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)

We report the case of a 9-year-old girl with multiple problems due to hypothalamic dysfunction of obscure origin: apnoeic spells, behavioural problems, developmental delay, hypodipsia with bouts of hypernatraemia, episodes of spontaneous hypothermia, obesity, petit-mal seizures, non-progressive precocious puberty, absence of respiratory response to CO2 and probably insensitivity of hyposensitivity to pain. She also had hyperprolactinaemia and decreased human growth hormone secretion. Hypothyroidism of central origin and hyposecretion of cortisol were also present. Multiple brain CT-scans failed to reveal any tumour or other anatomical abnormality. Her clinical course was improved initially by treatment with clomipramine, but she died suddenly, and the autopsy failed to disclose any anatomical lesion. We compare this case with three similar previously reported cases.
 ...
PMID:Hypothalamic dysfunction in a child: a distinct syndrome? Report of a case and review of the literature. 768 46

In order to examine the respiratory effects of tonic-clonic seizures and their treatment with i.v. diazepam or lorazepam, we utilized a spontaneously breathing piglet seizure model. A tracheostomy, arterial catheter, and epidural electrodes were inserted and pigs were maintained under ketamine anesthesia. After baseline recordings, seizures were induced with a pentylenetetrazol (PTZ) bolus and a 20 min infusion (5-6 mg/kg/min). After 10 min of PTZ infusion, randomly assigned animals received diazepam (D; N = 7; 0.5 mg/kg), lorazepam (L; N = 7; 0.2 mg/kg), or 0.9% saline (C; N = 7; controls) by rapid peripheral vein injection. Minute ventilation (Ve), Pa(CO2), and the pressure change in response to airway occlusion at end-expiration (P0.1) were measured at standard intervals. All groups had comparable increases in respiratory drive during untreated seizures. Changes in Ve and P0.1 were reduced to at or below baseline values in groups D and L, but not C, from 2 to 45 min after treatment (P < 0.05). No significant changes were observed in Pa(CO2) after either intervention. Following anticonvulsants, the cumulative duration of seizures was significantly reduced in L and D groups, compared to C (P < 0.05). We conclude that increases in respiratory drive occur during tonic-clonic seizures induced with PTZ. Amelioration of seizure activity with lorazepam or diazepam results in a reduction in respiratory drive, but not respiratory failure, in this tracheostomized model.
 ...
PMID:Respiratory drive during status epilepticus and its treatment: comparison of diazepam and lorazepam. 771 57

Subacute necrotizing encephalomyelopathy (Leigh's syndrome) is a rare neurodegenerative disease in the adult. The precise metabolic defect is unknown, but abnormalities of a mitochondrial enzyme system related to cytochrome-c oxidase or pyruvate dehydrogenase are described. The clinical picture usually consists of an altered breathing pattern, oculomotor paralysis, other signs of cranial nerve dysfunction, ataxia, myoclonic jerks, nystagmus, generalized seizures, optic atrophy and demyelinating peripheral neuropathy. Hypopnea leads to CO2-retention with consecutive loss of consciousness demanding mechanical ventilation. Respiratory failure is the most frequent cause of death. Here we describe two patients with adult onset Leigh's syndrome and we discuss the longterm treatment strategies including vitamin B1 and CPAP mask.
 ...
PMID:[Adult Leigh syndrome. A rare differential diagnosis of central respiratory insufficiency]. 771 56

The hemodynamic response to seizure has long been a topic for discussion in association with the neuronal damage resulting from convulsion. Electroconvulsive therapy (ECT) is an appropriate clinical model for the investigation of the cerebral physiology of seizure. In this study, we monitored the oxygenation state of brain tissue using near infrared (NIR) spectrophotometry, and flow velocity at the middle cerebral artery (MCA) using transcranial Doppler ultrasonography (tc-Doppler) in ninety cases where flow velocity at the middle cerebral artery (MCA) using transcranial Doppler ultrasonography (tc-Doppler) in ninety cases where ECT was prescribed to patients suffering from endogenous depression. Under general anesthesia with thiopental and succinyl choline, an electrical current was applied bilaterally at the minimal energy level. Throughout the therapy, end-tidal CO2 tension was maintained at 30-35 mmHg, and the SpO2 value was maintained above 98% by manual ventilation assistance. The total- and oxy-hemoglobin contents in the brain were reduced during the electrical shock, and then recovered to the pre-shock value (total-hemoglobin; 44.13 +/- 12.88 s after the shock, oxy-hemoglobin; 88.62 +/- 11.69 s after the shock). Subsequently, these values further increased beyond the preshock value. On the other hand, the deoxy-hemoglobin content increased for 90.73 +/- 15.88 s during and after the electrical shock, and decreased afterward. Reduction of cytochrome aa3 began 3.04 +/- 0.51 s after the electrical shock, and this was reoxygenated at 171.88 +/- 12.95 s after the shock.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:The cerebral hemodynamic response to electrically induced seizures in man. 775 84

