Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0026827 (hypotonia)
 5,860 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Apomorphine and the putative dopamine agonist, 2-(N, N-dipropyl)-amino-5, 6-dihydroxytetralin induced dose-dependent climbing behaviour in the mouse which was measured in wire mesh lined cages as the percentage of time spent climbing in the 30 min period following the first climb and as the maximum time spent in a single climb throughout the drug effect. These These two measures were generally found to parallel excepting when the interacting agent caused muscular hypotonia. All potential interacting agents were given as pretreatments to determine changes in motor function which may interfere with the climbing induced by 1.0 mg/kg s.c. apomorphine. The possibility of a change in the apomorphine response to a sterotyped biting, which would also interfere with climbing, was also considered. Excluding these non-specific changes, climbing behaviour was shown to be antagonised, dose-dependently, by low doses of typical and atypical neuroleptic agents (haloperidol, fluphenazine, loxapine, pimozide, oxiperomide, clozapin, thioridazine, sulpiride, tiapride and metoclopramide) but not specifically by other psychoactive agents. Climbing behaviour was modified by serotonergic agents; the agonist quipazine reduced or abolished, whilst the antagonists, methysergide and cyproheptadine, enhanced the response. Picrotoxin specifically reduced climbing behaviour but sodium valproate exerted non-specific effects, precluding conclusions as to a GABA involvement. Cholinergic and noradrenergic involvements with climbing were also apparently eliminated by the ineffectiveness of atropine, aceperone, piperoxan and propranolol. The involvement of serotonin with climbing was extended to the actions of the neuroleptics: the antagonistic effects of typical neuroleptics (haloperidol, fluphenazine, loxapine) were markedly enhanced by combination with methysergide or cyproheptadine whilst the effects of clozapine, sulpiride and thioridazine were significantly reduced. The actions of metoclopramide, oxiperomide, pimozide and tiapride were not generally modified by such combinations. These differences are discussed in terms of differential abilities to induce extrapyramidal disturbances and the mouse climbing model is forwarded as a test with potential to detect antipsychotic agents of different activity spectra.
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PMID:Climbing behaviour induced by apomorphine in mice: a potential model for the detection of neuroleptic activity. 2 33

Five patients suffering from choreo-athetotic syndromes of different genesis were treated with the benzodiazepine-derivative Ro 06-9098/000 (7-Nitro-1(methylmethoxy)-1,3-dihydro-5-phenyl-2 H-1,4-benzodiazepin-2-one). The existing hyperkinesias could be well influenced in four cases of male patients, sufficiently in one case of a female patient. The sedative effect, accompanied by a muscle hypotonia appearing simultaneously under the medication, did not represent and essential limiting factors at the chosen dose of 5--20 mg/die. The observed successes in therapy point at the result and effect of benzodiazepine derivatives on extra-pyramidalmotoric hyperkinesias which got little attention until now.
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PMID:[Influence of the Benzodiazepine-derivative Ro 06-9098/000 on choreo-athetotic syndromes (author's transl)]. 3 Jan 3

Two infants with lethargy, vomiting, convulsions, coma and marked metabolic acidosis were found to have very high concentrations of methylmalonic acid in their serum and urine. In vitro studies of fibroblasts demonstrated that the infants had different variants of methylmalonic acidemia.Vitamin B(12) was given in two different forms at 1 month of age and at 12 months of age. Each trial continued for 4 months but neither infant showed a clinical or biochemical response.In both infants hyperglycinemia, neutropenia and thrombocytopenia developed during acute metabolic crises only. Hypoglycemia was found in patient 2. Hyperammonemia was severe in patient 2 during acute crises but never appeared in patient 1. When clinically well, both infants continued to excrete abnormal amounts of methylmalonic acid in the urine and both had persistent compensated metabolic acidosis.Marked hyperuricemia developed in patient 1 at 18 months of age and led to progressive renal failure. Allopurinol therapy was necessary to keep the uric acid concentration within the normal range. Renal function returned to normal, as indicated by a marked increase in the renal clearance of creatinine and uric acid.Patient 1 is physically and mentally retarded, and has moderate hypotonia, hepatomegaly and persistent vomiting. Patient 2 has developed normally.The urine concentrations of methylmalonic acid in the four parents were normal.
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PMID:Methylmalonic acidemia: 6 years' clinical experience with two variants unresponsive to vitamin B12 therapy. 3 17

