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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mechanism of action of hypoxia on cerebral blood vessels and its role in the regulation of the cerebral circulation were investigated in anesthetized cats. Arterial hypoxia produced marked cerebral arteriolar vasodilation, which was partially reversed by perfusing the space under the cranial window with artificial cerebrospinal fluid (CSF) containing 6-94% oxygen. More marked increase in the local supply of oxygen, via perfusion of the space under the cranial window with fluorocarbon FC-80 equilibrated with 100% oxygen, completely eliminated the vasodilation induced by arterial hypoxia. Fluorocarbon equilibrated with 100% N2 had no effect on the vasodilation. The vasodilation associated with hypotension was completely reversed by perfusion with fluorocarbon equilibrated with 100% oxygen and was unaffected by perfusion with fluorocarbon or CSF equilibrated with gas not containing oxygen. The vasodilation associated with Metrazole-induced seizures was partially reversed by perfusion with fluorocarbon containing oxygen. The results show that hypoxia dilated cerebral blood vessels entirely via a local mechanism, that hypoxia is the dominant mechanism involved in the vasodilation associated with hypotension, and that it is, at least partially, responsible for the vasodilation associated with seizures.
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PMID:Role of tissue hypoxia in local regulation of cerebral microcirculation. 64 24

A variety of autonomic blocking agents, general anesthetics, and anticonvulsants have been shown to offer protection from seizures caused by hyperbaric oxygen. Amino-oxyacetic acid (AOAA) has been shown to offer rats only minimal protection from such seizures. This study investigated whether AOAA protected cats and mice from hyperbaric-oxygen-induced seizures. Cats and mice were exposed to 100% oxygen at 5 ATA until seizures occurred or for a period of up to 60 min. Approximately half of the animals were pretreated with AOAA either 30 or 240 min before oxygen exposure. Results showed that the interval between exposure and grand mal seizures increased significantly in cats pretreated 30 or 240 min before exposure with 17 to 25 mg/kg AOAA; the number of cats remaining seizure-free for 60 min also increased markedly. However, mice received little protection even at doses up to 40 mg/kg. At higher doses the AOAA itself caused seizures even in the absence of hyperbaric oxygen.
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PMID:Protection against high-pressure oxygen seizures by amino-oxyacetic acid. 70 42

The possible role of systemic physiological changes (occurring secondarily during status epilepticus) in the causation of epileptic brain damage has been evaluated in rats. Animals were anaesthetized, paralysed and mechanically ventilated; sustained electrocortical seizure discharges were induced by the intravenous injection of bicuculline, 1.2 mg/kg. After two hours of seizure activity brains were fixed by perfusion for histology. Physiological variables were maintained within certain limits from the end of the initial seizure phase (approximate duration twenty minutes) until two hours after onset of seizure to provide six groups: (1) Standard: mean arterial pressure above 120 mmHg, no hypoxia or hypoglycaemia, rectal temperature close to 37 degrees C. (2) Moderate Hypotension: mean arterial pressure at 70-75 mmHg. (3) Severe Hypotension: mean arterial pressure at 50 mmHg. (4) Hypoxia: arterial oxygen tension at 50 mmHg. (5) Hypoglycaemia: non-fed animals, with blood glucose close to 3.0 mumol/g. (6) Hyperthermia: rectal temperature at 40 degrees C. Microvacuolation and ischaemic cell change were identified by light microscopy in scattered neurons in the cortex (principally in the outer layers) in animals in three groups (Standard, Severe Hypotension and Hyperthermia). Similar neuronal changes were seen in the hippocampus (predominantly in the h1 or Sommer sector) in the Standard and Hyperthermia Groups. It is tentatively proposed that neuronal damage in animals with unrestricted cerebral oxygen and glucose availability is due to oxidative mechanisms in cells with excessively enhanced neuronal activity and that lesions caused by failing energy production do not appear until severe degrees of hypoxia are reached.
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PMID:Epileptic brain damage: the role of systemic factors that modify cerebral energy metabolism. 73 25

