Brain and nerve = Shinkei kenkyū no shinpo
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Pain is a common reason for seeking health care and chronic pain is a common comorbidity in psychiatric disorders. In clinical practice, we encounter many patients with chronic pain; however, before initiating pain treatment, we should conduct detailed analysis of psychiatric symptoms, such as perception, memory, thought and mood disturbances or behavioral problems. We should also determine the frequency of occurrence of mental disorders in patients with pain, especially those with chronic pain, such as in mood, anxiety, pain, personality, and developmental disorders, and dementia. Current understanding of the intricate relationship between chronic pain and psychiatric issues not only provides opportunities for designing appropriate treatment but also raises good and new questions for future pain research.
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Pain is classified into physical and psychological pain. Physical pain is nociceptive, inflammatory, or neuropathic. Pain can be categorized into acute or chronic pain depending on the duration of pain and mechanism of onset. ⋯ Chronic pain is caused by incurable conditions or requires a long time to heal and is persistent: it includes chronic nociceptive pain, established neuropathic pain, and psychogenic pain. The therapeutic strategies for pain depend on the underlying pathological conditions: (1) For nociceptive pain, analgesics, narcotic analgesics, and nerve block are indicated. (2) For neuropathic pain, supplementary analgesics, but not analgesics, are indicated, and some narcotic analgesics are also effective: the recommended supplementary analgesics include calcium channel alpha-2-delta ligands, tricyclic antidepressants (TCAs), and serotonin-noradrenaline reuptake inhibitors (SNRIs). (3) For psychogenic pain, analgesics and nerve block are not indicated, except in the setting of a placebo effect: in paticular, narcotic analgesics should not be used. Psychological therapy, tranquilizer administration, cognitive behavior therapy, and patient education are indicated for this kind of pain.
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Evidence regarding the effectiveness of nerve block in treating neuropathic pain is scarce. However, in actual clinical situations, nerve block has been used as a treatment in combination with other methods, such as pharmacotherapy, psychotherapy, and physiotherapy. The goal of neuropathic pain treatment is not a complete recovery but some improvement in the activities of daily living (ADL) as well as the quality of life. ⋯ Therefore, the use of nerve block should be considered from the onset of pain. In recent years, methods such as ultrasound-guided nerve block and thermocoagulation with pulsed radiofrequency have become more commonly used as safer and more accurate nerve block techniques. This article discusses the current clinical status of nerve block against neuropathic pain.
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Review
[Pathophysiology of neuropathic pain: Na⁺ channel and hyperexcitability of primary afferents].
Neuropathic pain occurs as a result of peripheral neuropathy or peripheral nerve injury. Voltage-gated Na⁺ channels are assumed to play a major role in the pathophysiology of neuropathic pain and have become important therapeutic targets, because they are critical determinants of the excitability of sensory neurons. Nerve injury or disease could induce changes in trafficking, gene expression, and kinetics of Na⁺ channels, resulting in ectopic discharge and increased neuronal excitability. ⋯ Na⁺ channels are attractive targets for studying the pathophysiology of neuropathic pain and for drug development. However, recent advances have been mostly based on basic research. Overcoming the challenges in directly approaching patients with neuropathic pain might advance our understanding of the pathophysiology of pain and aid the development of therapeutic strategies.
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Neuropathic pain syndromes are clinically characterized by spontaneous pain and evoked pain (hyperalgesia and allodynia). The optimal treatment approach for neuropathic pain is still under development because of the complex pathological mechanisms underlying this type of pain. ⋯ Central sensitization represents enhancement of the function of neuronal circuits in nociceptive pathways and is a manifestation of the remarkable plasticity of the somatosensory nervous system after nerve injury. This review highlights the pathological features of central sensitization, which develops because of (1) injury-induced abnormal inputs from primary afferents, (2) increase in the excitability of dorsal horn neurons, and (3) activated glial cell-derived signals.