66
Royal College of Psychiatrists Faculty of Neuropsychiatry Annual Conference 14 – 15 September 2017 Royal College of Psychiatrists London CONFERENCE BOOKLET
Royal College of Psychiatrists
Faculty of Neuropsychiatry
Annual Conference
14 – 15 September 2017 Royal College of Psychiatrists
London
CONFERENCE
BOOKLET
Dear colleague,
It gives us great pleasure to welcome you to the Faculty of Neuropsychiatry's annual conference.
Underlining our commitment to enhancing collaborative working with other institutions in various
countries, this year's event will continue to support global and transcultural perspectives.
With a host of distinguished international speakers, adopting various session formats, the
conference will cover important clinical and research topics. There will be no doubt lively debate
around how far services should investigate patients with mild cognitive impairment and exploration
of what the humanities can teach today’s clinicians about our contemporary understanding of the
mind.
We will also hear about Neuropsychiatry across the life span from affected families which will offer
another dimension and enrich our understanding and appreciation of key issues.
As always, our interactive seminars cover various clinical, legal and research topics addressing a
wide range of educational needs in a format that has never let us down!
We wish you a productive and enjoyable time.
Professor Eileen Joyce Dr George El-Nimr
Faculty Chair Academic Secretary
Contents Page(s)
General information 1
Programme Overview 2
Delegate List 7
Presentation abstracts and biographies 11
Thursday 14 September 11
Friday 15 September 19
Poster exhibition (alphabetically by surname) 28
Agenda for business meeting - Friday 15 September 2017, 13.20-
14.00 46
Business minutes from 16 September 2016 47
Notes 49
GENERAL INFORMATION
Certificates
Certificates of attendance will be sent to delegates after the conference.
Accreditation
This conference is eligible for up to 6 CPD hours on Thursday 14 September and up to 6 CPD hours
on Friday 15 September, subject to peer group approval.
Sessions
All sessions take place on the first floor.
Registration desk
The registration desk will be located in reception area, ground floor
Exhibition
An exhibition is available throughout the conference in member’s area, ground floor. The Royal
College of Psychiatrists would like to thank the following companies for their valuable support of
this conference:
St Andrew’s Healthcare
The presence of an exhibitor is not an endorsement of its products and exhibitors do not influence
the content of the meeting.
Feedback
A detailed online feedback form can be found at https://www.surveymonkey.co.uk/r/Neuropsych17
All comments received remain confidential and are viewed in an effort to improve future meetings.
If you wish to tweet about the conference use @RCPsych #NeuroConf
Lunch and refreshment breaks
Lunch and tea & coffee breaks will be served in the member’s area, ground floor.
Posters
Poster viewing is available throughout the conference on the mezzanine area, first floor.
Queries
Please come to the Conference Registration Desk on the ground floor if you require any assistance.
Cloakroom
The cloakroom can be found on the 1st floor.
Additional Meetings
Executive Committee Meeting (closed): Thursday 14 September 2017 in G7 (members area,
ground floor) from 13:30-14:30.
Wifi
Network: RCP Guest
Password: RCP2013!
1
Conference Programme
All sessions will take place in room 1.7 (main room), first floor
Seminars will take place in 1.1, 1.2-1.4, 1.6 and 1.7 – please see programme below for room
allocation Lunch and refreshments will take place in the members area, ground floor
Thursday 14 September
09:05-09:35 Registrstation and refreshments
09:35-09:45 Welcome and Introduction Professor Eileen Joyce, Faculty Chair
09:45–10:00 Neuropsychiatry within the College: A word from our new president
Professor Wendy Burn
Plenary 1: Image, imagery and imagination
Chair: Dr George El-Nimr
10:00-10:30 Phantasia: the neurology of visual imagery
Professor Adam Zeman
10:30-11:00 The mirror mechanism and its social and clinical implications
Professor Giacomo Rizzolatti
11:00-11:30 Neuropsychiatry of younger onset neurodegenerative disorders
Professor Dennis Velakoulis
11:30-12:00 Morning refreshments & Exhibition
11:30- 12:00
Plenary 2: Mild TBI and Post-concussion syndrome
Chair: Dr Niruj Agrawal
12:00-12:30
12:30-13:00
13:00-13:30
Neurological perspective and bio-markers Professor David Sharp
Neuropsychological perspective, chronicity and treatment
Dr Nigel King
Neuropsychiatric perspective and medico-legal dilemmas
Dr Robin Jacobson
Lunch, Exhibition and poster viewing
2
14:30-15:10
Room 1.7
Room: 1.2-1.4
Room: 1.6
Room: 1.1
Seminars
Seminar 1: Autoantibodies in Psychosis
Dr Mike Zandi
(Chair: Dr Tim Nicholson)
Seminar 2: Smart technology and Epilepsy management
Dr Craig Newman and Professor Stephen Brown
(Chair: Dr Rohit Shankar)
Seminar 3: Updates on the Neurobiology of Obsessive Compulsive
Disorder
Dr Himanshu Tyagi and Harith Akram
(Chair: Prof Eileen Joyce)
Seminar 4: The role of expert witness in Acquire Brain Injury claim
Ms Tracey Storey, Irwin Mitchell LLP
(Chair: Dr Mike Dilley)
15:10-15:40 Exhibition and refreshments and Poster viewing
Plenary 3: Epilepsy and the Mind: What the
humanities can teach us
Chair: Dr Jonathan Bird
15:40-16:10
16:10-16:40
16:40-17:10
17:10
19:00
‘A Matter of Life and Death': Phantom trains to quantum biology
Dr Ken Barrett
Music, Epilepsy and the Brain
Professor Steve Brown
Epilepsy in contemporary fiction: relevance to clinicians
Dr Maria Vaccarella
Close of day 1
Conference dinner, Brasserie Blanc Tower Hill
3
Friday 15 September
08.45-09.00 Registration and refreshments
09:00- 09:10 Welcome and Introduction
09:10 – 09:30
09:30 -09:50
09:50-10:00
10:00-10:25
10:25-10:50
10:50-11:05
Plenary 4: Caring for Neuropsychiatry patients across the life span;
the family perspective
Chair: Dr Czarina Kirk
Remembrance of Things Present – Making Peace with Dementia
Mr Peter Maeck
Neuropsychiatry – children on board: the Huntington’s
model
Dr Matthew Ellison
Q&A
Plenary 5: Cerebrovascular Disease & Brain Aging: Transcultural Lessons
Chair: Professor Eileen Joyce
The role of vascular factors in neuropsychiatric conditions. A global perspective
Professor Ingmar Skoog
Managing behavioural & psychological dysfunction: a novel integrative model
of care that blends psychological approaches with complimentary and
alternative medicine in India
Dr Ennapadam S Krishnamoorthy
International collaboration
11:05-11:35 Morning refreshments & Exhibition and Poster viewing
4
11:40-12:20
Plenary 6: Trainee award presentations
Chair: Mayur Bodani
Trainee award presentations
Is functional weakness associated with neural correlates in imaging studies?
A systematic review of the evidence.
Lori Black
The psychiatric phenotype of anti-NMDA receptor encephalitis
Dr Lucy Gibson
Quantitative EEG Findings are a Potential Prognostic Biomarker in Anti-
NMDA Encephalitis
Graham Blackman
Chemokines in Depression in Health and in Inflammatory Illness: a
systematic review and meta-analysis
Dr Louis Nerurkar
The psychiatric phenotype of anti-NMDA receptor encephalitis
Chemokines in Depression in Health and in Inflammatory Illness: a systematic review
and meta-analysis
Graham Blackman
Lucy Gibson
Louis Nerurkar
12:20-13:20 Lunch & Exhibition - Members area, ground floor Poster
viewing - Mezzanine, first floor
13:20-14:00
14:00- 14:40
Room: 1.2-1.4
Room: 1.7
Room: 1.1
Room: 1.6
Faculty of Neuropsychiatry Business Meeting
Seminars
Seminar 5: ECT in Neuropsychiatry
Dr Rupert McShane and Dr David Cousins (chair: Dr David Cousins)
Seminar 6: New and Future Drugs in Sleep Medicine
Guy Leschziner and Sue Wilson (chair: Dr Hugh Selsick)
Seminar 7: Neuropsychiatry on the shop floor: discussing difficult clinical
cases
Professor Hugh Rickards
Seminar 8: Neurological assessment and investigations: what do
psychiatrists need to know?
Dr Jan Coebergh
14:40-15:10
Exhibition and refreshments, Members area,
ground floor Poster viewing -
Mezzanine, first floor
5
15:10 – 16:30
16:30
Plenary 7: Debate
“This house believes that the investigation of patients with Mild Cognitive
Impairment is clinically unhelpful and economically unjustified’'
Chair: Dr Peter Byrne
For the motion: Dr Jeremy Isaacs
Against the motion: Dr Jonathan Schott
Announcing best presentation / poster winners and closing remarks
Professor Eileen Joyce, Faculty Chair
16:45 Close
6
DELEGATE LIST as at 11/09/2017
No Title Forenames Surname
1. Dr Talib Abbas
2. Dr Hosam Abed
3. Patrick Abela
4. Dr Jahnavi Acharya
5. Dr Kanu Achinivu
6. Dr Nyakomi Adwok
7. Dr Roohi Afshan
8. Dr Meenal Aggarwal
9. Dr Neeraj Aggarwal
10. Dr Niruj Agrawal
11. Dr Harith Akram
12. Dr Syed Ali
13. Dr Joyce Almeida
14. Dr Jacqueline Anderson
15. Dr Tom Anderson
16. Dr Mohammad Arbabi
17. Dr Abdolreza Ashtari Kiani
18. Dr Abdulkarim Awadh
19. Dr Nishanth Babu Mathew
20. Dr Vandana Balakrishna Menon
21. Dr Kenneth Barrett
22. Dr Alex Berry
23. Dr Nikhil Bhandari
24. Mrs Mitika Bhasin
25. Dr Rahul Bhattacharya
26. Miss Anum Bhatti
27. Dr Jonathan Bird
28. Dr Lori Black
29. Graham Blackman
30. Dr Mayurkumar Bodani
31. Dr Enrique Bonell Pascual
32. Dr Julius Bourke
33. Alan Breier
34. Dr Caroline Broadhurst
35. Prof. Stephen Brown
36. Dr Stefania Bruno
37. Dr Timothy Bullock
38. Prof. Wendy Burn
39. Dr Peter Byrne
40. Dr Julian Carr
41. Dr Matthew Castle
42. Dr Inderdeep Chana
43. Miss Lucia Chaplin
44. Dr Jan Coebergh
45. Prof. John Copeland
46. Dr Irene Cormac
47. Dr Bryan Corridan
48. Dr David Cousins
49. Miss Nadja Cox
50. Dr Tamsin Critchlow
51. Dr Adeline Cutinha
52. Dr Antonio D'Costa
53. Dr Samr Dawood
54. Dr Alexandra Day
55. Dr Gardiewasan De Silva
56. Dr Zenobia Deans
57. Dr Ian Dewar
7
58. Dr Michael Dilley
59. Dr Eoin Donohue
60. Dr George El-Nimr
61. Dr Thomas Elanjithara
62. Dr Matthew Ellison
63. Dr Francesca Falzon Aquilina
64. Dr Anjum Faridi
65. Osvaldo Fernandez
66. Dr Jacqueline Foong
67. Dr Kevin Foy
68. Dr Robert Fung
69. Dr Nimanpreet Gajebasia
70. Dr Nikhil Galgali
71. Dr Geetha Gandluru
72. Dr Premkumar Ganesan
73. Mr James George
74. Dr Ratna Ghosh
75. Dr Soumya Ghosh
76. Dr Lucy Gibson
77. Dr Jose Gonzalez
78. Dr Surya Goudaman
79. Dr Suren Govender
80. Dr Janet Grace
81. Dr Panthratan Grewal
82. Dr Soraia Guerra Sousa
83. Dr Sandra Hacker
84. Dr Alison Haddow
85. Dr Ali Hadi Al-Barazanchi
86. Dr Sheeba Hakeem
87. Dr Raissa Hamelmann
88. Dr Levente Herman
89. Dr Johanna Herrod
90. Dr Jason Holdcroft
91. Dr Timothy Howard
92. Dr Amanda Hukin
93. Dr Shahid Hussain
94. Dr Ioana Iordache
95. Dr Jeremy Isaacs
96. Dr Zehanah Izmeth
97. Dr Robin Jacobson
98. Dr Christopher Jagus
99. Miss Lottie James
100. Dr Jaiker Jani
101. Dr Gursharan Johal
102. Prof. Eileen Joyce
103. Dr Johan Jurgens
104. Miss Priya Kadam
105. Dr Peter Kanisius
106. Dr Samina Karamat
107. Dr Yana Kay
108. Dr Eric Kelleher
109. Dr Aubrey Kerr
110. Dr Rehan Khan
111. Dr Laxman Khatri
112. Dr Nigel King
113. Dr Czarina Kirk
114. Dr Ivan Koychev
115. Dr Ennapadam Krishnamoorthy
116. Dr Chetan Kuloor
117. Dr Mukesh Kumar
8
118. Dr Daniel Kwek
119. Dr Robert Lawrence
120. Dr Geoffrey Lawrence-Smith
Ellert
121. Dr Maria Lax-Pericall
122. Dr Patrick Leahy
123. Dr Eyal Lebovich
124. Dr Sean Lennon
125. Dr Guy Leschziner
126. Dr Jovita Lewis
127. Dr Omolade Longe
128. Dr Madeleine Love
129. Dr Collette Lowe
