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

A case of hemihypertrophy associated with multiple anomalies of the skin, bone and visceral organs is presented. A 31-year-old female was admitted for evaluation of her skin conditions. Her family history is noncontributory, while her past history discloses operations for syndactyly of the right foot, tonsillar hypertrophy, anal prolapse and ovarial cyst. Erythemas of the face and the left upper extremity were noticed during the neonatal period and hypertrophy of the right side of the body started at age 2 months. On admission, hemihypertrophy was observed in the face, trunk and extremities. Multiple faint nevi flammei were seen on the right half of the face and on the left side of the trunk and extremities. Telangiectasis and nevus anemicus were seen in the upper chest. The left upper extremity showed diffuse brown patches that was histologically basal pigmentation with some giant melanosomes. Visceral anomalies consisted of fibromatous tumors of the tip of the tongue and mitral prolapse. Angiography and computed tomography revealed a possible arteriovenous malformation of the right occipital region, small hemangiomas around the patella, dilation of the lateral ventricle, and calcification of the choroid plexus. Tortuous superficial veins were noted in the right leg. She had no seizure, but her IQ was 68. The bone disorders consisted of scoliosis, short forth metacarpus, hypoplastic mandible and peroneal exostosis. Examination revealed a slight diminution of urinary corticosteroid, but no other endocrinological disorders were found. The hemihypertrophy in this case is at least partially due to an arteriovenous shunt, suggested by elevated oxygen saturation of the blood obtained from the internal saphenous vein.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Congenital hemihypertrophy associated with cutaneous pigmento-vascular, cerebral, visceral and bone abnormalities]. 282 Feb 92

A series of 3-phenyl-2-piperazinyl-5H-1-benzazepines and related compounds were synthesized and evaluated for potential neuroleptic activity. The preparation of these compounds was carried out by 2,3-dichlorination of 3-phenyl-2,3,4,5-tetrahydro-1H-1-benzazepin-2-ones with phosphorus pentachloride followed by amination and concurrent dehydrochlorination. Compounds having the 4-chloro or 4-fluoro substituent in the 3-phenyl group were found to possess the neuroleptic-like activity. Among them, 2-(4-methyl-1-piperazinyl)-3-(4-fluorophenyl)-5H-1-benzazepine dihydrochloride (23) was comparable to chlorpromazine in inhibiting exploratory activity, conditioned avoidance response, and self-stimulation response and more potent than chlorpromazine in antagonizing apomorphine-induced emesis. These neuroleptic effects may be based on an antidopaminergic property of the compound. In causing catalepsy or ptosis, however, 23 was weaker than chlorpromazine. Therefore, this ring system is of interest as a novel class of neuroleptics. Some compounds having the 7-chloro or 7-bromo substituent showed potent anticonvulsant effects against maximal seizures induced by electroshock or pentylenetetrazole.
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PMID:A novel class of potential central nervous system agents. 3-Phenyl-2-(1-piperazinyl)-5H-1-benzazepines. 289 53

