Abstract Book
Organized by IMK Institute for medicine and communication Ltd
Neuroscience meets clinic
An update on headache
and orofacial pain
European Academy
of Craniomandibular Disorders
Annual Meeting
supported by the Swiss Society for the Study of Pain
September 18th – 20th, 2008
Zurich, Marriott Hotel
Welcome to Zurich
Dear Collegues
We are excited to invite you to the Annual Scientific Meeting of the European Academy
of Craniomandibular Disorders, which will be held in Zurich, Switzerland from September
18th - 20th, 2008. This meeting promises to be one of the most exciting meetings in recent
years on orofacial as well as head and neck pain, with an outstanding scientific program
and world’s leading experts sharing their thoughts, research and findings on these topics.
These will be discussed from a broad medical perspective so that this meeting should be
appealing not only to dentists and head and orofacial pain specialists but also to everyone
interested in pain therapy.
The meeting will provide a mix of basic and clinical science, starting on Thursday morning with
a symposium entitled “An update on head and neck pain”. The lecturers will lead us through
the latest information on the pathophysiology and therapy of primary headaches as well as
cervicogenic headache with new data on its relationship to whiplash and vertigo. The Friday
morning session “From the image of pain to pain imaging“ will be dedicated to the phenomenon of cortical reorganization and the discussion of some of the central processes and cortical
areas involved in pain modulation, while the afternoon session “Neuropathic orofacial pain“
will outline the genetic and neuropathic aspects of orofacial as well as persistent idiopathic
tooth pain. The lectures on Saturday morning session “From overuse to therapy“ will address
the question which is the optimal mechanical environment for the cartilage and the role that
mechanical overuse has in the etiology of muscle and joint disorders and how these disorders
should be managed. Finally, in the Saturday afternoon session “Orofacial pain therapy“ the
possibilities and limits of different orofacial pain therapy will be discussed.
We hope you can join us in Zurich for what will certainly be a stimulating, educational and
memorable event on orofacial pain and headache.
Cordially,
Sandro Palla
President Scientific Committee
2
Frank Lobbezoo
President European Academy of
Craniomandibular Disorders
Table of contents
4
General Information
6
Sponsors
Scientific Program
7
Thursday, September 18th
An update on head and neck pain
8
Friday, September 19th
Neuroscience meets clinic - From the image of pain to pain imaging
9
Saturday, September 20th
From overuse to therapy
10
Sunday, September 21st
EACD Candidate member presentations (only for EACD members)
Speakers / Abstracts
12
Thursday, September 18th
An update on head and neck pain
34
Friday, September 19th
Neuroscience meets clinic - From the image of pain to pain imaging
54
Saturday, September 20th
From overuse to therapy
76
Arrival
Supporting Instituts
3
General Information
Date
Congress venue
Homepage
September 18th - 20th, 2008
Zurich Marriott Hotel
Neumuehlequai 42
CH-8001 Zurich
Phone: +41 (0)44 360 70 70
Fax: +41 (0)44 360 77 77
Email: [email protected]
www.marriotthotels.com
www.imk.ch/eacd2008
Scientific Comittee
S. Palla, Zurich, CH, President
D. Ettlin, Zurich, CH
M. Farella, Zurich, CH
L. Gallo, Zurich, CH
Who should attend?
This meeting is designed for dentists, physicians, psychologists, physical therapists,
involved in the care of patients with head, neck, and orofacial pain.
Meeting Educational Objectives
To provide the meeting attendees with insight into
1.
2.
3.
4.
5.
6.
7.
8.
Administrative secretariat
Language
4
the pathophysiology and therapy of primary headaches as well as cervicogenic
headache
the phenomenon of cortical reorganization
the cortical mechanisms involved in pain modulation
the importance of genetic factors in orofacial pain
the mechanisms involved in neuropathic pain
possible mechanisms of persistent idiopathic tooth pain
the role of use and overuse in cartilage pathophysiology as well as muscle pain
the possibilities and limits of orofacial pain therapy
IMK - Institute for medecine and communication Ltd
Münsterberg 1
CH-4001 Basel
Phone: +41 (0)61 271 35 51
Fax: +41 (0)61 271 33 38
Email: [email protected]
www.imk.ch
The congress will be held in English with no simultaneous translation.
General Information
Credits
Swiss Society for Neurology: Thursday = 6 Credits
Friday = 5 Credits
Saturday = 4 Credits
Swiss Society for Anasthesiology: 6.5 SGAR-Credits
6 SGAR-Credits
Swiss Society for Rheumatology: accepted
Swiss Dental Societies:
Thursday = 6h
Friday = 8h
Saturday = 7.5h
Annual Meeting
2009
Registration
The meeting will be in Praia do Porte, Bahia, Brasil, August 26th - 30th, 2009.
Please find further information on:
www.icot2009.com
Days
1 day
2 days
3 days
EACD/SSSP members
230* 430* 570*
non EACD/SSSP members
260* 480* 620*
full-time university assistants
180* 320* 460*
*All prices stated in Euro.
Participation fees incl.: all scientific sessions, coffee and lunch breaks, congress certificate
and congress bag, welcome reception on Thursday.
Cancellation Policy
In the event your enrollment must be cancelled, your tuition less a 30,-€ administrative
fee will be refunded if we are notified by August 15th, 2008.
No refunds will be made after that date.
Social Events
Welcome drink
Gala dinner
Speakers dinner
All congress paricipants are invited to the welcome drink on
Thursday, September 18th, 2008, 18.00h - 20.00h, Zurich Marriott Hotel
Welcome address: Regierungsrätin R. Aepple, Zurich
sponsored by City Zurich
Friday, September 19th, 2008, from 19.30h,
Zunfthaus zur Meisen, Münsterhof 20, 8001 Zurich
Costs: 75,-€ per Person
supported by UCB Pharma AG
Saturday, September 20th, 2008, from 19.00h,
Restaurant Sinfonia, Bahnhofstrasse 29, 8703 Erlenbach
For invited guests only.
5
Sponsors
We would like to thank the following companies and instituts for their generous
support of our conference.
Main Sponsor
Sponsors
6
Scientific Program
Thursday, September 18th
An update on head and neck pain
Session 1: Tension Type Headache / Migraine
Chair: E. Alon, Zurich, CH
10:00-10:10
Opening remarks
10:10-10:30
The trigeminal complex symptoms of headache, facial pain, earache and neck pain
D. Ettlin, Zurich, CH
10:30-11:00
Pathophysiology of tension-type headache: an update
L. Bendtsen, Copenhagen, DK
11:00-11:30
Pathophysiology of migraine: an update
M. Ashina, Copenhagen, DK
11:30-12:00
Behavioral Aspects of Migraine
R. Agosti, Zurich, CH
12:00-12:30
Orofacial primary headaches
P. Sandor, Zurich, CH
12:30-13:00
Round table discussion
Chair: U. Büttner, Aarau, CH
13:00-14:00
Lunch
14:00-14:30
Modern treatment of trigeminal autonomic cephalgias
A. May, Hamburg, D
14:30-15:00
Neurostimulation in intractable headaches
J. Schoenen, Liège, B
Session 2: Cervicogenic Headache
Chair: M. Sturzenegger, Bern, CH
15:00-15:30
Cervicogenic headache: from nosography to clinical picture
F. Antonaci, Pavia, IT
15:30-16:00
Coffee break
16:00-16:30
Cervicogenic headache after whiplash injury
T. U. Schreiber, Rheinfelden, CH
16:30-17:00
Cervical and masticatory dysfunctions and their relationship with vertigo
D. Straumann, Zurich, CH
17:00-17:30
Round table discussion
Chair: H. Isler, Zurich, CH
18:00-20:00
Welcome drink
sponsored by City Zurich
7
Scientific Program
Friday, September 19th
Neuroscience meets clinic - From the image of pain to pain imaging
Session 1
Chair: P. Kemppainen, Turku, FI, I. Eli, Tel Aviv, IL
08:45-09:00
Congress opening: Introductory remarks
09:00-09:30
Cortical neuroplasticity: the musician’s brain
L. Jäncke, Zurich, CH
09:30-10:00
Teeth and the brain
D. Ettlin, Zurich, CH
10:00-10.30
Coffee break
supported by Kaladent AG
10:30-11:00
Pain modulation by anticipation
C. Porro, Modena, IT
11:00-11:30
Can behavioral therapy influence neuromodulation?
D. Linden, Gwynedd, UK
11:30-12:00
Neurobiological mechanisms of the placebo effect
F. Benedetti, Turin, IT
12:00-12:30
Round table discussion
Chair: P. Pionchon, Clermont-Ferrand, F
12:30-13:30
Lunch in the exhibition
supported by BIOMET 3i
Session 2: Neuropathic orofacial pain
Chair: C. Bodéré, Brest, F, J. De la Hoz, Madrid, ES
8
13:30-14:00
The role of genetic factors in orofacial pain
C. Stohler, Baltimore, USA
14:00-14:30
Can animal experiments on tooth deafferentation tell us something about atypical odontalgia?
E. C. Henry, Saint Louis, USA
14:30-15:00
Can herpes tell us something about neuropathic dental pain?
C. Miller, Lexington, USA
15:00-15:30
Coffee break
15:30-16:00
Quantitative neurosensory testing: A must for the diagnosis of orofacial neuropathic pain?
P. Svensson, Aarhus, DK
16:00-16:30
Post-implant pain. How to diagnose, what to do
G. Heir, Newark, USA
16:30-17:00
Round table discussion
Chair: J. Türp, Basel, CH
17:15-18:30
EACD General Assembly
from 19:30
Gala dinner at the Zunfthaus zur Meisen, Zurich
Scientific Program
Saturday, September 20th
From overuse to therapy
Session 1
Chair: M. Steenks, Utrecht, NL, B. Wenneberg, Gothenburg, SE
09:00-09:30
From TMJ biomechanics to cartilage mechanobiology
L. Gallo, Zurich, CH
09:30-10:00
What is the optimal mechanical environment for the cartilage?
P. Torzilli, New York, USA
10:00-10:30
The clinch about clenching
M. Farella, Zurich, CH
10:30-11:00
Coffee break
11:00-11:30
Overuse injuries as cause of muscle and tendon pain
A. Klipstein, Zurich, CH
11:30-12:00
Arthrogenous and myogeneous pain. Different pathologies, different therapies?
A. De Laat, Leuven, B
12:00-12:30
Round table discussion
Chair: F. Lobbezoo, Amsterdam, NL
12:30-13:30
Lunch
Session 2: Orofacial pain therapy
Chair: A. Michelotti, Napoli, IT , J.-P. Goulet, Québec, CA
13:30-14:00
The empathic brain: how, when and why?
S. Leiberg, Zurich, CH
14:00-14:30
Spinal GABAA receptor subtypes: new targets for the treatment of chronic pain?
H-U. Zeilhofer, Zurich, CH
14:30-15:00
Does topical capsaicin application have a role in the treatment of neuropathic pain?
M. Petersen, Mannheim, D
15:00-15:30
Coffee break
15:30-16:00
Limitations of pharmacotherapy: behavioral approaches to chronic pain
H. Flor, Mannheim, D
16:00-16:30
Coping, acceptance and orofacial pain: The outcome matters
P. Nilges, Mainz, D
16:30-17:00
TMD therapy: Efficacy or effectiveness? Or does it happens in the patient’s mind?
G. Mauro, Mantova, IT, G. Macaluso, Parma, IT
17:00-17:30
Round table discussion
Chair: A. De Laat, Leuven, B
End of congress
from 19:00
Speakers dinner
For invited guests only
9
Scientific Program
Sunday, September 21st
EACD Candidate member presentations (only for EACD members)
10
09:00-11:00
Oral Presentations
09:00-09:15
Effects of experimental jaw muscle pain on occlusal contacts
S. Catapano, N. Mobilio, IT
09:15-09:30
Temporomandibular disorders and orofacial pain: a competence based curriculum for the
physiotherapist in the Netherlands
A. de Wijer, C. van Maanen, M. H. Steenks, NL
09:30-09:45
Signs and symptoms of Temporomandibular Disorders and oral parafunctions among children
C. Goldsmith, A. Emodi-Perlman, P. Rubin-Friedman, E. Winocur, IL
09:45-10:00
Effects of prolonged chewing upon the reduction of anterior disc displacement of the
temporomandibular joint
S. I. Kalaykova, M. Naeije, F. Lobbezoo, NL
10:00-10:15
TMJ sound analysis with commercially available instrumentation and its discriminative
value in the internalderangements
A. Kanellopoulou, B. Droukas, GR
10:15-10:30
Single-needle arthrocentesis plus hyaluronic acid injections in the treatment of TMJ
osteoarthritis: preliminary data in the short-term period
D. Manfredini, L. Guarda-Nardini, IT
10:30-10:45
Relationship between craniofacial morphology and craniomandibular disorders:
a literature review
C. Micarelli, G. Calesini, IT
10:45-11:00
Treatment of Disc Displacement with Reduction by Restoring Overall Vertical Dimension
M. Sommerville, UK
Scientific Program
Sunday, September 21st
EACD Candidate member presentations (only for EACD members)
11:00-11:30
Poster Presentation
Effect of clonidine on sleep arousal pressure in sleep bruxism patients
M. C. Carrà, P. H. Rompré, G. M. Macaluso, N. Huynh, A. Smerieri, L. Parrino, G. Terzano,
G. J. Lavigne, IT
Oral malignancy masquerading as TMD
M. Di Giosa, D. Falace, L. Cunningham, USA
Time-frequency analysis of rhythmic masticatory muscle activity
M. Farella, L. M. Gallo, IT, CH
Prediction of Pain after Oral Surgery by Preoperative Nociceptive Responses to Cold
Stimulation
N. Mobilio, S. Catapano, IT
Saliva and anxiety in TMD patients: a preliminary study
M. Papa, D. Costanzo, G. Falsi, C. Di Paolo, IT
Reliability of an occlusal and non-occlusal tooth wear grading system: chair-side use
versus dental cast assessment
P. Wetselaar, F. Lobbezoo, M. Koutris, C. M. Visscher, M. Naeije, NL
11:30-12:00
Research Committee discussion
11
Speakers / Abstracts
Dominik A. Ettlin
MD and med. dent.
