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

Caffeine lengthens ECT seizures, perhaps by lowering the convulsive threshold. The authors assessed the impact of caffeine on the convulsive threshold and seizure duration. The convulsive threshold and seizure durations of 12 inpatients receiving right unilateral ECT were determined with and without caffeine pretreatment. Caffeine did not change the convulsive threshold, but it did lengthen seizure duration. Caffeine's lengthening of seizure duration without affecting the convulsive threshold is an uncertain benefit in right unilateral ECT.
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PMID:A reappraisal of the role of caffeine in ECT. 809 53

Thirty patients with major depressive disorder of melancholic subtype were randomly allocated to receive ECT either twice or thrice a week. Double-blind ratings on the Hamilton Scale for Depression and Clinical Global impression showed no differences in the outcome through 4 weeks of trial as well as at 6-month follow-up. Cumulative seizure duration was higher in the thrice weekly group but not significantly so in spite of having received a significantly greater number of ECTs. The results indicate that ECT given thrice a week conferred no advantage over ECT given twice a week.
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PMID:Twice versus thrice weekly ECT in melancholia: a double-blind prospective comparison. 850 27

Traditionally it has been thought that a grand mal seizure is both necessary and sufficient for the maximum efficacy of ECT. Recent important research, however, has demonstrated that both the electrical dosage above the seizure threshold, i.e. the suprathreshold dosage, and the electrode placement (unilateral or bilateral) determine the efficacy of this treatment, as well as the degree of cognitive impairment. This article reviews the development of these significant concepts and suggests specific practical recommendations for incorporating these into contemporary ECT practice.
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PMID:Fitting the treatment to the patient: recent advances in the practice of electroconvulsive therapy. 857 53

The neural basis underlying the cognitive side effects of ECT is unknown. Recent studies suggest that the memory dysfunction may be caused by alterations in hippocampal synaptic efficacy [20]. In situ hybridisation was used to examine the possible receptor mechanisms responsible for this effect. Repeated ECS markedly increased mRNA expression for the GluR1 subunit of the AMPA receptor, but not the NMDAR1A-G subtypes of the NMDA receptor, relative to control treatments. This effect was present 24 h after the last seizure and may be responsible for the expression of the ECS-induced increase in synaptic efficacy.
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PMID:Repeated ECS induces GluR1 mRNA but not NMDAR1A-G mRNA in the rat hippocampus. 871 76

The goal of this paper is to draw conclusions about the usefulness of the standard EEG in psychiatry. In general, two thirds of psychiatric referrals for an EEG are expected to provide useful information. The emphasis in schizophrenia is placed on left-sided abnormalities, especially on the left temporal area. In mood disorders the emphasis is on right-sided foci, in addition to the controversial 6/sec spike and wave complexes, small sharp spikes and positive spikes. In the acute stage of alcoholism, a relationship is seen between the degree of intoxication and the amount of slow activity, while in the chronic stage an increase in slow activity is seen, but another change is fast activity on the temporal areas. During withdrawal a low seizure threshold can be seen as irregular bilateral spike and wave complexes. During abstinence 2-4 yr may be required before slow wave sleep is normal in all regards. Among the organic mental syndromes, delirium shows slow activity, except in delirium tremens, which often is associated with a normal record with fast activity. In dementia the prevalence of EEG abnormalities is related to the degree of impairment. After five sessions of ECT diffuse slow waves are often seen. In other conditions, among developmental disorders about one half of autistic children show abnormalities and epileptiform activity is not uncommon. Mild nonspecific abnormalities are seen in about 40% of dyslexics and also in behavior disorders. Anxiety disorders include anorexia nervosa, showing abnormal background activity related to the effect of starvation on cerebral metabolism. In panic attacks paroxysmal activity can be seen. In borderline personality positive spikes have been (again) associated with impulsivity and 6/sec spike and wave complexes with interpersonal problems. Of the drugs of abuse psilocybin and phencyclidine are often associated with generalized epileptiform patterns and with marijuana the alpha shows a decreased frequency with increased amplitude. Typically, an increase in slow activity is seen with psychotropic drugs if there is a change in the level of awareness. Finally, distinctive personality traits are, at times, seen in temporal lobe epilepsy and the phenomenon of "forced normalization" may appear when seizures stop and psychotic symptoms appear.
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PMID:A review of the usefulness of the standard EEG in psychiatry. 871

Lithium (Li) has often been compared to ECT in therapeutic spectrum and mechanism. Inhibition of inositol monophosphatase and reduction of brain inositol are major mechanisms of Li action. Many Li effects in animals and humans are reversible by inositol. We therefore studied interactions of ECS and inositol. ECS in rats did not reduce brain inositol monophosphatase activity or brain inositol levels. Intracerebroventricular injection of 10 mg inositol, a dose that reverses Li effects, had no effect on seizure length or post-ictal length.
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PMID:Lack of effect of ECS on rat brain inositol monophosphatase activity and inositol levels and of i.c.v. inositol on ictal and post-ictal length. 873 65

Extreme obstruction of ECT seizure induction occurred in an elderly female with a low cardiac ejection fraction after a 20 to 25 s interval between the last ventilation and the electrical stimulus. Stimuli of 378 and 504 mC induced no motoric or EEG activity after an initial stimulus of 227 mC produced just 1 s of motoric seizure activity. After prolonged hyperventilation and immediate stimulation a seizure resulted with 33 s of motoric activity. This case suggests that patients with a low cardiac output might be particularly sensitive to the quality of ventilation.
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PMID:Obstruction of ECT seizure by submaximal hyperventilation: a case report. 874 47

