be considered (Allen et al, 2013, Bunnage 2013).
What is PTA?
The interval from the injury until the patient is orientated and can form and recall new memories. A person in PTA can often appear to be engaging normally with those around them but are unable to lay down new memories and, as a result, can subsequently appear confused or disorientated.
Why measure PTA?
The greatest accuracy is in using PTA as a continuous variable (Ponsford et al, 2016) where it is the strongest predictor of both productivity and functional outcome. It is important to establish whether or not a patient is in PTA, as there is no point in undertaking cognitive assessment or therapeutic treatment as the results would not be valid or reliable and the intervention would not be retained.
The onset of PTA begins at point of impact of the external forces so if the patient can describe a personal memory for the injury then the classification of the brain injury would be “mild” at worst. For PTA to exist, there must be a gap between impact and first recall post-injury. If there is delayed onset amnesia then factors other than the injury are likely mechanisms for the amnesia (eg: shock from fluid loss, hypoxia from respiratory distress). Having fleeting or isolated memories does not signify the end of PTA, as islands of memory are not uncommon during recovery from the confusion that typifies PTA.
Retrospective estimates of PTA are notoriously unreliable (Friedland & Swash, 2016) as consideration must be given to factors other than the traumatic brain injury which can impact on memory both at the time of injury and later on.
Problems with measuring PTA
It is possible that a patient may have no memory for the accident but be fully orientated (Ruff et al, 2009), “beware the orientated amnesiac” (Symonds & Russell, 1943). It is known that analgesia can induce memory “gaps”, even in patients with no underlying brain injury (McCarter et al, 2007; Kemp et al, 2010). It is possible that the patient may have full recall but be acutely stressed and appear forgetful or disorientated (Ruff et al, 2009). There is the possibility that healthcare Staff may not administer measures such as the Westmead Post Traumatic Amnesia Scales (WPTAS) consistently (inter-rater reliability) or not according to standardised instructions (intra-rater reliability and validity). Assessors need to be aware that the patient may be aphasic or lack the ability to communicate reliably but be fully orientated. This can confound measures of PTA which are administered and scored according to the verbal responses of the patient.
Poor performance on the WPTAS could be due to a number of other factors apart from post-traumatic amnesia. These include: poor motivation; malingering; medication effects; a further episode of head trauma, (such as falling whilst an inpatient); an undetected episode of hypoxia, (in cases where there has been emergency resuscitation); failure to diagnose premorbid difficulties or problems, like a previous learning disorder; or an undetected communication disorder like dysphasia or dyspraxia. These must be ruled out in order to convincingly demonstrate that the patient is still in PTA.
Classification of TBI
(The MAYO system, Malec et al, 2007)
Classify as Moderate–Severe (Definite) TBI if one or more of the following criteria apply:
• Death due to this TBI
• Loss of consciousness of 30 min or more
• Post-traumatic anterograde amnesia of 24h or more
• Worst Glasgow Coma Scale full score in first 24 h <13 (unless attributable to intoxication, sedation, systemic shock)
• One or more of the following present:
• Intracerebral haematoma, subdural haematoma, epidural haematoma, cere-bral contusion, haemorrhagic contusion, penetrating TBI (dura penetrated), subarachnoid haemorrhage, brainstem injury.
If none of the above criteria apply, classify as Mild (Probable) TBI if one or more of the following criteria apply:
• Loss of consciousness momentarily to less than 30 min
• Post-traumatic anterograde amnesia momentarily to less than 24 h
• Depressed, basilar or linear skull fracture (dura intact)
If none of the above criteria apply, classify as Symptomatic (Possible) TBI if one or more of the following symptoms are present:
• Blurred vision,
• Confusion (mental state changes)
• Daze
• Dizziness
• Focal neurological symptoms
• Headache
• Nausea
Classification of MTBI
The World Health Organisation (Carroll et al, 2004) define MTBI as occurring when at least one of the following apply:
• GCS of 13 or above at 30 minutes post-injury;
• Post-Traumatic Amnesia of less than 24 hours;
• Loss of consciousness of no more than 30 minutes;
• Temporary confusion; and
• Normal brain scan (this would include all types of scan)
This has to be in the absence of drugs, medication, alcohol or penetrating head injury. The WHO system is considered to be more helpful in considering milder brain injuries as the MAYO system is, “not able to get around some of the difficulties inherent in TBI classification especially at the milder end of the spectrum” (Friedland, 2013). It is also noted that, “...there is no guide as to long-term prognosis in the Mayo system” (Friedland & Hutchinson, 2013) and so it has little clinical utility.
