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Evaluation of Symptom Heterogeneity in Neuropathic Pain Using Assessments of Sensory Functions

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Evaluation of Symptom Heterogeneity in Neuropathic Pain Using Assessments of Sensory Functions Neurotherapeutics: The Journal of the American Society for Experimental NeuroTherapeutics Evaluation of Symptom Heterogeneity in Neuropathic Pain Using Assessments of Sensory Functions Kathrin Arning and Ralf Baron Division of Neurological Pain Research and Therapy, Department of Neurology, Christian-Albrechts-Universität Kiel, Germany Summary: Classification of neuropathic pain has been based can be elucidated in each patient. Moreover, in questionnaires on disease entities, anatomical localization, or histological ob- the verbal descriptors can depict the quality and intensity of the servations. Over the past decade, there has been an explosion in individual pain. The approach of classifying and subgrouping our understanding of the basic mechanisms of neuropathic pain. patients with neuropathic pain on the basis of symptoms or The exciting advances in basic science are paralleled by the signs opens up new possibilities for stratifying patients in clin- recognition from clinical investigations that neuropathic pain is ical trials. First, in clinical proof-of-concept trials the study not a monolithic entity, but instead presents as a composite of population can be enriched prospectively on the basis of entry pain and other sensory symptoms. Attempts are under way to criteria defined a priori. This enrichment with patients who supplement the traditional classification with a classification potentially require a specific treatment should increase the like- that links pain and sensory symptoms with neurobiological lihood for positive trial outcomes. Second, in clinical practice it mechanisms. This mechanism- or symptom-based classifica- becomes possible to establish an individualized therapy—that tion takes both negative and positive sensory symptoms into is, to identify the particular patients who require a specific account. By using a battery of several standardized quantitative treatment option. Key Words: Neuropathic pain, question- sensory tests, the characteristic profile of sensory symptoms naires, mechanism-based classification, symptom profiles. INTRODUCTION ETIOLOGY-BASED CLASSIFICATION Chronic pain is the reason for 40% of all visits to a It is common clinical practice to classify neuropathic general practitioner, causes severe suffering for many pain according to the underlying etiology of the disorder patients and presents a challenge to the doctor in terms of and the anatomical location of the specific lesion.2 Ac- adequate diagnostic work-up and management. There are cordingly, the majority of patients with painful lesions in two broad categories of chronic pain conditions: noci- the nervous system fall into three broad classes (Table 1).3 ceptive pain, which occurs after tissue disease or damage but in the presence of a functionally intact sensory ner- vous system (e.g., osteoarthritis), and neuropathic pain, 1) Neuropathic pain after peripheral nerve lesions. which arises when the afferent nervous system itself is Painful peripheral neuropathies may be of trau- diseased or damaged1 (e.g., postherpetic neuralgia). In matic, ischemic, inflammatory, toxic, metabolic, addition to nociceptive or neuropathic types, other or hereditary etiology. The anatomical distribu- chronic pain disorders should be distinguished, such as tion pattern of the affected nerves provides valu- somatoform pain disorders, pain associated with psycho- able differential diagnostic clues as to possible ses, or pain sine materia (diagnosed by exclusion), which underlying causes. Painful peripheral neuropa- are devoid of evidence for any nociceptive and neuro- thies are therefore grouped into symmetrical pathic processes. generalized polyneuropathies (diseases affecting many nerves simultaneously) and asymmetrical neuropathies (with a focal or multifocal distribu- tion, or processes affecting the brachial or lumbo- Address correspondence and reprint requests to: Prof. Dr. med. Ralf sacral plexuses). Baron, Division of Neurological Pain Research and Therapy, Department of Neurology, Christian-Albrechts-Universität Kiel, Arnold-Heller-Str. 3, 2) Neuropathic pain after lesions in the central ner- Haus 41, 24105 Kiel, Germany. E-mail: [email protected]. vous system. Central neuropathic pain syndromes 738 Vol. 6, 738–748, October 2009 © The American Society for Experimental NeuroTherapeutics, Inc. SYMPTOM HETEROGENEITY AND SENSORY FUNCTIONS 739 Table 1. Disease- and Anatomy-Based Classification of Table 1. Continued Neuropathic Pain Syndromes Abscesses Painful peripheral neuropathies Inflammatory diseases other than multiple sclerosis; Focal, multifocal myelitis caused by viruses, syphilis Phantom pain, stump pain, nerve