Brain Injury Group · change not only the functions but also the structure of the brain itself (Fuchs & Flügge, ... •Our brains are organised at every level according to function:

Brain Injury Group

Specialist training from brain injury experts

Brain Injuries

www.braininjurygroup.co.uk

0800 612 9660

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Chair

Claire Roantree

Boyes Turner


0800 612 9660

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Is It Ever Too Late To Undertake Rehabilitation?

Dr Edmund Bonikowski FRCP MRCGP MPhil (Cantab)

Consultant in Rehabilitation Medicine

Brain Injury Group - 9th October 2018

Quick Background

• Managing Partner - NNRC

• Honorary Consultant in Neurological Rehabilitation - T&S NHSFT

• Researcher – Cambridge University Department of Engineering

• Director – MedCan Training (Academy of Medical Cannabis)

• NHS Consultant posts in Neurological and Amputee Rehabilitation

• Chief Executive - Kynixa

What We Will Cover

• Rehabilitation of what?

• Why is the question important?

• What do we mean by rehabilitation?

• Where the idea of ”a two year window” came from.

• Predicting trajectory

• Sequence of brain recovery

• Mechanisms of recovery

• Neuroplasticity

• Connectome

• Studies

• Suggestions


No, it is (almost) never too late …

… and actually it is never too early!

Rehabilitation of what?

• Brain injury – mild to catastrophic?

• Physical • – paralysis/spasticity/pain/cranial nerves/bladder/speech/swallowing/phth …

• Cognitive and behavioural • - memory/concentration/executivefunction/irritability/aggression/obsessions• - initiation/perseveration/adjustment/depression/anxiety• - judgment/perception/fatigue

• Social • - family role/loss of friends and family/work/occupation ...

Why is it an important question?

• Ideal (ordeal) journey• Roadside/A&E/theatre/ITU/rehab ward/home/community rehab

• Goal of safe discharge only

• Causes of delay• Instruction/records access/expert availability/liability/adversarial process

• Consequence• Independent rehabilitation/case management/support - months to years late

• Funding• Payer reluctance/diminishing returns

What we mean by Rehabilitation

• The process by which an individual achieves functional gains

• Biological

• Psychological

• Social

• Neurosurgeons and neuropsychologists!

• Follow up trials

• Perpetuation of myth in the absence of alternative narrative

• What does common sense say?

• What does our experience tell us?

Where did 2 years come from?

Predicting trajectory

• Again common sense

• The concept of a plateau

• For better analysis – pattern recognition techniques

Sequence of brain recovery

Injury

AdaptationUse of compensatory strategies

NeuroplasticityFunctional recovery

Swelling subsidesEarly recovery

SwellingPressure on other areas

Mechanisms of recovery

• Plasticity: • brain repairs itself physically (hardware) • and functionally (software)

• Recovery is enhanced by environment (stimulation, repetition, motivation, explanation of purpose):

• Neuronal regeneration, collateral sprouting• Unmasking, restoration of goal-directed engrams, and re-organisation of motor pathways

• Functional recovery may seem only to start weeks and months after the injury, but that may be the final step in recovery, when motor function is restored

• Intact neurons establish synapses by dendritic and axonal sprouting throughout damaged areas

• Damaged hemisphere may temporarily shut down

Neuroplasticity

• 400 – 600 reps

• 1000 – 2000 steps

• Increased task reps after stroke to improve grasp-release

• Most therapy sessions do not contain sufficient reps

Current practice

• Kimberley TJ, Samargia S, Moore LG, Shakya JF, Lang CE. Comparison of amounts and types of practice during rehabilitation for traumatic brain injury and stroke. J. Rehabil Res Dev. 2010; 47(9):851-62.

• 40 – 60 reps per session

• Far below the hundreds required!

http://www.ncbi.nlm.nih.gov/pubmed/21174250

Neuroplasticity

• The physiological changes in the brain that happen as the result of our interactions with our environment.

• The connections among the cells in our brains reorganize in response to our changing needs.

• This dynamic process allows us to learn from and adapt to different experiences.

Neuroplasticity

• In the 1960s, it was discovered that neurons could “reorganize” after a traumatic event. Further research found that stress can change not only the functions but also the structure of the brain itself (Fuchs & Flügge, 2014).

• Neurogenesis, the brain’s ability to grow new neurons.

Neuroplasticity

• One could speculate that this process opens up the possibility to reinvent yourself and move away from the status quo or to overcome past traumatic events that evoke anxiety and stress. Hardwired fear-based memories often lead to avoidance behaviours that can hold you back from living your life to the fullest.

• We already use medications and chemicals to change the way our brain works, and psychology has certainly changed the way the brain works through modifying our thought patterns. What if we really can make permanent, significant changes to our brain structure and function through simple activities that we often do in a normal day?

• This is where the importance of learning comes in.

Neuroplasticity

• Children’s brains are constantly growing, developing, and changing. Each new experience prompts a change in brain structure, function, or both.

• At birth, each neuron in an infant’s brain has about 7,500 connections with other neurons; by the age of 2, the brain’s neurons have more than double the number of connections in an average adult brain (Mundkur, 2005). These connections are slowly pruned away as the child grows up and starts forming their own unique patterns and connections.

Neuroplasticity

• Recovery after brain injury: mechanisms and principles

• Randolph J. Nudo* Front Hum Neurosci. 2013; 7: 887

• It is now generally accepted that acquired brain injuries, such as occur in stroke or trauma, initiate a cascade of regenerative events that last for at least severalweeks, if not months.

• Many investigators have pointed out striking parallels between post-injuryplasticity and the molecular and cellular events that take place during normal brain development.

https://www.ncbi.nlm.nih.gov/pubmed/?term=Nudo RJ[Author]&cauthor=true&cauthor_uid=24399951https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3870954/

Neuroplasticity

• One important theme has persisted as the sophistication of clinicians and scientists in their knowledge of neuroplasticity mechanisms has grown: behavioral experience is the most potent modulator of brain plasticity.

• While there is substantial evidence for this principle in normal, healthy brains, the injured brain is particularly malleable.

• Based on the quantity and quality of motor experience, the brain can be reshaped after injury in either adaptive or maladaptive ways.

Neuroplasticity

• Immediately after the injury, neurons begin to die and cortical inhibitory pathways are decreased; this phase lasts one to two days, and may uncover secondary neural networks that have never been used or have been rarely used.

• After a few days, the activity of these cortical pathways changes from inhibitory to excitatory and new synapses are formed;

• After a few weeks, new synapses continue to appear and the “remodeling” of the brain is in full swing—this is the time when rehabilitation and therapy can help the brain to learn some helpful new pathways.

Neuroplasticity

• Andrew Weil:

• “Among other things, neuroplasticity means that emotions such as happiness and compassion can be cultivated in much the same way that a person can learn through repetition to play golf and basketball or master a musical instrument, and that such practice changes the activity and physical aspects of specific brain areas.”

