Behavioural and Cognitive Psychotherapy: page 1 of 7

doi:10.1017/S1352465817000832

A Novel Treatment Protocol (Nocebo Hypothesis Cognitive

Behavioural Therapy; NH-CBT) for Functional Neurological
Symptom Disorder/Conversion Disorder: A Retrospective
Consecutive Case Series

Matt Richardson, Gina Isbister and Brad Nicholson

ISIS Rehabilitation Centre, Southern District Health Board, Dunedin, New Zealand

Background: Theories concerning the aetiology of functional neurological symptom disorder

(FNSD; also known as conversion disorder) have historically inferred that psychological
factors or dissociative states underlie patients’ symptoms. Current psychological models of
functional neurological symptoms suggest that some type of ‘top-down’ representations/beliefs
are activated automatically (without conscious awareness), leading to symptoms. It is assumed
that these representations or beliefs are similar to the idea ‘I am neurologically damaged’,
as in our clinical experience, almost all patients have some reason to doubt the integrity of
their neurological system. Aims: It was hypothesized that FNSD arises from a belief of being
neurologically damaged (via a mechanism akin to a nocebo response), and an interdisciplinary
treatment protocol was developed consistent with this hypothesis, transparently sharing this
theory with participants. Method: A retrospective consecutive case series design was utilized,
measuring functional independence and symptom remission. Results: Of the 13 episodes
of care, 12 resulted in complete or almost complete symptom remission. Length of stay in
rehabilitation was also reduced compared with previous treatment attempts. Conclusions: It
appears as if the treatment protocol may be very effective, and further controlled study appears
warranted.
Keywords: somatization, beliefs, bodily sensations, cognitive behavioural interventions

Introduction
Functional neurological symptom disorder (FNSD; also known as conversion disorder) is
characterized by symptoms normally associated with neurological disorders, but with no
identified structural cause.
Neuroimaging and neurophysiological studies of patients with various functional
neurological symptoms suggest that neural networks and neurophysiological mechanisms
may mediate these symptoms (see Voon et al., 2016, for a review). However, no cause or
mechanism for FNSD has been firmly established, and treatment studies have generally shown
modest positive benefits at best (see Carson et al., 2012, for an overview). Relevant to this
study, there has been some degree of treatment success with in-patient physical rehabilitation,

Correspondence to Dr Matt Richardson, Clinical Psychologist, ISIS Rehabilitation Centre, Private Bag 1921, Dunedin
9054, New Zealand. E-mail: [email protected]

© British Association for Behavioural and Cognitive Psychotherapies 2018

2 M. Richardson et al.

incorporating some simple behavioural modification principles, e.g. Jordbru et al.

(2014).
Psychological models of functional neurological symptoms broadly focus on the idea of
the activation of some type of ‘top-down’ processing being important, such as the Integrative
Cognitive Model posited by Richard Brown and colleagues (e.g. Brown and Reuber, 2016).
This model suggests that some type of ‘rogue representation’/‘seizure scaffold’ is automatically
activated, in the context of a ‘high level inhibitory processing dysfunction’. Similar to this is
the account of functional symptoms described by Edwards et al. (2012), which suggests that
these symptoms autonomously arise from inferences based on prior beliefs and experience.
These accounts are consistent with our observation that almost every single person with
functional symptoms has some reason to doubt the integrity of their neurological system,
e.g. having received a neurological diagnosis unrelated to their symptoms, or having been
concussed shortly before symptom onset.
If there are representations or beliefs that lead to functional symptoms, one could assume
that they are similar to the idea ‘I am neurologically damaged’. The idea that such top-down
representations can trigger physical symptoms would be consistent with the idea of a nocebo
response, defined by Colloca and Miller (2011) as ‘the expectancy-induced changes in the
patient’s brain-body unit’. If present, such symptoms are almost certain to strengthen the belief
in one’s neurological impairment, which would then create a maintenance (i.e. ‘vicious’) cycle.
Clear demonstrations of the role of negative expectation or belief in functional neurological
symptoms are sparse. However, there are numerous reports in the literature of rapid
and/or dramatic placebo response (i.e. symptom reduction) in individuals with functional
neurological symptoms, further suggesting an important role of expectations/beliefs in this
population.
The aim of this study was to test the following hypothesis: if FNSD is the result of something
akin to a nocebo effect/response, a treatment protocol consistent with this theory should be
effective.

