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)

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.
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PMID:Phenytoin, electric, ionic, and metabolic responses in cortex and spinal cord. 19 41

The effect of experimentally induced generalized seizures on the relations between the various phases of sleep in the wakefulness--sleep cycle was studied in cats with chronically implanted electrodes. After generalized convulsions induced by electrical stimulation of the dorsal hippocampus, unlike those of amygdalar origin, clearly defined changes were observed in the structure of the wakefulness--sleep cycle. In the postseizure period, with increasing wakefulness sharp depression of paradoxical sleep takes place. However, in slow wave sleep only slight changes were observed. Instead of a rebound phenomenon, paradoxical sleep was sharply induced in cats after preliminary deprivation of paradoxical sleep as a result of generalized seizures induced by electrical stimulation of the neocortex. Nonspecific hyperactivation of the brain, in the form of epileptiform discharges, thus has a particularly marked effect on the structure of paradoxical sleep.
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PMID:Effect of experimentally induced generalized seizures on the wakefulness--sleep cycle. 21 49

A 62-year-old woman developed neurologic deficits 7 months after pulmonary lobectomy for alveolar cell carcinoma of the lung. CT scan of the head demonstrated two metastases with marked peritumoral edema. Administration of Decadron, chemotherapy and 3,000 rad cranial radiation resulted in dramatic improvement of dysphasia and right hand paresis. Almost 2 months later, rhythmic, involuntary movements of the left hand developed. There was progression to multifocal seizures, grand mal seizures, postictal depression, status epilepticus, and coma, with death 9 days after onset of the movement disorder. Bronchoalveolar carcinoma was widely disseminated in lungs and bones, and as three metastases in brain. Bland "ischemic" necrosis in a pseudolaminar pattern was present in the neocortex. Innumerable Cowdry type A intranuclear inclusion bodies were seen in neurons, astrocytes, and oligodenodroglia. Immunofluorescence demonstrated Herpes simplex virus type 2 antigen and electron microscopy revealed virions with the morphology of the Herpes group. The case is significant for (1) the concurrence of intracranial metastases and Herpes simplex encephalitis, and (2) the causal agent, Herpes simplex virus type 2. The implication for the clinical neurocientist is the potential in a patient with systemic cancer, for the causation of neurologic complications by more than one factor or mechanism.
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PMID:Herpes simplex type 2 encephalitis concurrent with known cerebral metastases. 22 22

Spreading depression (SD) elicited in the cerebral cortex of anaesthetized rats does not penetrate into epileptic foci (penicillin) or cortical regions subjected to repetitive electrical stimulation (6--10 Hz, 0.05--0.01 msec). The extent of the SD block, monitored by the absence of the slow potential change and preservation of spontaneous and evoked EEG activity, can be varied in certain limits by changing the stimulus parameters. When the diameter of the block in the parietal cortex is reduced at a time when its temporal boundary is circumvented by an SD wave, propagating in the rostral direction, a strip of cortical tissue between the block and sagittal sulcus is opened for SD which spreads through this route from the frontal to the occipital cortex and starts reverberating around the block. Other methods for eliciting SD reverberation employ removal of an additional block in a section of the circular pathway and directionally biased propagation around the stimulation point. SD reverberation lasting for at least 3 cycles was observed 109 times (median number of completed cycles 5.2, average cycle duration 4.4 +/- 0.1 min). It is suggested that SD reverberation around an epileptic focus can account for slow oscillations of ictal and interictal discharge and for recurrent seizures.
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PMID:Circulation of cortical spreading depression around electrically stimulated areas and epileptic foci in the neocortex of rats. 22 11

Steroid hormones, i.e., corticosteroids, estrogens, androgens and progestogens are formed in the adrenal cortex, male gonads, and the female placenta. Relatively little is known of their influence on behavior and their neuroendocrine function. On the cellular level, the rate of increase of RNA message to produce albumen and avidin is directly proportionate to the presence of steroids and their amount. Corticosteroid receptors are found in the thymus, liver, spleen and heart. The brain has receptors both for the corticosteroids and the sex hormones. These receptors are scattered throughout different regions of the brain, but the synthetic glucocorticoid dexamethasome is found only in the pituitary which accounts for its role in stopping the secretion of ACTH. Testosterone undergoes metabolic changes in the brain, affecting behavior. The A chain undergoes an enzyme reduction to 5aDHT and androstandiol. Following enzyme changes, the A chain of male testosterone can become female estradiol. Laboratory tests prove that sexual behavior in males is affected only by those androgens that can convert to estrogens, while in females it is dependent on the conversion of testosterone to estrogen. Lately psychiatrists have become very interested in the catechol estrogens, fairly new metabolites of estradiol which are produced in the hypothalamus and contain 2 hydroxyl groups (as compared with the 1 hydroxyl in estrogens). Catechol estrogens block estradiol receptors, behaving like antiestrogens. Researchers are investigating the possibility of signaling the desired neural messages without the concomitant effects that estrogen produces, through using catechol estrogens. They are examining this natural derivative of estradiol which may affect among others: sexual behavior, maturity, depression, migraines, and epileptic seizures.
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PMID:[Steroid hormones and the activity of the central nervous system]. 38 16

