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

A 12-year-old juvenile diabetic was inadvertently given 500 ml of hypertonic saline intravenously. He developed hypernatremia, hyperosmolality, metabolic acidosis, and hyperglycemia. Seizures and stupor ensued, followed by coma and death. Computerized cranial tomography revealed numerous small subcortical hemorrhages that were verified postmortem.
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PMID:Hypernatremic hemorrhagic encephalopathy. 47 54

Seizure susceptibility and GABA metabolism were altered in the substantia nigra [SN] of adult male Sprague Dawley rats when these animals were acclimating to an altered plasma osmolality. Changes in GABA metabolism were measured in vivo in SN of the freely moving rat. Suitable precautions were taken to avoid any post-mortem flux of glutamate to GABA and to correct for the underestimation of GABA build up in SN due to the finite diffusion rate of gamma-vinyl GABA [GVG] after stereotaxic injection of small amounts into one side of the brain. Control experiments provided evidence that changes in osmolality, within a normal physiological range, did not affect significantly gamma-aminobutyric acid transaminase [GABA-T]. Also kindling via the medial septum [MS], in the absence of electrical stimulation did not alter GABA metabolism in SN, thus providing a stable baseline for studies of osmotic effects. Hyperosmolality was associated with a rise in seizure thresholds, with a marked reduction of the rate of GABA synthesis in SN, and with a substantial increase in turnover time of the GABA pool. Hypoosmolality, of a degree known to be associated with mild cerebral edema and swelling localized to astrocytes, markedly reduced seizure threshold, and reduced GABA pool size in SN, but did not alter the rate of GABA synthesis significantly. These results demonstrate by new and independent means the relationship between GABA metabolism in the SN and seizure susceptibility in vivo.
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PMID:Alterations of GABA metabolism and seizure susceptibility in the substantia nigra of the kindled rat acclimating to changes in osmotic state. 178 28

Acute osmotic disturbances can lead to profound neurological problems, yet there has been little experimentation at a cellular level to assess if neurophysiological changes are induced by altered osmolality. Using extra- and intracellular recording in the rat neocortical slice preparation, we examined pyramidal neurons of layers II-III under changing osmotic conditions. Single cell properties, field potentials, synaptic transmission and epileptiform discharges were studied in control saline (295 mOsm) and compared with corresponding data collected during exposure to osmolalities between 245 and 375 mOsm. Single cell properties (resting membrane potential, cell input resistance, action potential threshold and duration) did not change significantly, but neuronal interactions were considerably influenced by osmotic change within minutes. Hyposmolality increased the amplitude of evoked field potentials and of excitatory postsynaptic potentials recorded intracellularly. Hyperosmolality, induced with mannitol, decreased these parameters. Electrotonic coupling, as gauged by the degree of dye coupling and by cell input resistance, was not influenced by shifts in osmolality. The clinical finding that overhydration promotes seizure onset was examined in slices made epileptogenic in Mg2(+)-free saline. Hyposmolality increased the frequency and decreased the duration of interictal bursts, whereas raising osmolality with mannitol had opposite effects. None of the aforementioned effects occurred when osmolality was increased with a freely permeable substance such as dimethylsulfoxide, nor could they be ascribed to changes in saline Na+ or Ca2+ concentrations. The results are consistent with hyposmotic solutions reducing extracellular space by causing cells to swell. Theoretically, during population discharge, this should both concentrate K+ released extracellularly and possibly increase field (ephaptic) interactions. How lowered osmolality strengthens spontaneous and evoked excitatory synaptic transmission in neocortex is not yet clear. However, it may be an important mechanism underlying the increased seizure susceptibility of patients and experimental animals with lowered plasma osmolality. Conversely, suppression of excitatory postsynaptic potentials by osmotically active substances may be involved in the lowered seizure susceptibility observed clinically.
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PMID:Osmotic effects upon excitability in rat neocortical slices. 227 Jan 33

We studied neonates with hyperosmolar syndrome using photo-evoked eyelid microvibration, a blink reflex elicited by photic stimuli. Patients with hyperosmolality showed disturbance of consciousness, convulsive seizures, hyperexcitability, and tachypnea. The latency of photo-evoked eyelid microvibration tended to be prolonged with an elevation of the plasma osmolality. Photo-evoked eyelid microvibration is believed to be a suitable method for monitoring brain disturbance due to hyperosmolality.
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PMID:Photo-evoked eyelid microvibration in neonates with hyperosmolality. 239 34

The schema in Table 1 illustrates the inter-relationship between the major fluid and electrolyte disturbances with their primary site of involvement, that is, the CNS or peripheral nervous system (PNS), their primary effect (nervous system depression or irritability), and the major symptom complex associated with these sites and mechanisms (obtundation, seizures, muscle weakness, and tetany). As can be seen, a pattern emerges. Disorders of sodium and osmolality, whether hypernatremia (hyperNa), hyponatremia (hypoNa), hyperosmolality (hyperOsm), or hypo-osmolality (hypoOsm), all produce CNS depression with encephalopathy as the major clinical manifestation. Disorders of potassium, whether hyperkalemia (hyperK) or hypokalemia (hypoK), produce PNS depression with muscle weakness as the major clinical manifestation. On the other hand, disorders of magnesium and calcemia produce both CNS and PNS manifestations. Hypercalcemia (hyperCa) and hypermagnesemia (hyperMg) produce CNS and PNS depression with encephalopathy and muscle weakness, respectively, being the major clinical manifestations. Hypocalcemia (hypoCa) and hypomagnesemia (hypoMg) produce CNS and PNS irritability with seizures and tetany, respectively, being the major clinical manifestations.
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PMID:Neurologic manifestations of fluid and electrolyte disturbances. 267 34