Method
This study has a retrospective consecutive case series design, with no control group. It is
essentially a summary of the results of a consistently applied treatment protocol in a neuro-
rehabilitation setting, supported by the rehabilitation unit’s routinely used outcome measures.
Whilst not specifically measured, it is estimated that the in-patient participants were treated
with the customary intensity of intensity (approximately 2–4 hours of therapy a day, for 5 days
a week, with nursing support available 24 hours a day).
For 17 months, every patient admitted with functional neurological symptoms (i.e. after a
full neurological assessment found no structural cause for the symptoms) was included in the
case series. There were no exclusions. Twelve participants (six males, six females; age range
19–63 years; mean 41.2 years) met this criterion, with one participant presenting twice. Eleven
participants were admitted as in-patients, and one was seen as an out-patient (3 hours total
input).
In terms of clinical presentation, the sample had a variety of functional symptoms. To
briefly describe the sample’s predominant (i.e. most disabling) symptom, seven presented with
weakness/reduced mobility, three with tremor, and two with non-epileptic seizures. Two of the
sample had mixed symptomatology.
 A novel treatment (NH-CBT) for FNSD 3

The following list outlines some of the participants’ circumstances that could be categorized
as ‘reasons to doubt the integrity of their neurological system’:
r A confirmed neurological diagnosis (that did not explain the symptoms), including epilepsy,
neurofibromatosis, an excised brain tumour as an infant, and multiple mild traumatic brain
injuries.
r Significant spinal surgery in the past.
r Initial diagnosis of multiple sclerosis, with a second neurological opinion (diagnosis of
functional symptoms) many months later.
r Taken to hospital in dramatic circumstances (e.g. in a helicopter), with paramedical and
medical staff initially suspecting serious structural neurological impairment.
r Intellectual disability or borderline intellectual disability.

The participants were treated using the following protocol:

r Medical staff explained key evidence regarding the improbability or impossibility of
structural changes to the neurological system.
r A clinical psychologist gathered information about their medical history, the onset and course
of symptoms, the participant’s understanding of the medical evidence, their personal belief
about the causes of their symptoms, and their understanding of the terms ‘subconscious’
and ‘placebo effect’. This was useful in helping judge how much, and what degree of
psychoeducation would be necessary in order to proceed. There was little or no conversation
about emotional factors.
r A formulation was then transparently and collaboratively developed with the participant
that incorporated relevant history within a ‘nocebo model’ (see Fig. 1). In essence, this
served to explain the discrepancy between the medical findings and the participant’s
subjective experience. It was hoped that this would engender in the participant an
alternative belief about their symptoms, to challenge the one currently held (often
something approximate to ‘the doctors have missed something’, or ‘this is being caused by
stress’).
r The participant was consequently encouraged to examine this different perspective on their
symptoms. This might commonly involve creating a new personal narrative about how events
transpired around the onset of symptoms, but this time assuming that the new ‘nocebo
model’ formulation was more accurate. Whilst every individual was different, the general
aim was to challenge participants’ beliefs that they were damaged, or in danger. Instead, a
narrative/metaphor such as e.g. ‘some simple misfiring of their intact neurological system’,
or ‘no more dangerous than a stutter’ was provided as psychoeducation. A hardware/software
metaphor was often used to this end.
r The participant was then given opportunities to experience themselves as functioning better.
This invariably involved physiotherapy sessions, e.g. focusing on getting their affected limbs
moving again. This was often done by varying what the participant attended to (e.g. trying to
get them to walk without attending to their body movement, using distraction such as music,
rhythm or attentionally absorbing video games), and using video recording/feedback to show
them any improvement in limb movement. Video feedback appeared essential, especially
given the observation that improved mobility appeared to accompany a lack of conscious
attention paid to one’s movements – the participant cannot notice their improvement in real
time, as when attention was directed towards particular parts of the body, symptoms usually
4 M. Richardson et al.

