Dr Nigel S King Consultant Clinical Neuropsychologist

Transcription

1 Dr Nigel S King Consultant Clinical Neuropsychologist Oxford Institute of Clinical Psychology Training University of Oxford, UK nigel.king@hmc.ox.ac.uk & Community Head Injury Service Bucks Healthcare NHS Trust Jansel Square, Aylesbury, Bucks, UK

2 1. Post concussion symptoms 2. Psychological and neuropsychological features of MHI and prolonged post-concussion symptoms 3. Other considerations 4. Sport related concussion 5. Conclusions

3 Post traumatic amnesia 0-24 hours. Glasgow Coma Scale Score Loss of consciousness of < 15 minutes. Absence of any evidence of inter or intra cerebral complications.

4 A cluster of cognitive, somatic and emotional symptoms, following a MHI which include: headache, dizziness, fatigue, irritability, reduced concentration, sleep disturbance, memory impairment, sensitivity to noise or light, nausea, blurred vision, anxiety and depression Caused by organic and/or psychological mechanisms which are poorly understood 4

5 hospital admissions a year per 100,000 of the population in Britain involve a head injury (Jennett et al 1981) 2. As few as 6% 8% of these may be severe (PTA 1 day) (Artiola et al 1980; Wade et al 1997) 3. At least 75% are mild or moderate (PTA 24 hours) (Kraus et al 1998)

6 The vast majority make a complete recovery within a few days or weeks of injury A minority still have significant symptoms at 6 months (up to 20-40%) A small minority still have significant symptoms 12 months and beyond (5-10%) (Karr 2014)

7 1. Psychological features best predictors of persisting PCS early on post injury (King 1996) and high co-morbidity of anxiety and depression symptoms 2. Poorer outcome with pre-existing psychopathology (Dencker, 1958) 3. Many if not all PCS could be caused by psychopathology only. 4. Stress exacerbates PCS (Moss et al 1994) 7

8 5. Poorer outcome with female sex (Rutherford et al 1979) 6. Many if not all PCS could be caused by pain only (whiplash, headache, orthopaedic) 7. Brief early psychological intervention significantly reduces PCS (Wade et al 1998) 8. Compensation factors 8

9 1. Positive correlation between PCS / time off work and seeking compensation (Binder & Rohling 1996) -? twice as many compensation seekers have symptoms at 1 year (Rutherford 1989) However 2. Remarkably few show significant improvement in PCS after settlement (Rutherford 1989) 9

10 Historically suggested that they do not co-exist (e.g. Mayou et al 1993) Later suggestions that they cannot co-exist (e.g. Sbordone & Liter 1995) PTSD and mild traumatic brain injury are mutually incompatible since patients who sustain PTSD simply cannot forget the traumatic event, whereas patients who sustain mild brain injury have no recollection of the traumatic event. (Based empirically on no cases of PTSD being found in their head injury samples)

11 1. Mild head injury where there is no or little PTA and retrograde amnesia and some memory of traumatic events. (Horton, 1993; Perceptive & Motor Skills) 2. Islands of traumatic memory during PTA (King, 1997; Journal of Neurology, Neurosurgery & Psychiatry) 3. Implicit conditioned fear response i.e. re-experiencing of event by the triggering of a conditioned fear response. (Layton & Wardi-Zonna, 1995; The Clinical Neuropsychologist) 4.? No memory for event but PTSD via imagined memory of what might have taken place/what the person has found out about what did happen (McMillan, 1996; Brain Injury)

12 Most more recent studies show PTSD incidence rates to be equal or higher in MTBI than non MTBI populations (e.g. Mayou et al 2000, Greenspan et al 2006) Hypothesised that MHI impede information processing at the time of trauma and therefore emotional processing later on King, N.S. (2008). PTSD and TBI. In Tyerman, A. & King, N.S. (Eds). Psychological Approaches to rehabilitation after traumatic brain injury. Blackwell. Oxford

13 1. Overlap of symptoms between the conditions 2. Psychogenic vs organic amnesia surrounding the event 3. Vicious cycle of PCS and PTSD symptoms

14 Helpful meta-analytic studies: Karr et al (2014) Systematic review of metaanalytic studies Belanger et al (2005) Best meta-analytic review Dougan et al (2014) Most recent meta-analytic review (sports injuries and acute effects only) Belanger et al (2010) Meta-analytic review of multiple MHIs

15 Cognitive domains typically affected are: i. New learning ii. Attention/speed of processing/working memory iii. Verbal fluency

16 Effect size is moderate to large initially but normally with complete recovery within 3 months, (7-10 days in sports injuries) Cognitive deficits have some correlation with reported PCS. Size of correlation reduces over time.

