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

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1. Early Interventions

2. Interventions for prolonged and long-term PCS

3. How this might be applied in practice

4. Other models that may be useful

5. Conclusions

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Sayegh, A., Sandford, D., Carson, A., (2011)

Psychological approaches to treatment of post

concussion syndrome: a systematic review. Journal of

Neurology, Neurosurgery & Psychiatry: 81: 1128 – 1134

Snell, D.L., Surgenor, L.J., Hay-Smith, E.J.C., Siegert,

R.J. (2009). A systematic review of psychological

treatments for mild traumatic brain injury: An update on

the evidence. Journal of Clinical & Experimental

Neuropsychology; 31 (1): 20-38.

Ponsford, J. (2005). Rehabilitation interventions after

mild head injury. Current opinion in Neurology; 18: 892-

697.

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Comper, P., Bischop, S.M., Carnide, N., Tricco, A.

(2005). A systematic review of treatments for mild

traumatic brain injury. Brain injury; 19 (11): 863 –

880

Borg, J., Holm, L., Peleso, P.M., Cassidy, J.D.,

Carroll, L.J., von Holst, H., Paniak, C., Yates, D.

(2004). Non-surgical intervention and cost of mild

traumatic brain injury: results of the WHO

collaborating centre task force on mild traumatic

brain injury. Journal of Rehabilitation Medicine;

Suppl. 43: 76-83.

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Vast majority of literature focuses on early intervention

Only one or two well conducted RCTs for

prolonged/long-term PCS

Supportive evidence for:

a) Brief written information for everyone following MTBI

in first few days and weeks

b) Tailored education, reassurance and CBT available to

those with persisting PCS in first few weeks and months

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Primary deficit after MTBI is a shaken sense of self If this occurs in a context where there is little or no

validation or understanding of this perceptions of predictability and stability are disrupted

This can lead to a cycle of fear, failure, avoidance, anxiety, depression, loss of self esteem and alienation (particularly if self esteem is heavily related to high levels of achieving or other vulnerable personality styles are present – perfectionism, obsessive-compulsive traits).

Psychological overlay accumulates with time These combine with physical (e.g. pain, fatigue,

sensory deficits, reduced balance/dizziness, medication) and neurological factors (e.g. age, previous MTBIs) to cause the presenting PCS.

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3

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Education/Information

Support/Reassurance

Graded Exposure to

Avoided Activity

Antidepressant

Medication

Cognitive therapy

82%

74%

56%

45%

44%

}

}

Mittenburg &

Burton (1994)

Middleboe et al

(1992)

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Main interventions are psychological

Predominately attempt to minimise vicious

cycle:

PCS PCS Stress

1. Validate and explain the experience of the

person

2. Do not prematurely confront any emotional

factors as primary

3. Re-establish shaken sense of self e.g. with

small successful challenges to achieve

4. Rebuild internal and external support systems

5. Help the family

6. Then treat emotional factors

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1. Early engagement helping client to develop an open mind to

alternative explanations for PCS which can be directly tested in

therapy, i.e. avoiding debate about “reality” of PCS and

aetiology

2. Identifying factors that improve or worsen PCS (e.g. poor sleep

fatigue, concentration problems)

3. Using Lishman’s 1988 model to explain reducing organic

factors and increasing psychological factors

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4. Minimising “boom-bust” oscillations between high &

low levels of activity to establish sustainable level of

activity to be built upon

5. Build on this level to aim for sustainable, graded

increases in activity (in intensity and/or duration)

6. ? Focus on how patients respond differently to

symptoms rather than dwelling on “good old days

biases”

7. ? Use of models of perfectionism

8. ? Reattribution of symptoms to take into account non-

organic factors

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9. Use of Yerkes-Dodson curve to illustrate non-linear

relationship between effort/arousal and performance,

e.g. trying harder on a task because you think you will

struggle with it may harm the performance

behavioural experiment of putting less effort and

concentration into a task

10.? Use of “re-investment” ideas – automatic skills

becoming deautomised particularly when under

stress/pressure, e.g. behavioural experiment of

focussing on walking

11.? Negative automatic thoughts regarding expectations

or perceptions of performance failures

12.Combine with cognitive rehabilitation strategies but

be careful they don’t become safety behaviours

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Preliminary investigations (e.g. Neuropsychological assessment, results feedback) Session 1

