Biomedical subjects

C W Bazil

Publications and source records attributed to C W Bazil.

15 recordsLinked to original sources

PubMed1999

Seizures in the life and works of Edgar Allan Poe.

Edgar Allan Poe, one of the most celebrated of American storytellers, lived through and wrote descriptions of episodic unconsciousness, confusion, and paranoia. These symptoms have been attributed to alcohol or drug abuse but also could represent complex partial seizures, prolonged postictal states, or postictal psychosis. Complex partial seizures were not well described in Poe's time, which could explain a misdiagnosis. Alternatively, he may have suffered from complex partial epilepsy that was complicated or caused by substance abuse. Even today, persons who have epilepsy are mistaken for substance abusers and occasionally are arrested during postictal confusional states. Poe was able to use creative genius and experiences from illness to create memorable tales and poignant poems.

Diagnosis, Differential↗

PubMed1998

Advances in the medical treatment of epilepsy.

Treatment options for epilepsy, especially using antiepileptic drugs, have increased substantially in the past five years. Since 1993, four novel antiepileptic drugs have been approved and marketed in the United States: felbamate, gabapentin, lamotrigine, and topiramate. Two others, tiagabine and vigabatrin, are likely to be approved in the near future. For many patients, these agents offer the realistic promise of improved seizure control, often with fewer adverse effects and less significant drug interactions compared with older agents. In addition, fosphenytoin, a water-soluble phenytoin prodrug with a number of advantages over intravenous phenytoin, has been released. There are new administration options for carbamazepine, diazepam, and valproic acid. For drug-resistant or -intolerant patients, there has been renewed interest in alternative therapies, especially the ketogenic diet. Taken together, these represent significant therapeutic advances that are benefiting patients with epilepsy. At the same time, improved understanding of the basic mechanisms of epileptogenesis, and of the cellular and molecular actions of available antiepileptic drugs, creates a framework for designing unique therapeutic strategies that are targeted at key sites of vulnerability involved in the development and maintenance of the epileptic state.

Acetates↗

PubMed1997

The predictive value of intraoperative electrocorticography in resections for limbic epilepsy associated with mesial temporal sclerosis.

OBJECTIVE: Prior studies on the predictive value of intraoperative electrocorticography (ECoG) have been performed on heterogeneous groups of patients with both temporal and extratemporal interictal spikes, lesional and nonlesional pathological findings, and variably extensive resections by different surgeons. METHODS: We performed both pre- and postresection intraoperative ECoG on 29 consecutive patients with medial temporal lobe epilepsy (17 left-sided) who underwent standard nontailored resections by one surgeon (RRG). All patients had only temporal interictal spikes (six bitemporal) and mesial temporal sclerosis diagnosed by preoperative magnetic resonance imaging and confirmed by pathological examination of resected tissue. RESULTS: After a mean follow-up of 24.8 months, there were 15 (52%) patients who were seizure-free, 6 (21%) who were seizure-free except for auras, and 8 (28%) who had any seizure after the 1st postoperative month. Fourteen patients (48%) had active interictal discharges outside the area of planned resection revealed by preresection ECoG. Neither the presence of these spikes nor their mean frequency correlated with seizure outcome. Eleven patients (38%) had residual spike discharges after resection, and 18 patients (62%) had new spikes revealed by the postresection ECoG. Neither of these findings nor the mean spike frequency of residual or new spikes related to seizure outcome. Persistent spikes increased in frequency after resection in all outcome groups. CONCLUSIONS: Electrocorticographic monitoring of interictal epileptiform activity intraoperatively is not useful in the surgical treatment of patients undergoing standard resection for medial temporal lobe epilepsy with magnetic resonance imaging evidence of mesial temporal sclerosis.

Adolescent↗

PubMed1997

Effects of sleep and sleep stage on epileptic and nonepileptic seizures.