Zentrum für Zahn-, Mundund Kieferheilkunde
Universität Zürich
Plattenstrasse 11
CH-8032 Zürich
T: +41 446 34 32 54
Email: [email protected]
Graduate Education:
• M.D.: Medical School, Univ. of Berne, CH 1982-89
• D.M.D.: School of Dental Medicine, Univ. of Pennsylvania, Philadelphia, USA 1992-94
Academic Appointments:
Assistant Professor and Director, Division of Oral Diagnosis / Oral Medicine, Northwestern
University Dental School, Chicago, USA 1996-2001
Oberassistent:
Clinic for Masticatory Disorders, Removable Prosthodontics and Special Care,
Center for Dental and Oral Medicine, University of Zurich, CH 2001-2005
Klinischer Dozent and Co-Director:
Interdiscipilinary Orofacial Pain Consulting Service
Clinic for Masticatory Disorders, Removable Prosthodontics and Special Care,
Center for Dental and Oral Medicine, University of Zurich, CH 2005-present
12
Speakers / Abstracts
The trigeminal complex symptoms of headache, facial pain, earache and neck pain
Thursday, September 18th
10:10-10:30
Patients evaluated for pain in the distribution of the three divisions of the trigeminal nerve
report distinctive pain histories. On specific questioning, symptoms for specific diagnoses
such as migraine, idiopathic persistent orofacial pain, ear and neck pathologies overlap and
thus complicate the diagnostic process. In this presentation, video recordings of patients
fulfilling diagnostic criteria for primary headaches according to IHS-II classification, but
associated with unusual pain locations, will be discussed.
13
Speakers / Abstracts
Lars Bendtsen
Senior consultant, MD, PhD, Dr Med Sci
Danish Headache Center
Department of Neurology
Glostrup Hospital
University of Copenhagen
DK-2600 Glostrup
Lars Bendtsen is a senior consultant at the Danish Headache Center and at the
Department of Neurology, Glostrup Hospital, University of Copenhagen. Lars Bendtsen has
published more than 90 scientific papers and book chapters. His main research interests
include the pathophysiological mechanisms underlying tension-type headache, in particular
central sensitization, and the treatment of tension-type headache.
14
Speakers / Abstracts
Pathophysiology of tension-type headache: an update
Thursday, September 18th
10:30-11:00
Tension-type headaches (TTH) are very prevalent and responsible for substantial costs both
for the individual and the society. In contrast with migraine no significant improvement
in treatment possibilities has been seen in TTH within the last decades. This may partly be
attributed to the fact that the understanding of TTH pathophysiology is less complete than
that of migraine. Fortunately, we have gained much new knowledge on pathophysiological
aspects of TTH within the last decade, and we are now beginning to understand some of
the complex mechanisms leading to this prevalent disease. This is the first step towards the
development of more effective treatments. Previously, the research into the mechanisms
leading to TTH mainly focused on muscular factors. More recently it has become clear that
central factors play a crucial role in particular in the more severe forms of the disorder.
The lecture will cover the most recent and exciting advances in the understanding of the
mechanisms leading to TTH, and discuss how these findings may lead to improved treatment
of this prevalent disorder.
15
Speakers / Abstracts
Messoud Ashina
Prof.
Danish Headache Center and
Department of Neurology
Glostrup Hospital
University of Copenhagen
DK-2600 Gloostrup
Copenhagen
Denmark
Email: [email protected]
Dr. Messoud Ashina is associate professor at the Department of Neurology, Glostrup Hospital,
and University of Copenhagen. Dr. Ashina has published more than 50 scientific papers
and book chapters. His main research interest includes experimental headache models and
functional neuroimaging.
16
Speakers / Abstracts
Pathophysiology of migraine: an update
Thursday, September 18th
11:00-11:30
Migraine is the most prevalent neurological disorder with an estimated 43 million
sufferers in Europe. It is a very painful condition that often leads to absenteeism from
work and more often to considerably decreased efficiency at work. The estimated cost of
migraine in Europe is 27,000 million Euros per year which, among the neurological disorders, ranks third after dementia and stroke. Migraine is considered to be a disorder of
neurovascular transmission without structural lesions. It is still uncertain, however, from
where the painful impulses in the trigeminal nerve arise. It has been suggested that the
problem is primarily one of CNS disorder and no abnormal peripheral input. However, there
is abundant evidence to refute this hypothesis. A solid body of evidence shows that the
input arises from perivascular sensory nerve terminals of the trigeminal nerve. In my lecture
I shall review the most important recent findings in human and animal studies.
17
Speakers / Abstracts
Reto Agosti
MD
Forchstrasse 424
CH-8702 Zollikon
T: +41 (0)43 499 13 30
Fax +41 (0)43 499 13 39
Email: [email protected]
www.kopfwww.ch
Reto Agosti studied Medicine at the University of Zurich and specialized in Neurology
at the same University in 1999. The period between 1991 and 1999 was characterized
by fellowships at several Universities in the USA (Lemuel Shattuk Hospital Boston; Mont
Sinai Hospital, New York; Boston University; Massachusetts General Hospital and Howard
Medical School, Boston). In 1999 he returned to the University Hospital Zurich as head
of the Headache and Pain Unit of the Neurology Departement. In 2002 he founded the
Headache Center of the Hirslanden Klinik in Zurich where he is currently working.
He published several papers in peer reviewed jourtnals and his main research interest is
the headache pharmacotherapy.
18
Speakers / Abstracts
Behavioral Aspect of Migraine
Thursday, September 18th
11:30-12:00
Migraine is known today a as a very special headache syndrome that includes mostly
temporal dysfunction of various neurological subsystems, such as pain regulation, autonomic and vegetative functions and, last but not least, dysfunction of the cerebral cortex,
leading to auras and various cognitive/behavioral phenomena. Neurological dysfunction
that can be clearly related to distinct cortical areas are usually understood as migraine
auras where positive and negative phenomena can be distinguished. Examples of positive
phenomena are zig-zag lines, scintiallation, tingeling and others. Negative phenomena are
typically blind spots, scotomas, numbness. It seems that when cortical migraine changes occur in other than visual and sensory areas a number of often rare, but nevertheless
distinct symptoms may occur. My presentation will focus on these experiences such as
aphasia, transient global amnesia, concentration difficulties, body dysmorphic experiences,
prosopagnosia etc. When systematically asked for these rare “auras” or behavioural symptoms are substantially more frequent then expected and reported in the literature. It is
important for the patient to discuss these phenomena with their physicians since many
patients are rather scarred by the occurrence of these symptoms. In addition, they an great
light on the pathophysiology of the highly complex disorder called migraine.
19
Speakers / Abstracts
Peter Sandor
PD Dr. med.
Neurologische Klinik
UniversitätsSpital Zürich
Frauenklinikstrasse 26
CH-8091 Zürich
T: +41 (0)44 255 55 60
Email: [email protected]
www.neurologie.usz.ch
Peter S. Sándor, MD, studied medicine in Ulm (Germany), Southampton (UK) and Zurich
(Switzerland). He specialized in Neurology at the University Hospital Zurich, with research
fellowships in the University of Liège, Belgium (Prof. Schoenen) and at the Institute of
Neurology, Queen Square, in London (Prof. Goadsby). Currently, he is heading the Headache and Pain Unit at the University Hospital in Zurich. His main research interests are the
pathophysiology of migraine, and the pharmacotherapy of headache and pain.
20
Speakers / Abstracts
Orofacial primary headaches
Thursday, September 18th
12:00-12:30
Background: Primary Headache syndromes like migraine and cluster headache are
described, according to International Headache Society criteria (ICHD-II, 1), with pain in
frontotemporal, orbital or supraorbital regions. Patients with “atypical dental pain” with
features otherwise reminiscent of primary headache syndromes presented to our clinics or
emergency units, some of them with a history of dental procedures without benefit.
Cases: We describe patients with pain manifestations in the second and/or third division
of the trigeminal nerve, but otherwise fulfilling ICHD-II criteria, for migraine (two patients,
2), and cluster headache (two patients, 3). Interestingly, all responded to pharmacotherapy
targeted at the suspected underlying primary headache syndrome.
Conclusions: Our patients suggest that otherwise typical primary headache syndromes can
present with a pain localization in the 2nd and 3rd rather than the 1st division of the
trigeminal nerve. This can be explained by the neuroanatomical convergence of trigeminal
with cervical afferents in the nucleus caudalis. These patients need to be recognized, also in
the dental context, as the appropriate treatment seems to be pharmacological rather than
dental.
References
1. International Classification of Headache Disorders, 2nd edition, 2004
2. Gaul et al. Orofacial migraine. Cephalalgia 2007
3. Gaul et al. Orofacial cluster headache. Cephalalgia 2008
21
Speakers / Abstracts
Arne May
PD MD
Institut für Systemische
Neurowissenschaften
Universitätsklinikum Hamburg-Eppendorf
Martinistrasse 52
D-20246 Hamburg
T: +49 404 280 391 89
Email: [email protected]
Arne May studied medicine at the University of Göttingen where he received his final degree
in 1991. From 1991 to 1995 Assistant and Registrarship at the Dpt. of Neurology, University
of Essen. 1996 to 1998 Postdoc Fellowship at the Institute of Neurology, London (Prof. PJ
Goadsby). 1998 to 1999 return to the University of Essen, Dpt. of Psychiatry. 1999 to 2004
consultant at the Dpt. of Neurology of the University of Regensburg. 2004 to 2005 Dpt.
of Neurology, University of Hamburg. Currently associated Professor of Neurology, Deputy
Director of the Dpt. of Systems Neuroscience and head of the headache outpatient clinic,
Dept. of Neurology, University of Hamburg. President of the DMKG.
Several publications in peer reviewed journals.
Modern treatment of trigemino-autonomic cephalgias
Thursday, September 18th
14:00-14:30
Following the IHS criteria, primary short-lasting headaches broadly divide themselves into those associated with autonomic symptoms, so called trigeminal autonomic cephalgias (TAC’s),
and those with little autonomic syndromes (1). The TAC’s include cluster headache, paroxysmal
hemicranias, and a syndrome called SUNCT (short lasting unilateral neuralgic cephalgias with
conjunctival injection and tearing). In these syndromes the half-sided head pain and cranial
autonomic symptoms are prominent. The paroxysmal hemicranias have, unlike cluster headaches,
a very robust response to indomethacin, leading to a consideration of indomethacin-sensitive
headaches. Despite the diagnostic challenges, the short- lasting primary headaches are important
to recognize because of their excellent but highly selective response to treatment.
The clinical picture
In 1997 Peter Goadsby and Richard Lipton documented a nosological analysis and definition of a
group of short-lasting headache syndromes (2). These paroxysmal hemicranias are characterized
by frequent short-lasting attacks of unilateral pain usually in the orbital, supraorbital or temporal region. The pain is severe and associated with autonomic symptoms such as conjunctival
injection, lacrimation, nasal congestion, rhinorrhoea, ptosis or eyelid oedema. Goadsby and Lipton
divided these short-lasting primary headache syndromes into those with marked autonomic activation and those without autonomic activation. The former group comprise chronic and episodic
paroxysmal hemicrania, SUNCT syndrome and cluster headache. These headache syndromes are
compared with other short-lasting headache disorders, such as hypnic headache, and a chronic
headache syndrome with milder autonomic features such as hemicrania continua. Idiopathic
stabbing headache, cough headache, exertional headache, sexual headache and trigeminal
neuralgia are not part of these syndromes as these short-lasting disorders have no autonomic
component (1,3).
22
Speakers / Abstracts
Prominent autonomic symptoms
Episodic Cluster Headache Chronic Cluster Headache
Episodic Paroxysmal Hemicrania
Chronic Paroxysmal Hemicrania
SUNCT Syndrome
Cluster TIC Syndrome
Sparse or no autonomic features
Trigeminal Neuralgia
Idiopathic stabbing headache
Cough Headache
Benign exertional headache
Headache associated with sexual activity
Hypnic Headache
Table1: primary short lasting headaches (after Goadsby and Lipton (2))
Episodic and Chronic Cluster Headache
Despite the fact, that the clinical picture of cluster headache is characteristic, making it probably the easiest idiopathic headache syndrome to diagnose, patients are often misdiagnosed
and undertreated (4). Cluster headache is characterized by recurrent, strictly unilateral attacks of
headache of great intensity and brief duration. The pain of cluster headache is perhaps the most
severe known to humans with female patients describing each attack as being worse than childbirth. The pain attacks are accompanied by local (ipsilateral) signs of autonomic dysfunction such
as ipsilateral parasympathetic (rhinorrhoe, lacrimation, impaired sweatening) and sympathetic
(miosis, ptosis) symptoms (5).
The prevalence is approximately 0.1 %, mostly affecting men. The attacks occur regularly and their
timing seems to be related to the sleep-wake cycle. Attacks most commonly appear in cluster
periods (episodic cluster headache) lasting from a week to several months. The periods are separated by clinical remissions of at least 2 weeks. About 15-20 % of patients suffer from chronic
symptoms (without remissions = chronic cluster headache). The most salient feature of cluster
headache is the reported seasonal variation and the clockwise regularity of the headache attacks.
Consequently a whole range of circadian irregularities have been reported in cluster headache
patients (6). The medical treatment of cluster headache includes both acute therapy aimed at
aborting individual attacks and prophylactic therapy aimed at preventing recurrent attacks during
the cluster period.
Acute therapy. Because of the rapid onset and short time to peak intensity of cluster headache
pain, fast-acting symptomatic therapy is needed. Oxygen (15min, 100%, 15L/min), subcutaneous
sumatriptan (6mg), and intramuscular dihydroergotamine (2mg) provide the most rapid, effective,
and reliable relief for cluster headache attacks.