• Elizabeth Thornton:

• “Because of the power of neuroplasticity, you can, in fact, reframe your world and rewire your brain so that you are more objective. You have the power to see things as they are so that you can respond thoughtfully, deliberately, and effectively to everything you experience.”

Neuroplasticity

• Santiago Ramón y Cajal:

• “Any man could, if he were so inclined, be the sculptor of his own brain.”

• Craig Krishna:

• “Meditation invokes that which is known in neuroscience as neuroplasticity; which is the loosening of the old nerve cells or hardwiring in the brain, to make space for the new to emerge.”

• Donald O. Hebb:

• “Neurons that fire together wire together.”

Mirrors and Connectomes

• Our brains are organised at every level according to function: • We learn (and re-learn) by refining engrams of skilled tasks

• Our brains are organised according to purposeful, goal-directed tasks, not muscle or joint movements

• Brain injury can therefore be understood as a disorder of large-scale neural connectivity

• So what? Does that have real-world implications?• We are starting to map connectomes, and they reveal deficits specific to TBI,

including mild TBI which has gone undiagnosed

Connectome

An Overview Study

• EVIDENCE FOR THE EFFECTIVENESS OF MULTI-DISCIPLINARY REHABILITATION FOLLOWING ACQUIRED BRAIN INJURY: A SYNTHESIS OF TWO SYSTEMATIC APPROACHES Lynne Turner-Stokes, DM, FRCP: J Rehabil Med 2008; 40: 691–701

• Conclusion: There is now a substantial body of high-quality research evidence for the effectiveness, and indeed the costeffectiveness, of rehabilitation. This reviewhighlights the importance of looking beyond the somewhat restrictive set of trial-based evidence.

Late rehabilitation (Papers 1&2)

• Malec 2001 (40) TBI Cohort analysis

• Day centre rehabilitation: time since injury ranging from 1 to >10 years

• Reduction in unemployment and need for supervision sustained at one year

• Quality Score 10 P1 High direct

• Powell et al. 2002 (14) TBI Cohort analysis (from an RCT)

• Home-based MD rehabilitation: mean 4 years since injury

• Gain in independence (BI) and community integration (BICRO-39)

• Quality Score 10 P1 High direct

Late rehabilitation (Papers 3&4)

• Gray & Burnham 2000 (46) TBI Cohort analysis

• Inpatient rehabilitation Mean 1.5 years post-injury

• Significant gains in independence (FIM+FAM)

• Quality Score 8 P1 High Direct

• Tuel et al. 1992 (45) TBI Cohort analysis

• Late inpatient rehabilitation -at least one year post-injury

• Significant gains in independence (BI) for about half the patients

• Quality Score 4 P1 Medium direct

An Overview Study

• Conclusions about “Late rehabilitation”

• Strong evidence (Grade A)

• Still make significant functional gains 5 – 10 years after injury

Other Studies

• Cost-efficiency of longer-stay rehabilitation programmes: Can they provide value for money?

• Brain Injury, September 2007; 21(10): 1015–1021

• LYNNE TURNER-STOKES

• There is no clear generalizable cut-off point beyond which rehabilitation will cease to bring about useful gain—this must be judged for each individual.

Other Studies

• BSRM abstract 2018

• BENEFITS OF REHABILITATION LATE AFTER STROKE: A MULTI-CENTRE COHORT ANALYSIS FROM THE UK REHABILITATION OUTCOMES COLLABORATIVE (UKROC) DATABASE.

• Turner-Stokes L1,2, Cardona A2, Alfonso E2

• Conclusions:

• This analysis of real-life data collected in routine clinical practice demonstrates that patients do continue to make functional gains from specialist rehabilitation even more than one year after stroke. Moreover, this intervention was highly cost-efficient, especially for the most dependent patients.

Other Studies

• Wood RLl, McCrea JD, Wood LM, Merriman RN. Clinical and cost effectiveness of post-acute neurobehavioural rehabilitation. Brain Injury 1999;13:69–88

• Differences between those who had been admitted less than two years, 2–5 years and more than five years post-injury

• The cost effectiveness of rehabilitation is greater for those who receive treatment within 2 years of injury. However, those who received rehabilitation at later stages also achieved significant social outcomes and savings on care hours.

Other Studies

• The clinical and cost-benefits of investing in neurobehaviouralrehabilitation: A multi-centre study

• Michael Oddy, & Sara da Silva Ramos

• Brain Inj, 2013; 27(13–14): 1500–1507

• Cost-benefits of up to £1.13 million were demonstrated for individuals admitted to rehabilitation within a year of sustaining a brain injury and of up to £0.86 million for those admitted more than 1 year after injury.

Other Studies

• Cost-efficiency of specialist inpatient rehabilitation for working-aged adults with complex neurological disabilities: a multicentre cohort analysis of a national clinical data set

• Lynne Turner-Stokes, Heather Williams, Alan Bill, Paul Bassett, Keith Sephton http://bmjopen.bmj.com/ on June 6, 2016

• … confirm the potential for substantial cost-savings to be made from appropriate provision of specialist rehabilitation services for patients with complex needs, even many months after the original injury.

FAM Splat

Suggestions

• Ask a consultant in neurological rehabilitation to see the patient as early as possible in hospital to provide a prognostic framework for the rehabilitation process and other reports

• Don’t wait for comprehensive medical records, just try to access admission/discharge summaries

• Engage a consultant in neurological rehabilitation to provide medical input to case managed rehabilitation programmes


No, it is (almost) never too late …

… and actually it is never too early!

PERIODICAL PAYMENTS & THE DISCOUNT RATE

Brain Injury Group

9 October 2018

About Nestor Financial Group Ltd

• Independent Financial Advisers

• Regulated by the Financial Conduct Authority

• Specialists in Personal Injury/Clinical Negligence

• Instructed by Claimants and Defendants (90%/10%)

• Periodical Payments – 150 instructions p.a.

• Manage lump sum investment portfolios c. £550m

• Manage Cash Accounts c. £150m +

• Personal Injury Trusts – 300 + implemented p.a.

• Court of Protection

• Accountancy Services & State Benefits advice

THE HISTORY OF THE 100% PRINCIPLE

‘Not a Penny more, not a Penny Less’

Damages Act 1996 – Lord Chancellor given the power to set rate - 1996

Wells –v- Wells – ‘4.5% down to 3.00% ILGS linking - 1999

Lord Irvine sets rate at 2.5% - 2001

Returns on ILGS reduce consistently over time - 2001 – 2007

Financial Crisis – 2007/08

ILGS continue to reduce significantly – 2007 -2009

Current Yields on ILGS between -1.6% to -1.8%

The Civil Liability Bill – 7 September 2017

‘Not working as fairly as it should’

‘Legislate Promptly’

‘Continue to support the 100% damages principle’

‘Claimants should be treated as more risk averse – but not NO risk

anymore’

David Lidington MP

THE REALITY OF THE RATE (REAL V NOMINAL RETURNS)

%

A Cautious Investor PA (nominal) 5.00

Less:

RPI (long-term) PA 2.70

Taxation Assumption 0.50

Investment Advice Costs (OCF) 1.25

Discount Rate 0.55

Less:

Wage Inflation v RPI differential 1.5

REAL DISCOUNT RATE -0.95

THE DISCOUNT RATE – Where are we now?

