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

Delirium tremens is linked with a chronic depression of the central nervous system by alcohol and a compensatory hyperactivity of neurotransmitters. A sudden stoppage of alcohol intake induces excessive production of these transmitters. Firstly appearing is a noradrenergic hyperactivity which may be responsible not only for reducing the magnesium blood level but also for activating the other transmitter systems. A magnesium blood level lower than 1 mmol.l-1 involves a risk of seizures and requires IV magnesium sulfate. Noradrenergic hyperactivity can be prevented by IV alcohol associated with sedation best achieved by IV clomethiazole in alcoholic solution. Should these preventive measures fail, noradrenaline action in the central nervous system can be blocked by clonidine. Should hallucinations become manifest, linked to dopaminergic hyperactivity, haloperidol is indicated. Benzodiazepines may be useful, particularly carbamazepine, for their depressing effect on gaba-ergic hyperactivity.
 ...
PMID:[Delirium tremens. Recent neurophysiologic concepts and therapeutic outlook]. 151 60

The influence of naloxone on the duration of the postictal depression was determined in 2 seizure models in the adult rats: hippocampal afterdischarges and maximal electroshock. For testing the intensity of postictal depression 2 subsequent stimulations were used. The interstimulation intervals were 3, 5, 10 and 60 min. Using interstimulation intervals 3, 5 and 10 min there was marked depression of the afterdischarge duration. Wet dog shakes accompanying hippocampal afterdischarges were suppressed only in 3- and 5-min intervals. Naioxone (1 mg/kg i.p.) abolished the suppression of afterdischarges when 10-min interstimulation interval was used. In maximal electroshock seizures where the duration of tonic flexion and extension was determined, no postictal depression was registered nor were any effects of naloxone present. The results suggest a limited role of the mu opioid receptor system in the late phases of postictal depression following hippocampal stimulation and different effects of the mu opioid system in tonic flexion/extension and behavioral depression induced by maximal electroshock.
 ...
PMID:Differential effects of naloxone on postictal depression. 152 27

The relation between depression and epilepsy was evaluated in 96 epileptic out-patients. We found that 50% of epileptic patients fulfilled the DSM-IIIR criteria for depression. The Hamilton Rating Scale for Depression, the Beck Self Depression Inventory and the Zung Anxiety Scale were also used in all patients. The patients with partial seizures with complex semiology (CPS) were more depressed than the patients with primary generalized epilepsy and with partial seizures with elementary semiology. A significant increase in the level of anxiety was also found in the group with CPS compared to the other two groups. No correlations were noted between severity of depression and duration of epilepsy, seizure frequency, socio-economic status, education, and family history of depressive illness. No relationship was observed between anticonvulsant drug levels and depression. We failed to confirm an association between side of epileptic lesion and severity of depression. We suggest that depression in epileptic patients does not represent a psychological reaction to a particular cognitive or physical impairment, but is in some way related to the type of epilepsy.
 ...
PMID:Interictal depression in epilepsy. 152 28

Spinal seizures evoked by sudden cooling (SSSC) were used to investigate the anticonvulsant activity of ketamine (KET) injected either intralymphatically (i.l., 5-40 mg/kg) or intrathecally (i.t., 0.5-1.0 mumol/20 microliters) using isolated spinal cord-hindleg preparation. KET inhibited the tonic phase and prolonged the clonic phase in a dose-dependent manner. The cionic phase was depressed or totally blocked at KET doses of 80-160 mg/kg, i.l. or 2 mumol/20 microliters, i.t. This depression was not prevented by i.t. administration of concanavalin A. The latency of onset of seizures was also increased by KET. KET abolishes the tonic-extensor phase of SSSC in which activation of N-methyl-D-aspartate-receptors may play a role.
 ...
PMID:Ketamine abolishes the tonic phase of the seizures evoked by sudden cooling of toad isolated spinal cords. 152 2

Paroxetine is a novel phenylpiperidine compound that acts as a selective serotonin reuptake inhibitor (SSRI). It is a more selective and potent SSRI than fluoxetine, sertraline, or fluvoxamine. Its pharmacokinetics are well suited to clinical use. Its half-life is approximately 24 hours, and it has no active metabolites. As with other SSRIs, there are few clinically significant drug interactions with paroxetine. Clinical studies consistently show that paroxetine alleviates moderate or severe depression and associated anxiety. It begins to act at least as rapidly as the tricyclic antidepressants. Animal data and limited human experience suggest relative safety in overdose and no evidence of teratogenicity. As with other SSRIs, the most common side effect of paroxetine is nausea, which is usually well tolerated. The nausea rarely leads to drug discontinuation or even dosage reduction. Little weight loss or weight gain occurs with paroxetine at doses used to treat depression, and the drug has no effect on the seizure threshold. Unlike other SSRIs, paroxetine has a relatively low incidence of anxiety and agitation. There is no evidence that paroxetine increases suicidal ideation. This supplement will contribute several important new papers to the literature on paroxetine.
 ...
PMID:An overview of paroxetine. 153 19

Depressive symptoms are common in medically ill patients although depressive disorders are considerably underdiagnosed and undertreated. Drug treatments for depression are reviewed in terms of a risk/benefit analysis. The main benefit is approximately to double the chance of recovery (from about 30 to 65%), with possible associated improvements in physical condition. The risks of treatment are considerable and include overdose, unwanted effects at therapeutic dose and interaction with other drugs. Among the risks associated with specific medical conditions are orthostatic hypotension, cardiotoxicity, deterioration of seizure control in epileptic patients and increased side effects in patients with renal and hepatic impairment. The available data suggest that there is relatively little to choose between antidepressants in terms of efficacy (although the quantity and quality of these data vary). It is therefore primarily the risks which should determine the choice of antidepressant, and these must be separately evaluated for each patient.
 ...
PMID:Drug treatment of depression in medically ill patients. 153 46