Preventive therapy. The importance of an effective preventive regimen during cluster periods cannot be overstated. During cluster periods, individual cluster attacks often occur daily for several
weeks to months. Since many patients have more than one attack a day (up to eight), treating
only the acute pain may result in overmedication or toxicity, and may unnecessarily prolong suffering. Corticosteroids (prednisone and dexamethasone) are the fastest-acting preventive agents.
Continued on next page
23
Speakers / Abstracts
Treatment is usually initiated with 60-80mg of prednisone per day for 2-3 days followed by 10mg
decrements every 2-3days. Dexamethasone at a dose of 4mg twice a day for 2 weeks followed by
4mg a day for 1 week has also been shown to be effective. Corticosteroids are primarily useful for
inducing a rapid remission in patients with episodic cluster headache, although long-term use of
corticosteroids must be resisted. Verapamil is often used as the first preventive therapy for both
episodic and chronic cluster headache. In doses up to 360mg it is generally well tolerated and can
be used safely in conjunction with sumatriptan, ergotamine, corticosteroids, and other preventive
agents. The initial starting daily dosage is 80mg three times a day or 240mg of sustained release
a day. Dosages employed range from 240g to 720g a day in divided dosages. Lithium carbonate
therapy is effective for cluster headache based mainly on open clinical trials. The initial starting
daily dosage is either 300mg three times a day or 450mg sustained release. Most patients will
benefit from dosages between 600g and 900mg a day. Methysergide is an effective preventive drug for the treatment of cluster headache. The daily dose is usually 2mg in three divided
dosages, but up to 12mg may be used if tolerated. Methysergide should be stopped after a treatment periode of 4-6 months. Topiramate and Gabapentin , are associated with rapid improvement
in recent studies.
Paroxysmal Hemicrania
Paroxysmal hemicrania is characterized by short bouts of severe unilateral pain in the area of
the orbit and temple. The characteristic attack frequency is >5 per day, but there are reports of
between 1 and 40 attacks per day. The age of onset is usually in the twenties with a 3:1 female
to male ratio. A chronic and episodic form that has been described is similar to cluster headache
and reflects a distinctive temporal pattern (7). The pain is associated with at least one autonomic
symptom such as ipsilateral conjunctival injection and tearing with nasal congestion and rhinorrhea. Treatment. Almost all reported cases respond to treatment with indomethacin, but respond
poorly to other treatments including other nonsteroidal anti-inflammatory drugs. In fact, the IHS
criteria require, that the attacks should rapidly resolve following treatment with indomethacin.
The dose is up to 150 mg/day orally and the response is usually within days of initiating an adequate dose. The standard treatment for CPH is indomethacin in a dose of 25 mg t.d.s., increasing
to 50 mg t.d.s. after a week if there is no response. Occasional patients require higher doses or
slow-release indomethacin preparations at night to treat break through headaches. In some
patients gastrointestinal side-effects require treatment with gastro-protective agents, such a
histamine-2 or proton pump blockers.
SUNCT-Syndrome
SUNCT is among the rarest idiopathic headache syndromes characterized by an extremely high
frequency of attacks (up to 200 attacks/day) with less severe pain but marked autonomic activation during attacks. Even though there are marked differences in the clinical pictures, such as the
frequency and duration of attacks and the different approach to treatment, many of the basic features of SUNCT, such as the episodic character, autonomic symptoms and unilaterality, are shared
by other headache types, such as cluster headache and CPH. This suggests a pathophysiological
similarity to these syndromes and prompted the suggestion to unify them on clinical grounds as
trigeminal-autonomic cephalgias (TAC‘s). The paroxysms of pain usually last between 5 and 250 s
although longer duller interictal pains have been recognized. Patients may have up to 30 episodes
per hour although more usually they would have 5–6 per hour. The frequency may also vary in
bouts. The conjunctival injection seen with SUNCT is often the most prominent autonomic feature
and tearing may also be very obvious.
Treatment. Unfortunately SUNCT syndrome is very hard to treat. Unlike CPH and EPH, which are
highly responsive to indomethacin, SUNCT is remarkably refractory to most treatments, though
recent reports point towards a good response to Lamictal. It is probably justified to use gabapentin
and topiramat as second line therapy.
24
Speakers / Abstracts
References
1. Headache Classification Committee of the International Headache Society: The International Classification of Headache Disorders, 2nd edition. Cephalalgia 2004; 24(Supplement 1):1-160
2. Goadsby PJ, Lipton RB: A review of paroxysmal hemicranias, SUNCT syndrome and other
short-lasting headaches with autonomic feature, including new cases.
Brain 1997; 120(Pt 1):193-209
3. Olesen J, Tfelt-Hansen P, Welch K: The Headaches. Philadelphia,
Lippincott Williams and Wilkins, 1999
4. May A: Cluster headache: pathogenesis, diagnosis, and management.
Lancet 2005; 366(9488):843-55
5. Sjaastad O (ed): Cluster Headache Syndrome. London, W B Saunders Company Ltd, 1992
6. Goadsby PJ: Pathophysiology of cluster headache: a trigeminal autonomic cephalgia.
Lancet Neurol 2002; 1(4):251-7
7. Sjaastad O, Apfelbaum R, Caskey W, Christoffersen B, Diamond S, Graham J, Green M,
Horven I, Lund-Roland L, Medina J, Rogado S, Stein H: Chronic paroxysmal hemicrania (CPH).
The clinical manifestations. A review. Ups J Med Sci Suppl 1980; 31:27-33
8. Goadsby PJ, Edvinsson L: Human in vivo evidence for trigeminovascular activation in
cluster headache. Neuropeptide changes and effects of acute attacks therapies.
Brain 1994; 117(Pt 3):427-34
9. Ekbom K: Patterns of cluster headache with a note on the relations to angina pectoris and
peptide ulcer. Acta Neurol. Scand. 1970; 46:225-237
10.Leone M, Patruno G, Vescovi A, Bussone G: Neuroendocrine dysfunction in cluster headache.
Cephalalgia 1990; 10(5):235-9
11.Waldenlind E, Gustafsson SA, Ekbom K, Wetterberg L: Circadian secretion of cortisol and
melatonin in cluster headache during active cluster periods and remission.
J Neurol Neurosurg Psychiatry 1987; 50:207-213
12.May A, Ashburner J, Buchel C, McGonigle DJ, Friston KJ, Frackowiak RS, Goadsby PJ:
Correlation between structural and functional changes in brain in an idiopathic
headache syndrome. Nat Med 1999; 5(7):836-8.
13.Sprenger T, Boecker H, Tolle TR, Bussone G, May A, Leone M: Specific hypothalamic activation
during a spontaneous cluster headache attack. Neurology 2004; 62(3):516-7
14.May A, Bahra A, Buchel C, Turner R, Goadsby PJ: Functional magnetic resonance imaging in
spontaneous attacks of SUNCT: short-lasting neuralgiform headache with conjunctival
injection and tearing. Ann Neurol 1999; 46(5):791-4
15.Sprenger T, Valet M, Platzer S, Pfaffenrath V, Steude U, Tolle TR: SUNCT:
bilateral hypothalamic activation during headache attacks and resolving of symptoms
after trigeminal decompression. Pain 2005; 113(3):422-6
16.Matharu MS, Cohen AS, McGonigle DJ, Ward N, Frackowiak RS, Goadsby PJ:
Posterior hypothalamic and brainstem activation in hemicrania continua.
Headache 2004; 44(8):747-61
17.Matharu MS, Good CD, May A, Bahra A, Goadsby PJ: No change in the structure of the brain
in migraine: a voxel-based morphometric study. Eur J Neurol 2003; 10(1):53-7.
18.Leone M, Franzini A, Bussone G: Stereotactic stimulation of posterior hypothalamic gray
matter in a patient with intractable cluster headache. N Engl J Med 2001; 345(19):1428-9.
19.Leone M, Franzini A, Broggi G, May A, Bussone G: Long-term follow-up of bilateral
hypothalamic stimulation for intractable cluster headache. Brain 2004; 127(Pt 10):2259-64
20.Schoenen J, Di Clemente L, Vandenheede M, Fumal A, De Pasqua V, Mouchamps M,
Remacle JM, de Noordhout AM: Hypothalamic stimulation in chronic cluster headache:
a pilot study of efficacy and mode of action. Brain 2005
25
Speakers / Abstracts
Jean Schoenen
Prof.
Neurobiology Research Center CNCM
Liège University
CHU-Sart Tilman, T4 (1+). B36
B-4000 Liège
T: +32 (0)43 66 51 90
Email: [email protected]
Qualifications :
• M.D. (Liège University - 1972)
• Certificate in Clinical Neurophysiology (Harvard Medical School - 1976)
• Residency in Neuropathology (Harvard Medical School - 1977)
• Internal Medicine (Liège University - 1978)
• Neurologist (1979)
• Agrégé de l‘Enseignement Supérieur (PhD) (1981)
Present Positions:
• Full Professor of Functional Neuroanatomy – Liège University (1998-..)
• Clinical Professor of Neurology (1996)
Coordinator of the Headache Research Unit – Dept of Neurology. Liège University
• Past-President and Secretary General (2002-..) Belgian Neurological Society
• President- Belgian Brain Council (2005-..)
• Past-President and Chairman Scientific Subcommittee-International Headache Society IHS (2001-..)
Past Positions:
• Research Director National Fund for Scientific Research Belgium (1990-1998)
• Maître de Conférences University of Liège (1987-1998)
• President (2000-2002) Belgian Neurological Society
• Chairman Research Group on Headache – World Federation of Neurology (WFN)
(2001-2005)
• Chairman Department of Preclinical Sciences-Morphology-Immunology. ULg (2002-2005)
Research Interests:
• Pathophysiology and therapy of migraine and headaches: clinical and animal research
• Plasticity and regeneration in the adult CNS: model of spinal cord injury and effects of
cellular and molecular therapies
Scientific Prizes:
• 14 (e.g. Cumings Lecture, Harold G. Wolff Award, Belgian Neurological Society,
Royal Academy of Medicine, MacDonald Critchley lecture, Cluster Headache Award ...).
26
Editorships:
• Associate Editor: Cephalalgia
• Past Associated Editor: Pain (Headache Section)
• Editorial Board: European Journal of Neurology, Functional Neurology,
New Trends in Clinical Neuropharmacology, Acta Neurologica Belgica,
Revue Médicale de Liège
• Ad Hoc reviewer: Annals of Neurology, Neuroscience Letters, Neuroscience, Neurology,
Stroke, Journal of Neuroscience Methods, Revue Neurologique, European Neurology,
Journal of Neurology, Clinical Neurophysiology, Biochemical Pharmacology,
Encyclopedia of Human Biology, Journal of Internal Medicine, Acta Clinica Belgica,
Medical Principles and Practice, Headache, Journal of Orofacial Pain, European Heart Journal,
Behavior Research Methods Instruments and Computers, European Journal of Neuroscience.
Speakers / Abstracts
Publications
Total : 749
• 331 articles; - 2 books; - 80 book chapters; - 336 abstracts
5 representative publications
• The effectiveness of high-dose riboflavin in migraine prophylaxis: results from a randomised controlled trial. Neurology 1998, 50: 466-470. (IF : 4.781)
• Effects of repetitive transcranial magnetic stimulation on visual
evoked potentials in migraine. - Brain 2002, 125, 1-11. (IF : 8.201)
• Retrograde Reactions of Clarke ’s Nucleus Neurons after Human Spinal Cord Injury.
Annals of Neurology 2003;54:534 –539 (IF. : 8.603)
• Delayed GM-CSF treatment stimulates axonal regeneration and functional recovery in
paraplegic rats via an increased BDNF expression by endogenous macrophages.
The FASEB Journal 2006, 20: 1239-1241 (F.I.: 7.064)
• Occipital nerve stimulation for drug-resistant chronic cluster headache:
a prospective pilot study.
The Lancet Neurology 2007, 6, 289-291 (F.I.: 12.167)
Neurostimulation for intractable headaches
Thursday, September 18th
14:30-15:00
A proportion of chronic headache patients become refractory to medical treatment and
severely disabled. In such patients various neurostimulation methods have been proposed,
ranging from invasive procedures such as deep brain stimulation to minimally invasive ones
like occipital nerve stimulation. They have been applied in single cases or small series of
patients affected with varying headache disorders: cervicogenic headache, hemicrania continua, post-traumatic headache, chronic migraine and cluster headache. Although favourable
results were reported overall, it is premature to consider neurostimulation as a treatment
with established utility in refractory headaches. At present, the most detailed clinical studies have been performed in intractable chronic cluster headache patients (iCCH), which
represent about 1% of all chronic cluster headache patients. Various lesional interventions have been attempted in these patients, none with lasting benefits. In recent years,
non-destructive neurostimulation methods have raised new hope. Hypothalamic deep brain
stimulation (hDBS) acts rather rapidly and has durable efficacy, but it is not riskless. Occipital nerve stimulation (ONS) was studied in 2 trials on a total of 17 iCCH patients. Clinical
efficacy was found very satisfactory by most patients and by the investigators. Although
slightly less efficacious than hDBS, ONS has the advantage of being rather harmless and
reversible. At this stage, it should be preferred as 1st line invasive therapy for iCCH. Recent
case reports mention efficacy of supraorbital and vagal nerve stimulation (VNS). Whether
these neurostimulation methods have a place in the management of iCCH patients remains
to be determined.
27
Speakers / Abstracts
Fabio Antonaci
Prof.
