Pain
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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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Neurogenic dysaesthetic pain in the neck following surgery for tumours in the neck is rare. Rarer still is the combination of pain following surgery with syncope. ⋯ Spinal cord stimulation was used successfully to treat the dysaesthetic pain and syncope in three of the patients while the fourth patient died from the effects of his tumour. Medical practitioners may wish to consider spinal cord stimulation in relation to treating neurogenic dysaesthetic neck pain with syncope.
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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.