The genetically epileptic-prone rat (GEPR) is a valuable model for the study of gene-linked abnormalities involved in epilepsy. In comparison with normal Sprague-Dawley controls, we found, in GEPRs, a marked depression in local cerebral glucose utilization, widespread throughout the brain. This depression was accompanied by a significant increase of blood-brain barrier permeability and a reduction in regional blood volume. Finally GEPRs showed lower plasma levels of total triiodothyronine than normal controls. One can speculate that alterations in cerebral metabolism and microvascular regulation and thyroid hormone imbalance may be gene-linked factors involved in seizure susceptibility.
 ...
PMID:Evaluation of local cerebral glucose utilization and the permeability of the blood-brain barrier in the genetically epilepsy-prone rat. 154 51

The role of seizures occurring with perinatal hypoxic-ischemic encephalopathies is unclear. We examined the relationships between the time course of parasagittal electroencephalographic (EEG) activity and pathological outcome following transient cerebral ischemia, which was induced in 33 chronically instrumented fetal sheep by occluding the carotid arteries after ligation of the vertebral-carotid anastomoses. The EEG was quantified with real-time spectral analysis. Histological outcome was assessed 72 hours later. After 10 or 20 minutes of ischemia, EEG activity was depressed and then progressively recovered and mild selective neuronal loss was seen. The length of this depression correlated with the duration of ischemia (r = 0.88). After 30 or 40 minutes of ischemia, EEG activity remained depressed for 8 +/- 2 hours, followed by a rapid transition to low-frequency epileptiform activity that reached maximum intensity at 10 +/- 3 hours. By 72 hours, EEG intensity had fallen below control levels. This sequence of prolonged depression, epileptiform activity, and then loss of intensity was associated with the development of laminar necrosis of the underlying cortex. These electrophysiological sequelae may have prognostic value. The results indicate that after a severe hypoxic-ischemic insult, the parasagittal cortex becomes hyperexcitable before the final loss of activity. Secondary neuronal death may occur in this phase.
 ...
PMID:Outcome after ischemia in the developing sheep brain: an electroencephalographic and histological study. 154 46

Increasing evidence implicates glutamate receptor over-stimulation in the neurotoxicity associated with a host of metabolic insults, including seizures and hypoxia-ischemia. To begin to understand more completely the role of energy metabolism in the mechanism of neuron death following excitatory amino acid exposure, we investigated the effects of kainic acid exposure on metabolic rate in cultured hippocampal cells using a recently developed silicon microphysiometer. The device gives a continual real-time measure of metabolism in relatively small numbers of cells, as assessed by efflux of protons generated at least in part by ATP hydrolysis and lactic acid production. In the first half of this report, we characterize the feasibility of using this device for measuring cellular metabolism in hippocampal cultures. Metabolic rate in both astrocytes and neurons was readily detectable, with a high signal-to-noise ratio. The rate was proportional to the number of cells and was sensitive to metabolic enhancement or depression. We then utilized this device to study metabolic responses to the excitotoxin kainic acid. We observed a receptor-mediated, dose-dependent increase in metabolic rate upon stimulation by kainic acid, with an EC50 of approximately 100 microM. Exposure to toxic levels of kainic acid for 10 min produced an initial elevation (for 2 hr) in metabolic rate and then a gradual decline in metabolism over the next 8 hr that preceded a measurable loss of cell viability. This study further delineates a time window for the onset of kainic acid-induced damage. The results clearly show the feasibility of using silicon microphysiometry for assessing metabolism of brain cultures and for exploring the relationship between metabolism and synaptic activation.
 ...
PMID:Effects of excitotoxin exposure on metabolic rate of primary hippocampal cultures: application of silicon microphysiometry to neurobiology. 154 39

Lidocaine (lignocaine) was given in 42 episodes of status epilepticus (SE) in 36 patients either because of limited pulmonary reserve (22 patients) or because of lack of response to diazepam (14 patients). Lidocaine (1.5-2 mg/kg) was given intravenously in two minutes. A further identical bolus was infused if no response had occurred or if seizures recurred. With the first bolus 11 episodes of SE did not stop, but 31 responded, always in less than one minute. In 19 episodes, however, this response lasted less than 30 minutes. Twelve episodes did not recur, but 30 needed a second bolus because of recurrence. Of these, 19 episodes responded at once but SE reappeared in seven. In these seven episodes the mean control time with the second dose was 102 minutes. Five of these subsequently responded to a continuous infusion of lidocaine. Eleven patients, who had not responded to the first bolus, had no response to the second. Lidocaine is a drug that may be epileptogenic at high doses. At the doses used here, however, lidocaine seems to be a rapid acting anticonvulsant, useful in the short term management of SE and may be indicated in patients in whom respiratory or consciousness depression is undesirable and in those with no response to diazepam. The absence of response to lidocaine indicates SE resistant to treatment and poor prognosis. These data show that prompt lidocaine administration may be worthwhile when management of respiratory depression is not possible.
 ...
PMID:Role of lidocaine (lignocaine) in managing status epilepticus. 154 99


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>