Centro Cefalee
Fondazione C. Mondino
Università di Pavia
Via Mondino 2
I-27100 Pavia
T: +41 (0)38 238 02 32 / 380315
Email: [email protected]
Fabio Antonaci is currently Aggregate Professor at the Headache Centre at the C. Mondino
Foundation, University of Pavia, Italy. Professor Antonaci re-ceived his degree in medicine
at the University of Siena. He then specialised in neurology and neurophysiopathology,
and obtained a PhD at the University of Trondheim in Norway. Professor Antonaci is currently President Elect of the European Headache Federation (EHF) and is the Editor of EHF
News. In addition, he is a member of several scientific bodies, including the Italian Society
of Neurology, Italian Society for the Study of Headache, IHS, EHF, BASH and the Swiss
Migraine Society.
Cervicogenic headache: from nosography to clinical picture
Thursday, September 18th
15:00-15:30
Since the first cases of cervicogenic headache were identified, considerable progress has
been made. Particularly in the last decade, there have been advances in therapeutic approach and in defining the clinical picture, diagnostic criteria. As repeatedly stated, cervicogenic headache (CEH) is a syndrome, not a disease or an entity sui generis. It constitutes a
“final common pathway” for pain stemming from several neck disorders. These may involve
such structures as nerves, nerve root ganglia, uncovertebral joints, intervertebral disks, facet
joints, ligaments, muscle, and so on. Pain may accordingly originate at different levels, including the lower part of the cervical spine. CEH comprises all headaches stemming from
the neck with the possible exception of specific headache entities (eg, a subgroup of chronic
paroxysmal hemicrania [CPH] with mechanical precipitation of attacks).
CEH has been defined, in principle, as a unilateral headache without sideshift. In the upgrading of the CEH diagnostic criteria, the strict unilaterality criterion has been softened.
In clinical practice, patients with bilateral headache may be acceptable (like “the unilaterality on two sides” in tic douloureux). Because CEH is a syndrome, the pathologic process
can, probably not so infrequently, be reproduced on the contralateral side. In these cases,
a positive response to appropriate anesthetic blockades might be essential also in clinical
practice (not only in scientific diagnostic work-up), mainly in order to exclude tension-type
headache (T-TH). Even in the more regular unilateral case, pain may eventually spread to the
opposite side when headache becomes severe, while remaining stronger on the original side.
The typical unilaterality may probably be most clear at attack/exacerbation onset. In CEH,
therefore, headache may be strictly unilateral in the most typical and dia­gnostic case, or it
may have a unilateral preponderance; as far as we are concerned, it will not occur solely on
the side opposite to the usual one.
28
Other, equally important, diagnostic features are the symptoms and signs of neck involvement. Such signs are mechanical precipitation of attacks (both iatrogenically and subjectively induced), reduced range of motion in the neck—in one or more directions, diffuse
ipsilateral neck/shoulder/arm pain of non-radicular nature or, occasionally, arm pain of
radicular nature. Iatrogenically induced pain similar to the spontaneous one may be elicited
by external pressure over tendon insertions in the occipital area. Pressure along the course
Speakers / Abstracts
of the major occipital nerve, over the groove immediately behind the mastoid process, and
over the upper part of the sternocleido-mastoid muscle on the symptomatic side may also
provoke similar pain. Intrinsic precipitation mechanisms may be activated by neck movements and/or sustained, awkward head positioning during sleep or during wakefulness (such
as when washing the ceiling, speaking to one’s neighbor at table during a party, and so
forth). Ipsilateral shoulder/arm symptoms may be even more frequent than they seemed to
be initially. One not infrequently encounters patients with marked, more or less constant
arm pain of a non-radicular nature. In these cases, the underlying pathology possibly resides
in the lower part of the cervical spine (C5 and so on). However, these phenomena are not
infrequently of low intensity, and may be more like a discomfort than a pain. Such phenomena may in the occasional case have their own temporal pattern, more or less independent
of the headache attacks. The side-locked unilaterality of the headache combined with the
ipsilaterality of the arm pain provides rather compelling evidence that headache on such
occasions stems from neck structures, but not necessarily only from bony structures.
The duration of attacks/exacerbations varies widely (from a few hours to a few weeks), with
a strong tendency toward chronicity; CEH is not infrequently episodic in the initial phase,
becoming chronic-fluctuating later on. The pain of attack starts in the neck, eventually
spreading to the oculofrontotemporal area, where, during the acme, it may be as strong
as or even stronger than in the occipital region. The duration of pain episodes is most frequently longer than in common migraine; the pain intensity is moderate, non-excruciating,
unlike cluster headache, and usually of a non-throbbing nature.
Autonomic symptoms and signs, like photo- and phonophobia, nausea, vomiting, and
ipsilateral periocular edema, are infrequent – and mild if present - and some of them,
like vomiting, are clearly less marked than in common migraine. Difficulties in swallowing
is another, rarely occurring associated phenomenon. There have also been cases with features consistent with a CEH picture, but with additional dizziness and even with vertebral
drop-attacks; such patients may benefit from surgical interventions, such as an anterolateral
approach toward the cervical spine, ad modum Jung. These patients may constitute
another clinical subgroup, namely the “vertebral artery type”.
29
Speakers / Abstracts
Thomas Uwe Schreiber
MD
Muskuloskelettale Rehabilitation
Rehaklinik Rheinfelden
Salinenstrasse 98
CH-4310 Rheinfelden
T: +41 (0)61 836 51 51
Email: [email protected]
Qualifications:
• Since 2008: Medical Error and Risk Analysis
• Since 2005: Critical Incident Reporting System
• Since 2001: Functional Capacity Evaluation
• Since 2000: Sports Medicine
• Since 1998: Evidence Based Medicine
• Since 1996: Pain Medicine
• Since 1993: Manual Medicine/ Chiropractor
• Since 1992: Naturopathic Medicine
• Since 1990: Physical Medicine and Rehabilitation
• 1990: graduation of Dr. med. (MD)
• 1986: license to practice medicine
• 1986: Degree of Medicine (Dipl-Med)
• 1980 – 1986 Study of Medicine at Friedrich-Schiller-University Jena
Positions:
• Since 2004: Vice Chief Physician, Reha Rheinfelden
• Since 2002: Physician in Charge, Muskuloskeletal Rehabilitation, Rheinfelden
• 1996-2001: Senior Physician, Vice Head of Experimental PMR; Jena
• 1990-2001: Physiatrist at the Department of Clinical and Experimental PMR, Jena
• 1986-1990: Assistant Physician at Institute of Physiotherapy, University of Jena
Fields of interest:
• Rehabilitation
• Pain Medicine
• Sports Medicine
• Manual Medicine
• 3D Motion analysis
• Evidence Based Medicine
• Performance Art Medicine
• Functional Capacity Evaluation
• Temporomandibular Joint Disorders
• Assessments and Outcome research
30
Speakers / Abstracts
Cervicogenic headache after whiplash injury
Thursday, September 18th
16:00-16:30
Whiplash injuries are the most frequently recorded trauma among insurance claimants.
One of the mainly difficulties in diagnosing whiplash is that the term whiplash primarily
describes a mechanism of bodily damage. Whiplash associated disorders (WAD) are often
accompanied by pain and stiffness of the neck, headache, brachialgia (pain radiating into
one or both arms), vertigo or dizziness, chewing and swallowing problems, visuomotor disturbances such as blurred vision and reduced coordination, fatigue and reduced energy,
neuropsychologic dysfunction, depression, irritability and sleep disorders.
According to the Quebec Task Force (QTF) classification WAD Grade I is characterized by
subjective neck complaints of pain, stiffness and tenderness without objective physical
signs. WAD Grade II is labelled by musculoskeletal signs such as decreased ROM and point
tenderness. In WAD grade III neurologic symptoms, such as muscle weakness or sensory
deficits, are integrated, whereas WAD grade IV is identified by cervical spine fractures or
dislocation.
Most WAD patients are assigned to WAD grade I and II, neurologic and/ or bony changes
are rarely found. In WAD grade I and II evidence from several studies has underlined the
importance of neuromuscular dysfunctions, but there remains a trenchant debate about the
frequency with which these dysfunctions cause chronic pain. It is important for clinicians to
be able to identify patients who are at risk of developing chronic impairment.
Spine studies done with specimens sectioned in thin slices have revealed a ratio of 60:1
of pathological findings at various structures to pathology detected by plain radiographs
respectively. Therefore notwithstanding the variety and the extent of lesions possible
after whiplash, X-ray as well as MRI have been shown to be profoundly insensitive. Hence
musculoskeletal findings remains of outstanding worth for clinical purposes.
Several trigger point studies has described abnormalities as identified at the motor endplate
of a skeletal muscle fiber. These pathologies appears to be stimulated by an abrupt cervical
movement and are followed by a release of excessive amounts of transmitters and a maximum of local muscle contraction.
As latest single case studies have shown, in patients with WAD a distinct pattern of trigger
point distribution have been found, which differed significantly from other patient groups
and healthy controls. The semispinalis capitis muscle seems to be more frequently affected
by trigger points in patients with WAD, whereas other neck and shoulder muscles and the
masseter muscle did not alter from distinct diseases. Cervicogenic headache may actually
arise from bony structures or soft tissues of the neck, but it is more common and prominent
as a adverse symptom of neck pain and cervical tenderness. In a vicious circle of strain and
pain primary and secondary headache is thought to be one of the end points in chronic WAD
conditions. For the most part natural history of whiplash injuries seems to be benign. On
the other hand a significant proportion of patients are at risk to develop chronic symptoms
already 6 month after accident within the following two years with very little prospect of
improvement after this.
31
Speakers / Abstracts
Dominik Straumann
Prof.
Neurologische Klinik und Poliklinik
Frauenklinikstrasse 26
CH-8091 Zürich
T: +41 (0)44 255 55 64
Email: [email protected]
Dominik Straumann, MD, studied medicine at universities of Fribourg and Zurich (19821988). He received his subsequent neurological training at the Neurology Department at
Zurich University Hospital before and after a postdoctoral fellowship (1994-95) at Johns
Hopkins Hospital, Baltimore, USA. Since 1998 he leads the Clinical Vestibulo-Oculomotor
Laboratory at the Neurology Department of Zurich University Hospital. Together with
colleagues from the ENT and Psychiatry Departments, he also heads the Interdisciplinary
Center for Vertigo and Balance Disorders founded in 2004.
32
Speakers / Abstracts
Cervical and masticatory dysfunctions and their relationship with vertigo
Thursday, September 18th
16:30-17:00
It is a well-recognized phenomenon that neck muscles in patients with vestibular disorders become stiffer. As a result, head movements get slower, causing less vertigo. Similarly,
muscle spindle input on the side of a vestibular deficit increases, which leads to a greater
effectiveness of cervico-postural and cervico-ocular reflexes. The neurophysiological basis
for these neck muscle changes in the presence of vestibular deficits may be found in the
disruption of oligosynaptic pathways from the vestibular labyrinths to the neck muscles. For
instance, in patients with a unilateral lesion of the sacculus, one finds missing inhibition of
the ipsilateral sterno-cleido-mastoid muscle upon clicks (so-called click-evoked vestibularevoked myogenic potentials, VEMP). Similar oligosynaptic pathways from the labyrinth have
been described to the masseter muscle, which could explain the frequent concurrence of
masticatory dysfunctions and vertigo. Such a hypothetical pathomechanism of disrupted
reflex pathways from the vestibular labyrinths to head and neck muscles implies that the
vestibular deficit is primary and the cervical and masticatory dysfunctions are secondary.
This conclusion, in turn, calls for neuro-otological investigations in patients with cervical
and/or masticatory disorders.
33
Speakers / Abstracts
Lutz Jäncke
Prof.
Psychologisches Institut
Lehrstuhl für Neuropsychologie
Universität Zürich
Binzmühlestr. 14/25
CH-8050 Zürich
T: +41 (0)44 635 74 00
Email: [email protected]
Prof. Lutz Jäncke studied first at the Technical University Braunschweig and thereafter at
the Heinrich Heine University in Düsseldorf where he received in 1984 his degree in psychology, brain-research. Afterwards he worked until 1988 – 1996 he worked at the Dpt. for
General Psychology at the University of Düsseldorf where he obtained his Dr. degree. This
period was interrupted by two one-year research-stays at the Yale University in Connecticut
and at Beth Israel Hospital of the Harvard Medical School in Boston. In June 1995 he received his PhD at the Heinrich-Heine University in Düsseldorf with the thesis „Funktionelle
und anatomische Hemisphärenasymmetrien“, that was awarded as the best thesis. 1997 he
was appointed as chairman at the Dpt. of Psychology at the Otto-von-Guericke-Universität
Magdeburg, a position he hold until his appointment 2002 as chair and director of Neuropsychology at the University of Zurich.
Prof. Jäncke received several honors and awards as well as numerous grants and he published
more than 170 peer reviewed papers in prestigious journals like Nature, Science, Cerebral
Cortex, Brain Research, Experimental Brain Research, Neuroimage.
34
Speakers / Abstracts
Cortical neuroplasticity: the musician’s brain
Friday, September 19th
09:00-09:30
One of the most important discoveries in “cognitive neurosciences“ is that the human brain
is more plastic than previously anticipated. A considerable contribution to this new research
discipline has been added to by a newly developed research area called “neuroscience of
music“ in which the brain of musicians is analyzed using modern brain imaging methods.
Professional musicians frequently start very early in life with musical training and they continue to practice their entire life. In my talk I will describe the many and fascinating findings
demonstrating that the brain of musicians is shaped by the particular experience of the musician. Thus, there is not only a strong difference in terms of neuroanatomical architecture
and neurophysiological functioning between professional musicians and non-musicians,
there are rather subtle and strong differences between the musicians themselves, depending on their particular experience and amount of practice. Based on these findings we can
infer the potential of specific training principles for shaping the human brain in terms of
anatomy and function. In addition, these findings open the door to new therapeutical and
rehabilitative approaches for neurological and psychiatric diseases. Even aging process can
benefit from music related experiences.
35
Speakers / Abstracts
Dominik A. Ettlin
MD and med. dent.
