Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Generalized tonic-clonic status epilepticus is a relatively common neurologic emergency. The differential diagnosis of this condition includes decerebrate spasms and hysterical seizures. Initial therapy includes establishing an airway and securing an intravenous line. Blood should be obtained for chemistries and anticonvulsant levels. Administration of anticonvulsants should not be delayed until laboratory results are obtained. Intravenous diazepam will usually stop continuous tonic-clonic seizure activity, but because of a rapid redistribution phase, it necessitates administration of a longer acting anticonvulsant such as phenytoin or phenobarbital. Intravenous phenytoin should be administered slowly at a dose of 15 mg/kg while carefully monitoring vital signs. Intravenous phenobarbital produces sedation and may cause respiratory depression. Occasionally, other anticonvulsants such as paraldehyde, lidocaine, and general anesthesia will be needed to break status epilepticus. Careful follow-up of the patient and monitoring of the anticonvulsant levels may prevent future bouts of status epilepticus.
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PMID:Current treatment of status epilepticus. 731 Mar 61

Flumazenil is a benzodiazepine receptor antagonist used to reverse sedation and respiratory depression induced by benzodiazepines. Seizures and cardiac arrhythmias have complicated its use in adult patients. Overdose patients who have coingested tricyclic antidepressants have a higher risk of these complications. Little information exists concerning adverse effects of flumazenil in children. We report the occurrence of a generalized tonic-clonic seizure in a pediatric patient following the administration of flumazenil.
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PMID:Seizure after flumazenil administration in a pediatric patient. 765 79

Although usually safe, retrobulbar anesthesia and peribulbar anesthesia have potentially sight- and life-threatening complications. Although it has been suggested that peribulbar anesthesia is as effective and safer than retrobulbar anesthesia, no large study has addressed the true rate of complications. To determine the efficacy and safety of peribulbar anesthesia, this study prospectively examined 16,224 consecutive peribulbar blocks. Twelve centers in the United States, Germany, and Chile participated in the study. After a peribulbar block was administered, the degree of akinesia, amaurosis, percentage of supplemental blocks required, and side effects and complications occurring after the block and for six weeks were recorded. Perioperative and late optic nerve complications were included. To approximate a real-life situation, ophthalmologists, anesthesiologists, and certified registered nurse anesthetists performed the blocks. Ninety-five percent of patients achieved a 95% or greater degree of akinesia. The incidence of complications in the consecutive cases was low. Orbital hemorrhage occurred in 12 cases (0.74%). There was one globe perforation (0.006%), two expulsive hemorrhages (0.013%), one grand mal seizure (0.006%), and no cases of cardiac or respiratory depression or deaths. Peribulbar is as effective as retrobulbar anesthesia and appears to lead to fewer sight- and life-threatening complications, even when slightly different peribulbar techniques are used. This is especially true when the anesthetic is administered with a 1 1/4-inch or shorter needle with the eye in the primary position, followed by ten to 15 minutes of ocular compression.
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PMID:Efficacy and complication rate of 16,224 consecutive peribulbar blocks. A prospective multicenter study. 772 98

Benign neonatal familial convulsions comprise a distinct epileptic syndrome with an autosomal mode of transmission. The electroclinical signs of seizures in this syndrome are not yet well defined. In 3 children from two families presenting with benign neonatal familial convulsions, 14 seizures were recorded during electroencephalographic (EEG)-video sessions. All seizures occurred during sleep, after a short arousal reaction. Seizures started with bilateral, symmetrical flattening of the EEG for 5 to 19 seconds; simultaneously there was apnea and tonic motor activity. The EEG flattening was followed by a long (1-2-minute) bilateral discharge of spikes and sharp waves; simultaneously, there were vocalizations, chewing, and focal or generalized clonic activity. The prominence of EEG and motor abnormalities varied between the left and the right from one seizure to the next in any given child. The seizures stopped without EEG or clinical postictal depression. These electroclinical observations suggest that the convulsions of benign neonatal familial convulsions are a form of generalized tonic-clonic seizure whose expression may be asymmetrical, probably because of the immaturity of the corpus callosum or other structures ensuring seizure synchronization.
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PMID:Electroclinical signs of benign neonatal familial convulsions. 825 May 33

The adverse stresses and injuries associated with epileptic seizures are prevented routinely when programmed, controlled grand mal seizures are administered. According to the described concepts of clinical benefit, symptoms of brain illnesses that are without substantial neuronal deterioration, but that have a sense of neurotransmitter dysregulation, are candidates for mitigation by administration of programmed seizures. Such symptoms include delirium, dementia, neuroleptic malignant syndrome, movement disorder, psychosis, and depression. Prior to recommending cortical excision for management of offtial complex epilepsy, a course of programmed seizures should be considered routinely.
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PMID:Seizure benefit: grand mal or grand bene? 844 67

