Pain
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Our aim was to asses the efficacy of deep brain stimulation in post-stroke neuropathic pain. Since 2000, 15 patients with post-stroke intractable neuropathic pain were treated with deep brain stimulation of the periventricular gray area (PVG), sensory thalamus (Ventroposterolateral nucleus-VPL) or both. ⋯ However, there is a wide variation between patients. This study demonstrates that it is an effective treatment in 70% of such patients.
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Randomized Controlled Trial
Mechanisms of placebo analgesia: rACC recruitment of a subcortical antinociceptive network.
Placebo analgesia is one of the most striking examples of the cognitive modulation of pain perception and the underlying mechanisms are finally beginning to be understood. According to pharmacological studies, the endogenous opioid system is essential for placebo analgesia. Recent functional imaging data provides evidence that the rostral anterior cingulate cortex (rACC) represents a crucial cortical area for this type of endogenous pain control. ⋯ BOLD-responses to the painful laser-stimulation during the placebo and no-placebo condition were assessed using event-related fMRI. After having confirmed placebo related activity in the rACC, a connectivity analysis identified placebo dependent contributions of rACC activity with bilateral amygdalae and the periaqueductal gray (PAG). This finding supports the view that placebo analgesia depends on the enhanced functional connectivity of the rACC with subcortical brain structures that are crucial for conditioned learning and descending inhibition of nociception.
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Clinical Trial
The relationship of adult attachment to emotion, catastrophizing, control, threshold and tolerance, in experimentally-induced pain.
Although insecure attachment has been associated with a range of variables linked with problematic adjustment to chronic pain, the causal direction of these relationships remains unclear. Adult attachment style is, theoretically, developmentally antecedent to cognitions, emotions and behaviours (and might therefore be expected to contribute to maladjustment). It can also be argued, however, that the experience of chronic pain increases attachment insecurity. ⋯ Of particular interest were findings that attachment style moderated the effects of pain intensity on the tendency to catastrophize, such that insecurely attached individuals were more likely to catastrophize when reporting high pain intensity. This is the first study to link attachment with perceptions of pain in a pain-free sample. These findings cast anxious attachment as a vulnerability factor for chronic pain following acute episodes of pain, while secure attachment may provide more resilience.
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The sensitivity of tendon and tendon-bone junction is not fully described although these tissues have high clinical impacts. This study assessed (1) pain intensity and referred pain caused by hypertonic saline injection to the proximal tendon-bone junction (PTBJ), tendon and muscle belly sites of tibialis anterior muscle and (2) pressure pain sensitivity, pre, during and post hypertonic saline injections. Eighteen subjects (14 males and 4 females) participated. ⋯ Hypertonic saline pain at the tendon and PTBJ caused significantly higher (P < 0.001) final VAS scores compared to the muscle belly site. The results indicate the PTBJ and tendon sites are more sensitive and susceptible to sensitisation by hypertonic saline than muscle belly. Furthermore, there may be site specific central changes reflected by the differences in the results regarding sensitivity and summation over time.
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Cold allodynia is a common complaint in patients with peripheral neuropathies. However, cold sensitivity of the different types of sensory afferents present in injured nerves is poorly known. We recorded activity evoked by cold in intact sensory fibers of the skin-saphenous nerve preparation and in axotomized sensory fibers of approximately 21 days-old neuromas of the saphenous nerve of mice, in vitro. ⋯ In conclusion, the transducing capacity to cold stimuli is substantially recovered in neuromas. Furthermore, axotomized fibers maintain the 4-AP-sensitive, voltage-activated, transient potassium conductance that counteracts the depolarizing effects of cold in the majority of intact, cold-insensitive primary afferents. Our results indicate that injured nociceptors do not develop abnormal cold sensitivity, suggesting that other mechanisms underlie the cold-induced allodynia following peripheral nerve injury.