The pharmacological actions of N-(2,6-dimethylphenyl)-8-pyrrolizidineacetamide hydrochloride hemihydrate (SUN 1165), a new antiarrhythmic agent, on the central nervous system were studied in various experimental animals as compared with those of disopyramide, mexiletine and lidocaine, and the following results were obtained. 1. Acute toxicity of SUN 1165 in mice was similar to that of mexiletine, and twice as potent as compared with that of disopyramide and lidocaine. Main acute toxic symptoms of SUN 1165 were muscle relaxation, ataxia, clonic convulsions, tremor and a decrease in spontaneous activity in mice, rats and rabbits. In addition to these symptoms, vomiting in dogs was observed. These toxic symptoms were similar to those of lidocaine. In the case of disopyramide, ataxia, tremor and a decrease in spontaneous activity were observed in mice and rats. On the other hand, mexiletine caused central nervous excitatory symptoms, that is, tremor, Straub tail, clonic convulsions, jumping, running and opisthotonus in mice and rats, and vomiting in dogs. 2. SUN 1165 even at large doses (50-100 mg/kg p.o.) exerted no significant effects on the following changes: hexobarbital-induced induced hypnosis, oxotremorine-induced tremor, apomorphine-induced hypothermia, reserpine-induced ptosis and hypothermia, 5-hydroxytryptophan syndrome and fighting behavior in mice, and conditioned avoidance response in rats. 3. An ineffective dose of SUN 1165 (12.5 mg/kg p.o.) on spontaneous locomotor activity was lower than of disopyramide and lidocaine, however, higher than that of mexiletine. 4. SUN 1165 at large doses showed antagonistic action on toxic extensor seizures induced by maximal electroshock, picrotoxin, or strychnine in mice, but anticonvulsive effects of SUN 1165 were less potent than those of mexiletine and lidocaine. SUN 1165 had no effect on clonic convulsions induced by pentetrazol and pictrotoxin in mice, while both mexiletine and lidocaine prolonged the duration of clonic convulsions. 5. The muscle relaxant effect of SUN 1165 (50%-toxic dose, TD50 = 30 mg/kg p.o.) was more marked than that of lidocaine (TD50 = 92 mg/kg p.o.) on traction test in mice. However, effect of SUN 1165 (TD50 = 62 mg/kg p.o.) on motor incoordination was similar to that of disopyramide, mexiletine and lidocaine on the rotarod test in mice. 6. The analgesic effect of SUN 1165 was as weak as that of disopyramide, mexiletine and lidocaine on chemically and mechanically-induced pain response in mice.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:General pharmacological studies on N-(2,6-dimethylphenyl)-8-pyrrolizidineacetamide hydrochloride hemihydrate. 1st communication: effect on the central nervous system. 319 80

In two sisters aged 36 and 38 years symmetrical calcifications were found in the vicinity of the pallidum in brain CT. In the younger sister epileptic seizures and transient focal signs were due to arrhythmias of the heart caused by mitral valve leaflet prolapse. In the second case no neurological signs were found. The calcifications were probably genetically determined suggesting an autosomal recessive inheritance. The described cases are another example of familial calcifications in basal ganglia without neurological changes.
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PMID:[Familial occurrence of calcinosis of the basal ganglia]. 324 17

Panic disorder with or without agoraphobia is dominated by the occurrence of panic attacks. However, panic attacks are also reported to occur as part of the clinical picture in several medical conditions, notably thyroid disease, hypoglycemia, and pheochromocytoma. The authors examine these conditions, review the relevant literature, and offer an evaluation strategy. Routine screening is not recommended. Panic disorder is also associated with mitral-valve prolapse and temporal lobe seizures. The authors explore the possible consequences of this association and outline an evaluation strategy. Again, routine screening is not recommended.
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PMID:Medical evaluation of panic attacks. 330 23

1. Benzyleugenol (BE), a phenylpropene derivative, protects rats and mice against maximal electroshock seizures and has a protective index superior to that of phenobarbital. The present paper describes experiments carried out to further characterize the pharmacological and toxicological profile of this compound. 2. BE, at a dose range of 100-400 mg/kg ip, was inactive when tested for the following effects: analgesia, as measured by the hot plate and acetic acid writhing methods; neuroleptic-like effects, when tested by the catalepsy and palpebral ptosis, conditioned avoidance response and apomorphine-induced stereotypies methods; and anxiolytic effects, measured by the shock-elicited aggressiveness of mice. In contrast, tolerance to the anticonvulsant effect of BE, at dose range of 240-800 mg/kg orally, developed in mice and rats after 10 to 40 days of continued treatment. 3. BE, at dose range of 104-800 mg/kg orally, proved to be remarkably safe when chronically administered to laboratory animals. Thus, 3 to 6 month administration of large BE doses to rats and mice did not affect body weight, behavioral measures, serum and blood tests, or hematological parameters. Anatomopathological examinations of viscera of BE-treated animals did not reveal alterations which could be attributed to drug treatment. 4. Daily treatment up to 3 months of male rats and mice with BE, at a dose range of 80-800 mg/kg orally, did not affect the reproductive capacity of the animals. Pregnant females treated with BE during different periods of gestation gave birth to litters similar to those of control females; when adult, BE and control litters performed equally well in a passive avoidance task. 5. These results were compared with those of known anti-epileptic drugs, such as phenytoin, phenobarbital and valproic acid, and it is suggested that BE deserves further research as a potential candidate for the treatment of epilepsy.
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PMID:Pharmacological and toxicological profile of benzyleugenol, a phenylpropene derivative possessing anticonvulsant properties. 333 Jun 76