The American Congress of Rehabilitation Medicine Diagnostic Criteria for MTBI (Silverberg et al, 2023) has recently developed a new classification system by consensus which only differentiates between "MTBI" and "suspected MTBI" but posits that there must be a biomechanically plausible mechanism of injury (including acceleration / deceleration injury with no contact to head). One or more of the following criteria must be met:
1. Clinical Signs: LoC; alteration of mental status following the injury; complete or partial amnesia for events immediately following injury; other acute neurological signs
2. Acute Symptoms: confusion / disorientation; physical symptoms; cognitive symptoms; emotional symptoms
3. Clinical Examination / Lab Findings: cognitive impairment; balance impairment; oculomotor impairment; elevated blood biomarkers indicative of intracranial injury
4. Neuroimaging: trauma-related intracranial abnormalities on CT or MRI
5. Not better accounted for by confounding factors (pre-existing or co-occurring health conditions)
As this system has only recently been published its clinical utility has yet to be established but the aim was to present a single taxonomy to promote a common understanding of MTBI.
What might "complicating" factors be in the context of MTBI? These were described by McCrea (2008) who differentiated between Uncomplicated MTBI where there is no neuroradiological evidence of injury and Complicated MTBI where there is positive neuroradiological evidence of traumatic injury. Recent research has upheld the clinical utility of this distinction but "the size of cognitive deficit (even) in complicated MTBI was small and unlikely to cause significant disability” (Hacker et al, 2023 p.3). This is a change of position from earlier research which had reported that complicated MTBI would lead to similar outcomes to moderate TBI by increasing the risk of slow or incomplete recovery (Williams et al, 1990 in McCrea, 2008) and by the patient taking considerably longer to return to work (Iverson et al, 2012).
The table at the end of this article summarises all of the key information required to classify a traumatic brain injury
Why is it that so many patients with such minor injuries report so many problems?
Bunnage (2013) referred to, “the role of psychological factors in the creation and perpetuation of symptoms following MTBI”. Researchers often comment upon the apparent disconnect between the relatively trivial nature of the index injury in such cases and the catastrophic symptoms that are reported by patients. Perrine & Gibaldi (2016) argued that, "Patients with relatively minor injuries can endorse a large number of severe post-concussion symptoms and complaints of long-term sequelae that reportedly disrupt daily functioning...if any physical disorder is present, such as minor and uncomplicated head injury, it does not explain the nature and extent of the symptoms or the distress of the patient...the frequency of somatoform disorder in patients presenting with post-concussion syndrome is significant" (2016, p5). Research has continued to report the same pattern and Phillips stated that, "in many ways, whether a claimant fulfils criteria for MTBI or not is not particularly relevant; persistent symptoms are likely to be functional, whether there has been an insult directly to the head or not" (2021, p.3).
What is the evidence for long-term or permanent consequences of mtbi?
Carroll et al (2014) review the literature and conclude that complete recovery may take six months or even up to a year but that full recovery would be expected. However, other researchers (Dean et al, 2012; McInnes et al, 2017; Nelson et al, 2019; and, Machamer et al, 2022) all attempt build a case for incomplete recovery up to and over a year after MTBI. But, there are several issues to consider:
1. The term MTBI is an over-inclusive descriptor which includes those who did not lose consciousness after a bump on the head and have clear CT and MRI scans, through to those who lost consciousness and have positive neuroradiological evidence of underlying brain injury: "one should consider subgroups of patients likely to vary in prognosis" (Nelson et al 2019 p.1050)
2. Most research or review studies have small sample sizes (eg: Dean et al, 2015, claim evidence of permanent white and grey matter changes after MTBI based on a sample size of 16).
3. Many studies use self-report measures such as the Rivermead Postconcussion Questionaire (RPQ) to positively diagnose MTBI yet it has weak content and construct validity. The RPQ lists symptoms which as non-specific such that a person with a chronic pain condition or an orthopaedic injury who has never sustained a head injury would score positively for symptoms of post-concussion.
4. Where comprehensive neuropsychological testing takes place, many commentators are unaware that inter-test scatter of scores occurs in the normal (healthy) population. Iverson & Gaetz (in Lovell et al, 2004) remind researchers that the more tests that are administered, the greater the probability that an individual will score in the “abnormal” range for one or more scores, even in the absence of a brain injury. This is a necessary caution as it avoids one pathologizing what is essentially a normal test profile.
5. McInnes et al (2017) argued that half the individuals with a diagnosis of MTBI have cognitive impairments on formal neuropsychological testing at 3, 6 or 12 months post-injury…BUT Iverson et al (2019) thoroughly debunked this paper concluding that, the impact of MTBI is undetectable on testing at 3 months post injury also arguing that McInnes et al “has the potential to misinform scientists, clinicians and the public…Clinicians who review and accept the findings of McInnes et al will be misinformed” (p.13).
In summary, there is no established evidence of objective, measurable, long-term adverse cognitive effects in a single MTBI.
