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

The syndrome of "painful legs and moving toes" is characterised by spontaneous causalgic pain in the lower extremities associated with peculiar involuntary movements of the toes and feet. It has been observed after a variety of lesions affecting the posterior nerve roots, the spinal ganglia and the peripheral nerves. The pathophysiology of the syndrome is unknown. I report a patient who developed the syndrome during treatment for schizophrenia with the antipsychotic agent molindone hydrochloride. The patient's response to the combination of clonazepam and baclofen suggests that the pathophysiology of the "painful legs and moving toes" may be linked to impairment of spinal serotonergic and GABA functions.
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PMID:Neuroleptic-induced "painful legs and moving toes" syndrome: successful treatment with clonazepam and baclofen. 208 81

Thiocolchicoside is a muscle relaxant which, due to its mainly spinal GABA-agonist activity, is used by the oral and intramuscular routes in the ambulatory treatment of painful contracture of the skeletal muscles. The effectiveness and acceptability of this drug in the treatment of acute low-back pain were evaluated in a multicentre, randomized, double-blind, drug versus placebo trial involving 98 patients. The effectiveness of thiocolchicoside was assessed on the following criteria: patients' overall opinion, pain intensity, number of analgesic tablets taken, vertebral rigidity and ability to resume ordinary daily tasks. The results obtained showed that thiocolchicoside significantly improves the principal criterion by the second day of treatment and the other criteria within 5 days.
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PMID:[Evaluation of thiocolchicoside as monotherapy in low back pain. Results of a randomized study versus placebo]. 214 31

Injection of GABA into the midbrain periaqueductal gray (PAG) activates medullary neurons that are involved in pain inhibition and potentiates morphine-induced analgesia. These observations suggest that GABAergic mechanisms in the PAG may modulate the descending pain inhibitory system that arises from this structure. In the present study, the effects of GABA and GABA antagonists on membrane properties and baseline activity of PAG neurons were examined using both in vitro and in vivo preparations. Application of bicuculline methiodide (BICM), at a dose that blocked the response to GABA, potently increased the baseline firing rate in 53% of cells recorded in vitro and 74% of cells recorded in the intact preparation. Application of BICM often yielded multiple or burst spiking episodes in both preparations. In 69% of cells the effect of BICM was diminished or totally abolished when the slice was perfused with high-magnesium, calcium-free, physiological saline solution. Intracellular recordings revealed that bicuculline caused depolarization of the membrane (70% of cells), increased the firing frequency (94% of cells) and increased the frequency of excitatory postsynaptic potentials (18% of cells). The effect of bicuculline on membrane resistance was not pronounced and in 64% of neurons it did not cause any measurable change in the resting membrane resistance. PAG neurons responsive to GABA and its antagonists were observed in all regions of the PAG. However, the highest number of neurons that responded to GABA and its antgonists was found in the medial and medioventral parts of the PAG. These results indicate that PAG may contain a tonically active GABAergic network that operates, at least in part, through GABAA receptors. This GABAergic system may modulate activity in descending pain inhibitory pathways emanating from PAG.
Pain 1990 Feb
PMID:The effect of GABA and its antagonists on midbrain periaqueductal gray neurons in the rat. 230 65

The effects of alfentanil on the midazolam dose-response curve for hypnosis was studied with response to the verbal command as an end point in 95 patients. The analgesic effect of alfentanil was studied by measuring the threshold for pain caused by pressure on the trapezius muscle with the use of a dolorimeter in 21 patients. The study was randomized, double-blind, and performed on the unpremedicated patients with ASA physical status I or II. Alfentanil was found to reduce the midazolam ED50 value for the induction of anesthesia in a dose-dependent fashion. The smallest dose of alfentanil (3 micrograms/kg) that caused a marked shift of the midazolam dose-response curve to the left along the dose axis (from the ED50 of 270 micrograms/kg to the ED50 of 142 micrograms/kg, P less than 0.0005) represents approximately 2% of the alfentanil ED50 for induction of unconsciousness (130 micrograms/kg). Alfentanil (10 micrograms/kg) caused only a tendency for increase in the pain threshold, whereas a dose of 15 micrograms/kg significantly increased the pain threshold by 37% (P less than 0.05). The results demonstrate that alfentanil potentiates the hypnotic effect of midazolam in very small doses. The high potency of alfentanil in this respect, as compared to its analgesic potency, suggests a very specific mechanism of alfentanil-midazolam hypnotic interaction, one that most likely is based on a functional relationship between the GABA receptor-benzodiazepine receptor system and the opioid receptor system in mediation of hypnosis.
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PMID:Alfentanil potentiates midazolam-induced unconsciousness in subanalgesic doses. 236 31

