Pain
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A cold plate apparatus was designed to test the responses of unrestrained rats to low temperature stimulation of the plantar aspect of the paw. At plate temperatures of 10 degrees C and 5 degrees C, rats with either chronic constriction injury (CCI) of the sciatic nerve or complete Freund's adjuvant (CFA) induced inflammation of the hindpaw displayed a stereotyped behavior. Brisk lifts of the treated hindpaw were recorded, while no evidence of other nociceptive behaviors could be discerned. ⋯ At 60 days, neither morphine nor naltrexone affected cold-induced paw lifting in CFA rats, suggesting that the neuronal circuit mediating cold hyperalgesia in these animals had become opiate insensitive. In conclusion, the cold plate was found to be a reliable method for detecting abnormal nociceptive behavior even at long intervals after nerve or inflammatory injuries, when responses to other nociceptive stimuli have returned to near normal. The results of pharmacological studies suggest that cold hyperalgesia is in part a consequence of altered sensory processing in the periphery, and that it can be independently modulated by opiate and adrenergic systems.
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Styles of catastrophic thinking about pain have been related to an inability to divert attention away from pain. We investigated whether pain catastrophizers displayed high attentional interference during a threatening low-intensity electrocutaneous stimulus (ES). In Experiment 1, 44 undergraduates performed a tone discrimination task whilst experiencing several times an ES on the left or right arms. ⋯ In Experiment 2, threat was induced in 36 undergraduates by informing them that an ES excites pain fibres. Again, catastrophizers had marked interference immediately after onset. The results are discussed in terms of how catastrophizing amplifies somatosensory information and primes fear mechanisms.
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Case Reports
Epileptic seizure associated with intracerebroventricular and intrathecal morphine bolus.
We report on two patients with morphine-related seizures associated with either intrathecal or intracerebroventricular administration. Both patients had a history of malignant tumor and both experienced the seizures following bolus application of morphine, while even higher dosages were well tolerated when continuously infused. ⋯ Initiation of intrathecal morphine therapy and bolus application should be performed carefully and only when constant monitoring is provided for at least 12 h. Animal data and possible mechanisms for morphine-related seizures are discussed.
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The paradoxical combination of sensory loss within the area where pain is felt together with pain evoked by non-noxious stimuli (allodynia) is a characteristic feature of neuropathic pain. This study examined the relationship between (mechanical and thermal) pain thresholds and dynamic and static hyperalgesia in 15 patients with traumatic nerve injury and brush-evoked pain. Sensory tests were carried out both in the allodynic skin area and in the unaffected contralateral mirror image skin. ⋯ There was no relationship between dynamic and static evoked hyperalgesia. These findings suggest a differential processing of repetitive thermal and mechanical stimuli in the central nervous system. Both dynamic and static mechanical hyperalgesia are maintained by activity in heat-sensitive nociceptors, but they are probably mediated by distinct mechanisms.
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This is the first neural imaging study to use regional cerebral blood flow (rCBF) in an animal model to identify the patterns of forebrain nociceptive processing that occur during the early and late phase of the formalin test. We measured normalized rCBF increases by an autoradiographic method using the radiotracer [99mTc]exametazime. Noxious formalin consistently produced detectable, well-localized and typically bilateral increases in rCBF within multiple forebrain structures, as well as the interpeduncular nucleus (Activation Index, AI = 66) and the midbrain periaqueductal gray (AI = 20). ⋯ The hindlimb region of somatosensory cortex was significantly activated (AI = 31), and blood flow increases in VPL (AI = 8.7) and the medial thalamus (AI = 9.0) exhibited a tendency to be greater in the late phase as compared to the early phase of the formalin test. The spatial pattern and intensity of activation varied as a function of the time following the noxious formalin stimulus. The results highlight the important role of the limbic forebrain in the neural mechanisms of prolonged persistent pain and provide evidence for a forebrain network for pain.