ISSN:0148-639X    

DOI:10.1002/mus.880161002

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1993

数据来源: WILEY

摘要:

AbstractThis is an overview on aspects of structure, function and pathology of the primary sensory unit in man, emphasizing concepts which form the basis for understanding the nature of neuropathic sensory syndromes and the rationale for special clinical physiologic testing. © 1993 John Wiley&Sons, Inc

ISSN:0148-639X    

DOI:10.1002/mus.880161003

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1993

数据来源: WILEY

摘要:

AbstractCentral pain syndrome is defined as pain associated with a lesion of the central nervous system. It has a low incidence but is frequently intractable and does not have effective treatment. The cause of central pain is speculative; however, the single common sensory abnormality in patients with central pain is interruption of spinothalamocortical nociceptive pathways. It appears that severe central nervous system lesions, with total destruction of ascending sensory systems, do not lead to a central pain syndrome; and that setting of mild, moderate, or severe disruption of the anterolateral ascending system with partial or complete preservation of the dorsal column/medial lemniscus functions is most frequently associated with central pain syndrome. Furthermore, even during remission, dysesthesias and pain could be triggered by additional afferent input to the large fiber/dorsal column/medial lemniscus system and, once established, they may not be abolished byadditional deafferentation. © 1993 John Wiley&Sons, Inc

ISSN:0148-639X    

DOI:10.1002/mus.880161004

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1993

数据来源: WILEY

摘要:

AbstractIt is possible to learn more about peripheral nerve function in human subjects than is obtainable with routine nerve conduction studies, and thereby to study the basis of “positive” symptoms, such as paresthesias. Using microneurography, ectopic impulse activity in cutaneous afferents has been recorded in patients suffering from neurologic disorders and in normal subjects in whom paresthesias were provoked by hyperventilation, prolonged tetanization of cutaneous nerves and ischemia. Using relatively simple modifications of standard nerve conduction techniques, the increases in axonal excitability responsible for this ectopic activity have been documented in human volunteers. Hyperventilation increases axonal excitability butdoes not change supernormality, probably because Na+channels are activated by the decrease in [Ca2+] on the axonal membrane. Prolonged tetanic stimulation and ischemia probably share similar mechanisms. At least in motor axons, postischemic ectopic activity occurs when the hyperpolarization that results from activation of the Na+/K+pump lowers the membrane potential below the equilibrium potential for K+. A high extracellular [K+] can then result in an inward current producing depolarization and possibly triggering regenerative processes. © 1993 John Wiley&Sons,

ISSN:0148-639X    

DOI:10.1002/mus.880161005

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1993

数据来源: WILEY

摘要:

AbstractThe search for the identification of the sensory apparatus encoding muscle pain sensation in humans is recounted. Basic neurophysiologic animal studies, leading to a description of slowly conducting afferent from muscle and definition of high threshold polymodal muscle nociceptors, and pioneer psychophysic human studies together with recent microneurographic experiments in humans are described. The phenomena of muscle pain broad localization and distant referral are discussed, and clinical implications are extrapolated to interpret muscle pain as a localizing sign of mononeuropathy or radiculopathy. The identification of human muscle nociceptors has defined the scientific standard to test emerging clinical descriptions having muscle pain as a symptom. © 1993 John Wiley&Sons, Inc

ISSN:0148-639X    

DOI:10.1002/mus.880161006

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1993

数据来源: WILEY

摘要:

AbstractRecent work has succeeded in producing models of painful peripheral neuropathies in laboratory animals. There is evidence that the animals experience both abnormal spontaneous pain and abnormal evoked pains (allodynia and hyperalgesia). Experimental analyses of these models have demonstrated potential pathophysiologic mechanisms in both the peripheral and central nervous systems; it is likely that the model neuropathic pain syndromes are due to several different mechanisms. One line of evidence suggests that these pain states gradually become centralized due to an excitotoxic effect on spinal cord dorsal horn inhibitory interneurons. The role of the sympathetic nervous system appears to vary, depending on the type of nerve injury and the temporal evolution of the syndrome. There is evidence indicating that theabnormality of cutaneous temperature regulation that often accompanies painful peripheral neuropathy is not necessarily due to the activity of sympathetic vasomotor efferents. © 1993 John Wiley&Sons, Inc

