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Query: UMLS:C0423716 (Neuropathic pain)
 1,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neuropathic pain is caused by lesions in the peripheral and/or central nervous system. Patients with pain due to nerve damage after operations are often misinterpreted and met with suspicion of malingering. Neuropathic pain typically presents with a characteristic set of sensory disorders independent of the cause. The sensory dysfunction may manifest itself as hypo- and/or hyperesthesia to one or more modalities, increased pain to painful stimuli (hyperalgesia) and/or pain to non-painful stimuli (allodynia). Conventional analgesics such as acetaminophen, non-steroidal anti-inflammatory drugs and opioids are often ineffective. Instead, antidepressants and anticonvulsants may be tried. The pain condition is unknown to most physicians. This may result in mistreated patients having undergone several unnecessary and ineffective investigations and treatments.
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PMID:[Diagnosis and treatment of postoperative nerve damage. Chronic neuropathic pain]. 1048 32

Neuropathic pain is accompanied by both positive and negative sensory signs. To explore the spectrum of sensory abnormalities, 1236 patients with a clinical diagnosis of neuropathic pain were assessed by quantitative sensory testing (QST) following the protocol of DFNS (German Research Network on Neuropathic Pain), using both thermal and mechanical nociceptive as well as non-nociceptive stimuli. Data distributions showed a systematic shift to hyperalgesia for nociceptive, and to hypoesthesia for non-nociceptive parameters. Across all parameters, 92% of the patients presented at least one abnormality. Thermosensory or mechanical hypoesthesia (up to 41%) was more frequent than hypoalgesia (up to 18% for mechanical stimuli). Mechanical hyperalgesias occurred more often (blunt pressure: 36%, pinprick: 29%) than thermal hyperalgesias (cold: 19%, heat: 24%), dynamic mechanical allodynia (20%), paradoxical heat sensations (18%) or enhanced wind-up (13%). Hyperesthesia was less than 5%. Every single sensory abnormality occurred in each neurological syndrome, but with different frequencies: thermal and mechanical hyperalgesias were most frequent in complex regional pain syndrome and peripheral nerve injury, allodynia in postherpetic neuralgia. In postherpetic neuralgia and in central pain, subgroups showed either mechanical hyperalgesia or mechanical hypoalgesia. The most frequent combinations of gain and loss were mixed thermal/mechanical loss without hyperalgesia (central pain and polyneuropathy), mixed loss with mechanical hyperalgesia in peripheral neuropathies, mechanical hyperalgesia without any loss in trigeminal neuralgia. Thus, somatosensory profiles with different combinations of loss and gain are shared across the major neuropathic pain syndromes. The characterization of underlying mechanisms will be needed to make a mechanism-based classification feasible.
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PMID:Quantitative sensory testing in the German Research Network on Neuropathic Pain (DFNS): somatosensory abnormalities in 1236 patients with different neuropathic pain syndromes. 2063 44

Neuropathic pain may develop after a variety of injuries to peripheral nerves and roots. Most injury models have included a direct injury to primary afferent fibers or neurons. Recently, it has been demonstrated that injury to motor fibers in ventral roots may also result in neuropathic pain. A lumbosacral ventral root avulsion injury results in acute and persistent mechanical allodynia, but not thermal hyperesthesia. Interestingly, an acute replantation of the avulsed ventral roots into the spinal cord results in amelioration of the neuropathic pain. A detailed description of this injury and repair model is provided.
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PMID:A lumbosacral ventral root avulsion injury and repair model for studies of neuropathic pain in rats. 2235 Oct 91