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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pain syndromes in elderly patients are seldom psychogenic or due merely to "old age." Careful differential diagnosis is important, as judicious use of nerve blocks as adjunctive therapy often can relieve pain and restore activity. In the acute phase of shoulder pain, intrabursal injection of local anesthetic and steroid inhibits the inflammatory process. In the later stages, suprascapular nerve block relieves pain and interrupts afferent pain pathways. The occipital pain and headache of cervical arthritis also often respond to injection of 2 to 3 ml of long-acting anesthetic into the greater and lesser occipital nerves at the sites where they pierce the trapezius. Minor causalgia, shoulder-arm syndrome, or chronic traumatic edema may follow either forearm fracture or inflammation around the shoulder joint. Five stellate ganglion blocks with 1% lidocaine on alternate days, followed by 3 to 4 months of active and passive exercise, is the most effective treatment. This regimen usually produces a fully functional extremity. In degenerative disk disease, osteoarthritis, and metastatic disease, the cause of back pain is essentially the same--edema and inflammation of nerve roots at the intervertebral foramina. Injection of local anesthetic and steroid into the epidural space usually reduces swelling and inflammation. Patients are evaluated in 2 weeks and reblocked if improvement has plateaued. Pain relief most often is prompt and persists for an indefinite period.
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PMID:Relieving pain with nerve blocks. 14 96

Cephalalgia (1st century AD), nostalgia (1678), neuralgia (18th century), causalgia (1872) were terms followed in the 1950's by Bonica's 'algology... a disease state of its own', addressed by ever-growing numbers of pain clinics, strongly foreshadowed by Leriche's douleur maladie in the 1930's. (Hence also 'algotherapy'). Philosophers first, then early academic physiologists began to exhibit interest in pain, that all too common phenomenon, only too often unyielding to theoretical as well as practical efforts. Was it, after all, an instance of built-in self-preservation, a reflex? Identification of the nervous energy and its anatomical pathways in the 19th century, endless arguments as to their 'specificity', led to new surgical attempts to control and interpret pain, by now supported by general, then local anesthesia. Early in this century Henry Head's much-discussed notion of 'epicritic' sensation exerting some control over 'protopathic' pain was soon followed by Otfried Foerster's insistence on a central role of inhibition providing pain relief. Almost forgotten, Foerster's idea found expression in Melzack and Wall's 'gate control theory' of 1965. Gasser and Erlanger's classification of sensory nerve fibers began to dominate research in the 1930's thanks to the cathode ray oscillograph invented in 1897. The pain inhibition concept was given another boost in the seventies when the role of the midline mesencephalic and oblongata nuclei was established as both opium receptors and producers of opioids. Finally, inhibition may also be seen as the principle underlying the age-old therapeutic effect of 'counter-irritation', mostly in the form of electrical stimulation.
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PMID:The history of algology, algotherapy, and the role of inhibition. 224 24

Recent data indicate that 25 to 30% of the population in industrialized countries suffers from benign chronic pain. Among these patients, 50 to 75% are professionally incapable for varied lengths of time, from a few days to some weeks or months, or even definitively. The aetiology and clinical presentation of chronic benign pain are enormously varied because this definition includes such different pathologies as headache, pain of rheumatologic, postsurgical, organic, and post-zoster origin, lombalgia, radiculalgia, post-amputation pain, neuropathologic pain, causalgia, algoneurodystrophic pain, psychosomatic and idiopathic pain. Since these syndromes and causes of pain could not be discussed individually, they have been grouped according to their neurophysiology and pathophysiology.
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PMID:[Benign chronic pain]. 793 80

Complex Regional Pain Syndrome (CRPS) is the new name for entities formerly known mostly as Reflex Sympathetic Dystrophy and Causalgia. Treatment of CRPS with either the calcium channel blocker nifedipine or the alpha-sympathetic blocker phenoxybenzamine was assessed in 59 patients, 12 with early stages of CRPS, 47 with chronic stage CRPS. In the early stage CRPS patients, 3 of 5 were cured with nifedipine and 8 of 9 (2 of whom had earlier received nifedipine) with phenoxybenzamine, for a cure rate of 92% (11 out of 12). In the chronic stage CRPS patients, 10 of 30 were cured with nifedipine; phenoxybenzamine cured 7 of 17 patients when administered as a first choice and another 2 of 7 patients who received nifedipine earlier, for a total late stage success rate of 40% (19 out of 47). The most common side effects necessitating discontinuing the drug were headaches for nifedipine and orthostatic dizziness, nausea and diarrhoea for phenoxybenzamine. All male patients on phenoxybenzamine experienced impotence, but this did not lead to discontinuing this agent and immediately disappeared after stopping the drug. These results once again stress the importance of early recognition of CRPS, and treatment with either of these drugs could be considered as a first choice for early CRPS, especially because in this series this treatment was not combined with physical therapy making it very cost-effective. In the chronic stage of CRPS, treatment with these drugs was much less successful (40%), even though it was always combined with physical therapy, but it can still be considered, either as a first choice or when other types of treatment have failed.
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PMID:Complex regional pain syndrome (reflex sympathetic dystrophy and causalgia): management with the calcium channel blocker nifedipine and/or the alpha-sympathetic blocker phenoxybenzamine in 59 patients. 910 64