1. Focal electrographic seizures arose in the CA1 region of rat hippocampal slices bathed in elevated (8.5 mM) external potassium [( K+]o). High [K+]o also induced spontaneous interictal bursts that originated in area CA3 and propagated to CA1. To examine the contribution to electrographic seizure initiation of excitatory mechanisms that are influenced by extracellular volume, we studied the effect of hyperosmotic expansion of interstitial volume on seizure occurrence, interictal bursts, and excitatory synaptic transmission. The tissue electrical resistance was also measured leading up to and during seizures. 2. Media made 5-30 mosmol/kg hyperosmotic by addition of agents restricted to the extracellular space (mannitol, sucrose, raffinose, L-glucose, dextran) rapidly and reversibly abolished [K+]o-induced spontaneous CA1 seizures in 86% of slices tested. However, similar increases in osmolality effected by agents that access the intracellular compartment (D-glucose, glycerol) did not influence electrographic seizure occurrence. Hyperosmotic changes with plasma membrane impermeable compounds, but not permeable compounds, produced significant concentration-dependent decreases (1-10%) in the electrical resistance of CA1 stratum pyramidale. Because tissue resistance is proportional to extracellular volume, these results suggest that hyperosmotic suppression of electrographic seizures is associated with expansion of the extracellular space in hippocampal slices. 3. Measurement of electrical resistance of the CA1 stratum pyramidale during spreading depression and electrographic seizure revealed an increase in tissue resistance to 122% and 108% of control, respectively. Furthermore, a slight (approximately 2%) but significant increase in electrical resistance gradually occurred over the 20 s immediately preceding seizure generation. The observed increase in tissue resistance suggests extracellular space is decreased during these events. 4. Hyperosmolality did not alter CA3 interictal burst frequency. However, burst intensity, estimated from the total length of the burst waveform, was significantly reduced in both the CA3 (83% control) and CA1 region (67% control) when osmotic changes were imposed by plasma membrane impermeant compounds. Additionally, media made hypoosmotic by removal of 7.5 mM NaCl reversibly increased burst intensity. 5. High [K+]o potentiated excitatory synaptic transmission and excitatory postsynaptic potential (EPSP) spike coupling.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Role of extracellular space in hyperosmotic suppression of potassium-induced electrographic seizures. 272 35

In some unknown manner, water uptake by brain cells (hyposmolality) promotes generalized seizure in humans and experimental animals, whereas cell dehydration (hyperosmolality) protects against it. We have replicated both scenarios in slices of hippocampus undergoing electrographic seizures. Surprisingly, a shift in osmolality does not change the excitability of individual neurons but rather, it alters the degree to which neurons interact. Hyposmolality enhances both excitatory synaptic transmission in neocortex and field (ephaptic) effects, the latter arising when cortical cells fire as a population. We propose that these increased excitatory interactions promote the synchrony that characterizes epileptiform activity.
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PMID:Seizure susceptibility and the osmotic state. 279 Apr 71

Blood plasma hypo- or hyperosmolality alters significantly the concentration of some amino acids in brain tissues of the medial septum and hippocampus of adult Sprague-Dawley rats. With some notable exceptions, brain amino acid concentrations decreased under hypoosmotic conditions and increased under hyperosmotic conditions. Osmotic changes and brain amino acid changes appear to be related to each other in an almost linear fashion. A comparison of rats and toads indicates that the patterns of changes in brain amino acid concentrations in response to a hypoosmotic plasma osmolality were almost identical for both species. Changes achievable under hyperosmotic conditions were considerably greater in toads. When rats with kindled epileptogenic foci were made hypoosmotic by water-loading, seizure thresholds decreased dramatically. Our data suggest a possible relationship between the hypoosmotically induced biochemical changes in brain tissues (especially some amino acid neurotransmitters and neurotransmitter precursors) and the hypoosmotically induced increase in seizure susceptibility.
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PMID:Effect of altered blood plasma osmolalities on regional brain amino acid concentrations and focal seizure susceptibility in the rat. 309 Feb 5

In 21 patients, epilepsia partialis continua (EPC) was an early symptom of nonketotic hyperglycemia and occurred during an initial phase of hyponatremia and mild hyperosmolality. EPC persisted for an average of 8 days, and its duration correlated predominantly with the degree of hyponatremia. Depression of consciousness and cessation of seizures occurred with increasing severity of hyperglycemia and hyperosmolality. In 9 patients, EPC was the first symptom leading to the diagnosis of diabetes mellitus. Four patients died of serious associated illness. The majority of the patients had evidence of a localized structural cerebral lesion. Metabolic disturbances including hyperglycemia, mild hyperosmolality, hyponatremia, and lack of ketoacidosis contribute to the development of EPC in areas of focal cerebral damage.
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PMID:Epilepsia partialis continua associated with nonketotic hyperglycemia: clinical and biochemical profile of 21 patients. 677 82

Hyperosmolality complicating the management of burned patients has multiple etiologies. Sepsis, hyperglycemia, renal failure, electrolyte disturbances, shock, and substances absorbed from the burn wound may be contributing factors. Chemicals, such as propylene glycol, within bacteriostatic topicals may also lead to hyperosmolality. This report describes a patient who developed severe hyperosmolality after 5% Betadine-glycerin therapy for a 60% partial-thickness burn. Status epilepticus developed 36 hours later, and triglycerides were 9,700 mg/dl. After Betadine-glycerin was stopped the central nervous system status slowly improved but pre-seizure function was never regained.
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PMID:Hyperosmolality caused by percutaneously absorbed glycerin in a burned patient. 706 13


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