Experiments reported in this study have been performed in order to investigate cholinergic and GABA-ergic neurotransmitter systems and substance P in the realization of internal inhibition and pain reinforcement. This was accomplished during the elaboration of inhibitory and defensive conditioned reflexes to light flashes in alert, nonimmobilized rabbits. Present results together with a review of past research indicate that the cholinergic system is directly involved in transmitting the effects of pain reinforcement to neocortical neurons. Substance P, a neuropeptide, reduces the background activity of neocortical and hippocampal neurons and the response of cortical neurons to pain and positive conditioned stimuli. The cholinergic system and substance P exert a modulating effect on the elaboration of internal inhibition. Phenybut, a GABA derivative capable of penetrating the blood-brain barrier, enhances inhibitory hyperpolarization in the cerebral cortex and improves discrimination between the inhibitory and reinforcing light flashes. It appears, therefore, that the GABA-ergic system plays a leading part in the elaboration of internal inhibition. Neuronal activity and slow potential changes in response to positive conditioned and pain stimuli occur in the same direction after administering the preparations, and the dynamics of these changes is different from that in responses to inhibitory stimuli. It may be supposed on these grounds that the neurotransmitter and neuromodulator systems studied possess a considerable degree of plasticity.
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PMID:On neurotransmitter mechanisms of reinforcement and internal inhibition. 243 77

An isolated spinal cord-tail preparation of the newborn rat was developed and used for studying the effects of various drugs. The cord and the tail were separately perfused with oxygenated artificial cerebrospinal fluid. Application of capsaicin in a small amount to the tail induced a depolarizing response of the lumbar ventral root (L3-L5) lasting for about 30 sec. The stimulating action of capsaicin was potentiated by previous perfusion of the tail with a medium containing prostaglandin E1 or E2. The capsaicin-induced nociceptive reflex was depressed by application to the spinal cord of morphine, Met-enkephalin, dynorphin (1-13), somatostatin, adenosine, GABA and a substance P (SP) antagonist [D-Arg1, D-Pro2, D-Trp7,9, Leu11]SP, and potentiated by bicuculline. The present preparation will be useful for the future studies on pain and analgesic drugs.
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PMID:Effect of a substance P antagonist on capsaicin-induced nociceptive reflex in the isolated spinal cord-tail preparation of the rat. 244 68

Recent electrophysiological evidence shows that rostral levels of the trigeminal spinal complex are concerned with pain processing from receptive fields in the face and oral cavity. The ventrolateral quadrant of the subnucleus interpolaris contains concentrations of enkephalin, dynorphin, serotonin, substance P and GABA [Matthews M. A., Hernandez T. V. and Liles S. L. (1987) Synapse 1, 512-529; Matthews M. A., McDonald G. K. and Hernandez T. V. (1988) Somatosensory Res. 5, 205-217]. These transmitters have also been localized to the fusiform and stalked cells in Laminae I and II of the subnucleus caudalis [Basbaum A. I. and Fields H. L. (1984) A. Rev. Neurosci. 7, 309-338]. The present study compares Golgi impregnations of the subnucleus interpolaris with sections at the same levels immunoreacted against enkephalin to determine if comparable cells exist in the subnucleus interpolaris and if they occur predominantly in the ventrolateral quadrant of the subnucleus. Twelve, young adult cats were killed by perfusion, the brainstems removed and either processed for rapid Golgi impregnation or sectioned and immunoreacted for enkephalin using the avidin-biotin Vectastain method. Golgi impregnated tissue was sectioned in the coronal, transverse or sagittal plane to insure the most advantageous visualization of cells with a directional bias in their dendritic arbors. The subnucleus interpolaris contained several distinctive cell types. The predominant neuron throughout the subnucleus was the smooth pyramidal cell or multipolar cell, characterized by a large round soma (15-25 microns diameter) and a spherical dendritic arborization which allowed its identification in all planes of section. The second cell type was the fusiform cell which had a smaller ovoid soma (10-15 microns) with narrow, less ramified, dendritic arbors oriented dorsoventrally, thus giving a bipolar appearance. Fusiform cells were most concentrated along the lateral margin of the subnucleus interpolaris. Examination of sections at the same level reacted for enkephalin revealed cells with a bipolar appearance in these same locations. An additional cell population which tended to predominate in the lateral zone was the stalked cell. These displayed a rounded soma (12-20 microns) and were evident only in the transverse or sagittal plane. Two to four primary dendrites arose from the soma and extensively ramified into a dense spiny arbor directed into the body of the subnucleus interpolaris. Many examples contained enkephalin. Islet cells, characterized by a very small oval soma (6-12 microns) and dense, rostrocaudally oriented dendrites, were less common than stalked cells and were located deeper in the nucleus.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Golgi and immunocytochemical analysis of neurons in trigeminal subnucleus interpolaris: correlations with cellular localization of enkephalin. 247 85