17 Clinical and litigation populations often show deficits (with large effect sizes) beyond 3 months Some deteriorate neuropsychologically and litigation effects remain even when effort/symptom validity factors are accounted for Deficits predominantly in attention /speed of processing/working memory (although probably not restricted to these) and are permanent for some

18 Attention and /or vigilance Working memory Executive function Episodic memory Semantic memory Visual memory Verbal memory Fear extinction Processing speed Procedural memory Social cognition (theory of mind) Language Major depression +(+) (+) 0/+? ++(+) + +(+) + Bipolar disorder ++(+) ? Schizophrenia (+) ASD (+) +(+) +++ 0/ ADHD / /+ OCD +++( ) +(+) /+ + 0/ /+ PTSD +++( ) +(+) +(+) (+) /+ 0 Panic Disorder +++ ( ) + 0/+ + 0/+ 0/ GAD /+ 0 Parkinson s disease Alzheimer s disease ++ ++(+) / ? (+) +(+) +(+) +(+) +(+) (+) 0? Millan et al (2012), Nature Reviews, 11,

19 Parameter Fibromyalgia Chronic fatigue syndrome Memory Attention/concentration Executive functions Vulnerability to distraction Explicit worse than implicit memory* Selective/divided attention* Bias towards emotionally negative information** Cognitive inhibition** Impaired registration and consolidation* Working memory disruption by abnormal attention/information processing* Divided attention Executive function of attention** Bias towards threatening stimuli* Functional neurological disorder Working memory** Attention** Attentional bias towards social threating stimuli** Information processing Slow Slow** Language Verbal fluency* Verbal fluency** Social cognition Factors related with cognitive deficits Alexithymia** Recognising others emotions* Alexithymia* Affect expression and recognition** Pain* Fatigue** Psychopathology**

20 Time after injury Possible emerging factors 0-24 h (immediate symptoms) Mainly organic factors 1 day 4 weeks (early symptoms) Overdoing and failing tasks Increase in life demands following recuperation Misattribution of symptoms to malignant causes that have been missed Difficulties coping with cognitive impairments Initial concerns regarding longevity of symptoms/disabilities Dissonance regarding severity of head injury and severity of symptoms/disabilities 1-6 months (medium-term symptoms) Unhelpful pre-morbid schemas and coping responses related to managing abnormal life events; inability to complete tasks; frustration and mind over matter coping Concerns regarding potential permanence of symptoms Unhelpful strategies for coping with uncertainty (particularly uncertain aetiology of symptoms) Misperception of having suffered a severe brain injury Over 6 months (long-term or possibly permanent symptoms) Lack of understanding/belief from others Compensation-claim factors Issues relating to adjustment to long-term disability Unhelpful secondary coping strategies (those employed following failure of initial strategies) British Journal of Psychiatry, 183,

21 It is increasingly evident that although a percentage of mild head injury patients remain chronically symptomatic rather than making the expected full recovery, this is for psychological not organic reasons, for example, adoption of sick role or frank malingering. Powell, 2012

22 Everything should be made as simple as possible but not simpler. Albert Einsten

23 1. Diffuse microscopic axonal injury. From post-mortem studies on humans and animals (Oppenheimer 1968; Povlishok & Coburn 1989). 2. Macroscopic lesions on CT and MRI scans 8%-20% of MHI show CT abnormalities (Sekino et al, 1981; Jacobs, 2009) (however no correlation with PCS) MRI abnormalities primarily in frontal and temporal areas after MHI (Levin et al 1987; Levin et al 1992) (however resolved over 3 months in line with PCS and neuropsychological correlates) 23

24 3. Cellular damage and metabolic abnormalities in frontal white matter in MHI patients with normal MRIs within the first few weeks of injury (Garnett et al 2000) 4. Subtle abnormal EEG and ABER findings within 48 hours of MHI (Schoenhuber & Gentilini, 1989; Montgomery et al, 1984) (however have no prognostic value re PCS and neuropsychological sequelae) 5. Abnormal regional cerebral blood flow and reduced glucose metabolism in frontal and temporal areas in MHI patients with persisting PCS (5 years post injury) on PET & SPECT despite normal CT& MRI findings (Ruff et al 1994; Varney et al 1995) 6. Diffuse Tensor Imaging high resolution imaging revealing microstructural abnormalities in white matter. 24