Zentrum für Zahn-, Mundund Kieferheilkunde
Universität Zürich
Plattenstrasse 11
CH-8032 Zürich
T: +41 446 34 32 54
Email: [email protected]
Graduate Education:
• M.D.: Medical School, Univ. of Berne, CH 1982-1989
• D.M.D.: School of Dental Medicine, Univ. of Pennsylvania, Philadelphia, USA 1992-1994
Academic Appointments:
Assistant Professor and Director, Division of Oral Diagnosis / Oral Medicine, Northwestern
University Dental School, Chicago, USA 1996-2001
Oberassistent:
Clinic for Masticatory Disorders, Removable Prosthodontics and Special Care, Center for
Dental and Oral Medicine, University of Zurich, CH 2001-2005
Klinischer Dozent and Co-Director:
Interdiscipilinary Orofacial Pain Consulting Service
Clinic for Masticatory Disorders, Removable Prosthodontics and Special Care, Center for
Dental and Oral Medicine, University of Zurich, CH 2005-present
36
Speakers / Abstracts
Teeth and the brain
Friday, September 19th
09:30-10:00
Toothache is subjectively seen, without doubt, undesirable.“ (Wilhelm Busch; lib. trans.). In
Günter Grass’s novel “Local Anaesthetic“, there are even speculations about possible effects
of toothaches on world history, as the question is raised if Nero set fire on Rome simply because he was suffering from a severe toothache? It can thus be noted that toothaches have
left lasting imprints in world literature, but what about imprints in the brains of subjects
affected? This presentation will discuss data on our recent experimental explorations of this
topic. We analyzed neural activation in cortical and subcortical structures of human volunteers. Upon electrically induced dental nociception, a wide cortical network distributed over
several areas was found being significantly activated, collectively representing a “dental
pain matrix“. Specific brain structures revealed distinct lateralization patterns. With regard
to emotional processing of dental pain, it is remarkable that the amygdala responds more
strongly to contralateral stimuli, which may reflect a peculiarity of dental pain processing.
37
Speakers / Abstracts
Carlo Adolfo Porro
Prof.
Dipartimento Scienze Biomediche
Sezione Fisiologia
Università di Modena e Reggio Emilia
Via Campi 287
IT-41100 Modena
T: +39 059 205 53 41
Email: [email protected]
Born in Modena (Italy) on December 24, 1954.
Present position:
• Full Professor of Physiology, School of Medicine of the Univ. of Modena and Reggio Emilia, Italy.
Education:
• PhD 1989 University of Parma (Italy) Neuroscience
• Specialist 1983 University of Modena (Italy) Anesthesiology
• MD 1979 University of Modena (Italy) Medicine
Research Experience :
• 2004- present University of Modena Full Professor of Physiology
• 2001-2004 University of Udine Full Professor of Neurophysiology
• 1992-2001 University of Udine Associate Professor of Neurophysiology
• 1990-1992 University of Modena Research Assistant of Physiology
• 1987-1990 University of Modena Postdoctoral fellow (Neuroscience)
• 1983-1987 University of Parma and Modena Doctoral Fellow (Neuroscience)
• 1980-1983 University of Modena Trainee Anesthesiology
Research interests:
A first line of research concerns the functional organization of the pain system and its modulation by endogenous antinociceptive and cognitive mechanisms, studied with metabolic mapping
techniques in experimental animals and in humans. These studies unraveled the spatio-temporal
dynamics of the activity of spinal cord and brain nociceptive networks during acute pain states,
in parallel with time-related changes in pain perception or in different behavioral endpoints. His
studies have shown also that anticipation of pain by itself can induce changes in cortical nociceptive networks, thus demonstrating a powerful top-down modulation of the pain system.
More recently, he has been investigating the neural circuits underlying the placebo analgesic
effects and the neural counterparts of observation of painful scenes.
A second line of research is devoted to the mechanisms of cognitive modulation of the cortical
motor system, specifically during action observation or willed, first person internal representation
of different kinds of action. These studies showed that motor imagery activates a parieto-frontal
circuit similar to that active during action observation, plus frontal-mesial areas and, at least for
some tasks, the primary motor area. Thus, mental representations involve to a large extent the
same circuits engaged in actual perceptual or motor tasks. This conclusion is strengthened by
recent results, showing that repeated observation of simple intransitive finger movements led to
increases in maximal voluntary force during the same kind of movements. These results suggest
a powerful, specific training effect of action observation, which may prove useful in physiological
and rehabilitative conditions.
38
Speakers / Abstracts
A third and more recent line of research concerns the functional organization of spinal sensorimotor circuits, studied with advanced functional magnetic resonance imaging (fMRI) techniques.
The results have provided evidence for side- and rate- dependent BOLD fMRI signal changes in
the cervical spinal cord during a simple finger-to-thumb opposition task in healthy volunteers.
This suggests that, thanks to recent technological advances, fMRI can be used to obtain novel and
quantitative physiological information on the activity of spinal circuits.
Since 1995 he has been leading a group on the functional mapping on cortical systems in humans,
by means of functional magnetic resonance imaging.
Since 2006 he has been Coordinator of the PhD Program in Neuroscience, Dept. of Biomedical
Sciences, University of Modena and Reggio Emilia.
Pain modulation by anticipation
Friday, September 19th
10:30-11:00
Anticipation is a highly complex condition where different factors such as attention, preparation and motivation, fear or anxiety can come into play. Such mechanisms allow anticipatory adaptation and coping with emotional stimuli, thus influencing subsequent behaviour,
and have been shown to modulate basal and evoked activity in different regions of the pain
system. Given its unique role at the interface of cognitive, affective, and motor functions
the cingulate cortex is a likely substrate for anticipatory mechanisms. Indeed, physiological
and functional imaging studies have disclosed the role of cingulate regions in different experimental models of anticipation. It may be hypothesized that anticipation of pain and of
analgesia share at least in part common sites within the rostral cingulate cortex, taking part
in a cortico-subcortical network involved in modulating the response of the pain matrix.
39
Speakers / Abstracts
David Linden
Prof. MD
School of Psychology
Bangor University
Adeilad Brigantia
Penrallt Road
Gwynedd LL57 2AS
United Kingdom
T: +44 (0)12 483 825 64
Email: [email protected]
Research interests:
Mechanisms of working memory and its interaction with attention at behavioural and
physiological levels (fMRI and EEG). Functional imaging studies with schizophrenia patients looking at cognitive deficits accompanying the disorder. Functional and anatomical
brain connectivity abnormalities and their relationship to the psychopathology of schizophrenia and the neural mechanisms of mental imagery (fMRI and TMS). Imaging correlates
of memory deficits in Alzheimer‘s disease and the neural meachnisms of number processing.
Website:
www.psychology.bangor.ac.uk/research/staff_detail/linden.php
Publications:
Please visit the publications page of Professor David Linden to view recent publications.
40
Speakers / Abstracts
Can behavioural therapy influence neuromodulation?
Friday, September 19th
11:00-11:30
Current functional neuroimaging techniques allow us to assess the brain changes produced
by behavioural therapy and other psychological interventions and to evaluate whether psychotherapy and pharmacotherapy operate through the same neural channels. This approach
has already provided important insights into the mechanisms of therapies for anxiety disorders, obsessive-compulsive disorders, depression and pain. The standard procedure for
studying these effects is to induce symptoms in an experimental setting before and after the
intervention while patients undergo fMRI (functional magnetic resonance imaging) or PET
(positron emission tomography) scanning. For example, nociceptive stimuli produced less
activation of brain areas that process the sensory and affective components of pain during
a hypnosis protocol, in parallel to its attenuating effect on perceived pain. The recent development of fMRI-based neurofeedback now opens up the possibility of direct modulation
of brain regions. Again, first applications in the field of chronic pain are promising, but its
wider clinical applicability and duration of therapeutic effects still need to be explored.
41
Speakers / Abstracts
Fabrizio Benedetti
Prof.
Dipartimento di Neuroscienze
Università di Torino
Corso Raffaello 30
IT-10125 Torino
T: +39 011 670 77 09
Email: [email protected]
Fabrizio Benedetti, MD, is Professor of Physiology and Neuroscience at the University of Turin Medical School, Consultant for the Placebo Project at the National Institute
of Health in Bethesda, MD (USA), and Member of the Mind-Brain-Behavior Initiative at
Harvard University in Cambridge, MA (USA). In the 80s he joined the Postdoctoral School
of Psychiatry and Biobehavioral Sciences at the University of California in Los Angeles, and
in the 90s he was appointed Assistant Professor at the Southwestern Medical Center of the
University of Texas in Dallas. His current scientific interests are the placebo effect across
diseases, pain in dementia, and intraoperative neurophysiology for mapping the human
brain.
42
Speakers / Abstracts
Neurobiological mechanisms of the placebo effect
Friday, September 19th
11:30-12:00
The placebo effect is a rapidly growing research field, whereby sophisticated neurobiological research tools have recently been applied, such as neuropharmacology, brain imaging,
in vivo receptor binding, and single-neuron recording in awake humans. These techniques
have allowed a better understanding of the mechanisms underlying the placebo effect, with
the most secure and promising results in the field of pain and analgesia and movement
disorders. Both placebo analgesia and nocebo hyperalgesia have been investigated and the
underlying biochemical mechanisms have been identified. It is fundamental to understand
that the study of placebo and nocebo effects is basically the study of the psychosocial
context around the patient and the treatment, and has immediate clinical implications that
embrace both clinical trials methodology and clinical practice. For example, as placebos
induce opioid and dopamine release in the brain, any drug may potentially interact with
these placebo-activated endogenous opioids, thus confounding the interpretation of clinical
trials. Likewise, nocebos may activate cholecystokinin through the induction of anticipatory
anxiety. Besides pain, a recent interesting medical condition for the study of the placebo
effect has emerged in the field of movement disorders. In fact, patients with Parkinson’s
disease have been found to activate endogenous dopamine following placebo administration. In addition, single-neuron recording from awake Parkinson patients has shown changes
in neuronal activity during the placebo response. A key question is whether the loss of these
placebo mechanisms may represent a point of vulnerability for the expression and maintenance of a pathological condition and for the response to its therapeutic intervention.
To answer this question, the disruption of placebo-related mechanisms has recently been
obtained experimentally by means of hidden administrations of treatments and has also
been described in dementia of the Alzheimer type, whereby prefrontal executive control is
disrupted. Importantly, in both these cases, the effectiveness of a therapy has been found to
be reduced. These findings have important clinical implications in all medical conditions.
43
Speakers / Abstracts
Christian S. Stohler
MD
Baltimore College of Dental Surgery
650 W Baltimore St
Baltimore, MD 21201
USA
T: +1 410 706 74 61
Email: [email protected]
Trained at the Medical Faculty, University of Bern [1969-1979], Switzerland (DDS, graduate
studies, doctoral degree); joined the University of Michigan [1979-2002], Dental School
and Center for Human Growth and Development - (Visiting Professor, Research Scientist,
Professor, Research Director, Department Chair), moved to University of Maryland, Baltimore
[2003] (Dean).
44
Speakers / Abstracts
The Role of Genetic Factors in Orofacial Pain
Friday, September 19th
13:30-14:00
Not unlike diabetes, cardiovascular disease, schizophrenia, or Parkinson’s disease, today’s
knowledge of orofacial pain states presents a compelling case for studies aimed at
identifying disease genes that confer liability. Discovery of vulnerability genes, combining
positional and candidate approaches, is considered the first step towards understanding and
managing persistent pain. Ultimately, it leads to the discovery of important proteins that
influence the development and course of these pain conditions.
Although diagnostic taxonomies with explicit operational criteria allow reliable case
assignment (e.g., Research Diagnostic Criteria for TMD), ignorance of the underlying pathogenesis and the absence of established disease-defining biomarkers make these conditions, notably the TMJ diseases effectively syndromic, not different from other complex
diseases noted above. The Human Genome Project and recent biotechnological advances
have expanded our views of such complex diseases and facilitates the rational discovery of
vulnerability genes. The emerging thinking is to accept the persistent orofacial pain states
as conditions with a genetic underpinning that mediates either resiliency or alternatively,
susceptibility to disease through a host of genes.
Here, to illustrate the new conceptual thinking of the causation of clinically relevant orofacial pain, the role of gene variants (1) affecting the function of the catechol-O-methyltransferase, an enzyme involved in the degradation of catecholamines, and (2) the vulnerability mediated by gene variants influencing the function of neuropeptide Y, will be used
as illustration of the new conceptual framework of disease that shapes the discovery process in the 21st Century.
45
Speakers / Abstracts
Erin C. Henry
Ph.D.
Genentech, Inc
10 N. Kingshighway #9C
Saint Louis, MO 63108
USA
T: +1 314 361 88 72
Email: [email protected]
Erin Henry, Ph.D., received her B.S. in Biochemistry from Virginia Tech in Blacksburg, VA
and her Ph.D. in Neuroscience from Vanderbilt University in Nashville, TN. She completed
a post-doctoral fellowship in Anatomy and Neurobiology at Washington University in St.
Louis School of Medicine. Dr. Henry’s research focused on investigating mammalian sensory system organization, connectivity, and plasticity using neurophysiology, neuronal tract
tracing, and histological methods.
Dr. Henry is currently a Medical Science Liaison in the department of Immunology, Tissue
Growth, and Repair at Genentech, Inc. (South San Francisco, CA).
46
Speakers / Abstracts
Can animal experiments on tooth deafferentation tell us something about atypical
odontalgia?
Friday, September 19th
14:00-14:30
Naked mole-rats (Heterocephalus glaber) are subterranean rodents with reduced eyes and
limited auditory capabilities. They rely heavily on their large incisors for digging and moving
objects and have a greatly magnified cortical representation of the dentition, accounting for
30% of their primary somatosensory area (SI). The representation of the contralateral lower
incisor alone accounts for more than half of this cortical dentition area.