Complex regional pain syndromes (CRPS) (formerly reflex sympathetic dystrophy and causalgia) are neuropathic pain conditions that are initiated by an extremity trauma or peripheral nerve lesion. Clinical definition and scientific understanding of CRPS are still evolving; however, both the clinical picture and therapeutic options are significantly influenced by a dysfunction of the sympathetic nervous system. Recent investigations suggest functional central abnormalities and a peripheral inflammatory component in the pathophysiology of CRPS. Interdisciplinary treatment includes physical, pharmacologic, and invasive interventional therapy, as well as stimulation techniques.
Curr Pain Headache Rep 2001 Apr
PMID:Complex regional pain syndromes. 1125 45

Complex regional pain syndrome (CRPS) is clinically characterized by pain, abnormal regulation of blood flow and sweating, edema of skin and subcutaneous tissues, active and passive movement disorders, and trophic changes. It is classified as type I (reflex sympathetic dystrophy) and type II (causalgia). CRPS cannot be reduced to one system or to one mechanism only. In the past decades, there has been absolutely no doubt that complex regional pain syndromes have to be classified as neuropathic pain disorders. This situation changed when a proposal to redefine neuropathic pain states was recently published, which resulted in an exclusion of CRPS from neuropathic pain disorders. We analyzed the strength of the scientific evidence that supports the neuropathic nature of complex regional pain syndromes.
Curr Pain Headache Rep 2010 Jun
PMID:Complex regional pain syndrome type I: neuropathic or not? 2046 75

Historically, complex regional pain syndrome (CRPS) was poorly defined, which meant that scientists and clinicians faced much uncertainty in the study, diagnosis, and treatment of the syndrome. The problem could be attributed to a nonspecific diagnostic criteria, unknown pathophysiologic causes, and limited treatment options. The two forms of CRPS still are painful, debilitating disorders whose sufferers carry heavy emotional burdens. Current research has shown that CRPS I and CRPS II are distinctive processes, and the presence or absence of a partial nerve lesion distinguishes them apart. Ketamine has been the focus of various studies involving the treatment of CRPS; however, currently, there is incomplete data from evidence-based studies. The question as to why ketamine is effective in controlling the symptoms of a subset of patients with CRPS and not others remains to be answered. A possible explanation to this phenomenon is pharmacogenetic differences that may exist in different patient populations. This review summarizes important translational work recently published on the treatment of CRPS using ketamine.
Curr Pain Headache Rep 2011 Jun
PMID:Advances in translational neuropathic research: example of enantioselective pharmacokinetic-pharmacodynamic modeling of ketamine-induced pain relief in complex regional pain syndrome. 2136 34

Occipital neuralgia is defined by the International Headache Society as paroxysmal shooting or stabbing pain in the dermatomes of the greater or lesser occipital nerve. Various treatment methods exist, from medical treatment to open surgical procedures. Local injection with corticosteroid can improve symptoms, though generally only temporarily. More invasive procedures can be considered for cases that do not respond adequately to medical therapies or repeated injections. Radiofrequency lesioning of the greater occipital nerve can relieve symptoms, but there is a tendency for the pain to recur during follow-up. There also remains a substantial group of intractable patients that do not benefit from local injections and conventional procedures. Moreover, treatment of occipital neuralgia is sometimes challenging. More invasive procedures, such as C2 gangliotomy, C2 ganglionectomy, C2 to C3 rhizotomy, C2 to C3 root decompression, neurectomy, and neurolysis with or without sectioning of the inferior oblique muscle, are now rarely performed for medically refractory patients. Recently, a few reports have described positive results following peripheral nerve stimulation of the greater or lesser occipital nerve. Although this procedure is less invasive, the significance of the results is hampered by the small sample size and the lack of long-term data. Clinicians should always remember that destructive procedures carry grave risks: once an anatomic structure is destroyed, it cannot be easily recovered, if at all, and with any destructive procedure there is always the risk of the development of painful neuroma or causalgia, conditions that may be even harder to control than the original complaint.
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PMID:Neuralgias of the Head: Occipital Neuralgia. 2705 Dec 29

The trauma of World War I had a lasting impact on clinician and physiologist Jules Tinel (1879-1952). His treatment of peripheral nervous system injuries led him, in 1917, to describe the eponymous sign that he linked to activity of the sympathetic nervous system. Among the sequelae of nerve injuries, he was confronted with causalgia that he attributed, here again, to the autonomic nervous system, the main focus of his laboratory research throughout his career. Tinel's sign became so well known that it eclipsed the originality of his seminal descriptions of exertional headache and of hypertensive emergency caused by pheochromocytoma, which could also have been associated with his name. He was always able to marry his clinical practice of neurology and psychiatric consultations with his anatomicopathological, physiological and pathophysiological research, which was based on his daily practice as a physician. At the same time, he directed the work of numerous assistants in his research laboratory, which has since been unjustly forgotten. Several hundreds of scientific publications, including three seminal works, bear witness to his intense activity, which he combined with a genuine talent for teaching and making his findings accessible to a wider public. Those publications alone would fully justify the historical value of extending his renown beyond the existing eponym.
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PMID:Jules Tinel (1879-1952): Beyond the eponym, the man and his forgotten neurological contributions. 2837 88