PURPOSE: Previous studies of patients with epilepsy and animal models of epilepsy suggest that sleep increases the frequency, duration, and secondary generalization of seizures. This information is, however, incomplete. METHODS: We retrospectively examined video-EEG monitoring reports from our comprehensive epilepsy center. We recorded seizure type, site of onset (for partial seizures), sleep state at onset, and whether partial seizures secondarily generalized. Seizures arising from sleep were then reviewed to determine sleep state. RESULTS: We analyzed 1,116 seizures in 188 patients. Thirty-five percent of complex partial seizures (CPSs) starting during sleep underwent secondary generalization compared with 18% in wakefulness (p < 0.0001). Frontal lobe CPSs secondarily generalized at equal rates during sleep (22%) and wakefulness (20%), but temporal lobe CPSs generalized much more frequently during sleep (45%) than in wakefulness (19%; p < 0.0001). Frontal lobe seizures were more likely to occur during sleep (37%) than were temporal lobe seizures (26%; p = 0.0068). CPSs were more frequent in stages 1 and 2 and occurred rarely during REM. Seizures starting during slow-wave sleep were significantly longer than seizures starting during wakefulness or stage 2 sleep. Psychogenic nonepileptic seizures (PNESs) were rare between midnight and 6 a m. and never occurred during sleep. CONCLUSIONS: Sleep has a pronounced effect on secondary generalization of partial seizures, especially those of temporal lobe origin. Frontal lobe seizures occur more often during sleep than do temporal lobe seizures, and occurrence during sleep helps to distinguish PNESs from CPSs.

Brain↗

PubMed1997

Recognition and classification of seizures in infants.

PURPOSE: We wished to assess the reliability of the International League Against Epilepsy (ILAE) seizure classification system applied to infantile seizures and to test a proposed new classification. METHODS: We first analyzed 39 seizures in 20 infants (aged 1-26 months) recorded with simultaneous closed-circuit television and EEG (CCTV/EEG). EEGs and videotapes of all seizures were independently analyzed by two epileptologists blinded to clinical histories. Videotapes of each seizure were reviewed without simultaneous EEG (phase 1), and printouts of ictal EEGs were assessed without behavioral correlates (phase II). The observers classified seizures according to ILAE criteria. Interrater agreement was assessed by the kappa statistic. RESULTS: Agreement on EEG features (phase II) was moderate (= 0.54) in identifying focal ictal onsets and substantial (= 0.79) in identifying generalized onsets. In contrast, analysis of videotapes showed substantial disagreement between observers in terms of classifying seizures as partial or generalized. Therefore, agreement between observers for partial was slight (= 0.14) and fair for generalized seizures (= 0.26). Similarly, conclusions of the observers as compared with those of a consensus panel were divergent for both partial (= 0.18) and generalized seizures (= 0.30). We therefore developed an alternative classification scheme and retested interrater agreement in a review of 50 seizures in 25 other infants. With this classification scheme, there was substantial agreement between observers (= 0.72). CONCLUSIONS: With clinical observations and interictal EEGs, seizures in infants cannot be reliably classified by current ILAE criteria. In contrast, a proposed new classification scheme based solely on semiology showed substantial reliability.

Age Factors↗

PubMed1996

Sphenoidal electrode insertion using topical anesthesia.

Sphenoidal electrodes are frequently used in epilepsy centers, but ins ertion can be painful. We used a topical anesthetic cream on patients (2.5% lodocaine, 2.5% prilocaine) before inserting electrodes and had patients rate their discomfort on an analogue pain scale. As a comparison, the same patients rated the pain caused by inserting a heparin lock. There was no significant difference between the pain of sphenoidal electrode insertion with use of topical anesthesia and that of heparin lock insertion. We suggest that when a topical anesthetic is used, the discomfort of inserting sphenoidal electrodes is minimal and comparable to that of inserting a heparin lock.

Administration, Cutaneous↗

PubMed1994

Migraine and epilepsy.

A relationship between epilepsy and migraine has been postulated for over a hundred years, but the nature of this interaction is still debated. This article reviews the physiologic arguments for a relationship between the two disorders. Specific clinical syndromes where epilepsy and migraine seem to be related are also discussed.

Brain↗

PubMed1989

Clinical concentrations of volatile anesthetics reduce depolarization-evoked release of [3H]norepinephrine, but not [3H]acetylcholine, from rat cerebral cortex.

We compared the potencies of halothane, enflurane, and methoxyflurane in producing unconsciousness in vivo and in inhibiting the release of [3H]norepinephrine and [3H]acetylcholine in vitro. Rats were anesthetized with various concentrations of each anesthetic, and responsiveness was determined by a hemostat tail pinch. Slices of cerebral cortex were equilibrated with similar concentrations of each agent in vitro, and potassium-evoked release of [3H]norepinephrine and [3H]acetylcholine was determined. For both studies, brain concentrations of the anesthetics were determined by heptane extraction and gas chromatography. Using this method, we found that brain concentrations of all three agents which caused unconsciousness in vivo also reduced depolarization-evoked release of [3H]norepinephrine by approximately 30% in vitro. The release of [3H]acetylcholine was unaffected by similar concentrations of these anesthetics. Such selective interference with stimulus-secretion coupling in central noradrenergic, and possibly other, neurons might contribute to the depressant actions of volatile anesthetics. The differential effects on norepinephrine and acetylcholine release also suggest differences in the mechanisms by which these two transmitters are released.