So, what about Post Concussion Syndrome?
This term used to be used frequently in clinical practice but there has always been difficulty in establishing exactly what symptoms are referred to. Since the revision of the major diagnostic taxonomies, it no longer exists as a diagnosis.
DSM-V (May 2013 & TR version March 2022, American Psychiatric Association)
Post-concussion syndrome was considered to be a controversial and (scientifically) poorly defined entity. PCS was used by clinicians to describe and refer to all sorts of different symptoms and presentations. The DSM-IV criteria for PCS were for research use, not clinical use, and were never generally accepted. DSM-V, therefore, dropped the diagnostic construct and indicated that persistent symptoms after a concussion should lead to consideration of neurocognitive impairment, somatic symptom disorder, or non-psychiatric causes.
ICD-11 (World Health Organisation, January 2022)
What was previously referred to as PCS is now classified as "mild neurocognitive disorder due to TBI". There needs to be less than one month between injury and symptom onset and the symptoms should not be sufficiently severe to significantly interfere with independence or activities of daily living.
What is the evidence for long-term or permanent consequences of mtbi?
There are researchers and clinicians who are seeking the "holy grail" of pathophysiological evidence within the brain to explain those with MTBI who report persistent symptoms for months or even years after injury – often in the face of no biological evidence of injury. They refer to published evidence of blood biomarkers (inflammatory markers; tau proteins, neurofilament light – the latter is an axonal protein) in support of this position. However, as recently as 2022, Mayer & Quinn critically examined the strengths and limitations of neuroimaging for establishing TBI related microstructural changes, neuroinflammation, proteinopathies, blood-brain barrier damage and disruptions in cellular signalling. They concluded that, “neuroimaging biomarkers do not yet exist for the definitive in vivo diagnosis of cellular pathology”(p.459). Rajesh et al (2023) call for further research into the potential role of biomarkers in prognosis following head injury.
The Lancet supports this position and states that: "when compared with more severe TBI, biomarkers were less predictive of outcomes in mild TBI and of incomplete recovery overall" (2022, p.1025). Other researchers are also unconvinced. Huovinen et al, (2021) found that, “in MTBI, traumatic microbleeds do not seem to be a significant prognostic factors of RTW (return to work)”
Those who argue for long-term consequences of MTBI suggest that there is a need for increasingly sophisticated brain imaging, suggesting that they just need to look harder and they will find the biological basis of perpetuating symptoms following such injuries. Bunnage had urged caution in that such a link has yet to be established, "to what extent (imaging abnormalities) can actually explain the disability experienced by patients" (2013, p.72) even where they exist. More recently, it has been pointed out that, "this is a type of diagnostic bias where undue emphasis is placed on one aspect of the presentation (the initial injury), which has the effect of obscuring other elements of the diagnostic process" (Sharp & Jenkins, 2015, p.174).
It is the case that pursuing this exclusively physical / medical explanation misses the relative and significant contribution of psychological and personality factors, past medical history, systemic issues, secondary gain (usually, but not always, financial) and confounding health issues (pain, iatrogenic effects of medications):
There is "increasing recognition by clinicians and policy makers of the relevance of a multifactorial bio-psycho-socio-ecological model to TBI (The Lancet, 2022, p.1029) "prognosis in mild TBI is driven to a greater extent by what the patient brings to the injury (eg: pre-injury co-morbidities and mental health)..." (The Lancet, 2022, p.1037). This latter argument echoes a similar view expressed by Lingsma et al (2015) who had suggested that, “in moderate and severe TBI outcome is determined by what the injury brings to the patient whereas in MTBI it is what the patient brings to the injury and our data support this statement….the combination of pre-existing psychiatric conditions, low education, and assault as a cause of injury as predictors of 6 month outcome poses the question of whether persistent complaints are fully attributable to the TBI” (p.92). This was followed up by Van Der Naalt (2017) who remarked that, "the risk of both cognitive and psychological symptoms co-exist from the beginning and that those most at risk of poor outcome at 6 months post injury are those who express emotional distress and maladaptive coping style at 2 weeks (when combined with pre-accident mental health problems, low education and older age)……" . These views were taken up and echoed by Yeates et al (2017) who considered that, “recovery from the injury is....shaped by pre-injury, comorbid and contextual factors”.
A comprehensive explanation of persisting symptoms had been suggested by Waljas et al (2015) who had found that patients with greater injury severity do NOT report more persistent symptoms, that patients with a pre-injury history of mental health problems are more likely to have persistent symptoms at one-month post-injury, and that although some patients with MTBI show differences on DTI imaging compared with controls, these patients did not report more symptoms than those with “normal” white matter. This led the authors to conclude that there is, therefore, no direct association between the presence of white matter changes and the presence of persisting symptoms.
