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)

To define the time course of the metabolic acidosis that follows a single grand-mal seizure, we obtained serial blood samples from eight consecutive patients. Immediately after a seizure, the mean (+/- S.E.M.) venous lactate concentration was 12.7 +/- 1.0 meq per liter, the mean carbon dioxide content 17.1 +/- 1.1 mmol per liter, and the mean arterial pH 7.14 +/- 0.06. Sixty minutes later their values were 6.6 +/- 0.7 meq per liter (P less than 0.005), 23.6 +/- 1.1 mmol per liter (P less than 0.005) and 7.38 +/- 0.04 (P less than 0.005) respectively. The spontaneous resolution of the acidosis was due, in large part, to the metabolism of lactate and to the concomitant removal of hydrogen ion. There was no change in the serum potassium concentration, despite the development of a severe systemic acidemia and the subsequent return to normal of the pH. We suggest that the patient with seizures may serve as a unique model of lactic acidosis.
 ...
PMID:Natural history of lactic acidosis after grand-mal seizures. A model for the study of an anion-gap acidosis not associated with hyperkalemia. 1 2

Paroxysmal activity in ventral roots induced by penicillin in decapitate cat spinal cords is associated with waves of depolarization of primary afferent fiber terminals. These paroxysmal depolarizations can be detected as spontaneously occurring negative dorsal root potentials (DRPs) and are associated with antidromic discharge of nerve impulses in dorsal root fibers; they can also be detected by testing the excitability of afferent nerve terminals by focal stimulation. Negative DRPs evoked by afferent nerve volleys are altered in waveform but not in amplitude during seizures induced by penicillin, although they are blocked by the administration of picrotoxin. While blocking afferent-evoked DRPs, picrotoxin does not interfere with paroxysmal DRP'S, INDICATING DIFFERENCES IN THE GENERATION OF THE Two phenomena, which nevertheless have some link in common, for the paroxysmal waves occlude the evoked DRP. Such occlusion would appear as blockade, if DRPs were recorded by condenser-coupled amplifiers. In the presence of pentobarbital penicillin suppresses evoked DRPs, but under such circumstances seizure activity is not observed. Extracellular potassium activity within spinal gray matter transiently increases during seizure activity. Such increments of potassium activity are maximal in the ventral horns. This and several other observations suggest that in decapitate spinal cords systemically administered penicillin induces seizures which originate in the ventral gray matter. Accumulation of excess potassium may be the cause of paroxysmal depolarization of afferent nerve terminals. Excess potassium while not playing a principal role in initiating seizures, may influence the course of seizures by depolarizing afferent terminals. Such depolarization probably enhances tonic background release of transmitter substance, may modify the effect of synaptic input, and may favor synchronization of waves of neural excitability through extrasynaptic mechanisms.
 ...
PMID:Functions of primary afferents and responses of extracellular K+ during spinal epileptiform seizures. 6 Feb 13

70 chronic alcoholics in the withdrawal state, 45 with convulsions and 25 controls without convulsive seizures, were tested with respect to electrolyte changes and acid base balance in serum or blood and cerebrospinal fluid (CSF). It was of special interest to note that there was a partial independence between magnesium levels in serum and CSF. Thus the serum level has only a limited liability as to magnesium depletion suggested to be responsible for seizure precipitation. In the seizure group a slightly but significantly lower magnesium, potassium and calcium in CSF and a significant decrease of potassium and calcium in serum were revealed. In the nonzeizure controls a similar decrease of magnesium in serum and potassium in CSF was observed while serum potassium and calcium in CSF and serum remained in low normal range. In both groups there was a prominent respiratory alkalosis. The role of magnesium depression for seizure precipitation is discussed with respect to the concomitant changes of other electrolytes and acid base disturbances.
 ...
PMID:Electrolyte changes and acid base balance after alcohol withdrawal, with special reference to rum fits and magnesium depletion. 6 5