Using a scoring system designed to assess the severity of neurologic deficit in gerbils during and after temporary unilateral carotid occlusion, the effects of large doses of methylprednisolone sodium succinate (MPSS: Solu-Medrol sterile powder) on experimental stroke have been examined. By scoring gerbils hourly for torso curvature, circling, inability to walk, ptosis, barrel rolling, opisthotonus, generalized seizures, and loss of righting reflex, their level of neurologic deficit can be easily, quantitatively, and reproducibly evaluated. Approximately 37% of gerbils subjects to a 3-hour unilateral carotid occlusion attained average scores of 4.0-4.5 during the first hour. There was a slight, though not significant, worsening (increase) of scores over the 3-hour occlusion period that was not altered by pretreatment of gerbils with 60 mg/kg of MPSS 10 minutes before occlusion. Following removal of occlusion at 3 hours, gerbils recovered only minimally during the ensuing 4-hour period, with deficit scores remaining around 3.2 +/- 0.3. Pretreatment of gerbils with 60 mg/kg of MPSS, however, resulted in a striking improvement in their deficit scores to 1.6 +/- 0.2 (p less than 0.05) by 2 hours after occlusion removal. Treatment of gerbils with lower (30 mg/kg) or higher (100 mg/kg) doses of MPSS was not as effective in promoting improvement. The survival of 3-hour occluded gerbils was significantly enhanced by pretreatment with 60 mg/kg of MPSS. Vehicle-treated gerbils had survival rates of 41.7%, 16.7%, and 16.7% at 24 hours, 48 hours, and 7 days, respectively, compared with 90.9%, 72.7%, and 45.4%, respectively, for MPSS-treated gerbils.
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PMID:The effects of large doses of methylprednisolone on neurologic recovery and survival in the Mongolian gerbil following three hours of unilateral carotid occlusion. 376 81

Cyclopiazonic acid (CPA) was found to have many pharmacological properties in common with the antipsychotic drugs chlorpromazine and reserpine. Thus, in mice CPA at ip doses of 5-14 mg/kg body weight produced hypokinesia, hypothermia, catalepsy, ptosis, sedation without loss of righting reflex, tremor, gait disturbance, dyspnoea, opisthotonus, atypical convulsion and prolonged barbiturate-induced sleep. The ip LD50 of CPA was found to be 13 +/- 0.05 mg/kg. The tremors induced by near-lethal doses of CPA were associated with voluntary or forced movements (action tremors); they worsened during the days following treatment, but they were weak compared with the exhausting and continuous tremors of the whole body caused by 20 mg tremorine/kg (used for comparison). When death occurred only 24-259 min after administration of CPA (11-14 mg/kg), it was preceded by dypsnoea, cyanosis, opisthotonus and clonic leg movements and tonic extension of hind legs (convulsions). When death was delayed (2-6 days after CPA administration), it was preceded by prostration, ptosis, hypothermia, tremor and cessation of food and water intake resulting in cachexia; convulsions were not seen in this group of mice. CPA did not affect the rate of convulsion or death caused by either maximal electroshock or metrazol administration but it did delay the onset of metrazol-induced seizures. In rabbits, 10 mg CPA/kg body weight initially produced tachycardia, tachypnoea and sedation with an activated electroencephalogram. Of three rabbits given 10 mg CPA/kg one died, and in this rabbit slow delta waves were seen just before and during a brief period with clonic leg movements. In this animal death was accompanied by tonic extension of the hind legs, respiratory arrest and cardiac fibrillation; and epileptiform EEG was not seen at any time. The unexpected EEG activation with sedation in rabbits treated with CPA was similar to the effect of reserpine on EEG.
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PMID:Toxicity and neuropharmacology of cyclopiazonic acid. 404 83