Acetylcholine↗

PubMed1989

Anaesthetic concentrations of enflurane and methoxyflurane in rat brain in-vivo and in-vitro.

We measured concentrations of enflurane and methoxyflurane in brains of anaesthetized rats and established conditions for reproducing these concentrations in brain tissue in-vitro. Despite a 12-fold difference in inspired potency, brain concentrations resulting in anaesthesia were similar for both compounds. However, substantially lower concentrations in the equilibrating gas were necessary to achieve similar tissue concentrations in-vitro, probably because anaesthetic-induced respiratory depression or changes in cardiac output causes incomplete equilibration in-vivo. These studies provide direct evidence that brain concentrations associated with anaesthesia are similar for anaesthetics with different inspired potencies. They also suggest that lower concentrations in the equilibrating gas should be used in-vitro to reproduce clinically relevant tissue concentrations that are necessary to cause anaesthesia in-vivo.

Anesthesia, General↗

PubMed1989

Effects of clinically effective concentrations of halothane on adrenergic and cholinergic synapses in rat brain in vitro.

The effects of clinically relevant concentrations of halothane on various synaptic events in rat brain were examined in vitro. Slices or membranes prepared from various brain regions were equilibrated with 1.25% halothane at 37 degrees C, resulting in tissue concentrations greater than those found in brains of completely anesthetized animals (greater than 40 nmol/mg of lipid). Under these conditions, no effects of halothane were observed on agonist or antagonist binding to alpha-1 adrenergic, beta adrenergic, alpha-2 adrenergic or muscarinic cholinergic receptors, or on the ability of 5'-guanylylimidodiphosphate to reduce agonist binding affinity. This concentration of halothane also had no effect on norepinephrine-stimulated cyclic AMP accumulation, or inositol phosphate accumulation in response to norepinephrine, carbachol, histamine or 5-hydroxytryptamine. Halothane did reduce potassium-evoked release of [3H]norepinephrine from slices of rat cerebral cortex although it did not affect potassium-evoked release of [3H]acetylcholine. These results suggest that halothane may be relatively specific in its synaptic actions and may affect depolarization-evoked release of norepinephrine at concentrations achieved clinically.

Acetylcholine↗

PubMed1987

Equilibration of halothane with brain tissue in vitro: comparison to brain concentrations during anesthesia.

A method was devised for reproducing anesthetic concentrations of halothane in slice and membrane preparations of rat brain in vitro. Rats were anesthetized with varying concentrations of halothane, responsiveness was tested, and brain halothane content was determined by heptane extraction and gas chromatography. The inspired concentration of halothane at which half of all animals were unresponsive was 1.05%. At 1.25% halothane, all animals were unresponsive and brain halothane was determined to be 41 +/- 1.3 nmol/mg lipid. No significant differences in halothane concentration between whole brain and a variety of brain regions were detected. To obtain similar concentrations in vitro, membranes or slices of cerebral cortex were incubated in Krebs-Ringer bicarbonate buffer (KRB) that had been preequilibrated with anesthetic. Halothane equilibrated rapidly with the buffer and the tissues. The partition coefficient between gas and KRB was found to be 0.78, and between brain slices and KRB approximately 12. Slightly lower gas concentrations were necessary in vitro than in vivo to obtain the same tissue levels of anesthetic. Using this method, it was shown that there was no effect of anesthetic concentrations of halothane on the uptake of [3H]norepinephrine or [3H]choline into slices of rat cerebral cortex.

Anesthesia↗

PubMed1986

An investigation of the low intrinsic activity of adenosine and its analogs at low affinity (A2) adenosine receptors in rat cerebral cortex.

