Pain
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The involvement of the basal ganglia in motor functions has been well studied. Recent neurophysiological, clinical and behavioral experiments indicate that the basal ganglia also process non-noxious and noxious somatosensory information. However, the functional significance of somatosensory information processing within the basal ganglia is not well understood. ⋯ Frequently, these patients have intermittent pain that is difficult to localize. Collectively, these data suggest that the basal ganglia may be involved in the (1) sensory-discriminative dimension of pain, (2) affective dimension of pain, (3) cognitive dimension of pain, (4) modulation of nociceptive information and (5) sensory gating of nociceptive information to higher motor areas. Further experiments that correlate neuronal discharge activity with stimulus intensity and escape behavior in operantly conditioned animals are necessary to fully understand how the basal ganglia are involved in nociceptive sensorimotor integration.
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Review Historical Article
The role of psychological factors in chronic pain. I. A half century of study.
This review examines a half century of thought about the role of psychological factors in chronic pain. Changing views are discussed, and representative examples of pain research based on psychoanalytic, behavioural, cognitive, and psychophysiological theories are presented and evaluated. ⋯ Studies reviewed show that an earlier concept, based on simple formulations of psychological causation, has been replaced by more comprehensive explanations comprising both physical and psychological influences. Further methodological and conceptual problems are discussed in the second paper of this 2-part review.
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Review Case Reports
Reflex sympathetic dystrophy treated by electroconvulsive therapy: intractable pain, depression, and bilateral electrode ECT.
An adult female patient without previous history of pain or psychiatric disorder developed reflex sympathetic dystrophy (RSD) in her left hand and arm after 2 separate injuries, and subsequent arthroscopy and arthroscopic surgery. Traditional management with systemic medications, nerve blocks, and behavioral pain management were unsuccessful. With subsequent development of depression and suicide attempt, electroconvulsive therapy (ECT) was administered using bilateral lead placement. ⋯ A review of the literature from the 1940s revealed numerous cases of chronic, intractable pain treated successfully by ECT, although none of the case series were controlled studies. More recent literature questions if 'modified' ECT, using unilateral lead placement, is less effective than bilateral lead placement, in treating pain syndromes. Resolution of the vascular changes of RSD after ECT raises questions of possible cerebral contributions to the pathophysiology of RSD.
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Peripheral tissue damage or nerve injury often leads to pathological pain processes, such as spontaneous pain, hyperalgesia and allodynia, that persist for years or decades after all possible tissue healing has occurred. Although peripheral neural mechanisms, such as nociceptor sensitization and neuroma formation, contribute to these pathological pain processes, recent evidence indicates that changes in central neural function may also play a significant role. ⋯ We also assess the physiological, biochemical, cellular and molecular mechanisms that underlie plasticity induced in the central nervous system (CNS) in response to noxious peripheral stimulation. Finally, we examine theories which have been proposed to explain how injury or noxious stimulation lead to alterations in CNS function which influence subsequent pain experience.
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The prevalence of major depression in patients with chronic low back pain (CLBP) is approximately three to four times greater than that reported in the general population. In spite of these high prevalence rates, there have been few systematic attempts to investigate the efficacy of treatment for major depression in patients with CLBP. ⋯ Clinical issues related to diagnostic confounds, rehabilitation outcome, and conceptualizations of the relation between pain and depression are discussed. It is argued that, in patients with clinical levels of depression, treatment modalities specifically targeting depressive symptomatology deserve serious consideration as an integral component of pain management programs.