Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The subacute toxicity of compound 1 was investigated in rats and dogs. Compound 1 was administered orally to rats of both sexes at daily doses of 0.5, 1.0 or 2.5 g/kg for 3 months. No change attributable to the administration of compound 1 was found either in blood count or in histopathological examination. Decreases in SGPT, alkaline phosphatase and lactic acid dehydrogenase and an increase in serum cholesterol were detected. Compound 1 was mixed with food and given to dogs of both sexes daily at doses of 0.2 or 0.5 g/kg for 3 months. Severe toxic symptoms including anorexia, emesis, ataxia and convulsive seizures were observed. A decrease in SGPT and increase in alkaline phosphatase were also detected. Hyperemia of the duodenal mucosa and severe kidney lesions were found in histopathological examination. Neither abnormality of appearance nor histopathological change was found in a pig receiving compound 1 at the daily dose of 0.1 g/kg for 3 months. The results suggest that there are differences of compound 1 metabolism among the species used in this study.
 ...
PMID:[Species differences in subacute toxicity of pyrrole aldehyde N4-(4-methoxyphenyl) semicarbazone]. 215 Dec 66

Knowledge of side effects associated with different cephalosporins may be of help to prescribers. There are several side effects that are common to all cephalosporins, but overall, cefotaxime and ceftizoxime cause the fewest adverse reactions. Bleeding is probably the most common serious side effect of cephalosporins. Moxalactam causes coagulopathy and bleeding more often than do other cephalosporins, probably because it is carboxylated and has a methylthiotetrazole side chain. Cefoperazone also has a methylthiotetrazole side chain and may cause bleeding, particularly when used in doses greater than 4 g per day. Ceftriaxone has a similar side chain and there is some evidence that it can induce a coagulopathy. Coagulation tests should be monitored when any of the third-generation cephalosporins are given to patients with a high risk of bleeding. Disulfiram-like reactions are also related to the side chains associated with coagulation defects and have been reported when patients receiving cefoperazone, moxalactam, or ceftriaxone have ingested alcohol. Seizures have been reported with ceftazidime, but are uncommon. Hematologic reactions are rare with all third-generation cephalosporins. Benign diarrhea and Clostridium difficile colitis probably occur most often with moxalactam, cefoperazone, ceftazidime, and ceftriaxone, but there are few good data on this issue. Ceftriaxone has the unique ability to cause sludge (also referred to as pseudolithiasis) to form in the gallbladder, particularly in children. This may be associated with nausea, anorexia, epigastric distress, and colic, and is usually detected using ultrasonography. The sludge dissolves and symptoms subside after therapy is discontinued. None of the third-generation cephalosporins is clearly significantly nephrotoxic, even when combined with aminoglycosides. Most of the third-generation cephalosporins have surprisingly few serious side effects, which make them attractive for use in the treatment of a wide variety of serious infections.
 ...
PMID:Safety of parenteral third-generation cephalosporins. 218 9

Triple bromide elixir was used as an adjunctive antiepileptic drug in 11 children whose seizure disorders were intractable to other antiepileptic therapy. The patients' ages ranged from 2 to 17 years. The seizure disorders treated included photosensitive epilepsy (one case), acquired epileptic aphasia (one case), Lennox-Gastaut syndrome (three cases), and symptomatic localization-related epilepsies (six cases). Two patients' seizures completely stopped with bromide therapy. Four patients had a significant and sustained improvement on bromide therapy, while three more had a transient improvement. In these six patients with complete or significant control, the mean therapeutic dose was 33 mg bromide/kg daily, and the mean therapeutic serum concentration was 14.1 mmol/L (range, 4 to 30.5 mmol/L). The combination of bromide with valproate appeared to be particularly effective in these patients. Toxicity was minimal, and in only one patient was the medication stopped, because of anorexia and weight loss. Given the low cost, long half-life, and minimal toxicity when serum bromide concentrations are followed, bromide therapy should be considered as adjunctive antiepileptic drug therapy for patients whose seizures are intractable to other drugs.
 ...
PMID:Bromide therapy for pediatric seizure disorder intractable to other antiepileptic drugs. 229 42

