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 11,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have investigated the effects of the local administration into the periaqueductal gray matter of thiorphan, a selective inhibitor of endopeptidase 24.11 "enkephalinase", kelatorphan, (R)-3-(N-hydroxy-carboxamido-2-benzylpropanoyl)- L-alanine, and RB 38 A, (R)-3-(N-hydroxy-carboxamido-2-benzylpropanoyl)-L-phenylalanine, two almost complete inhibitors of enkephalin metabolism, on the naloxone-precipitated morphine withdrawal syndrome in rats. Local administration of these inhibitors decreased the severity of the withdrawal syndrome. Jumping, chewing, diarrhea, piloerection, salivation and hypothermia were decreased by all drugs. Lacrimation and weight loss were reduced by kelatorphan and RB 38 A whereas teeth chattering, tremor, eye twitch and rhinorrhea were decreased only by RB 38 A. The rise in plasma corticosterone levels was only slightly reduced by the three inhibitors. Wet dog shakes and ptosis remained unchanged. These results indicate that during the morphine withdrawal syndrome in rats there is a tonic or/and naloxone evoked release of opioid peptides, presumably enkephalins, into the periaqueductal gray matter and that inhibition of their degradation strongly decreases the severity of the withdrawal syndrome.
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PMID:Attenuation of the morphine withdrawal syndrome by inhibition of catabolism of endogenous enkephalins in the periaqueductal gray matter. 162 Feb 46

Noradrenergic neuronal hyperactivity following chronic morphine administration has been postulated to cause withdrawal signs and symptoms. Suppression of this hyperactivity, for example, by clonidine attenuates withdrawal. It might follow, therefore, that the prevention of suppression of noradrenergic systems during chronic morphine administration might diminish hyperactivity and prevent withdrawal. If the normalization of noradrenergic activity during opioid administration did not also suppress analgesia, it might be of medical and theoretical interest. To test this hypothesis, we gave the alpha-2-antagonist yohimbine to rats in order to increase noradrenergic activity during morphine treatment and then subsequently precipitated morphine withdrawal with naloxone. Six groups were examined: saline controls (N = 11), morphine (N = 11), morphine + 2.0 mg/kg/day yohimbine (N = 15), morphine + 3.0 mg/kg/day yohimbine (N = 5), 2.0 mg/kg/day yohimbine (N = 11) and 3.0 mg/kg/day yohimbine (N = 5). Subjects received 75 mg morphine pellets implanted on day 1,4 and 6 of the treatment or sham implantation. Yohimbine was delivered throughout the morphine treatment by subcutaneously implanted osmotic pumps. On day 7, all subjects were given 1.0 mg/kg naloxone and rated for behavioral signs of withdrawal. Analgesia was measured by observing tail flick latencies (TFL) before and after chronic drug treatments. Naloxone-precipitated withdrawal was characterized by irritability, ptosis, penile erection, diarrhea, rhinorrhea, abnormal posture, wet-dog shakes, jumping, and teeth chattering, none of which were observed in groups receiving only saline or yohimbine. Withdrawal behavior was attenuated in a dose-dependent manner when yohimbine was administered during morphine treatment but analgesia was not attenuated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Yohimbine co-treatment during chronic morphine administration attenuates naloxone-precipitated withdrawal without diminishing tail-flick analgesia in rats. 205 41

We report the case of a woman with short nocturnal attacks of peri- and retro-orbital pain, diplopia, ptosis, rhinorrhea and lacrimation of five months evolution. Neurological examination was normal between attacks. The latter presented with partial third nerve palsy, which finally became complete and permanent. Brain CT showed a sellar and supraseller tumor with parasellar extension to the right side. We stress the atypical clinical presentation and evolution of this case, and discuss its pathophysiology.
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PMID:Pituitary adenoma presenting as painful intermittent third nerve palsy. 275 52

A subcutaneous injection of 6 mg sumatriptan rapidly and effectively stopped attacks of cluster headache. After a time lag of 4-14 minutes (mean 7 minutes) pain dramatically dropped to zero within seconds to single minutes (mean 56 seconds). This rapid effect may indicate that mere vasoconstriction is the mechanism behind the beneficial effect of sumatriptan in cluster pain. The findings support a scenario in cluster headache where an inflammation in the cavernous sinus affects the sympathetic fibers traversing the cavernous region. This leads to the miosis, ptosis and forehead anhidrosis but also to a dilated internal carotid arterial tree distal to the lesion. The dilatation, in combination with an obliterated drainage of the cavernous sinus by the inflammatory process, leads to progressive stasis in the sinus, to cause the painful attack. The attack terminates when the enhanced load on the sinus is reduced by constriction of vessels supplying the sinus, as is achieved by administration of sumatriptan. The present observation that other accompanying symptoms during attacks (nasal congestion, rhinorrhea, lacrimation and swelling of eyelids) disappeared in parallel with the pain points to the possibility that these symptoms may be directly related to venous stasis or activation of pain fibers, rather than resulting from a primary parasympathetic activation.
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PMID:Subcutaneous sumatriptan in cluster headache: a time study of the effect on pain and autonomic symptoms. 838

Two patients suffering from SUNCT syndrome are presented. Some features are remarkable. The first patient was a 69-year-old man whose first crisis was located in the right supraorbital region. After a 4-month spontaneous remission, the pain returned to the upper part of the cheek, radiating to the supraciliary region on the same side, with lacrimation and conjunctival injection. Rhinorrhea was absent. The painful attacks were triggered by head movements. Clinical improvement occurred with carbamazepine treatment. The second patient was a 48-year-old woman whose painful attacks lasted from 30 to 45 seconds followed by a burning sensation lasting 2 hours. Autonomic signs such as conjunctival injection, lacrimation, and edema and ipsilateral ptosis of the upper lid were rather marked. There was never any rhinorrhea. Her attacks were triggered by head and eye movements. She responded to the administration of corticosteroids and carbamazepine. According to these features, the two patients had SUNCT syndrome, and the positive carbamazepine response suggests a relationship with trigeminal neuralgia.
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PMID:SUNCT syndrome. Two cases in Argentina. 963 Jul 90

Postnatal day-14 (P14) infant rats remained naive or were implanted with osmotic minipumps infusing saline or fentanyl (50 microg kg(-1) h(-1)). Fentanyl was administered 72 h later for measurement of antinociception in the tail-flick test. The potency of fentanyl was 3.0-fold lower in fentanyl-infused compared to saline-infused P17 rats. Fentanyl-infused P17 rats injected with naloxone underwent withdrawal characterized by increases in spontaneous activity, wall climbing, diarrhea, abdominal stretching, forepaw treading/tremors, wet-dog shakes, jumping, ptosis, rhinorrhea and hypothermia. Other naive, saline-infused and fentanyl-infused P17 rats not challenged with fentanyl or naloxone were housed until maturing into P42 juveniles. Fentanyl's potency was equal among each treatment group. However, morphine's potency was reduced in juveniles tolerant to fentanyl as infants. Morphine was also less potent in P90 adults tolerant to fentanyl as infants. Thus, chronic opiate exposure during infancy may affect the developing central nervous system, and desensitize animals and humans to opiate analgesia throughout life.
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PMID:Long-term alterations in opiate antinociception resulting from infant fentanyl tolerance and dependence. 988 76

We present a review of 60 cases of cluster headache. Most patients were males, ranging from 19 to 65 years of age at the time of the first visit. Headaches consisted of short-lasting (from 15 to 210 minutes), intense, unilateral pain attacks, most frequently in the periorbital area, with ipsilateral autonomic signs (rhinorrhea, ptosis, tearing and conjunctival injection). Between attacks, patients were completely free of pain. The attacks occurred in bouts lasting 1 to 6 months, in which patients had daily headaches (one to three times a day). Headaches responded well to oxygen or ergotamine. Prophylactic therapy in most cases consisted of verapamil, also with a good response. We present this review in order to draw attention to this relatively rare form of headache with a specific therapy.
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PMID:[Cluster headache]. 1102 46

The syndrome of short-lasting unilateral, neuralgiform attacks of pain in the peri orbital area associated with conjunctival injection and tearing (SUNCT) is a rare disorder affecting mainly males. We report two French patients (1 male and 1 female) with SUNCT syndrome, 27 and 28 years of age respectively. Both patients had short (30 sec), frequent (30-100/day) excruciating pain located at the peri orbital area, associated with conjunctival injection, tearing, rhinorrhea, ptosis and others vasomotor symptoms. Clinical examination and imaging were normal. Most drugs used in the treatment of migraine, cluster headache, trigeminal neuralgia, and other short-lasting headaches were not successful.
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PMID:[Idiopathic SUNCT (short lasting unilateral neuralgiform headache attacks with conjunctival injection, tearing, sweating and rhinorrhea) syndrome: 2 new cases]. 1192 48

A total of 26 episodes of V-1 trigeminal neuralgia attacks have been recorded in two female patients. Autonomic phenomena were assessed according to a semiquantitative scale. Attacks lasted 17 +/- 5 s. Mild lacrimation without conjunctival hyperaemia, rhinorrhea or ptosis was observed, even in relatively long lasting episodes. This is in clear contradiction with SUNCT (shortlasting, unilateral, neuralgiform headache with conjunctival injection, tearing and rhinorrhea) attacks that are always dramatically accompanied by both lacrimation and conjunctival injection of the symptomatic side from the very onset of symptoms. Carbamazepine provided complete and sustained relief of symptoms in both patients. Herein we will show differential autonomic features of V-1 trigeminal neuralgia vs. SUNCT that will both aid the clinician to distinguish both syndromes and stress that both entities are nosologicaly different.
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PMID:Objective assessment of autonomic signs during triggered first division trigeminal neuralgia. 1210 85

This is the first case report of a chinese patient with SUNCT (shortlasting, unilateral, neuralgiform headache attacks with conjunctival injection and tearing) presenting with persistent Horner's syndrome. She had episodic, brief, right periorbital pain in association with ipsilateral eye injection, lacrimation and rhinorrhea as well as persistent ipsilateral miosis and ptosis. She had partial response to a combination of indomethacin and carbamazepine therapy.
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PMID:SUNCT syndrome in association with persistent Horner syndrome in a Chinese patient. 1501 64


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