130. Mr Peter Maeck
131. Dr Kadhem Majeed
132. Dr Haider Malik
133. Dr Osman Malik
134. Dr Negibe Mankir
135. Dr Hester Mannion
136. Dr William Mansvelt
137. Dr John Mason
138. Dr Shevonne Matheiken
139. Dr Benjamin Mcloughlin
140. Dr Rupert McShane
141. Dr Seth Mensah
142. Dr Sarah Mercieca
143. Dr Katerina Miloseska
144. Mr Adrian Mohit
145. Dr Venkatesh Muthukrishnan
146. Dr Abdul Muzaffar Shah
147. Dr Paul Myatt
148. Miss Yafit Nahari
149. Dr Krishnendu Nandy
150. Stefan Nasir
151. Mr Louis Nerurkar
152. Dr Craig Newman
153. Dr Timothy Nicholson
154. Dr Chidinma Nwosu
155. Dr Geetha Oommen
156. Dr Roshini Oommen
157. Dr Henry Oraekwute
158. Dr Meritxell Oto Llorens
159. Dr Ashish Pathak
160. Dr Jerson Pereira
161. Dr Panayiota Petrochilos
162. Dr Lorien Porter
163. Dr Baljinder Powar
164. Dr Gary Price
165. Dr Lakshmanan Ramachandran
166. Dr Gianetta Rands
167. Prof. Hugh Rickards
168. Prof. Giacomo Rizzolatti
169. Dr Pauline Robertson
170. Dr Silvia Rodriguez-Ferrera
Massons
171. Dr Sheelagh Rogan
172. Dr Jonathan Rogers
173. Prof. Maria Ron
174. Dr Anneka Rose
175. Dr Yvain Rumalean
176. Dr Jose Saez Fonseca
177. Dr Mohammad Saidi
9
178. Dr Bruce Scheepers
179. Dr Jonathan Schott
180. Dr Hugh Selsick
181. Dr Jordi Serra Mestres
182. Dr Ruth Seton
183. Dr Rohit Shankar
184. Dr Puja Sharma
185. Prof. David Sharp
186. Dr Stephen Sherwin
187. Dr Gregory Shields
188. Dr Shaheen Shora
189. Dr Inderbir Sidhu
190. Dr Meetu Singh Sonsati
191. Prof. Ingmar Skoog
192. Dr Gabrielle Smith
193. Dr Henk Smith
194. Dr Richard Soppitt
195. Dr Robert Spalding
196. Dr Penny Spencer
197. Dr Thomas Stevens
198. Ms Tracey Storey
199. Dr Ian Stout
200. Dr Senthil Subramanian
201. Dr Anar Suriya
202. Dr Richard Symonds
203. Dr Hina Tahseen
204. Dr Thomas Tennent
205. Dr Thanakumar Thanulingam
206. Dr Khinezar Tint
207. Dr Michal Tomek
208. Dr Brian Toone
209. Dr Ognyan Trendafilov
210. Dr Peter Trimble
211. Prof. Michael Trimble
212. Dr Himanshu Tyagi
213. Miss Stephanie Upton
214. Dr Maria Vaccarella
215. Prof. Dennis Velakoulis
216. Dr Srilakshmi Velandy
217. Dr Stephanie Velential
218. Dr Rosemarie Vella Baldacchino
219. Dr Vivek Vijay
220. Dr Farazdak Wahab
221. Mr Robert Walsh
222. Miss Alexandra Welford
223. Prof. Malcolm Weller
224. Dr Steven White
225. Dr Jacqueline Wiggins
226. Dr Gintotage Wijesiri
227. Mr Charles Williams
228. Mr Tim Williams
229. Dr Sue Wilson
230. Dr Graeme Wood
231. Dr Gerald Woolfson
232. Prof. Graeme Yorston
233. Dr Syeda Zaidi
234. Dr Mike Zandi
235. Dr Adam Zeman
10
PRESENTATION ABSTRACTS AND BIOGRAPHIES (LISTED BY PROGRAMME ORDER)
Abstracts and biographies not included here were not available at the time of going to print.
14 September
Neuropsychiatry within the College: A word from our new president
Professor Wendy Burn
Professor Wendy Burn became a Consultant Old Age Psychiatrist in Leeds in West Yorkshire in
1990. She currently works in a community post.
She has been involved in the organisation and delivery of postgraduate training since she started as
a consultant. She has held many roles in education including College Tutor, Training Programme
Director, Director of Postgraduate Medical Education, Chair of Specialty Training Committee and
Associate Medical Director for Doctors in Training. She set up the Yorkshire School of Psychiatry and
was the first Head of School.
On behalf of the Royal College of Psychiatrists she has been an examiner, a Senior Organiser of clinical
examinations, a Deputy Convenor, Regional Co-ordinator for CPD and the Deputy Lead for National
Recruitment. She was College Dean from 2011 to 2016. She became the Co-chair of the Gatsby
Wellcome Neuroscience Project in 2016. In 2017 she was elected as President of the College and took
office in June.
Phantasia: the neurology of visual imagery
Professor Adam Zeman
Professor Adam Zeman is Professor of Cognitive and Behavioural Neurology, University of Exeter
Medical School, Exeter.
The mirror mechanism and its social and clinical implications
Professor Giacomo Rizzolatti
Mirror mechanism is a basic neural mechanism that transforms sensory representations of others’
actions into motor representations of the same actions in the brain of the observer. In the first
part of my talk I will describe the functions of the mirror mechanism located in the parieto-fontal
network of monkeys and humans. I will show that this mechanism enables one to understand
others in an immediate, phenomenological way, without recourse to cognitive inferential
processing. In the second part of my talk I will discuss the role of the mirror mechanism in
understanding basic Darwinian emotions. I will focus on disgust, fear and joy and will demonstrate
the role of the mirror mechanism in empathic experience of these emotions, contrasting it to mere
recognition. The data on emotions will lead me to the last part of my talk where I will present
stereo-EEG data on action recognition. Stereo-EEG allows one to go beyond the static three-
11
dimensional maps obtained with fMRI a providing a four dimensional picture (space plus time) of
brain activations during different types of actions
Giacomo Rizzolatti was born in Kiev in 1937. He studied in Padua where he graduated in Medicine
(1961) and Neurology (1964). He received his training in Physiology at the University of Pisa (1965-
68) and in Psychology at the McMaster University, Hamilton, Ontario, Canada (1970-71). Most of his
scientific career has been done at the University of Parma where he is, at present, responsible of the
“Brain Center for Motor and Social Cognition”, Italian Institute of Technology (IIT) and Professor
Emeritus of Human Physiology.
He has been “Visiting professor” at the Department of Anatomy of the University of Pennsylvania,
Philadelphia (1980), and “Sage Professor” at University of California, Santa Barbara (2007). An early
part of his research on the mirror mechanism in humans has been carried out in collaboration with
the Department of Computer Science of the University of Southern California and with the Ahmanson
Lovelace Brain Mapping Centre of UCLA, Los Angeles.
The main focus of his research concerns the motor system and its role in cognitive functions. He is
the discoverer of the mirror neurons.
He has been President of the European Brain Behaviour Society, of the Italian Society for
Neuroscience, and former director the European Training Program in Brain and Behaviour Research
(ETP) sponsored by the European Science Foundation.
He is Member of Academia Europaea, of Accademia dei Lincei, of the Institute de France (Académie
des Sciences), and Honorary Foreign Member of the American Academy of Arts and Sciences.
He received many awards are among which "Golgi Prize for Physiology", "George Miller Award" of the
Cognitive Neuroscience Society, the "Feltrinelli Prize for Medicine" of Accademia dei Lincei, the
Herlitzka Prize for Physiology, Accademia delle Scienze di Torino, Prix IPSEN, Neuroplasticity,
Fondation IPSEN Paris 2007, the Grawemeyer Award for Psychology, Luiseville and Prix Signoret,
Neuropsychology, Fondation IPSEN Paris 2010. He recently (2011) received the prestigious “Prince of
Asturias Award” for Science and Technology (Spain).
He is recipient of Honorary Degrees from the University Claude Bernard of Lyon, from the University
of St. Petersburg, St. Petersburg and from KU Leuven.
Giacomo Rizzolatti has 369 cited publications (Google: total citations for Rizzolatti G. 100.535). The
original articles describing the mirror mechanism and a review on this topic, received more than 2000
citations, 8 other recent publications on this topic largely exceed 1000 citation. His H-index is 92.
12
Neuropsychological perspective, chronicity and treatment
Dr Nigel King
Very large numbers of people sustain a mild head injury (MHI) and the vast majority make a complete
recovery from any post-concussion symptoms (PCS) experienced within 3 months at the most. A small
minority however go on to experience persisting and possibly permanent PCS. This presentation
review the neuropsychology of MHI and PCS, in both the early stages after injury and when problems
are chronic. It addresses the factors which contribute to persisting symptoms and the evidence base
for psychological interventions for PCS in the early stages post injury and for when the symptoms
persist.
Dr Nigel King is a Consultant Clinical Neuropsychologist specialising in head injury at the Community
Head Injury Service (CHIS), Aylesbury and Clinical Tutor at The Oxford Institute of Clinical Psychology
Training. He has published widely on mild traumatic brain injury and the post-concussion syndrome
and regularly speaks at national and international conferences on the subjects. His recent self-help
book ‘Overcoming Mild Traumatic Brain Injury and Post-concussion Symptoms’ has been very well
received by patients and clinicians alike, and was shortlisted for the BMA Book of the Year Award 2016
in their Popular Medicine category. He is a Fellow of Harris Manchester College, University of Oxford
and the Head of Clinical Neuropsychology Module and the Expert Witness and Court Work teaching on
the Oxford Doctoral Course in Clinical Psychology. In addition to Dr King’s National Health Service
work he regularly conducts medico-legal assessments on mild head injured clients for solicitors acting
for claimants or defendants, or as a single-joint expert.
Neuropsychiatric perspective and medico-legal dilemmas
Dr Robin Jacobson
Since the definition of mild Traumatic Brain Injury (mTBI) changed in 1993 (ACRM), the spectrum of
mTBI is now wide. The Post Concussional Syndrome is no less controversial than it was 100 years
ago, with its exclusion from DSM-5 and probably from ICD-11. The non-specificity of the Post
Concussional Syndrome is reviewed, along with the predominant model suggesting early
physiogenesis and perpetuation of symptoms on a predominantly psychological basis. The importance
of DTI in predicting outcome of MTBI will be discussed. Finally, medico-legal aspects of MTBI will be
reviewed, including the assessment of the duration of post-traumatic amnesia and the use of effort
tests in neuropsychological examination.
Dr Robin Jacobson is a Consultant Neuropsychiatrist in private practice at Keats House, London. He
was formerly a Senior Lecturer in Neuropsychiatry at St George’s, University of London. From 1993
to 2016 he chaired the Paper A Sub-Committee of the MRCPsych Examination and was a member of
the Examinations Sub-Committee of the Royal College of Psychiatrists. He has extensive medico-legal
experience.
13
Seminar 1: Autoantibodies in Psychosis
Dr Michael Zandi and Dr Tim Nicholson
Dr Michael Zandi will discuss the role of auto-antibodies to brain proteins in neuropsychiatric disease,
with a focus on NMDAR autoantibodies and their possible causal role in some cases of acute psychosis.
Subjects with the NMDAR antibody encephalitis syndrome have symptoms which do not respect the
neurology-psychiatry divide. The relevance of NMDAR-targetted and related auto-antibodies in the
serum of those with relatively pure psychotic disease remains unclear. We have developed a placebo-
controlled randomised trial to help assess whether these antibodies are causal or simply
epiphenomena. This work represents a key advance and first step in the evaluation of re-purposing
immune therapies beyond conventional autoimmune neurological disease.