Three methods of electroconvulsive therapy (ECT) were compared in respect of therapeutic effect in 69 attacks of endogenous depression in 65 patients, not previously treated by ECT during the actual period of illness. The treatments were given under barbiturate narcosis, with full muscular relaxation, administration of oxygen and electroencephalographic recording of the seizure discharge. In two methods grand mal seizures were evoked by supraliminal (A) and liminal stimulation (B), in the third (C) lidocaine (3 mg/kg i.v.) was given before the application of liminal stimulation. The seizure discharges in C were markedly shortened and their pattern modified, while between A and B the duration and pattern of the seizures were similar (Table 1). The patients were referred to the three treatments at random and the groups may be regarded as having a similar prognosis (Table 2-5, 7). The therapeutic outcome was estimated by rating several depressive symptoms according to a rating scale worked out for the purpose. The rating was performed before treatment, one week after the fourth treatment (a treatment pause was then made) and one week after the completed series. To obtain more reliable measures the scores for the various symptoms were added together to form a total score, which was then divided into a depression score and a retardation score, presumably measuring mainly depressive mood and psychomotor retardation. Differences in rating scores on two rating occasions were taken as measures of improvement. In addition, a global rating of improvement was made. The rating procedure was double blind. The principal results were: 1. After four treatments (three patients who recovered after three treatments included) the degree of improvement was in the rank order ABC with significant group differences for a few scores. After the completed series of treatments improvement in groups A and B did not differ significantly whereas in group C it was significantly smaller for some scores (Table 9). 2. The total number of treatments was significantly higher in group C than in group A and B, which did not differ significantly between themselves (Table 10). 3. A measure of therapeutic efficiency, improvement per treatment, was computed by dividing the degree of improvement as obtained from the differences in the combined scores and from the global score of improvement, by the number of treatments. After four treatments the improvement per treatment was highest in group A and lowest in group C, although in the comparisons AB and BC most differences did not reach significance. After the completed series the improvement per treatment did not differ significantly in groups A and B whereas in group C it was significantly less (Table 10). 4. In comparison with groups A and B, the total duration of seizure discharges was significantly shorter in group C both after four treatments and, in spite of the higher number of treatments, after the completed series. The improvement per second of seizure discharge was not significantly different in the groups although there was a tendency to a lower effect per second in group B (Table 11). It is concluded from these results that shortening of the seizure discharge decreases the therapeutic efficiency of ECT. Increase of the stimulus intensity, which apparently does not change the seizure discharge, possibly gives a more rapid therapeutic response but does not change the final degree of improvement or the number of treatments required to reach it. The depression-relieving effect of ECT is bound to seizure activity and not, or only slightly, to other effects of electrical stimulation.
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PMID:Experimental studies of the therapeutic action of electroconvulsive therapy in endogenous depression. The role of the electrical stimulation and of the seizure studied by variation of stimulus intensity and modification by lidocaine of seizure discharge. 887 6

We present the case of a 71-year-old female suffering from bipolar affective disorder type 2 and an old lacunar brain infarct who, under the combined treatment of fluoxetine for depression and low dose trazodone for the accompanying insomnia, developed a toxic delirium. The subject presented with mental state changes (confusion and agitation), hyperreflexia, diaphoresis, nausea, vomiting, fever, and a general tonic-clonic seizure which developed soon after an increase in the trazodone dose. One year prior to the above episode, she was hospitalized for a transient episode of agitated confusion while being treated with fluvoxamine for depression, alprazolam and brotazolam for the accompanying anxiety and insomnia. Both episodes subsided spontaneously when treatment was discontinued. This case reports the possible existence of increased vulnerability to hyperserotonergic states in elderly patients suffering from concomitant psychiatric and neurological disorders.
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PMID:Recurrent toxic delirium in a patient treated with SSRIs: is old age a risk factor? 923 73

