Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028738 (nystagmus)
 7,431 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Despite the widespread use of non-steroidal anti-inflammatory drugs (NSAIDs), the current number of reported cases of poisoning is small. However, with the introduction of 'over-the-counter' preparations of NSAIDs in some countries (e.g. ibuprofen in the UK and USA) an increased incidence of acute poisoning from this group of drugs can be expected. Conventionally, NSAIDs are divided into the following groups based on their chemical structure: arylpropionic acids, indole and indene acetic acids, heteroarylacetic acids, fenamates, phenylacetic acids, pyrazolones and oxicams. Unless NSAIDs are ingested in substantial overdose, acute poisoning with these agents does not usually result in significant morbidity or mortality. In most cases the clinical features are mild and confined to the gastrointestinal and central nervous systems, though acute renal failure, hepatic dysfunction, respiratory depression, coma, convulsions, cardiovascular collapse and cardiac arrest may complicate severe poisoning. Arylpropionic acid derivatives were thought initially to have a low order of toxicity in overdose but, in addition to anticipated gastrointestinal symptoms, headache, tinnitus, hyperventilation, sinus tachycardia, hypoprothrombinaemia, haematuria, proteinuria and acute renal failure have been described. In addition, drowsiness, coma, nystagmus, diplopia, hypothermia, hypotension, respiratory depression and cardiac arrest have been reported in severe cases of poisoning. Oxyphenbutazone and phenylbutazone are considerably more toxic in overdose. Complications of severe poisoning include coma, convulsions, hepatic dysfunction, acute renal failure, sodium and water retention, haematuria, cardiovascular collapse, respiratory alkalosis, metabolic acidosis, hypoprothrombinaemia and thrombocytopenia. In contrast, indomethacin appears to be much less toxic. In addition to gastrointestinal symptoms, indomethacin taken in overdose induces headache, tinnitus, dizziness, lethargy, drowsiness, confusion, disorientation and restlessness. Only 1 case of acute sulindac poisoning has been reported in the literature. A 16-year-old boy was admitted with hypokalaemia (2.2 mmol/L), transient granulocytosis and 'scanty' haematemesis after ingesting 12 g sulindac. No case of acute tolmetin poisoning have been reported. The fenamates (flufenamic acid, meclofenamic acid, mefenamic acid, tolfenamic acid) are, with the exception of mefenamic acid, not as widely prescribed as other groups of NSAIDs. In overdose, mefenamic acid may result in nausea, vomiting, diarrhoea, muscle twitching, convulsions and coma.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acute poisoning due to non-steroidal anti-inflammatory drugs. Clinical features and management. 353 13

A multicenter survey of adverse drug reactions (ADR) to anticonvulsants was conducted in 15 university and hospital departments, including six epilepsy centers in Italy. Five hundred and nine patients undergoing chronic anticonvulsant therapy (greater than 3 months) were admitted to the study. Details of the main characteristics of the underlying disease, drug schedules, and ADR (including date of onset, type, involved tissue or organ, severity, duration, acceptability by the patient, clinical significance, referral pattern, and clinical implications) were provided. One or more ADR were recorded in 157 cases (31%), with a wide range of referrals among centers (6-79%). Of the 232 recorded ADR, 109 were definite, 84 were possible, and 26 were doubtful. In 54.5% of the cases ADR were reported by the patient, 52.5% were clinically important, 49.5% were permanent, and 67% were tolerable. In 53% of patients having ADR no decisions had been taken. Plasma levels of anticonvulsants were determined in 47% of cases and for 49% of the prescribed drugs. The proportion of cases with ADR was 22% in patients receiving monotherapy, 34.2% in patients treated with two drugs, and 44.4% in patients receiving three or more drugs. Thirty-three percent of patients taking phenytoin as the only drug had ADR as compared with 23, 15, and 12% of patients treated with phenobarbital, carbamazepine, and sodium valproate or depamide. Somnolence was the commonest complaint (51 cases), followed by gingival hyperplasia (34 cases), nystagmus (23 cases), and ataxia (16 cases). These findings provide a real-life profile of the ADR to anticonvulsants, with inclusion of the factors likely to influence the behavior of the practicing physicians.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adverse reactions to antiepileptic drugs: a multicenter survey of clinical practice. Collaborative Group for Epidemiology of Epilepsy. 372 Jun 93

