Pain
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Controlled Clinical Trial
Increased taste intensity perception exhibited by patients with chronic back pain.
There is overlap between brain regions involved in taste and pain perception, and cortical injuries may lead to increases as well as decreases in sensitivity to taste. Recently it was shown that chronic back pain (CBP) is associated with a specific pattern of brain atrophy. Since CBP is characterized by increased sensitivity to pain, we reasoned that the sense of taste might also be enhanced in CBP. ⋯ There was no difference between CBP and control subjects for visual grayness rating. On the other hand, CBP patients in comparison to control subjects rated gustatory stimuli as significantly more intense but no more or less pleasant and showed a trend towards a lower detection threshold (i.e. increased sensitivity). The selectivity of the taste disturbance suggests interaction between pain and taste at specific brain sites and provides further evidence that CBP involves specific brain abnormalities.
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Controlled Clinical Trial
Neural correlates of individual differences in pain-related fear and anxiety.
Although individual differences in fear and anxiety modulate the pain response and may even cause more suffering than the initiating physical stimulus, little is known about the neural systems mediating this relationship. The present study provided the first examination of the neural correlates of individual differences in the tendency to (1) feel anxious about the potentially negative implications of physical sensations, as measured by the anxiety sensitivity index (ASI), and (2) fear various types of physical pain, as indexed by the fear of pain questionnaire (FPQ). ⋯ These functional relationships cannot be wholly explained by generalized anxiety (indexed by STAI-T scores), which did not significantly correlate with activation of any regions. The present findings may help clarify both the impact of individual differences in emotion on the neural correlates of pain, and the roles in anxiety, fear, and pain processing played by medial and orbitofrontal systems.
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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.
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Randomized Controlled Trial
Chronobiological characteristics of painful diabetic neuropathy and postherpetic neuralgia: diurnal pain variation and effects of analgesic therapy.
Clinical impressions suggest that neuropathic pain is often worse at night and significantly impairs sleep. However, the temporal pattern of neuropathic pain during waking hours has not been clearly characterized. Using clinical trial data, we have evaluated the diurnal variation of pain intensity before and during analgesic treatment in patients with diabetic neuropathy (DN) and postherpetic neuralgia (PHN). ⋯ Neuropathic pain intensity progressively increases throughout the day and this temporal profile appears to be unaffected by treatment with gabapentin and/or morphine. Advancing our understanding of the chronobiology of neuropathic pain may shed new light on various neurohormonal and neurophysiologic influences and lead to the identification of novel therapeutic targets. Furthermore, recognizing diurnal pain patterns may guide treatment strategies such as the targeted timing of analgesic therapies.