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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 20-year-old man suffered head, chest, and abdominal trauma in an auto accident resulting in a traumatic dissecting aneurysm of the thoracic aorta. Hypotension developed. The aneurysm was resected and replaced with a prosthetic graft. Postoperatively, the patient was found to be paraplegic below T-9, areflexic and anesthetic to pain and temperature, with preservation of vibration and position senses. In the ensuing nine months, the patient regained considerable sensory function in his lower extremities and had severe constant hyperhydrosis below the T-9 dermatome. The exaggerated sweating was unaffected by temperature change and anxiety. It was diminished by methantheline bromide treatment but never abolished. The spinal cord lesion is postulated to be anterior horn cell loss, with preservation of interneurons and intermediolateral gray columns. Disinhibition of sympthetic circuits or sprouting of axons are proposed mechanisms.
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PMID:Hyperhydrosis in paraplegia. 88 95

The synaptic relationships between gamma-aminobutyric acid (GABA)-immunoreactive and enkephalin-immunoreactive profiles in the cat spinal cord were examined using combined pre-embedding immunoperoxidase and post-embedding immunogold electron microscopic immunocytochemistry. Although colchicine was not used, enkephalin-immunoreactive somata and dendrites were detected in regions associated with nociceptive transmission, including laminae I, II, V and X. In each of these laminae, many GABA-immunoreactive terminals were found presynaptic to enkephalin-immunoreactive cell bodies and dendrites. We propose that disinhibition of opioid-containing neurons may be a common feature of pain-related circuits in the cat spinal cord.
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PMID:Ultrastructural evidence for GABA-mediated disinhibitory circuits in the spinal cord of the cat. 140 60

The quantitative somatosensory thermotest (QST) assesses the function of afferent channels concerned with sensory submodalities served by small calibre fibres. Measured ramps of ascending or descending temperature are applied to the skin through a Peltier contact thermode, and detection thresholds are recorded as the subject signals the onset of a particular sensation. The present study describes underlying principles, methodological aspects and normal reference values for the QST. In patients, measurement of thresholds for cold sensation, warm sensation, cold-induced pain and heat-induced pain, applied to 465 individuals, yielded 13 abnormal patterns segregated into three main groups: (i) thermal (cold or warm) hypoaesthesia; (ii) thermal hyperalgesia (abnormally reduced threshold for cold and/or heat induced pain); (iii) thermal hypoaesthesia combined with thermal hyperalgesia. Critical analysis of these results yielded a number of observations of general relevance: (i) thermal specific (warm or cold) hypoaesthesia and thermal (heat or cold) hyperalgesia may occur in the absence of hypoaesthesia for tactile submodalities served by large calibre afferents; (ii) cold hypoaesthesia and warm hypoaesthesia may dissociate from each other; (iii) thermal pain hyperalgesias may occur in the absence of hypoaesthesias for specific cold or warm sensations; (iv) cold hyperalgesia and heat hyperalgesia may dissociate from each other. Thus, a negative routine sensory examination and unimpaired sensory nerve action potentials do not exclude possible somatosensory dysfunction. Furthermore, while most methods of sensory testing only document normality or deficit, the QST permits additional documentation of hyperalgesia, a positive sensory phenomenon that implies unusual pathophysiologies such as sensitization of receptors, central hyperexcitability, disinhibition or, possibly, ectopic nerve impulse discharge. This psychophysical test does not specify the level within afferent channels, between skin and brainmind, where the abnormality resides. It is recommended that the QST for all four thermal specific and thermal pain functions be incorporated in routine neurological assessment.
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PMID:Quantitative somatosensory thermotest. A key method for functional evaluation of small calibre afferent channels. 162 7

When a peripheral nerve is severed, damaged sensory fibers emit a barrage of impulses that lasts for many seconds, or even several minutes ('injury discharge'). We have shown in rats that local anesthetic blockade of this discharge suppresses autotomy (a behavioral model of neuropathic pain). Correspondingly, mimicking prolonged injury discharge with electrical stimulation, especially of C-fibers, increased autotomy. These data support the hypothesis that injury discharge plays a role in the triggering of neuropathic pain. The mechanism of triggering autotomy was investigated using intrathecal injection of agents affecting glutamatergic transmission. A single intrathecal injection at the lumbar enlargement of the NMDA receptor blockers MK-801 and 5-APV, just prior to neurectomy, significantly suppressed autotomy. Blocking glycinergic inhibition just prior to neurectomy with a single strychnine injection strikingly enhanced autotomy. Strychnine enhancement of autotomy was prevented by prior injection of MK-801 or 5-APV. These results suggest that the expression of autotomy in rats, and by inference neuropathic pain in humans, is affected by injury discharge, possibly mediated by long-lasting, NMDA receptor-related, spinal disinhibition.
Pain 1991 Apr
PMID:Modulation of neuropathic pain behavior in rats by spinal disinhibition and NMDA receptor blockade of injury discharge. 167 50