“The manifestation of Post Concussion symptoms likely represents the cumulative effect of multiple variables, such as genetics, mental health history, current life stress, general medical problems, chronic pain, depression and substance abuse.....How people report their symptoms can also be influenced by personality factors and the presence of possible future financial gain (Waljas et al, 2015, p.544)
Despite the well-touted figure of 15% of the MTBI population being the “miserable minority” (Ruff et al, 1996) who do not fully recover, a closer analysis of the data reveals that the actual figure of those with poorer outcomes is between 1 and 5% This over-calculation which has been mistakenly perpetuated throughout the MTBI literature for many years occurred primarily because the operational definition of MTBI in a large number of reported studies required only a momentary loss of consciousness and was, therefore, over-inclusive. The figure was also elevated by a patient endorsing a single, non-specific symptom after 1 year (eg: headache) which led to study authors considering them to have an unresolved MTBI (Iverson, 2005, p.307). Ruff’s data were reviewed (Rohling et al, 2012) and it was concluded that there was compelling evidence against the existence of a chronically impaired sub-group of MTBI with significant continued deficits. Rohling et al further concluded that, “misidentifying common daily cognitive, somatic, and affective phenomena, which covary with stress as post-concussive, can reify these symptoms and in someone prone to being excessively focused on bodily sensations may create a disorder where none would otherwise exist” (p.210). This point is further reinforced by research by Waljas et al (2015) who reported a 31% false positive rate for persisting symptoms in a normal control group.
What about symptom exaggeration?
Lippa et al (2016, p.271) state that, “concern regarding symptom exaggeration is particularly warranted in situations where primary or secondary gain is involved such as medicolegal evaluations..”. Whilst it is for the Court to judge what an individual’s motivations might be in bringing a personal injury claim, the Expert is expected to provide an opinion and can certainly point to incongruities and inconsistencies in a clinical presentation, based on both clinical experience and knowledge of published literature (Slick et al, 1999). It is worth bearing in mind that two separate investigations have reported a substantial base rate of 40% of malingering in MTBI cases (Larrabee, 2003; Mittenberg et al, 2002 – reported in Rohling et al, 2012).
What about Functional Neurological Disorder as an explanation?
Picon et al (2021) stated that, “fear avoidance behavior was most strongly related to unexpected neurological symptoms and anxiety was most strongly related to unexpected somatic symptoms” after a concussive injury (p.3).
More recently, Mavroudis et al (2023) have reported that, “the lack of objective evidence for structural brain damage in PCS, combined with evidence of psychological factors contributing to PCS symptoms and similarities with other FNDs, suggests a strong case for considering PCS as an FND…PCS symptoms may be influenced by psychological and behavioral factors, which can exacerbate underlying neurological impairments and contribute to persistent symptoms” (p.6).
Summary
• Most head injuries are "mild"
• Full recovery is expected from a single MTBI. There is no objective, measurable evidence of long-term cognitive effects of a concussive injury.
• Definition and classification of MTBI can be problematic. It pays to be aware of the weaknesses in different taxonomies and to be mindful of over-inclusivity of non-specific symptoms.
• PCS is no longer a diagnostic classification.
• Persisting symptoms after MTBI are more than likely to be psychological, to be linked to secondary gain or be due to pre-existing vulnerabilities and impoverished coping skills than to a persisting underlying organic injury.
• The answer lies in the complex interaction of a bio-psycho-social-environmental factors not an exclusively medical model where increasingly sophisticated pathophysiological investigations are being pursued in the hope of uncovering a unidimensional (biological) substrate to prolonged symptoms post MTBI.
• Always review published research from a position of curiosity. Consider the methodology of any research published in the area of MTBI (definition / sample size / potential confounding factors).
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About the author
Dr. Tracey Ryan-Morgan
Dr. Tracey Ryan-Morgan is a Lead Consultant Clinical Neuropsychologist, and Clinical Director of Talis Consulting Limited (www.talisconsulting.co.uk), as well as an Associate Fellow of the British Psychological Society. Tracey was Registrar and Chief Supervisor to the Clinical Neuropsychology Qualifications Board for the post-doctoral Qualification in Clinical Neuropsychology (Q.i.C.N.) from 2010 to 2022 and is now Chair of the Committee for Training in Clinical Neuropsychology that sets the accreditation standards for post-doctoral university routes to the Specialist Register of Clinical Neuropsychologists. Tracey is a Regional Fellow of the Royal Society of Medicine and a Chartered Scientist. She works out of bespoke Consulting Rooms in Carmarthen and at 10, Harley Street, London.
Tracey was the Consultant and Clinical Lead for the Brain Injury Rehabilitation Trust 24 bed unit in Llanelli, Carmarthenshire from October 2013 to January 2017, establishing it as a new service.