We investigated cortical reorganization in naked mole-rats after tooth extraction, revealing a possible mechanism for the occurrence of atypical odontalgia. The naked mole-rats
had their lower right incisor extracted on postnatal day 7 or 21. After approximately 4-8
months, the response properties of the deactivated tooth zone in SI were investigated with
multiunit microelectrode recordings. The results revealed a dramatic reorganization of the
oral-facial representation in SI. The deactivated tooth zone became activated by stimulation of surrounding oral-facial structures, including the contralateral upper incisor, the
ipsilateral lower incisor, the tongue area, and the buccal pad. These results suggest that the
representation of the dentition in mammals is capable of significant reorganization after
the loss of sensory inputs from the teeth and these data parallel plasticity findings in the
somatosensory hand area of primates.
47
Speakers / Abstracts
Craig S. Miller
DMD, MS
Oral Medicine
College of Dentistry
Lexington, KY 40536
USA
T: +1 859 323 55 98
www.mc.uky.edu/microbiology/miller.asp
Professor Miller is the Past-President of the American Academy of Oral Medicine and the
Oral Medicine and Pathology Group (American Association of Dental Research), and is
the editor of the Oral Medicine Section of Oral Surgery, Oral Medicine, Oral Pathology,
Oral Radiology and Endodontics. His 16 years of funding from the National Institutes of
Health has resulted in more than 100 scientific articles, textbook chapters, and monographs in the areas of oral viral infections, dental management and oral manifestations of
systemic disease, and dental pharmacology. He is the recipient of numerous awards and is
internationally recognized for his knowledge of herpesviruses.
48
Speakers / Abstracts
Can herpes tell us something about neuropathic dental pain?
Friday, September 19th
14:30-15:00
Eight members of the herpesviradae family infect humans. These highly successful viruses
have different biological characteristics, but similar basic properties such as morphology of the virion, highly regulated transcription, establishment of latency and periodic reactivation. Herpesviruses important to the neurosciences belong to Alphaherpesvirinae. This
subfamily contains pseudorabies virus (PRV), herpes simplex virus (HSV) and varicella zoster
virus (VZV). PRV and HSV have been extensively used as models for unraveling basic viral
lytic processes, and for exploring neural networks and brain circuitry. These neurotropic
viruses are taken up by nerve terminals that interact with dynein molecules in the axoplasm
and migrate along axonal microtubules before establishing long-term persistent infections
within primarily sensory ganglionic neurons. Beta and gamma herpesviruses, in contrast,
enter latency within white blood cell lineage and endothelial cells, and during immunesuppression are known to induce tumors and nociceptive (i.e., odontogenic) pain.
Alphaherpesviruses reactivate spontaneously and after physical/emotional stress resulting
in subclinical (i.e., shedding) or clinical disease. The molecular and physiological changes
that occur during stress and the inter-relationships between neurological disease and reactivation, virus replication and antiviral therapy will be explored in this lecture. The clinical
manifestations of recurrent infections are often associated with acute pain, but rarely is the
pain persistent unless herpes zoster is involved. Differing pathophysiological responses to
HSV and VZV contribute to the latter’s ability to cause persistent neurological disease. Interestingly, the primary afferent neurons that synapse with second order neurons in sensory
ganglia during central sensitization can harbor quiescent or active herpesvirus genomes
that may modulate the perception of pain. Finally, gene therapy offers the possibility to
achieve pain relief by interfering with pain neurotransmission. The advantages of using
recombinant alpha herpesviruses for the delivery of transgene products with analgesic potential to neurons of the dorsal root/trigeminal ganglia will be discussed.
49
Speakers / Abstracts
Peter Svensson
Prof.
School of Dentistry
Aarhus University
Tandlægeskolen
Vennelyst Boulevard 9
DK - 8000 Århus C
Denmark
T: +45 894 241 91
Email: [email protected]
Graduated from the School of Dentistry, University of Aarhus 1987 (DDS). Earned his Ph.D.
degree in 1993 and Doctor of Odontology in 2000 at University of Aarhus. In 2001 promoted
to full professor and chairman of Department of Clinical Oral Physiology. Appointed clinical
consultant at Department of Oral Maxillofacial Surgery, Aarhus University Hospital in 2002
and consultant at Danish Headache Center, University of Copenhagen in 2005. Appointed
honorary adjunct professor at Aalborg University in 2005. The research has focused on orofacial pain, physiology and temporomandibular disorders with more than 215 contributions
to peer-reviewed journals and book chapters. Presented more than 150 lectures, talks and
courses on orofacial pain mechanisms and TMD problems around the world. Awarded the
Codan Young Investigator Research Prize in 1995, the Strathmann Research Award in 1998
and the Zendium-Hoogendoorn Award in 2000 and Bagger-Soerensen Grant 2004. Editorial board member and reviewer for several international dental and neuroscience journals
including Pain and Journal of Orofacial Pain. Editor-in-Chief of Journal of Oral Rehabilitation (2004-present). Co-editor of textbook on Clinical Oral Physiology, Quintessence 2004.
Supervised 15 completed Ph.D.-projects (6 as main-supervisor). Main-supervisor of 4 ongoing Ph.D.-projects and co-supervisor of 4 other ongoing Ph.D.-projects and has an extensive
network of national and international collaborations.
50
Speakers / Abstracts
Quantitative neurosensory testing: A must for the diagnosis of orofacial neuropathic pain?
Friday, September 19th
15:30-16:00
Pain is not just pain but comes in different types and with different clinical manifestations and underlying neurobiology. It has been proposed that pain can be: 1) transient or
nociceptive, 2) tissue-injury or inflammatory, 3) nervous system injury or neuropathic or 4)
functional (Woolf 2004). Progress has also been made in the classification of neuropathic
pain which now is recognized as “pain arising as a direct consequence of a lesion or disease
affecting the somatosensory system (Loeser and Treede 2008). In addition, a new grading
system has been introduced outlining criteria for 1) definite, 2) probable, 3) possible and 4)
unlikely neuropathic pain (Treede et al. 2008). The importance of quantitative neurosensory
testing for the diagnosis of orofacial neuropathic pain will be discussed. Finally, a survey of
which tests can be done in the clinic and in the laboratory will be presented (Svensson et
al. 2004).
References
1. Loeser JD, Treede R-D. The Koyto protocol of IASP basic pain terminology. Pain 2008;137:473-477.
2. Svensson P, Baad-Hansen L, Thygesen T, Juhl GI, Jensen TS. Overview on tools and
methods to assess neuropathic trigeminal pain. J Orofac Pain 2004;18:332-338.
3. Treede RD, Jensen TS, Campbell JN, Cruccu G, Dostrovsky JO, Griffin JW,
Hansson P, Hughes R, Nurmikko T, Serra J. Neuropathic pain: redefinition and a grading
system for clinical and research purposes. Neurology 2008;70:1630-1635.
4. Woolf CJ. Pain: moving from symptom control toward mechanism-specific
pharmacologic management. Ann Intern Med 2004;140:441-451.
51
Speakers / Abstracts
Gary M. Heir
DMD
Clinical Professor, Clinical Director
Department of Diagnostic Sciences
Division of Orofacial Pain
UMDNJ, New Jersey Dental School
110 Bergen Street
Newark, New Jersey 07103
USA
718 Broadway
Bayonne, NJ 07002
T: +1 201 339 48 47
Fax: +1 201 339 48 50
Email: [email protected]
Dr. Heir a past President and a Fellow of the American Academy of Orofacial, and Immediate
Past-President and a Diplomate of the American Board of Orofacial Pain.
Having pursued his undergraduate studies at Temple University, Philadelphia, Pennsylvania,
Dr. Heir graduated from the University of Medicine and Dentistry of New Jersey with the
degree of Doctor of Medical Dentistry. He is currently a Clinical Professor of the University
of Medicine and Dentistry of New Jersey in the Department Diagnostic Sciences / Division
of Orofacial Pain and a Co-Director of the Orofacial Pain Graduate Program, and Director of
the Orofacial Pain Clinic. The University of Medicine and Dentistry of New Jersey has one
of the few Masters in Dental Science / Orofacial Pain programs in the United States. He is
the director of the oral biology post graduate core module on orofacial pain and director of
the second year undergraduate orofacial pain lecture series. Dr. Heir is a member of many
professional organizations devoted to the study and diagnosis of pain disorders.
Dr. Heir has published papers, chapters and abstracts on topics related to the field of temporomandibular disorders and orofacial pain and has authored a chapter on the assessment
of the temporomandibular disorder patient in an upcoming edition text on oral surgery. Dr.
Heir has contributed to other chapters on TMJ surgery and neuropathic pain.
Dr. Heir’s other interests have been recognized, and he is considered an authority on orofacial pain in Lyme disease, a debilitating disorder seen in the United States and other parts
of the world. In 1996, the Governor of New Jersey appointed him to the Governor’s Lyme
Disease Advisory Council for the State of New Jersey. Dr. Heir to served as the Council’s Vice
Chair for four years and continues as one of its members.
52
Speakers / Abstracts
Post-implant pain. How to diagnose, what to do
Friday, September 19th
16:00-16:30
Endosseous implants have become a standard of care. Implant placement in the mandibular molar and premolar zone is sometimes associated with damage to peripheral branches
of the mandibular division of the trigeminal nerve. This presentation will review the basic
science of nociception and nerve injury, how to recognize when things go wrong during and
after the placement of an implant, and what action to take when they do.
53
Speakers / Abstracts
Luigi M. Gallo
Prof.
Zentrum für Zahn-, Mundund Kieferheilkunde
Universität Zürich
Plattenstrasse 11
CH 8032 Zürich
T: +41 446 34 32 26
Email: [email protected]
With a PhD in biomedical engineering, Luigi Gallo joined the Clinic for Masticatory Disorders at UZH as senior researcher. He has been active on instrumental assessment of TMD,
in particular by means of “Dynamic Stereometry“, i.e. 3D-reconstructing TMJ anatomy and
animating it with corresponding real kinematics. In 2003/2004, Gallo was Research Fellow
at the Soft Tissue Research Lab in New York. Besides authoring round 50 journal papers and
some book chapters, Luigi Gallo is associate editor of “Cells, Tissues, Organs”. In August 2007
he was appointed Professor for Physiology and Biomechanics of the Masticatory System at
the University of Zurich.
54
Speakers / Abstracts
From TMJ biomechanics to cartilage mechanobiology
Saturday, September 20th
09:00-09:30
The analysis of TMJ biomechanics is important for understanding degenerative disease of
this joint. Indeed, TMJ osteoarthritis could be related to articular cartilage overloading,
possibly due to masticatory muscles hyperactivity, often occurring during sleep. Prolonged
static loading of disc cartilage seems to modify its mechanical response, increasing not only
compressive stresses but also tractional forces. Since animal models have shown that TMJ
disc displacement and/or failure induce osteoarthritis, we are interested in the in vivo analysis of the forces due to disc deformation during jaw movement. These forces, if abnormal,
could initiate disc displacement and/or damage.
Dynamic stereometry studies on TMJ space variation during mastication indicate that both
TMJs are loaded during chewing, the balancing joint more than the working one. Also studies on the dynamics of compression areas in the TMJ show that plowing forces can occur
through the disc during functional movements, due to stress-field translation. The energy
spent in the TMJ is primarily influenced by the velocity and distance of mediolateral stressfield translation, with a great inter-individual variability. Furthermore, disc loading patterns
appear to be related to condyle and fossa anatomy. The loading patterns might contribute
to cartilage wear and fatigue because of the anisotropic material properties of the disc,
which is weaker mediolaterally. A greater mechanical energy density might also elicit a
biological response of the tissue. This is the topic of an ongoing project aimed at the benchtop dynamic replication on live tissue of the strains measured in vivo with a subsequent
biochemical analysis.
55
Speakers / Abstracts
Peter A. Torzilli
Ph.D.
Laboratory for Soft Tissue Research
Hospital for Special Surgery
535 East 70th Street
New York, NY 10021-4892
USA
T: +1 212 606 10 87
Email: [email protected]
Peter A. Torzilli, Ph.D. is a Senior Scientist and Director of the Tissue Engineering, Regeneration and Repair Program at Hospital for Special Surgery and Professor of Applied
Biomechanics in Orthopaedic Surgery, Department of Orthopaedics at the Weill Medical
College of Cornell University, in New York City. He heads the Laboratory for Soft Tissue
Research, a multi-disciplinary research group of scientists, engineers and physicians
studying soft tissue injuries to the musculoskeletal system. Dr. Torzilli’s principle research interest is in studying the mechanobiology of articular cartilage in health and
disease, and the role of mechanical stimuli in the development of osteoarthritis.
56
Speakers / Abstracts
What is the Optimal Mechanical Environment for Cartilage
Saturday, September 20th
09:30-10:00
Osteoarthritis (OA) is one of the leading causes of disability in the United States, with more
than 20 million people having the disease. OA is a disease of the articular cartilage covering movable joints. While the exact etiology of the disease is not known, most believe it
is caused by mechanical factors such as from joint trauma, long-term wear-and-tear, and
obesity. In normal healthy tissue the cellular metabolic rate is fairly low but the synthesis
and degradation of proteoglycan (PG) is stable, maintaining mechanical function. However
in OA there is a loss of PG and collagen rupture due to mechanical and biological factors,
and a concomitant loss of mechanical function leading to an inability to act as a bearing
material for load distribution and lubrication. Clinical evidence indicates that the initial
damage to the articular cartilage occurs at or just below the articular surface. How surface breakdown occurs is not well understood but believed a combination of mechanical
damage and cellular catabolism by enzymes. The field of mechanobiology can be used to
study how each of these factors, mechanical and biological, can lead to an imbalance in
cartilage hemostasis and the eventual destruction and eroding of the extracellular matrix.
Eventually repair of the tissue damage will have to involve surgical intervention, such as
with a tissue engineered constructs or total joint replacement.
