Hindlimb muscle atrophy occurs from peripheral nerve damage in a rat neuropathic pain model.
ABSTRACT The purpose of this study was to examine the effect of neuropathic pain produced by peripheral nerve damage on mass, myofibrillar protein content, and cross-sectional areas of Type I and II fibers of rat hindlimb muscles.
Adult male Sprague-Dawley rats were assigned to one of three groups: a pain group (n = 10) that underwent ligation and cut of the left L5 spinal nerve, a sham group (n = 10) that underwent a sham cut procedure, or a control group (n = 10) that underwent no procedures. The withdrawal threshold test was done to assess pain threshold on each of Days 1-7 and 14. Activity, body weight, and food intake were measured daily for 2 weeks. At 15 days, rats were anesthetized and the bilateral soleus, plantaris, and gastrocnemius muscles dissected.
At 15 days post-ligation, the pain group had significant decreases in total dietary intake, body weight, activity, and muscle weight as compared to sham and control animals. Muscle weight and cross-sectional area of Type II fiber of the ipsilateral soleus, plantaris, and gastrocnemius muscles decreased as did myofibrillar protein content of the ipsilateral plantaris and gastrocnemius muscles. Muscle weight of the contralateral gastrocnemius muscle decreased, as did myofibrillar protein content and cross-sectional area of Type II fiber of the contralateral plantaris muscle.
Hindlimb muscle atrophy occurs in both ipsilateral and contralateral sides following induction of neuropathic pain by unilateral peripheral nerve damage. Muscle changes of the ipsilateral side are more pronounced than those of the contralateral side.
Article: Defining neuropathic pain.[show abstract] [hide abstract]
ABSTRACT: Clinical research and practice have suffered because of lack of specificity when clinical diagnoses of pain are made. Distinction between neuropathic and inflammatory pain mechanisms is suggested, as well as the distinction between neuropathic pain from hypersensitivity pain disorders, previously termed neuropathic pain due to neurological dysfunction. Neuropathic pain is in this case defined as pain occurring in the ara of body affected by neurological disease or injury. This type of pain manifests not only with positive sensory phenomena such as pain, dysesthesia, and different types of hyperalgesia, but also with negative sensory phenomena and negative and positive motor and autonomic symptoms and signs.Anesthesia & Analgesia 10/2003; 97(3):785-90. · 3.30 Impact Factor
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ABSTRACT: Chronic neuropathic pain, caused by lesions in the peripheral or central nervous system, comes in many forms. We describe current approaches to the diagnosis and assessment of neuropathic pain and discuss the results of recent research on its pathophysiologic mechanisms. Randomized controlled clinical trials of gabapentin, the 5% lidocaine patch, opioid analgesics, tramadol hydrochloride, and tricyclic antidepressants provide an evidence-based approach to the treatment of neuropathic pain, and specific recommendations are presented for use of these medications. Continued progress in basic and clinical research on the pathophysiologic mechanisms of neuropathic pain may make it possible to predict effective treatments for individual patients by application of a pain mechanism-based approach.JAMA Neurology 12/2003; 60(11):1524-34. · 7.58 Impact Factor
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ABSTRACT: A common complaint among pain patients is that they lose their appetite. These accounts are anecdotal, however, and the neural mechanism underlying pain-induced loss of appetite remains unknown. In this study, we documented the occurrence of appetite loss in patients under migraine attack and investigated the neuronal substrate of pain-induced anorexia in our animal model of intracranial pain. We found that loss of appetite during the migraine attack in humans coincided strongly with the onset and duration of the head pain in 32/39 cases, and that brief noxious stimulation of the dura in conscious rats produced a transient suppression of food intake. Mapping of neuronal activation in the rat showed that noxious dural stimulation induced a 3- to 4-fold increase in the number of Fos-positive neurons in medullary dorsal horn areas that process nociceptive signals (laminae I, V) and in parabrachial and hypothalamic neurons positioned to suppress feeding behavior. In the parabrachial area, activated neurons were localized in the superior-lateral subnucleus, and 40% of them expressed the mRNA encoding the anorectic neuropeptide cholecystokinin. In the hypothalamus, activated Fos-positive neurons were found in the dorsomedial area of the ventromedial nucleus, and 76% of them expressed the mRNA for cholecystokinin type-B receptor. Based on these findings, we suggest that at least one of several groups of hypothalamic neurons that normally inhibit appetite in response to metabolic cues is positioned to mediate the suppression of food intake by pain signals.Proceedings of the National Academy of Sciences 09/2001; 98(17):9930-5. · 9.74 Impact Factor