25 Waljas et al 2014 review of MTBI & DTI (50 studies): 9/12 found abnormalities at 18+ months post injury in those with prolonged PCS 9/10 found a correlation between abnormalities and cognitive dysfunction at 18+ months post injury in those with prolonged PCS Corpus callosum most commonly affected (internal and external capsule and centrum semiovale also often affected). Journal of Neurotrauma 31:

26 1. Poorer outcome (slower and less complete recovery) with increased age (cut off at around 40 years) (Binder et al 1986). DSM-V - In older individuals with depleted cognitive reserve mild TBI is more likely to result in incomplete recoveries. 2. Poorer outcome with previous MHI (Gronwall & Wrightson 1975) 3. Poorer outcome with alcohol or substance misuse (Carlsson et al 1987) 26

27 King & Kirwilliam, 2010, Brain Injury, 25 (5), An exploratory study of a representative sample of long term/permanent PCS patients examining the extent to which a wide range of variables (demographic, cognitive, emotional and psychosocial), known to be important in the development of early PCS apply to this group, both in terms of describing the sample and in predicting the severity of PCS.

28 Participants: All patients referred to the Community Head Injury Service (CHIS), Aylesbury, UK with a MHI and persisting PCS between , and who were at least eighteen months post injury at the time of the study. CHIS is a specialist head injury service for the whole of Buckinghamshire, UK. It serves patients with all severities of head injury (mild, moderate, severe, very severe) in a mixed rural and urban population of approximately 725,000. Referrals come from a wide range of sources GPs, Brain Injury Clinical Nurse Specialists, Neurologists, Social Services, Family, Patient, other Clinicians.

29 Procedure: 100 participants were identified and invited by letter to take part in the study. They were asked to consent to take part and complete a Rivermead Post Concussion Symptoms Questionnaire (RPQ) (King et al., 1995) if they wished to participate 30 participants consented (all of whom had at least three PCS) 6 withdrew The total sample was 24 Assessed with wide range of neuropsychological, emotional, demographic and quality of life measures

30 1. Patients with long term/permanent PCS are associated with: a) Older age b) Very high levels of PCS c) High post injury unemployment d) Pre and/or post morbid factors which might exacerbate PCS e) Elevated levels of anxiety and depression symptoms f) Mildly reduced scores on tests of short-term memory and speed of information processing

31 2. Older age as a vulnerability factor suggests that organic factors operate in long term/permanent PCS 3. Additional compromises to an individual s emotional or cognitive capacities may play a significant role in long term/permanent PCS 4. Anxiety can play a significant role in long term/permanent PCS 5. Very high levels of PCS, high post injury unemployment and measurable cognitive deficits can be the permanent effects of a MHI 6. Quality of life is directly related to PCS severity

32 1. Identification of factors implicating secondary complications 2. Avoidance of return to play during the period of time when a second MHI could have a very serious effect e.g. Second Impact Syndrome 3. However how long is the Window of Cerebral Vulnerability (McCrea et al 2017) and what are the risks?

33 1. Metabolic and microstructural recovery commonly lags behind symptomatic recovery (Kamins et al 2017) 2. Metabolic and microstructural complications often extend to 4 weeks post injury even when compete symptomatic recovery has occurred within the first few days (Vagnozzi et al 2008)

34 May not be conservative enough in those who are quickly asymptomatic.

35 1. Lee et al (1995) 1812 MHI cases: 1.5% went on to develop secondary complications 50% of these occurred within 24 hours 75% of these occurred within 7 days 96% of these occurred within 3 weeks N=1 (4%) of these occurred within 3 months (a chronic subdural haematoma) (Drowsiness and motor weakness were very strong predictors and >60 years, vomiting and headaches were also predictive.)

36 2. Full metabolic and microstructural recovery is normally complete within 2 months of a MHI even after a second injury is suffered i.e. there is a cumulative effect but it is finite (Vagnozzi et al 2008). 3. Rat studies indicate that two MHIs within 3 days leads to metabolic effects similar to a severe HI but two MHIs within 5 days leads to no difference compared to a single MHI (Vagnozzi et al 2005).