18 months at - 0.75%.

The Civil Liability Bill:

Not ‘no-risk’

But ‘low-risk’

Yet still supporting the 100% principle

The Civil Liability Bill

Section 4 (3):

d): the assumption that the relevant damages are invested using an

approach that involves:

i): more risk that a very low level of risk, but:

ii): less risk than would ordinarily be accepted by a

prudent and properly advised individual investor who

has different financial aims.

The Civil Liability S2

The ‘Other’ research – Pen ‘case study’ research

The Government Actuaries’ (GAD) Report – July 2017

‘Low risk portfolio of investments’

Cost inflation at 2.7% PA (30 year average)

30 year damages/investment term

Portfolio A : ‘typical’ PI investor

Portfolio B: ‘highest’ risk for a PI investor

The GAD Report

Asset Class Portfolio A

%

Portfolio B

%

UK Shares 13 29

Overseas Shares 15 28

TOTAL SHARES 28 57

FI Gilts 15 7

ILGS 5 3

Corp Bond 21 14

Cash 10 5

Property 4 5

Alternatives 18 8

The GAD Report

% probability of being under compensated at various discount rates:

Discount

Rate

5% or more

under

compensation

10% or more under

compensation

Portfolio A 1% 30% 22%

Portfolio A 0.5% 19% 12%

Portfolio B 1% 26% 21%

Portfolio B 0.5% 9% 6%

The GAD Report (ex investment advice costs & taxation):

Money

Weighted

Real Return

% PA

5 years 10 years 15 years 20 years 30

years

50 years

Portfolio A 0.0% 0.6% 1.0% 1.2% 1.3% 1.6%

Portfolio B 0.0% 1.3% 1.7% 1.9% 2.0% 2.3%

The GAD Report

No account of expenses and tax – further work needed………….

‘based on an initial high level assessment, we believe that a

deduction of around 0.5% is likely to be reasonable’.

Highly sensitive to a number of key assumptions.

Economics

Investment Strategy

Term

Mortality

Inflation

CJC Report – November 2017

Does past claimant investment behaviour potentially skew the data?

‘It may seem intuitive that the discount rate should reflect actual

investment behaviour. But we conclude that this proposition should

not be adopted without some further critical examination’.

‘We advise caution in considering evidence of claimants’

Investment behaviour to set the discount rate. Investment by

claimants in higher risk portfolios could indicate they are under-

compensated and forced into higher-risk investments to generate

sufficient return for their future living expenses’.


Evidence in support of a change is not yet adequate:

‘We recommend that clear and unambiguous evidence is gathered

about the way claimants invest their lump sum damages before

legislation changes the basis on which the discount rate is

calculated’.

‘There does not appear to be a consensus about what type of

portfolio would be suitable to set a discount rate for claimants’.


Evidence in support of a change is not yet adequate:

‘We recommend that instead of targeting 100% compensation,

neither “under” or “over” compensation, the Government should

consider adopting as a target the median level of compensation to

tend towards over-compensation; or should at least ensure that

there are adequate safeguards to prevent significant under-

compensation of the most vulnerable claimants’.

Investment Advice Costs – A New Head of Future Loss

If claimant has to invest with risk to achieve 100% compensation

Future recurring investment advice costs?

Lump sum or PPO?

Significant head of future loss.

‘make such allowances for taxation, inflation & investment advice costs as

the Lord Chancellor thinks appropriate’

Likely Timetable

Sent to Commons : 28th June 2018

Second Reading : 4th September 2018

Committee : 11th September 2018

Report & Third Reading : TBC

Royal Assent likely Spring 2019 (subject to Brexit), then 90 day review

To be reviewed at least every 5-years by Lord Chancellor and Expert Panel

Where do we go??

Clear that current -0.75% rate will likely end

The end of Wells et al

Difficult to maintain the 100% principle

Will likely end up at 0%-1% as per GAD report

Accommodation issues still need resolution – Get Expert Advice

‘Rough & Ready’ investment approach in setting the rate

Claim future loss investment advice costs

Where do we go??

‘The assumption that the recipient of the relevant damages is

properly advised on the investment of the relevant damages’

Lawyers/Counsel are NOT FCA approved persons –can’t and should not

give advice.

Most Deputies/Trustees are not FCA approved persons.

Take extreme care when advising claimants on investments (don’t do it!!!).

Instruct Expert Financial Advisers

Summing Up

Sad to see the end of Wells et al

Claimants are put in difficult financial position

Get, and document advice

But, that said, better than 2.5%!!!!

Thank you for listening

Nestor, Controlled House, Waterfold Business Park, Bury, BL9 7BR

DX20511, Bury

T: 0161 763 4800 F: 0161 763 4809 E: [email protected] W: nestor.co.uk

Authorised and Regulated by the Financial Conduct Authority

Nick Martin, [email protected]

REFRESHMENT BREAK


0800 612 9660

[email protected]


Joint Working in Neurologic Music Therapy Provisions

Why use music?

Chiltern Music Therapy

Multi-Award Winning!

Research Committee of International Academics

Only Licensed Trainers in the Music Therapy Outcome Star

Royal Society of Public Health board for Social Prescribing

Allied Health Professions Public Health Strategy Board

Public Health England’s Arts in Health Special Interest Group

Music Therapists

High level of musicianship

in 2 instruments

Must have

Masters level in Music

Therapy

Registered with the Health &

Care Professions Council &

BAMT

Relevant clinical

experience with client

groups

Additional training for

NMT, MATADOC and NICU-

MT

Neurologic Music Therapy

Functional:

helping develop skills in cognition, speech & communication, motor skills.

Psychological:

working on emotional needs & mental health issues.

Sensorimotor training

Speech and language training

Cognitive training

Music Therapy approaches differ according to the client group and aim of the therapy:

NMT is an evidence based, neuro-scientific model of practice:

Music Therapy

What client groups can NMT work with?

Acquired Brain injury

Dementia

Multiple Sclerosis

Parkinson’s Disease

Autism

Stroke

Motor Neurone Disease

Huntingdon's Disease

Spinal Cord Injury

Cerebral Palsy

Hypoxic brain injury

Developmental delay

www.chilternmusictherapy.co.uk

Standard Music Therapy Neurologic Music Therapy

Community Programme

Music Producers DJs

Let’s Sing

Jammin’ Group

Silver Singers

Community Musicians

Therapy Programme

1:1 sessions

Group sessions

Group sessions

1:1 or group rehab

1:1 sessions

NMT or MATADOC

Assessment

Continuing care

Home Programme

Assessment 1:1 sessions

Group sessions

Client

Observing and Evaluating

How we observe and record……

Working with Speech & Language Therapists

Brain Injury: Compensatory

strategies

• Enhance functional and spontaneous speech

• Improving functional breath support

• Improve social interaction skills

• Improve initiation and rate of speech

• Improving articulation

Neuro-disability:

Maintaining skills

• Maintaining respiratory strength and breath support

• Maintaining articulation

• Maintaining functional speech


Joint working in the Community

• Community Support Group – Aphasia Focus

www.chilternmusictherapy.co.uk | make music. make change.

