Neuroimaging methods have become widely used byresearchers and clinicians interested in better under-standing the functioning of the human brain in healthand disease. For the field of pain advances have beenmade in understanding how nociceptive processingwithin the healthy human central nervous system gener-ates a conscious perception of pain. The focus hasrecently shifted towards patient-related research, har-nessing earlier developments to test specific hypothesesin a broad range of chronic pain disorders includingneuropathic. Results to date strongly support the notionthat neuroimaging will aid our understanding of basicmechanisms contributing to the generation of chronicpain states. Furthermore, these techniques might helpdiagnose a patient’s pain condition in a more objectiveand robust way. This could enable better targeting oftherapies and more rapid development of compoundsto alleviate pain. The timing is therefore ideal to assessthe utility of data generated from studies utilising differ-ent methodological approaches to assess human CNSstructure and function in neuropathic pain states: (1)brain morphometry, (2) functional MRI, and (3) neuro-receptor imaging for acute and chronic pain, and forneuropathic pain. What is fact rather than fiction?

doi:10.1016/j.ejpain.2007.03.073

60WHAT TO LEARN FROM LIGAND-PET IMAGINGSTUDIES?

T.R. Tolle*, M. Valet, G. Henriksen, T. Sprenger

Neurologishe Klinik, Munich, Germany

Over the last decades, functional imaging studieshave fostered our knowledge about cerebral pain pro-cessing in humans. Great interest has focussed on possi-ble opioidergic mechanism of pain transmission andmodulation. Today, reliable knowledge about in vivodistribution of opioid receptors in healthy human sub-jects is available from PET studies of opioidergic neuro-transmission. Gender dependent differences in receptordistribution and ligand metabolism have been docu-mented. Moreover, an increasing number of studiesare reporting alterations of receptor distribution pat-terns in painful disease states. Various acute painfulchallenges have also been shown to induce measurablechanges in receptor availability in multiple brain areas.The perigenual anterior cingulate cortex (ACC) hasbeen identified as one brain region of major impact inopioidergic pain modulation. Thereby, the ACC appar-ently executes cortical top-down control on brainstemstructures in (exogenous) pharmacological opioid anal-gesia. In addition, accumulating evidence suggests that

also non-pharmacological treatment approaches utilizesimilar endogenous opioid dependent pathways to exertpain modulation. Moreover, it was recently shown thatopioids modulate neurotransmission in the nigrostriataldopaminergic pathway and that in turn dopaminergicchanges such as increases or decreases in COMT enzymeactivity affect opioidergic neurotransmission.

doi:10.1016/j.ejpain.2007.03.074

61FUNCTIONAL MRI AS A TOOL FOR DIAGNOSIS

IN NEUROPATHIC PAIN

I. Tracey *, P. Schweinhardt, H. McQuay, K.Wartolowska

Oxford University, UK

Most functional MRI studies have focussed on acutenociceptive processing in normal, healthy subjects. Thecerebral signature that reflects the painful experience isreasonably well identified and brain regions that are mod-ulated during manipulations of the pain experience in dif-fering circumstances increasingly understood. Onlyrecently have laboratories started to translate these find-ings and hypotheses generated to chronic pain patients.The cerebral pattern that reflects central processing insuch patients, particularly those of a neuropathic classifi-cation, is now emerging. Furthermore, the use of capscai-cin as a model of key neuropathic pain symptomscombined with FMRI in healthy controls is contributingto a greater knowledge regarding signals that possiblyreflect central sensitisation. Pharmacological studies usinggold-standard agents in the treatment of neuropathic painare further helping understand what regions are key inboth the generation and maintenance of this pain state.The prefrontal cortex, thalamus, insula and brainstemseem to play particularly important roles in the contextof chronic, neuropathic pain, however, the field is stillemerging. Combined, these studies provide strong evi-dence that our knowledge regarding this condition is mov-ing towards a point where the information available mightenable a better diagnosis of an individual patient’s paincondition in the years to come. In this talk examples willbe given to illustrate all the points discussed above.

doi:10.1016/j.ejpain.2007.03.075

62WHAT CAN BRAIN MORPHOMETRY TELL USABOUT CHRONIC PAIN?

M.C. Bushnell *, A. Kuchinad, P. Schweinhardt, D.A.

