Corticalization of chronic pain?

Abstract

p ain, the barking watchdog of our health, is normally temporary. It immobilizes the damaged muscle or joint so that healing can occur and forces us to see the doctor. This acute and subacute pain is soon and completely forgotten once it has passed. Otherwise, as has been speculated, every family would have but one child. Acute pain normally has a reason, and is then treated by removing that cause. Similarly, we can mimic pain by inducing a cause experimentally, for example, by noxious stimulation. This way we get evidence about the pain receptors and afferents, pain pathways, its central processing, thalamic contributions, and about cortical involvement. In the same manner, mechanisms of pain relief, endogeneously through diffuse noxious inhibitory control or endorphin release, exogeneously through analgesic drugs or treatments, have well been studa destructor. Pain, formerly a symptom, becomes a disease. Physicians are normally trained to cure acute illness and are often frustrated by those patients with vague pain that refuses to go. As a consequence, the patient is despaired of seeking help in vain by the fami]ydoctor, the neurologist, the psychiatrist, the psychologist, at last by alternative medicine, and even by quackery. In parallel to the derailment of pain into chronification, the scientific attempts to explain chronic pain are poor. Physiological, anatomical, or biochemical developments involved in sustained chronic pain are broadly missing. This is already true for the peripheral end. How can a brief damage induce a permanent pain? Dissection of a nerve produces only a short barrage of impulse trains for a very short period of a~couple of minutes, not days, months, or years like in the phantom limb pain. Persistent dental pain, ied with experimental pain models. The most importoo , is not necessarily coupled to correspondingly tant pain response to these stimuli in man is, of course, the verbal report. Other pain reactions, measurable in man and in animal, are withdrawal reflexes or vegetative responses, e.g., changes in blood pressure, heart action, respiration rate, and local blood circulation. Phasic pain stimuli allow the monitoring of normal and disturbed pain pathways, by microelectroneurographic recordings or scanning through surface electrodes, especially over the scalp in the form of pain-relevant changes in the spontaneous electroencephalogram. 1 All these approaches are useful to uncover the puzzle of phasic pain. Chronic pain, however, is different. It persists, day after day and night after night, leading to the endless circle of sleeplessness, depression, agony, and social isolation. Pain, the protector of life, turns into