Acromegaly was diagnosed in 14 middle-aged to old cats of mixed breeding. Thirteen (93%) of the cats were male and one was female. The earliest clinical signs in the 14 cats included polyuria, polydipsia, polyphagia, all of which were associated with untreated diabetes mellitus. All developed severe insulin resistance within a few months; peak insulin dosages required to control severe hyperglycemia ranged from 20 to 130 U per day. Other clinical findings weeks to months after diagnosis included enlargement of one or more organs (e.g., liver, heart, kidneys, and tongue) (n = 14), cardiomyopathy (n = 13), increase in body size and weight gain (n = 8), nephropathy associated with azotemia and clinical signs of renal failure (n = 7), degenerative arthropathy (n = 6), and central nervous system signs (i.e., circling and seizures) caused by enlargement of the pituitary tumor (n = 2). The diagnosis of acromegaly was confirmed by demonstration of extremely high basal serum growth hormone concentrations (22 to 131 micrograms/l) in all cats. Computerized tomography disclosed a mass in the region of the pituitary gland and hypothalamus in five of the six cats in which it was performed. Two cats were treated by cobalt radiotherapy followed by administration of a somatostatin analogue (octreotide), whereas two cats were treated with octreotide alone. Treatment had little to no effect in decreasing serum GH concentrations in any of the cats. Eleven of the 14 cats were euthanized or died four to 42 months (median survival time, 20.5 months) after the onset of acromegaly because of renal failure (n = 2), congestive heart failure (n = 1), concomitant renal failure and congestive heart failure (n = 3), progressive neurologic signs (n = 2), persistent anorexia and lethargy of unknown cause (n = 1), the owner's unwillingness to treat the diabetes mellitus (n = 1), or unknown causes (n = 1). Results of necropsy examination in ten cats revealed a large pituitary acidophil adenoma (n = 10), marked left ventricular and septal hypertrophy (n = 7), dilated cardiomyopathy (n = 1), arthropathy affecting the shoulder, elbow, or stifle (n = 5), and glomerulopathy characterized by expansion of the mesangial matrix and variable periglomerular fibrosis (n = 10).
 ...
PMID:Acromegaly in 14 cats. 240 66

Because hypothermia and anorexia were previously found to be more sensitive indices of the effects of lindane than were convulsions, these endpoints were used to quantify the ability of benzodiazepines (BDs) and phenytoin either to ameliorate or exacerbate the toxicity of lindane in the rat. After administration of lindane (40 or 50 mg/kg) in oil per os, toxicity was counteracted by phenytoin and the "central" BD agonists diazepam and clonazepam, but was worsened by Ro 5-4864 a "peripheral" BD agonist. Clonazepam and diazepam were each more effective in counteracting lindane-induced anorexia than in stimulating food intake, presumably because the animals had been fasted and probably even controls ate maximally when food was presented. Diazepam alone (3 injections in 1 day) produced withdrawal-induced decreased food intake the following day. Clonazepam and diazepam alone each transiently decreased colonic temperature, yet effectively blocked the more severe hypothermia produced by lindane. Ro 5-4864 by itself did not produce any measurable effects, yet exacerbated all of the effects, including lethal effects, of lindane. The present findings are compatible with other evidence that lindane and Ro 5-4864 act at the picrotoxinin receptor of the GABAA-activated chloride channel and that systemic administration of agents acting at this site may produce a constellation of effects, including seizures, hypothermia and anorexia.
 ...
PMID:"Central" and "peripheral" benzodiazepines and kinetics of lindane-induced toxicity. 247 Dec 14

Teething does not appear to cause diarrhea, fever, rashes, seizures or bronchitis. It may be associated with some daytime restlessness, thumb sucking, gum rubbing, drooling and temporary loss of appetite. It is not clear whether these signs are developmental in origin or are actually related to tooth eruption. Illness occurring with teething should be thoroughly evaluated so that a serious systemic disturbance is not overlooked.
 ...
PMID:Teething. 281 81