We evaluated seven children who had been exposed to sodium valproate (or valproic acid) in utero. A consistent facial phenotype was observed in all seven in addition to other birth defects in four. The facial changes consisted of epicanthal folds which continued inferiorly and laterally to form a crease or groove just under the orbit, flat nasal bridge, small upturned nose, long upper lip with a relatively shallow philtrum, a thin upper vermillion border, and downturned angles of the mouth. Hypospadias, strabismus, and psychomotor delay were found in two males; two children had nystagmus and two had low birth weight.
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PMID:The fetal valproate syndrome. 643 41

The safety of administering phenytoin sodium by intermittent intravenous infusion was evaluated. Twenty-eight adult patients in a neurosurgical intensive-care unit were studied; most patients had head trauma. Ninety-three doses of phenytoin sodium 300 mg in 0.9% sodium chloride injection 50 ml were administered according to hospital-approved guidelines, which included administration over 30-60 minutes, initiation of infusion within one hour of solution preparation, and use of a 5-microns inline filter. All patients were monitored for adverse reactions and were on continuous ECG monitoring. Analysis of clinical data before and immediately after phenytoin infusions showed no statistically significant change in blood pressure and a small but significant drop in mean heart rate. There were no cases of hypotension, arrhythmias, bradycardia, or phlebitis. Single occurrences of hypertension, nystagmus, and pain at the i.v. site were noted. It is concluded that careful infusion of phenytoin sodium in 0.9% sodium chloride injection is safe. The use of approved written guidelines to govern important factors of preparation and administration are recommended.
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PMID:Clinical use of intravenous phenytoin sodium infusions. 688 41

Salt poisoning/water deprivation has been described under various circumstances in adult cattle. The signs and lesions in cattle are somewhat different from those in swine, which are frequently affected. This report describes several cases of salt poisoning in veal calves. The calves were fed milk replacer and were housed without access to water. Presenting signs were mostly referrable to dysfunction of the central nervous system and included hyperesthesia, opisthotonus, nystagmus, muscle twitching and intermittent convulsions. Although the serum sodium concentration in some of these calves was over 200 mEq/1, no remarkable brain lesions were noted at necropsy. The salt content of the milk replacer was 10 times the level recommended by the National Research Council. This salt may have come from the whey included in the formula. The syndrome produced in the veal calves was similar to that seen in infant children given only a nursing formula containing too much salt, and limited water.
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PMID:A case of presumptive salt poisoning (water deprivation) in veal calves. 708 63

We evaluated the effects of Ca2+ entry blockers, nilvadipine and flunarizine, on microcirculatory disorders of the inner ear and on blood flow in the inner ear of rats. Under sodium pentobarbital anesthesia, the middle ear was opened by a ventrolateral approach. A green light (wave length 540 nm) was applied to the cochlea or the vestibule to induce a hearing disturbance or equilibrium dysfunction as a result of inner ear microcirculatory disorders, while rose bengal solution was infused intravenously. In a hearing disturbance model, a compound cochlear nerve action potential was recorded by electrocochleography every minute after the beginning of illumination. The sound stimulus was an 8 kHz sine wave 100 dB normal hearing level. The action potential was calculated 128 times. The action potential disappeared about 12 min after the beginning of illumination. In another model of equilibrium dysfunction, the photoillumination was applied for 40 min under the infusion of rose bengal. The behavior of rats was observed in the swimming test and nystagmus was recorded 24 h after the completion of photoillumination. In a separate experiment, blood flow in the inner ear was measured with a laser Doppler flowmeter under sodium pentobarbital anesthesia. In this study, both nilvadipine and flunarizine prolonged the time required for complete suppression of the action potential, prevented equilibrium dysfunction in the swimming test and reduced the occurrence of nystagmus. Flunarizine significantly increased inner ear blood flow and nilvadipine failed to decrease blood flow in the inner ear, despite a reduced systemic blood pressure. In conclusion, Ca2+ entry blockers may prevent microcirculatory disorders of the inner ear in rats.
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PMID:Effect of a Ca2+ entry blocker, nilvadipine, on hearing disturbances and equilibrium dysfunction caused by microcirculatory disorders of the rat inner ear. 822 91