Secondary metabolic encephalopathy is a diffuse disorder of the brain caused by an extracerebral process. Underlying causes include oxygen deprivation, systemic metabolic disease, and drug intoxication. Symptoms and signs usually suggest a generalized disturbance of brain function: alterations in the level of consciousness; diffuse and, occasionally, focal motor abnormalities; and seizures. Electroencephalography in most instances gives evidence of generalized neuronal disturbance. Early diagnosis is important because encephalopathy secondary to an extracerebral process is potentially reversible. Treatment is directed toward reversal or control of the underlying process, supportive care, and prevention of complications such as infection, electrolyte imbalance, and cerebral edema.
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PMID:Secondary metabolic encephalopathy. Diagnosis and treatment. 77 43

Coma and other neurologic abnormalities are present in patients with either diabetic ketoacidosis (DKA) or nonketotic coma (NKC), and the cause of such phenomena are not known. Patients with NKC also manifest seizures and focal neurologic changes. Treatment of diabetic coma with insulin may induce cerebral edema by as yet undefined mechanism(s). In patients with DKA, cerebral oxygen utilization is impaired, and there is hyperviscosity of the blood. A substantial part of the brain's energy source is derived from ketones, which in themselves can depress sensorium. Extracellular hyperosomolality is present, which may also contribute to the genesis of coma. In addition, most ketoacidotic patients have associated medical conditions, which may further impair consciousness. Biochemical changes in the brains of animals with DKA include impairment of both phosphofructokinase activity and pyruvate oxidation, and accumulation of citrate. The net effect upon sensorium in ketoacidotic patients probably represents the interaction of most of the above factors and differs markedly among individuals. Patients with NKC manifest not only depression of sensorium, but also focal motor seizures, hemiparesis, and other neurologic changes, such as aphasia, hypereflexia, sensory defects, autonomic changes, and brainstem dysfunction. Most of the aforementioned changes revert to normal after correction of hyperosomolality. Gamma amino butyric acid, which has been shown to elevate the seizure threshold, is normal in brains of ketoacidotic animals, but may be low in nonketotic coma. Also, hyperosomolality per se may produce seizures. Cerebral edema may complicate the treatment of either DKA or NKC. The available experimental evidence suggests that many of the commonly held theories for the production of such brain swelling probably do not occur. There is no breakdown of the sodium pump, sorbitol or fructose do not accumulate in brain, and brain glucose is only about 25 percent of that in plasma; Cerebral edema is probably produced largely by a direct action of insulin on brain at a time when plasma glucose is approaching normal values. Cerebral edema can thus theoretically be avoided by stopping insulin when plasma glucose has been lowered to values approaching normal.
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PMID:Neurologic manifestations of diabetic comas: correlation with biochemical alterations in the brain. 80 37

The knowledge that GABA is an inhibitory neurotransmitter substance in brain has spurred a prodigious research effort to implicate GABA in the etiology of seizures. Such an involvement for GABA can occur theoretically at either of two levels, at the level of its metabolism or at the level of its functioning. Convulsant agents such as picrotoxin and bicuculline appear to act by impairing the functioning of GABA at the postsynaptic receptor site, but virtually nothing is known about the attendant molecular events although a major expansion of knowledge in this area may be expected within the next decade. In contrast, a vast amount of data has accumulated with respect to changes in GABA metabolism induced by convulsant agents such as the hydrazines, hydrazides, and hyperbaric oxygen. The problem in this case lies in the interpretation of the data. Are the changes in GABA metabolism the cause of the seizures? There is clearly no simple relationship between seizure activity and any single parameter of GABA metabolism, be it the GABA content of the brain, or the rate of uptake of GABA by cellular components, or the activity of the GABA-synthesizing and degrading enzyme systems, GAD and GABA-T respectively. This finding may, however, be illusory since the parameters of GABA metabolism were in most cases measured using preparations from intact brain tissue. Observed changes in the parameters may not accurately reflect events at a critical subcellular location such as the synaptic cleft. Thus there may well be a simple relationship between the concentration of GABA in the synaptic cleft and seizure activity. Unfortunately the limitations of current technology preclude the testing of this possibility. The author has, however, developed an equation on an empirical basis which provides an excellent relationship between the excitable state of the brain and a function of GABA metabolism which incorporates both changes in GABA level and changes in GAD activity. This equation has been used successfully to explain and rationalize previously anomalous results with respect to changes in GABA metabolism associated with the action of both convulsant and anticonvulsant agents. The concept embodied in the equation is that the excitable state of brain is determined primarily by the rate of synthesis of GABA but that reflects changes in the concentration of GABA in the synaptic cleft has been suggested.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The role of gamma-aminobutyric acid in the mechanism of seizures. 83 81