Dr Michael Zandi is an honorary consultant neurologist at the National Hospital for Neurology and
Neurosurgery, and honorary senior lecturer and principal investigator at the UCL Department of
Molecular Neuroscience. I see patients in an encephalitis and neuroimmunology clinic at the National
Hospital. I trained in medicine at Cambridge, with neurology training in Cambridge, Norwich and
London. My PhD in neuropsychiatric SLE and NMDAR antibody encephalitis was in Cambridge with
time in the laboratory of Angela Vincent in Oxford. I also work in the UCLH neuroimmunology and CSF
laboratory, developing biomarkers of inflammation in brain disease.
Seminar 2: Smart technology and Epilepsy management
Towards improved safety for people with epilepsy: Can technology such as smart apps be
a cost effective method to monitor risk, improve patient empowerment and safety?
Dr Craig Newman and Professor Stephen Brown
About 600,000 people in the UK have epilepsy, and approximately 1200 die as a result of it each year.
Half of these deaths are due to Sudden Unexpected Death in Epilepsy (SUDEP) and at least 42% are
potentially avoidable. In clinical settings the approach to communicating and managing risk is diverse,
yet evidence is growing that due attention to risk management can reduce mortality.
In the UK over 45 million people (76% of population) own a smartphone. They are a way of life to
many in developed and developing countries. Evidenced based mobile applications such as EpSMon
(www.epsmon.com) are being designed to help people with epilepsy (PWE) take charge of their
condition. EpSMon has been received positively by both health and patient communities and is part
of the national commissioning tool kit for epilepsy in UK, winner of the SUDEP Challenge USA award
2016, BMJ Neurology award 2016, National Patient Safety Award 2016 and Business Health awards
2016. EpSMon is one of the 8 projects selected in for the 2017 National Innovations Accelerator
programme. It is developed from the validated and evidenced based communication tool ‘SUDEP and
Seizure Safety Checklist’ (www.sudep.org/checklist) which is being used by over 330 clinicians
nationwide. The Checklist enables clinicians to discuss and monitor epilepsy risks, & known risk factors
14
for SUDEP with their patients, to support risk reduction over time. Both tools can be used in
conjunction to provide a holistic approach to epilepsy risk communication and management.
The session will explore the potential benefits of smart technology as a method of risk management
and present the potential advantages and barriers to use of risk discussion and management tools. It
will explore the interface between clinicians and PWE with regard to safety and responsibility through
use of the Checklist, and EpSMon as a useful record for patients to open discussion with their clinician.
The cost benefits of using such technology and its potential preventive nature will also be discussed.
The session will demonstrate how the project collaboration (involving 2 Cornwall NHS Trusts, Plymouth
University and SUDEP Action, the UKs only Epilepsy Charity dedicated to tackling epilepsy mortality)
has produced a model which can be implemented across a range of clinical and community settings
to standardise epilepsy risk management.
Professor Stephen Brown trained in Psychiatry at the Maudsley and in Neurology at King’s. He was
medical director of the David Lewis Centre for Epilepsy from 1984-1996 and Professor of
Developmental Neuropsychiatry at the Peninsula Medical School until retiring in 2010. He was one of
the first UK clinicians to speak about and publish on sudden unexpected death in epilepsy (SUDEP).
His other research interests have included non-pharmacological and non-surgical treatments for
epilepsy and cognitive aspects of epilepsy. He was chair of the UK Epilepsy Task Force, and is a former
chair of Epilepsy Action and founding trustee of the Epilepsy Research Fund (now Epilepsy Research
UK). He was appointed Ambassador for Epilepsy by the International League against Epilepsy in 1999
and received the Epilepsy Action Award in 2004 "in recognition of his significant contribution to
improving the lives of people with epilepsy".
After retiring from clinical work he became chair of trustees of SUDEP Action. He is also a musician.
Seminar 3: Updates on the Neurobiology of Obsessive Compulsive Disorder
Dr Himanshu Tyagi and Harith Akram
Over the past 100 years, the construct of the obsessive-compulsive disorder (OCD) as an illness has
curiously tracked every significant milestone in the field of psychiatry. OCD was at the cornerstone of
psychoanalytic theories of mind in early 1900s, its presumed ‘untreatability’ contributed to the
psychosurgical omnipotence seen in the 1930s, it changed from a ‘rarest of rare’ disorders to the third
most common in psychiatry once we figured out the methods to treat it with cognitive-behavioural
transformation of 1970s and the second psychopharmacological revolution of 1980s. Now in early 21st
century, it is widely considered as a prototypical neuropsychiatric disorder. Last two decades have led
to a reasonable consensus over the cortico-thalamic-striatal-cortical circuitry as being the core
neurological model for OCD. However there still are many more questions than answers. This session
would look at the questions and controversies raised by recent research about the neurobiology of
OCD and frame these findings it in relevant historical contexts. It would be followed by a session
reporting new findings from probabilistic tractography in a small cohort of severe treatment refractory
OCD.
15
Dr Himanshu Tyagi MRCPsych, is medical psychotherapist and clinical academic psychiatrist in the
field of obsessive-compulsive and related disorders. He coordinated UCL led and MRC funded research
trial investigating Deep Brain Stimulation (DBS) in severe and treatment refractory OCD between
2012-2016. At present he is a Consultant Psychiatrist at National Hospital for Neurology and
Neurosurgery and runs a specialist Tourette syndrome clinic. He received Higher Psychiatric Trainee
of the Year award from the Royal College of Psychiatrists, UK in 2012 and British Neuropsychiatric
Association’s Alwyn Lishman prize in 2017. He is also a co-founder and vice chair of the Royal College
of Psychiatrists network for Obsessive-Compulsive and Related Disorders (OCARD) and routinely
tweets about the latest OCD research and clinical practice tips at @himanshutyagi
Seminar 4: The role of expert witness in Acquire Brain Injury claim
Ms Tracey Storey, Irwin Mitchell LLP
The presentation will focus on the role of the expert witness in personal injury cases. It will look at
what makes a great expert, how they fit into the litigation process, why they are needed and the rules
and framework for working as an expert. It will also look at the practicalities of being an expert
witness, the contents of the expert report, what lawyers want to know in a personal injury claim,
issues of liability, causation, quantum, limitation and capacity and the importance of rehabilitation in
personal injury claims
Tracey Storey is a solicitor and partner in national law firm, Irwin Mitchell. She heads up 5 teams
of Serious Injury lawyers in IM’s London office and she also has considerable experience of psychiatric
cases involving child abuse, Her practice now focuses on brain injury cases, amputation claims and
spinal cord cases. She is a Fellow with the Association of Personal Injury Lawyers and is also
accredited by APIL as a brain injury specialist. She regularly presents on serious injury cases, abuse
cases and rehabilitation.
Plenary 3: Epilepsy and the Mind: What the humanities can teach us
Chair: Dr Jonathan Bird is a Consultant Neuropsychiatrist and Past Chair of RCPsych Section of
Neuropsychiatry.
‘A Matter of Life and Death’: Phantom trains to quantum biology
Dr Ken Barrett
The 1946 movie 'A Matter of Life and Death' is a wartime love story in which the principal character,
Squadron Leader Peter Carter, experiences temporal lobe seizures and peri-ictal psychosis, clinical
features that have evaded reviewers as the words ‘epilepsy, ‘seizure’ and ‘psychosis’ remain
unspoken. This talk will explore the film's unusual origin, and consider three of its key themes, the
perception of time, peri-ictal psychosis and post-traumatic epilepsy, in light of cutting edge
neuroscience.
16
Dr Ken Barrett studied neuropsychiatry at the Burden Neurological Institute in Bristol, where he also
gained an MD in cognitive psychophysiology. He moved to moved to Keele University as a senior
lecturer, and subsequently created the North Staffordshire neuropsychiatry service. Following
retirement from clinical practice he obtained and MA in contemporary visual art and has since worked
on a variety of projects, the most recent combining the arts and neuroscience. He is currently working
on ‘Wavecraft’, an exhibition for the Institute of Neurology based on two pioneers of the EEG.
Music, Epilepsy and the Brain
Professor Steve Brown
The subject of human language and communication encompasses a spectrum from verbal language,
music, dance, movement & gesture as well as the visual arts. Music forms part of this spectrum and
overlaps with these other functions. As such it contributes to internalised thought and external social
interactions, as do other art and language forms. Music academics such as Derek Cook have written
about the specific language functions of western diatonic music and others have produced speculative
notions of the origins and early functions of musical performance in courtship display and ritual. More
scientific approaches have emphasised the crucial importance of music and music-related skills in
general cognitive development. Music can also induce particular mood states which in turn may modify
behaviour and cognitive function. As with other parts of the communication spectrum, things can go
wrong, and music can also, it seems, be used to help things go right. The usual example is musicogenic
epilepsy. Here music is one of a large number of sensory experiences that may evoke seizures in
those so predisposed. Studies of such specific seizure evocation help inform not only the mechanisms
of epilepsy, but also the neural pathways and interactions that play a part in music.
Music has also been postulated as an anti-epileptic tool, though it is not entirely clear how this relates
to specific pieces of music such as Mozart K448, which also improve intelligence if some researchers
are to be believed. Research has tended to concentrate on diatonic western art music with a
preponderance of Mozart though in this talk we may also hear some modified Prokofiev. More recently
there seems to be a growing interest in also studying other, non-western musical traditions.
The potential positive importance of exposure to music and music education in basic cognitive and
emotional development now has a an impressive evidence base beyond any self-evident statements
we might make about cultural growth and the importance of adding beauty to people’s lives. It’s a
pity politicians don’t see this - but then we’ve had enough of experts.
Since retiring as Professor of Developmental Neuropsychiatry at the Peninsula Medical School in 2010
Stephen Brown has divided his time between being chair of trustees of the charity SUDEP Action,
and being a musician. A beneficiary of free instrumental teaching through the schools’ music service,
he studied the ‘cello with William Roskelly in London and as a teenager had conducting lessons from
Sir Adrian Boult. He has written four string quartets and various song settings for chamber and
orchestral groups which have been performed in various venues including Truro Cathedral and the St
Ives Festival. He is currently researching a book on the history of peripatetic music teaching.
17
Epilepsy in contemporary fiction: relevance to clinicians
Dr Maria Vaccarella
Literary authors have long used epilepsy as a characterization or plot device, but usually in a
stereotypical way. More recent epilepsy narratives, instead, provide compelling insight into the stigma
and difficulties associated with this condition, as they often incorporate first-hand observation and
research. In my presentation, I will survey a selection of these narratives to demonstrate how literary
texts can help us better understand patients’ views on controversial issues, such as poor adherence
to anti-epilepsy drugs. In particular, I will illustrate examples from my research on literary
representations of epilepsy surgery (from pre-operative hesitation to postsurgical alleviation of
symptoms) and its application in a clinical context.
Dr Maria Vaccarella is Lecturer in Medical Humanities at the University of Bristol. She works on
literature and medicine, narrative medicine, critical disability studies, and narrative bioethics. She has
published in The Lancet, Literature and Medicine and Medical Humanities. Together with Mark Davis
and Silvia Camporesi, she has recently edited the special issue “Investigating Public Trust in Expert
Knowledge: Ethics, Narrative, and Engagement” of the Journal of Bioethical Inquiry (2017).
18
15 September
Remembrance of Things Present – Making Peace with Dementia
Mr Peter Maeck
"Remembrance of Things Present: Making Peace with Dementia" combines Peter Maeck's
poetry, prose, and photographs to celebrate his father's brave, good-humored struggle with
Alzheimer's Disease, while recounting Peter's own journey while his father's condition
progressed. Initial feelings of depression yield ultimately to a realization that dementia’s grip is
loosened by the power of poetry, pictures, music, and love which can break down cognitive
boundaries by freezing time initially then melting it, enabling a coming-together in a lyrical
middle realm between what has gone before and what is yet to be.
Peter Maeck is an American writer and photographer. His plays and dance scenarios, including
for Pilobolus and MOMIX Dance Theatres, have been produced in New York City, Europe, and
Africa. Peter served as a U.S. State Department Cultural Specialist in Tanzania and Morocco.
His photographs have been exhibited internationally. Peter has addressed mental health issues
at multiple TEDx and Alzheimer's Association events. "Remembrance Of Things Present: Making
Peace with Dementia," is published by Shanti Arts Publishing. Peter has a B.A. in English from
Dartmouth College and an M.F.A. in Playwriting from Brandeis University. More at
www.petermaeck.com.
Neuropsychiatry – children on board: the Huntington’s model
Dr Matthew Ellison
Dr Matt Ellison is Project Coordinator at the Huntington's Disease Youth Organization.