The potencies and intrinsic activities of adenosine analogs for stimulating cyclic AMP accumulation in slices of rat cerebral cortex were examined. 5'-N-Ethylcarboxamidoadenosine (NECA) caused the greatest increase in cyclic AMP accumulation (19.2-fold). 2-Chloroadenosine (2-CAD) induced a similar increase, but adenosine and six other analogs caused much smaller increases. All agonists tested had similar potencies in activating this response. Inhibition of adenosine uptake with 10 microM dipyridamole did not affect the maximal response to any agonist, although the potency of adenosine was increased approximately threefold. Each analog was also able to block partially the stimulation of cyclic AMP accumulation caused by NECA. Levels of cyclic AMP accumulation in the presence of NECA plus another analog were similar to those observed when the analog alone was present, as expected for partial agonists. Furthermore, the EC50 value for R-(-)-N6(2-phenylisopropyl)adenosine in increasing cyclic AMP accumulation was similar to the KI value for inhibiting the response to NECA. The EC50 value for adenosine was substantially higher than the KI value for inhibiting the response to NECA; however, in the presence of dipyridamole, the two values were more closely correlated. The response to NECA was blocked by 8-phenyltheophylline, 1,3-diethyl-8-phenylxanthine, and 8-p-sulfophenyltheophylline, with KI values from 1 to 10 microM. The results suggest that adenosine analogs stimulate cyclic AMP accumulation in cerebral cortex through low-affinity receptors, but that some analogs only partially activate these receptors. Adenosine itself may also be a partial agonist, or its actions may be obscured by simultaneous activation of another receptor.

2-Chloroadenosine↗

PubMed1984

Caffeine injection raises brain tryptophan level, but does not stimulate the rate of serotonin synthesis in rat brain.

Acute caffeine injection (100 mg/kg) elevates brain levels of tryptophan (TRP), serotonin (5HT), and 5-hydroxyindoleacetic acid (5HIAA). Experiments were performed to determine if the increases in 5HT and 5HIAA result from a stimulation of the rate of 5HT synthesis. Both the rate of 5-hydroxytryptophan (5HTP) accumulation following NSD-1015 injection, and the rate of 3H-5-hydroxyindole synthesis from 3H-tryptophan were measured in vivo following caffeine administration and found to be normal. Tryptophan hydroxylase activity, as measured in vitro in brain homogenates, was also unaffected by caffeine. The results suggest that the elevations in brain 5HT and 5HIAA levels produced by caffeine do not reflect enhanced 5HT synthesis, despite significant elevations in brain TRP level. Some other mechanism(s) must therefore be responsible for these elevations in brain 5-hydroxyindole levels.

5-Hydroxytryptophan↗

PubMedDate not supplied

Recent advances in the pharmacotherapy of epilepsy.

The therapeutic options for the treatment of epilepsy have expanded during the 1990s. Since 1993, four novel agents (felbamate, gabapentin, lamotrigine, and topiramate) have been approved by the US Food and Drug Administration, primarily for adjunctive treatment of partial seizures. In addition, a water-soluble pro-drug of phenytoin, fosphenytoin, and a sustained-release preparation of carbamazepine have been introduced. The novel anticonvulsants represent a potential improvement for patients whose seizures are incompletely controlled or who experience significant adverse effects with older anticonvulsants. Felbamate, lamotrigine, and topiramate appear to have a broad spectrum of action in seizure control, but felbamate use is limited by the potential for serious adverse effects. Gabapentin, lamotrigine, and topiramate are all well tolerated. Gabapentin has no known drug interactions, whereas lamotrigine and topiramate have limited interactions compared with older agents. The sustained-release preparation of carbamazepine may decrease the incidence of adverse effects and increase patient compliance. Fosphenytoin offers a safer method for intravenous administration of phenytoin and the added flexibility of intramuscular administration. Taken together, these recent advances in treatment may bring about improved efficacy and decreased adverse effects for many patients with epilepsy.

Animals↗

PubMedDate not supplied

Provocation of nonepileptic seizures by suggestion in a general seizure population.

Nonepileptic seizures (NES) are common and are often diagnosed at epilepsy centers by video-EEG recording of both spontaneous and suggestion-induced episodes, but no study has evaluated provocative testing in a general seizure population. We studied consecutive patients with a tentative diagnosis of epilepsy using saline provocation during video-EEG recording, suggesting that this could produce a typical seizure. Of 52 patients, 40% had no response, 23% had responses unlike their seizures, and 37% had typical episodes (positive test). Patients whose usual episodes resembled complex partial seizures (CPS) were more likely to have NES than were patients with a history of generalized tonic-clonic seizures (GTC). Of patients with positive provocations, the primary physician predicted NES in 68% of cases. This preliminary study suggests that NES are frequent in a general neurology setting, and that saline provocation is a sensitive method of identifying NES.

Adult↗