Seminowicz

Centre for Research on Pain, Montreal, Canada

S24 Invited Presentations / Workshop – Assessment And Diagnosis 3 / European Journal of Pain 11(S1) (2007) S1–S57

There is accumulating evidence that chronic pain isassociated with changes in brain anatomy, most com-monly a decrease in gray-matter. Gray-matter decreaseshave been described for chronic low back pain andheadache, and we now have similar results for fibromy-algia (FM). The decreases in gray-matter are related toduration and intensity of symptoms, suggesting thatthe structural changes may be an important componentof the chronification of pain. Similar neuroanatomicalabnormalities are found in stress-related disorders,including chronic fatigue syndrome and posttraumaticstress disorder (PTSD). In contrast to the decreasedgray-matter observed in the older patients examined inmost of these studies, we found that a group of youngwomen with a chronic pain condition (vulvovestibulitis)had greater gray-matter density than controls. Similarly,our youngest FM patients had more gray-matter thanage-matched controls. This biphasic effect is consistentwith other disorders. Whereas adults with PTSD havereduced gray-matter volume, children and adolescentswith PTSD have increased gray-matter volume. Simi-larly, adults with bipolar disorder have decreased gray-matter in the orbitofrontal cortex, whereas adolescentgirls with bipolar disorder show the opposite effect.Thus, there is accumulating evidence that abnormalgray-matter density at a young age may be predictiveof various disorders, including chronic pain. Althoughthis idea is speculative, the available data suggest thatthe examination of differences in brain anatomy mightprovide a useful tool for predicting and diagnosingchronic pain states, including neuropathic pain.

doi:10.1016/j.ejpain.2007.03.076

Workshop – Epidemiology And Health Care

Systems 3: ASSESSMENT AND TREATMENT

OF NEUROPATHIC BACK PAIN

63Workshop Summary: ASSESSMENT AND TREAT-

MENT OF NEUROPATHIC BACK PAIN

R. Rolke

Department of Neurology, University of Mainz, Germany

Back pain seems to be the most common chronic paincondition. The current assessment of back pain com-prises clinical examination, pain questionnaires andimaging techniques. Especially pain questionnairesallow profiling of ongoing pain or evoked pain intensi-ties. Moreover, some of these questionnaires are helpfulto distinguish between nociceptive and neuropathic backpain components. In the recent years, other methods areemerging from the laboratory to the clinical environ-ment like quantitative sensory testing (QST). This

expansion of the classical clinical armamentariumallows more detailed insights into the symptom profilesand possible underlying neurobiological mechanisms ofback pain syndromes. Based on these assessment resultsdifferent psychological, pharmacological or interven-tional treatment procedures are available.

The first lecture will address the use of pain question-naires in the diagnosis of neuropathic pain in general.The LANSS scale allows characterizing different painsyndromes based on pain descriptors distinguishingbetween a more nociceptive or neuropathic pain with ahigh sensitivity and specificity.

The second lecture will cover the use of the QST pro-tocol of the German Research Network on NeuropathicPain (DFNS) in the assessment of different groups ofback pain patients. Using QST it is possible to examinethe complete somatosensory phenotype, namely the per-formance of different peripheral and central somatosen-sory channels to the brain.

The third lecture will focus on treatment strategies,whenever back pain presents with a predominantly neu-ropathic pain component. While pharmacological treat-ment algorithms do not differ from those of otherneuropathic pain syndromes, several interventional pro-cedures allow a causal treatment, e.g. nucleotomy afterlumbar disc herniation.

doi:10.1016/j.ejpain.2007.03.077

64QUESTIONNAIRES IN NEUROPATHIC PAIN:

WHAT HAVE WE LEARNED FROM THE LANSS

PAIN SCALE?

M.I. Bennett

St. Gemma’s Hospice, Leeds, UK

In most cases of chronic pain, it is difficult to estab-lish the presence or absence of nerve dysfunction,regardless of symptoms. Many clinicians that managepatients with chronic pain do not have adequate skillor time for a thorough neurological examination. Nei-ther do they have easy access to quantitative sensorytesting and so treatment decisions are supported bybasic clinical evidence alone.

The Leeds Assessment of Neuropathic Symptomsand Signs (LANSS) pain scale was the first validatedscreening tool for neuropathic pain. Clinical studiesdemonstrated around 80% sensitivity and specificityfor distinguishing neuropathic pain from non-neuro-pathic pain. Further independent validation studies indifferent pain contexts have confirmed the utility of theLANSS as a reliable screening tool.

This presentation will focus on the use of the LANSSand other screening tools in identifying back pain with a

Invited Presentations / Workshop – Epidemiology And Health Care Systems 3 / European Journal of Pain 11(S1) (2007) S1–S57 S25