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The Elephant in the Jungle (as it relates to a traumatic brain injury)

Special Reports

by Dr. Michael Bourke, Consultant Psychiatrist, FRCPsych (UK), FRCP (Canada), PCPsychl (Ireland) - Psychiatric and Psychological Consultant Services Ltd (PPCS)


Introduction

As most in the profession will realise, medicine is often like the elephant in the jungle, where we are like pigmies, viewing a set of symptoms through the eyes of our own specialty.

One pigmy describes what he sees as big and round with nails on the end. Another describes what he sees as long and thin with two holes in the end through
which air passes. Another describes what he sees as round but long and thin with a tuft of hair in the end and you really shouldn’t stand there too long.

If the pigmies could stand back and view the entirety of what they each see, they would realise it was an elephant, but that is hard to do in a jungle dark with
foliage.

How often does that happen in medicine too? A young man presents to A&E having been thrown through the air by a car. He is an irritated and troubled youth who should not have been on the road in the first place. He is understandably somewhat disoriented, but there is no obvious loss of consciousness. He accepts a lift in the ambulance to A&E, where he is assessed neurologically due to the evidence of a head injury and the decision is taken to keep him in overnight.

Because he is an irritated and troubled youth, he finds staying in overnight for observation boring and discharges himself, his notes are written up correctly with a summary sent to his GP.

Two weeks later, his mother brings him to the GP saying that he is anxious and could he be given  something. His General Practitioner takes an appropriate history and registers the symptoms of anxiety, offering advice and treating appropriately.

Four months later the young man appears at the surgery again and on this occasion, he is complaining of being depressed. The notes suggest there may be a connection with his accident and he is referred to his local psychiatric service.

Some months later, the diagnosis of PTSD is given and he is offered a number of sessions of CBT to deal with it.

So far so good – his General Practitioner has registered anxiety and depression. The psychiatric service has registered depression and PTSD for which he is
receiving psychotherapy and later he is put on an antidepressant. Six months post-accident it is thought prudent to have a neurological opinion, due to his complaint of headaches and difficulty to quantify lapses in memory. His CT scan showed a frontal suprorbital contusion with a repeat being reported as normal and the Neurologist queries post traumatic migraine.

Nine months later, the young man is on propranolol, requesting tranquilizers and given to bursts of unpleasant behaviour while complaining of panic attacks. Twelve months later, with little change in his condition, the history of his grandfather’s Huntington’s disease brings the question of whether a similar process might be taking place. He is referred to a Neuropsychiatrist where eventually the diagnosis of Huntington’s is discounted. He is discharged and continues on the antidepressant.

He is referred back to his local psychiatric service with the query diagnosis of an emerging psychosis, due to his excited, over-active behaviour, disregard for other people’s needs, pressure of speech and insomnia. The diagnosis of bi-polar affective disorder is given and neuroleptic medication is introduced. The young
man is non-concordant with medication and he appears to become more floridly psychotic.

Around this time, going into his third year, the question of organic mania (ICD 10 – F30.8) is questioned but depending who is looking, the alternative diagnosis of an emerging schizophrenic illness due to his paranoid delusions is also thought to be a valid alternative. He eventually agrees to be treated with the neuroleptic Olanzapine 15 mgs nocte, which in turn appears to be helpful. The diagnosis of schizophrenia becomes established and his irritating and troubled behaviour pre-accident is put down to prodromal symptoms in the slow development of this disorder.

What actually happened was that the young man suffered a bi-lateral, frontal lobe supraorbital contusion with some temporal lobe involvement on the left. That brain injury led to impaired concentration, attention and memory, anxiety, headaches, depression and eventually psychosis with delusions of interference (somatic passivity), delusions of reference (being observed by cameras) and the belief that his flat was being entered during the night.

As each symptom group led to what were reasonably appropriate referrals, the diagnosis was questioned according to the discipline of the observer. However, he did not have anxiety and depression, did not have PTSD, traumatic migraine, a neurodegenerative disease or a bi-polar illness.

