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

Serotonin (5HT) binds in a saturable and specific manner to high affinity binding sites present on the surfaces of human lymphocytes and monocytes. We reported that migraine patients have an increase in 5HT binding parallel to the progression of the attack, with the appearance of a subsequent phenomenon of cellular deactivation. The same experiment previously carried out in cluster headache patients revealed a lack of high affinity binding sites, independently of the pain period. Low levels of plasma 5HT were recently described by Anthony in chronic tension-type headache. The implication of 5HT in tension headache was also hypothesized by Shukla with the demonstration of an increased 5HT uptake by platelets. We studied the 5HT binding on surfaces of lymphocytes and monocytes in 26 tension-type headache patients (16 affected by chronic form (CTH) of the disease and 10 by episodic form (ETH]. Fourteen clinically healthy subjects were used as controls. Circulating lymphocytes and monocytes were tested for their ability to specifically bind 5HT, using (3H) labeled 5HT. The "in vitro" 5HT binding curves to lymphocytes and monocytes of tension-type headache patients show a constant trend; during headaches, both CTH and ETH patients present a desensitization phenomenon with a complete loss of high affinity binding sites for 5HT. The 5HT binding curve observed in controls is indistinguishable from that of ETH patients studied outside the attack period. The total amount of 5HT bound appeared to be more markedly raised in CTH patients than in ETH patients when compared to control values.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Impairment of 5HT binding to lymphocytes and monocytes from tension-type headache patients. 233 75

Inhibition of the second exteroceptive suppression of temporalis muscle activity (ES2) produced by a preceding electrical stimulus applied at the index was studied in patients suffering from migraine without aura (MO), chronic (CTH) or episodic (ETH) tension-type headache. Each patient group comprised of 12 subjects was compared to a group of healthy controls. Mean duration of unconditioned ES2, measured on 10 averaged rectified responses after labial stimulation at a 0.1 Hz frequency, was reduced in CTH only. From stimulation intensities of 20 mA onward, peripheral-induced inhibition of temporalis ES2 was significantly more pronounced in both subtypes of tension-type headache compared to migraineurs or controls. After an index finger stimulus of 20 mA, temporalis ES2 was abolished in 83% of CTH, 67% of ETH, 25% of MO patients and 8% of controls, whereas unconditioned ES2 was present in all patients. Among 9 ETH patients with normal (> or = 32 msec) unconditioned ES2, 5 had total disappearance of ES2 after a 20 mA index stimulation. These results demonstrate that peripheral conditioning at 20 mA increases the diagnostic sensitivity of ES2 studies. They suggest that the changes observed in tension-type headache are due to hyperexcitability of the reticular nuclei which inhibit the medullary inhibitory interneurons mediating ES2.
Pain 1994 Dec
PMID:Reduction of temporalis exteroceptive suppression by peripheral electrical stimulation in migraine and tension-type headaches. 770 6

Clinical trials have been conducted of a new therapeutic semiconductor laser from the Mustang series which generates laser radiation in red light range (0.63-0.65 mcm) in impulse mode. Laser therapy was given to 75 patients with different ENT diseases with good effect. A surgical laser unit CTH-10 (YAG-Ho laser, 2.09 mcm) has undergone pilot tests with good results in 12 patients with pain maxillofacial syndromes. Photodynamic therapy was used in upper respiratory tract cancer in 27 patients, the results are analysed.
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PMID:[Updated laser technologies in otorhinolaryngology]. 1169 90

The mechanisms by which stress contributes to CTH are not clearly understood. The commonly accepted notion of muscle hyper-reactivity to stress in CTH sufferers is not supported in the research data. We propose a neural model whereby stress acts supra-spinally to aggravate already increased pain sensitivity in CTH sufferers. Indirect support for the model comes from emerging research elucidating complex supra-spinal networks through which psychological stress may contribute to and even cause pain. Similarly, emerging research demonstrates supra-spinal pain processing abnormalities in CTH sufferers. While research with CTH sufferers offering direct support for the model is lacking at present, initial work by our group is consistent with the models predictions, particularly, that stress aggravates already increased pain sensitivity in CTH sufferers.
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PMID:A neural hypothesis for stress-induced headache. 1954 31

Stress is the most commonly reported trigger of an episode of chronic tension-type headache (CTTH); however, the causal significance has not been experimentally demonstrated to date. Stress may trigger CTTH through hyperalgesic effects on already sensitized pain pathways in CTTH sufferers. This hypothesis could be partially tested by examining pain sensitivity in an experimental model of stress-induced headache in CTTH sufferers. Such examinations have not been reported to date. We measured pericranial muscle tenderness and pain thresholds at the finger, head and shoulder in 23 CTTH sufferers (CTH-S) and 25 healthy control subjects (CNT) exposed to an hour-long stressful mental task, and in 23 CTTH sufferers exposed to an hour-long neutral condition (CTH-N). Headache developed in 91% of CTH-S, 4% of CNT, and 17% of CTH-N subjects. Headache sufferers had increased muscle tenderness and reduced pain thresholds compared with healthy controls. During the task, muscle tenderness increased and pain thresholds decreased in the CTH-S group compared with CTH-N and CNT groups. Pre-task muscle tenderness and reduction in pain threshold during task were predictive of the development and intensity of headache following task. The main findings are that stress induced a headache in CTTH sufferers, and this was associated with pre-task muscle tenderness and stress-induced reduction in pain thresholds. The results support the hypothesis that stress triggers CTTH through hyperalgesic effects on already increased pain sensitivity in CTTH sufferers, reducing the threshold to noxious input from pericranial structures.
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PMID:Central mechanisms of stress-induced headache. 1961 6