57
Speakers / Abstracts
Mauro Farella
Dr. PhD
Zentrum für Zahn-, Mundund Kieferheilkunde
Universität Zürich
Plattenstrasse, 11
8032 Zurich, Switzerland
T: +41 446 34 32 63
Email: [email protected]
Mauro Farella is a dentist specialized in orthodontics and in biostatistics, with a special
interest in masticatory muscles and orofacial pain research. During his PhD training, he had
been working on many research projects carried out at the University of Naples, Copehnagen,
Amsterdam, Uthrect, and Zurich. Since 2002, he has been appointed as Assistant Professor
at the University of Naples “Federico II”, and since 2007 he is working at the University of
Zurich. He has authored or co-authored more than 30 papers published in international
peer-reviewed journals and serves as an active reviewer for many international dental and
non-dental journals.
58
Speakers / Abstracts
The clinch about clenching
Saturday, September 20th
10:00-10:30
Epidemiological research has consistently shown that patients affected by masticatory
muscle pain (MMP) report tooth clenching habits more frequently than normal subjects.
This was also confirmed by longitudinal controlled studies, in which the frequency of tooth
contact in MMP patients has been repetitively assessed over several consecutive days. Nevertheless, the possible causal role of hyperactivity conditions for the development of MMP
contrasts with experimental data, which indicate that motor changes observed in masticatory muscles, can be the consequence rather than the cause of orofacial pain. Previous
attempts to overload the masticatory system under laboratory controlled conditions have
consistently shown that subjects performing moderate to strong clenching efforts, experience unbearable pain and fatigue, so that the intensity of contraction cannot be longer sustained. After these efforts, however, the masticatory muscles recover very quickly, without
late consequences such as pain and tenderness. On the other hand, the occurrence of TMDlike pain and muscle tenderness has been reported after prolonged low-level contractions
of the masticatory system, which can be even sustained for several hours. Clenching efforts
can be performed using different individual neuromuscular motor strategies. It was recently
found that in some individuals, several masticatory motor units are continuously active
during prolonged low-level clenching efforts. Selected muscle fibers that are contracted
for long periods may be therefore damaged, and this, in turn, may lead to muscle pain
through nociceptor sensitization. A critical review of neurobiological mechanisms involved
in tooth clenching, especially prolonged low-level clenching, supports the hypothesis that
this parafunction might play an important role in the pathogenesis of MMP.
59
Speakers / Abstracts
Andreas Klipstein
Dr, MSc
Dept. of Rheumatology and Institute of Physical Medicine
University Hospital Zurich
Gloriastr. 25
Ost A 150
CH-8091 Zurich
T: +41 (0)44 255 51 22
Email: [email protected]
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60
Medical school, University of Zurich 1980-1986
Specialising on FMH Physical Medicine, Rehabilitation and FMH Rheumatology 1987-1995
Master of Science in Health Ergonomics, University of Surrey, UK 2001
Lecturer Dpt. Of Rheumatology and Institute of Physical Medicine,
University Hospital, Zurich
Full time 1994-1999
Part time since 1999
AEH, Centre for Occupational Health, Ergonomics and Hygiene AG,
member of leading board since 1999
Research fellow, Swiss Federal Institute of Technology, Centre of Occupational science and Work Organisation, Zurich since 2004
PI of Swiss National Foundation project
“Prevention of Work-Related neck pain in computer work” 2000-2003
Member of consortium of EU project PROCID
(Prevention of work-related disorders in computer input devices) 1999-2002
Member of Working Group Ergonomy of the Swiss Association Of Rehabilitation (SAR)
since 1994
Member of the scientific commission musculoskeletal of ICOH
(int. commission of occupational health) since 2006
Speakers / Abstracts
Overuse injuries as cause of muscle and tendon pain
Saturday, September 20th
11:00-11:30
Musculoskeletal disorders are common in the working population. The pathomechanism
depends on the localization, the type of tissue involved, the force-levels and the possibility of recovery. Even with computer work characterized by low force demands, extensive
health problems have been documented. Factors, such as constrained postures, repetitive
work tasks, mental demands, and improper workstation ergonomics may contribute to the
development of these disorders. Psychosocial stress has also been implicated as a risk factor
for musculoskeletal disorders. There is evidence that mental stress or cognitive factors, even
in the absence of physical demands, can increase muscle activity.
Epicondylitis is very common and usually self-limiting condition with a reported prevalence
of between 3 and 12%, partly depending on the occupational risk or leisure time activities.
Lateral is much more prevalent than the medial epicondylitis with nearly equal risk for
both arms. Similar expressions for Epicondylitis are “tennis elbow”, gulf-elbow”, Epicondylopathia, local fibro-osteitis, insertion tendonitis, work-related upper limb disorder and repetitive strange injury. Pathomechanism is discussed controversially and may depend also
on the reason (occupational, leisure-time actitivity), the localisation (medial and lateral),
the force-levels and the demands /individual properties addressing intra- and intermuscular
co-ordination. Change of local metabolism and microlesions may be more important than
real (partial) ruptures, as they are well known in the rotator-cuff in the shoulder. Nevertheless, histological findings in form of an alteration of the structure of the insertion of
the tendon are common. In the development of occupational epicondylitis, the incidence
of Epicondylitis depends on the relation of exerted relative force (percentage of maximal
voluntary capacity) and the relative duration (percentage) of recovery time Model by Moore
and Gar (1994).
In the case of work-related muscular neck pain (“tension neck syndrome”) with respect to
repetitive work with low-force levels, the Cinderella hypothesis (Hägg) tries to explain this
discrepancy by postulating that overload may be attributable to prolonged, singer motor
unit activity not detected by the surface EMG. We developed advanced intramuscular EMG
techniques under dynamic conditions and new algorhythms in order to follow single motorunit activities over a longer time. We found a limited number of continuously active motor
units despite of a lack of biomechanical demand, of a relationship to the pain history over
the previous year. Furthermore, results were inversely related to the correct adjustment of
the working desk. Some results supporting the Cinderella hypothesis will be discussed in the
presentation.
61
Speakers / Abstracts
Antoon De Laat
Prof.
Afd. Stomatologie and Maxillo-fac. Heelk.
Kapucijnervoer 7 blok a – bus 07001
B-3000 Leuven
T: +32 216 33 24 54
Email: [email protected]
Prof. Antoon DE LAAT , DDS, PhD is responsible for the Clinic for Temporomandibular Disorders (Dept. Oral and Maxillofacial Surgery) and for teaching oral physiology and pathophysiology at the School of Dentistry, Oral Pathology and Maxillofacial Surgery of the Catholic
University Leuven, Belgium. He deals with temporomandibular disorders and orofacial pain
on a full-time basis. His scientific work led to over 160 papers and abstracts. He lectured
all over Europe, North and South-America, the Middle and Far East. He was Associate Editor of the Journal of Orofacial Pain, the European Journal of Oral Sciences and the European Journal of Pain. Currently he serves on the Editorial Boards of Douleur et Analgésie,
Prosthodontic Research and Practice and the Leuven Dental Journal. He is Past-President
of the IADR/Neuroscience group, the European Academy of Craniomandibular Disorders, the
Belgian Pain Society, and founding Chair of the Special Interest Group on Orofacial Pain
of the International Association for the Study of Pain (IASP). At this moment he is council
member of the IASP and chairs the Research Committee. His research interests are trigeminal neurophysiology, jaw reflexes, orofacial pain and quantitative sensory testing.
62
Speakers / Abstracts
Arthrogeous and myogenous pain. Different pathologies, different therapies?
Saturday, September 20th
11:30-12:00
The introduction of the research diagnostic Criteria for Temporomandibular disorders (RDCTMD) in 1992 aimed at a better definition of subgroups of patients, and this by the use of
clear inclusion and exclusion criteria. Soon, this classification, which allowed the use of
more homogeneous patient groups in clinical studies, was translated in clinical diagnostic
criteria facilitating clinical diagnosis too. The distinction between myofascial pain (with or
without limitation of movement) and arthralgia is mainly made on the basis of positive signs
upon palpation of the tissues involved, and was certainly inspired by the presumed underlying etiological factors, like e.g. overloading muscles by parafunctions, or disc displacements
causing inflammation/irritation of joint tissues. With regard to the genesis of pain, however, these etiological factors are not completely clear and the term “arthromyopathy” to
denominate this kind of pain is still in use. The underlying pathophysiological mechanism
for these nociceptive pains appear similar, and in clinical reality, also the management approach appears very comparable. The present lecture will address some of these points of
discussion from the perspective of general musculoskeletal pain. Does it make any sense –
from a pathophysiological point of view – to make a distinction between myogenous and
arthrogenous pain ? Is there a need for a differential treatment approach ?
•
•
•
•
Dworkin SF, LeResche L. Research diagnostic criteria for temporomandibular disorders:
review, criteria, examinations and specifications, critique.J Craniomandib Disord.
1992; 6 :301-355.
Truelove EL, Sommers EE, LeResche L, Dworkin SF, Von Korff M. Clinical diagnostic
criteria for TMD. New classification permits multiple diagnoses.J Am Dent Assoc.
1992 ;123 :47-54.
Woolf CJ, Bennett GJ, Doherty M, Dubner R, Kidd B, Koltzenburg M, Lipton R, Loeser JD,
Payne R, Torebjork E. Towards a mechanism-based classification of pain?
Pain. 1998 ;77 :227-9.
Türp JC. Myoarthropathy of the temporomandibular joint and masticatory muscles.
Pain therapy management and relaxation instead of aggressive surgery.
MMW Fortschr Med. 2003;145:33-35.
63
Speakers / Abstracts
Susanne Leiberg
MD
Institut für Empirische
Wirtschaftsforschung
Universität Zürich
Blümlisalpstrasse 10
CH-8006 Zürich
T: +41 (0)44 634 52 34
Email: [email protected]
I am a postdoctoral fellow at the Center for the Study of Social and Neural Systems at
the University of Zurich. I studied psychology at the Technical University Dresden and received a PhD in neuroscience from the Max Planck International Research School at the
University of Tuebingen. Since my PhD time my research centers on the investigation of
empathy, its link to prosocial behaviour and mediating regulatory processes with fMRI, EEG,
MEG and psychophysiological measures. Currently I am studying the trainability of empathy
and the concurrent behavioural and functional brain changes.
64
Speakers / Abstracts
The empathic brain: How, when and why?
Saturday, September 20th
13:30-14:30
The ability to share and understand other’s emotions is called empathy. It is essential for
successful interactions in our inherently social environment. In this talk I will present recent
research pertaining to the neural underpinnings of empathy, with a focus on empathy for
pain. First, I will show that overlapping brain regions are activated when we experience
emotions ourselves and when we observe someone else in an emotional state. A crucial role
in understanding our own and others’ emotions falls to the insula. Second, I will present
evidence that empathic responses do not strictly occur automatic but can be modulated
by contextual factors. Perceiving another person as unfair reduces empathic responses in
the insula to this person. Third, I will introduce results on differences in empathic brain
responses in healthy populations and populations with deficient empathic abilities and how
they might be alleviated by training. It is suggested that impaired empathic abilities are associated with insula hypofunction.
65
Speakers / Abstracts
Hans Ulrich Zeilhofer
Prof.
Institut für Pharmakologie und Toxikologie
Winterthurerstrasse 190
8057 Zürich
T. +41 44 635 59 12
Email: [email protected]
Present Position:
• Professor of Pharmacology
Organization:
• Institute of Pharmacology and Toxicology, University of Zürich
• Institute of Pharmaceutical Sciences, ETH Zürich
Major Field:
• Neuropharmacology, Pain research
Professional history:
• 1990MD, University of Erlangen-Nurnberg, Germany
• 1990-1991 Postdoctoral training in electrophysiology,
Max-Planck-Institute of Biophysical Chemistry, Göttingen, Germany
• 1992-1997 Postdoctoral training in Pharmacology,
University of Erlangen-Nürnberg, Germany
• 1997/1998 Habilitation and board exam in Pharmacology and Toxicology
• 2001Professor of Molecular Neuropharmacology, University of Erlangen-Nürnberg
• 2005Professor of Pharmacology, University of Zürich
• 2006Professor of Pharmacology,
ETH Zürich (double appointment with University of Zürich)
66
Speakers / Abstracts
Spinal GABAA Receptor Subtypes: New Targets for the Treatment of Chronic Pain
Saturday, September 20th
14:00-14:30
Inflammatory diseases and neuropathic insults trigger signaling cascades, which frequently
lead to intense and long-lasting pain syndromes in affected patients. Such pain syndromes
are characterized not only by an increased sensitivity to painful stimuli (hyperalgesia), but
also by a qualitative change in the sensory perception of other, tactile stimuli (allodynia)
and the occurrence of spontaneous pain in the absence of any sensory input. A loss of
inhibitory control by GABAergic and glycinergic spinal dorsal horn neurons is a major factor in this pathology in particular in the generation of allodynia and spontaneous pain.
In inflammatory diseases, spinally produced prostaglandin E2 inhibits strychnine-sensitive
glycine receptors (Ahmadi et al., Nat. Neurosci. 2002; Harvey et al., Science 2004), and
factors released from activated microglia impair the chloride homeostasis in dorsal horn
neurons rendering GABAergic and glycinergic input less inhibitory or even excitatory (Coull
et al., Nature 2005). Assuming that a loss of synaptic inhibition in the spinal dorsal horn is
a major factor of chronic pain, a facilitation of inhibitory synaptic transmission should reverse pathological pain sensitivity. Indeed, intrathecally injected benzodiazepines do reverse
heightened pain sensitivity in inflammatory and neuropathic pain states without interfering
with normal pain sensitivity. Spinal GABAA receptors containing the α2 and/or α3 subunits
are particularly relevant for the antihyperalgesic action of benzodiazepines. Importantly,
the α1 subunit, which mediates the sedative action of benzodiazepines is not involved.
Subtype-selective benzodiazepine site ligands, which spare activation of the α1 subunit, do
exert pronounced anti-hyperalgesic actions without producing sedation, motor impairment
or tolerance development. Such compounds might be useful for the treatment of chronic
pain syndromes, which have become unresponsive to classical analgesic drugs (Knabl et al.,
Nature 2008).
