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)

Kainic acid (KA), in various concentrations, was applied iontophoretically into the central nucleus of the amygdala. Microlesions with this cell specific neurotoxin caused body weight loss, hypo- or aphagia and hypo- or adipsia in a dose-dependent manner. EEG-examinations proved that even low doses of KA produced seizure activity; however, these epileptiform symptoms disappeared within the first 48 h after the operations. Thus, the lasting feeding disturbances produced by iontophoretic KA applications to the central nucleus of the amygdala (i.e., even these fine microlesions) were not related causally to the pathological EEG activity changes. Our findings, along with previous data, indicated that the body weight loss and feeding deficits were due to the KA-induced impairment of complex regulatory mechanisms.
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PMID:Feeding disturbances and EEG activity changes after amygdaloid kainate lesions in the rat. 147 23

The characteristics and consequences of limbic seizures evoked by single peripheral injections of lithium (3 mEq/kg) and pilocarpine (30 mg/kg) were investigated over a three-year period. The seizures occurred when 3 mEq/kg of lithium was followed 4 to 28 hours later by 30 mg/kg of pilocarpine. The seizures did not occur if the intervals were shorter or longer or if the pilocarpine preceded the lithium. The acute mortality or persistent aphagia and adipsia could be compensated by postseizure injections of acepromazine and a special milk-bread diet. Gender, age and preinjection environmental effects, but not hybrid genetics, influenced the seizure onset latency. Fifty to 100 days after the seizures massive lesions were found in the entorhinal-pyriform cortices, amygdala and selected thalamic groups.
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PMID:Characteristics of limbic seizures evoked by peripheral injections of lithium and pilocarpine. 285 77

Primary adipsia and defective osmoreceptor function were diagnosed in a 7-month-old female Miniature Schnauzer. Also, the dog was noted to be dehydrated and to have chronic hypernatremia. On multiple occasions the dog's urine osmolality: plasma osmolality was greater than 4. The dog had inappropriate responses to isoosmotic and hypertonic NaCl infusions. Chlorpropamide administration initiated water intake but the volume was insufficient to avoid hypernatremia. The chronic hypernatremia and dehydration were treated successfully by mixing the calculated maintenance fluid volume in canned food. At 25 months of age, the dog died several days after becoming dehydrated and severely hypernatremic. Astrogliosis and neuronal degeneration were noted in both the thalamic and hypothalamic regions, but were believed to be nonspecific degenerative lesions compatible with seizures and severe dehydration.
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PMID:Hypernatremia and adipsia in a dog. 672 16

Systemic administration does not allow a clear differentiation between the anticonvulsant properties of GABAA (gamma-aminobutyric acid) modulators. For this reason, various GABAA modulators have previously been micro-infused into seizure controlling substrates (area tempestas, substantia nigra) in the rat brain as a screening method for potential systemic administration. The purpose of the present study was to examine the anticonvulsant impact of the GABAergic modulators muscimol, ethanol, and propofol (screened by micro-infusions) when each drug was combined with procyclidine and administered systemically. The results showed that all 3 combinations could effectively terminate soman-induced (100 microg/kg s.c.) seizures when administered 30-35 min after onset. Procyclidine and propofol were considered as the most relevant double regimen to replace a previous triple regimen (procyclidine, diazepam, pentobarbital) against soman-induced seizures. Additionally, it was shown that unilateral implantation of hippocampal electrodes resulted in increased resistance to aphagia/adipsia and neuropathology, but not to lethality following soman. Efficient pharmacological treatment of soman-induced seizures at an early stage (< 20 min) is crucial to avoid neuropathology and cognitive deficits.
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PMID:Pharmacological therapies against soman-induced seizures in rats 30 min following onset and anticonvulsant impact. 1694 71

In nerve agent research, it is assumed that the regions from which seizure activity is triggered may offer clues for the designing of effective anticonvulsive therapy. In the present study, selective brain lesions were made to identify critical cholinergic pathways and seizure controlling areas involved in the induction of epileptiform activity in rats challenged with soman. The results showed that rats with bilateral aspiration lesion of the seizure controlling substrate, area tempestas (AT) in the piriform cortex, displayed marked anticonvulsant effects, whereas such effects were not seen when substantia nigra was destroyed. Aspiration lesion of the medial septal area (MS) including the vertical limb of the diagonal band nucleus (DBN) caused increased latency to the onset of convulsions, whereas damage to the nucleus basalis magnocellularis (NBM), nucleus accumbens, or both MS and NBM did not cause anticonvulsant effects. Saporin lesion of MS, DBN (horizontal limb), or MS+DBN had no anticonvulsant effects, suggesting that aspiration lesion of MS disrupted pathways beyond cholinergic ones. Severe aphagia/adipsia and reduced body weight occurred in rats with lesions in the septal area. In separate sham operated rats, a strong positive correlation was found between body weight and latency to onset of convulsions in response to soman. Thus, weight loss and a relatively high dose of soman (1.6 x LD(50)) in this context may have masked potential anticonvulsant effects among some lesioned animals. It is inferred that MS and AT/piriform cortex occur as prime target areas for induction of seizures by soman.
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PMID:Anticonvulsant effects of damage to structures involved in seizure induction in rats exposed to soman. 1751 81

