Journal Article10.1016/0304-3959(92)90259-E
Painful neuropathy: altered central processing maintained dynamically by peripheral input.
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TL;DR: A model of neuropathic pain is proposed in which ongoing nociceptive afferent input from a peripheral focus dynamically maintains altered central processing that accounts for allodynia, spontaneous pain, and other sensory and motor abnormalities.
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Abstract: We performed sensory assessments before and during diagnostic tourniquet-cuff and local anesthetic blocks in 4 patients diagnosed with reflex sympathetic dystrophy (RSD). All patients complained of mechano-allodynia; lightly touching the skin evoked an intense pain sensation. At detection levels, electrical stimuli were perceived as painful, suggesting that the mechano-allodynia was mediated by A beta low-threshold mechanoreceptor afferents. A beta-mediated allodynia was further supported by reaction time latencies to painful electrical stimuli at threshold for A-fiber activation and, in 1 patient, by differential cuff blocks which abolished A beta function and allodynia while thermal sensation (warm and cold) were preserved. Local anesthetic block of painful foci associated with previous trauma abolished mechano-allodynia, cold allodynia, and spontaneous pain in all patients and relieved the motor symptoms in 1 patient with tonic contractures of the toes. Tactile and thermal perception in the previously allodynic area was preserved. When the local anesthetic block waned, spontaneous pain, allodynia, and motor symptoms returned. We propose a model of neuropathic pain in which ongoing nociceptive afferent input from a peripheral focus dynamically maintains altered central processing that accounts for allodynia, spontaneous pain, and other sensory and motor abnormalities. Blocking the peripheral input causes the central processing to revert to normal, abolishing the symptoms for the duration of the block. The model accounts for sympathetically maintained (SMP) and sympathetically independent (SIP) pain. The peripheral input can be independent of sympathetic activity or driven completely or in part by activity in sympathetic efferents or by circulating catecholamines. The shared final common pathway may explain the common features of SMP and SIP.
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References
Evidence for a central component of post-injury pain hypersensitivity
TL;DR: An animal model is developed where changes occur in the threshold and responsiveness of the flexor reflex following peripheral injury that are analogous to the sensory changes found in man, and shows that it in part arises from changes in the activity of the spinal cord.
2.2K
The induction and maintenance of central sensitization is dependent on N-methyl-D-aspartic acid receptor activation; implications for the treatment of post-injury pain hypersensitivity states.
TL;DR: Results indicate that NMDA receptors are involved in the induction and maintenance of the central sensitization produced by high threshold primary afferent inputs and have a bearing both on the potential role of NMDA antagonists for pre‐emptive analgesia and for treating established pain states.
2K
Peripheral nerve injury triggers central sprouting of myelinated afferents
TL;DR: It is shown that after peripheral nerve injury the central terminals of axotomized myelinated afferents, including the large Aβ fibres, sprout into lamina II, a structural reorganization in the adult central nervous system that may contribute to the development of the pain mediated by A-fibres that can follow nerve lesions in humans.
1.1K
Neurogenic hyperalgesia: psychophysical studies of underlying mechanisms.
TL;DR: It was postulated that there exist special chemosensitive primary afferent nerve fibers that are more effective in producing mechanical hyperalgesia than are the known thermo- and mechanosensitive nociceptive nerve fibers.
967
Method for quantitative estimation of thermal thresholds in patients.
TL;DR: A quantitative method for the examination of thermal sensibility was applied in 26 normal subjects and in patients with various neurological disorders, and the resulting temperature curve enables a quantitative description of the subject's Thermal sensibility and of the degree of impairment displayed by neurological patients.
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