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)

A 13-year-old boy, with the diagnosis of congenital adrenocortical unresponsiveness to ACTH (ACTH insensitivity) at age 7, developed a steppage gait, when under glucocorticoid replacement therapy at age 13. The parents were healthy and not consanguinous. On general physical examination, a mild diffuse skin hyperpigmentation was noted. Neurological examinations revealed that all the muscle stretch reflexes of both limbs were absent without pathologic reflexes. Pes cavus was found bilaterally. A slight decrease of tactile sensation was noted distal to the ankle joints. Pain sensation was slightly decreased in the toes. On laboratory examination, the conduction velocities of the left ulnar and median motor nerves were 51 and 45 m/sec, respectively, which are normal. No M-wave responses were obtained by electrical stimulation of the tibial and peroneal nerves. The coefficient of the variation of the R-R interval from ECG recordings was normal. Orthostatic hypotension was not observed. Achalasia was negative on the barium swallow esophagram. Therefore, it was concluded that he had motor and sensory polyneuropathy, and a right sural nerve biopsy was performed. A 12-year-old girl, a sister of the boy described above, with the diagnosis of ACTH insensitivity at age 5, noted a pain on the medial aspect of the left sole after skating. On general physical examination, a mild diffuse skin hyperpigmentation was discovered. On neurological examination, a spontaneous pain with dysesthesia was noted on the plantar aspect of the 1st, 2nd and 3rd left toes and on the anterior and medial aspect of the sole. Otherwise she was normal. A diagnosis of the left tarsal tunnel syndrome was made.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Two siblings with congenital adrenocortical unresponsiveness to ACTH showing peripheral neuropathy--morphometric evaluation of the sural nerve]. 792 65

The sex-dependent effects of acute restraint (RT) on nociceptive and pituitary-adrenal responses were investigated in the rat. In a first experiment, the effect of 30 min RT on pain sensitivity was evaluated through repeated use of the tail withdrawal test during and after treatment. RT induced an increase in the nociceptive threshold, i.e., analgesia, in males and females, but the duration and time-course of this effect varied between sexes. The latencies returned to approximately control values in females in the second half of RT, but in males they remained higher for the whole period of RT and immediately afterwards. Twenty-four hours later, males displayed longer latencies than controls in response to simple reexposure to the environment. In a second experiment, ACTH and corticosterone plasma levels were measured immediately after 15 or 30 min of RT. ACTH and corticosterone were higher in restrained animals than in controls after both periods of treatment, and in both sexes; however, females showed higher basal and stress corticosterone levels than males. The role played by corticosteroids in the nociceptive responses of the two sexes is discussed.
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PMID:Sex-dependent effects of restraint on nociception and pituitary-adrenal hormones in the rat. 802 95

After intraperitoneal injection of ACTH, the content of GABA in hippocampus and the pain threshold were increased. This effect could be decreased by cyclosporin. ACTH decreased SI of MSBT and production of IL-II, and this suppression could be reversed by GABA synthesis inhibitor isoniazid, or GABA receptor blocker picrotoxin. These results suggest that: the analgesic effect of ACTH is related with the increase of GABA content in hippocampus, and cell immunity could be involved the regulation of GABA content in the brain regions. ACTH inhibited the effect of cell immunity, and this effect related to GABA content. Above effect is at least partly mediated by GABA synthesis and GABA receptor.
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PMID:[Interaction between r-aminobutyric acid content of the brain regions and cell immunity in the analgesic effect of adrenocorticotropic hormone in rats]. 808 82

We investigated whether the anti-aversive effects of salmon calcitonin (SCT) was induced by increasing ACTH and beta-endorphin and/or by decreasing of prostaglandin E2 (PGE2) levels in plasma of mice to elucidate the mechanisms responsible for the analgesic effects of SCT. Intracerebroventricular (i.c.v.) injections of SCT inhibited acetic acid-induced aversive behavior (writhing) in a U-shaped dose response curve, the most effective dose being 0.1 IU/mouse. Intraperitoneal (i.p.) injections of acetic acid increased, but not significantly, the levels of plasma ACTH and PGE2, but not beta-endorphin, which are considered to be psychoneuroendocrines correlated with pain. SCT (0.1 IU/mouse, i.c.v.) significantly increased plasma ACTH levels (p < 0.05) and tended to increase beta-endorphin levels (p = 0.052) in acetic acid-treated mice, whereas no change in PGE2 level was observed (p > 0.1). These results suggest that the anti-aversive effects of SCT may be mediated, at least in part, by the activation of ACTH.
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PMID:Relationship between anti-aversive effects of salmon calcitonin and plasma levels of ACTH, beta-endorphin and prostaglandin E2 in mice. 816 65