Central pontine myelinolysis (CPM) has been reported in women with severe hyperemesis gravidarum-induced hyponatremia followed by rapid correction. Gestational diabetes with adipsia complicated by acute hypernatremia resulting in CPM has never been reported. Here is a case of a disabled female who presented with polydipsia, polyuria, seizures, fetal death in utero, hyperglycemia, and hyper-osmolar hypernatremia on her 31st gestational week. The dead fetus was delivered and the patient's plasma glucose and sodium were later stabilized. When the patient developed quadriplegia and respiratory failure 5 days later, brain magnetic resonance imaging showed central pontine and extra-pontine myelinolysis. Gestational diabetes complicated by hyper-osmolar crisis may cause fetal death and severe neurologic sequela. Early recognition and delivery of the fetus and placenta may improve the electrolyte and fluid imbalance.
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PMID:Gestational diabetes and central pontine myelinolysis with quadriplegia: a case report. 1965 45

The present investigation envisages the toxic effects of aluminium on the cholinergic system of male albino rat brain. Aluminium toxicity (LD(50)/24 h) evaluated as per Probit method was found to be 700 mg/kg body weight. One-fifth of lethal dose was taken as the sublethal dose. For acute dose studies, rats were given a single lethal dose of aluminium acetate orally for one day only and for chronic dose studies, the rats were administered with sublethal dose of aluminium acetate once in a day for 25 days continuously. The two constituents of the cholinergic system viz. acetylcholine and acetylcholinesterase were determined in selected regions of rat brain such as cerebral cortex, hippocampus, hypothalamus, cerebellum, and pons-medulla at selected time intervals/days under acute and chronic treatment with aluminium. The results revealed that while acetylcholinesterase activity was inhibited, acetylcholine level was elevated differentially in all the above mentioned areas of brain under aluminium toxicity, exhibiting area-specific response. All these changes in the cholinergic system were subsequently manifested in the behavior of rat exhibiting the symptoms such as adipsia, aphagia, hypokinesia, fatigue, seizures, etc. Restoration of the cholinergic system and overt behavior of rat to the near normal levels under chronic treatment indicated the onset of either detoxification mechanisms or development of tolerance to aluminium toxicity in the animal which was not probably so efficient under acute treatment.
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PMID:Cholinergic system under aluminium toxicity in rat brain. 2117 Feb 57

Hyperosmolar hyperglycemic state (HHS) is a disorder that occurs most frequently in type 2 diabetics and is associated with high mortality - up to 50%. Hypernatremia, when associated with HHS, worsens the prognosis. Encephalopathy is evident at a serum sodium level greater than 160 mOsm/kg. Additional symptoms include lethargy, weakness, seizures, and coma. Rhabdomyolysis can rarely occur in hyperosmolar states. Here we describe a case of severe hypernatremia in the setting of HHS leading to profound encephalopathy and report to the best of our knowledge the highest serum sodium level published in the literature. A 50-year-old female with no past medical history (PMH) of diabetes presented to the ED obtunded and found to have a glucose level of 1400 mg/dL without metabolic acidosis or ketosis. Her sodium on presentation was 169 mOsm/kg but subsequently rose to 200 mOsm/kg when corrected for hyperglycemia. Plasma osmolality was 340 mOsm/kg. She developed pre-renal acute kidney injury (AKI) secondary to the osmotic diuresis from severe hyperglycemia as well as rhabdomyolysis with a peak creatine kinase(CK) level of 2493. The free water deficit was 14L which was corrected. New-onset anisocoria raised concern for osmotic demyelination which was further investigated with MRI. An acute ischemic stroke in the right caudate was found. Fortunately, the patient survived the endocrine emergency. This case emphasizes the importance of an appropriate rate of sodium correction. This case is particularly unique because the degree of hypernatremia seen here was in the absence of intentional salt loading (for example by the administration of hypertonic saline), or psychiatric disease (as psychogenic adipsia). In conclusion, we report the case of severe hypernatremia and the highest documented serum sodium level was seen in literature in the background of HHS, rhabdomyolysis and septic shock.
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PMID:Salty, Sweet and Difficult to Treat: A Case of Profound Hypernatremia in the Setting of Hyperosmotic Hyperglycemic State. 3230 Apr 98