The role of vascular factors in neuropsychiatric conditions. A global perspective
Professor Ingmar Skoog
Professor Ingmar Skoog is Director at the Centre for Ageing and Health, AGECAP, at University of
Gothenburg, Sweden and Professor in Social Psychiatry and Epidemiology, Leader of the research
group Epinep, Neuropsychiatric Epidemiology.
Managing behavioural and psychological dysfunction: a novel integrative model of
care that blends psychological approaches with complimentary and alternative
medicine in India
Dr Ennapadam S Krishnamoorthy
Prof. Dr. Ennapadam S Krishnamoorthy (ESK) MBBS, MD, DCN (Lond), Ph.D (Lond), FRCP
(Lond, Edin & Glas), MAMS (India), FIMSA, FIPS
Founder and Director - NEUROKRISH and TRIMED
19
President Elect of the International Neuropsychiatric Association (2015)- the first person
working in a developing nation to be so elected.
Adjunct Professor- Public Health Foundation of India and Manipal University, India
An Internationally recognized Neuropsychiatrist with special interests in epilepsy & dementia;
integrative medicine; models of comprehensive care and rehabilitation he has founded and leads a
hub-spoke model of comprehensive care for chronic diseases in Chennai that blends western
objectivity with eastern mindfulness; modern scientific knowledge with ancient clinical wisdom, and
the fine art of patient care.
Career Highlights:
Rich and diverse two-decade long background of clinical and senior management experience
across 3 countries
Over 75 scientific publications, 40 articles in the lay press, two edited books & two coffee
table books
Has lectured to diverse audiences across 4 continents; and has organized and led over 100
workshops/ symposia.
A teacher with past and current academic appointments: Public Health Foundation of India,
TN Dr. MGR Medical University, Indian Institute of Technology, Madras, University of Madras,
University College London.
Youngest Indian Neurologist & first Indian Psychiatrist to be elected Fellow of all three Royal
Colleges of Physicians in the UK (Glasgow, Edinburgh & London)
Recipient of the prestigious President’s Medal of the Royal College of Psychiatrists for
contributions to community neuropsychiatry
An academic leader who has chaired the International League Against Epilepsy- Commission
on Psychobiology; the World Health Organization- World Health Report 2012 (Dementia),
Executive Committee Member of the International Neuropsychiatry Association (since 2004)
and Asian Society Against Dementia (since 2005).
A healthcare industry leader- chaired the Confederation of Indian Industry- Healthcare Panel
(Tamil Nadu, India) for 3 consecutive terms.
Social Impact Leader: Was Honorary Secretary of the prestigious Voluntary Health Services,
Chennai for a full and productive 3-year productive term
Many other awards and honors of significance
Seminar 5: ECT in Neuropsychiatry
Dr Rupert McShane and Dr David Cousins
Dr Rupert McShane is Consultant Psychiatrist at Oxford Health NHS Foundation Trust.
Dr David Cousins is the MRC Clinician Scientist at the University of Newcastle.
20
Seminar 6: New and Future Drugs in Sleep Medicine
Dr Hugh Selsick, Dr Guy Leschinzer and Dr Sue Wilson
Dr Hugh Selsick is a consultant in psychiatry and sleep medicine and lead clinician at the
Insomnia Clinic, UCLH. He also works as a consultant at the Sleep Disorder Centre at Guy’s
Hospital. He runs the sleep special interest group in the Faculty of Neuropsychiatry and is a
council member of the Sleep Section at the Royal Society of Medicine. His special interest is the
role of sleep disorders in mental psychiatric disorders.
Seminar 7: Neuropsychiatry on the shop floor: discussing difficult clinical cases
Professor Hugh Rickards
Professor Hugh Rickards MD FRCPsych is a Consultant in Neuropsychiatry and Hon. Professor of
Neuropsychiatry, University of Birmingham and National Centre for Mental Health, Birmingham.
Seminar 8: Neurological assessment and Investigations: what do psychiatrists need
to know
Dr Jan Coebergh
The neurological examination in neuropsychiatry is as essential as the mental state examination
in neurology. The neurological examination includes the whole nervous system and is part of
the wider physical examination. Many neurological signs have limited sensitivity, specificity,
intra- and interobserver reliability so need to be interpreted in the context of the assessment
as a whole. Misinterpretation of the neurological examination can lead to unnecessary
investigations and treatment or delay diagnosis and management. A focused neurological
examination in neuropsychiatry however is essential for patient satisfaction, diagnosis and can
be part of treatment. The same caveats of limited sensitivity, specificity, intra- and
interobserver reliability also apply to neurological investigations. Severeal case examples will
be used to illustrate this.
Dr Jan Coebergh MBBS FRCP studied undergraduate medicine at Newcastle University. His
neurology training, he undertook in The Hague, The Netherlands. He has worked as a Consultant
Neurologist at Ashford St Peter’s Hospitals since January 2012 where he has a specialist
Movement Disorders clinic. He also works as a Honorary Consultant Neurologist St Georges
Hospital where he has a clinic in functional neurological symptoms (as part of Prof Edward's
group). He is a honorary senior lecturer at St George's university.
Recent research projects are studying musical hallucinations and the recognition of sound in
dementia. He recently co-authored a chapter in the upcoming Oxford Handbook of
Neuropsychiatry on the neurological examination in neuropsychiatry.
21
Plenary 6: Trainee award presentations
Is functional weakness associated with neural correlates in imaging studies? A
systematic review of the evidence.
Lori Black
Introduction
Functional neurological disorders (FNDs) are common disorders defined by the presence of
neurological symptoms which have no organic cause. By definition, they have no signs on
structural imaging. However, it is not impossible that there are neural correlates to be found
using SPECT, PET and fMRI. The purpose of this systematic review is to evaluate all literature
regarding functional imaging of functional weakness to see if functional weakness has neural
correlates to inform further research.
Methodology
I followed the PRISMA guidelines to conduct a systematic review, searching MedLine, Embase
and PsychInfo. I searched for “functional”, “psychogenic”, “somatoform”, “somatization”,
“somatisation”, “FND”, “conversion” OR “non-organic” and Medical Subject Headings (MeSH)
for somatoform disorder and conversion disorder.
I then made another search for “neuroimag*”, “fMRI”, “MRI”, “SPECT”, “PET”, “positron
emission tomography” OR “single photon emission computed tomography” and MeSH for
neuroimaging and functional neuroimaging. I combined this search with the other searches
using the word OR.
This gave 42237, refined to 39651 by only using articles with abstracts in the English language.
Using a highly time consuming strategy of reading the titles and abstracts of the papers this
was reduced to 29. Most articles were easily rejected because they contained no information
regarding imaging or functional neurological disorders (often being rheumatological conditions
and other neurological problems).
I read all of these in full, excluding articles not specific to functional imaging in functional
weakness. This left 7 articles for review.
Results
7 studies were included in my systematic review. Most studies used fMRI to image the patients
and comparison groups in their studies. All of the studies examined patients with unilateral
weakness. 4 studies purely researched patients with unilateral upper limb weakness.
Most studies found some neural correlates in patients with functional weakness and those that
compared their subjects with those feigning weakness found the results were usually different.
22
Areas found specifically to be deficient were the SMA contralateral to the affected side, and
precuneus. The prefrontal cortex had either diminished or increased activity depending on the
study looked at.
Discussion
The findings of this systematic review suggest that there may be some neural correlates on
functional imaging of patients with functional weakness. It should particularly be noted that
there was universally decreased activation in the areas specific to movement on the affected
cortex. However, the few studies looked at are small, pilot studies and, therefore, work in this
area in inconclusive.
Lori Black is a core trainee in Cardiff with a strong interest in neuropsychiatry. During a year
out before commencing psychiatric training she completed an MSc in Clinical Neuropsychiatry
and the University of Birmingham whilst working at the National Centre for Mental Health at
Cardiff University. Her subspecialist interest within the area of neuropsychiatry is functional
neurological disorders.
The psychiatric phenotype of anti-NMDA receptor encephalitis.
Dr Lucy L Gibson, Academic Foundation Year 2, Kings College Hospital NHS Foundation Trust, Dr
Thomas Pollak, Clinical Research Training Fellow, Institute of Psychiatry, Psychology and
Neuroscience, Professor Anthony S David, Consultant, Institute of Psychiatry, Psychology and
Neuroscience.
INTRODUCTION
NMDAR encephalitis classically presents with cognitive deficits and psychiatric symptoms which
progress to loss of consciousness with dystonic movements. However, the condition is
heterogeneous and isolated psychiatric presentations occur, causing delays in diagnosis and
treatment. Clearer definition of the psychiatric phenotype is needed to differentiate these patients.
METHODS
An observational retrospective cohort study: 86 patients identified with positive serum NMDAR
antibodies between July 2010 and May 2017 at Kings Health Partners. Inclusion criteria: over 18
years; meeting internationally accepted criteria for anti-NMDAR encephalitis. Electronic patient
records were reviewed to identify demographics and clinical features. Psychiatric symptoms
assessed using the Positive and Negative Syndrome Scale (PANSS).
RESULTS
47% (n=22) of adults with a positive antibody met criteria for encephalitis.
22 encephalitic patients included in analysis: 73% female; mean age 44; 55% acutely psychotic
and 32% admitted to psychiatric units.
23
Patients presenting with psychotic symptoms were significantly younger than those without
(33.8 vs 57.2 years t(15.2)=3.50, p<0.005) and were more likely to have a psychiatric
admission (p=0.005).
No significant difference in gender (p=0.4) or severity at nadir (p=0.8) in patients with or
without psychosis.
For the 12 patients with psychosis, PANSS scores indicated severe psychopathology (mean
total=125.8). PANSS five factor analysis showed some symptomatic domains are
disproportionately affected; ANOVA indicated more significant cognitive symptoms than
depressive or positive features (F(4,44)=10.7, p<0.005). Patients also exhibited high negative
symptom scores.
DISCUSSION
More prominent psychotic features in younger adults suggests greater susceptibility of the young
brain to exogenous psychosis. Negative symptoms and severe cognitive disturbance are seen in
anti-NMDAR encephalitis with sparing of some symptomatic domains. This is an unusual construct of
psychosis, distinct from the typical presentation of ‘functional psychoses’. Given the difficulty in
diagnosing anti-NMDAR encephalitis in psychiatric inpatients, this constellation of psychiatric
features should prompt further investigation.
Quantitative EEG Findings are a Potential Prognostic Biomarker in Anti-NMDA Encephalitis
Graham Blackman (1), Anthony David (1), Tom Pollak (1), Anthony Dalrymple (2), John Hanrahan
(2)
Institute of Psychiatry, Psychology and Neuroscience, Kings College London, London, United Kingdom
(1) Faculty of Life Sciences and Medicine, Kings College London, London, United Kingdom (2)
Background: Over the last decade there has been an increasing recognition of encephalopathy
syndromes caused by autoantibodies. One of the most investigated of these are antibodies acting
against the N-methyl-D-aspartate receptor (NMDAR). Outcomes from patients with anti-NMDAR
encephalitis are extremely variable, ranging from complete recovery to death. There is little
evidence available to predict which patients will have a favorable outcome. Patients often have
abnormal EEG findings and an important, yet unanswered question is whether EEG may have
prognostic value in this patient group.
Method: A single center retrospective review of patients with anti-NMDAR encephalitis over a 6-
year period was employed. Patients were identified from a hospital electronic register database and
were included if they had confirmed anti-NMDAR antibodies with, one or more neuropsychiatric
symptoms and an admission EEG. Peak power for the four main frequency bands (beta, alpha, theta
and delta) were calculated between two scalp electrodes (C3-C4) using spectral analysis. Outcome
measures were admission duration and Modified Rankin Scale (MRS) at discharge and last follow up.
24
Results: The commonest presenting symptoms were confusion, followed by psychosis. Average
time from symptom onset to EEG was 179 days and average admission length was 25 days with a
follow up of 2.1 years. Qualitative analysis revealed generalised slowing and electrographic seizures
as the most common features. There was a highly significant correlation between poor outcome, at
last follow up, and peak power in the theta and delta ranges only. There was no association between
peak power and admission length or outcome at discharge.
Conclusion: This is the first study to demonstrate that EEG may be a potentially useful prognostic
tool in patients with anti-NMDAR encephalitis. In particular, early findings suggest patients with anti-
NMDAR encephalitis with greater slow wave activity on their admission EEG have a worse long term
outcome.
Dr Graham Blackman gained a Psychology degree from the University of Bath before completing a
medical degree at the University of Birmingham.
He has held academic posts at the University of Nottingham, University of Birmingham and Harvard
University.
He is currently an Academic Clinical Fellow in General Adult Psychiatry on the Maudsley Training
Programme and the Institute of Psychiatry, Psychology and Neuroscience.