A 19-year-old woman presented with severe carbon monoxide poisoning resulting in coma, brain stem signs, cerebellar syndrome, anterograde memory disorder and some frontal signs. Nine years later, generalized seizures appeared. At the age of 31, the cerebellar syndrome and memory disorders persisted. MRI showed cerebellar and internal temporal atrophy with high-intensity signals, and hippocampal and callosal atrophy. SPECT (Xe133) showed a low cerebellar blood flow.
 ...
PMID:[Cerebellar syndrome after carbon monoxide poisoning. Magnetic resonance imaging and single photon emission tomography]. 799 44

Although preischemic hyperglycemia is known to aggravate damage due to transient ischemia, it is a matter of controversy whether or not this is a result of the exaggerated acidosis. It has recently been reported that although tissue acidosis of a comparable severity could be induced in normoglycemic dogs by an excessive rise in arterial CO2 tension, short-term functional recovery was improved, rather than compromised. In the present experiments we induced excessive hypercapnia (PaCO2, approximately 300 mm Hg) in normoglycemic rats before inducing forebrain ischemia of 10-min duration. This reduced the brain extracellular pH to values normally encountered in hyperglycemic rats subjected to ischemia. The events induced by hypercapnia clearly enhanced ischemic brain damage, as assessed histologically after 7 days of recovery. We hypothesize that the decisive event was an exaggerated decrease in extra- and intracellular pH and that the results thus demonstrate an adverse effect of acidosis. However, since postischemic seizures did not occur in the hypercapnic ischemic rats, the results also demonstrate that changes in intra-extracellular pH and bicarbonate concentrations modulated ischemic damage in an unexpected way.
 ...
PMID:Acidosis induced by hypercapnia exaggerates ischemic brain damage. 811 21

The imidazobenzodiazepine 6-(2-bromophenyl)-8-fluoro-4H-imidazo-[1,5-a] [1,4]benzodiazepine-3-carboxamide (imidazenil) is a new anxiolytic and anticonvulsant ligand of the benzodiazepine recognition site that possesses the characteristics of a partial allosteric modulator of the gamma-aminobutyric acid (GABA) type A receptor. The effects of imidazenil on GABAA receptor function were examined both in vitro and in vivo. Imidazenil inhibited [3H] flumazenil binding to mouse cerebral cortical membranes in vitro with an IC50 of 0.9 nM, showing that this compound binds with high affinity to benzodiazepine receptors. However, imidazenil failed to modify t-[35S]butylbicyclophosphorothionate ([35S]TBPS) binding to washed or unwashed mouse cortical membrane preparations. Furthermore, imidazenil injected i.p. into mice failed to affect [35S]TBPS binding subsequently measured in unwashed cortical membranes. In contrast, imidazenil reduced in a dose-dependent manner the increase in [35S]TBPS binding elicited by isoniazid (200 mg/kg s.c.), an effect mimicked by lorazepam and abecarnil++ but not by bretazenil. As expected, i.p. administration of lorazepam or abecarnil induced within 30 min a marked reduction in [35S]TBPS binding subsequently measured in unwashed cortical membranes of control mice. Moreover, imidazenil at a dose as low as 0.05 mg/kg (i.p.) delayed the onset of convulsions and death elicited by isoniazid and reduced significantly the number of mice exhibiting seizures. Accordingly, imidazenil also showed great potency in antagonizing the convulsions induced by pentylenetetrazole in rats. Imidazenil also completely abolished the increase in [35S]TBPS binding induced by foot-shock or exposure to carbon dioxide. Finally, imidazenil antagonized both in vitro and in vivo the effects of bretazenil or lorazepam on GABAA receptor function.
 ...
PMID:Imidazenil, a new partial agonist of benzodiazepine receptors, reverses the inhibitory action of isoniazid and stress on gamma-aminobutyric acidA receptor function. 816 38

Carbon monoxide causes one third of all poisoning deaths in Denmark, but is probably grossly underdiagnosed. We present a case where an elderly couple was admitted on several occasions to local hospitals with a variety of symptoms and signs; e.g. flu-like symptoms, generalized seizures, polycythaemia, chest pain, and ventricular tachycardia. The correct diagnosis, carbon monoxide poisoning, was made when the dog in the family was found dead; examination of the natural gas boiler revealed sooting, clogging of the flue, and a carbon monoxide concentration above 0.2 percent. The natural gas boiler had not been checked after installation five years earlier. Natural gas installations are becoming still more prevalent in Danish homes, but present regulations regarding the installations are apparently not yet able to prevent new incidents of carbon monoxide poisoning.
 ...
PMID:[Carbon monoxide poisoning due to lack of maintenance of a natural gas boiler]. 829 26