The next question became whether the symptoms satisfied the criteria for the diagnosis of schizophrenia. Was he arguably showing prodromal symptoms of
irritability, troubled behaviour and detachment that had now passed through a natural progression and resulted in a schizophrenic illness or could the head injury precipitate schizophrenia in a case where there was no pre-existing disorder (or prodroma) or can such a head injury produce a psychosis with all the symptoms of delusions or hallucinations that one might find in schizophrenia, but attributable to the head injury alone, so that he had neither the natural progression of a schizophrenic illness independent of the head injury, nor had he developed schizophrenia precipitated out by the head injury.

Discussion

A good place to start is with “Psychosis following head injury: a critical review”. David, A. S., J. Neurol. Neurosurge Psychiatry 2005; 76: 153 – 160. This paper
states what we know about schizophrenia, that it has a multi-factorial aetiology e.g. an important heritable (genetic) component but where environmental exposures are relevant. The paper concludes it is unlikely that head injury causes schizophrenia. It does however carry an addendum, citing the paper “Psychiatric illness following traumatic brain injury in an adult health maintenance organisation population”. Fann, J. R. et al., Arch Gen Psychiat 2004; 61: 53- 61 in which they conclude their findings are consistent with other reports of delayed psychosis after traumatic brain injury.

That brings us to the paper “Is traumatic brain injury a risk factor for schizophrenia?” A meta-analysis of case controlled population-based studies. Molloy, C. et al., Schizophrenia Bulletin. 37 (6): 1104 -1110. In this paper Molloy does raise the question of whether TBI is a risk factor for psychosis and, in particular, schizophrenia. We are now into two possibilities. Is TBI a precipitating factor for the development or expression  of schizophrenia or can it bring about a psychosis independent of the genetic disorder of schizophrenia. Molloy found an increased risk of schizophrenia following TBI of about 60%, but that did not mean association was established and that, as discussed in the paper by David and Prince above, it is difficult to tease apart whether the TBI causes the psychosis or whether a particular individual is already on a trajectory toward psychosis before the injury occurred. Certainly those vulnerable to schizophrenia have a greater contribution from TBI as a precipitating event much the same as, for example, substance
abuse.

If we then look in more detail at the paper “Psychiatric illness following brain injury in an adult health maintenance organisation population” Fann, J.R. et al. Arch Gen. Psychiatry 2004: 61: 53 – 61. The paper concludes both moderate to severe and mild TBI are associated with an increased risk of psychiatric illness. The paper notes that high rates of mood, psychotic and substance abuse disorders following TBI have been found in hospitalised trauma and tertiary care referral populations. For our purposes, the paper supports TBI as precipitating psychosis.

It is to be remembered that the genetic disorder of schizophrenia is only one form of psychosis and the question now becomes, can TBI cause psychosis in individuals with a non genetic predisposition to schizophrenia? If we move on to the paper “Characteristics of Psychotic Disorder Due to Traumatic Brain Injury. An Analysis of Case Studies in the Literature” by Fujii, D. et al., J. Neuropsychiatry Clin. Neurosci. 2002 Spring; 14 92): 130 – 40. The authors analysed data
from 69 published case studies of psychotic disorder due to traumatic brain injury (PDTBI) in order to describe its common characteristics and assist in its diagnosis and differentiation from schizophrenia. The authors contend that their findings demonstrated that patients with PDTBI have a psychotic profile that
distinguishes itself from schizophrenia. Delusions appear to be more common than hallucinations and the most common delusion is the persecutory etc.

Conclusion

It is not so long ago that DSM I (1952) and DSM II (1968) gave very little in the way of diagnosis. Thanks to Robert Spitzer, DSM III (1980) began to separate out and define various categories of psychiatric illness. It may seem that the above attempt to tease out the relationship between TBI (especially frontal lobe, supra-orbital and temporal-lateral) and psychosis is intuitive. The very same argument occurred with late onset schizophrenia and late onset schizophrenia-like psychoses due to failing sensorium in the elderly. In this brief vignette each specialist was diagnosing the symptoms that he saw before him and that were viewed according to his special interest, however, while standing back and trying to see the entirety is something we all endeavour to do, Henri Bergson’s (1859-1941) famous quote that the eye only sees what the mind is prepared to comprehend, remains as true as ever.

Michael P. Bourke - 18/01/2017.
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