Relationship between pain symptoms and referred sensory and trophic changes in patients with gallbladder pathology.
ABSTRACT The relationship was investigated between algogenic potential of gallbladder pathology and occurrence/extent of sensory and trophic changes in the referred area. Five groups of subjects were studied, with: symptomatic gallbladder calculosis (3-20 colics); asymptomatic calculosis; symptomatic gallbladder shape abnormality (8-18 colics); asymptomatic shape abnormality; normal gallbladder/no symptoms. At the cystic point (CP) and contralaterally, all underwent measurement of: pain thresholds to electrical stimulation of skin, subcutis and muscle; thickness of subcutis and muscle via ultrasounds. Contralaterally to CP, all thresholds were not significantly different in the five groups. At CP, subcutis and muscle thresholds were significantly lower in symptomatic vs asymptomatic patients and/or normals (0.0001<P< 0.05). In symptomatic cases, at CP compared to contralaterally, subcutis and muscle thresholds were significantly lower (0.0001<P<0.02), subcutis thickness was significantly higher and muscle thickness significantly lower (0.006<P<0.02). Subcutis and muscle thresholds at CP in symptomatic patients were significantly and inversely correlated linearly to the number of colics (P<0.0004; P<0.0001). Patients with symptomatic calculosis were re-evaluated after 6 months; those not presenting further colics showed a significant increase in subcutis and muscle thresholds at CP, while those who continued presenting colics showed a further significant threshold decrease (0.01<P<0.05); tissue thickness did not vary. Referred hyperalgesia and altered trophism from the gallbladder only occur in painful pathology, their extent being modulated by the amount of perceived pain. The results suggest different mechanisms by which visceral nociceptive inputs trigger sensory vs trophic changes in the referred area.
Article: Is altered central pain processing related to disease stage in chronic pancreatitis patients with pain? An exploratory study.[show abstract] [hide abstract]
ABSTRACT: The most dominant feature in chronic pancreatitis is intense abdominal pain. Changes in spinal and/or supraspinal central nervous system pain processing due to visceral nociceptive input play an important role in this pain. How altered pain processing is related to disease stage still needs study. Sixty chronic pancreatitis patients were compared to 15 healthy controls. Two subgroups of pancreatitis patients were defined based on the M-ANNHEIM severity index of chronic pancreatitis; i.e. moderate and severe. Pain detection and tolerance thresholds for pressure and electric stimuli were measured in six selected dermatomes (C5, T4, T10, L1, L4 and T10BACK). In addition, the conditioned pain modulation response to cold pressor task was determined. These measures were compared between the healthy controls and chronic pancreatitis patients. Severe pancreatitis patients showed lower pain thresholds than moderate pancreatitis patients or healthy volunteers. Healthy controls showed a significantly larger conditioned pain modulation response compared to all chronic pancreatitis patients taken together. The present study confirms that chronic pancreatitis patients show signs of altered central processing of nociception compared to healthy controls. The study further suggests that these changes, i.e. central sensitization, may be influenced by disease stage. These findings underline the need to take altered central pain processing into account when managing the pain of chronic pancreatitis.PLoS ONE 01/2013; 8(2):e55460. · 4.09 Impact Factor
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ABSTRACT: Long-term potentiation (LTP) in nociceptive spinal pathways shares several features with hyperalgesia and has been proposed to be a cellular mechanism of pain amplification in acute and chronic pain states. Spinal LTP is typically induced by noxious input and has therefore been hypothesized to contribute to acute postoperative pain and to forms of chronic pain that develop from an initial painful event, peripheral inflammation or neuropathy. Under this assumption, preventing LTP induction may help to prevent the development of exaggerated postoperative pain and reversing established LTP may help to treat patients who have an LTP component to their chronic pain. Spinal LTP is also induced by abrupt opioid withdrawal, making it a possible mechanism of some forms of opioid-induced hyperalgesia. Here, we give an overview of targets for preventing LTP induction and modifying established LTP as identified in animal studies. We discuss which of the various symptoms of human experimental and clinical pain may be manifestations of spinal LTP, review the pharmacology of these possible human LTP manifestations and compare it to the pharmacology of spinal LTP in rodents.Molecular Pain 03/2011; 7:20. · 3.53 Impact Factor
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ABSTRACT: Objectives. This study was done to evaluate three bedside tests in discriminating visceral pain from somatic pain among women with chronic pelvic pain. Study Design. The study was an exploratory cross-sectional evaluation of 81 women with chronic pelvic pain of 6 or more months' duration. Tests included abdominal cutaneous allodynia (aCA), perineal cutaneous allodynia (pCA), abdominal and perineal myofascial trigger points (aMFTP) and (pMFTP), and reduced pain thresholds (RPTs). Results. Eighty-one women were recruited, and all women provided informed consent. There were 62 women with apparent visceral pain and 19 with apparent somatic sources of pain. The positive predictive values for pelvic visceral disease were aCA-93%, pCA-91%, aMFTP-93%, pMFTP-81%, and RPT-79%. The likelihood ratio (+) and 95% C.I. for the detection of visceral sources of pain were aCA-4.19 (1.46, 12.0), pCA-2.91 (1.19, 7.11), aMTRP-4.19 (1.46, 12.0), pMFTP-1.35 (0.86, 2.13), and RPT-1.14 (0.85, 1.52), respectively. Conclusions. Tests of cutaneous allodynia, myofascial trigger points, and reduced pain thresholds are easily applied and well tolerated. The tests for cutaneous allodynia appear to have the greatest likelihood of identifying a visceral source of pain compared to somatic sources of pain.Pain research and treatment. 01/2011; 2011:692102.