Human status epilepticus (SE) is consistently associated with cognitive problems, and with widespread neuronal necrosis in hippocampus and other brain regions. In animal models, convulsive SE causes extensive neuronal necrosis. Nonconvulsive SE in adult animals also leads to widespread neuronal necrosis in vulnerable regions, although lesions develop more slowly than they would in the presence of convulsions or anoxia. In very young rats, nonconvulsive normoxic SE spares hippocampal pyramidal cells, but other types of neurons may not show the same resistance, and inhibition of brain growth, DNA and protein synthesis, and of myelin formation and of synaptogenesis may lead to altered brain development. Lesions induced by SE may be epileptogenic by leading to misdirected regeneration. In SE, glutamate, aspartate, and acetylcholine play major roles as excitatory neurotransmitters, and GABA is the dominant inhibitory neurotransmitter. GABA metabolism in substantia nigra (SN) plays a key role in seizure arrest. When seizures stop, a major increase in GABA synthesis is seen in SN postictally. GABA synthesis in SN may fail in SE. Extrasynaptic factors may also play an important role in seizure spread and in maintaining SE. Glial immaturity, increased electronic coupling, and SN immaturity facilitate SE development in the immature brain. Major increases in cerebral blood flow (CBF) protect the brain in early SE, but CBF falls in late SE as blood pressure falters. At the same time, large increases in cerebral metabolic rate for glucose and oxygen continue throughout SE. Adenosine triphosphate (ATP) depletion and lactate accumulation are associated with hypermetabolic neuronal necrosis. Excitotoxic mechanisms mediated by both N-methyl-D-aspartate (NMDA) and non-NMDA glutamate receptors open ionic channels permeable to calcium and play a major role in neuronal injury from SE. Hypoxia, systemic lactic acidosis, CO2 narcosis, hyperkalemia, hypoglycemia, shock, cardiac arrhythmias, pulmonary edema, acute renal tubular necrosis, high output failure, aspiration pneumonia, hyperpyrexia, blood leukocytosis and CSF pleocytosis are common and potentially serious complications of SE. Our improved understanding of the pathophysiology of brain damage in SE should lead to further improvement in treatment and outcome.
 ...
PMID:Pathophysiological mechanisms of brain damage from status epilepticus. 838 2

Intracellular pH and ammonium ion concentration are potent modulators of cerebral amino acid metabolism. Furthermore, intracellular acidosis and hyperammonemia accompany conditions such as ischemic encephalopathy and seizures and may contribute to the pathological sequelae observed. In vivo NMR spectroscopy permits multiple, non-destructive measurements of important cerebral metabolic intermediates in the same animal. We describe here the use of 1H, and 31P NMR spectroscopy to investigate the effects of acute changes in intracellular pH and ammonium ions on cerebral glutamate, glutamine, and lactate levels in vivo. We then show how 1H NMR can be used to indirectly follow the flow of 13C label from [1-13C] glucose into the cerebral glutamate pool, allowing us to measure cerebral TCA activity in normal and chronically hyperammonemic rats. Male Sprague-Dawley rats (160-210 gm), fasted 24-hours, were tracheotomized, paralyzed and ventilated on 30% O2/70% N2O. NMR spectroscopy was performed at a field strength of 8.4 Tesla using a Bruker AM-360 wide bore spectrometer. An elliptical surface-coil (8 x 12 mm) was double-tuned to either the 1H and 31P or 1H and 13C frequencies. After retraction of extracranial tissues, the coil was positioned over the skull 2 mm posterior to the bregma. Tail arteries and veins were cannulated allowing periodic measurements of PO2, pCO2, pH and glucose in arterial blood and intravenous infusions. Respiratory acidosis was induced in rats by the addition of CO2 to the ventilation gas mixture. Arterial pCO2 increased within 5 min from a pre-hypercarbic value of 36.4 +/- 6.1 mm Hg to 200-220 mm Hg and was maintained at this level for over 1 hour. Hypercarbia led to rapid cerebral acidification. Intracellular pH decreased from 7.18 +/- 0.08 (pre-hypercarbic period) to 6.68 +/- 0.06 (n = 4) at 10 min and remained stable throughout the NMR observation period. Glutamate decreased to 53 +/- 4% of control after 60 min of hypercarbia, while glutamine increased to 126 +/- 7% of control. Acute hyperammonemia was produced by a programmed intravenous infusion of 250 mM ammonium acetate, which rapidly raised and maintained the concentration of ammonium ions in the blood at approximately 500 microM. Shortly after the start of the infusion (10-20 min), the levels of glutamine and lactate rose continuously throughout the experiment, reaching levels of 170 +/- 25% and 260 +/- 60% of control, respectively (n = 12) after 50 min. Glutamate decreased during the same time interval to 80 +/- 4% of control (n = 12).(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Cerebral metabolic studies in vivo by combined 1H/31P and 1H/13C NMR spectroscopic methods. 842 59


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