Pain
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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
The NMDA-receptor antagonist ketamine abolishes neuropathic pain after epidural administration in a clinical case.
A 14-year-old male patient developed severe right limb pain after traumatic sciatic nerve injury. His pain was diagnosed as neuropathic pain (complex regional pain syndrome, type II). He did not respond to any conventional therapy for limb pain including non-steroidal antiinflammatory drugs, antidepressants, anticonvulsants, continuous epidural administration of local anesthetics and psychotherapy. ⋯ There has been no recurrence of pain for 8 months after discontinuation of epidural ketamine. The symptoms related to dysfunction of the sympathetic nervous system still remained after complete pain relief. We discuss pain mechanisms, pain relief and the use of ketamine in this case.
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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.
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Comparative Study
Effects of systemic carbamazepine and gabapentin on spinal neuronal responses in spinal nerve ligated rats.
There are few pharmacological studies of central neuronal measures in animal models of neuropathic pain. In the present study we have compared the effects of two anticonvulsants, carbamazepine and gabapentin, on spinal neuronal responses of nerve injured rats (selective ligation of spinal nerves L5 and L6, SNL) and sham-operated rats. The development and maintenance of cooling and mechanical allodynia of the lesioned hindlimb of SNL rats was followed with behavioural indices. ⋯ The peripheral nerve dysfunction reveals an effect of carbamazepine which is maintained throughout the observation period, validating this experimental approach. Gabapentin, a novel treatment for neuropathic pain states, also reduced neuronal responses, but the actions of the drug were not dependent on nerve injury. Further studies at the spinal level may shed light on the physiology and pharmacology of the aberrant processes associated with neuropathic pain.
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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.