Pain
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Comparative Study
Pattern-reversal visual-evoked potentials in children with migraine and other primary headache: evidence for maturation disorder?
Recently, evidence for a disturbed maturation of cerebral information processing in migraine came from studies investigating the auditory-evoked contingent negative variation and the auditory-evoked potential from childhood to adulthood. This study is to clarify whether age-dependent development is altered also for the processing of visual stimuli in migraine. Components of pattern-reversal visual-evoked potentials at four different spatial frequencies (which can preferentially activate the magno- and the parvocellular visual system) were compared between children aged 6 and 18 years with primary headache (N = 123; 67 migraine without aura, MO; 32 migraine with aura, MA; 24 tension-type headache, TH) in the headache-free interval and healthy controls (N = 82). ⋯ In headache-free controls, N135 latency reduction between pre- and post-puberty age was most pronounced at high spatial frequency. The main 'decline' of N135 latency with increasing age was shifted to lower spatial frequencies in the headache subgroups. The results give evidence that maturation of visual processing is partly disturbed in migraineurs.
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Comparative Study
Central poststroke pain and reduced opioid receptor binding within pain processing circuitries: a [11C]diprenorphine PET study.
Based on concepts that endogenous opioids participate in neural transmission of pain, the present study in central poststroke pain (CPSP) patients investigated changes in opioid receptor (OR) binding in neural structures centrally involved in the processing of pain. Five patients with central pain after lesions in the brain stem, thalamus or parietal cortex and twelve healthy volunteers underwent a [11C]diprenorphine positron emission tomography study. Binding potentials were calculated using a reference region model in all subjects. ⋯ Individual extracted binding values disclosed a reduced binding in these regions in all patients independent from the particular lesion site. The poststroke pain syndrome is associated with a characteristic pattern of reduced OR binding within the neural circuitry processing pain. It is suggested that an imbalance of excitatory-inhibitory mechanisms in certain brain structures, as evidenced in decreased [11C]diprenorphine binding, is one of the causes or the consequences of poststroke pain.
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Comparative Study
Changes in the expression of tetrodotoxin-sensitive sodium channels within dorsal root ganglia neurons in inflammatory pain.
Nociceptive neurons within dorsal root ganglia (DRG) express multiple voltage-gated sodium channels, of which the tetrodotoxin-resistant (TTX-R) channel Na(v)1.8 has been suggested to play a major role in inflammatory pain. Previous work has shown that acute administration of inflammatory mediators, including prostaglandin E2 (PGE2), serotonin, and adenosine, modulates TTX-R current in DRG neurons, producing increased current amplitude and a hyperpolarizing shift of its activation curve. In addition, 4 days following injection of carrageenan into the hind paw, an established model of inflammatory pain, Na(v)1.8 mRNA and slowly-inactivating TTX-R current are increased in DRG neurons projecting to the affected paw. ⋯ The results demonstrate that, following carrageenan injection, there is increased expression of TTX-S channels Na(v)1.3 and Na(v)1.7 and a parallel increase in TTX-S currents. The previously reported upregulation of Na(v)1.8 and slowly-inactivating TTX-R current is not accompanied by upregulation of mRNA or protein for Na(v)1.9, an additional TTX-R channel that is expressed in some DRG neurons. These observations demonstrate that chronic inflammation results in an upregulation in the expression of both TTX-S and TTX-R sodium channels, and suggest that TTX-S sodium channels may also contribute, at least in part, to pain associated with inflammation.
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Case Reports
Some cases of severe post-mastectomy pain syndrome may be caused by an axillary haematoma.
Post-mastectomy pain syndrome (PMPS) is experienced by 20-65% of patients who undergo breast surgery for cancer. The etiology of this chronic neuropathic pain syndrome is unclear and most likely multi-factorial. Symptoms may be mild, not requiring treatment, or severe, considerably restricting quality of life. ⋯ In these cases the symptoms were completely relieved by the aspiration or formal drainage of an encapsulated haematoma in the axilla. The removal of a minimal amount of blood brought instant improvement suggesting that pressure within the haematoma could be an etiological factor. An axillary haematoma, which may not be clinically obvious, should be considered as a possible cause of PMPS.
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Comparative Study
Development and validation of the Neuropathic Pain Symptom Inventory.
This study describes the development and validation of the Neuropathic Pain Symptom Inventory (NPSI), a new self-questionnaire specifically designed to evaluate the different symptoms of neuropathic pain. Following a development phase and a pilot study, we generated a list of descriptors reflecting spontaneous ongoing or paroxysmal pain, evoked pain (i.e. mechanical and thermal allodynia/hyperalgesia) and dysesthesia/paresthesia. Each of these items was quantified on a (0-10) numerical scale. ⋯ It included: (i) assessment of the test-retest reliability of each item, (ii) determination of the factorial structure of the questionnaire and analysis of convergent and divergent validities (i.e. construct validity), and (iii) evaluation of the ability of the NPSI to detect the effects of treatment (i.e. sensitivity to change). The final version of the NPSI includes 10 descriptors (plus two temporal items) that allow discrimination and quantification of five distinct clinically relevant dimensions of neuropathic pain syndromes and that are sensitive to treatment. The psychometric properties of the NPSI suggest that it might be used to characterize subgroups of neuropathic pain patients and verify whether they respond differentially to various pharmacological agents or other therapeutic interventions.