Totteridge Stroke Support Group's Version of What a Wonderful World.mp4

Joint-working in medical settings -NICU

• Neonatal Dysphagia

SLTs and MTs work together to provide:

- External pacing during feeding (suck-swallow-breath pattern)

- This reduces the risk of aspiration pneumonia and increase intake with reduced effort


Medical Settings – Acute Stroke Ward


SLT: “patient was engaged and responded to questions in the

session. He maintained attention for 10 minutes which is

meeting his goal.

SLT: the session had a positive effect on mood – patient was

engaged, participated and attended. The patient was able to

make verbal choices with songs which he is struggling with

previously (making choices). We (SLT’s) have been able to

use the singing in our sessions which has been very helpful.”

SLT: “It has encouraged patients to join in when other

techniques have failed. The patients I have been with have

enjoyed the sessions but we have also seen positive effects

on their participation/attention/communication e.g.

vocalising/automatic speech.”

Aphasia23%

Apraxia31%

Dysfluency15%

Volume15%

Clarity8%

Not known8%

SPEECH AND LANGUAGE REASONS FOR REFERRAL WITHIN ACUTE STROKE

Working with Physiotherapists

Possible difficulties:

• Gait deviations

• Kinaesthetic sense, proprioception

• Poor strength and balance, coordination

• Spasticity

• Decreased or poor strength and endurance, range of motion, flexibility

• Ataxia

NMT can improve

• Gait plus additional improvements in gross & fine motor skills

• Improved nerve and muscle control

• Balance, coordination, posture

• Range of motion

• Trunk control


NMT for Spinal Cord Injury

Existing research points towards use of Rhythmic Auditory Training (for those

with incomplete spinal injury),

Vocal Intonation Therapy and Therapeutic Singing to support respiration,

increasing vital capacity and volume, and pacing of breathing.

• de l'Etoile, S.K. (2008). The effects of rhythmic auditory stimulation on the gait parameters of

patients with incomplete spinal cord injury: an exploratory pilot study. International Journal of

Rehabilitation Research, 31, 155-7.

• Johansson K M, Nygren-Bonnier M, Klefbeck B, and Schalling E (2011). Effects of glossopharyngeal

breathing on voice in cervical spinal cord injuries. International Journey of Therapy and

Rehabilitation, 18, 501-12.

• Tamplin J et al. (2013). The effect of singing on respiratory function, voice, and mood after

quadriplegia; a randomized controlled trial. Archives of Physical Medicine and Rehabilitation, 94,

426-34.

• Tamplin, J. et al. (2011). The impact of quadriplegia on muscle recruitment for singing and

speech. Archives of Physical Medicine and Rehabilitation, 92, 250-56.

Non-Musical Goal:

• Example of how music is used to increase strength, co-ordination and control in movement.

• Non-musical aim:

- For the client to be able to reach forward and also to increase the strength in his core muscles.

- To be able to self-propel in his wheelchair.

• Music instruments are placed in the appropriate positions and a tempo is set.

Setting tempo, adding live music and rhythm



Siting balance15%

Sit to stand12%

Standing balance8%

Walking8%

Shoulder and arm15%

Leg and foot19%

Motivation for movement

15%

Left side neglect8%

PHYSIOTHERAPY REASONS FOR REFERRALPT: “this particular patient has been struggling to access traditional therapy. In this session he exceeded his goal and we will continue to use the techniques to ensure generalisation.”

PT: we have been struggling with this patient and they are highly distractible. The minute the music started the patient moved to the rhythm and he walked across the gym with a significantly improved gait pattern”

PT: “for this patient the music therapy has really helped us turn a corner.”

Working with Clinical Psychologists and Occupational Therapists

Difficulties with:

• Attention and concentration

• Memory

• Sensory processing

• Difficulties with multi-tasking

• Problem solving and decision making

• Learning to use switches

NMT can improve:

• Memory difficulties, decision-making and problem solving skills

• Improving difficulties with attention and focus

• Promotes adaptive responses to environmental demands.



OT: “significantly improved sustained attention to task and client ability to engage in the task. Initially requiring increased prompts to follow tasks and to attend to left side but with music was able to start following the task independently. Increased bilateral integration of upper limb when initially not engaging his left arm”

OT assistant: “patient engaged in music therapy very well,

demonstrated ability to use her left hand to the rhythm of

the beat. Patient previously has disengaged/got sleepy

when using her left hand in activities such as

cards/dominoes. Patient’s mood was also noted to improve,

stating that sh had enjoyed herself”

OT: “clients were engaging in session and with music

therapist. It improved mood and motivation. It provided a

physical and cognitive element which was graded.”

Transfers11%

Sitting balance22%

Upper body strength

22%

Standing balance17%

Grip and release11%

Motivation for movement

5%

Attention and focus

6%

Left-side neglect

6%

OCCUPATIONAL THERAPY REASONS FOR REFERRAL

Bringing it all together

Client Background

• Injury at birth followed by seizures and sedation.

• Parents noticed delayed milestones and at 18 months he received a diagnosis of

Cerebral Palsy

• With input from Physiotherapy 3 x a week, he could walk, unaided at 3 ½ years old.

• Attended mainstream primary school with input from Physio, OT, and (limited) Speech

and Language Therapy.

• Attended mainstream secondary school and referred to Music Therapy by his parents

at 14 years old to see whether NMT could improve his speech intelligibility.

Initial NMT goals focused on Speech and Language:

• Improving respiratory strength and oral motor control (essential for articulation)

• To increase fluency of speech and to facilitate intelligibility of speech.

Appropriate NMT techniques:

Oral Motor and Respiratory Exercises (OMREX)

Rhythmic Speech Cueing

OMREX

• Wind instruments support breathing exercises

• Choose songs with lyrics that repeat target sounds

(e.g. /v/.... “All you need is love”)

• Sing melodies using one vowel

- Open jaw: “a”

- Lips rounded: “o”

- Lips closed: “m”

- Elevated tongue tip: “l”

- Back of tongue elevated: “g”

Rhythmic Speech Cuing (RSC)

1.Slow down with metronome and then speed up (compensatory strategy)

2.Ask / answer questions

3.Free speech

“My favourite car is a jaguar e-type

It’s very fast and it glides like air

My favourite programme is Top Gear

My favourite food is chocolate cake!”