His academic interests include the neurophysiology and psychopathology of autoimmune
encephalitis and the role of the immune system in psychosis.
Chemokines in Depression in Health and in Inflammatory Illness: a systematic review and
meta-analysis
Leighton SP*, Nerurkar L*, Krishnadas R, Johnman C, Graham GJ, Cavanagh J.
Presenting Author
*Joint first authors
Depression is a heterogeneous psychiatric disease whose pathogenesis remains unclear. Despite this,
inflammatory illness is associated with depressive illness and there is evidence for alterations of pro-
inflammatory cytokines in depressive disorders. Pre-clinical work has identified that chemokines,
chemotactic cytokines, may play a role in depressive behaviours. In this meta-analysis, we aimed to
establish if there is evidence of an association between blood or cerebrospinal fluid (CSF) chemokine
levels and depressive disorder. Following PRISMA guidelines, we performed systematic searches of
EMBASE, PsycINFO and MEDLINE databases. Participants with comorbid physical illness were included
for subgroup analysis. Subjects with psychiatric illnesses that would preclude a diagnosis of depression
as per conventional nosological thinking (e.g. schizophrenia or mania) were excluded. 72 studies met
25
the inclusion criteria. Meta-analysis identified significant increases in blood CCL2, CXCL4, CXCL7,
CXCL8 and CXCL12 and significant decreases in blood CCL4 in patients with depressive illness
compared to controls. Sensitivity analysis of studies with only physically healthy participants also
revealed significant increases in blood CCL3 and CCL11 in patients with depressive illness. However,
in this analysis blood CXCL4 did not retain significance. No chemokine retained significance when
considering only those studies with a comorbid physical illness. No other chemokine examined differed
significantly between depressed patients and controls (blood CCL5, CCL7, CCL15, CCL18, CCL24,
CCL27, CXCL1, CXCL9, CXCL10 and CSF CCL2, CXCL8, CXCL10). Analysis of the clinical utility of
CXCL8 found a negative predictive value (NPV) of 93.5% given a population prevalence of depressive
disorder of 10%. Overall these data provide significant evidence for an association between alterations
in circulating chemokine levels and depressive disorders, with evidence of possible clinical utility.
Future work should aim to examine these molecules in prospective longitudinal studies and to identify
putative mechanisms through which the chemokine family of molecules can drive depressive illness.
Louis Nerurkar is a medical student at the University of Glasgow who has just completed a
PhD in the Cavanagh lab at the Institute of Infection, Immunity and Inflammation. Our group’s
primary interest is understanding the mechanisms through which inflammation drives changes
in the brain and how these changes may lead to behavioural alterations, ultimately in the hope
of further clarifying molecular pathways that drive psychiatric disease.
Plenary 7: Debate “This house believes that the investigation of patients with Mild
Cognitive Impairment is clinically unhelpful and economically unjustified”
Chair: Dr Peter Byrne
For the motion
Dr Jeremy Isaacs
Dr Jeremy Isaacs is a Consultant Neurologist and Dementia Clinical Lead at St George's
University Hospitals NHS Foundation Trust, Consultant Neurologist and Neurology Clinical Lead:
Kingston Hospital NHS Foundation Trust and Honorary Senior Lecturer: St George's University
of London.
Against the motion
Dr Jonathan Schott
Jonathan Schott is Professor of Neurology at the Dementia Research Centre, UCL Institute of
Neurology, and Honorary Consultant Neurologist at the National Hospital for Neurology and
Neurosurgery, Queen Square. He runs a busy cognitive disorders clinic with a particular
emphasis on young onset and unusual dementias, and he has an extensive portfolio of
translational clinical research in the dementias, with particular interests in how clinical
assessment, biomarkers and genetics can be combined to improve differential diagnosis and
identify pre-symptomatic Alzheimer’s disease. He has published over 180 paper on dementia,
and edited the Oxford Textbook of Cognitive Neurology and Dementia. He serves on a number
26
of national and international bodies influencing clinical practice and research in the dementias,
and is committed to translating research advances to improve patient care.
27
POSTER EXHIBITION (ALPHABETICALLY BY SURNAME)
1. Tardive dystonia: a case report and literature review
Dr Alex Berry, CT1 Psychiatry, Camden and Islington Mental Health Trust
Dr Samina Karamat, Consultant Psychiatrist, North East London Foundation Trust
AIM:
We present a case of tardive dystonia (TDt) caused by risperidone in a 68-year-old female with
probable Lewy body dementia. We also aimed to perform a non-systematic literature review of TDt
(associated with psychotropic medication) published within the last 10 years.
METHOD:
We searched PubMed titles and abstracts using the search terms: “tardive” in combination with
“dystonia”, “camptocormia” “blepharospasm”, “torticollis”, “Meige syndrome” and “Pisa syndrome”.
Articles published since 2007 describing individual patient characteristics with documented TDt were
included. We excluded articles we were unable to access, or were not relevant (including those
focusing on TDt unrelated to psychotropic medication). We collated information about patient age,
indications for medication, causative medication, duration of exposure, dystonia phenotype and
treatment strategies used.
RESULTS:
We identified 94 articles, 34 of which were excluded. 141 cases were identified, with a mean age of
42.5, 56% being male. The most frequently reported indication for medication was schizophrenia
(n=51), followed by depression (n=17). The most frequently reported causative medications were
haloperidol (n=23), risperidone (n=19), chlorpromazine (n=9), olanzapine (n=8) and aripiprazole
(n=6). Duration of reported exposure to implicated medication was available in 83 cases (average of
27.9 months exposure prior to dystonia-onset). Cervical dystonia was the most frequently reported
TDt phenotype (n=51), followed by orofacial/oromandibular (n=23), blepharospasm (n=13) and
truncal dystonia (n=14). 29 separate treatments were reported, with deep brain stimulation (DBS,
n=39) being one of the most frequently reported treatments utilised.
CONCLUSIONS:
Haloperidol and risperidone are frequently reported as causative agents of TDt. Antidepressants are
rarely implicated in TDt. Use of DBS for TDt is highly represented in the case-report literature
published in the last decade.
28
2. Use of mood stabilisers in the management of aggression secondary to a traumatic
brain injury.
Ms Anum Bhatti, Medical Student, Keele University. Dr George El-Nimr, Consultant Neuropsychiatrist,
North Staffordshire Combined Health NHS Trust.
Aims: Review the available literature regarding the efficacy of mood stabilisers for the treatment of
post- traumatic brain injury (TBI) aggression.
Methodology: A literature search was conducted using Research Gate, the Cochrane Library, PubMed
and Google Scholar using the search terms “traumatic brain injury”, “aggression”, “drug treatment”,
“mood stabilisers” and names of individual drugs. Exclusion criteria were 1) studies involving
paediatric patients and 2) publications prior to 1980.
Results: 4 reviews and 1 trial were identified that met the inclusion criteria. There is compelling
evidence for the efficacy of carbamazepine and valproate in reducing post- TBI aggression however
several trials have contested this. Adverse effects associated with their use include impaired
psychomotor function, sedation and impaired cognition although valproate has been associated with
a decreased incidence of the latter. One trial demonstrated that oxcarbazepine is effective in reducing
aggression whilst having milder side effects compared to carbamazepine. Gabapentin has yielded
mixed results whilst one case study provides promising evidence regarding lamotrigine use.
Topiramate is discussed in one review to reduce aggression however it is not recommended due to its
side effects of psychosis and cognitive impairment. Additionally, lithium presents a heightened risk of
neurotoxic effects at lower doses to brain injury patients and is not recommended.
Conclusion: There is insufficient evidence regarding the efficacy of mood stabilisers in treating post-
TBI aggression. Of the available trials, carbamazepine and valproate have been shown to be the most
effective drugs with minimal side effects. There is a need for more trials investigating the effectiveness
of mood stabilisers, particularly lamotrigine and oxcarbazepine, in the management of post- TBI
aggression.
3. Psychosis in wilson’s disease: an unusual presentation of bipolar affective disorder
Lori Black, Cardiff University
Psychosis is a rare but recognised symptom of the neurological effects of Wilson’s Disease.[1] We
report on the presentation of a 55 year old woman, C, admitted after displaying a decline in mental
state. On initial assessment in the Emergency Department she was restrained by security and police
and was aggressive in her behaviour. She was quietly spoken, voicing paranoid persecutory delusions,
euthymic with labile affect, alternating between anger, tearfulness and displayed disinhibited affection,
29
behaving in a frontal manner. She lacked insight completely. She was detained under for a period of
assessment under Section 2 of the Mental Health Act (MHA) 2007.
C had multiple previous admissions under the MHA. Past primary diagnoses included Wilson’s Disease
and Bipolar Affective Disorder (BPAD). Secondary to her Wilson’s Disease she had developed Liver
Cirrhosis, abdominal varices, portal and pulmonary hypertension (WHO functional class II) with
massive splenomegaly. She has a history of behavioural outbursts; acquiring a forensic history for
assault on staff, police and family members, and drunken and disorderly behaviour. In the weeks
leading to admission she had stopped taking all of her medication including her Penicillamine.
A neurological examination showed ataxia with a wide-based gait and minor bradykinesia. C did not
have a wing-flapping tremor, dystonia or myoclonus. All other findings on neurological examination
were normal. She had a copper level of 1.7umol/L, caeruloplasmin of 0.04g/L and a bilirubin of
50umol/L. Full blood count demonstrated pancytopaenia, and extended blood screen highlighted low
calcium with vitamin D deficiency. A CT of her head displayed hypodensity in the putamen, which was
worse on the left. There was no mass, infarct or infectious process obvious to explain the lesions. This
was consistent with an MRI brain performed a number of months prior to the admission, which
demonstrated hyperintensity of both putamina. Such changes are recognised to be associated with
Wilson’s Disease.[2]
These findings, along with C’s behaviours indicative of frontal lobe involvement, suggested to the
managing team a diagnosis of psychosis secondary to neurological Wilson’s Disease. She was treated
effectively with Paliperidone depot (100mg monthly), 4mg Risperidone ON and Penicillamine (750mg
BD) along with her usual medication for liver cirrhosis. To date she remains stable and has not been
readmitted.
The MRI and CT brain findings along with C’s longstanding Wilson’s Disease brought into question her
diagnosis of BPAD. Upon casenote review her previous presentations had included behavioural and
neurological examination findings consistent with neurological sequelae of Wilson’s Disease.
Psychiatric symptoms within Wilson’s Disease are common, with one study finding 20% of WD patients
had seen a psychiatrist.[3] Predominantly personality change and depression are typical features,
psychosis being a rare but recognised feature.[1,2] Psychiatric symptoms are a recognised side effect
of Penicillamine, clouding diagnostic clarity.[1] Literature reviews suggest that Wilson’s Disease may
present with only psychiatric symptoms for many years before neurological or hepatic symptoms
develop.[1,2] Wilson’s Disease should therefore not be discounted in unusual presentations of
psychosis such as C’s case.
1. Bandmann O, Weiss KH, Kaler SG. Wilson’s disease and other neurological copper disorders. Lancet
Neurol. [Internet]. 2015 [cited 2017 Apr 2];14:103–13. Available from:
http://www.sciencedirect.com.abc.cardiff.ac.uk/science/article/pii/S1474442214701905
2. Zimbrean PC, Schilsky ML. Psychiatric aspects of Wilson disease: a review. Gen. Hosp. Psychiatry
30
[Internet]. 2014 [cited 2017 Apr 2];36:53–62. Available from:
http://www.sciencedirect.com.abc.cardiff.ac.uk/science/article/pii/S0163834313002454
3. TR D, GE B. Wilson’s disease: Psychiatric symptoms in 195 cases. Arch. Gen. Psychiatry [Internet].
1989;46:1126–34. Available from: http://dx.doi.org/10.1001/archpsyc.1989.01810120068011
4. Is functional weakness associated with neural correlates in imaging studies? A
systematic review of the evidence.
Lori Black
Introduction
Functional neurological disorders (FNDs) are common disorders defined by the presence of
neurological symptoms which have no organic cause. By definition, they have no signs on structural
imaging. However, it is not impossible that there are neural correlates to be found using SPECT, PET
and fMRI. The purpose of this systematic review is to evaluate all literature regarding functional
imaging of functional weakness to see if functional weakness has neural correlates to inform further
research.
Methodology
I followed the PRISMA guidelines to conduct a systematic review, searching MedLine, Embase and
PsychInfo. I searched for “functional”, “psychogenic”, “somatoform”, “somatization”, “somatisation”,
“FND”, “conversion” OR “non-organic” and Medical Subject Headings (MeSH) for somatoform disorder
and conversion disorder.