Intrathecal administration of glycine (strychnine) or GABA (bicuculline) but not opioid (naloxone), adrenergic (phentolamine) or serotonin (methysergide) receptor antagonists resulted in a dose-dependent organized agitation response to light tactile stimulation. This effect was maximally evoked by oscillating but not continuous stimulation applied to a dermatome corresponding to the levels of spinal cord acted upon by the intrathecal antagonist. Similar results were observed in chloralose-urethane anesthetized rats in which tactile stimulation evoked hypertensive responses following local tactile stimuli. The effects were only mildly depressed by even high doses of spinal morphine or DADL and not at all by ST-91 or baclofen. In contrast, intrathecal injections of glutamate receptor antagonists resulted in a dose-dependent depression of the strychnine evoked hyperesthesia with the ordering of activity being MK-801, AP-5, kynurenic acid, SKF10047 and ketamine. At doses below those which produced motor dysfunction, however, these agents had no effects on the hot-plate response latency. These data emphasize that low threshold afferent input is likely subject to an ongoing modulation, the loss of which results in a miscoding of the afferent stimulus yielding a pain relevant message. The lack of effect of agents having a powerful effect on somatic pain stimuli and the converse effects of glutamate receptor antagonists on the strychnine hyperesthesia at doses which do not affect the somatic pain response indicate discriminable processing systems, the characteristics of which resemble the clinical phenomenon observed in patients suffering from sensory dysesthesia following central and peripheral horn injury.
Pain 1989 Apr
PMID:Behavioral and autonomic correlates of the tactile evoked allodynia produced by spinal glycine inhibition: effects of modulatory receptor systems and excitatory amino acid antagonists. 254 67

The spinal mechanism of the phantom pain origin is proved. The underlying factors are: segmentary spinal denervation hypersensitivity and attenuation of the descending inhibitory influence. The pathogenetic treatment of phantom pains is proposed by means of an associated treatment by GABA-ergic drug--Baclofen and alpha-2--adrenomimetic--Clofelin. Good effects of the proposed scheme of treatment confirm the correctness of the presented ideas of pathogenesis of phantom pains.
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PMID:[Pathogenesis of phantom limb syndrome and its treatment]. 260 7

The emotional-pain stress (EPS) in C57BL mice with Lewis carcinoma was studied for its influence on serotoninergic, noradrenergic, dopaminergic, glutamatergic, aspartatergic, glycinergic, taurinergic, GABA-ergic and cholinergic mediator mechanisms of the hypothalamus, the level of corticotropin, free and bound 11-corticosteroids, insulin, thyroxin and testosterone in blood plasma as well as on the content of catecholamines, their precursors and catabolites in urine. EPS contributed to a long-term activation of stress-realizing systems resulting in generalization of decompensation in them. The stimulating effect of EPS on the incidence and growth of metastases is established depending on the terms of its application.
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PMID:[The effect of emotional-pain stress syndrome on the biochemical characteristics of the stress-realizing system and metastasis of Lewis lung carcinoma in mice]. 279 54


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