The effect of thiopentone 0.5 and 1.0 mg/kg on the enflurane-induced cortical spike discharge has been examined. Seven cats were anaesthetized with enflurane in oxygen and ventilation was controlled to maintain eucapnia during e.e.g. recording. End-tidal enflurane concentrations of between 1.2 and 2.2% provoked dose-dependent spontaneous spike discharges reproducibly. It was found that, during light enflurane anaesthesia, intravenous thiopentone could exacerbate e.e.g. signs of seizure activity. However, at a greater depth of anaesthesia spike activity was suppressed. The e.e.g. changes following thiopentone resembled the effects of still greater concentrations of enflurane.
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PMID:The effect of thiopentone on enflurane-induced cortical seizures. 83 45

The electroretinogram (ERG) was measured in lightly anaesthetised rats exposed to 4-7 atm O2 until death. An initial increase and later decrease in amplitude with increase in latency was seen which, although not consistently related to the appearance of seizures characteristically seen above 4.5 atm 02, appeared closely linked to systemic factors. A fall in respiration rate always preceded the fall of the ERG, and apnoea preceded ERG extinction. When blood pressure and ERG were measured in two comparable groups of rats exposed to 5.76 atm O2, both records showed similar time courses. The cerebral visual evoked response (VER) was measured at 5.76 atm O2 simultaneously with the ERG. The later VER waves showed a degree of enhancement at the time of seizures, but otherwise amplitude and waveform were maintained until late in toxicity. EEG spiking gave the earliest indication of toxicity, and it is concluded that the primary projection to the rat visual cortex is comparatively resistant to high-pressure oxygen.
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PMID:Influence of systemic factors on hyperbaric oxygen toxicity in the rat visual system. 92 72

A longitudinal study of 1553 infants, designed to provide early indicators of gross developmental problems by using a behavioral assessment scale, included 12 infants who later died suddenly and unexpectedly. In a retrospective examination of neonatal records, considerable evidence of central nervous system damage was found. Anoxic conditions and even possible seizure activity were implicated. Abnormalities of muscle tonus, skin color and cry were found, together with some visual problems. These findings on behavioral assessment in the neonatal period appear to identify a population which is at greater risk of sudden death in infancy. The need for oxygen therapy as a high-risk indicator of sudden unexpected death has been reported in a previous study and is further substantiated by the present findings: they are also compatible with thos of Naeye (1973), who found long-term hypoxic conditions in autopsy studies on the sudden infant death syndrome. It is suggested that the possibility of central nervous system involvement in the aetiology of the sudden infant death syndrome should be more thoroughly investigated.
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PMID:Central nervous system damage as a possible component of unexpected deaths in infancy. 95 12

l-Propranolol was found to protect mice from hyperbaric oxygen-induced seizures. The disposition of effective doses of propranolol isomers in mice was followed using stereospecific antibodies with a radioimmunoassay procedure. Serum and tissue concentrations were determined and correlated with the protective effect. Following racemic administration, there were no differences in serum disposition of d- and l-propranolol, although there was initially a preferential uptake of the 1-isomer both into cardiac and brain tissue. The d-isomer exerted synergistic action on the 1-isomer protective effect.
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PMID:Disposition of propranolol isomers in mice. 99 31


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