ISSN:0148-639X    

DOI:10.1002/mus.880161007

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1993

数据来源: WILEY

摘要:

AbstractCausalgia, reflex sympathetic dystrophy, and sympathetically maintained pain (SMP) are a complex group of disorders, with symptoms of spontaneous/stimulus‐induced pain and vasomotor, sudomotor or skeletomotor dysfunction of the involved area. Sympatholysis has been recommended for diagnosis/classification and treatment of these patients. Lack of adequate placebo control makes the physiologic response to this intervention unclear. Sensitization of wide dynamic range (WDR) neurons in the central nociceptive pathway has been proposed as a key element in pathophysiologic mechanisms of these disorders. Low threshold mechanoreceptors and nociceptors have been implicated as the primary afferents transmitting signals to or maintaining sensitization of WDR neurons in SMP. Vasomotor disturbances may result from antidromic vasodilatation, vasoparafytic dilatation, normal somatosympathetic reflexes, and denervation supersensitivity. There is conflicting information regarding the use of phentolamine and clonidine in these pain syndromes. Treatment of these patients remains a challenge given the many potential underlying mechanisms. © 1993 John Wiley&Sons, I

ISSN:0148-639X    

DOI:10.1002/mus.880161008

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1993

数据来源: WILEY

摘要:

AbstractA number of laboratory tests are critically important in the quest to diagnose presence or absence of organic neuropathic dysfunction and to establish the relevance of such to the subjective pain complaints. However, none of these tests has absolute diagnostic value and their results must be interpreted in the light of the clinical picture. Conventional electrophysiology evaluates function of large caliber afferent and motor fibers leaving the function of small caliber afferent fibers unexplored, and cannot explore the basis for positive sensory phenomena. The quantitative somatosensory thermotest is the best test available to explore function of small caliber afferents. It allows documentation of positive sensory phenomena in the form of thermal hyperalgesia. Because it is a psychophysical test, it lacks localizing value. Thermography sensitively detects and precisely delineates areas of cutaneous thermal change of neural origin. Three types of diagnostic neurologic blocks are used in the clinic: compression‐ischemia, local anesthetic and sympathetic blocks. Although they may provide important information about the pathophysiology of pain and hyperalgesias, adequate placebo control is of the essence because chronic neuropathic pain patients may express a high incidence of placebo response. © 1993 John Wiley&Sons, I

ISSN:0148-639X    

DOI:10.1002/mus.880161009

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1993

数据来源: WILEY

摘要:

AbstractPsychophysical experiments in combination with microneurography and intraneural microstimulation in awake human subjects have yielded some useful information on somatosensory functions under normal and pathologic conditions. Normally, pain is signaled by nociceptive afferents, and tactile sensations are evoked from activation of low‐threshold mechanoreceptors. Following tissue injury, nociceptors are sensitized, and their enhanced responsiveness correlates with hyperalgesia to heat and in some cases to mechanical stimuli. In addition, ongoing activity in sensitized nociceptive afferents may lead to central sensitization in such a way that normally nonpainful gentle stroking the skin evokes pain from activation of low‐threshold mechanoreceptors. This particular change in signal processing in the central nervous system is restored when the ongoing nociceptive input is interrupted, whereas other forms of central sensitization can outlast the duration of the nociceptive input. © 1993 John Wiley&Sons,

ISSN:0148-639X    

DOI:10.1002/mus.880161010

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1993

数据来源: WILEY

ISSN:0148-639X    

DOI:10.1002/mus.880161011

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1993

数据来源: WILEY