Pre-disposing factors, i.e.

some persuasive reason to
doubt the integrity of one’s
neurological system, e.g. family
history

Belief that one’s neurological

system is vulnerable to damage,
dysfunction or disease

Trigger – situation or bodily

sensation consistent with above
belief, strengthening that belief
past a certain threshold

Changes in neurological
functioning, creating physical
symptoms

Further strengthening of belief

regarding neurological damage,
dysfunction or disease.

Figure 1. A simple hypothesized model for the creation and maintenance of functional neurological
symptoms.

worsened. A treadmill was often used with those with weakness/movement difficulties, due
to the frequent observation that this led to a more reliable production of improved limb
movement.
r Improved functioning was framed as further evidence that the participant’s symptoms were
caused by a nocebo response (e.g. ‘you have improved, yet we only changed your beliefs
about the symptoms/what you attended to – we didn’t touch your legs’).
r This treatment cycle (varying attention, creating improved, more ‘automatic’ movement,
giving feedback of some sort, such as video, and then reflecting on what that means about
the cause of symptoms) was repeated, with more and more complex or effortful tasks. Any
use of walking aids was reduced or eliminated at the earliest possible opportunity, with the
attending physiotherapist ensuring safety precautions were taken.
r For the majority of participants, an occupational therapist was also involved, utilizing any
increase in physical functioning in order to support them to return to any activity that they
had not been able to perform whilst symptomatic.
r In the case of those participants who believed that their symptoms were triggered by aspects
of their environment (typically those with non-epileptic seizures or tremor), graded exposure
principles/treatments were incorporated.
 A novel treatment (NH-CBT) for FNSD 5

r Once symptom elimination was achieved, participants were encouraged to push themselves
to their physical limits to further prove to themselves that they were not neurologically
damaged. This idea originated from the first participant in the case series who, of their own
volition, decided to run up some stairs once they felt able to walk up them.

The functional independence measure (FIM) is completed on admission and discharge as

part of normal practice at the rehabilitation centre. This is essentially a validated measure of
disability/burden of care in rehabilitation patients (see Mackintosh, 2009), consisting of 18
items (13 motor, five cognitive), each scoring between 1 (total assistance) and 7 (complete
independence), with any item score of 5 or less indicating some level of dependence on others.
The total FIM score therefore ranges from 18 to 126. In this retrospective study, it was completed
for 11 of the 13 episodes of care, i.e. all except the out-patient, plus one other.
To assess relapse rate, participants were followed up (predominantly by telephone) between
12 and 26 months post-discharge.

Results
Of the 13 treatment episodes, 12 resulted in complete or almost complete remission of
functional symptoms (i.e. fully independent). To qualify that statement further, ten episodes
of care concluded with complete symptom remission, one participant was discharged with a
slight limp that was probably linked to chronic pain following previous discectomy, and one
self-discharged with a slight limp, but was walking normally after a week at home. The other
participant dropped out of treatment, with no clear improvement.
The mean improvement in FIM scores was 28.1, achieved in an average of 14.3 days.
Typically, an improvement of this magnitude reflects someone who was initially dependent
to some extent on other people or aids (such as a walking frame or wheelchair) for mobility
and/or personal care, but was discharged fully mobile and independent.
Using the definition of reliable and significant change as postulated by Jacobson and Truax
(1991), seven of the twelve episodes of care measured by the FIM resulted in reliable and
significant change, with all of the other five episodes being unable to reach significance as the
admission scores were all within 20 points of a maximum FIM score (a 20 point gain being
necessary for a reliable and significant change).
With regard to symptomatic relapse, the mean follow-up time was 17 months post-discharge.
Three participants (25%) had experienced no symptoms whatsoever in that time, five (42%)
had experienced either fleeting symptoms (e.g. for 2 days, with subsequent full remission) or
clinically insignificant symptoms (e.g. a very slight twitch), three (25%) had experienced
symptomatic relapse, but still had significantly improved functioning compared with first
presentation, and one (8%) showed no improvement – this was the participant who dropped
out of treatment.