The pharmacology and pharmacokinetics of clonidine and the symptoms and treatment of acute clinidine overdosage are reviewed. Clonidine, a relatively safe and effective antihypertensive agent when used at therapeutic dosages, reduces blood pressure through a centrally mediated reduction in vasomotor tone. The primary symptoms of clonidine overdosage are central nervous system depression, bradycardia, hypotension, miosis, hypotonia, respiratory depression and possibly seizures. Gastric lavage followed by administration of activated charcoal is used to decrease absorption following acute oral ingestion. Intravenous fluid therapy and dopamine infusion are recommended for severe hypotension, and atropine sulfate is used to manage persistent bradycardia. Treatment of hypotension with alpha-adrenergic blocking agents (e.g., tolazoline) is not recommended unless patients fail to respond to dopamine infusion and administration of i.v. fluids.
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PMID:Clonidine overdose: a review. 38 42

The clinical and electroencephalographic (EEG) effects of sodium valproate were studied in four patients by means of serial 24-hour EEG recordings and simultaneous hourly determinations of serum drug concentrations. The patients all had frequent clinical seizures and generalized spike-wave discharges. Valproate appeared to reduce diurnal paroxysmal discharges (PD) and clinical seizures, but the effect on nocturnal PD was less marked. The extent and duration of the depression of PD and seizures varied. Altering the distribution of the total daily dose may change the pattern of clinical seizures and PD. Valproate concentrations fluctuated widely over 24 hours, and the significance of single estimations often cited in the literature appears dubious. Peak serum concentrations above 100 micrograms per milliliter may be necessary in some patients to achieve clinical and EEG improvement.
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PMID:Sodium valproate: serial monitoring of EEG and serum levels. 38 50

Two cannabinoids, delta9-tetrahydrocannabinol and cannabidiol, and several reference drugs were compared relative to their effects in a recently developed anticonvulsant test system, the after-discharge potentials of the visually evoked response; the potentials were recorded electrophysiologically from electrodes permanently mounted over the visual cortices of conscious rats. In anticonvulsant doses, trimethadione and ethosuximide produced an extensive depression of after-discharge activity, whereas diphenylhydantoin and cannabidiol exerted no such effect. In contrast, anticonvulsant doses of delta9-tetrahydrocannabinol and subconvulsant doses of pentylenetetrazol markedly increased after-discharge activity, which may represent a manifestation of their central nervous system excitatory properties. The data from the present study support our previously published ovservations from several other anticonvulsant tests that indicate the anticonvulsant characteristics of cannabidiol resemble those of diphenylhydantoin rather than those of trimethadione and that the central excitatory properties of delta9-tetrahydrocannabinol distinguish it from cannabidiol. The results consistently suggest that the cannabinoids will be effective against grand mal but not absence seizures.
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PMID:Influence of delta9-tetrahydrocannabinol and cannabidiol on photically evoked after-discharge potentials. 40 6

The possibility that epileptic seizures and classic migraine episodes may occur in the same patient is discussed. The probable relationship between the neurophysiological mechanisms which underlie both types of attacks has not yet been agreed upon. The case of a young man who suffered from classic migraine and who presented two convulsive epileptic attacks, preceded by visual aura is described. The EEG showed an epileptogenic occipito-temporal focus which corresponded to the region of the scotoma origin. A possible connection between scotoma in migraine and epileptic discharge is discussed. It is proposed that spreading depression, as the basis of the migraine prodomata, was preceded by a moment of intense neuronal excitation which changed the epileptic intercritical activity into a critical one.
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PMID:Possible interference between migrainous and epileptic mechanisms in intercalated attacks. Case report. 45 90

Seven infants developed mepivacaine intoxication secondary to accidental injection during paracervical or pudental blocks or both. All presented with unexplained neonatal depression at birth, tonic seizures (often with apnea) within six hours, and characteristic neurologic findings. Twenty-four-hour urinary excretion produced 12.7 to 37.4 mg, exchange transfusions less than 1.02 to 3.5 mg, and gastric drainage or lavage or both 0.63 to 1.26 mg of mepivacaine. Thus promotion of urinary excretion is the treatment of choice. All six survivors are seizure free and neurologically and developmentally normal at one to 4 1/2 years. With early diagnosis and prevention of severe perinatal hypoxia, the prognosis from intoxication alone is very good.
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PMID:Diagnosis, treatment, and follow-up of neonatal mepivacaine intoxication secondary to paracervical and pudendal blocks during labor. 46 77


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