Org 6368 is a homologue of pancuronium bromide. Its interactions with other agents in the cat sciatic nerve-gastrocnemius muscle preparation revealed that paralysis was of the non-depolarizing type. This was confirmed in experiments using avian muscle. Org 6368 is a potent muscle relaxant being 2-4 times as potent as (+)-tubocurarine in the cat. Paralysis in the cat is rapid in onset and of appreciably shorter duration than that of pancuronium and (+)-tubocurarine. Repeated injections of the same dose of Org 6368 show no cumulative effect. Muscle relaxant doses generally cause a slight increase in both blood pressure and heart rate. Although its histamine-releasing capacity is greater than that of pancuronium it is less than that of (+)-tubocurarine. Org 6368 shares with pancuronium a very weak effect on both the muscarinic receptor and ganglionic transmission. Differences in the muscle relaxant profiles of Org 6368 and pancuronium are discussed.
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PMID:On the pharmacology of Org 6338 (2beta, 16beta-dipiperidino - 5alpha - androstan - 3alpha - ol acetate dimethobromide), a new steroidal neuromuscular blocking agent. 5 4

A newborn, whose mother had been treated with lithium carbonate for a manic-depressive illness suffered from hypotonia, poor feeding, weak Moro reflex, hyperexcitability, thyroid enlargement and cyanosis. Symptoms resolved within a few weeks. No malformations could be detected. The psychomotor development of the child was normal up to the age of 18 months.
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PMID:[Lithium-intoxication in a newborn (author's transl)]. 7 34

A female child with brachycephaly, hypertelorism, convergent strabismus, interstitial keratitis, analgesia on both sides of the face, absent corneal reflexes, and focal congenital alopecia of a zone of the occipital and posterior parietal scalp is presented. The patient also had generalized hypotonia in early life, and at age 4 years 9 months, she was found to be moderately mentally subnormal and to have severe cerebellar deficit consisting of gait and truncal ataxia. There was no clinical evidence of other cranial nerves being affected. It is postulated that the patient has a cerebellotrigeminal and focal dermal dysplasia due to a development arrest of the ectoderm, which gives rise to the alar plate of the rhombencephalon, the overlying epidermis, the motor nucleus of V, and the trigeminal placodes.
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PMID:Cerebellotrigeminal and focal dermal dysplasia: a newly recognized neurocutaneous syndrome. 9 27

Clobazam, an anxiolytic 1,5-benzodiazepine, has been evaluated as an anticonvulsant in 2 animal models. In mice showing sound induced seizures, clobazam, 1--4 mg/kg, i.p., blocked seizure responses for 1--2 hr. In Senegalese baboons Papio papio showing photically induced myoclonus or seizures, clobazam, 2--12 mg/kg, i.v., totally prevented such responses for up to 6 hr. In baboons pretreated with allylglycine, 170--185 mg/kg, a similar but briefer protection was induced by clobazam. Neurological toxicity was not prominent (transient, slight nystagmus after clobazam, 2--6 mg/kg; muscular hypotonia after clobazam, 12 mg/kg). The possibility that 1,5-benzodiazepines are superior to 1,4-benzodiazepines in the therapy of epilepsy requires clinical investigation.
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PMID:Anticonvulsant action of a 1,5-benzodiazepine, clobazam, in reflex epilepsy. 9 17