1. Agenda setting

2. CBT rationale for persistent PCS

3. Discussion of CBT format (collaborative, goal-focused, homework, focus on links between thoughts and feeling)

4. Problem and goal list

5. Homework: read Recovery from Post-concussion Syndrome: A Guide for Patients (adapted from Mittenberg et al., 1993)

Session 2

1. Agenda setting

2. Review of previous session and homework

3. Discuss probable treatment techniques

4. Identify initial problem area and initiate appropriate techniques

5. Review and homework

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Session 3

1. Agenda setting

2. Review previous session and homework

3. Identify the day’s “problems area(s)” and initiate/develop appropriate techniques

4. Review and homework

Session s 4-12

1. As with session 3

3. Summarise techniques that have worked, and clarify reasons why

4. Summarise techniques that have not worked, and clarify reasons why

5. Introduce other problem areas as applicable

Sessions 9-12

1. Increasing focus on relapse prevention/coping with possible symptom flare-ups in final quarter of session series (“What happens if ...?”)

2. Focus on continuation of therapy beyond final sessions: Devising action plans/behavioural experiments for the future

3. Review what has and has not helped, and discuss why

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24% significant improvement (RPQ <13 points)

44% moderate improvement (reduction of ≥ 8

points)

56% little to no improvement on RPQ scores

Overall effect sizes: ◦ Large – QOLAS (Quality of life) Hedges g=0.95

◦ Moderate – RPQ (PCS symptoms) – Hedges g=0.54

◦ Moderate – C15 20R (Fatigue) – Hedges g=0.50

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Main limitations:

o N = 45 (25 treatment, 20 waiting list control)

o 28% PTA > 1 day, 20% PTA > 1 week.

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The other RCT (Tiersky et al 2005) – Archives of Physical

Medicine & Rehabilitation (86), 1565 - 1574

o 1 – 20 years post injury (mean = 5 – 6 years)

o 50 mins CBT + 50 mins cognitive rehabilitation,

3x week for 11 weeks

o Significant improvements in anxiety and depression

and scoring on PASAT and Ray Auditory Verbal

Learning Task

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o Small sample size (N = 20 – 11 treatment, 9 waiting

list control)

o Included patients with GCS 9 – 12 and LOC up to 4

hours

o Very high levels of input

o Mixed input

o Cognitive rehabilitation involved both compensatory

and remediation approaches

o Only brief description of interventions

Early Symptoms

Assessment 1. Severity of head injury

Post traumatic amnesia

Loss of consciousness

Glasgow Coma Scale

Neurological investigations, e.g. CT, MRI

2. Extent and severity of post concussion symptoms

e.g Rivermead Post Concussion Symptoms Questionnaire (RPQ – King et al 1995)

3. Emotional status

e.g. Hospital Anxiety & Depression Scale (HADS – Zigmond & Smith, 1983), Impact of Event Scale-Revised (IES-R Weis & Marmar, 1997)

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Intervention

Education/Reassurance

1. Normality of symptoms & non malignant nature

2. Likely recovery time & optimistic prognosis

3. Reduced speed of information processing

4. Graduated return to work

5. Symptoms as ‘temperature gauge’ re: doing too much

6. Minimizing vicious circle:

PCS Stress PCS

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a) Common problems following mild head

injury

b) Reduced speed of information processing

c) Memory problems

d) Post traumatic stress reactions

(King et al 1997)

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1. Full assessment of symptoms vs symptoms

via expectation

2. Realistic and optimistic prognosis vs bland

reassurance (if unrealistic

anger, worry & disillusionment)

3. Using symptoms as ‘temperature gauge’ vs

over- focusing on symptoms

Late Symptoms

Assessment 1. Severity of head injury

Post traumatic amnesia

Loss of consciousness

Glasgow Coma Scale

Neurological investigations, e.g. CT, MRI

2. Extent and severity of post concussion symptoms

e.g Rivermead Post Concussion Symptoms Questionnaire (RPQ – King et al 1995)

3. Emotional status

e.g. Hospital Anxiety & Depression Scale (HADS – Zigmond & Smith, 1983), Impact of Event Scale-Revised (IES-R Weis & Marmar, 1997)

