Maija Haanpää1 & Rolf-Detlef Treede2 1 Department of Neurosurgery, Helsinki University Hospital, Helsinski, Finland 2 Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany Neuropathic pain (NP), defined as “pain arising as a direct consequence of a lesion or disease affecting the somatosensory system” [1] is a challenge to healthcare providers as it is common, often under‐diagnosed, under‐treated and, when severe, associated with suffering, disability and impaired quality of life. Standard treatment with conventional analgesics does not typically provide effective relief of pain. The most common reasons for NP are radiculopathy, diabetic polyneuropathy and nerve trauma including postoperative neuralgia. Population prevalence of pain with neuropathic characteristics is 6.9–10% [2]. Incidences of painful diabetic neuropathy, postherpetic neuralgia and trigeminal neuralgia are 5.3–72.3/100,000 person‐years (PY), 3.9–42.0/100,000 PY and 0.2–0.4/100,000 PY, respectively [2]. NP follows spinal cord injury in 53 % of patients [3] and stroke in 11 % of patients [4]. As the population is aging and the prevalence of diabetes is increasing, prevalence of NP is expected to rise. In the ICD‐11 classification, NP is first organized into peripheral and central neuropathic pain based on the location of the lesion or disease in the peripheral or central somatosensory nervous system [5]. Within each of these categories, pain is classified into different NP conditions based on the underlying disease. Peripheral NP includes: (1) trigeminal neuralgia, (2) NP after peripheral nerve injury, (3) painful polyneuropathy, (4) postherpetic neuralgia, (5) painful radiculopathy and 6) other specified and unspecified peripheral NP. Central NP includes: (1) central NP associated with spinal cord injury, (2) central NP associated with brain injury, (3) central post‐stroke pain, (4) central NP caused by multiple sclerosis and (5) other specified and unspecified central NP. This classification covers the epidemiologically most relevant conditions and provides clear diagnostic criteria that are backed by literature [5]. Unlike nociceptive pain, which is caused by physiological activation of peripheral nociceptive nerve terminals in response to tissue damage or threat of such damage, chronic NP has no beneficial effect. It can arise from damage to the nerve pathways at any point from the terminals of the peripheral nociceptors to the cortical neurons in the brain. It is not known why the same condition is painful in some patients and painless in others. Currently, a mechanism‐based classification of NP is not possible, as the detailed pain mechanisms in an individual case cannot be identified. Furthermore, one mechanism can be responsible for many different symptoms and the same symptom in two patients can be caused by different mechanisms [6]. Our understanding of the underlying pathophysiology has increased considerably in the last decades, although not to the extent that treatment has improved [7]. As NP can coexist with nociceptive pain, clinicians should try to identify different pain components and treat each of them according to the best available evidence. Damage to the somatosensory system leads to negative sensory symptoms (feeling of numbness) and signs (sensory loss to the somatosensory submodalities touch, proprioception, thermoreception, nociception or visceroreception). Damaged neurons, however, can also develop spontaneous activity (e.g. by altered expression of ion channels at a neuroma or in the dorsal root ganglion). When ectopically generated action potentials are transmitted to the nociceptive network in the brain, this results in a pain sensation that is projected to the receptive field of the damaged neural structure (Figure 36.1). Peripheral nerve damage can also lead to secondary changes within the central nervous system, including altered synaptic connectivity and receptive field reorganization. These secondary changes involve local excitatory and inhibitory neurons, ascending and descending pathways, as well as microglia and astrocytes [8]. When the neural damage is partial, the remaining neural connections may be facilitated as a result of these secondary changes, leading to positive sensory symptoms (paraesthesia and spontaneous pain) and signs (hyperalgesia and allodynia, mostly to mechanical or cold stimuli) (For further discussion of mechanisms see Chapter 3). Figure 36.1 Projected pain. Damage to a peripheral nerve may lead to action potential generation at the site of damage. When these action potentials reach the nociceptive network in the brain, the resulting pain sensation is projected into the peripheral receptive field of the damaged nerve, where this activity would normally originate. Thus, pain in a body part may result from damage to that body part itself or to any site along the neural pathways connecting that body part with the brain. Based on Treede (2001) Kapitel A3, In: Zenz, Jurna (Hrsg.) Lehrbuch der Schemerztherapie, Fig . 