Speech & Language Goals

Goal: To increase fluency and intelligibility of speech

Objectives: Client will decrease rate of speech to 70 BPM, with

external rhythmic cueing.

Client will demonstrate intelligibility in 3 out of 4

spoken phrases at the end of each session following

completion of Vocal intonation Therapy exercises by November

15th

Goal: To increase oral and motor control and

coordination

Objectives: Client will imitate simple syllables (ba, ha, kuh,

tee etc) sung by the therapist in 7 out of 10 trials by session 6

Client will demonstrate the ability to direct air flow through

the mouth using a musical instrument (recorder or kazoo)

Moving into NMT Cognitive goals to assist with day to day difficulties:

• To improve working memory and recall


Musical Mnemonics Training

Cognition Goal

Goal: To improve working memory

and recall

Objective: Client will recall and

carry out a 5 step instruction with no prompting by

January 17th.

There was particular concern about roadsafety and J needing to memorise usefulinstructions for road safety.

Therapist created a song with 5 linesincluding simple instructions such as waiting,looking, and listening before crossing.

Both the therapist and J came up with themelody line and lyrics. Repetition was key toensure the song would be easily recalled andremembered at the right time.

NMT motor skills goals for improving independence and self-confidence:

• To increase functional motor skills of the upper limb


Therapeutic Instrumental Music Performance

Patterned Sensory Enhancement

Motor Goals

Goal: To increase functional motor skills of the upper limb

Objective: The client willindependently complete 3minutes of instrumentalplaying requiring bilateraluse of hands with finemotor movement.

Music Therapy to support emotional needs, independence and transition…

“So what’s the point of nothing,When you have everything to look forward to?

And what’s the point of looking backwards,When everything in your life kicks off.

It’s the small things that change your lifeAnd if it’s free, it’s better for me

It’s the passion that changes your lifeSo join us and you will see”

Community Music Provision

Neurologic Music Therapy

Community Programme

Music Production Skills

Therapy Programme

1:1 sessions

1:1

sessions

Assessment

Client


Music Volunteer in the Community for CMT

Client’s transition and ‘Journey of Change’

Mentor for Chicken Shed

CONTACT

ROSIE AXON

Chiltern Music Therapy, Office A, Irfon House, Stones Courtyard, High Street, Chesham, Buckinghamshire HP5 1DE

07968 395794

01442 780541

[email protected]


mailto:[email protected]

Reuben GlynnManaging Director at Partners in Costs

Email: [email protected]: 01302 343666

LinkedIn: pic-legal | Twitter: @PIC_Legal

mailto:[email protected]://www.linkedin.com/company/pic-legalhttp://twitter.com/PIC_Legal

• Rules

• 3.12-3.18 CPR & PD 3E

• Timing Mitchel [2013] EWCA civ 1537

• Abuse

• Findcharm [2017] EWHC1108(TCC)

• Tucker [2017] SCCO case number JR 1607217

• Cost Recovery

• Merrix [2017] EWHC 346 QB

• Harrison [2017] EWCA 792

• POA Cleveland Bridge [2018] EWHC 827 (TCC)

• Security for Costs SARPD OIL [2016] EWCA civ120

• Revising Budgets SHARP [2017] EWHC 3390(ch)

• Proportionality

• New Bill of Costs

Cost Budgeting Update

Any Questions?...

Reuben GlynnManaging Director at Partners in Costs

Email: [email protected]: 01302 343666

LinkedIn: pic-legal | Twitter: @PIC_Legal

mailto:[email protected]://www.linkedin.com/company/pic-legalhttp://twitter.com/PIC_Legal

LUNCH BREAK

Afternoon session will

resume at 14.00


0800 612 9660

[email protected]


Dementia after Head Injury

Dr Mike DilleyConsultant Neuropsychiatrist

St George’s NHS [email protected]

mailto:[email protected]

This lecture will aim to:

• Provide an update on the evidence for a relationship between traumatic brain injury (TBI) and Alzheimer’s Disease (AD)

• Consider the risk factors for AD after head injury and particularly the role of APO E

• Consider the risks of developing dementia after multiple concussions

• Discuss neuropsychiatric presentations that may mimic dementia

‘While dementia is sometimes the outcome of severe head injuries, the role of CNS trauma as a provocative agent in the

pathogenesis of Alzheimer’s Disease is controversial.’

Posttraumatic Premature Alzheimer’s Disease Rudelli et al. 1982

• 22 year old steel worker in RTA

• Left frontotemporal skull fracture and LOC

• Burr hole evacuation of SDH; 4/52 admission

• Dysphasia, amnesia, impaired judgement and abstract thinking –improved 18/12 – work

• Deterioration 5 years later – develops apraxia, challenging behaviour

• Enlarged ventricles; Δ AD and died in 30’s; no FH

What is Dementia?

• Multiple cognitive deficits• Amnesia, disorientation, aphasia (language), apraxia (motor tasks), agnosia

(sensory input), executive dysfunction

• Functional impairment

• Clear consciousness• i.e. cognitive deficits are not only during delirium

• Change from previous level

• Long duration• >6 months

Alzheimer’s Disease

• 60-70% of dementia diagnoses Fratiglioni & Rocca, 2001• Dementia with Lewy bodies, vascular dementia

• Insidious onset

• Gradual progression

• No focal neurological signs

• No evidence for a systemic or brain disease sufficient to cause dementia

Epidemiology

• Exponential increase in prevalence of AD with age Fratiglioni et al. 1999; Lobo et al. 2000

• Suggestion that over next 50 years cases will increase by 4x Mortimer 1997

• Multiple risk factors including TBI Levin & Goldstein, 1995; Spear, 1995

• Insidious increase in TBI alongside advances in neurotrauma management Sosin et al. 1995

WHAT IS THE EVIDENCE FOR AN ASSOCIATION BETWEEN TBI & AD?

What is the evidence for an association between TBI & AD?

• Largely studied using case-control methods• Proportion of patients with AD and a history of head injury vs. the proportion

of controls of same age and gender who report having had a head injury

• This method at risk of recall bias• Matched informant history

• Needs to ensure that controls do not have dementia

• Prospective cohort studies

Odds Ratios

• Quantifies an inferred association in terms of strength and direction

• Approximates to the relative risk in AD i.e. the degree to which the disease is more likely to occur in exposed, as compared unexposed, individuals

• e.g. Heyman et al. 1984 identify OR of 5.31 as measure of association between TBI & AD

• The odds of prior TBI were 5.31 times higher in AD cases than in controls

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Mortimer et al. 1991 (EURODEM)

• Conflicting results between case-control studies• Misdiagnosis of AD cases or false positives

• Lack of agreed diagnostic standard for TBI

• Recall bias – AD informants may be more motivated than control informants to recall TBI

• Poor statistical power of individual studies

• Head injury with LOC of any duration

• Meta-analysis of case-control studies allowing for more powerful statistical investigation of association

Mortimer Results

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Pooled RR for 7 studies 1.82 (1.26-2.67)

