‘The needs of the walking wounded are being ignored’

We meet Dr Priyanka Pradhan.

Dr Priyanka Pradhan is a Consultant Clinical Neuropsychologist at St George’s University Hospital and is holding a workshop on mild traumatic brain injury later this year. Our journalist Ella Rhodes spoke to her.

Can you tell me about how mild traumatic brain injuries were dealt with in the past?
Historically, a mild traumatic brain injury – an mTBI – was not commonly associated with longstanding physical or cognitive sequelae. The general consensus was that symptoms should abate within three months followed by complete recovery by six months, with the individual being able to return to pre-injury work and social function.

If this trajectory was not followed, then any ongoing and persistent physical symptoms were thought to be ‘functional’, and persistent cognitive and emotional symptoms thought to be of ‘psychological’ or ‘psychogenic’ origin. Such individuals were not deemed appropriate for neurological services due to the perception of their symptoms being of non-organic causation. If referred to and accepted by mental health services, the array of issues associated with mTBI were poorly understood and, in many cases, formulated and treated incorrectly.

And we’re not talking about concussion here?
No. For a long time the term ‘concussion’ has been used interchangeably with mTBI. But they are not the same thing. In 2015 David Sharp and Peter Jenkins, from the Division of Brain Sciences at Imperial College London, suggested that the term ‘concussion’ should be abandoned, as it has no clear definition or pathological meaning. Instead they propose that ‘neurologists and other healthcare professionals should classify the severity of the traumatic brain injury and then attempt to precisely diagnose the underlying cause of post-traumatic symptoms’.

So what do we know about the effects of mTBI now?
Whilst there has been a shift in our understanding of the impact of mTBI on physical, cognitive, emotional, behavioural and psychosocial functioning, for a long time presenting symptoms were subject to dichotomous categorisation of either ‘organic’ or ‘psychological’. This black-and-white view of symptoms fails to fully account for the complexity and interplay of biopsychosocial and cognitive factors and, most importantly, the day-to-day experience of the individual. Basically, it falls short of a comprehensive neuropsychological formulation.

For many years, services in the UK that accepted individuals with mTBI for treatment were scarce. I am pleased to say that there is some change in our understanding of the impact of mTBI, but due to issues around commissioning and strains on NHS services, provision is yet to catch up. Also because of the variable understanding of mTBI amongst GPs and physicians in A&E, the two main points of entry, referral to specialist services and subsequent treatment can vary immensely. Essentially the needs of the ‘walking wounded’ are being ignored for those with more serious physical injuries: understandably so, many would say. However, the emerging long-term outcome of not identifying and treating mTBI is proving to be a substantial strain on health and social care services as well as the welfare and the criminal justice systems… individuals experience family and relationship breakdown, loss of jobs, poor health, substance misuse and, in some cases, engagement in criminal behaviour.

Whilst there is growing evidence that symptoms individuals are experiencing following mTBI are a direct result of a pathological process within the brain, there is yet to be a general acceptance amongst clinicians working in the field. Challenging long-held belief systems of clinicians is, in many ways, our first and biggest hurdle in the appropriate treatment of individuals following mTBI.

What injury mechanisms trigger mTBI?
There are two main causes of traumatic brain injury. The first is when direct forces are applied to the head. This is referred to as ‘impact’ injury and can be caused by a blow to the head or the head hitting something. This mechanism of injury usually results in a loss of consciousness, in some cases, very briefly. The second mechanism of traumatic brain injury is caused by acceleration/deceleration of the brain in the skull. This is often the type of injury that individuals experience in road traffic collisions and has previously been termed ‘whiplash’. However, what has gone undetected until recently is that the acceleration/deceleration of the brain within the skull can lead to diffuse axonal injury (DAI). DAI results in the shearing of neural pathways in the connective white matter, which forms the subcortical regions of the brain. It results in a metabolic cascade that evolves over minutes, hours and days. In essence, a disruption occurs in the brain’s ability to efficiently and effectively relay messages between neurons. The effect on function is cumulative over time rather than immediate.  

This trajectory is likely to have given rise to the misinterpretation that evolving cognitive symptomatology is psychological rather than organic. However, physical symptoms also evolve over time, and despite being initially discharged from A&E due to being medically fit, individuals may return with symptoms that can include vomiting and headaches. Of course, over time, as individuals get the feedback that their brain and body is not functioning as it once did, their mood will be affected, which results in reactionary psychological issues.

I have assessed a wide variety of patients following what has been classified as mTBI. What is striking is the undeniable similarity and consistent patterns of what people report, which does not seem to be influenced by gender, age, social strata, ethnicity or which referral path they have come through.

What are some of the limitations of brain-imaging techniques in this context?
A CT scan is used to detect skull fractures, injuries that are focal in nature, as well as intrarcerebral bleeding, all of which would be classified as moderate/severe brain injury according to the Mayo criteria. A CT scan, such as is routinely used in emergency departments when individuals present with a head injury, would be normal for mTBI.

A standard MRI produces a more detailed picture of the brain, but, like a CT scan, they are insensitive to subtle vascular or diffuse axonal injury. There are more sophisticated MRI techniques that show vascular and white matter damage such as gradient-echo and susceptibility weighted imaging. These scanning techniques can show micro-bleeds, which is an indication of white matter injury (including DAI) but unfortunately are not routinely available, especially for those that have no overt signs of a brain injury. Diffusion-tensor imaging (DTI) is another tool that is often used in research but not clinically, despite its being a sensitive marker for white matter injury.