11. The coexistence of negative and positive sensory phenomena within the same region is prototypical for patients with NP. The spatial distribution of these symptoms and signs and the distribution of the projected pain sensation provide information on the neuroanatomic site of neural damage. Current and future therapies for NP are directed at central and peripheral nociceptive signal processing (centrally and peripherally acting analgesics, modulators of endogenous pain control systems), ectopic impulse generation (local anesthetics) and at the pathophysiological processes of degeneration, regeneration and reorganization [9]. In general, systemic NP medication has to pass the blood–brain barrier in order to reach its target. Such a barrier is also present in the peripheral nervous system, but the blood–nerve barrier is leaky in the dorsal root ganglion and in peripheral nerve inflammation. NP can be spontaneous (stimulus‐independent) or elicited by a stimulus (stimulus‐evoked pain). Spontaneous pain is often described as a constant burning sensation, but it may also include intermittent shooting lancinating sensations, electric shock‐like pain and dysesthesia (i.e. an unpleasant abnormal sensation). The pain may also be accompanied by paresthesia, an abnormal sensation that is not unpleasant. Stimulus‐evoked pains are elicited by mechanical, thermal or chemical stimuli. Hyperalgesia consists of an increased pain response to a stimulus that is normally painful and activates peripheral nociceptive terminals, whereas allodynia has been introduced as a term to describe pain sensation from a stimulus that does not normally provoke pain and that does not activate nociceptors (such as gentle stroking by a brush) and thus implies a change in central neural processing [10]. Additionally, there may be other symptoms and clinical findings (e.g. motor paresis, muscle cramps, autonomic nervous system signs) depending on the site of the lesion. It is not possible to conclude the etiology of NP from the clinical characteristics of pain. Once present, NP pain tends to be long‐lasting. However, some patients may recover from their pain completely and others may obtain relief by pharmacotherapy or learn to cope with their symptoms by attending interdisciplinary treatment or self‐management programs. Assessment of a patient with suspected NP aims at: (i) recognition of NP; (ii) localizing of the lesion as far as possible (peripheral or central and further whether the lesion is in the brain hemisphere, brainstem, spinal cord, nerve root, plexus, peripheral nerve or its branches); and (iii) diagnosing the causative disease or event. In addition, assessment of psychosocial aspects is necessary for an individually tailored management strategy. Possible comorbidities such as impaired sleep, anxiety, depression, disability and secondary impairment in work, family and social life should also be taken into account [11]. The clinical examination of the patient presenting with NP is the same as that described for any patient presenting with chronic pain (Chapter 8). The neurosensory examination is particularly important. Sensory testing at the bedside can be accomplished with simple tools [12]. Touch is tested with a finger or cotton wool, pinprick with a wooden cocktail stick, warm and cold with a cold and a warm object and vibration with a tuning fork. The response to each stimulus can be graded as normal, decreased or increased. The findings in the painful area are compared with the findings in the contralateral area in unilateral pain and in other sites on the proximal–distal axis in bilateral pain. Identifying a neurological disease or a nervous system lesion is based on a systematic search of neurological abnormalities in the clinical examination. In the neurological examination the signs are repeatable and the location of lesion is concluded on the basis of the neurological signs. In addition to the sensory examination, the motor assessment (muscle strength, tonus, coordination and fluency of movements), examination of tendon reflexes and examination of cranial nerves are performed. Assessment of the peripheral autonomic nervous function (warmth and color of skin, sudomotor function) is important especially when a complex regional pain syndrome is suspected. Sometimes the diagnosis is straightforward (e.g. NP after an obvious nerve lesion during surgery or post‐herpetic neuralgia after shingles). In these cases no additional tests are needed. If a patient has stocking and glove‐type pain location (Figure 36.2), then one might consider nerve conduction studies (NCS) and electromyography (EMG). As presented in more detail in Chapter 11
Chapter 36
Neuropathic pain
Introduction
Basic mechanisms
Clinical picture
Clinical examination
Other diagnostic procedures
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