Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In an 11-year-old girl with congenital insensitivity to pain, diagnosis depended on three diagnostic features: pain sensation absent from birth; entire body affected; all other sensory modalities and deep tendon reflexes present. The cause of this disease is unknown. Other diseases to be considered when insensitivity to pain is present are diabetes, lues, and syringomyelia. Less common neurologic diseases are congenital sensory neuropathy with or without anhidrosis, familial dysautonomia (Riley-Day syndrome), and sensory radicular neuropathy. The three orthopedic manifestations of congenital insensitivity to pain are recurrent fractures, neuropathic (Charcot's) joints, and osteomyelitis. Management is based on proper appreciation of the disease. Prevention of complications is important. Treatment of fractures and osteomyelitis is straightforward. However, the treatment of neuropathic joints demands caution and is done best nonsurgically.
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PMID:Orthopedic aspects of congenital insensitivity to pain. 618 64

Mutilated foot (mf) is a mutant rat with an autosomal recessive sensory neuropathy. Affected animals become ataxic and their feet become mutilated. Morphological and quantitative studies have shown a reduced number of sensory ganglion cells and of cells of secondary sensory neurons. No degeneration was seen in the peripheral nervous system. Substance P (SP) is an undecapeptide which is thought to be involved in transmission of nociceptive information. Since mf rats show, in addition to ataxia, a decreased response to painful stimuli, SP immunoreactivity was examined. The density of SP staining was decreased at all levels of the spinal cord, mainly at cervical and lumbar levels and only in areas related to sensory pathways. In other areas of the spinal cord and in the substantia gelatinosa of the trigeminal tract, no reduction of SP staining was observed. The results further support the relationship between SP and transmission of pain stimuli. There are also many similarities between the appearance in mf rats and those in animals in which sensory afferents from dorsal root ganglia had been impaired with various methods, particularly in those treated from birth with capsaicin.
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PMID:Reduced substance P in hereditary sensory neuropathy in the mf rat. 618 15

Thirty-one patients with chronic HBV infection were randomized to receive a short or long course of ARA-AMP. Fifteen completed a 4 week course of treatment and 16 completed longer courses varying from 7 to 12 weeks. Eighteen patients did not experience any neurological side effects. Six patients had myalgia. This was not associated with any neurological deficit. Seven patients developed a sensory neuropathy with distressing pain and dysesthesiae in the feet and abnormalities in nerve conduction. The development of neurotoxicity was related to a long duration of treatment and a correspondingly higher total dose but there was no association with the severity of liver disease.
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PMID:Neurotoxicity associated with adenine arabinoside monophosphate in the treatment of chronic hepatitis B virus infection. 620 58

Peripheral blood flow is known to be qualitatively increased in diabetic patients with neuropathy. We have measured the actual blood flow in the feet of diabetic patients with neuropathy using non-invasive mercury strain gauge plethysmography and Doppler sonogram techniques and shown that it is increased on average five times above normal at an ambient temperature of 20 degrees-22 degrees C. Moreover, reduction of this high flow by sympathetic arousal stimuli proved possible in those with severe painful neuropathy contrasting strongly with failure to reverse it in those with severe non-painful sensory neuropathy. Reduction of blood flow was associated with reduction in neuropathic pain. We studied 22 diabetic patients with severe sensory neuropathy and eight with painful neuropathy. High resting foot blood flows were demonstrated in both groups with neuropathy. The big toe flow in those with severe sensory neuropathy was 29.3 +/- 9.2 ml X min-1. 100 ml-1 (mean +/- SD) and in the painful neuropathy group, 25.9 +/- 7.5, compared with 5.2 +/- 2.4 ml X min-1 X 100 ml-1 in the non-diabetic control subjects (p less than 0.001). High foot skin temperatures were also recorded in the groups with neuropathy, reflecting the high blood flow. The subjects with painful neuropathy retained the ability to constrict peripheral blood vessels in response to arousal stimuli, and reduce peripheral flow on average by 32% compared with the patients with sensory neuropathy who responded on average by only 10%. The demonstration of a peripheral sympathetic defect, responsible for the high blood flow and the potential reversal of such flow in painful neuropathy may be important in our further understanding of the aetiology of such pain and its treatment.
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PMID:Blood flow patterns in painful diabetic neuropathy. 653 51

A young woman had chronic symptoms of "burning feet" but no clinical or neurophysiologic findings of neuropathy. These symptoms were aggravated by warmth and ameliorated by cooling. Extensive pathologic grading of teased sural nerve fibers, however, provided suggestive evidence of a low-grade pathologic abnormality. Other kin were discovered to have similar symptoms in an autosomal-dominant pattern, and some of these relatives had evidence of a subclinical sensory neuropathy. From this experience, we infer that a mild subclinical neuropathy may underlie the symptom of burning feet; burning pain of the feet may be dominantly inherited; hereditary sensory neuropathy may, therefore, manifest with only positive symptoms of burning pain, restless legs, and lancinating pain, rather than with mutilating acropathy, neurotrophic arthropathy, or severe distal sensory loss as is usually reported; and temperature may modulate physiologic mechanisms related to the experience of burning pain.
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PMID:"Burning feet" as the only manifestation of dominantly inherited sensory neuropathy. 657 33