Nonketotic hyperglycinemia (NKH) is an inborn error of glycine degradation causing muscular hypotonia, seizures, apnea, and lethargy; it has a poor prognosis. Accumulation of glycine in the brain is thought to cause excessive stimulation of the N-methyl-D-aspartate receptor. Dextromethorphan (DM), an N-methyl-D-aspartate receptor antagonist, in doses of 5 to 35 mg/kg per day has been shown to have beneficial therapeutic effects in some patients with NKH. We report the case of a 1-year-old infant with NKH, seizure disorder, and psychomotor delay who was clinically seizure free during treatment with sodium benzoate, arginine, benzodiazepam, and phenobarbital. Although sodium benzoate normalized serum glycine levels (103 to 125 mumol/L), cerebrospinal fluid glycine levels remained elevated (42 to 47 mumol/L), with epileptiform activity on electroencephalography. The addition of low-dose DM (0.25 mg/kg per day) to the treatment led to improvement of electroencephalographic activity, resolution of nystagmus with increased eye contact, and modest progression of developmental milestones. These data suggest that DM at doses significantly lower than previously reported may be beneficial in some patients with NKH. Treatment with low-dose DM needs further evaluation.
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PMID:Efficacy of low-dose dextromethorphan in the treatment of nonketotic hyperglycinemia. 865 42

The objective of this study was to determine the effects of ouabain, a Na+,K+-ATPase inhibitor, in inner ears. Administering ouabain locally through the round window and vestibule, resulted in degenerative changes in cochlear and vestibular sensory cells and limbal fibrocytes, but the stria vascularis and spiral ligament were less affected. The position of Reissner's membrane was rarely changed. Vacuolar spaces in the sensory epithelia of cristae, maccula utriculi and macula sacculi increased in number. Nystagmus was a common occurrence with or without demonstrating degeneration of vestibular sensory cells. By administering ouabain systemically, the course of developing endolymphatic hydrops could not be altered in the ears with endolymphatic duct blockage. Edema of nerve endings of inner hair cells and vestibular sensory cells was frequently observed with administration of a high concentration of ouabain in both normal and hydropic ears, but edema was reversible. Degeneration of some vestibular sensory cells were observed in hydropic ears with a long survival time. The mechanism of selective sensitivity or non-sensitivity of inner ear tissues to ouabain is discussed.
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PMID:Morphological changes induced by administration of a Na+,K+-ATPase inhibitor in normal and hydropic inner ears of the guinea pig. 1068 35

The effects of nitric oxide on the vestibular function recovery following unilateral labyrinthectomy were studied. Male Sprague-Dawley rats treated with N-omega-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase (NOS) inhibitor, were subjected to destruction of the unilateral vestibular apparatus and spontaneous nystagmus was observed. To explore the role of nitric oxide on the potassium current, the whole cell patch clamp technique was applied on isolated medial vestibular nuclear neurons. The frequency of spontaneous nystagmus that appeared in L-NAME-treated rats was higher and maintained longer than in control animals. Potassium currents in the isolated medial vestibular nucleus were inhibited by nitric oxide liberating agents, sodium nitroprusside and S-nitroso-N-acetylpenicillamine. After blockade of calcium dependent potassium currents by high EGTA (11 mM)-containing pipette solution, sodium nitroprusside did not inhibit the outward potassium currents. 8-Bromoguanosine 3,5-cyclic monophosphate, a membrane-permeable cGMP analogue, produced similar effects to inhibit the outward potassium currents as sodium nitroprusside. These results suggest that nitric oxide production after unilateral labyrinthectomy would help to facilitate vestibular compensation by inhibiting calcium-dependent potassium currents through increasing intracellular cyclic GMP, thereby increasing excitability in ipsilateral vestibular nuclear neurons.
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PMID:Effects of nitric oxide on the vestibular functional recovery after unilateral labyrinthectomy. 1120 15

Epileptic nystagmus (EN) is a rare form of nystagmus that occurs only during epileptic seizures. We report a case in which EN was first noted in an 8 year-old boy. Neuro-imaging was normal. Sharp waves from the left occipital lobe characterised the interictal EEG. Ictal video-EEG showed the aspects of electric seizures during clinical manifestations e.g. nystagmus. Ambulatory EEG displayed numerous diurnal and nocturnal seizures, but exclusively in REM sleep. After two weeks of sodium valproate treatment, the seizures, EEG focus spikes and nystagmus, as well as the squint, disappeared. During a two-year follow-up the child had no further seizures, EEG was normal and the school performance was unaffected. This case has the main features of benign epilepsy, although there are unusual features such as epileptic nystagmus, permanent squint, reduction of EEG paroxysmal abnormalities during NREM, and the presence of seizures during REM sleep. The observation and the significance of EN are discussed with reference to the literature.
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PMID:Epileptic nystagmus: electroclinical study of a case. 1131 21


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