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

We investigated the blood pressure response elicited by microinjection of various hypertonic solutions into the area of the nucleus tractus solitarii (NTS) of the brainstem, an area rich in catecholaminergic neurons. Equiosmolar solutions of NaCl, dextrose, LiCl and KCl were employed. NaCl produced a prolonged blood pressure rise; LiCl and normal saline produced a similar rise of short duration; and KCl produced epileptic-type seizures with postictal hypertension. Dextrose had no effect and neither had NaCl microinjection in areas relatively distant from the NTS. The rise in blood pressure was not reversed by a vasopressin antagonist injected systemically, but was totally abolished by systemic alpha-adrenergic blockade with phentolamine. These findings suggest that sodium can cause hypertension by direct stimulation of the central sympathetic nervous system without participation of peripheral mechanisms such as fluid volume expansion or alteration of the vascular wall.
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PMID:Hypertensive response to saline microinjection in the area of the nucleus tractus solitarii of the rat. 299 26

Carbamazepine (CBZ)-induced water intoxication occasionally limits its usefulness in refractory seizures and trigeminal neuralgia. Fluid restriction, CBZ dose reduction, or concomitant phenytoin therapy may be impractical or ineffective. Demeclocycline (7-chloro-6 demethyl tetracycline) (DMC) corrected the CBZ-induced water intoxication in a 51-year-old man with refractory complex partial seizures and a normal antidiuretic hormone (ADH) level. DMC inhibits ADH-sensitive adenylate cyclase activity in the renal collecting duct and may be useful in correcting the ADH-like or renal antidiuretic effect of CBZ.
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PMID:Perspective on carbamazepine-induced water intoxication: reversal by demeclocycline. 309 19

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.
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PMID:Management of the syndrome of inappropriate secretion of antidiuretic hormone. 312 Dec 40

A case of hyponatremia is presented with water intoxication due to treatment with oxcarbazepine (OxCZ). The patient was admitted because of exceeding dullness and increasing seizures. Low values for serum sodium and osmolality were found. Simultaneously with the reduction in OxCZ, values of sodium and osmolality increased, normalizing on discontinuation of the drug, and the exceeding tiredness as well as the generalized seizures disappeared. Low values of arginine-vasopressin were found, suggesting that the mode of action of OxCZ was directly or indirectly at the level of the kidney.
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PMID:Hyponatremia induced by oxcarbazepine. 314 48

Kindling of seizures with stimulation of anterior neocortex was examined in control rats and in Brattleboro rats deficient in arginine-vasopressin (AVP). There were no significant differences between control rats, homozygous Brattleboro rats, and heterozygous Brattleboro rats in the rate and pattern of kindling of generalized seizures. Thus AVP is not critically involved in anterior neocortical kindling.
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PMID:Anterior neocortical kindling in vasopressin-deficient rats. 319 27

The onset of therapeutic effectiveness of carbamazepine is generally very rapid in the treatment of seizure and paroxysmal pain disorders, shows some lag in the treatment of mania, and exhibits the longest lag in depression. These time course variations may indicate that different mechanisms underlie the efficacy of carbamazepine in the differential neuropsychiatric syndromes. Biochemical and pharmacological data suggest that the anticonvulsant effects of carbamazepine are related to "peripheral-type" benzodiazepine and alpha 2-noradrenergic receptor systems and to its ability to stabilize sodium channels. GABAB (baclofen-like) actions appear to be involved in antinociceptive, but not anticonvulsant, effects. The relatively acute time course of antimanic efficacy may be related to the above-mentioned mechanisms or to other effects related to systems postulated to be altered in the manic syndrome. These effects might include carbamazepine's ability to increase acetylcholine in the striatum, decrease probenecid-induced levels of CSF homovanillic acid (HVA) in man and dopamine turnover in animals, decrease CSF norepinephrine in manic patients, inhibit adenylate cyclase activity (in response to norepinephrine, dopamine, adenosine, or ouabain), decrease GABA turnover, or act as a vasopressin agonist. Efficacy in depression may be related to actions in man that take time or chronic drug administration to develop, such as increases in plasma tryptophan, decreases in CSF somatostatin, decreases in thyroid indices, and increases in urinary free cortisol excretion and, in animals, increases in substance P sensitivity and increases in brain adenosine receptors. The ability of carbamazepine to block the development of lidocaine- and cocaine-induced seizures also requires chronic administration, suggesting that these seizure models may provide a unique perspective for understanding mechanisms of time-dependent effects.
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PMID:Time course of clinical effects of carbamazepine: implications for mechanisms of action. 328 May 60