37 However: Return-to-sport protocols typically emphasise a six stage graduated increase in exercise and sporting activity but with progression to each step predicated on no PCS being present or exacerbated by the activity at each stage i.e. PCS used as a proxy measure of organic recovery. Therefore PCS as a proxy measure of cerebral recovery is often too conservative for those with persisting PCS.

38 and may cause additional psychological factors to operate regarding: a) Cerebral vulnerability b) Self identity c) Unavailability of stress-reducing activities.

39 1. Roberts (1969) Professional boxers > 50 years: 50% incidence of Dementia Pugilistica with > 150 fights 7% incidence of Dementia Pugilistica with <150 fights 2. High incidence rates of Chronic Traumatic Encephalopathy (CTE) in ex Professional / College Level American Footballers (Mez et al 2017)

40 Later life problems associated with SRC: a. Anxiety/depression/sleep problems - Dose Dependant Effect (2-9 SRCs) b. PCS (DDE >2) c. Diagnosis of Mild Cognitive Impairment (DDE >2) d. Diagnosis of Multiple Sclerosis (DDE >1) e. Tagged Magnetic Resonance Imaging changes f. Measured cognitive deficits

41 But in the context of: 1. Non-significant findings of other studies and conclusions that effects are subtle or detectable but non-clinical even with those with high numbers of career SRCs (means of 5 14). 2. CTE/Dementia studies limited due to: a. Unreliability of diagnosis. b. Unreliable base rate data of diagnosis. c. Use of convenience samples. d. Mortality odds ratios being quoted at the expense of a substantial reduction of such within the same samples (due to the health benefits of taking part in sport).

42 3. Little evidence of any later-life effects outside of studies of professional/elite level athletes. 4. No bio-markers yet identified to determine those who might be susceptible to any such effects. 5. Little evidence from studies of athletes with very high numbers of sub-concussive blows to the head (e.g. heading a football).

43 Also within the context of broader MHI studies: a. No universal agreement of increased risk of later life effects even with a severe head injury (although odds ratios of are often reported). b. Odds ratios of up to 2 for single or multiple MHIs but with very little universal agreement of increased risk.

44 c) Even recent Danish population study (2.8 million) (Fann et al 2018) with statistically significant effects of a single MHI had a modest odds ratios of 1.2 (4.0% vs. 4.3%).

45 i) older age was an important factor: highest odds ratios (4.1) were obtained for those developing dementia within 6m of their injury. ii) Gardner 2014 study of over 55 y.o showed increased odds ratios for MHI only in those over 65 y.o with independent cumulative factors of poor sleep and psychopathology contributing (both more common after MHI).

46 The SRC literature can therefore imply that MHI is a dangerous condition that causes a complex neuropsychiatric disorder and that even heading a football may cause dementia. Carson, 2017

47 An athlete who is symptomatic from a head injury must not participate in contact or collision sports until all cerebral symptoms have subsided and preferably not for at least a week after. Whether it takes days, weeks or months to reach the asymptomatic state, the athlete must never be allowed to participate or compete while still suffering post-concussion symptoms. Contu vs. It is increasingly evident that although a percentage of mild head injury patients remain chronically symptomatic rather than making the expected full recovery, this is for psychological, not organic reasons, for example the adoption of a sick note or frank malingering. Powell 2013.

48 1. Highly serious intracerebral complications, in all but the rarest of circumstances, last for hours, days and occasionally weeks but not months. 2. The increased risk of cumulative metabolic and microstructural deterioration due to a second MHI during the window of cerebral vulnerability is unlikely to extend beyond 3 months even if PCS exist or are made worse by exercise. 3. After this time the primary risk is an exacerbation of PCS due to a second injury but not of serious intracerebral complications. 4. There is little evidence of any long-term risk for amateur athletes and equivocal evidence for professional athletes. However if MHIs become more frequent and the severity of PCS/cognitive deficits increases each time or the recovery time lengthens retirement from that sport should be considered.

49 1. Many people, non-specific symptoms, multiple causes and possible changes in causes and presentations. 2. Neuropsychological deficits common in first 3 months predominantly in attention/speed of processing, new learning and fluency and normally ameliorate alongside PCS 3. Small minority likely to have prolonged/ permanent symptoms and neuropsychological deficits will often also remain in this group. 4. Organic factors reducing over time, psychological factors increasing over time. However prolonged symptoms may be exclusively due to one or the other for some individuals. 5. Mixed messages between MTBI and SRC literature may have to be addressed as part of intervention 49

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