Fleminger et al. 2003

• Inclusion criteria• Head injury with loss of consciousness

• Matched case and control subjects

• Diagnostic criteria for AD

• Inclusion criteria for controls

• Informant history from cases and controls

• Exclusion criteria• Studies with psychiatric controls

• Head injury prior to onset of AD

• 15 studies (8 pre-Mortimer; 7 post)

Fleminger Results

Odds Ratio 1.58 (1.21-2.06); Males 2.26 vs. Females 0.92

Fleminger et al. 2003

• Did not review the relationship with APO E

• Did not consider the nature and severity of injury

• Sensitivity analyses to consider bias– Specified period after TBI before onset of AD to reduce bias of AD

causing TBI – little effect on OR

– Matched informant relationships to reduce bias of spouse vs. all comers – non-significant reduction of OR

Perry et al. 2015

• Metaanalysis of all studies reporting mTBI as a risk factor for psychiatric and neurological diagnoses

• 57 studies

• OR for any illness 1.67: neuro 1.55; psych 2.00

• Higher odds of AD, PD, depression, BPAD

• No impact of repeated injury demonstrated

Cohort Studies

• No increased risk of AD associated with TBI

– Katzman et al 1989 – prospective– Williams et al. 1991 – prospective – problems with standardization of AD onset– Mehta et al. 1999 – prospective– Dams-O’Connor et al. 2013 – prospective– Crane et al. 2016 – prospective– Weiner et al. 2017 - prospective

• Increased risk of AD associated with TBI

– Scholfield et al. 1997 – incidence study; dependent on duration of LOC >5mins– Nemetz et al. 1999 – retrospective population – time to AD shorter in TBI– Plassman et al. 2000 – retrospective – increased risk stratified by severity– Wang et al. 2012 – 2x increased risk; high rates of CVD; unclear if deteriorated since TBI i.e. poor criteria for

dementia– Kaprio et al. 2017 – retrospective – OR 1.8 for AD but not for PD/ALS– Nordstrom 2018 – prospective, OR 1.81 strongest in Y1 but continues to Y30

Fann et al. 2018

• Observational cohort study, prospective• n= 2 794 852 subjects

• 36 year follow up

• All dementia in TBI group OR higher (1.24) than no TBI/trauma controls

• AD OR 1.16; highest in first 6 months (4.06) and associated with injury severity

• Increased OR with multiple TBI’s (2.85 with >5 TBI’s)

Does brain injury accelerate the onset of AD?

• All documented episodes of TBI between 1935 – 1984 in Olmsted County, Minnesota

• Community medical records used to follow TBI cases aged 40+ until last contact or death

• n = 1283: 31 developed AD i.e. similar to background incidence

• Time from TBI to AD less than expected (10 vs. 18 years; p = 0.015) Nemetz et al. 1999

THEORETICAL CONSIDERATIONS

Cognitive Reserve & Threshold Theory

• Inbuilt reserve in neuronal circuitry Teuber, 1974

• Reduced by maturation and degenerative changes of aging Glassman & Smith, 1988

• Hypothesis that function is maintained until a critical threshold of neuronal loss is surpassed Satz, 1993

• Brain Reserve Capacity varies between individuals – but hard to quantify

• Education may afford higher baseline

What links TBI & AD pathologically?

• Neuronal loss

• Persistent inflammation

• Cytoskeletal pathology

• Amyloid-β (Aβ) deposition

– Hallmark of AD found in 30% of all age groups who die from TBI but only in elderly with no TBI Roberts et al. 1994

• Role of APO E ε4 allele

APO E ε4

• Associated with Aβ deposition

• Those who are ε4 positive are at greater risk of developing AD post-TBI Mayeaux et al. 1995

• Of 10% of cohort of TBI patients developing AD, 100% ε4 positive cf. 32% base rate Koponen et al. 2004

• Non-significant trend toward stronger associationbetween AD and TBI in men with more ε4 alleles Plassman et al. 2000

• Finding is not consistent O’Meara et al. 1997

Can multiple concussions lead to dementia?

• Repetitive mTBI can trigger development of chronic traumatic encephalopathy McKee et al. 2012

• Previously described as punch drunk, dementia pugilistica and boxers encephalopathy

• Associated with irritability, impulsivity, aggression, STM-loss 8-10 years after repetitive mTBI. APO E ε4 status implicated.

• With advancing disease develop dementia, gait and speech abnormalities and parkinsonism

WHICH NEUROPSYCHIATRIC PRESENTATIONS CAN MIMIC DEMENTIA?

When it looks like dementia… but isn’t

• Consider complications of head injury such as SDH or hydrocephalus

• Neuropsychiatric conditions such as depression, anxiety, psychosis and substance misuse can present with apparent cognitive deterioration

• Performing worse than chance on tests of effort can be related to these conditions as well as malingering

• Interestingly long term increased disability may be impacted by effect of self perception and illness beliefs McMillan et al. 2012

Summary

• Head injury is a probable risk factor for developing AD, although likely only slight

• Injury severity probably increases risk• Greater risk in males? Recent studies suggest not• In part related to the APO E status of the patient• Attributable risk for Alzheimer’s disease as a result of head

injury is small• At most only a small proportion of AD could be prevented by

eliminating head injury – although some authors more optimistic!

Malingering, Conscious and Unconscious Exaggeration

Dr Karren Towgood

Clinical Neuropsychologist

What is malingering?

• DSM-IV TR defines the term malingering as:

• A conscious process that involves the intentional production of false or grossly exaggerated physical or psychological symptoms and which is motivated by external incentives.

• Distinguished from similar presentations that are not volitional, and not aimed at gaining external incentives.

• Much criticism of the DSM criteria, especially when applied to neuropsychological function.

Secondary Influences: Section Title : What is Malingering

• Slick et al (1990) have proposed criteria for diagnosing malingering of neuropsychological dysfunction.

• Criteria specifically avoid the necessary establishment of intent to diagnosis malingering.

• Criteria have levels of diagnostic certainty – possible, probable, definite.

• Definite malingering:– Presence of substantial external incentive;

– Definite negative response bias – below chance performance on one or more forced choice measures of cognitive function;

– Negative response bias is not accounted for by Psychiatric, Neurological or Developmental factors.


• Slick et al (1999) note that where there are potentially motivating external incentives, but there are also other possible motivations for exaggeration or fabrication, such as to communicate distress, “it is rarely possible to apportion intent”.

• Suggests in this case a diagnosis of possible malingering should be considered if other criteria are met.


• What does malingering look like:

• Symptom feigning can appear in discrete cognitive skills, such as in memory or processing speed, or can be seen as global cognitive impairment.

• Symptom exaggeration can also be seen in report of psychological symptoms, pain etc.

• The choice of which symptoms to feign and how to feign will be based on the individual’s beliefs about the cognitive disorders they are attempting to feign.

• Two strategies have been identified:

• To intentionally diminish or reduce capacity.