Ciliochoroidal detachments were produced in rhesus monkeys by injecting glutathione bicarbonate Ringer's solution, autologous serum, or silicone oil into the anterior suprachoroidal space. Silicone oil detachments, like sham operations, caused a transient 2 mm Hg reduction in intraocular pressure. Detachments with glutathione bicarbonate Ringer's solution or serum caused a 6 mm Hg reduction in intraocular pressure, which normalized in three weeks. Aqueous humor flow in serum-detached eyes was normal, indicating that the hypotonia does not result from reduced aqueous humor formation. Blood was present in Schlemm's canal in most eyes with hypotonia, which suggests that hypotonia is not the result of enhanced conventional aqueous humor outflow. Therefore, it is postulated that hypotonia might result from enhanced aqueous humor outflow from the anterior chamber into the suprachoroidal space and out of the eye through the emissarial channels of the sclera (uveoscleral outflow).
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PMID:Experimental ciliochoroidal detachment. Effect on intraocular pressure and aqueous humor flow. 10 96

The Northwest Regional Screening Program to detect congenital hypothyroidism in infants born in Oregon, Montana, Alaska, and Idaho (combined birthrate of 69,000/ yr) was added to our ongoing screening program in 1975. The program utilizes dried blood filter paper specimens collected routinely in the first few days of life in all four states and again at about 6 weeks of age in Oregon only. The screening test consist of an initial thyroxine (T4) measurement; a thyroid-stimulating hormore (TSH) determination is performed on those specimens with T4 concentrations in the lowest 3% group. Serum samples obtained by venipuncture are requested for confirmation of the diagnosis. In the first two years of the program, 25 infants with primary hypothyroidism were detected amont 110,667 infants screened, a frequency of 1:4,430. Fourteen cases of thyroxine-binding globulin deficiency were also detected, a frequency of 1:7,900. Using the T4 followed by TSH testing approach, the frequency of request for repeat specimens was 0.4% in Oregon and 0.05% in the other states. The cost per specimen was $1.96. The majority of infants lacked clinical signs or symptoms of hypothyroidism; only one infant was clinically suspected of having hypothyroidism prior to detection. The most common neonatal symptoms were constipation, lethargy, and prolonged jaundice, while the most common physical signs were hypotonia, umbilical hernia, and large fontanels. Thyroid scans showed the most common etiology to be thyroid aplasia, followed by an ectopic gland, hypoplasia, and goiter. Serum T4 concentrations were lowest in those infants with aplasia, intermediate in infants with an ectopic gland or hypoplasia, and normal in the infant with the goiter. Neonatal hypothyroidism varies in degree and has several different causes; the capacity to secrete thyroid hormone, the duration before hypothyroidism becomes clinically manifest, and possibly the eventual prognosis for intellectual function depend on the nature of the underlying cause. While the mean age at treatment was 59 days, the goal of diagnosing congenital hypothyroidism and treating affected infants by 1 month of age seems realistic.
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PMID:Neonatal hypothyroidism detected by the Northwest Regional Screening Program. 10 59

Two new 1,5 benzodiazepines have been evaluated acutely as anticonvulsants in baboons, Papio papio, with photosensitive epilepsy. BAU 426 (8-Chlor-6-[2-chlorphenyl]-4H-s-triazolo-[4,3-a] [1,5-benzodiazepin-5-[6-H]on) and BAU 500 (analogue of BAU 426 with [2-trifluor methylphenyl] substituted for [2-chlorphenyl]), 0.1--5.0 mg/kg, were administered i.v. to baboons with and without priming with D,L allylglycine. BAU 426 or BAU 500, 0.1--0.2 mg/kg, produced partial or transient protection against photically induced myoclonus or epileptic responses. Complete protection, in the absence of signs of sedation or acute neurological toxicity, was seen 1--4 h after 0.5--2 mg/kg. EEG changes typical of benzodiazepines were seen for 1--3 h and clinical signs of sedation with some muscular hypotonia were evident for 1 h after either drug, 5 mg/kg. Clinical trials are required to determine if these compounds are superior to 1,4 benzodiazepines as anticonvulsants.
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PMID:Anticonvulsant activity in photosensitive baboons, Papio papio, of two new 1,5 benzodiazepines. 10 5


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