Discussion
It appears that the treatment protocol is highly effective, in that it reliably and quickly
eliminated symptoms in the vast majority of participants. This treatment protocol involves
a cognitive behavioural intervention, with a focus on a particular maladaptive belief (akin to
‘I am neurologically damaged’) with behavioural activation or graded exposure provided via
6 M. Richardson et al.

interdisciplinary team input. The results were surprising given the current dearth of compelling
evidence for treatment that leads to consistent full symptom remission in people with FNSD.
The improvements were well maintained for the majority of participants over a considerable
period of time.
Aspects of the protocol have clear similarity to the ‘Hypothesis A/Hypothesis B’ concept
often used in treating health anxiety (Salkovskis and Bass, 1997), where Hypothesis A is that
the person has a health condition, and Hypothesis B is that the person simply believes that they
have a health condition.
However, in the case of FNSD, one has to explain how such a belief can actually lead
to symptoms, otherwise ‘Hypothesis B’ will not be accepted by people with the condition.
The success of this intervention is not proof that a nocebo-like mechanism is responsible for
functional neurological symptoms, although this seems plausible. The explanatory theories
put forward by Brown and Reuber (2016) or Edwards et al. (2012) may have greater empirical
grounding, but are not ‘user friendly’. Our experiences with delivering this treatment protocol
revealed that the concept of a placebo effect is well known to most of the general public, and
the related idea of a nocebo response therefore becomes a readily believable ‘Hypothesis B’
when transparently shared.
Another key observation is the almost total absence of conversation about emotional factors
during the treatment protocol, which did not appear to affect its success, and most likely led
to substantially decreased episode of care duration. This raises questions about whether or
not traditionally labelled ‘psychological’ or ‘mental health’ difficulties are key aspects of the
aetiology of the disorder, with many researchers noting the sizeable percentage of people with
functional symptoms who have no discernible or diagnosable mental health issues.
A crude comparison could be made with the findings of Jordbru et al. (2014), who also
used an in-patient multi-disciplinary rehabilitation approach, also used the FIM as an outcome
measure, but appeared to use a straightforward behavioural intervention for the psychological
component of their treatment (attending to good function, ignoring poor function). Their study
only treated people with psychogenic gait disorder, and there were other exclusions applicable
(including those with diagnosed organic neurological conditions). The mean FIM gain in their
cohort was 8.4 in 3 weeks, compared with the 28.1 point gain in 2 weeks achieved by the
current study, although it should be noted that the vast majority of participants in both studies
achieved full functional independence by the end of the treatment.
There are numerous methodological limitations to this study, including the retrospective
design, lack of control group, small sample size, lack of independent or blind assessment, as
well as the inherent difficulties in diagnosing functional neurological symptoms. However, the
clinical outcomes were substantial enough for a controlled study of the treatment protocol to
appear warranted.

Acknowledgements
The authors would like to acknowledge the support of the staff team at the ISIS Rehabilitation
Centre, Dunedin, New Zealand, and also Professor Graeme Hammond-Tooke for his help with
this submission.
Ethical statement: The authors assert that all procedures contributing to this work comply
with the ethical standards of the relevant national and institutional committees on human
 A novel treatment (NH-CBT) for FNSD 7

experimentation and with the Helsinki Declaration of 1975, and its most recent revision. The
study was approved by the Human Ethics Committee, University of Otago, New Zealand
(reference no: H13/070).

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