• To intentionally exaggerate symptom complaints.


• Important to realise that malingering is not static and typically fluctuates across an evaluation depending on patients beliefs and attentional focus.

• No clear pattern, as it depends on beliefs of patient, for example:

• May produce better effort on harder tests because don’t appreciate which tests are harder or easier.

• Also, harder tests may take up more attention so will forget they are supposed to be feigning as their attention is captured.

• May produce odd patterns because of their beliefs – for example, producing digits backwards when supposed to be doing them forwards (but this takes a huge amount of effort!).

• Also can see a mix of genuine and malingered performance.


• Because it can be so difficult to be sure that symptom production is intentional it has been argued that we (neuropsychologists) should disregard the term malingering in all but the most rare conditions when there is incontrovertible evidence of malingering (Boone et al 2007).

• It there is usually considered to be a matter for the courts to decide if there is incontrovertible evidence of malingering.


• But - some argue that we should be less reticent about diagnosing malingering based on concern about inferring internal states as clinicians often do this in practice – ie with regard to hallucinations in schizophrenia.

• Slick et al (1999) argues that the essence of clinical diagnosis is the expert judgement in the absence of a definitive test and that diagnosing malingering is no different than this.

• Relies on training and experience.


• Factors which may inform a decision about malingering:– Performance on “effort testing” – but important to note that equating

failure of effort testing with proof of malingering is an over-simplification (Heilbrooner et al 2009);

– Consideration of whether there are any alternative explanation for the “failed” effort testing, for example other mental health factors, pain, medications, fatigue etc;

– Consistency of evidence;– Consistency of symptom presentation;– Performance as a witness;– Confession or direct evidence such as from surveillance – difficult to gather

direct evidence to support malingering of cognitive or mood difficulties.


How do we assess malingering?

: Assessment of Effort

: How do we assess malingering?

•Evidence from neuropsychological testing:•Below chance performance on symptom validity tests (SVTs)•Discrepancies between test data and observed behaviour

•Evidence from self report, questionnaires:•Self-reported history discrepant with documented history•Self-reported symptoms discrepant with known patterns of brain functioning•Behavioural observations•Information from collateral sources


: AACN Consensus Statement

•In diagnosing poor effort need to consider overall presentation of client, background information, history taken during clinical interview, observations, neuropsychological performance and performance on SVTs.•Research has found that experienced experts are not accurate in identifying valid from invalid performances on the basis of behavioural observation and test scores alone.


: What are effort tests?

•Key to diagnosing malingering, particularly in the Slick et al criteria, are the effort tests, which are more appropriately called performance or symptom validity tests•They are empirically based methods which aim is to help identify individuals who may not be putting in the required “effort” to perform at their best on tests.


: Symptom Validity Tests

•Basic rationale is that they appear to measure a particular ability, for example memory.•However, in reality they are so simple that even a person with significant cognitive impairment should be able to perform well on them. Whilst typically called ‘effort tests’, the reality is they require little effort to achieve 100% performance.•Two basic categories of SVT

•Free standing•Embedded


: Symptom Validity Tests

•Free standing measures are additional measures specifically designed to test validity. Can be time consuming but have the best evidence base.

•Forced choice – if perform below chance this suggests they knew the correct answer and deliberately chose incorrect answer.•Non forced choice – for example tapping speed, dot counting etc.

•Embedded measures are calculations derived from standard neuropsychological tests already included in the battery – for example reliable digit span.


: BPS Guidance

•Effort testing should be routinely carried out except in exceptional circumstances (ie severe learning disability).•A multi-method and multi-test approach is recommended.•Careful interpretation of failure on effort testing is required.•Knowledge of sensitivity and specificity of tests of effort is crucial.

: Secondary Influences: Section Title : Assessment of Effort

: Example – Dot Counting


: Example –15 Item Test


: Example – Forced Choice Test


: Examples – Forced Choice Test


: Example – Forced Choice Test


: How do we interpret findings?

•Below chance performance does not necessarily equate to conscious control – for example Boone et al (2007) note that in a study of hypnotized individuals who were asked to feign amnesia 25% performed below chance. Presumably this was not due to conscious control as individuals were hypnotized.

•To aid in interpretation of results it is important to understand the psychometric properties of the tests, and in particular their sensitivity and specificity – as well as looking at false positive rates. For example, below chance performance on two or more effect indicators is often set to be the gold standard for detecting malingering, but is generally associated with a 10% false positive rate.

Conscious or Unconscious

: Conscious or Unconscious

• One of the key requirements for a diagnosis of malingering is that the behaviour is conscious and intentional, and this helps to distinguish it from other clinical disorders that may also involve symptom exaggeration or fabrication, for example:

• Somatization disorder – unintentional, involuntary• Conversion disorder – unintentional, involuntary• Dissociative disorder – unintentional, involuntary

•Another key element is that there is evidence of external incentives, which helps distinguish it from disorders that are also conscious, but not externally motivated, for example:

• Factitious disorder – intentional, voluntary, internal incentive (sick role)


•Also important to think about why a patient may be inconsistent.

•Variable attention due to pain, fatigue, mental health difficulties etc.

• Given that human behaviour is so complex, how can we ever be certain that a patient has malingered without direct evidence or confession? Is probable or possible malingering enough, or do we need to be certain?


•It is also important to understand why a person may (genuinely) exaggerate cognitive or mood symptoms in a medico legal setting.

•In a context where beliefs about cognitive/mood difficulties are reinforced – such as can frequently occur in medico legal settings where a diagnosis may have been given about brain dysfunction – suggestible individuals may be prone to exaggerate symptoms.

•In the context of litigation, an attentional bias may lead some individuals to overly focus on common cognitive complaints, interpret them as reflecting significant brain dysfunction (possibly supported by the opinion of other experts), and then possibly act out these beliefs in daily life and in an assessment.

175hardwicke.co.uk @hardwickelaw||© Hardwicke, Hardwicke Building, New Square, Lincoln’s Inn, London WC2A 3SB

FUNDAMENTAL DISHONESTY

LITIGATION LIFE AFTER SINFIELD AND S.57

Colm Nugent

9 October 2018

http://www.hardwicke.co.uk/http://www.hardwicke.co.uk/http://www.twitter.com/hardwickelawhttps://www.google.co.uk/maps/place/London+WC2A+3SB/@51.5160786,-0.114498,17z/data=!3m1!4b1!4m5!3m4!1s0x48761b4b4364ec3f:0xc99fbd022b845732!8m2!3d51.5160198!4d-0.1124534?hl=en


The implications of dishonesty

•The finer points of Fundamental Dishonesty

•Recent case decisons

•Tactical implications



LOCOG v Sinfield [2018] EWHC 51

• Mr Sinfield faked the gardening invoices to support an (arguably)

genuine claim for gardening assistance. This meant that …

• the SOT on the disclosure was false

• The SOT on the schedule of loss was false

• The SOT on the witness evidence was false.