A 1-month-old boy was admitted because of failure to thrive. He was floppy and had bilateral ptosis, diminished reflexes, and poor suck. He had aspiration pneumonia, developed seizures, and died at age 3 1/2 months. Laboratory data showed lactic acidosis, proteinuria, glycosuria and generalized aminoaciduria. He was an only child, and family history was negative. Muscle biopsy showed large clumps of granules positive with oxidative enzyme stains and increased lipid droplets. Ultrastructural studies showed large aggregates of mitochondria, many of which were greatly enlarged and contained disoriented or concentric whorls of cristae and paracrystalline inclusions. Cytochrome c oxidase was absent in fresh frozen sections by histochemical staining. By biochemical assay, cytochrome c oxidase (cytochrome aa3) was 6% of normal in muscle biopsy and undetectable in autopsy muscle; spectra and content of cytochromes showed lack of cytochrome aa3, decreased cytochrome b and normal cytochrome cc1. In kidney, cytochrome-c-oxidase activity was 38% of normal and spectra showed decreased cytochromes aa3 and b. The association of fatal infantile mitochondrial myopathy, lactic acidosis and renal dysfunction was previously reported by Van Biervliet et al and appears to be a distinct nosologic entity, one of the few biochemically defined mitochondrial myopathies.
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PMID:Fatal infantile mitochondrial myopathy and renal dysfunction due to cytochrome-c-oxidase deficiency. 625 6

The anticonvulsant action of various aporphine derivatives that act on dopamine receptors has been investigated in two genetically determined animal models--DBA/2 mice with sound-induced seizures and baboons Papio papio with photically-induced seizures. Protection against the clonic and tonic phases of the seizures response in DBA/2 mice was seen for 15-60 min after (-)2,10,11-trihydroxy-N-n-propylnoraporphine (1.25 mg/kg) and (-)10,11-methyl-enedioxy-N-n-propylnoraporphine (0.625-1.25 mg/kg) and for 30-60 min after (-)2,10,11-trihydroxyaporphine (31.25 mg/kg). Short-lasting protection (up to 30 min) was seen following (-)2,10,11-trihydroxy-N-ethyl-noraporphine (1.25-6.25 mg/kg). Changes in audiogenic seizure susceptibility were accompanied by piloerection, ptosis and loss of spontaneous locomotor and exploratory behaviour. No protection was seen after (-)norapomorphine (0.05-18.75 mg/kg). All the compounds (including norapomorphine) significantly lowered rectal temperature, although the time course of this effect was often longer than that of protection against audiogenic seizures. In baboons, marked reductions in photomyoclonic responses were seen following (-)10,11-methylenedioxy-N-n-propylnoraporphine (0.25 mg/kg, lasting up to 2h); (-)2,10,11-trihydroxy-N-n-propylnoraporphine (0.5-2.5 mg/kg, lasting up to 7 h); (-)2,10,11-trihydroxyaporphine (5 mg/kg, duration of action 1-4 h) and (-)2,10,11-trihydroxy-N-ethylnoraporphine (6.25 mg/kg, lasting 2 h). Little change in responsiveness followed administration of (-)norapomorphine 1.25 or 6.25 mg/kg. Changes in photosensitivity were accompanied by yawning and pupil dilatation. (-)10,11-Methylenedioxy-N-n-propylnoraporphine (0.5-6.25 mg/kg) was also administered orally in baboons.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparative assessment of dopamine agonist aporphines as anticonvulsants in two models of reflex epilepsy. 641 43


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