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  • 1
    Electronic Resource
    Electronic Resource
    USA/Oxford, UK : Blackwell Science Ltd
    Cephalalgia 14 (1994), S. 0 
    ISSN: 1468-2982
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: A patient with typical trigeminal neuralgia involving the first branch of the nerve developed short-lasting unilateral attacks in the same area which were associated with severe vasomotor phenomena consistent with the recently described SUNCT syndrome. This evolution suggests that SUNCT might correspond, at least in this case, to a “transformed” trigeminal neuralgia and emphasizes the close relationship between these unilateral facial pain syndromes.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background and Aim: Gastric hypersensitivity to mechanical distension has been observed in functional dyspepsia, but no drug is available that specifically acts on gastric afferent pathways to decrease gastric nociception. The aim of this study was to assess the effect of fedotozine, a synthetic ligand for peripheral kappa receptors, on human gastric sensitivity. Methods: Twenty-seven healthy volunteers were randomized to receive either fedotozine (30 mg t.d.s.) or a placebo, for 7 days. On day 7, the effects of fedotozine were tested on discomfort threshold and gastric compliance during graded isobaric and isovolumic distensions. In 16 of these subjects, the effect of this drug was tested on somatic sensitivity. In 10 other healthy volunteers the effect of fedotozine on gastric distension-induced inhibition of the RIII reflex, a process closely related to visceral sensitivity, was also studied. Results: During isobaric distensions, the discomfort threshold was significantly higher in subjects on fedotozine than in those on placebo (14.4±0.92 vs. 12.0±1.13 mmHg; P=0.04). Compared to placebo, fedotozine did not modify gastric compliance and somatic sensitivity. Fedotozine also reduced the inhibition of the RIII reflex induced by gastric distension. Conclusion: Fedotozine decreases gastric sensitivity to distension by exerting specific action on gastric afferent pathways.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Alimentary pharmacology & therapeutics 17 (2003), S. 0 
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background : Tegaserod reduces the symptoms associated with irritable bowel syndrome, and anti-nociceptive effects have been demonstrated in animals. Its effect on the rectal sensitivity in humans has not been delineated clearly.Aim : To evaluate the action of tegaserod on rectal sensitivity in response to distension by means of a reflexological technique based on electrophysiological recordings of the RIII nociceptive reflex.Methods : A randomized, double-blind, placebo-controlled study, performed in 20 healthy women, quantified the effects of slow or rapid rectal distensions on the RIII reflex at baseline and on day 8 following treatment with either placebo or tegaserod (6 mg b.d.).Results : At baseline, slow distensions performed up to the pain threshold induced gradual inhibitions of the RIII reflex. On day 8, these inhibitory effects were significantly reduced in the tegaserod group, but not in the placebo group (P = 0.0001). The effects of rapid distensions were not significantly modified by tegaserod or placebo. The intensity of subjective pain perception and rectal compliance were not altered by either treatment.Conclusion : These results suggest that tegaserod reduces the sensitivity to rectal distension in healthy subjects and interacts with the processing of sensory visceral information.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Experimental brain research 80 (1990), S. 54-62 
    ISSN: 1432-1106
    Keywords: Anterior thalamic nuclei ; Sleep-waking cycle ; Theta ; Cats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In contrast with most dorsal thalamic nuclei, the anterior thalamic (AT) complex is devoid of input from the reticular (RE) thalamic nucleus. Instead, it is interposed in a limbic circuit linking the mammillary bodies (MB) to various allo- and periallocortical fields. To investigate the electrophysiological consequences of this peculiar pattern of connectivity, a sample of 92 AT cells, physiologically identified by their short-latency response to MB stimulation, was recorded in chronically-implanted animals and compared to a group of rostral intralaminar centralis-paracentralis (CL-PC) thalamic neurons receiving a dense innervation from the RE nucleus. Numerous similarities were found between the state-related fluctuations in spontaneous and evoked activities of AT and CL-PC neurons. For instance, both types of cells displayed stereotyped, high-frequency (250–300 Hz) bursts of 2–4 spikes in S and a more tonic discharge pattern in W and D. However, the high-frequency bursts of the S state occurred randomly in AT cells, whereas in CL-PC neurons they appeared rhythmically in clusters closely related to spindle waves. In addition, we found that a period of decreased responsiveness consistently followed the ortho- or antidromic activation of AT an CL-PC cells. This inhibitory period lasted less than 80 ms in AT cells and contrasted with the much longer (⩽120ms) period of decreased excitability observed in CL-PC neurons during S. We suggest that these differences reflect the lack of RE input to the AT group. Since the AT complex is, through the MB, intimately linked to the hippocampal formation, it was expected that such prominent hippocampal activities as the theta rhythm would be channeled to the AT nuclei. Surprisingly, no theta-related modulation of neuronal activity was observed in identified AT cells during D epochs. This finding suggests that dramatic transformations are made on the signals emitted by the hippocampal formation somewhere along the pathway linking the hippocampal formation to the AT complex.
    Type of Medium: Electronic Resource
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