The etiology, pathophysiology, clinical features, diagnosis, and medical treatment of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) are reviewed. SIADH is a common cause of hyponatremia in hospitalized patients. Increased concentrations of antidiuretic hormone (ADH) result in retention of free water, increased excretion of sodium, and hyponatremia. Symptoms generally occur only when hyponatremia is severe (less than or equal to 125 meq/L) and may include anorexia, vomiting, and confusion, followed by seizures, coma, and death. SIADH may result from a variety of diseases, as well as from the use of drugs such as chlorpropamide, carbamazepine, diuretics, and some antineoplastic agents. Diagnosis of SIADH is confirmed by demonstration of a high urine osmolality with a low plasma osmolality, in the absence of diuretic use. Immediate treatment of the symptomatic patient with SIADH includes intravenous furosemide and 3% sodium chloride injection to produce a negative free-water balance. If the underlying cause of SIADH cannot be corrected, the treatment of choice for chronic SIADH is fluid restriction. If this is not tolerated by the patient, demeclocycline can be used to induce a negative free-water balance. Urea, lithium, phenytoin, and loop diuretics have been reported to be effective, but there are few data to support their use. Future research into the treatment of SIADH must be directed at developing effective antagonists of ADH. Treatment of SIADH consists of elimination of underlying causes and restriction of fluid intake; if these measures are unsuccessful or poorly tolerated, long-term drug therapy may be indicated.
 ...
PMID:Management of the syndrome of inappropriate secretion of antidiuretic hormone. 312 Dec 40

Thirty-six children with epilepsy resistant to conventional treatment were treated with bromides in addition to the current therapy. Six out of 19 cases with prevailingly or exclusively generalized tonic-clonic seizures became seizure-free and in 9 cases a reduction in seizure frequency of more than 50% was achieved. Freedom from seizures could not be obtained in 13 cases, who had frequent minor seizures in addition to generalized tonic-clonic seizures. In some, minor seizures were even activated. Tonic and focal seizures showed no response. Side effects were observed in one-third of the cases (acne, loss of appetite, loss of weight, fatigue) but in no case they did become intolerable. Fifty to 80 mg potassium bromide per kg body weight seems to be an effective daily dose range. There is a preferential indication of bromides for patients suffering from early onset epilepsy with generalized tonic-clonic seizures and/or alternating hemi-grand mal, for whom other treatment is ineffective. This disorder is characterized by a high familial incidence of epileptic seizures, onset between 6 months and 3 years of age, normal development until the onset of seizures, generalized tonic-clonic seizures and often alternating hemi-grand mal, seizure precipitation by fever, and occasional combination with or transition to myoclonic-astatic and/or myoclonic seizures. EEG is often normal or shows slight slowing in the initial phase; later it shows theta rhythms and generalized spikes and waves. Especially, if the onset is during the first year of life, the course of the epilepsy is often unfavourable.
 ...
PMID:Bromides were effective in intractable epilepsy with generalized tonic-clonic seizures and onset in early childhood. 321 12

Two dogs were examined because of anorexia, lethargy, muscle tremors, weakness, and seizures that were associated with an acute onset of hypocalcemia. Both dogs had histories of chronic hypercalcemia. Examination of the parathyroid glands revealed infarction of focal parathyroid adenomas, with atrophy of the remaining parathyroid glands. It was concluded that the acute onset of hypocalcemia was caused by infarction of functional parathyroid adenomas that were previously responsible for the cause of persistent hypercalcemia. Infarction of a parathyroid adenoma should be included in a list of differential diagnoses of acute hypocalcemia in the dog, especially if hypercalcemia has been diagnosed previously.
 ...
PMID:Acute hypocalcemia associated with infarction of parathyroid gland adenomas in two dogs. 335 Jul 46

The paroxysmal (px) chick is a mutant White Leghorn (Gallus domesticus) which appears normal at hatching and during the subsequent week. By ca. 8 days posthatching, various symptoms develop, of which the most obvious are depressed food intake (anorexia) and audiogenic seizures. Histological evidence suggests that central auditory and vestibular nuclei and fiber tracts begin to degenerate prior to seizure onset. This degeneration, which affects central and peripheral components of both systems, becomes increasingly severe over time although auditory stimulation continues to elicit seizures. Characterization and analysis of peripheral and brainstem auditory response to auditory stimuli indicated that major response differences between px and normal chicks exist in peaks reflecting brainstem activity (P3A, P3B, P4A, P5A). In 5 of 8 px chicks, these later response peaks were either grossly abnormal in terms of amplitude and latency (including amplitude input/output functions) or often entirely absent. Early peaks (P1A and P2A), however, in px waveforms were normal in morphology and amplitude, indicating normal function of peripheral auditory structures. Although lower body temperature of px chicks may account for some of the longer latencies observed, other abnormalities (e.g. absence of peaks) could not be produced in normal birds by induced hypothermia.
 ...
PMID:Peripheral and brainstem auditory function in paroxysmal (px) White Leghorn chicks. 356 41


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>