transection pain Epilepsy (partial or complete) Parkinson’s disease Neuroma (posttraumatic or postoperative) Mixed pain syndromes Posttraumatic neuralgia Chronic low back pain with radiculopathy Entrapment syndromes Cancer pain with malignant plexus invasion Mastectomy Complex regional pain syndromes Post thoracotomy Morton’s neuralgia Painful scars may develop after stroke, multiple sclerosis, or Herpes zoster and postherpetic neuralgia spinal cord injury. Diabetic mononeuropathy, diabetic amyotrophy Ischemic neuropathy 3) Mixed pain syndromes. In these entities, both no- Borreliosis ciceptive and neuropathic processes contribute to Connective tissue disease (vasculitis) the pain. In particular, patients with chronic low Neuralgic amyotrophy back pain and cancer pain seem to fit into this Peripheral nerve tumors theoretical framework.4,5 Radiation plexopathy Plexus neuritis (idiopathic or hereditary) Trigeminal or glossopharyngeal neuralgia RATIONALE FOR A NEW CLASSIFICATION Vascular compression syndromes Generalized (polyneuropathies) For centuries, clinicians have been taught to examine Metabolic or nutritional and classify patients on the basis of the topography of the Diabetic, often “burning feet syndrome” Alcoholic lesion and the underlying pathology. In most clinical Amyloid specialties, such an approach has been a key element in Hypothyroidism understanding the pathophysiology of diseases and has Beri beri, pellagra led to progress in terms of finding disease-modifying or Drugs: Antiretrovirals, cisplatin, disulfiram, even disease-curing therapies. There are multiple exam- ethambutol, isoniazid, nitrofurantoin, thalidomide, thiouracil, vincristine, ples, including bacterial meningitis, neuroborreliosis, os- chloramphenicol, metronidazole, taxoids, gold teoarthritis, cancer, rheumatoid arthritis, ischemic heart Toxins: Acrylamide, arsenic, clioquinol, disease, and stroke. In most of these disorders, pain can dinitrophenol, ethylene oxide, pentachlorophenol, be a major complaint, a symptom that rapidly disappears thallium after the relevant therapy has been administered. Hereditary Amyloid neuropathy But what happens if the symptom itself becomes a Fabry’s disease disease? When pain persists and becomes a chronic prob- Charcot–Marie–Tooth disease type 5, type 2B lem, and when the underlying disease such as diabetes, Hereditary sensory and autonomic neuropathy cancer or vasculitis is known and cannot be cured? Clin- (HSAN) type 1, type 1B ical experience and decades of rather discouraging sys- Malignant: Carcinomatous (paraneoplastic), myeloma Infective or postinfective, immune system: Acute or tematic research related to therapy in chronic pain have inflammatory polyradiculoneuropathy (Guillain- shown that a strategy directed at examining, classifying, Barré syndrome), borreliosis, HIV and treating pain on the basis of anatomy or underlying Other polyneuropathies disease is of little or no help to the patients and their Erythromelalgia pain.6 This has become desperately clear in some recent Idiopathic small fiber neuropathy Trench foot (cold injury) randomized clinical trials in painful diabetic neuropathy. Central pain syndromes In these trials, the study medications failed to demon- Vascular lesions in the brain (especially brainstem and strate efficacy even though the compounds had shown thalamus) and spinal cord encouraging results in preclinical and early clinical stud- Infarct ies.7 Do these negative results really indicate lack of Hemorrhage Vascular malformation efficacy? Or is it possible that specific characteristics of Multiple sclerosis the study population, the selected patient group, or the Traumatic spinal cord injury including iatrogenic defined primary outcome have obscured a positive re- cordotomy sponse?8 Traumatic brain injury These observations have raised the question of Syringomyelia and syringobulbia Tumors whether an entirely different strategy, in which pain is analyzed on the basis of underlying mechanisms, could Neurotherapeutics, Vol. 6, No. 4, 2009 740 ARNING AND BARON be an alternative approach to examining and classifying Many patients with neuropathic pain also have evoked patients to obtain a better outcome. Increasing under- types of pain (stimulus-induced pain, hypersensitivity), standing of mechanisms underlying chronic pain, to- which are characterized by several sensory abnormali- gether with the discovery of new molecular targets for ties. They may be adjacent to or intermingled with skin modifying pain, has strengthened the demand for other areas of sensory deficit. Patients most often report me- ways to treat pain. Woolf and other authors3,9 have em- chanical hypersensitivity, followed by hypersensitivity to phasized the rationale for a treatment approach directed heat and cold. at one or more mechanisms rather than at diseases be- Two types of hypersensitivity can be distinguished. cause
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