Extracellular potassium activity (ak) and field potentials (fp) were measured in the nucleus ventro-postero-lateralis (VPL) thalami in order to assess the extent of thalamic participation in cortical seizure activity. Small increases (up to 0.7 mmole/l) or decreases (up to 0.2 mmole/l) in ak were induced by electrical stimulation of the contralateral forepaw. These changes in ak were spatially more limited than the simultaneously recorded fp. Similar observations were made during weak electrical stimulation of the somatosensory cortex and during interictal spikes in a cortical penicillin focus. Large and widespread increases in ak to levels of 11.6 mmoles/l and slow negative fps of 8 mV accompanied seizure generation either in a cortical penicillin focus or during intense repetitive electrical stimulation of the cortical surface. Subsequent to such increases ak fell to subnormal levels. The amplitudes and durations of such undershoots were correlated with the amplitudes of the preceding increases in ak. Sometimes thalamic seizures ceases before cortical epileptic episodes. This resulted in a decrease of cortical EEG amplitudes. After ablation of the sensorimotor cortex seizures in forepaw-VPL could be induced by stimulation of the somatosensory cortex. These results further support the conclusion that specific thalamic nuclei participate in seizure generation and may serve as a subcortical route of seizure spread.
 ...
PMID:Stimulus induced and seizure related changes in extracellular potassium concentration in cat thalamus (VPL). 9 Jun 3

Neuronal and potassium activities (ak) were measured in the nucleus ventro-posterolateralis thalami (VPL) during propagated epileptiform activity from the somatosensory cortex of cats. Seizures were induced by repetitive electrical stimulation of the cortical surface or by topical application of penicillin. The recruitment of VPL into a seizure resulted in large increases of ak to levels of up to 11.6 mmoles/l, accompanied by increased in neuronal discharge rate to 300/sec. Sometimes the rise in ak preceded active participation of a given thalamo-cortical relay (TCR) neuron in the seizure. After reaching a peak level, ak and neuronal discharge rate slowly declined during an ictal episode. After cessation of seizures all TCR neurons were inhibited, while ak fell to subnormal levels. The duration of these postictal depressions increased with the amplitude of preceding increases and subsequent undershoots in ak and could last up to 120 sec. During decay and undershoot in ak, relay capability of TCR neurons was reduced. Also the probability that action potentials elicited in intracortical endings of TCR cells would antidromically invade their cell bodies was decreased. The duration of these periods varied with the amplitude of undershoot in ak. Seizure threshold was increased during undershoots. These observations are consistent with a long-lasting postictal hyperpolarization of neuronal membranes. The hyperpolarization may be caused by the action of an electrogenic pump, which is probably involved in termination of seizure discharge.
 ...
PMID:Relation between extracellular potassium concentration and neuronal activities in cat thalamus (VPL) during projection of cortical epileptiform discharge. 9 Jun 4

In thin hippocampal slices, paroxysmal epileptiform discharge was generated in high potassium medium. Removal of chloride from the high potassium medium caused explosive potentiation of the paroxysmal discharge and emergence of clonic relapsing discharges. Evolution of the paroxysm to regenerative seizure was attributed to the reduction of inhibitory postsynaptic potentials.
 ...
PMID:Possible explanation for interictal-ictal transition: evolution of epileptiform activity in hippocampal slice by chloride depletion. 10 Mar 40

Clinical studies indicate that early epilepsy after injury may be associated with some transient and reversible pathophysical processes of the brain. It has been proposed that epileptogenesis in the neocortex and hippocampus may be related to potassium ion accumulation in extracellular spaces. To investigate this hypothesis, we measured [K+]0 using potassium-sensitive microelectrodes in the sensorimotor cortex of cats during early seizures induced by trauma. The [K+]0 increases associated with seizure activity ranged from 14.6 to 25.1 mM, and these were significantly higher than those unassociated with spikes or seizure discharges. Moreover, high K+ solutions (15 mM or more) directly applied to the cortex produced spiking and seizures. These results seem to support the hypothesis that accumulation of [K+]0 is related to development of early epilepsy.
 ...
PMID:The role of extracellular potassium in early epilepsy. 12 51