4. Pre-morbid factors (family, psychological, educational, occupational and clinical history).

5. Detailed chronological development of symptoms

6. ?? Neuropsychological assessment

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Accident

Mild head injury and

post concussion symptoms Neck injury

Reduced: concentration,

stress tolerance,

multi-tasking,

day-to-day memory,

speed of processing

Post traumatic

stress

• Nightmares

• Increased

arousal/

jumpiness

• Flashbacks

• Anxiety near

reminders of

accident

• Avoidance of

reminders

• Flashbacks

Decreased ability to

manage daily demands

leading to reduced confidence ++

Stress ++

• “I’m going mad”;

• “I’m a different person”;

• “Why am I like this?”;

• “Something serious has

been missed”

Loss of life:

structure/routine/

purpose/meaning

Intervention Formulation

Pain

Reduced

mobility

Depression

Irritability Reduced

quality/

quantity

of sleep

Loss of job

Life assumptions changed regarding: control, predictability, purpose, safety/ vulnerability

Fatigue

Agoraphobia/

panic attacks

Financial

difficulties

Compensation claim

Reduced quality of

close relationships

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Neuropsychological rehabilitation principles and

treatment to slowly reclaim normality

CBT principles to minimise emotional sequelae

CBT models from other areas

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I must rest to get

better

Avoid activity

Reduction in fatigue but failure to live up

to expectations

‘I should try harder’

Burst of activity

Some achievement but fatigue

Surawy et al 1995

Cognitive Behavioural Model of Chronic Fatigue

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1. Pain – depression cycle

Pain

Social withdrawal Decreased Activity

Depression

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2. Pain – agitation cycle

Pain

Sleeplessness Muscle Tension

Anger

Hardin 1998

Characteristics of trauma / sequelae /

prior experiences / beliefs / coping state

of the individual

Cognitive processing

during trauma +

Matching Triggers

Nature of Trauma Memory Negative Appraisal of Trauma

and/or sequelae

Current Threat

(Intrusions, arousal symptoms, strong emotions)

Strategies intended to control threat / symptoms

(Ehlers & Clark 2000)

Cognitive Model of PTSD

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Irritability, anger

outbursts

Neuropsychological

problems

‘My personality has changed for the worse’

‘My marriage will break-up’

‘I can’t trust myself with my own children’

‘My brain has been damaged’

‘I’ll lose my job’

‘I’m going mad’

‘I can’t cope with stress anymore’

Examples

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Functional symptoms: Generalized pain

Fatigue

Excessive / misdirected

attention

Reduced

attentional reserve

Slow information processing

↑ Controlled (effortful) / ↓ automatic cognitive processing?

High cognitive effort

Heightened self-monitoring of cognitive processes and errors

Memory perfectionism

Over-interpretation of cognitive failures – abnormal beliefs

Predominant interference with real-life multi-tasking?

Cognitive symptoms (e.g. memory lapses,

distractibility and word-finding difficulties)

Illness experience

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1. “One size fits all” early interventions may be adequate for

providing effective initial information and reassurance, with tailored reassurance and CBT for persisting symptoms.

2. Individualised formulations and interventions essentials for prolonged/long-term PCS.

3. Emerging evidence that CBT can be an effective treatment for some patients with permanent PCS, but not for all.

4. Formulation normally to include all potential non-organic factors alongside the possibility of brain injury factors

5. Emphasis that problems and symptoms are real regardless of cause

6. Emphasis that the more they are due to non-organic factors the better – as greater scope for successful treatment and full recovery

7. Treat all non-organic factors maximally e.g minimising boom-bust approach to symptom management, establish a baseline activity level and increase it in a graduated way (including physical exercise), emphasis that worsening symptoms do not mean physical harm is occurring, attend to threatened sense of self, minimise hyper-attention to deficits.

8. ? Treat residual cognitive difficulties with cognitive rehabilitation approaches

9. ? Postpone judgement regarding contribution of organic factors until all non-organic factors have been maximally addressed

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Overcoming Mild

Traumatic Brain Injury

and Post-concussion

Symptoms: A self-help

guide using evidence-

based techniques

King 2015 –

Constable & Robinson. London

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