Impact of shock on pain reactivity:  II. Evidence for enhanced pain.

King, Tamara; Joynes, Robin L.; Meagher, Mary W.; Grau, James W.

doi:10.1037/0097-7403.22.3.265

Cited by 52 publications

(100 citation statements)

References 59 publications

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“…In particular, there appears to be an association between unconditioned pain modulation and expression of the immediate-early gene c-fos in the entorhinal cortex. Pain of moderate intensity leads to hyperalgesia (King et al, 1996) and increased entorhinal c-fos expression (Funahashi et al, 1999), whereas strong pain leads to hypoalgesia (King et al, 1996) and decreased entorhinal c-fos expression (Funahashi et al, 1999). Our finding provides an experimental demonstration of the apparent association between entorhinal activity and pain modulation and shows that the entorhinal cortex mediates not only unconditioned, but also conditioned hyperalgesia.…”

Section: Discussionmentioning

confidence: 50%

Exacerbation of Pain by Anxiety Is Associated with Activity in a Hippocampal Network

et al. 2001

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It is common clinical experience that anxiety about pain can exacerbate the pain sensation. Using event-related functional magnetic resonance imaging (FMRI), we compared activation responses to noxious thermal stimulation while perceived pain intensity was manipulated by changes in either physical intensity or induced anxiety. One visual signal, which reliably predicted noxious stimulation of moderate intensity, came to evoke low anxiety about the impending pain. Another visual signal was followed by the same, moderate-intensity stimulation on most of the trials, but occasionally by discriminably stronger noxious stimuli, and came to evoke higher anxiety. We found that the entorhinal cortex of the hippocampal formation responded differentially to identical noxious stimuli, dependent on whether the perceived pain intensity was enhanced by pain-relevant anxiety. During this emotional pain modulation, entorhinal responses predicted activity in closely connected, affective (perigenual cingulate), and intensity coding (midinsula) areas. Our finding suggests that accurate preparatory information during medical and dental procedures alleviates pain by disengaging the hippocampus. It supports the proposal that during anxiety, the hippocampal formation amplifies aversive events to prime behavioral responses that are adaptive to the worst possible outcome.

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Section: Discussionmentioning

confidence: 50%

Exacerbation of Pain by Anxiety Is Associated with Activity in a Hippocampal Network

et al. 2001

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“…Although the results from the hotplate and formalin tests (Experiments 2 and 3) are consistent with the PDR model, the results from the tailflick test (Experiment 1B) are not. It could be argued that decreased tailflick latencies are not indicative of increased pain sensitivity (see, e.g., Illich, King, & Grau, 1995;King, Joynes, Meagher, & Grau, 1996;but see McNally, 1999), and therefore are not relevant to the PDR model. Further experiments are required to address this issue and to determine whether exposure to the LiCl-associated context provokes additional behavioral and autonomic changes consistent with conditioned arousal of a fear or defensive motivational system.…”

Section: Discussionmentioning

confidence: 99%

Effects of contextual cues previously paired with footshock or illness on behavior and pain sensitivity in the rat

McNally

Gorrisen

Low

et al. 1999

Animal Learning & Behavior

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Rats were used in four experiments to study the effects on behavior and pain sensitivity of exposure to a context previously paired with footshock or injection of the emetic drug lithium chloride (LiCl). Exposure to a context previously paired with footshock or injection of LiCl provoked the speciestypical defense response of freezing (Experiments 1A and 1B). Exposure to a context previously paired with footshock additionally produced hypoalgesia when rats were tested using the tailflick test (Experiment 1A). By contrast, exposure to a context previously paired with injection of LiCl produced hyperalgesia when rats were tested using the tailflick test (Experiment 1B). However, exposure to a context previously paired with injection of LiCl did provoke hypoalgesia when rats were tested for pain sensitivity using either the hotplate or formalin tests (Experiment 2), which was mediated by the release of endogenous opioid peptides (Experiment 3). These results are discussed with reference to the processes governing associative regulation of defensive behavior and pain control.

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“…The rats were then injected with an assigned dose of morphine sulfate (Sigma-Aldrich, St. Louis) and, 30 minutes later, were placed in the restraining tubes and nociceptive reactivity was assessed. Nociceptive reactivity was assessed with gradually incremented shock and radiant heat, as described in prior studies [e.g., 9,16,17]. Briefly, subjects were placed in the restraining tubes, and the apparatus used to assess reactivity was attached to the tail.…”

Section: Assessment Of Motor/sensory Recoverymentioning

confidence: 99%

“…Separate groups received nothing (0 s) or 30 min of uncontrollable, intermittent tailshock. The shocks were 1.5 mA, 0.08 s in duration, and occurred on a variable time schedule (range 0.2 to 3.8 s) with a mean interstimulus interval of 2.0 s. (Shock at an intensity of 1.5 mA [AC, constant current] is known to engage antinociceptive mechanisms within the spinal cord [18,19], vigorous defensive behavior in intact rats, and pain in humans [see 8,9].) An experimenter blind to the subject's drug treatment recorded whether the shocked rats vocalized during the first minute of stimulation.…”

Section: Shock Treatmentsmentioning

confidence: 99%

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The impact of morphine after a spinal cord injury

Hook

Liu

Washburn

et al. 2007

Behavioural Brain Research

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Nociceptive stimulation, at an intensity that elicits pain-related behavior, attenuates recovery of locomotor and bladder functions, and increases tissue loss after a contusion injury. These data imply that nociceptive input (e.g., from tissue damage) can enhance the loss of function after injury, and that potential clinical treatments, such pretreatment with an analgesic, may protect the damaged system from further secondary injury. The current study examined this hypothesis and showed that a potential treatment (morphine) did not have a protective effect. In fact, morphine appeared to exacerbate the effects of nociceptive stimulation. Experiment 1 showed that after spinal cord injury 20 mg/kg of systemic morphine was necessary to induce strong antinociception and block behavioral reactivity to shock treatment, a dose that was much higher than that needed for sham controls. In Experiment 2, contused rats were given one of three doses of morphine (Vehicle, 10, 20 mg/kg) prior to exposure to uncontrollable electrical stimulation or restraint alone. Despite decreasing nociceptive reactivity, morphine did not attenuate the long-term consequences of shock. Rats treated with morphine and shock had higher mortality rates, and displayed allodynic responses to innocuous sensory stimuli three weeks later. Independent of shock, morphine per se undermined recovery of sensory function. Rats treated with morphine alone also had significantly larger lesions than those treated with saline. These results suggest that nociceptive stimulation affects recovery despite a blockade of pain-elicited behavior. The results are clinically important because they suggest that opiate treatment may adversely affect the recovery of function after injury.

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Impact of shock on pain reactivity: II. Evidence for enhanced pain.

Cited by 52 publications

References 59 publications

Exacerbation of Pain by Anxiety Is Associated with Activity in a Hippocampal Network

Exacerbation of Pain by Anxiety Is Associated with Activity in a Hippocampal Network

Effects of contextual cues previously paired with footshock or illness on behavior and pain sensitivity in the rat

The impact of morphine after a spinal cord injury

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