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

The role of physiological changes occurring during prolonged seizures in the causation of epileptic brain damage has been investigated experimentally in baboons and rats. Prolonged drug-induced myoclonic seizure activity is associated with initial arterial hypertension and subsequent hypotension, increased venous pressure, early hyperglycaemia and subsequent hypoglycaemia, variable arterial hypoxia and lactacidosis, and hyperpyrexia. Cerebral metabolic rate for oxygen and glucose is increased 2--3 fold throughout prolonged seizures provided the physiological status of the animal is well maintained. Ischaemic neuronal change is found after seizures lasting 1.5--7 hours, involving the small neurones of the third cortical lamina, Purkinje and basket cells in the cerebellum, and pyramidal neurons in the endfolium and Sommer sector of the hippocampus. Muscular paralysis and artificial ventilation minimise late physiological changes such as arterial hypotension and hyperpyrexia, and protect against cerebellar damage, but only slightly against neocortical and hippocampal damage. When arterial hypotension, hypoxia or hypoglycaemia lead to a reduction in the intensity of seizure discharge in paralysed, ventilated rats, there is also a reduction in hippocampal and neocortical damage. Factors intimately related to the intensity and duration of the neuronal discharge are responsible for neocortical and hippocampal lesions.
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PMID:Physiological changes during prolonged seizures and epileptic brain damage. 58 96

Studies were carried out to determine the effect of high oxygen pressure (OHP) on brain and blood glucose. OHP increased cerebral glucose in mice killed at various stages of oxygen toxicity. This included times which corresponded to 75% and 100% of the CT50, the hyperactive state, and at seizure onset. Blood glucose also was increased but only when mice were exposed to oxygen for times which produced stress-related responses. These were at 100% of the CT50,during hyperactivity, and at the onset of seizures. The increase in cerebral glucose was due to the increased oxygen pressure and not to the pressure per se. Adrenalectomy blocked the oxygen-induced increase in blood glucose but not in cerebral glucose. Disulfiram, an effective oxygen protectant, markedly increased both brain and blood glucose.
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PMID:Cerebral and blood glucose in central oxygen poisoning. 63 77

The clinical, laboratorial and radiological features of a 3-month-old child with neurocutaneous melanosis are described. The patient was born with multiple disseminated benign cutaneous nevi, proven by skin-biopsy, and presented with drug-resistant seizures and psycho-motor retardation. Serial cerebrospinal fluid studies showed high protein and low glucose levels, with pleocytosis and malignant cells in the fluid. Pneumoencephalogram showed mild non-obstructive hydrocephalus. Immunological studies showed normal immunological activity at three months of age and very poor activity at one year. The patient died at 16 months of age, after the sudden onset of intracranial hypertension and meningeal signs. Immunotherapy and chemotherapy were suggested but not accepted by the family. Some comments are made based on this and other 43 cases described in the literature; the value of laboratory studies in detecting malignant transformaiton in the meninges in patients with benign skin nevi is stressed.
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PMID:[Neurocutaneous melanosis. Report of a case]. 65

Glucose and insulin injections both decrease seizure susceptibility in C57BL/6J mice subjected to audiogenic priming at 16 days of age and tested at 21 days of age. These data support an hypothesis of defect in immediately available energy reserves in brains of audiogenic seizure prone mice.
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PMID:Time course of protection from audiogenic seizures by glucose and insulin in audiogenically primed C57BL/6J mice. 67 68

Anatomical structures demonstrating increased glucose uptake during the various stages of amygdaloid kindling in rats were identified by the 14C-2-deoxyglucose (DG) autoradiographic technique. Partial (stages 1 and 2) seizures were correlated with increased DG uptake in the ipsilateral amygdala and its direct projection fields. The appearance of generalized motor (stages 3,4, and 5) seizures was accompanied by less limbic involvement and recruitment of a bilateral system including substantia nigra, specific and nonspecific thalamic nuclei, globus pallidus, and neocortex. Increased hippocampal DG uptake was correlated with prolonged amygdaloid after discharge duration but not with the behavioral seizure stage. This study does not reveal which of these structures are responsible for the observed behavioral and electrical events and which are activated by them. It does suggest, however, that three discrete anatomical systems underlie the generation of partial seizures, generalized motor seizures, and local after discharge.
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PMID:Anatomical correlates of electrical and behavioral events related to amygdaloid kindling. 67 19