We measured simultaneously the oxidative metabolic activity, monitored as the tissue fluorescence attribute to intramitochondrial NADH, the extracellular potassium level with ion-selective microelectrodes, and the focal extracellular electrical potential, of one site in intact cerebral cortex of cats. When the cerebral was stimulated by trains of repeated electric pulses applied either directly to its surface or to an afferent pathway, the corrected cortical fluorescence (F-R) declined indicating oxidation of NADH, the activity of extracellular potassium [K+]o increased, and the extracellular potential (Vec) shifted in the negative direction. When mild to moderate stimuli not exceeding 10-15 sec in duration were used, a 3-fold correlation was found between these three variables. The regression of F-R over either Vec, or over log [K+]o had a positive ordinal intercept. The results are in agreement with earlier suggestions 4,24,25,43,45,46 that (a) much but not all the oxidative metabolic response of cortex to electrical stimulation is expended in restoring disturbed ion balance; and (b) that sustained shifts of potential (SP) in response to repetitive electrical stimulation are generated by glia cells depolarized by excess potassium. The magnitude of SP shifts associated with a given elevation of [k+]o are smaller in cerebral cortex than in spinal cord48,49. The correlation of F-R with [K+]o breaks down when pathologic processes of either seizure activity or spreading depression set in. During paroxysmal activity [K+]o tends to remain confined below 10-12 mM, a level observed in non-convulsing cortex as well, but oxidation of NADH progresses beyond that seen in non-convulsing cortex as well, but oxidation of NADH progresses beyond that seen in non-convulsing tissue. This observation is hard to reconcile with the suggestion that excess potassium is a factor in the generation of seizures, at least of the type observed in this study. When [K+]o levels exceeded 10-12 mM, spreading depression invariably followed at least under the unanesthetized condition in these experiments. During spreading depression [K+]o levels rose to exceed 30 mM, sometimes 80 mM. NADH was oxidized during spreading depression to a level comparable to that seen in seizures. The observations are compatible with the suggestion13 that spreading depression occurs whenever the release of potassium into extracellular fluid is overloading its clearance therefrom.
 ...
PMID:Responses of electrical potential, potassium levels, and oxidative metabolic activity of the cerebral neocortex of cats. 16 65

Reviewed is the author's investigation of potassium in extracellular fluid of cerebral neocortex and spinal cord determined with ion-selective microelectrodes, and of oxidative metabolism monitored by fluorometric determination of intramitochondrial NADH in intact cortex. When gray matter is excited by afferent input, or by direct electrical stimulation, the logarithm of the rise of extracellular potassium concentration ([K+]0), the sustained shift of electrical potential, and the response of oxidative metabolism are linearly correlated. However, during seizures and during spreading depression, the correlation is broken, suggesting that the demand for oxidative energy exceeds that corresponding to the elevation of [K+]0. There exists a critical concentration of [K+]0 at which spreading depression inevitably erupts (12 mM for cat cerveau isole), but no such critical level could be detected for seizures. The rate of clearance of excess potassium from extracellular fluid is slower for high concentrations than for low; this rate is further slowed by the administration of phenobarbital, and possibly also of diphenylhydantoin. Changes of membrane potential of glia cells in the mammalian spinal cord can adequately be described by the Nernst equation.
 ...
PMID:Potassium, neuroglia, and oxidative metabolism in central gray matter. 17 18

Post-tetanic potentiation (PTP) of monosynaptic reflex was estimated in spinal cords in the drug-free state after the administration of a convulsant dose of penicillin and after the administration of phenytoin. There was no apparent correlation between the degree of depression of PTP and the efficacy of controlling seizure activity by phenytoin. Extracellular potassium levels were measured with ion-selective microelectrodes. The post-stimulation clearing of [K+]0 was not accelerated by phenytoin, and frequently it was slowed. Post-stimulus undershooting of [K+]0 was diminished. Oxidation of NADH in cortex and of cytochrome a, a3 in spinal cord were measured by optical methods. Stimulus-evoked transient oxidation responses evoked by electrical stimulation were depressed by phenytoin. It is concluded that systemic administration of phenytoin in therapeutic doses does not stimulate Na+-K+-activated membrane ATPase in cortex and spinal cord. Unlike other depressants, phenytoin did not cause a reduction of "resting" redox levels of respiratory enzymes. The local regulation of blood flow remained unaltered after phenytoin administration. Phenytoin caused a moderate but consistent depression of the stimulus-evoked responses of potassium activity, electric potential, and oxidative enzymes, consistent with diminished outflow of potassium from cells, owing either to lesser activation of cells or to a lesser exchange of ions.
 ...
PMID:Phenytoin, electric, ionic, and metabolic responses in cortex and spinal cord. 19 41


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