Based on a review of numerous studies conducted on normal, neurosurgical and brain-injured individuals, the right cerebral hemisphere appears to be dominant in the perception and identification of environmental and nonverbal sounds; the analysis of geometric and visual space (e.g., depth perception, visual closure); somesthesis, stereognosis, the maintenance of the body image; the production of dreams during REM sleep; the perception of most aspects of musical stimuli; and the comprehension and expression of prosodic, melodic, visual, facial, and verbal emotion. When the right hemisphere is damaged a variety of cognitive abnormalities may result, including hemi-inattention and neglect, prosopagnosia, constructional apraxia, visual-perceptual disturbances, and agnosia for environmental, musical, and emotional sounds. Similarly, a myriad of affective abnormalities may occur, including indifference, depression, hysteria, gross social-emotional disinhibition, florid manic excitement, childishness, euphoria, impulsivity, and abnormal sexual behavior. Patients may become delusional, engage in the production of bizzare confabulations and experience a host of somatic disturbances such as pain and body-perceptual distortions. Based on studies of normal and "split-brain" functioning, it also appears that the right hemisphere maintains a highly developed social-emotional mental system and can independently perceive, recall and act on certain memories and experiences without the aid or active reflective participation of the left. This leads to situations in which the right and left halves of the brain sometime act in an uncooperative fashion, which gives rise to inter-manual and intra-psychic conflicts.
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PMID:The right cerebral hemisphere: emotion, music, visual-spatial skills, body-image, dreams, and awareness. 246 90

Migraine is a psychobiological disorder in which a recurrent failure of opioid and adrenergic systems might occur, as plasma and CSF studies suggest. In order to elucidate the relationship between noradrenergic and opioidergic functions, the plasma beta-endorphin (beta-EP) response to clonidine and the cortisol response to dexamethasone were evaluated together in 25 patients suffering from migraine without aura, and with chronic tension headache (MTH). Baseline beta-EP plasma levels and beta-EP response to clonidine were significantly lower in MTH subjects than in controls, suggesting a postsynaptic hypothalamo-pituitary impairment. Forty-four percent of the MTH subjects showed either a lack of suppression of plasma cortisol following dexamethasone administration, or basal cortisol concentrations higher than controls and suppressors, suggesting a disinhibition of the hypothalamopituitary-adrenal (HPA) axis. An inverse correlation was found between pain severity and beta-EP secretion induced by clonidine (delta max), and no relationship was found between beta-EP and mood. These data suggest a failure of central noradrenergic activity, or perhaps an impaired secretion of beta-EP not related to HPA axis hyperactivity or to affective state.
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PMID:Neuroendocrine evidence of deranged noradrenergic activity in chronic migraine. 255 58

Clonazepam is a high-potency benzodiazepine labeled for use as an anticonvulsant. Increasingly, clonazepam has been used in the treatment of a variety of psychiatric disorders. The authors discuss its potential clinical applications, including (1) use as an adjunct to neuroleptics for treating psychosis, (2) management of specific psychotropic side effects, (3) alternative treatment for certain pain syndromes, and (4) a primary treatment for severe agitation, atypical psychosis, and anxiety disorders. Apparent treatment-emergent side effects including depression, disinhibition, and sexual dysfunction are also discussed.
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PMID:Clonazepam: new uses and potential problems. 288 24

The possibility that GABAergic neurons in the ventral periaqueductal gray matter modulate the analgesic effects of morphine microinjected into this brain area was investigated in the rat. Microinjection of 4,5,6,7-tetrahydroisoxazolo[5,4-c]pyridin 3-ol (THIP) (0.4 microgram in 0.2 microliter), a GABA agonist, in the ventral periaqueductal gray matter significantly reversed the increase of tail-flick latency induced by a prior injection of morphine sulfate (4 micrograms in 0.2 microliter) at the same site. Conversely, microinjection in the same region of picrotoxin (10 ng in 0.2 microliter), a GABA antagonist, significantly potentiated the analgesic effect of the same dose of morphine. These results suggest the existence of GABAergic neurons that tonically inhibit periaqueductal gray output neurons involved in centrifugal pain inhibition. The analgesic effects of opiates may, at least in part, result from disinhibition of these GABAergic neurons.
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PMID:GABAergic modulation of the analgesic effects of morphine microinjected in the ventral periaqueductal gray matter of the rat. 343 24