I then made another search for “neuroimag*”, “fMRI”, “MRI”, “SPECT”, “PET”, “positron emission
tomography” OR “single photon emission computed tomography” and MeSH for neuroimaging and
functional neuroimaging. I combined this search with the other searches using the word OR.
This gave 42237, refined to 39651 by only using articles with abstracts in the English language. Using
a highly time consuming strategy of reading the titles and abstracts of the papers this was reduced to
29. Most articles were easily rejected because they contained no information regarding imaging or
functional neurological disorders (often being rheumatological conditions and other neurological
problems).
I read all of these in full, excluding articles not specific to functional imaging in functional weakness.
This left 7 articles for review.
31
Results
7 studies were included in my systematic review. Most studies used fMRI to image the patients and
comparison groups in their studies. All of the studies examined patients with unilateral weakness. 4
studies purely researched patients with unilateral upper limb weakness.
Most studies found some neural correlates in patients with functional weakness and those that
compared their subjects with those feigning weakness found the results were usually different.
Areas found specifically to be deficient were the SMA contralateral to the affected side, and precuneus.
The prefrontal cortex had either diminished or increased activity depending on the study looked at.
Discussion
The findings of this systematic review suggest that there may be some neural correlates on functional
imaging of patients with functional weakness. It should particularly be noted that there was universally
decreased activation in the areas specific to movement on the affected cortex. However, the few
studies looked at are small, pilot studies and, therefore, work in this area in inconclusive.
5. Quantitative EEG Findings are a Potential Prognostic Biomarker in Anti-NMDA
Encephalitis
Graham Blackman (1), Anthony David (1), Tom Pollak (1), Anthony Dalrymple (2), John
Hanrahan (2)
Institute of Psychiatry, Psychology and Neuroscience, Kings College London, London, United Kingdom
(1) Faculty of Life Sciences and Medicine, Kings College London, London, United Kingdom (2)
Background: Over the last decade there has been an increasing recognition of encephalopathy
syndromes caused by autoantibodies. One of the most investigated of these are antibodies acting
against the N-methyl-D-aspartate receptor (NMDAR). Outcomes from patients with anti-NMDAR
encephalitis are extremely variable, ranging from complete recovery to death. There is little
evidence available to predict which patients will have a favorable outcome. Patients often have
abnormal EEG findings and an important, yet unanswered question is whether EEG may have
prognostic value in this patient group.
Method: A single center retrospective review of patients with anti-NMDAR encephalitis over a 6-
year period was employed. Patients were identified from a hospital electronic register database and
were included if they had confirmed anti-NMDAR antibodies with, one or more neuropsychiatric
symptoms and an admission EEG. Peak power for the four main frequency bands (beta, alpha, theta
and delta) were calculated between two scalp electrodes (C3-C4) using spectral analysis. Outcome
measures were admission duration and Modified Rankin Scale (MRS) at discharge and last follow up.
32
Results: The commonest presenting symptoms were confusion, followed by psychosis. Average
time from symptom onset to EEG was 179 days and average admission length was 25 days with a
follow up of 2.1 years. Qualitative analysis revealed generalised slowing and electrographic seizures
as the most common features. There was a highly significant correlation between poor outcome, at
last follow up, and peak power in the theta and delta ranges only. There was no association between
peak power and admission length or outcome at discharge.
Conclusion: This is the first study to demonstrate that EEG may be a potentially useful prognostic
tool in patients with anti-NMDAR encephalitis. In particular, early findings suggest patients with anti-
NMDAR encephalitis with greater slow wave activity on their admission EEG have a worse long term
outcome.
6. Predictors of Poor Outcome in Functional Neurological Disorders
Dr Sara Castro, Dr Balam Budwal, Dr Parviz Bahadoran, Dr David Hall, Dr Sarah Cope, Dr Norman
Poole and Dr Niruj Agrawal, Atkinson Morley Regional Neurosciences Centre, ST George’s
University Hospital NHS, London.
Aims: The present study was intended to establish predictors of poor outcome in a sample of patients
with functional neurological disorders at a regional neuroscience centre.
Methods: A descriptive retrospective analysis was undertaken of the psychiatric medical records for
all outpatients with confirmed Functional Neurological Disorder (FND) assessed at a regional
neuropsychiatry service over the preceding 18 months. Sociodemographic and clinical data was
collected, including type and duration of FND, comorbidity, and response to treatment. Patients were
categorised according to a dichotomous treatment outcome: good (complete/partial recovery) or poor
(minimal improvement or deterioration). Categorical or ordinal variables were compared using the χ2
test with Bonferroni post hoc tests.
Results: Poor outcome was reported in 70 of 169 patients (41%). A statistically significant difference
in terms of response was found for age, marital status, education, employment status, type of
treatment, plus type and duration of FND. Poor outcomes were associated with age 45-64 years
compared to younger patients (p=0.035) and married or divorced/separated status compared to
single patients (p=0.035 and p=0.031 respectively); being in receipt of long-term compared to
employment (p=0.016); and having lower educational status compared to people with higher
education (p=0.048). Lack of psychological based intervention was also associated with poor recovery
(p=0.026). Considering all FNDs, non-epileptic attack disorder (NEAD) was associated with better
outcome.
Comments: Some results were similar to previous findings, but the study failed to confirm previously
established correlations and found some new associations. There is still considerable uncertainty about
the predictors of good and bad outcome in FND supporting the relevance of this study. Greater
33
understanding of predictors of outcome should lead to greater targeting of interventions and perhaps
a more tailored and individualized approach with increased likelihood of positive results.
7. Depression and suicidality in Korsakoff’s Syndrome: a literature review and brief case
series
Ms Nadja Cox, Assistant Psychologist, Ms Alexandra Welford, Psychology Student, Professor Graeme
Yorston, Consultant Forensic Neuropsychiatrist, St Matthew’s Healthcare, Northampton.
Aims: The current published literature on the care and treatment needs of people with Korsakoff’s
syndrome (KS) living in long-term care facilities in the UK is extremely limited as previous research
has focussed largely on describing their neuropsychological deficits. Anecdotally, depressive
symptoms and impulsive suicide attempts are common in this group and they can often lead to
individuals being admitted, in crisis, to an acute mental health hospital bed and later being referred
on to a specialist rehabilitation service. The aim of this literature review and descriptive case series is
to highlight some of the difficulties clinicians face in assessing, treating and monitoring mood disorders
and suicidal behaviour in this group of patients and to propose further research in this area.
Method: A systematic literature review will be conducted exploring suicidality, hopelessness and
depressive symptoms in people with Korsakoff’s syndrome. A case series of five male KS patients
being treated in a slow stream rehabilitation service will be reported.
Results: The outcome of the literature review will be reported. The case series will describe the clinical
issues experienced by this complex patient group, focussing on their affective symptoms, feelings of
hopelessness, suicidal thoughts and self-harming behaviour.
Conclusion: Depressive symptoms and self-harming behaviour are common in people with Korsakoff’s
syndrome and the impact of these on their quality of life and care needs has been largely overlooked
in previous research . It is hoped that this presentation will act as a stimulus to further research into
the non-cognitive symptoms of this complex patient group.
8. INFLUENCE OF HORMONAL CHANGES ON SEIZURES IN WOMEN WITH EPILEPSY
Dr Antonio D’Costa, ST5, Neuropsychiatry, Brain Injury Rehab., Merseycare NHS Trust, Liverpool; Dr
Dimple D’Costa, SpR, Obstetrics and Gynaecology, Whiston Hospital, Prescott
Aim:
The original concept of Catamenial epilepsy (CE) was defined as seizures occurring during menses.
But this definition was challenged by clinical observations of increase in seizures frequency in other
phases of the Menstrual Cycle (MC) as well, depending on hormonal fluctuations. The primary aim of
this review is to understand the influence of hormonal changes in females on seizures frequency.
34
METHODS:
A search of Medline, Embase and PubMed with the keywords ‘female’, ‘seizure’, ‘epilepsy’, ‘hormones’
‘catamenial’ generated predominantly studies in relation to estrogen and progestrone. A total of 11
primary studies were chiefly included in this review.
RESULTS:
Bäckström T, (1976) found a positive correlation between increased seizure and E/P ratio. John
Jacono(1986) demonstrated effect of gonadal hormones and ionized calcium on seizure frequency,
attributing low calcium having a stabilizing influence on seizures. Rościszewska, D et al. (1986) found
estrogen levels not having a significant effect on the seizure frequency. Herkes et al. (1993) found
increase seizure frequency during menses, 2 days prior and also at the time of ovulation. Herzog et
al.(1997) strongly supported the concept of CE, proposing the existence of three patterns of its
occurrence in relation to MC. Herzog et al. (2015) found a 2 fold difference in average daily seizure
frequency between the highest(day 1) and lowest (day 8) days of the MC.
DISCUSSION:
The general consensus was the increase in seizures frequency in relation to hormonal fluctuations.
There was large heterogeneity in studies and their findings, which can be attributed to lack of a correct
definition for CE. While, older studies relied generally on an increased incidence in seizures during a
particular phase to define their criteria; the studies by Herzog et al used a strict two fold increase
incidence as the basis for inclusion. In conclusion adopting a strict criterion would have ensured
uniformity in the findings.
9. The Role of Traumatic Events in Conversion Disorder: A Psychodynamic Perspective
Dr. Francesca Falzon Aquilina & Dr Joseph Cassar , Mount Carmel Hospital, Attard, Malta.
Aim:
To highlight the significance of traumatic events and the key psychodynamic concepts involved in the
recognition, understanding and treatment of such a conversion disorder.
Method:
The case of J.T, a 22 year old male suffering from long standing pseudoseizures was modelled on
Freud’s and Breuer's psychodynamic model of hysteria. The latter suggested that symptoms pertinent
to conversion disorder resulted from intrusion of “memories connected to psychical trauma” into the
somatic innervation. With this a primary and secondary gain is derived by the patient himself.
Results:
Several major and recurrent minor traumatic events in the patient’s history were pivotal in explaining
the significance of these events in some of the most fundamental concepts of psychodynamic theory.
The major traumatic event identified was the discovery that the patient’s brother had a spinal nerve
tumour. This incident diverted most of the family attention normally given to the patient onto his
35
brother. Thus, primary gain, manifesting itself as pseudoseizures, allowed the patient to express the
conflict that had been unconsciously suppressed. Moreover, the secondary gain made it possible for
the patient to garner support from his family and friends, which would otherwise have been
unobtainable.
Moreover, according to sociocultural theories, the direct expression of emotion is at times
impermissible, with somatization being the only option. This was adequately illustrated in J.T’s case,
who grew up in a very protective and close knit family were emotions were not liberally expressed.
Conclusions
Understanding the role of traumatic events in conversion disorder leads to a better understanding of
the defense mechanisms implicated in the development and maintenance of such a diagnosis. We
conclude that in such a case, breaking the cycle of secondary gain would only be possible if the
enmeshment with his family dissolves and the patient lives independently.
10. The psychiatric phenotype of anti-NMDA receptor encephalitis.
Dr Lucy L Gibson, Academic Foundation Year 2, Kings College Hospital NHS Foundation Trust, Dr Tom
Pollak, Clinical Research Training Fellow, Institute of Psychiatry, Psychology and Neuroscience,
Professor Anthony S David, Consultant, Institute of Psychiatry, Psychology and Neuroscience.
INTRODUCTION
NMDAR encephalitis classically presents with cognitive deficits and psychiatric symptoms which
progress to loss of consciousness with dystonic movements. However, the condition is heterogeneous
and isolated psychiatric presentations occur, causing delays in diagnosis and treatment. Clearer
definition of the psychiatric phenotype is needed to differentiate these patients.
METHODS
An observational retrospective cohort study: 86 patients identified with positive serum NMDAR
antibodies between July 2010 and May 2017 at Kings Health Partners. Inclusion criteria: over 18
years; meeting internationally accepted criteria for anti-NMDAR encephalitis. Electronic patient
records were reviewed to identify demographics and clinical features. Psychiatric symptoms assessed
using the Positive and Negative Syndrome Scale (PANSS).
RESULTS
47% (n=22) of adults with a positive antibody met criteria for encephalitis.
22 encephalitic patients included in analysis: 73% female; mean age 44; 55% acutely psychotic
and 32% admitted to psychiatric units.
Patients presenting with psychotic symptoms were significantly younger than those without (33.8
vs 57.2 years t(15.2)=3.50, p<0.005) and were more likely to have a psychiatric admission
(p=0.005).
36
No significant difference in gender (p=0.4) or severity at nadir (p=0.8) in patients with or without
psychosis.
For the 12 patients with psychosis, PANSS scores indicated severe psychopathology (mean
total=125.8). PANSS five factor analysis showed some symptomatic domains are
disproportionately affected; ANOVA indicated more significant cognitive symptoms than
depressive or positive features (F(4,44)=10.7, p<0.005). Patients also exhibited high negative
symptom scores.