Ictal EEG indices show promise for separating individual ECT seizures on the basis of treatment electrode placement (ELPL), relative stimulus intensity (Dose), and expected therapeutic response. One factor impeding the effective clinical implementation of ictal EEG indices for these purposes is uncertainty as to the relative utility of lower and higher frequency EEG activity. Recent articles are contradictory in this regard, but no data exist addressing this issue. As a result, we reanalyzed data from 44 subjects in two studies and compared the relative ability of ictal EEG data in three frequency bands to differentiate seizures as a function of ELPL, Dose, and therapeutic response. We found that the frequency band that best differentiated these groups depended on the EEG measure used, the temporal portion of the seizure, and whether ELPL, Dose, or therapeutic response was being compared.
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PMID:The relative ability of three ictal EEG frequency bands to differentiate ECT seizures on the basis of electrode placement, stimulus intensity, and therapeutic response. 877 48

Electrically induced seizures with anesthesia and muscle relaxation (ECT) is commonly used in the therapy of psychotic depression in humans. Unmodified electroshock (ECS) is used as a model for epilepsy in the rat. In several seizure models of epilepsy, in particular the dentate hilar somatostatin-containing (SSergic) neurons have been found to undergo degeneration. To assess the potential loss of SSergic hilar neurons after repeated ECS, 10 rats were given 110 ECS, one per day, 5 days a week. One day after the last ECS the rats were anesthesized, perfused, the brains cut on a vibratome and prepared for nonradioactive in situ hybridization for somatostatin along with five control rats. Like rats given 10-36 ECS in earlier studies, the ECS-treated rats displayed a markedly increased neuronal hybridization labeling when compared with control rats. The total number of dentate hilar SSergic neurons of each rat was estimated using the optical disector technique. The mean number of hilar SSergic neurons in the ECS-treated rats was 12,785, compared to 12,392 in the control rats. The total number of hilar SSergic neurons in ECS-treated versus control rats was not significantly different (Student's t test; t value = .35; p = .74). We conclude that repeated ECS treatment does not cause loss of hilar SSergic neurons.
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PMID:No loss of hippocampal hilar somatostatinergic neurons after repeated electroconvulsive shock: a combined stereological and in situ hybridization study. 878 Aug 55

ENM is an etiologically heterogeneous disorder clinically evident as brief (less than 500 msec) lapses of tonic muscular contraction which seems to be related to lesions or dysfunction of different anatomofunctional levels of the CNS (Fig. 13). ENM can occur in heterogeneous epileptic disorders, ranging from benign syndromic conditions (such as BECTS) to focal static lesional epilepsy, as in neuronal migration disorders, and even to severe static or progressive myoclonic encephalopathies (PMEs). Neurophysiological studies in patients with ENM lead to the following conclusions: 1. A cortical origin of ENM is supported by EEG mapping and dipole analysis of spikes related to the ENM. In particular, our data suggest that the focal spike is a paroxysmal event involving, primarily or secondarily, the centroparietal and frontal "supplementary" motor areas. 2. A cortical inhibitory active mechanism for the genesis of ENM is supported by the occurrence of a decreased motor response to TMS, with preserved spinal excitability as demonstrated by the persistence of F waves. A "cortical motor outflow inhibition" related to spike-and-wave discharges was suggested by Gloor in his Lennox lecture (34). The cortical reflex negative myoclonus, described by Shibasaki et al. (16) in PME, is also consistent with a cortical active inhibitory mechanism. The spike associated with ENM raises new issues about the definition of "interictal" versus "ictal" EEG paroxysmal activity. A single spike on the EEG can be clinically silent (therefore, "interictal") or clinically evident as ENM (then viewed as "ictal"), depending on whether a given group of muscles is at rest or is showing tonic activity (see Fig. 4). These data, from a more general perspective, imply that the motor manifestation related to EEG paroxysmal events can depend not only on amplitude, topography, or intracortical distribution of seizure activity (35), but also on plasticity (36) and on the functional condition of the motor system (37). The variability of latency between the spike and the onset of the muscular inhibition (ranging from 15 to 50 msec, for the upper limbs), and the variability of duration of the ENM itself (from 50 to 400, or more, msec) indicate that ENM could be the result of inhibitory phenomena arising not only from a single cortical "inhibitory" area, but also from subcortical and pontine structures, as discussed by Mori et al. (this volume). The neurophysiological distinction between ENM and postmyoclonic periods of muscular suppression, mainly related to an EGG slow wave, as described by Lance and Adams (2) in the postanoxic action myoclonus is still a matter of discussion (38, 39). This is also the case for other movement disorders combining action myoclonus and epilepsy-as described in Ramsay Hunt syndrome (30), now better referred to as Unverricht-Lundborg syndrome (40) (Fig. 14). In these conditions, myoclonia and muscular silent periods are inconstantly associated with paroxysmal EEG discharges, suggesting a possible thalamocortical mechanism rather than a purely cortical one. In the most prolonged muscular inhibitions, both cortical and thalamocortical mechanisms might be implicated. Clearly, our knowledge of ENM is still very limited and gaining further insights into this complex phenomenon is a challenging problem.
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PMID:Epileptic negative myoclonus. 884 69


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