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 a prospective study, 14 out of 49 patients presenting to a Regional Neurosurgical Unit with sudden headache suggestive of subarachnoid haemorrhage had normal CSF and a normal CT scan: it did not prove possible, on clinical grounds alone, to distinguish these from those that had bled. We have now followed all these patients for a minimum of 18 months. Only one has had no further headache, 4 have had musculoskeletal pain, 5 psychogenic pain, and 4 migraine type symptoms. None went on to have an unequivocal subarachnoid haemorrhage, and we conclude that angiography cannot be justified in patients with this type of "thunderclap headache".
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PMID:Thunderclap headache: is it migraine? 274 16

Fentanyl (1 microgram/kg body weight) was administered intravenously and via a lumbar epidural catheter (in random order) on 2 separate occasions to 6 patients with chronic pain associated with non-terminal disease states. Frequent blood samples were collected from an indwelling intravenous catheter and CSF samples were collected via spinal needles inserted in the cervical (C7-T1 interspace) and lumbar (L3.4 interspace) regions at 0, 5, 10, 20, 30 and 45 min after fentanyl administration. The concentration of fentanyl in blood and CSF samples were quantified by a sensitive and selective gas-liquid chromatography assay. Visual analogue pain scores (VAPS) were recorded every 5 min for the first hour. Coded syringes (one containing the appropriate fentanyl dose while the other contained an equivalent volume of saline) allowed the investigator administering the fentanyl and assessing VAPS to remain blinded as to which route of administration actually contained the fentanyl. There was minimal vascular uptake of fentanyl following epidural administration. Similarly, the permeation of fentanyl into cervical and lumbar CSF following intravenous administration was minimal and erratic such that only 4 of the 60 CSF samples had detectable fentanyl concentrations. In contrast, there was a rapid penetration of fentanyl across the dura mater following lumbar epidural administration. There was significantly fentanyl in lumbar CSF samples by 10 min in 5 patients, and by 20 min in all 6 patients. The mean maximum lumbar CSF concentration was 19.1 ng/ml, while the time associated with these maximum concentrations was 22.5 min. The mean maximum cervical CSF fentanyl concentrations were 10% of the lumbar CSF concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)
Pain 1989 Sep
PMID:Pharmacokinetics of fentanyl in lumbar and cervical CSF following lumbar epidural and intravenous administration. 281 36

We report a case of syphilitic lumbosacral polyradiculopathy in an HIV-positive, 22-year-old bisexual man with a recent history of secondary syphilis treated with intramuscular penicillin. He presented with rapidly progressive pain and weakness, and muscle wasting in the legs. CSF was under increased pressure and showed a marked pleocytosis (1,130 cells/mm3), hypoglycorrhachia (19 mg/dl), and very elevated protein (1,000 mg/dl). Serum and CSF VDRL serologies were positive. In the legs, nerve conduction studies and needle EMG were consistent with an asymmetric lumbosacral polyradiculopathy with active denervation. His clinical state, CSF, and electrophysiologic studies all improved promptly and markedly after intravenous penicillin. This report documents an uncharacteristically aggressive case of neurosyphilis accompanied by marked changes in the CSF in an HIV-positive patient. While the immunologic effects of HIV and syphilis in combination are not yet fully understood, the cellular immunity defect associated with HIV may alter the natural history of syphilis in patients with concomitant infection, producing unusually aggressive forms or atypical presentations of neurosyphilis.
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PMID:Syphilitic polyradiculopathy in an HIV-positive man. 284 Jun 6

Total opioid peptide receptoractivity in human cerebrospinal fluid is measured in patients who are experiencing lower back pain. Desalted CSF is eluted from a C18 Sep-Pak and is subjected to a radioreceptorassay (RRA) that employs tritiated etorphin, which is a ligand that is effectively displaced by opioids from several different types of opioid receptors. Three clinical groups have significantly different endogenous levels of 2.4, 4.5, and 6.4 pmol of methionine enkephalin-equivalents per mL CSF. Those three levels indicate that more opioid activity is correlated with the amount of drug to relieve the patient's perception of pain. When the total opioid content exceeds an empirical threshold, the sample is further fractionated with gradient reversed phase HPLC, and the opioid receptoractivity in each HPLC fraction is measured to determine the characteristic pattern of those receptoractive opioid peptides present in that patient's CSF. Different HPLC RRA patterns are found for different clinical categories. A possible interpretation of these two different sets of data.is that a lesion exists in one or several of the opioid peptidergic systems (metabolism, receptors) in this particular patient population.
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PMID:HPLC receptorassay of opioid peptides in the cerebrospinal fluid of lower back pain patients. 285 11

The spinal administration of opioids may provide analgesia of long duration to patients with bilateral or midline lower abdominal or pelvic cancer pain. However, cross-tolerance to orally and parenterally administered narcotics and the rapid development of tolerance to spinal narcotics have limited their usefulness. Opioids have extensive distribution in the CSF and plasma when administered into the epidural or intrathecal space, and delivery of drug to brain stem sites may account for many of the toxic and therapeutic effects of spinal opioids. Further clinical and pharmacokinetic studies are required to provide the information regarding: the optimal opioids for use as spinal analgesics; equieffective dose ratios of spinal opioids in comparison to parenteral or oral opioids; strategies useful to forestall the development of tolerance of spinally administered opioids; the analgesic efficacy of this therapy in opioid-tolerant patients; and the role of spinally administered nonopioid analgesics in the management of cancer pain in the tolerant patient. These questions will need resolution before this therapy can be recommended for routine use in the management of cancer pain.
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PMID:Role of epidural and intrathecal narcotics and peptides in the management of cancer pain. 288 Oct 34

The role of opioid peptides in modulating the nervous system adaptability has been demonstrated recently; proopiomelanocortin (POMC)-related peptides, in particular, serve in pain perception, in adaptation to stress, and in modulating higher brain functions. Primary headaches, besides pain, involve neuroendocrine/autonomic/adaptive processes as well as mood and personality factors. The view that primary headaches can be taken as a possible model of POMC-related peptides dysfunction led us to evaluate the resting plasma and CSF peptide levels and their plasma changes in response to various stimuli affecting their release. The data obtained from basal and dynamic studies agree with the concept that primary headaches are sustained by opioid system disturbance. In particular the reduced release of endogenous opioids by anterior pituitary in response to physical, endocrine or pharmacological stimuli agrees with a weak adaptive ability of headache sufferers. This impairment of endorphin responsiveness could play a key role in headache susceptibility to environmental stimuli. Primary headaches constitute a wide, intriguing field, including several subgroups bordering on "ischemic" and behavioral/affective disorders. The development of neuroendocrine techniques could be a useful means for supporting the clinical criteria identifying subpopulations of headache sufferers.
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PMID:Endorphin patterns within the headache spectrum disorders. 299 Jul 21

Pain-alleviating effects of epidural spinal cord stimulation (ESCS) were assessed in patients with chronic intractable pain including cancer pain, and some aspects concerning its mechanisms were discussed. The temporary ESCS with percutaneously inserted electrodes was employed in 105 patients, and the implantable systems for long-term use in 19 patients. The ESCS had satisfactory effects especially in patients suffering from cancer pain, causalgia, facial and nape pain. The conditioning stimuli applied to the cervical dorsal cord exhibited interactions with the segmentally evoked spinal cord potential (SCP). The N1 wave of the SCP was inhibited up to 120 ms, while the P2 wave was facilitated for more than 100 ms, suggesting that the presynaptic inhibitory action at the dorsal horn is responsible for mechanism of the ESCS. CSF concentration of norepinephrine was significantly decreased by the ESCS therapy, indicating the existence of the relationship between norepinephrinergic descending inhibitory system and the ESCS in pain-alleviating mechanism.
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PMID:[Epidural spinal cord stimulation: its efficacy and mechanisms]. 299 94

The use of intraspinal narcotics has been widely accepted as pain relief treatment for intractable cancer pain. Intraspinal low doses of morphine induce a potent selective long lasting analgesia. To avoid repetitive lumbar puncture, a drug delivery device was surgically implanted in 41 patients. The surgical procedure is described. The mean amount of morphine needed was 1.48 +/- 0.25 mg per day at time of surgery, rising to 6.86 +/- 1.47 mg per day after a mean survival time of 65 days. Tolerance became a major problem in 18 patients, which nearly all were selected at a late disease stage and previously received narcotics for pain relief. However, no clear-cut prognostic factor had a predictive value for the appearance of tolerance. In some cases, it could be successfully treated by intraspinal injection of local anaesthetics or clonidine. CSF leakage was noted in 11 patients; this was a challenge for us, as no other authors reported such a high rate for this complication. Aseptic meningitis was noted three times. In all cases but one, the symptoms resolved with appropriate treatment.
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PMID:[Analgesia with an implanted device for repetitive intrathecal injections of morphine]. 300 65

Radio-immunoassayable methionine-enkephalin (ME) and radioreceptor-active opiate peptide levels (OP) were determined in CSF from patients, both with and without chronic pain, under investigation for vertebral disk disease. This study showed: that there was no direct correlation between ME and OP levels in CSF; OP levels were negatively correlated with the ME/OP ratio; migraine patients had higher levels of ME; ME concentrations were reduced in patients receiving anti-inflammatory drugs (nonsteroidal): patients with chronic pain (non migraine, no anti-inflammatory drug therapy) had lower ME levels than patients without pain. The data are discussed in relation to animal models of chronic pain.
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PMID:Simultaneous determination of radio-immunoassayable methionine-enkephalin and radioreceptor-active opiate peptides in CSF of chronic pain suffering and non suffering patients. 301 4

The availability of rhGM-CSF has allowed the in vivo treatment of patients with cytopenia. Therefore, a phase I-II trial was initiated to study the effect of rhGM-CSF in patients with myelodysplastic syndromes who were not eligible for other kinds of therapy. rhGM-CSF has been tested in 10 patients in doses from 15 micrograms/m2 to 150 micrograms/m2 given intravenously over 8 hours for a cycle of 7 days followed by an interval of 14 days and a second 7-day treatment course. A dose-dependent increase in leukocyte count was observed in 9 of 10 patients. No change in reticulocyte numbers was seen and only one patient experienced an increase in platelet count. Toxicity mainly consisted of mild phlebitis at the site of infusion and sternal pain after bolus injection. An increase in blast cell counts in some patients necessitated the start of low-dose Ara-C therapy.
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PMID:In vitro and in vivo action of recombinant human GM-CSF (rhGM-CSF) in patients with myelodysplastic syndromes. 306 85


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