DISCUSSION
More prominent psychotic features in younger adults suggests greater susceptibility of the young brain
to exogenous psychosis. Negative symptoms and severe cognitive disturbance are seen in anti-NMDAR
encephalitis with sparing of some symptomatic domains. This is an unusual construct of psychosis,
distinct from the typical presentation of ‘functional psychoses’. Given the difficulty in diagnosing anti-
NMDAR encephalitis in psychiatric inpatients, this constellation of psychiatric features should prompt
further investigation.
11. Early onset Dementia: A Conundrum for Professionals
Dr Sheeba Hakeem and Dr Chidinma Nwosu ,Kent and Medway NHS and Social care partnership trust;
Dr Jaleel Khaja, South Essex Partnership Trust
Abstract: Cognitive impairment can range from something mild and transient to severe and
progressive, with a large spectrum of presentations in-between. It can be a primary disorder as in
dementia or secondary to other psychiatric disorders such as depression. In clinical practice
establishing a definitive diagnosis for cognitive impairment is fraught with challenges particularly when
the impairment occurs in younger adults and secondly there is a background psychiatric history, not
to mention the symptomatic overlap among various psychiatric disorders. Often in such cases the
professionals are more inclined to consider cognitive impairment to be secondary to a primary
psychiatric disorder than a primary diagnosis with secondary psychiatric symptoms. We describe a
case report highlighting the challenges of disentangling the diagnoses of depression and dementia,
with differing views from various professionals.
Ms X, a 56 year old lady with a past history of depression presented with cognitive impairment which
was attributed to a recurrence of a severe depressive disorder. Ms X presented with marked cognitive
impairment, anxiety, anxiety congruent tearfulness, atypical features of motor symptoms of
Parkinson’s disease, perhaps a pointer towards the dementia in Lewy body. Due to differing views
over the atypicality of these features and the past history of severe depression Ms X was considered
to be suffering from recurrence of depressive disorder for months prior to a definite diagnosis.
Following numerous assessments, she received a diagnosis of Lewy Body Dementia and did relatively
well on Rivastigmine at least for a brief period.
37
This case emphasizes the need, among other things, for a better collaboration of various specialities
i.e psychiatry, neurology and radiology, especially in view of very few, if any, designated young onset
dementia services locally. We believe this case highlights the need to do more to ensure that the right
and timely information about the diagnosis, management and prognosis is available to the patients
and their families to help them make informed decisions regarding care and help reduce the impact
of the time spent waiting which is easily underestimated.
12. Characteristics and cognitive outcomes for patients with anti-NMDA receptor
encephalitis in Ireland
Eric Kelleher1,2, Helen Barry3, Daniel Costello4, Patricia McNamara5, April Hargreaves1, Shane
Smyth6, Killian O’Rourke6, Peter Boers7, David Columb3, Richard Walsh5, Elijah Chaila7, Jean
Dunne8, Tim Lynch6, Niall Tubridy9, Michael Gill1,2, Angela Vincent10, David Cotter3, Colin
Doherty11, Aiden Corvin1,2
1. Department of Psychiatry, Trinity College Dublin, 2. Department of Psychiatry, St James’s University
Hospital, Dublin, 3. Department of Neuropsychiatry, Beaumont University Hospital Dublin, 4.
Department of Neurology, Cork University Hospital, Cork, 5. Department of Neurology, Tallaght
University Hospital, Dublin, 6. Department of Neurology, Mater Misericordiae University Hospital,
Dublin, 7. Department of Neurology, Limerick Regional University Hospital, Limerick, 8. Department
of Immunology, St James’s University Hospital, Dublin, 9. Department of Neurology, St Vincent’s
University Hospital, Dublin, 10. Department of Neuroimmunogy, John Radcliffe Hospital, Oxford, 11.
Department of Neurology, St James’s University Hospital, Dublin
Background:
NMDAR-Ab encephalitis is an autoimmune disorder characterised by prominent early psychiatric
features including psychosis. I aimed to assess the presentation, care pathway and long term cognitive
outcomes of such patients in the republic of Ireland (2014-2016).
Methods:
Collaborators identified all individuals with NMDAR-Ab encephalitis. Participants were invited to a semi-
structured intervew and neurocognitive test battery using tests selected from CANTAB and the WMS-
III. Tests selected were for working memory (letter number sequencing and spatial working memory),
executive functioning (stockings of Cambridge), episodic memory [logical memory immediate and
delayed) and visual memory (faces immediate and delayed task and paired associate learning). Cases
who participated in cognitive follow up were matched with previously collected healthy controls and
schizophrenia for age, gender and full scale IQ (FSIQ). Ethical approval was obtained at each
institution.
Results:
38
19 individuals were diagnosed with NMDAR-Ab encephalitis. Mean (s.d.) time at follow up was 48.72
(20.55) months. Participants were predominantly female (15:4). Mean (s.d.) age of 34.74 (14.79)
years. 68.42% (N=13) had initial psychiatric diagnosis (invariably psychosis). 57.89% (N=11) were
referred for psychiatric admission 78.94% (N=15) developed neurological features within two months.
36.8% (N=7) required ICU admission.
Investigations that lead to diagnosis included abnormal EEG (15/19, 78.94%), MRI brain (15.78%,
3/19), inflammatory CSF (10/19, 52.63%). NMDAR-Ab in the CSF of 7 cases. 73.68% (14/19) treated
with first line immunotherapy only and 5/19 receiving second line. 4 patients had ovarian teratomas.
One case died secondary autonomic dysfunction.12 patients (11F:1M) participated in cognitive test
battery at 55 months. Cognitive deficits were observed for working memory and visual memory
subtests. However there was a wide degree of variability in performatnce.
Conclusions
Anti-NMDA encephalitis is a rare disorder that usually presents with psychotic features.. Some deficits
are observed in working memory in the longer term. Awareness by psychiatry and liaison with neuro-
immunology services are important for prompt diagnosis and early treatment.
13. Neuropsychiatric symptoms associated with Peramapnel usage in people with
pharmacoresistant epilepsy: a case series of 10 patients
Dr Ivan Koychev1 PhD MRCPsych, Dr David Okai2 MD MRCPsych, Dr Arjune Sen3 PhD MRCP
1 Department of Psychiatry, University of Oxford, Warneford Hospital, Oxford, UK
2 Psychological Medicine Service, The John Radcliffe Hospital, Oxford University Hospitals NHS
Foundation Trust, Oxford, UK
3 Oxford Epilepsy Research Group, NIHR Biomedical Research Centre, Nuffield Department of Clinical
Neuroscience, The John Radcliffe Hospital, Oxford University Hospitals NHS Foundation Trust, Oxford,
UK
Aims
Perampanel is an anti-epileptic drug (AED) licensed in 2012 for the treatment of focal epilepsy with
or without secondary generalisation. Perampanel is a second/third line AED and therefore used often
in those who are treatment resistant to other AEDs. Pooled analyses have shown a consistent efficacy
in terms of seizure frequency reduction. As with many novel AEDs, Perampanel can have an adverse
effect on mood and associates with significant psychiatric and behavioural change. These side effects
appear to be dose-dependent: irritability is a prime example affecting 4% of patients taking
perampanel at the lowest dose (2 mg per day), increasing to 12% in those taking 12 mg per day
(Rugg-Gunn 2014, Epilepsia). In the current presentation we aim to summarise a case series of
patients treated with perampanel where irritability, aggression, psychosis and/or self-referential ideas
were major psychiatric side effects.
39
Methods
A case series of 10 patients treated with perampanel at the Department of Neuroscience, Oxford
University Hospitals NHS Foundation Trust.
Results
We illustrate the neuropsychiatric side effects with case report examples alongside the pooled
characteristics of the whole case series. We discuss the relationship between the emergence of these
side effects and drug dose, time from initiation of perampanel, patient demographics and seizure
semiology. We also present data on resolution of symptoms with perampanel dose
modification/cessation as well as addition of agents to control neuropsychiatric symptoms.
Conclusions
The incidence and characteristics of perampanel-associated psychiatric symptoms, requires awareness
among neurologists and psychiatrists to inform risk management and appropriate treatment.
14. Akathisia in a cohort of female psychiatric inpatients
Dr Benjamin C Mcloughlin, Radbourne Unit, Derby.
Aims: The prevalence of akathisia amongst an inpatient cohort of female psychiatric patients was
assessed using the Barnes Akathisia Rating Scale (BARS). Patients deemed suitable were trialled on
propranolol or procyclidine with a view to evaluating improvements in akathisia.
Methods: Data was collected from 19 female inpatients using BARS. 4 symptomatic patients were
placed on therapeutic agents: 2 on propranolol, 2 on procyclidine. These 4 patients were re-assessed
using BARS following 7 days of therapy.
Results: At baseline, objective akathisia was present in 3 of 19 patients, subjective akathisia in 7 of
19, subjective distress in 7 of 19. Of those on typical neuroleptics +/- atypicals, objective akathisia
was found in 2 of 5, subjective akathisia in 2 of 5 and subjective distress in 3 of 5. At 7 days 4 of 19
patients were re-assessed following commencement of procyclidine or propranolol. Akathisia reduction
was observed globally in objective and subjective terms, with distress reduction in 3 of 4 patients.
Conclusion: It is recognised that neuroleptic-induced akathisia is amenable to attenuation in both
objective and subjective terms by widely available therapeutic agents. Use of these medications should
be considered routinely in clinical practice alongside when prescribing neuroleptics.
40
15. Chemokines in Depression in Health and in Inflammatory Illness: a systematic
review and meta-analysis
Leighton SP*, Nerurkar L*, Krishnadas R, Johnman C, Graham GJ, Cavanagh J.
Presenting Author
*Joint first authors
Abstract
Depression is a heterogeneous psychiatric disease whose pathogenesis remains unclear. Despite this,
inflammatory illness is associated with depressive illness and there is evidence for alterations of pro-
inflammatory cytokines in depressive disorders. Pre-clinical work has identified that chemokines,
chemotactic cytokines, may play a role in depressive behaviours. In this meta-analysis, we aimed to
establish if there is evidence of an association between blood or cerebrospinal fluid (CSF) chemokine
levels and depressive disorder. Following PRISMA guidelines, we performed systematic searches of
EMBASE, PsycINFO and MEDLINE databases. Participants with comorbid physical illness were included
for subgroup analysis. Subjects with psychiatric illnesses that would preclude a diagnosis of depression
as per conventional nosological thinking (e.g. schizophrenia or mania) were excluded. 72 studies met
the inclusion criteria. Meta-analysis identified significant increases in blood CCL2, CXCL4, CXCL7,
CXCL8 and CXCL12 and significant decreases in blood CCL4 in patients with depressive illness
compared to controls. Sensitivity analysis of studies with only physically healthy participants also
revealed significant increases in blood CCL3 and CCL11 in patients with depressive illness. However,
in this analysis blood CXCL4 did not retain significance. No chemokine retained significance when
considering only those studies with a comorbid physical illness. No other chemokine examined differed
significantly between depressed patients and controls (blood CCL5, CCL7, CCL15, CCL18, CCL24,
CCL27, CXCL1, CXCL9, CXCL10 and CSF CCL2, CXCL8, CXCL10). Analysis of the clinical utility of
CXCL8 found a negative predictive value (NPV) of 93.5% given a population prevalence of depressive
disorder of 10%. Overall these data provide significant evidence for an association between alterations
in circulating chemokine levels and depressive disorders, with evidence of possible clinical utility.
Future work should aim to examine these molecules in prospective longitudinal studies and to identify
putative mechanisms through which the chemokine family of molecules can drive depressive illness.
16. What is the evidence that Tetrabenazine is effective and well tolerated in
Huntington’s Disease?
Dr Baljinder Powar, Consultant in Neuropsychiatry, CAS Behavioural Healthcare, Nottinghamshire, and
MSc student, Clinical Neuropsychiatry, University of Birmingham.
Aim
The aim of this work was to review the literature on the effectiveness and tolerability of Tetrabenazine
in HD.
41
Methods
The search terms ‘Tetrabenazine’, ‘Huntington’s disease’ and ‘Huntington’s chorea’ were used.
Searches were conducted using Cinahl, Embase classic, Medline, Science Direct, PsycInfo, Proquest
Neurosciences, Pubmed and the Cochrane library. Grey literature was searched through google
scholar. Reference lists of pertinent articles were cross checked for inclusion.
381 articles were found through database searches, and a further 69 through google scholar. 285
remained after duplicate removal. 148 were excluded after title and abstract review.