A tabular synopsis is presented for articles concerned with the effects of peptides on the central nervous system that appeared in the journal Peptides from 1980-1985. A table arranged alphabetically by peptide and one arranged by effects, both listing routes of injection, species, direction of change, and qualifying notes, provides easy cross-referencing of peptides and their effects. Over 80 peptides and over 135 effects are listed. The list of peptides includes, but is not limited to: ACTH, angiotensin, bombesin, bradykinin, calcitonin, casomorphin, CCK, ceruletide, CGRP, CRF, dermorphin, DSIP, dynorphin, endorphins, enkephalins, GRF, gastrin, LHRH, litorin, metkephamid, MIF-l, motilin, MSH, NPY, NT, oxytocin, ranatensin, sauvagine, substances P and K, somatostatin, TRH, VIP, vasopressin, and vasotocin. The list of effects includes, but is not limited to: aggression, alcohol, analgesia, attention, avoidance, behavior, cardiovascular regulation, catalepsy, conditioned behavior, convulsions, dopamine binding and metabolism, discrimination, drinking, EEG, exploration, feeding, fever, gastric secretion, GI motility, grooming, learning, locomotor behavior, mating, memory, neuronal activity, open field, operant behavior, rearing, respiration, satiety, scratching, seizure, sleep, stereotypy, temperature, thermoregulation and tolerance.
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PMID:Central nervous system effects of peptides, 1980-1985: a cross-listing of peptides and their central actions from the first six years of the journal Peptides. 353 8

I retrospectively describe 20 episodes of water intoxication in 19 infants, with hypothermia, seizures, and hyponatremia. Overdilution of formula or aggressive supplementation with water or clear juices were documented in 16 of the 20 episodes. Seizures and respiratory distress were severe enough in six cases to require intubation and ventilatory support. Marked diaphoresis was noted as a premonitory symptom to seizures in eight children. The children were an average of 5.1 +/- 4.3 months of age; serum sodium values averaged 118 +/- 4.3 mmol/L. No evidence of excess production of antidiuretic hormone was found. Water intoxication in infants is common, and I discuss its possible relationship to demyelinating disease of the central nervous system.
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PMID:Seizures and hypothermia due to dietary water intoxication in infants. 356 73

A 17-month-old boy presented with 10% to 12% first- and second-degree burns secondary to scald injury. He rapidly developed hyponatremia secondary to inappropriate antidiuretic hormone secretion, manifested by the occurrence of seizures. After appropriate therapy was instituted, the child had an uneventful recovery. To the best of the authors' knowledge, this problem has not been reported previously in a child with a relatively mild burn.
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PMID:Early syndrome of inappropriate secretion of antidiuretic hormone in a child with burn injury. 372 8

Homozygous and heterozygous Brattleboro rats deficient in central vasopressin and Long-Evans control rats were electrically kindled in the ventral hippocampus or lateral septum. The homozygous and heterozygous Brattleboro groups stimulated in the ventral hippocampus or lateral septum kindled significantly faster than the respective Long-Evans control groups. The accelerated kindling rate of the Brattleboro groups is attributed to faster seizure development during the early seizure stages. These results suggest that vasopressin may be involved in the kindling of convulsions from limbic structures where it is normally found.
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PMID:Kindling of the hippocampus and septum in vasopressin-deficient rats (Brattleboro strain). 394 5


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