The study was performed on 94 urological patients, aged 15 to 78 years, subjected to planned operations. The initial autonomic tone, autonomic reactivity, autonomic maintenance of the activity, ACTH and cortisol content have been investigated in the ward and in the operation room with concomitant premedication with pipolphen in combination with promedol and diazepam in combination with promedol. Tactile and pain thresholds were studied in patients on premedication in the ward and the operation room. It has been noted that positive effect of premedication, an increase in the pain threshold and adequate neuroautonomic protection do not only depend on the presence or absence of diazepam in premedication, but also on the initial autonomic tone, autonomic reactivity, and autonomic maintenance of the activity. The above parameters in their turn depend on the functional state of the autonomic nervous system, the patient's age, concomitant diseases, and other factors determining general physical status of the patient.
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PMID:[Correlation between the effectiveness of premedication and neuroanatomic protection during surgery with NLA and the initial state of the autonomic nervous system]. 818 83

A 67-year-old man was admitted to the orthopedic ward, complaining of severe pain in his right greater trochanter. He was diagnosed as spinal cord tumor and underwent laminectomy for extirpation of the tumor. Histological examination revealed bone metastasis of unknown origin. Laboratory data revealed hypokalemia and hyperglycemia. Endocrinological data showed elevation of plasma cortisol and ACTH, and increased excretion of urinary 17-OHCS. Ten specimens needle biopsy of the prostate showed poorly differentiated adenocarcinoma, thus patient was diagnosed as prostate cancer with bone metastasis (stage D2) and perhaps ectopic ACTH production. Castration was performed, however 2 days after the surgery he died suddenly. We suspected that cerebral hemorrhage was the cause of his death. On autopsy ectopic ACTH production in the prostate was confirmed.
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PMID:[A case of prostatic carcinoma with ectopic ACTH syndrome]. 825 41

Amongst the spinal peptide candidates believed to be involved in the mediation of analgesia, only somatostatin fulfills the criterium of a real analgesia substance. Spinal somatostatin specifically blocks the transmission of painful stimuli. Spinal calcitonin may lower the opioid dose requirement in patients with bone metastases but it fails to relieve acute pain. The usefulness of ACTH and CRF for treatment of pain remains to be established. The role of CCK-8, vasopressin and neurotensin is unclear. The contradictory findings on antinociception using simple rodent withdrawal reflex tests (e.g. the tail flick test), or more complex behavioral tests in which supraspinal sensory processing is involved, (e.g. the hot plate test), indicate that these tests are inappropriate when neuropeptides are employed. Furthermore, due to their inability to predict analgesia in humans, they do not fulfill the guidelines proposed by the IASP that animal test procedures have to be for the benefit of humans.
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PMID:Non-opioid peptides for analgesia. 831 62

Plasma levels of beta-endorphin (beta-EP), met-enkephalin (met-ENK), ACTH, cortisol, and prolactin were measured in 20 patients who underwent extracorporeal gallstone lithotripsy (ESWL) before the treatment, at 500 shock waves (SW) (15-20 min), at 1000 SW (40-50 min), and 10 min after the end of ESWL. According to the Visual Analog Scale, nine patients had no pain, seven patients had pain from level 1 to 5, and four patients had pain from 5 to 10. No complications were observed. Plasma beta-EP values increased during the treatment, both in patients without pain and in those with pain. Only in the former group was the increase significant (baseline values (pmol/L): no pain = 4.04 +/- 1.3; pain 1-5 = 3.6 +/- 1.06; pain 5-10 = 2.9 +/- 0.5. Peak values: no pain = 6.6 +/- 1.2 (p < 0.005); pain 1-5 = 4.6 +/- 2.5; pain 5-10 = 4.5 +/- 2.2). Moreover, a negative correlation between beta-EP levels and individual pain scores during ESWL has been observed (CC = -0.64, p < 0.003). Plasma met-ENK levels reached the peak at 1000 SW and declined 10 min after the end of the treatment, although they were always higher than basal values (baseline values (pg/ml): no pain = 45 +/- 12; pain 1-5 = 38 +/- 10; pain 5-10 = 48 +/- 8. Peak values: no pain = 112 +/- 42 (p < 0.005), pain 1-5 = 114 +/- 48 (p < 0.005), pain 5-10 = 85 +/- 10 (p < 0.005). This behavior has been the same, regardless of the presence or absence of pain. We conclude that during ESWL, a rise of beta-EP and met-ENK occurs, and the increase of the former can be responsible for induction of analgesia because of its inverse correlation with pain intensity.
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PMID:Plasma opioid levels during extracorporeal gallstone lithotripsy. 839 Dec 10