It is now possible to develop a dynamic neuronal network model for generalized convulsive seizures because of in vivo data recently obtained in a naturally occurring epilepsy model--the genetically epilepsy-prone rats (GEPR-9s). GEPR-9s exhibit audiogenic seizures (AGS) that consist of a sequence of discrete behavioral phases (i.e., wild running, clonus-tonus, and post-ictal depression). The neuronal firing changes in most nuclei implicated in the network during each phase of AGS in behaving GEPR-9s have been examined. The inferior colliculus is critical in AGS initiation, because extensive firing increases in inferior colliculus are observed preceding seizure initiation. The deep layers of superior colliculus (DLSC) are crucial to wild running, based on the emergence of tonic firing of DLSC neurons just preceding this phase. The pontine reticular nucleus (PRF) and periaqueductal gray (PAG) are critical to the clonic-tonic phase, because tonic firing patterns appear in these neurons just prior to this phase. During post-ictal depression all areas except the PRF are quiescent. These temporal relationships suggest that each nucleus plays a specific hierarchic role in each discrete convulsive behavior. Generalized tonic-clonic seizure behavior observed in human epilepsy, in GEPR-9s, and in other seizure models is likely to involve similar neuronal network components. The neurotransmitter mechanisms subserving the abnormal neuronal responses in the GEPR-9 neuronal network involve an increased availability of glutamate and a decrease in the effectiveness of gamma-aminobutyric acid (GABA) in many brain regions. Focal modification of the effects of GABA, glutamate, norepinephrine, or serotonin also modulates the nuclei of the network differentially. Together, these data reveal the anatomic, neurotransmitter, and neurophysiologic mechanisms of the neuronal network hierarchy in GEPR-9s, which is currently the most completely developed of any generalized convulsive model. Differential effects of anticonvulsants on the AGS phases and concomitant differential modifications of neuronal firing are observed on neurons in these network nuclei. With nearly complete identification of the network nuclei, the differential effects of these anticonvulsant drugs on different aspects of neuronal firing in different brain sites indicate that this experimental approach can likely identify the most sensitive therapeutic target for these agents. This concept is potentially vital to developing the most selective treatment of different convulsive behaviors occurring in human epilepsy. The neuronal network for AGS does not require brain structures rostral to the midbrain for seizure expression. However, the forebrain is recruited into an expanded seizure network through AGS repetition ("kindling"), resulting in prolonged AGS, post-tonic clonus, and epileptiform electrographic cortical abnormalities. AGS kindling produces network expansion into medial geniculate body (MGB) and amygdala and involves neuronal firing increases in MGB.
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PMID:Neuronal networks in the genetically epilepsy-prone rat. 1051 23

Ramsay Hunt syndrome (RHS) is a rare condition within the progressive myoclonic epilepsies syndrome (PME), with a triad of action myoclonus, grand mal seizure and severe cerebellar ataxia. There are few reports about the psychiatric disturbances associated with PME or RHS. The present study examines the evidence that RHS may accompany an organic mental syndrome, ethanol's effective suppression of myoclonus, and the possible resultant problem of alcohol dependence in RHS patients. Two brothers with the previous long-standing diagnosis of RHS and their mental symptoms of persecutory delusion and depression are reported, as well as the additional problem of alcohol dependence in one of them. The cerebellar dysfunction found in RHS may be associated with an underlying organic condition. Determination of the relationship between cerebellar dysfunction and psychosis in RHS will require further study. Although the mechanism of the suppression of myoclonus by alcohol remains unclear, patients should be allowed to drink socially, and alcohol consumption should not be totally prohibited. However, effective treatment of the problems of alcohol tolerance, abuse, or dependence requires the cooperation of both neurologists and psychiatrists.
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PMID:Progressive myoclonic epilepsies syndrome (Ramsay Hunt syndrome) with mental disorder: report of two cases. 1059 82

Sustained inward currents in neuronal membranes underlie tonic-clonic seizure discharges and spreading depression (SD). It is not known whether these currents flow through abnormally operating physiological ion channels or through pathological pathways that are not normally present. We have now used the NEURON simulating environment of Hines, Moore, and Carnevale to model seizure discharges and SD. The geometry and electrotonic properties of the model neuron conformed to a hippocampal pyramidal cell. Voltage-controlled transient and persistent sodium currents (I(Na,T) and I(Na,P)), potassium currents (I(K,DR) and I(K,A)), and N-methyl-D-aspartate (NMDA) receptor-controlled currents (I(NMDA)), were inserted in the appropriate regions of the model cell. The neuron was surrounded by an interstitial space where extracellular potassium and sodium concentration ([K(+)](o) and [Na(+)](o)) could rise or fall. Changes in intra- and extracellular ion concentrations and the resulting shifts in the driving force for ionic currents were continuously computed based on the amount of current flowing through the membrane. A Na-K exchange pump operated to restore ion balances. In addition, extracellular potassium concentration, [K(+)](o), was also controlled by a "glial" uptake function. Parameters were chosen to resemble experimental data. As long as [K(+)](o) was kept within limits by the activity of the Na-K pump and the "glial" uptake, a depolarizing current pulse applied to the cell soma evoked repetitive firing that ceased when the stimulating current stopped. If, however, [K(+)](o) was allowed to rise, then a brief pulse provoked firing that outlasted the stimulus. At the termination of such a burst, the cell hyperpolarized and then slowly depolarized and another burst erupted without outside intervention. Such "clonic" bursting could continue indefinitely maintained by an interplay of the rise and fall of potassium and sodium concentrations with membrane currents and threshold levels. SD-like depolarization could be produced in two ways, 1) by a dendritic NMDA-controlled current. Glutamate was assumed to be released in response to rising [K(+)](o). And 2) by the persistent (i.e., slowly inactivating) Na-current, I(Na,P). When both I(NMDA) and I(Na,P) were present, the two acted synergistically. We conclude that epileptiform neuronal behavior and SD-like depolarization can be generated by the feedback of ion currents that change ion concentrations, which, in turn, influence ion currents and membrane potentials. The normal stability of brain function must depend on the efficient control of ion activities, especially that of [K(+)](o).
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PMID:Simulated seizures and spreading depression in a neuron model incorporating interstitial space and ion concentrations. 1089 22


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