Some patients with radiologic findings of neurogenic arthropathy or multiple fractures do not exhibit overt neurologic signs. Results of nerve conduction velocity, computer-assisted sensory examination, periosteal nociception, and morphometric and graded teased-fiber evaluation of cutaneous nerves allowed us to recognize a mild neuropathic abnormality. Neurogenic arthropathy and subclinical neuropathy were also found in relatives. In three kinships, the underlying disorder was probably hereditary sensory neuropathy type 1 and in several others, it was recessively inherited sensory neuropathy. These arthropathies were often painful, and overt loss of superficial and deep pain sensation was not a prominent or necessary condition. An interplay of multiple factors including insensitivity, trauma, obesity, activity, abuse, personality, mental subnormality, and metabolic joint and bone disease are probably involved in the development of the bony lesions and thus provide further evidence that environmental factors affect expression of human mutant genes for inherited neuropathy.
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PMID:Neurogenic arthropathy and recurring fractures with subclinical inherited neuropathy. 668 82

Small fiber sensory neuropathy is one of the most common complications of diabetes mellitus. Currently there is no adequate therapy to prevent this often debilitating problem. Nerve growth factor (NGF) is a protein that promotes the survival and integrity of a large percentage of sensory neurons including the small fiber pain transmitting neurons which are often prominently affected in diabetic neuropathy. We report here that exogenously administered NGF is capable of preventing the behavioral and biochemical manifestations of diabetic sensory neuropathy in a streptozocin induced rat model. NGF administration prevented the elevation of tailflick threshold (a measure of the rat's response to a thermal noxious stimulus) which occurred in streptozocin-induced diabetic rats. Further, it prevented the induced reduction in levels of the neuropeptides substance P and calcitonin gene related peptide measured from cervical dorsal root ganglia. Finally, NGF did not ameliorate the prolonged latency of the compound action potentials measured from the caudal nerve of the tail. In view of these results, a clinical trial of NGF in diabetic neuropathy has now commenced.
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PMID:Nerve growth factor administration protects against experimental diabetic sensory neuropathy. 751 29

The exact nosological status of "congenital insensitivity to pain" remains in doubt. Possible pathological correlates of this clinical syndrome include sensory neuropathy, central lesions at the level of the reticular formation or dorsal horn of the spinal cord, or a central indifference to, or asymbolia for, pain. The reassessment of two members of a kindred previously reported more than 20 years ago as having congenital insensitivity to pain indicated that they in fact had an inherited sensory and autonomic neuropathy. Prolonged follow up and morphometric analysis of sequential nerve biopsies may be necessary to definitively establish this diagnosis.
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PMID:Congenital insensitivity to pain: a 20 year follow up. 752 56

Digital fractures are a common injury in the forefoot. Most fractures, however, do not present relatively free of pain. When they present without pain or with few symptoms, they may be overlooked or misdiagnosed. The following is a case presentation of a patient who presented to Franklin Delano Roosevelt Hospital after trauma to the right fifth toe. The case was atypical in that the patient was asymptomatic despite the recent injury. Rapid conservative intervention by the patient at home, coupled with sensory neuropathy secondary to diabetes, can alter the clinical presentation as witnessed in this case. An appropriate history and physical examination combined with radiographs were essential to an otherwise ordinary clinical presentation.
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PMID:Fracture of the fifth digit. An atypical presentation. 777 8

Measurements of skin blood flow (by laser Doppler flowmetry) and temperature were made under environmental conditions promoting peripheral vasodilatation at the fingertips of a disfigured 'clawed' hand in 12 leprosy patients long-resident at Baba Baghi Leprosy Hospital, Tabriz, Iran. Sensory function was assessed by measuring the responses to light touch, pain and temperature of each finger, and peripheral autonomic function was gauged by estimating palmer sweating and by measuring skin vasomotor reflexes in response to inspiratory gasp. In 2 patients all measured fingers had laser Dopper flux (LDFlux) values and skin temperatures lower than the 95% confidence limits for the mean of 20 healthy controls, i.e. were impaired; in 2 patients all fingers had normal values for LDFlux and temperature; and in 8 patients there was a combination of impairment with most fingers normal for these parameters but with the small finger most commonly impaired. There were 10 (67%) fingers with impaired LDFlux and temperature values who had significant sensory impairment, whereas only 5 (18%) of the fingers with normal LDFlux values and temperatures had a similar sensory deficit. Overall, the fingers with the most impaired sensation had significantly (P < 0.05) lower LDFlux and temperature values than those with no sensory deficit. Microcirculatory impairment was not related to disordered skin vasometer reflexes or dysfunction of sweating. We concluded that the relationship between motor (skeletal muscle) nerve paralysis and any subsequent sensory neuropathy and/or microcirculatory impairment is more complex than might be expected from previous understanding of the disease.
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PMID:Circulation and sensation at the fingertips of claw hands. 786 20


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