In sum, standard neuroimaging lacks the sensitivity to identify damage at a microscopic level, which is the level at which DAI occurs. Individuals are reassured, albeit falsely, that the scans and therefore their brains are normal. This is at odds with their experience and clinical outcome. Thus DAI is often a ‘diagnosis of exclusion’ for those with persisting symptoms following a head injury but no radiological findings.

What kinds of neuropsychological assessments can reveal mTBI?
For me as a diagnostician, it is about identifying tests that highlight the brain regions that are most susceptible to being affected. I am reluctant to name specific neuropsychological tests in an effort to keep them (as much as possible) out of the public domain. Whilst I assess all cognitive domains, I interrogate frontal and subcortical functions more heavily. In terms of memory assessment, I look at the pattern of performance to help differentiate whether there is a deficit in encoding, retention or retrieval and whether there is any benefit gained from cueing. Furthermore, I assess post-traumatic amnesia, albeit retrospectively. This line of questioning helps to elucidate what information the individual recalls minutes, hours and days after the injury. This information is important in the classification of brain injury severity.

There are limitations in solely basing neuropsychological formulation on neuropsychological tests alone. Many people with mTBI perform within normal limits on a range of standard neuropsychological tests… but of course this doesn’t mean they do not experience a change in their cognitive functioning post-mTBI, given the sterile nature of a testing environment. Our understanding of executive functioning, in particular is evolving – seek out recent research by Donald Stuss and by Rodger Wood and Andrew Worthington. It is being more widely recognised that observed neurobehavioural changes indicate executive dysfunction even when performance on standardised neuropsychological tests is not significantly different from the individual pre-morbid level. For many years this discrepancy between ‘normal’ neuropsychological test results and what the individual and family members reported in terms of persisting symptoms was labelled ‘psychological’ and in some cases, unfortunately, ‘malingering’.

Having spent a large proportion of my 20-year career in neuro-degenerative differential diagnosis, I use the same principles when assessing those with brain injury. I use a breadth and range of information to test hypotheses and inform my formulation. That includes clinical interview of the individual and someone who knows them well, neuropsychological assessment, standardised mood questionnaires, observations of behaviour before, during and after testing. It is well recognised by neurologists who work in neurodegenerative services that cognitive problems can present prior to neuro-radiological changes. So brain scans are just one part of the puzzle, rather than the main source of evidence of brain pathology and cognitive dysfunction.

‘Effort testing’ is important. However, the value of this can be misunderstood in a personal injury claim. I am aware of cases where the individual has performed within normal limits on most neuropsychological tests but then failed tests of effort. To me, this indicates that the test of effort was not fit for purpose rather than being an indication of poor effort on the part of the individual, as they are capable of applying normal effort on other tests. Many of the most popular tests of effort load heavily on attention and also give feedback about an incorrect response. This in itself can result in elevated levels of stress, which then further impedes performance. I tend, therefore, to use a mix of embedded and overt tests of effort that tap into a variety of cognitive domains.

What implications might this changing awareness of mTBI have on clinical practice?
In the first instance I think the term ‘mild TBI’ is misleading. From my clinical experience, there is nothing mild about the impact on people’s lives. People fail to return to work successfully, their relationships and support systems break down. A recent review by Huw Williams and colleagues explored the link between violent crime and brain injury, revealing that a high proportion of those with brain injury, whatever the severity, end up in the criminal legal system.

The first step for clinicians is to allow their belief systems around mild TBI to be challenged with the growing evidence base. This will then allow individuals to be properly assessed, and understood and for their symptoms to be taken seriously and treated appropriately. This has significant implications for primary care service provision in the short term, but should ultimately ease the long-term impact of secondary and tertiary care service provision.

What are the treatment options for mTBI?  
The first step is acceptance that there has been a change in brain functioning. This will allow the individual, with the support of experienced professionals, to make adjustments. So that involves psycho-education for the individual, family and workplace. In my medico-legal work, there is the argument that telling someone they have a brain injury will then result in their behaving in a way that supports this diagnosis and inhibits them from improving: but there’s limited evidence for this ‘misattribution bias’. Whether or not an individual is told their brain is injured, recovery is slow and treatment needs to be far more holistic than it currently is.

Within statutory services, there is significant variability in provision. Some individuals receive a neuropsychological assessment with some feedback and recommendations. Some may receive a few sessions of occupational therapy and physiotherapy input. When involved in a personal injury claim, treatment can be much more comprehensive in terms of professional time, but it still falls short in terms of breadth and scope. This is partly due to the evidence base for talking therapies and medication being much larger than that for options such as neurofeedback, music and art therapy, acupuncture and hormone replacement therapy, to name just a few. There is, however, growing evidence for the use of more brain–body based approaches, such as yoga, tai chi and qigong. These can also help to combat fatigue, which is a significant inhibitor to recovery. 

- Dr Pradhan’s workshop, run jointly with Consultant Neurologist Dr Steven Allder, is being held at the British Psychological Society’s London offices on 21 September.
See tinyurl.com/pradhanallder

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