• Sinfield asserted that the invoices were not created dishonestly



So what if C believes that his actions were honest?

Even if they weren’t…



“Dishonesty can easily be recognised by juries, so too can it be by Judges”

• Ivey v Genting Casinos Ltd [2017] 3 WLR 1212

• Dishonesty is subjective, but

• The standard applied by the court is objective, therefore

• A dishonest mental state is measured by ‘ordinary standards’

• [In other words: you can’t claim you genuinely thought it was ok to act dishonestly]



Approach is echoed in insurance claims

• Versloot Dredging v HDI [2017] AC 1

• ‘Fraudulent Claim Rule’ (per. Lord Hughes [95,96])

• A genuine insurance claim supported by false/fraudulent evidence should fail even if it is otherwise valid in law.

• The ‘rule’ is not limited by how dishonest the fraud was, if it was material –otherwise it would leave the rule “hopelessly vague”



Core ingredients of Fundamental Dishonesty



What are the core ingredients of F.D.?

• The criteria appears to be remarkably wide (looking at Sinfield)

• That C made dishonest misrepresentations.

• That the defendant may have settled at a figure to which C was not entitled. [para 84]

• The sums involved need not be high – apparently £3,000 may be enough [para 85] -£14,000 certainly was.

• That the greater part of the claim is honest “is neither here nor there”. [para 86]



Fundamental dishonesty - a comparison

CPR 44.16 S.57

Claim has been fundamentally

dishonest

Claimant has been fundamental

dishonest

Applies whether C is entitled to

some damages or not

Only applies where C is entitled to

damages

Only relevant to costs Relevant to both costs and

damages

Saving provision: the court “may” –

significant discretionary element

Saving provision: unless C would

suffer “substantial injustice”

D may enforce costs order to full

extent

D’s costs reduced by sum Court

would have awarded C



What now amounts to ‘F.D.’?

1. A false assertion in witness evidence.

2. A false assertion in a schedule.

3. A false assertion on a disclosure statement.

The effect/purpose of which is to recover damages to which C is otherwise not entitled



Molodi - groundbreaking?

• Molodi v Aviva [2018] EWHC 1288 (QB)

• The first extension of s.57 and the principles in Sinfield?

• M claimed minor whiplash. M told expert he’d one previous accident.

• Turned out he’d had at least six.

• J said that it meant the medical report could not be relied upon by court.

• Held to be Fundamentally Dishonest: C had failed to prove his case.



Not everything is fundamentally dishonest

• (1) Richards (2) McGrann v Morris [2018] EWHC 1289 (QB)

• The lesser known relative of Molodi.

• No F.D. - Claimants just failed to prove their case on injury.

• “Hopeless inconsistencies” as opposed to dishonesty.



So where are we headed?

• Howlett v Ageas [2017] EWCA 1696 - FD did not need to be specially pleaded.

• Pinkus v Direct Line [2018] EWHC 1671 (QB) 02.07.18 HHJ Coe QC

• C’s presentation at trial, his Facebook entries, inconsistencies to experts = conscious exaggeration



Discontinuing the claim

• Alpha Insurance v Roche [2018] EWHC 1342 Mrs Justice Yip QC

• 44PD12 para 12.4 deals – allows court to deal with allegations of FD even after

discontinuance and even if Notice not set aside.

• No “exceptionality” test said the Judge

• Discretion unfettered – ‘all relevant considerations’ and the Overriding Objective is the

appropriate test

• Discontinuing shortly before trial without explanation “weighed heavily” in favour of granting

D’s application (and appeal).



The real impact of these cases is the uncertainty they create

1. Legal teams must now advise any C very carefully, if there are matters which may amount to fundamental dishonesty, and which may result in C losing all damages and zero costs recovery.

2. Any Deft. offers – even modest ones – will now have to be looked at in that context.

3. Most importantly: how many legal teams will really going to take the chance if C is challenged? [Pinkus, anyone?]



Faced with s27, legal teams need to reappraise our approach to the evidence

1. Did Mr. Sinfield’s solicitors think they needed to interrogate what seemed to be a completely genuine invoice?

2. Did Molodi’s solicitor think they needed to check what Molodi told the expert was true, or not?

3. Did Mr Pinkus’ solicitor think they needed to challenge his account in his extensive

witness evidence?



How will courts now view ‘everyday’ matters such as…

• Inconsistent accounts of disability given to medics, experts or claims assessors?

• Does this merely inhibit C from proving the claim?

• Or does it undermine the credibility of the expert report to the point where it is abandoned (e.g. Molodi)

• Claims for Aids & Equipment that have never been acquired, notwithstanding an interim.



How will courts now view surveillance evidence…?

• Patel v Arriva Midlands [2018] (Lawtel only)

• C succeeded on liability-only trial in establishing 60% liability

• D argued FD and sought s.57 declaration (after split trial) when inconsistent surveillance

evidence was disclosed.

• Judge refused to allow C to recover any costs of split trial until issue of FD was

determined, based on surveillance evidence.

• C argues that full quantum trial is now required.

• D says no additional evidence required.



Claims now more vulnerable?



Claims by the self-employed



There is now a shift in the balance of risk

• Where do the dividing lines between embellishment – exaggeration – and dishonesty now lie?

• Is there an irreducible minimum of fraud needed?



But let’s not get too zealous, or too paranoid

Allegations should be deployed carefully and appropriately



What is fair warning?

• Courts do not require FD to be formally pleaded.

• But will expect to see it in the C-Schedule (at a minimum) - see Wright and Pinkus.

• Taking C by surprise will only lead to adjournments and delay to enable C to obtain rebuttal evidence.

• In Pinkus, J refused a declaration that D was unable to advance a FD/fraudulent exaggeration claim because it was not set out in the Defence.



Forewarned is forearmed

• C may well demand to know what case they have to meet, if D is being coy or is havering.

• C will need the medical experts to address it in evidence.

• C will say that their client should know whether they have a exaggerated or fraudulent allegation to meet.

• C may well try to counter (or swamp) an allegation of exaggeration with multiple independent witnesses.

• C may well point out at a CCMC that an ‘exaggeration/dishonesty’ defence is more expensive to deal with, and should be reflected in costs and the input of Grade A solicitor and counsel.



Questions? Observations?



Thank you! Any questions?

Colm Nugent

[email protected]

@wigapedia

http://www.hardwicke.co.uk/http://www.hardwicke.co.uk/http://www.twitter.com/hardwickelawhttps://www.google.co.uk/maps/place/London+WC2A+3SB/@51.5160786,-0.114498,17z/data=!3m1!4b1!4m5!3m4!1s0x48761b4b4364ec3f:0xc99fbd022b845732!8m2!3d51.5160198!4d-0.1124534?hl=enmailto:[email protected]

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Documents

Brain Injury Group · change not only the functions but also the structure of the brain itself (Fuchs & Flügge, ... •Our brains are organised at every level according to function: