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)

Twenty-five patients with nonhaemorrhagic infarcts of the thalamus were studied clinically and by neuropsychological testing, computerized tomography and somatosensory evoked response (SER) recordings. Our aim was to determine whether the findings in these different tests would form distinct symptom clusters associated with different anatomical territories of the thalamus. Infarction conforming to the tuberothalamic arterial territory caused a facial paresis for emotional movements, severe neuropsychological deficits and a delay of the SER after P14. Infarction conforming to the interpeduncular profundus arterial territory caused a supranuclear vertical gaze paresis, severe neuropsychological deficits and a delay in the P60 component of the SER. Infarction conforming to the anterior choroidal territory caused a hemiparesis, moderate neuropsychological deficits and varied sensory evoked responses. Patients with infarctions conforming to the entire geniculothalamic territory had sensory loss in multiple modalities, minimal neuropsychological deficits and absence of sensory evoked responses after P14. A lacune in this territory caused pure hemisensory loss involving part of the body for the modalities of pain and light touch but not proprioception or vibration. Neuropsychological deficits were uncommon and N32 and N60 were delayed in the SER.
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PMID:Nonhaemorrhagic thalamic infarction. Clinical, neuropsychological and electrophysiological findings in four anatomical groups defined by computerized tomography. 400 33

Dermatomal somatosensory evoked potentials (DSEPs) were recorded in 62 healthy volunteers aged from 15 to 65 years (mean 36.8 +/- 12.9 years) with height from 1.5 to 1.92m (mean 1.69 +/- 0.10m). The aim of the study was to establish normal values for L3, L4, L5 and S1 dermatomes and to introduce this method for the neurophysiological diagnosis of chronic lumbosacral pain and disc disease. The signature areas of dermatomes in both legs separately were stimulated according to the method described by Sedgwick and Katifi (1985). DSEPs were recorded from the scalp electrodes placed at Cz', referred to Fpz. The latencies and amplitudes of consecutive components of DSEPs: N33, P40, N50, P60, N75 and side to side differences were measured and evaluated. Statistical analysis of the results revealed significant positive correlation of DSEPs latencies as a function of height. The correlation of amplitudes with height was less significant. Age, on other hand, showed only negative correlation with amplitudes of later DSEP components. On the basis of the performed analysis the latency of P40 and amplitude of P40-N50 seem to be the best parameters for the evaluation of pathological DSEPs. The range of normal value of latencies for stimulated roots should be calculated from regression equation with the subject's height. As regards amplitude, side to side mean value difference above two standard deviation appears to be more useful.
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PMID:[Dermatomal somatosensory evoked potentials from L3, L4, L5 and S1 spinal roots in healthy subjects]. 786 33

We investigated the effect of a tonic discharge of muscle nociceptive afferents on somatosensory evoked potentials (SEPs) in humans in response to stimulation of non-nociceptive afferents arising from the same muscle. Conditioning nociceptive muscle stimulation was achieved by local injection of 50 mg levo-ascorbic acid (in a volume of 0.3 ml) in the body of the extensor digitorum brevis muscle (EDB). The test stimulus for SEPs was an electrical pulse applied to the EDB nerve at an intensity below the motor threshold. The main finding was that tonic muscle nociceptive stimulation strongly depressed the middle-latency P60-N75 complex without modifying the size of the early P40-N50 complex of SEPs. Depression of the P60-N75 complex was correlated with the pain-induced loss of proprioception of the foot, making it plausible that this cortical complex reflects neuronal processes leading to perception.
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PMID:Interactions between nociceptive and non-nociceptive afferent projections to cerebral cortex in humans. 965 32

We examined the long-term effects of a short-lasting (approximately 24 h) inflammatory insult generated by injections of 0.25% carrageenan (1 microl/g) into the hindpaws of newborn (P0) rat pups. At P60 animals which experienced this early inflammatory insult showed significant alterations in the withdrawal responses to noxious stimulation of the affected paws. Furthermore, in the absence of ongoing inflammation, the withdrawal latencies to heat stimulation and withdrawal thresholds to mechanical stimulation were increased by such experience. In the presence of ongoing CFA-induced inflammation, however, the same early experience decreased these parameters of response to noxious stimulation. These data suggest that early inflammatory insult may differentially affect the aspects of nociceptive circuitry involved in transient pain sensitivity and in inflammation-induced hyperalgesia.
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PMID:Long-term effects of short-lasting early local inflammatory insult. 1120 57

The cortically generated P60 component of the posterior tibial nerve somatosensory evoked potential (PTSEP) is occasionally found to be absent in neurological patients,while the preceding P40 is preserved ("Absent P60" pattern). A retrospective analysis of 24 such cases showed them to represent a different clinical population from that represented by 24 age- and sex-matched but otherwise unselected patients with entirely normal PTSEPs. The most frequent diagnoses of the patients with normal PTSEPs (conversion disorder and definite or suspected multiple sclerosis) were significantly less prevalent in the patients with the Absent P60 pattern, while miscellaneous other diseases affecting the peripheral and/or central sensory pathways were more frequent. In comparison with a second matched patient group with abnormal P40 in addition to P60, the patients with the Absent P60 pattern had a significantly lower incidence of "large fibre" sensory deficits (impaired vibration and/or joint-position sense). The incidence of "small fibre" deficits (impaired pain and/or temperature sensation) was similar in both groups with PTSEP changes. In conjunction with previously published findings in normal subjects, the data suggest that the P60 is a late response of the primary sensorimotor cortex due to activation of large diameter myelinated sensory fibres, but which is also tonically influenced by small fibre input. The Absent P60 pattern may be recognized as a distinct PTSEP abnormality, although its occurrence in some normal individuals should be noted.
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PMID:Neurological associations of absent P60 component of the posterior tibial nerve somatosensory evoked potential. 1467 74

Neonatal noxious insult produces a long-term effect on pain processing in adults. Rats subjected to carrageenan (CAR) injection in one hindpaw within the sensitive period develop bilateral hypoalgesia as adults. In the same rats, inflammation of the hindpaw, which was the site of the neonatal injury, induces a localized enhanced hyperalgesia limited to this paw. To gain an insight into the long-term molecular changes involved in the above-described long-term nociceptive effects of neonatal noxious insult at the spinal level, we performed DNA microarray analysis (using microarrays containing oligo-probes for 205 genes encoding receptors and transporters for glutamate, GABA, and amine neurotransmitters, precursors and receptors for neuropeptides, and neurotrophins, cytokines and their receptors) to compare gene expression profiles in the lumbar spinal dorsal horn (LDH) of adult (P60) male rats that received neonatal CAR treatment within (at postnatal day 3; P3) and outside (at postnatal 12; P12) of the sensitive period. The data were obtained both without inflammation (at baseline) and during complete Freund's adjuvant induced inflammation of the neonatally injured paw. The observed changes were verified by real-time RT-PCR. This study revealed significant basal and inflammation-associated aberrations in the expression of multiple genes in the LDH of adult animals receiving CAR injection at P3 as compared to their expression levels in the LDH of animals receiving either no injections or CAR injection at P12. In particular, at baseline, twelve genes (representing GABA, serotonin, adenosine, neuropeptide Y, cholecystokinin, opioid, tachykinin and interleukin systems) were up-regulated in the bilateral LDH of the former animals. The baseline condition in these animals was also characterized by up-regulation of seven genes (encoding members of GABA, cholecystokinin, histamine, serotonin, and neurotensin systems) in the LDH ipsilateral to the neonatally-injured paw. The largest aberration in gene expression, however, was observed during inflammation of the neonatally injured hindpaws in the ipsilateral LDH, which included thirty-six genes (encoding numerous members of glutamate, serotonin, GABA, calcitonin gene-related peptide, neurotrophin, and interleukin systems). These findings suggest that changes in gene expression may be involved in the long-term nociceptive effects of neonatal noxious insult at the spinal level.
Mol Pain 2005 Sep 22
PMID:Neonatal local noxious insult affects gene expression in the spinal dorsal horn of adult rats. 1617 88

Premature infants are routinely exposed to invasive medical procedures during neonatal intensive care treatment that are largely performed in the absence of anesthetics or analgesics. Data collected to date suggest that exposure to early insult during this time of increased plasticity alters the development of the CNS and influences future pain responses. As previous studies examining the impact of neonatal injury on nociception have been conducted primarily in males, the potential adverse effects on females are not known. Therefore, the present studies were conducted to determine whether neonatal injury differentially impacts male and female sensory thresholds in adulthood. A short lasting inflammatory response was evoked in male and female rats on the day of birth with an injection of carrageenan (CGN; 1% or 2%) into the right hindpaw. Nociceptive thresholds were assessed using a noxious thermal stimulus at both adolescence (P40) and adulthood (P60). A more persistent inflammation was subsequently evoked in adult rats with an intraplantar injection of Complete Freund's adjuvant (CFA). Neonatally injured females exhibited significantly greater hypoalgesia at P60, and displayed enhanced inflammatory hyperalgesia following re-injury in adulthood compared to neonatally injured males and controls. These results demonstrate that the long-term adverse effects of neonatal injury are exacerbated in females, and may contribute to the higher prevalence, severity and duration of pain syndromes noted in women compared to men.
Pain 2007 Nov
PMID:Female rats are more vulnerable to the long-term consequences of neonatal inflammatory injury. 1790 45

To gain an insight into the developmental characteristics of neuropathic pain induced by peripheral nerve injury during neonatal period, we employed three groups of rats suffering from peripheral nerve injury at different postnatal times, and compared the onset time, severity and persistency of neuropathic pain behaviors, such as mechanical and cold allodynia. The first group (P0 group) was subjected to partial injury of tail-innervating nerves within 24 h after birth, the second group (P10 group) underwent nerve injury at postnatal day (P) 10, and the third group (P60 group) was subjected to injury at P60. Although mechanical allodynia was readily detectable in the P60 group even 1 day after nerve injury, the signs of neuropathic pain were observed from 6 or 8 weeks after nerve injury in the P0 or P10 groups, respectively. Compared with the P60 group, the P0 group showed more robust mechanical and cold allodynia, whereas the P10 group exhibited rather milder pains. In addition, while the P0 and P60 groups showed long-lasting signs of mechanical allodynia, the P10 group exhibited shorter persistency. These results indicate that peripheral nerve injury during neonatal period leads to neuropathic pain with distinct developmental characteristics later in life.
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PMID:Developmental characteristics of neuropathic pain induced by peripheral nerve injury of rats during neonatal period. 1853 29

Studies in both rodents and humans have shown that acute inflammatory pain experienced during the perinatal period produces long-term decreases in pain sensitivity (hypoalgesia) (Grunau et al., 1994a, 2001; Ren et al., 2004; LaPrairie and Murphy, 2007). To date, the mechanisms underlying these long-term adaptations, however, have yet to be elucidated. The present studies tested the hypothesis that neonatal inflammatory pain induces an upregulation in endogenous opioid tone that is maintained into adulthood, and that this increase in opioid tone provides the underlying mechanism for the observed hypoalgesia. On the day of birth (P0), inflammatory pain was induced in male and female Sprague-Dawley rats by intraplantar administration of carrageenan (CGN; 1%). In adulthood (P60), these animals displayed significantly increased paw withdrawal latencies in response to a noxious thermal stimulus in comparison to controls. Systemic administration of the brain-penetrant opioid receptor antagonist naloxone HCl, but not the peripherally restricted naloxone methiodide, significantly attenuated the injury-induced hypoalgesia. Direct administration of naloxone HCl or antagonists directed at the mu or delta opioid receptors into the midbrain periaqueductal gray (PAG) also significantly reversed the injury-induced hypoalgesia in adult rats. Parallel anatomical studies revealed that inflammatory pain experienced on the day of birth significantly increased beta-endorphin and met/leu-enkephalin protein levels and decreased opioid receptor expression in the PAG of the adult rat. Thus, early noxious insult produces long-lasting alterations in endogenous opioid tone, thereby profoundly impacting nociceptive responsiveness in adulthood.
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PMID:Neonatal injury alters adult pain sensitivity by increasing opioid tone in the periaqueductal gray. 1986 48

Considering the importance of studies in animal models that are focused on systems involved in pain mechanisms, this investigation aimed to evaluate the effects of pharmacological treatments on the behavioral responses of younger animals. To this end, we evaluated the effect of an acute dose of fentanyl (FEN) or S(+)-ketamine (KET) at postnatal day 14 (P14) upon behavioral responses in the short- (P14), medium- (P30) and long-term (P60) using the open field (OF), elevated plus-maze (EPM) and formalin tests (FT) and tail-flick latency. Fourteen-day-old male Wistar rats were divided into three groups: control (CT), fentanyl (FEN) and S(+)ketamine (KET) groups for statistical analysis, it was performed two-way ANOVA followed by Bonferroni. We found that, regardless of the test performed (OF or EPM), between-group differences occurred over time in all behaviors analyzed, including in the second phase of FT. In addition, EPM showed significant differences in behavioral responses related to acute administration (at P14) of fentanyl or S(+)-ketamine, in behaviors such as number of entries in open and closed arms, time spent in open and closed arms, and number of head-dipping. In relation to nociceptive response, the FEN group exhibited a decrease in the first phase of FT. These results indicate that unique administration of fentanyl or S(+)ketamine in an early period of life (P14) can promote changes in behavioral responses. In addition, our findings highlight the importance of extending the investigation of the effect of drug administration in young rats into adulthood.
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PMID:Fentanyl administration in infant rats produces long-term behavioral responses. 2202 20


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