The full text of the remaining 137 articles was reviewed, leading to the inclusion of 8 studies in the
results. At this stage articles were excluded if the number of patient subjects were less than 10, they
were systematic reviews, retrospective studies, conference proceedings, editorials and case series.
Results
8 studies were located for qualitative review. Two were double blind, one single blind and the
remaining open label. Sample size varied from 10-84.
Comments/Conclusions
7 of the 8 studies showed an improvement on Tetrabenazine, or deterioration off it depending on the
study design. The main adverse events reported were depression, sedation and akathisia across 5
studies. No adverse effects were reported in 3 studies.
The studies were of varying quality. Some used study subjects as their own controls.
More double blind placebo controlled trials are needed in this area. Future studies could employ a
head to head comparison of drugs to explore efficacy in chorea. Although of variable quality the studies
do point to the conclusion Tetrabenazine is effective for chorea. However, evidence of its usefulness
in cognitive and other functional aspects of the disease is less robust. The tolerability is under studied,
and more evidence is needed to explore impact on mood and cognition.
17. Vestibular dysfunction impairs visuospatial working memory independently of co-
morbid depression, anxiety, fatigue and sleep disturbance.
L J Smith, Dr D T Wilkinson and R Bicknell, The University of Kent; Dr M Bodani, Kent and Medway
NHS and Social Care Partnership Trust; Dr S Surenthiran, Medway NHS Foundation Trust.
Aims
Beyond the acute effects of vertigo and unsteadiness, disease or injury to the human vestibular system
is commonly accompanied by subjective reports of memory loss and problems concentrating. The co-
morbid presence of psychiatric illness, fatigue and difficulty sleeping, coupled with the lack of
comprehensive, validated neuropsychological assessment, has left questions unanswered about the
origin and nature of these underlying memory and attentional impairments.
42
Methods
100 patients diagnosed with primary vestibular disorder (mostly vestibular migraine) at their initial
neuro-otology appointment completed validated neuropsychological assessments of depression,
anxiety, depersonalisation, fatigue, sleep, memory and attention. Vestibular pathology was
characterised using a range of behavioural and physiological assessments.
Statistical analyses first calculated the prevalence of cognitive and other comorbid impairments. A
series of structural equation models then tested whether vestibular function exerted a direct influence
on cognition, or influenced performance indirectly via psychiatric, fatigue/ sleep mechanisms. All
models were adjusted for age-related effects on cognition.
Results
The majority of patients presented with a combination of anxiety, depression, sleep disturbance,
fatigue, working memory impairments and problems sustaining attention. Most important, balance
function, assessed via balance platform (a measure of unassisted posture), influenced visuospatial
memory performance independently of any age, psychiatric or fatigue/ sleep-related effects.
Conclusions
The present findings identify new clusters of impairment in vestibular patients and highlight a direct
effect of vestibular dysfunction on short-term visuospatial memory. We suggest that the most likely
anatomical route is via the vestibulo-thalamo-cortical pathway which passes vestibular signals to
several areas associated with working memory and visuospatial processing including the
hippocampus, parietal cortex, frontal cortex and basal ganglia. From a clinical perspective, the results
suggest that psychiatric treatments may do little to reduce co-morbid cognitive symptoms.
18. Review and redesign of the neuropsychiatric outpatient pathway to reduce non-
attendance rates
Charles Williams, Medical Student at Newcastle University, Dr Christopher Symeon, South London and
the Maudsley NHS Foundation Trust.
Aim: High rates of non-attendance to assessments have a profoundly negative impact on the
department’s capability to efficiently process new referrals which, in turn, increases patient waiting
times. This audit forms part of a wider quality improvement project in creation of a streamlined
pathway for new neuropsychiatry outpatient referrals with the aim of reducing the amount of time
between the receipt of referrals to initial assessment and also minimising non-attendance rates.
Methods: We carried out a retrospective review of case files for 30 patients who were yet to be seen
following their referral to neuropsychiatry outpatients at Kings College Hospital. We collected data on
the time taken to receive referrals, referral routes, time between receiving referrals and contacting
43
the patients and time between receiving referrals and initial assessment. We also collected data on
non-attendance rates, the reasons given for non-attendance and the action taken by staff following
non-attendances.
Results: We found that the documented initial assessment non-attendance rate was 85.7% (66.7%
DNA by client, 25% cancelled by client, 8.3% cancelled by SLaM). Following non-attendance 53.8%
of patients were offered a rescheduled assessment. The mean time between referrals being sent by
clinicians and being received by the neuropsychiatry team was 28 days (range = 0 – 86). Referrals
came from neurologists (70%) psychiatrists (17%) and GPs (13%). Mean time between receiving
referrals and contacting patients regarding their initial assessment was 56 days (range = 0 – 141).
Mean time between receiving referrals and initial assessment date was 68 days (range = 3 – 153).
Comments: Our findings highlight the need to address high non-attendance rates and increase
efficient processing of new referrals. We are currently implementing an innovative referral hub for
neuropsychiatry outpatients with the aim of reducing patient wait-times and non-attendance rates,
which will be audited over the next 6 months.
19. Whac-a-neuropsychiatry-mole: the problems of treating multiple comorbid
disorders
Professor Graeme Yorston, Consultant Forensic Neuropsychiatrist, Dr Sidney Munonyedi, Associate
Specialist, St Matthew’s Healthcare, Northampton.
Aims: It is not uncommon for patients to have multiple mental health and neuropsychiatric disorders
at the same time, yet most research relating to treatment and management in psychiatry is based on
less complex patients. The aim of this poster is to highlight the difficulties of trying to target one
disorder for treatment without destabilising other disorders.
Method: An anonymised single case description is used for which the patient has given consent.
Results: The diagnoses and treatment of Gilles de la Tourette syndrome, Hypersomnia with
somnambulism, obsessive compulsive disorder, social anxiety and rapid cycling bipolar affective
disorder will be discussed and how trying to improve the symptoms in one disorder by making changes
to a complex medication regime has often led to a worsening of other symptom clusters – which the
patient himself likened to the whac-a-mole fairground game.
Conclusion: The importance of considering drug and pharmacokinetic interactions in patients with
complex medication regimes is emphasised. It is hoped that this presentation will also remind
clinicians of the value of reading about and discussing complex cases, as quantitative research can
never address all of the issues in such cases.
44
20. Atypical cognitive and psychotic symptoms as an unusual initial presentation of
sporadic Creutzfeldt-Jacob disease
Dr Zehra Zaidi and Dr Owain Baker, Abertawe Bro Morgannwg University Health Board,
Swansea.
Aims A case is presented with the purpose of highlighting an important rare differential diagnosis of
memory impairment and psychosis, with the aim of promoting early investigation and diagnosis.
Case report A previously fit and well 59-year-old gentleman presented to memory clinic with sudden
onset confusion, behavioural changes and memory impairment. He rapidly became manic with
psychotic symptoms and required formal admission to a psychiatric hospital. Psychotropic medication
was ineffective in controlling his psychosis. Within days he deteriorated physically; he became ataxic,
incontinent and progressively akinetic. Global triphasic sharp waves were present on
electroencephalography (EEG) and diffusion weighted magnetic resonance imaging (MRI) of the brain
demonstrated cortical ribbon sign. Cerebrospinal fluid (CSF) analysis detected protein 14:3:3
confirming the working diagnosis of sporadic Creutzfeldt–Jakob disease (CJD). The patient was
palliated and died less than three months after the onset of symptoms.
Discussion Psychotic symptoms are not commonly seen in the early stages of sporadic CJD, which
more typically presents initially with rapid progressive dementia, myoclonus, visual disturbance and
other non-specific symptoms. Evidence is emerging that indicates early psychiatric symptoms are
more common than historically considered. This has raised the possibility of reviewing the diagnostic
criteria of CJD, which currently focuses heavily on neurological aspects of the disease. Case reports
such as this one can aid our understanding of the presentation and progression of sporadic CJD in the
hope of working towards a treatment.
Comments This presentation in memory clinic is unusual and clinicians should be mindful of atypical
cognitive and psychotic symptoms to ensure prompt investigation and diagnosis of CJD.
45
There will be a
BUSINESS MEETING
of the Neuropsychiatry Faculty
on Friday 15 September 2017, 13.20-14.00
21 Prescot Street, London E1 8BB
AGENDA
1. Welcome
2. To approve the previous minutes (attached)
3. Chair’s report (Prof E Joyce)
4. Vice-chair’s report (Dr M Bodani)
5. Finance report (Dr M Mohan)
6. Academic Secretary’s Report (Dr G El-Nimr)
7. Any other business
46
MINUTES
of the BUSINESS MEETING
of the Neuropsychiatry Faculty
held on 16 September 2016
Royal College of Psychiatrists
No Subject
1 Attendance
Prof Eileen Joyce (Chair)
Dr Monica Mohan (Finance Officer)
Dr George El-Nimr (Academic Secretary)
Approximately 100 members were in attendance.
Prof Joyce welcomed everyone to the meeting.
2 Minutes
The minutes of the meeting held on 10 September 2015 were approved as a
correct record.
Matters arising
Prof Besag reported that the article by the International Child
Neuropsychiatry in Epilepsy group had been published in the Epileptic
Disorder Journal. It would become accessible to all in May 2017.
It was noted that the chapters of the Neuropsychiatry textbook were
being finalised.
The Faculty would be updating its database on Neuropsychiatry services.
Prof Joyce would email members for data on their services.
3 CHAIR’S REPORT
3.1 Education and training
Prof Joyce reminded members that a few years ago the GMC had rejected
Neuropsychiatry’s application to become a sub-specialty. The GMC was now
encouraging specialties to set up post-CCT credentials.
The College was in the process of piloting a Liaison Psychiatry Credential. The
Faculty was hoping to set up a neuropsychiatry credential in the future, guided
by feedback from the liaison pilot. The College would help with setting this up
and the GMC would need to approve it. A credential would take a year to
complete in order to acquire neuropsychiatry competencies. The Faculty was
setting up a Faculty Curriculum Committee to work on this project, chaired by
Prof Joyce.
3.2 Working groups
Prof Joyce reported that the Faculty has a number of active working groups:
Childhood Onset Neuropsychiatric Conditions and Early Life Brain
Injury(CONCEBI), chaired by Dr Gul
Epilepsy: If anyone is interested in chairing this, please let Prof Joyce
know.
47
Movement disorders, chaired by Dr Sridharan
Neurorehabilitation, chaired by Dr Faruqui (The Complex Neurodisability
working group and Brain Injury working group were merged to create this
new group)
Sleep, chaired by Dr Selsick
3.3. Neuroscience project
Prof Joyce reported that the College had received £250K from the
Wellcome/Gatsby foundation to introduce more neuroscience into the core
curriculum. She is a member of the commission.
3.4 Commissioning
Prof Joyce reported that the Commissioning Reference Groups had recently
changed their structures. There are 3 CRGs relevant to Neuropsychiatry. Dr
Faruqui had been appointed to the Mental Health CRG. Dr Dilley had been
appointed to the Specialist Neurosciences and Complex Rehabilitation CRGs
within the Trauma group. They would both feed back to the Faculty executive.
3.5 Neurodevelopmental SIG
The College was in the process of setting up a new Neurodevelopmental special
interest group. All members would be offered the opportunity to join once it had
been set up.
4 Finance Officer’s report
Dr Mohan reported that the Faculty’s balance was £71K as of July 2016. The
Faculty would carry on supporting students and trainees by offering bursaries
and prizes. Funds would be available for outcome measures work and the
Neuropsychiatry Quality Network.
Dr Faruqui suggested setting up a Travelling Fellowship for Trainees.
5
5
Academic Secretary's report
Dr El-Nimr reported that the current conference was very successful and
oversubscribed.
The next residential conference would be held at the College on 14-15
September 2017. Dr El-Nimr asked for topic suggestions and the following were
suggested:
Non-epileptic attacks
Update on the neurology of epilepsy across the age-range
Stress
Neuroimaging for neuropsychiatrists
Cognition, schizophrenia
Abnormal Circadian rhythms
The next workshop day would be held in Cardiff on 27 January 2017 and
organised by the RCPsych Wales office. Details would be circulated shortly.
Dr El-Nimr reported that members of the Faculty were planning to submit
various sessions for the 2017 International Congress.
The Faculty gave a vote of thanks to Dr El-Nimr for his outstanding work as
Academic Secretary.
6 AOB
Prof Joyce thanked Dr Rafey as the outgoing Chair.
7 Future meetings
Business meeting during the Faculty conference, 14-15 September 2017, at the
College
48
NOTES
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
49
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
50
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
51
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
52
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
53
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
54
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
55
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
56
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
_________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
57
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
58
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
59
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
60
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
_________________________________________________________________
61
62
