Articles: pain-clinics.
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Following head trauma many different forms of headache can develop. Complaints in the early post-traumatic period appear to be organic in most cases. Later in the course post-traumatic headache frequently shows a psychogenic picture. Describing the causative factors and discussing the therapeutic guidelines, the authors explain how psychological influences can form chronic pain syndromes.
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During the long-term treatment with opioids it is sometimes important to switch the opioid or change the route of administration. The estimation of morphine-equivalents can be helpful in this range because it clarifies the dose in milligramm required for different clinical situations. The basis of this estimation is the equianalgesic potency of opioids. ⋯ Useful starting point for calculation an effective dose when changing from one opioid or route of administration to another can result in improved pain control that is more responsive to patient need. The limitations are 1. individual differences in the response to opioids, especially during long-term treatment and in the development of analgesic tolerance, 2. individual differences in the response to alternatives routes of administration, and 3. the unknown degree of cross tolerance among opioid drugs. The scientific meaning of the estimation of i.m. morphine-equivalent is discussed.
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Since 1982, a total of 88 patients with refractory fibrositis have received treatment as part of an integrated group program within a psychiatric outpatient clinic working closely with the department of rheumatology. The best arrangement proved to be a series of 15 weekly two-hour sessions with groups of 8 patients. The program has three main elements: information, instruction in pain control strategies, and group discussion. ⋯ Our program makes it possible for a greater proportion of patients to learn one or more techniques affording some measure of pain relief. It is important for the therapists to adopt a positive and convincing attitude while restricting themselves to helping the patients to help themselves and avoiding power struggles. They should also be ready to accept the patients and their view of the illness, and not attempt to interpret the illness as the expression of something else.
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A central antinociceptive effect of calcitonin has been well established in animal experiments. Owing to the lack of appropriate studies, however, a final judgement cannot be made regarding the value of calcitonin in pain therapy. Positive clinical experiences have been reported in the following cases. (1) In isolated osseous tumor pain and in pain caused by tumorous infiltration of peripheral nerve tissue or acute malignant transverse lesions of the spinal cord (with paraplegia), calcitonin can be a suitable supplement to opiate therapy. (2) In algodystrophy calcitonin can be administered in addition to physical therapy. ⋯ Dangerous side-effects have not been reported to date. However, dose-dependent side-effects occur frequently, which the patients often consider very distressing. The disadvantages and the "escape" phenomenon that occur during longterm use restrict the value of calcitonin as an analgesic.
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Migraine is more than the pain involved in the "migraine attack." Before the onset of pain many clinical symptoms can be observed. These symptoms may be classified as vegetative, affective, and vascular. Brain perfusion is altered during migraine attacks as well as during the intervals between attacks. ⋯ It may be assumed that platelet serotonin is a potent vasoregulating substance that may interact in the brain vessels with the neurotransmission controlled perfusion. The hypothesis of an (inborn) instability of the interaction of cerebral neurotransmission systems in patients suffering from migraine is in accordance with the vegetative and affective symptoms in migraine, the observed imbalance of neurotransmission mediated cerebrovascular autoregulation and the irritation of platelets in migraine attacks, as well as in the interval between attacks. The "modern" treatments of migraine with acetylsalicylic acid, ergotamin and/or beta blockers are discussed in relation to this proposed hypothesis of a migraine pathophysiology.