Autoradiography with [14C]deoxyglucose was used to study the architectural pattern of glucose utilization in the motor cortex of rats during focal penicillin seizures. The seizure focus was characterized by a well circumscribed area whose metabolic activity was increased 2-3 times normal. This was tightly surrounded by cortex that was normal or slightly depressed. The posterior third of the focus showed an increase in glucose utilization in a columnar pattern with particular accentuation of activity in lamina V. There was a loss of normal activity in lamina IV within the focus and in somatosensory and occipital cortex far behind the focus. This depression was particularly prominent in the ipsilateral barrel field. Increased metabolic activity was found in a small area in contralateral homotopic cortex, in lamina Vb with columns extending above this from lamina IV to the surface. Glucose utilization was accentuated 1.2-1.8 fold in the ipsilateral secondary somatosensory area, but was normal in the contralateral cortex. The intensity of focal seizures was increased by the intracortical injection of more penicillin or by giving intravenous metrazol. Both of these methods resulted in an increase in the size of the focus as determined with [14C]deoxyglucose. This was most prominent on the lateral border in lamina I-II and V. In addition, there was an accentuation of the columnar pattern in the posterior part of the focus, ipsilateral somatosensory cortex, and contralateral motor cortex. The architectural pattern of glucose utilization in the cortex during focal seizures is discussed with reference to corticocortical, commissural, and corticothalamic circuits that have been identified by others in anatomical studies. Superimposed on this structure are physiological principles of recurrent excitation, lateral spread, and surround inhibition that characterize basic electrophysiological mechanisms of epilepsy, and influence the intensity of activity within the architectural design.
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PMID:Use of cortical circuits during focal penicillin seizures: an autoradiographic study with [14C]deoxyglucose. 67 86

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

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

Seizures in the neonatal period are usually concomitants of serious neurological disease. The convulsive phenomena take certain distinctive and often subtle forms because of the status of the neuroanatomical and neurophysiological development of the neonatal brain. The predominant etiological process is hypoxic-ischemic encephalopathy, but intracranial hemorrhage, intracranial infection, development defects and metabolic disorders are also responsible for a considerable proportion of cases. Prognosis is related primarily to the neurological disease that underlies the seizures. Treatment may be specific for the underlying disorder, e.g., glucose, calcium, magnesium, pyridoxine, but whatever the cause, urgent control of the convulsions is important because they may have deleterious consequences. Phenobarbital is the single, most important anticonvulsant in the management of neonatal seizures.
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PMID:Management of neonatal seizures. 83

A dramatic decrease in mortality from Hemophilus influenzae meningitis has occurred in recent years. Morbidity and long-term sequellae remain significant problems. A follow-up investigation of 73 cases of H. influenzae meningitis seen over a three-year period revealed: 2 deaths, 6 children with major sequellae (retardation, spastic quadriplegia, blindness, persistent seizure disorder), 10 with minor residua, and 55 with no detectable disability. Statistical analysis of clinical parameters demonstrated a significant risk of death or major morbidity in those patients who, at the time of admission, had seizures, coma, hypothermia, shock, age less than 12 months, hemoglobin less than 11 gm/100 ml, pretreatment symptoms for longer than three days, a spinal fluid white blood cell count less than 1,000/cu mm, or a spinal fluid glucose value less than 20 mg/100 ml. Using these parameters, those patients at highest risk of having lasting major morbidity with H. influenzae meningitis can be predicted, allowing more vigorous intensive care which may reduce the mortality and morbidity further.
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PMID:Prediction of morbidity in Hemophilus influenzae meningitis. 84 May 37


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