67
Speakers / Abstracts
Marlen Petersen
Prof. MD
Klinik für Anästhesiologie und
Operative Intensivmedizin
Experimentelle Schmerzforschung
Fakultät für Klinische Medizin Mannheim
Ruprecht-Karls-Universität Heidelberg
Theodor-Kutzer-Ufer 1-3
D-68167 Mannheim
T: +49 (0)62 138 356 16
Email: [email protected]
Education and academic positions:
• 1975 - 1980, study of Biology and Chemistry, Universities Marburg and Kiel
• 1982, Dr. rer. nat. degree in Animal Physiology, Marburg
• 1998, Habilitation for Physiology, Würzburg
• 2004, apl. Professor, Würzburg.
• 1983 - 1987, Wissenschaftliche Mitarbeiterin (post-doc),
Max-Planck-Institut für Physiologische und Klinische Forschung,
Bad Nauheim, Germany
• 1987 - 1989, Hochschulassistentin (assistant professor),
Institute of Physiology, Marburg
• 1989 - 1993, Associate Research Scientist,
Yale University School of Medicine, Department of Anesthesiology, New Haven (USA)
• 1993 - 1998, Hochschulassistentin (assistant professor),
Institute of Physiology, Würzburg
• 1998 - 2004, Professor of Physiology (C3, holding), Institute of Physiology, Würzburg
Current position:
• 2004-present, Wissenschaftl. Angestellte, Dept. of Anesthesiology and Intensive Care Medicine, Experimental Pain Research, Faculty of Medicine Mannheim, University of Heidelberg; apl. Professor, Institute of Physiology, Würzburg.
Research interests:
• Peripheral sensory transduction mechanisms in nociception.
Honors and awards:
• 1997, 1st Prize “Förderpreis für Schmerzforschung“
of the German Society for the Study of Pain
68
Speakers / Abstracts
Does topical capsaicin application play a role in the treatment of neuropathic pain?
Saturday, September 20th
14:30-15:00
For many years, capsaicin, the active pungent ingredient in hot peppers, has not only been
used as a tool to study the function of sensory neurons, but also to treat peripheral neuropathic pain. Neuropathic pain is characterized by damage to peripheral nerves, in contrast
to nociceptive pain caused by tissue injury. One mechanism that may underlie peripheral
neuropathic pain is the appearance of abnormal, spontaneous activity in peripheral nociceptive neurons, which may contribute to central sensitization in the pain pathway.
The action of capsaicin is mediated by activating the ‘capsaicin receptor’ TRPV1, leading
to membrane depolarization. Topical application of capsaicin to the skin or mucosa first
evokes burning sensation or pain and neurogenic inflammation (vasodilatation and plasma
extravasation). After repeated, long-lasting application of high doses the treated area becomes desensitzed to noxious stimuli, thus less pain sensitive. The mechanisms underlying
excitation, desensitization and neurotoxicity through capsaicin on the cellular basis are
reviewed.
The desensitizing action has made capsaicin attractive for use as a peripherally acting
analgesic for chronic painful syndromes. Desensitization of capsaicin-sensitive afferent
fibres involves a continuum of physiological and morphological changes that are dependent
on the capsaicin dose and route of administration. However, the use of capsaicin is limited
by the fact that before desensitization occurs, nociceptors are activated, i.e. pain is experienced.
In an outlook, recent approaches involving capsaicin for pain treatment are presented. For
example, new pathways for focused administration of local anaesthetics via capsaicin action are being developed. Furthermore, an in vitro model to investigate peripheral endings
of nociceptors isolated from there somata is presented.
69
Speakers / Abstracts
Herta Flor
Prof.
Zentralinstitut für Seelische Gesundheit
Institut für Neuropsychologie und
Klinische Psychologie
Ruprecht-Karls-Universität Heidelberg
68159 Mannheim
T: +41 (0)49 621 17 03 63 02
www.zi-mannheim.de
After receiving her doctorate in psychology at the University of Tübingen, Germany, Herta
Flor has worked as a post-doctoral fellow at Yale University and as visiting professor at
the University of Pittsburgh. In 1995, she became Full Professor of Psychology at the Humboldt University, Berlin, Germany. Since 2000, she is Full Professor at the Ruprecht-KarlsUniversity Heidelberg and Scientific Director of the Department of Clinical and Cognitive
Neuroscience at the Central Institute of Mental Health, Mannheim, Germany. Her research
focuses on the role of neuronal plasticity and learning and memory in chronic pain, anxiety
and mood disorders, substance abuse and neuropsychological rehabilitation. She has received more than 33 research grants and numerous prestigious awards and has more than
350 publications.
70
Speakers / Abstracts
Limitations of pharmacotherapy: behavioral approaches to chronic pain
Saturday, September 20th
15:30-16:00
Pharmacotherapy is most appropriate in acute pain whereas in chronic pain states behavioral approaches or a combination of behavioral treatment and pharmacotherapy is more
appropriate. In this chapter we first describe the role of learning and memory as well as
other psychological factors in the development of chronic pain and emphasize that chronic
pain must viewed as the result of a learning process with resulting central neuro­plastic
changes. We then describe operant behavioral and cognitive-behavioral treatments as
well as biofeedback and relaxation techniques and present innovative treatment procedures aimed at altering central pain memories. We complete the section with a discussion
of combined behavioral and pharmacological approaches and an interdisciplinary view.
Key words
• operant conditioning in acute and chronic pain, learning, memory, physical training, cognitive and behavioral therapeutic approaches, multidisciplinary rehabilitation
71
Speakers / Abstracts
Paul Nilges
MD
DRK Schmerz-Zentrum Mainz
Auf der Steig 16
D-55131 Mainz
T: +49 (0)61 319 885 50
Email: [email protected]
Degrees in psychology and educational science (University of Mainz), Ph.D. in psychology
(natural science doctorate, University of Trier); since 1985 clinical psychologist in the German Red Cross Pain Center Mainz, head of psychological department; clinical work with
pain patients in an interdisciplinary team, research and scientific work in cooperation with
various universities; university lecturer in clinical psychology, instructor and supervisor in
behavioral therapy and pain psychotherapy, member of the leading committee and treasurer
of the German Society for psychological pain treatment and research (DGPSF).
72
Speakers / Abstracts
Coping, acceptance and orofacial pain: The outcome matters
Saturday, September 20th
16:00-16:30
In the “fight against pain” a great coalition of various medical specialists including dentists,
physiotherapist, psychologists and other health care providers are assisting the patients’ effort
to get rid of the nagging experience of pain. Whether back pain, headache or orofacial pain: the
return to normal life is at stake, pain reduction, preferably abolition is the goal of treatment. In
the stage of acute pain this is a necessary and mostly successful strategy. Especially Dentistry is
exemplary among the medical disciplines concerning perfect pain control: regarding acute dental
pain. Rapid reduction to zero is the usual result of treatment. Patients expectations are formed by
this standards and expectations.
With reference to chronic pain the attempts to control pain and to finally abolish the problem
turns into being a problem by itself: While the focus is still on eliminating pain by all means and
a return into normal life, the cumulative attempts to do so are associated with psychological
distress, increasing deficits and losses in core domains of life.
If conventional treatment fails and pain turns into becoming a persistent problem Interdisciplinary pain management seems to be a promising alternative. This shift in concept is characterized
by transferring the responsibility to the patient and by supporting means of coping with the
challenging situation. Preferably active coping strategies (e.g. exercise, physical therapy, relaxation, distraction and other means of treatment) are applied. This so called assimilative coping involves active attempts (e.g. instrumental activities, selfcorrective actions, compensatory
measures) to alter unsatisfactory life circumstances and situational constraints in accordance
with personal preferences. This has demonstrated a substantial positive effect in terms of improving central aspects of life (e.g. activity, mood, work, family, social life). Active coping is
considered an effective agent in doing so.
However, the success is limited and studies have proven an inconsistent relation between the
amount of effort, pain reduction and the improvement of core outcome domains (e.g. reduced
disability and distress). The central question (and principal target) of treatment is simply spoken:
does the patient feel better? It is usually taken for granted that this is achieved via pain control.
Studies with various pain syndromes failed to confirm this concept: There is no clear link between
well being and amount of active coping.
Conversely, accommodative coping (e.g. downgrading of aspirations, positive reappraisal, exploring and pursuing realistic goals and self-enhancing comparisons) is directed towards a revision of
self-evaluative and personal goal standards in accordance with perceived deficits and losses. The
pain specific application is the acceptance based concept. Our research is based on the assumption that chronic pain can be described as a major source of threat or impediment to personal
goals. In various groups of pain patients two main components of acceptance have repeatedly
been measured: Pain willingness (acknowledging the chronicity of pain) and activity engagement
(allocate motivational resources towards other than pain-related goals). These two factors are
closely related to indicators of psychosocial functioning. Correlations between these factors with
the affective dimension of pain are moderate and with the sensory dimension low. No correlation is found with heat pain thresholds (thermal sensory analyzer), a finding that confirms that
acceptance is not merely an expression of a physiologically based indolence. Pain willingness might
inhibit any further effort to fight pain and, thus, reduce negative affect due to recurring treatment failure. Activity engagement additionally produces positive affect. Our results suggest that
flexibility and acceptance when facing pain operate as a protective resource and help to maintain
a positive life perspective. Most important, the ability to flexibly adjust personal goals attenuates
the negative impact of the pain experience (pain intensity, pain related disability) on psychological well-being (depression). Well being despite pain requires the readiness to give up excessive
preoccupation with the fight against pain as a prerequisite and furthermore to engage in activity
despite pain.
73
Speakers / Abstracts
Guido M. Macaluso
Prof.
Sezione di Odontostomatologia
Università degli Studi di Parma
via Gramsci 14
IT-43100 Parma
T: +39 052 198 67 22
Email: [email protected]
Functions:
• Full Professor at the University of Parma, Faculty of Medicine
• In charge of the teachings of Orofacial Pain and of Periodontology at the Dental School, University of Parma
• Director of the postgraduate course Master in Implantology, University of Parma
• Past-president of the European Academy of Craniomandibular Disorders
Education:
• Degree in Medicine, University of Parma, Italy
• Degree in Dentistry, University of Parma, Italy
• Specialization in Neurology, University of Parma, Italy
• Master of Dental Sciences, Catholic University of Leuven, Belgium
Research interests:
• Sleep medicine and physiology applied to dentistry
• Trigemino-facial neurophysiology
• Oro-facial movement disorders
• Orofacial pain
• Implant biomaterials
• Clinical portocols in implant dentistry
• Funding: MIUR (Italian Ministry of University and Research), RER (Emilia-Romagna Region), University of Parma, private fundings
Giovanni Mauro
MD
Sezione di Odontostomatologia
Università degli Studi di Parma
via Gramsci 14
IT-43100 Parma
T: +39 052 198 67 22
Email: [email protected]
Functions:
• Visiting professor and clinical instructor at the University of Parma, Faculty of Medicine
• Teacher of Clinical Gnatology course at the Dental School, University of Parma
• Teacher at postgraduate course Master in Implantology, University of Parma
• Secretary of the European Academy of Craniomandibular Disorders (2008-2010)
74
Speakers / Abstracts
Education:
• Degree in Medicine, University of Verona, Italy
• Specialization in Odontostomatology, University of Verona, Italy
• Diplome de Stomatologie, University of Nancy (France)
• Postgraduate in Cranio-Cervical-Mandibular Dysfunctions, University of Sassari, Italy
• Diplomate American Board of Orofacial Pain (ABOP)
• Full personal psychoanalytic training for the trainee
Research interests:
• Psychosocial aspects in Orofacial Pain
• Treatment of Temporomandibular Disorders
• Clinical protocols in Implant Dentistry
TMD therapy: Efficacy or effectiveness? Or does it happen in the patient’s mind?
Saturday, September 20th
16:30-17:00
It has been proposed to separate “efficacy” and “effectiveness” by defining the first as the
real therapeutic impact, while the second term explains the subjective, perceived impact
of a given successful treatment experience. A placebo is by definition a treatment without
efficacy, i.e. which produces no specific biologic effects on the medical condition or symptoms that a patient is experiencing. Nevertheless increasing evidences suggest that placebos have, under certain conditions, a great effectiveness. Also in TMDs placebo analgesia
seems to be therapeutically relevant. We performed a literature search aiming at gaining
information on how placebos work (the placebo effect) and how patients react to them
(the placebo response) in TMDs. A qualitative assessment of papers was possible, given the
uneven design of papers, mostly not expressly designed at investigating placebo.
Concepts about placebo effects and responses have changed dramatically over the years,
particularly in recent years. This has occurred primarily as a result of the evolution of experimental protocols using placebos in clinical studies of patients in pain, as well as of the
results of various studies involving normal subjects. Our understanding of the biological and
psychological mechanisms underlying placebo effects has expanded significantly due to
recent developments in the technology of brain imaging. Based on findings from functional
MRI and PET scan analyses, we now know that placebo analgesia is definitely a real (i.e.,
biologically measurable) phenomenon. It can be pharmacologically blocked and behaviorally
enhanced, and these responses have been demonstrated to be similar to those elicited by
administration of real anti-pain substances. Psychological mechanisms involved in placebo
analgesia include expectancy, meaning response and classical conditioning. Based on these
findings reconceptualization of the placebo response is proposed.
Present knowledge suggests that every treatment for pain contains a placebo component,
which sometimes is as powerful as the so-called ‘active’ counterpart. While the deceptive
use of placebos must be considered unethical, every health provider who is treating pain patients must be aware of this important phenomenon in order to harness its huge potential.
Keywords
• Placebo effect, expectancy, TMDs, splints, acupuncture
75
Arrival
Zurich Marriott Hotel
Neumuehlequai 42
CH-8001 Zurich
Phone: +41 (0)44 360 70 70
Fax: +41 (0)44 360 77 77
Email: [email protected]
www.marriotthotels.com
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