The view that the two cerebral hemispheres of the human brain are characterized by different cognitive processing modes that handle information received in various forms is commonly accepted by neurobehavioral scientists and neuropsychologists. Selected neuroanatomical, electrophysiological, neurochemical, biochemical, and neuropsychological data that bear on a cognitive information-processing model of the brain are presented. Processes involved in memory functions are discussed in regard to the nature of thought and the characteristics of mental life, e.g., internalization of thought, perception, arousal, attention, cognitive development, problem solving, the development of cognitive encoding, and selective recall. We present a position that argues for the brain as being flexible vs. fixed in its characteristics and limitations, drawing from various theories and viewpoints. We also present a review of selected mechanisms believed to be involved in brain-behavior processes, e.g., learning, cognition, pain, emotion, reward, cognitive development, and memory formation. A major theme addressed in terms of human information processing is that cognitive functioning, in a variety of instances, comprises subsets of more general processes, e.g., selective recall, cueing that is capable of addressing schemas, notions of inhibition and disinhibition, and the modulation of excitatory properties of certain neural transmitter substances. Questions such as "how is information stored in memory in the first place?" and "how do elements of motivation (i.e., goal orientation) get connected and then send their messages to appropriate inbound behaviors?" are addressed from the point of view that learning, although not understood completely, is somehow involved. Another unresolved question of theoretical and practical significance that we address is "how does learning result in neural connections?" Such questions are discussed in light of their implications for human memory, thought, and behavioral events.
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PMID:Cognitive information processing and learning mechanisms of the brain. 612 96

The medial prefrontal cortex has been implicated in pain perception by recent anatomical, physiological, and functional imaging data demonstrating that frontal and anterior cingulate cortices receive inputs related to nociception; neurosurgical case reports suggest that lesions involving these areas may specifically reduce the affective or emotional component of chronic intractable pain. We examined this hypothesis more closely by assessing psychophysical ratings of (1) warmth, pain intensity, and unpleasantness evoked by phasic thermal stimuli, (2) tolerance to tonic cold stimuli, and (3) perceived intensity of visual stimuli, both before and after neurosurgical lesions of the fiber tracts connecting the frontal lobes to subcortical structures. A 22-year-old male, with no history of chronic pain, underwent psychophysical testing 3 days before, 5 days after, and 6 months after receiving bilateral lesions of the anterior internal capsule (aIC), performed as treatment for obsessive-compulsive disorder. In each session, the patient rated the intensity and unpleasantness of 5-sec cutaneous heat stimuli (39-47 degrees C); pain tolerance was measured by means of a cold-pressor test (hand immersion in 1 degrees C water). The patient was able to differentially rate the intensities of heat stimuli during both pre- and postsurgical testing sessions (p < 0.001). However, he rated heat stimuli as less intense 5 days after surgery than during presurgical testing (p < 0.001), with significant decreases in both pain intensity (p < 0.005) and unpleasantness (p < 0.05). Likewise, the patient described the cold-water immersion as less painful following surgery, although his tolerance times were substantially shorter than those of the presurgical evaluation. Ratings of visual stimulus intensity did not differ across the pre- and postsurgical testing periods, suggesting that changes in pain perception were not related to attentional or cognitive deficits. Magnetic resonance imaging 5 days following surgery revealed bilateral lesions and edema centered in the aIC, with some edema in the left frontal lobe. Those 6 months later showed substantially smaller lesions involving less than half of the aIC and no edema; pain ratings and cold-water tolerance measured at that time indicated a substantial return toward the patient's presurgical values. These data suggest that blocking subcortical input to the anterior cingulate and frontal cortices reduces both the perceived intensity and the unpleasantness of noxious stimuli; reduced cold tolerance times--in the face of decreased pain perception--may reflect a disinhibition of cortical control on spinal reflexes.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Evaluation of pain perception after anterior capsulotomy: a case report. 750 2


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