A 60-year-old man presented with waste, muscle weakness and pain of knees and shoulders. Endocrinological investigations revealed low plasma cortisol and ACTH levels, delayed response of plasma cortisol to ACTH, no response of plasma ACTH to CRF and normal response to other pituitary hormone to corresponding stimulate test. He was diagnosed as isolated ACTH deficiency. Then we examined plasma type IV collagen 7S and fibronectin, because experimentally, corticosteroid regulates the extracellular matrix structure composed of type IV collagen, fibronectin and so on. These parameters were elevated and rapidly decreased to the normal range with the replacement of hydrocortisone, simultaneously his arthralgia was improved. These parameters can reflect the biochemistric change in cortisol deficiency state.
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PMID:[Changes of type IV collagen 7S and fibronectine in a patient with isolated ACTH deficiency]. 852 45

The hypothalamic-pituitary adrenocortical (HPA) system and sympathoneural and adrenomedullary systems are major effector systems that serve to maintain homeostasis during stress. Corticotropin-releasing hormone (CRH) in the paraventricular nucleus (PVN) of the hypothalamus, a determinant of both HPA and autonomic responses to stress, is under the control of many neurotransmitters and neuropeptides. Norepinephrine (NE) potently stimulates CRH neurons in the PVN; however, the physiologic role of NE in stress-induced activation of the HPA is unknown. In the present study we exposed animals to various stressors (immobilization (IMMO), cold (COLD), hemorrhage (HEM), hypoglycemia elicited by insulin administration (INS), pain and tissue damage caused by formalin injection (FORM) and sc injection of physiological saline (SAL), all of which are known to activate the HPA axis. Injection of physiological saline iv was used as a control. In vivo microdialysis was used to assess stressor- and intensity-specific activation of the PVN noradrenergic system, based on measurements of NE, its intraneuronal metabolite dihydroxyphenylglycol (DHPG), and the dopamine metabolite, dihydroxyphenylacetic acid (DOPAC). Simultaneously with microdialysate collections, blood samples were obtained via catheters in the femoral artery to measure plasma ACTH and corticosterone (CORT) levels as dependent measures, to assess stress-induced activation of the HPA axis. At their highest intensities, all the stressors significantly increased levels of PVN microdialysate NE, DHPG, and DOPAC, and plasma ACTH and CORT. PVN NE levels varied across stressors, with IMMO and FORM more potent than INS, COLD, or HEM. INS and HEM evoked proportionately larger plasma ACTH responses than did IMMO, FORM, and COLD. Plasma CORT responses were largest during IMMO, FORM, and HEM. Except for COLD and HEM, there was a strong correlation of plasma ACTH levels with levels of NE, DHPG, and DOPAC in PVN microdialysate. The data suggest that, except for COLD or HEM, there is a strong positive correlation of PVN noradrenergic activation and activity of the HPA axis. With stressors such as IMMO and FORM, NE synthesis, reflected by DOPAC changes, is strongly positively correlated with activity of the HPA axis. Furthermore, the results indicate substantial stressor specificity of PVN catecholaminergic and of HPA responses to different stressors and are inconsistent with a founding tenet of Selye's stress theory, the doctrine of nonspecificity, which defines stress as the nonspecific response of the body to any demand.
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PMID:Effects of various stressors on in vivo norepinephrine release in the hypothalamic paraventricular nucleus and on the pituitary-adrenocortical axis. 859 92


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