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)

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

1. An attempt was made to evaluate the pathophysiology of symptoms of hyponatremia as related to changes in brain water and electrolytes. Studies were carried out in 66 hyponatremic patients and 5 groups of experimental animals. 2. In hyponatremic patients, symptoms (depression of sensorium, seizures) correlated well with plasma Na+ (r = 0.64, p less than .001), but there was substantial overlap. In patients with acute hyponatremia, all were symptomatic and 50% died. Among patients with hyponatremia of at least 3 days duration, sympatomatic patients had plasma Na+ (115 +/- 1 mEq/L) which was significantly less (p less than .001) than that of asymptomatic patients (plasma Na+ = 122 +/- 1 mEq/L). Among symptomatic patients, mortality was 12% and 8% had seizures, while none of the asymptomatic patients died or had seizures. 3. Among 14 patients with acute (less than 12 hrs) hyponatremia, the mean plasma Na+ was 112 +/- 2 mEq/L. All such patients had some depression of sensorium and four had grand male seizures. Seven of these patients were treated with hypertonic (862 mM) NaCl, while four were treated only with fluid restriction. Of the seven patients treated with hypertonic NaCl, five survived, while three of four patients treated with fluid restriction died. There was no evidence of circulatory congestion or cerebral damage in the patients treated with hypertonic NaCl. 4. Among rabbits with acute (2-3 hours) hyponatremia (plasma Na+ = 119 +/- 1 mEq/L), all had grand mal seizures and 86% died. All such animals had cerebral edema (brain H2O content 17% above control value) but brain content of Na+, K+ and Cl- was normal. 5. Rabbits with 3 1/2 days of hyponatremia (plasma Na+ = 122 +/- 2 mEq/L) appeared to be asymptomatic, even though brain water content was 7% above normal (p less than .01). 6. Rabbits with 16 days of more severe hyponatremia (plasma Na+ = 99 +/- 3 mEq/L) were weak, anorexic, lethargic and unable to walk. Brain water content was 7% above normal, although brain osmolality (218 +/- 12 mOsm/kg H2O) was similar to plasma (215 +/- 8 mOsm/kg). Brain content of Na+, K+, Cl- and osmoles was 17 to 37% less than normal values, so that the brain established osmotic equilibrium with plasma primarily by means of a loss of electrolytes. 7. These studies suggest that in patients with hyponatremia, symptoms and morbidity are only grossly correlated with either magnitude or duration of hyponatremia. Symptoms appear to correlate best with the interplay between a net increase in brain water versus a loss oof brain electrolytes. However, even asymptomatic animals have subclinical brain edema when plasma Na+ is below 125 mEq/L, and such edema may cause permanent brain damage. Thus, many patients with similar levels of plasma Na+, particularly when they are symptomatic, should probably be treated with hypertonic NaCl infusions.
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PMID:Neurological manifestations and morbidity of hyponatremia: correlation with brain water and electrolytes. 125 11

Psychiatric disorders in epilepsy are frequently encountered. Contradictory reports are given in literature about the phenomenology of such disturbances and their relationship to seizure frequency. Depression has been described as mostly like "endogenous" with a family history of psychiatric illness or mostly "reactive". 32 patients with idiopathic Grand mal-seizures were studied using the Inpatient Multidimensional Psychiatric Scale (IMPS). They showed significant higher levels in scales of anxious depression and impaired functioning, no signs of hostility or delusion. Severity of depression was moderate compared with groups of inpatients suffering from endogenous and neurotic-depressive disorders. It was correlated with frequency of epileptic seizures and history of behaviour disturbances in infancy (Spearman-rang correlation).
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PMID:[Depressive disorder of the epilepsy patient--symptoms and factors of influence]. 169 87

Generalized tonic-clonic seizures are a neurologic emergency. Duration of ictal activity has been associated with neurologic sequelae. The purpose of this study was to determine if midazolam, a short-acting benzodiazepine, could effectively ablate ictal activity in an animal model without significant cardiorespiratory compromise. Ten domestic swine (10 to 20 kg) were ventilated and hemodynamically monitored. Bifrontal craniotomies were performed and electrocortical activity was recorded throughout the experiment. Pentylenetetrazol (100 mg/kg) was administered iv to induce seizures. Midazolam (0.1 mg/kg) was administered iv and serum levels were drawn at 1, 2, 5, 10, 15, and 20 min after administration. There was no significant difference between the baseline and postmidazolam vital signs. Seizure activity was seen periodically as generalized spikes, as well as individual spikes for 29 +/- 5 sec after midazolam administration. A period of attenuation of 24 +/- 7 sec was seen before returning to baseline electrocortical activity. Our study demonstrates that midazolam effectively ablated induced ictal activity without significant cardiorespiratory depression and with similar EEG effect as other benzodiazepines.
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PMID:Intravenous midazolam suppression of pentylenetetrazol-induced epileptogenic activity in a porcine model. 210 74

Overdose of pentazocine (Talwin), an agonist/antagonist opioid analgesic, is relatively uncommon. Fifty-seven cases occurring over ten years are reported. Twenty-three patients (40%) had ingested only pentazocine and did not have the classic opioid toxidrome of CNS and respiratory depression with miosis. Most patients were awake, and no patient had a respiratory rate below 12/minute. Other findings included: grand mal seizures, hypertension, hypotonia, dysphoria, hallucinations, delusions, and agitation. Eleven of 23 patients received IV naloxone (0.4-2.4 mg), but only two showed improvement. Thirty-four patients (60%) had coingested pentazocine with one to five additional substances. Patients who had ingested pentazocine with alcohol, a sedative/hypnotic drug, or an antihistamine, showed increased toxicity, including apnea, deep coma, and recurrent seizures. One patient developed opioid pulmonary edema. One patient died. Three of five patients with coma and inadequate respirations responded to IV naloxone in doses of 0.4 to 1.2 mg.
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PMID:Pentazocine (Talwin) intoxication: report of 57 cases. 235 1

This report describes the investigation of a spontaneous grand mal seizure in a 55-year old woman, being treated with drugs and ECT for depression. The spontaneous seizure was due to hyponatremia caused by self-induced water intoxication, although psychotrophic medication may have contributed by lowering the seizure threshold. The diagnosis of hyponatremia is discussed.
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PMID:Hyponatremic seizure following ECT. 250 79

A sequential sample of 101 patients hospitalized for ethanol withdrawal and requiring sedation for evolving withdrawal syndromes was assigned randomly according to a double-blind protocol to treatment with either alprazolam or chlordiazepoxide administered orally. The data from one patient were unevaluable due to acute bleeding, leaving a sample of 100 (50 in each condition). At discharge, three independent ratings of diaphoresis, tremor, hallucinations, nausea/vomiting, and overall severity of withdrawal were obtained, and the occurrence of delirium tremens and grand mal seizures was noted. Patients also completed the Beck Depression Inventory, and their disposition following discharge was recorded. There were no statistically significant differences between the two treatment groups on any of the dependent variables studied. It was concluded that the choice between alprazolam and chlordiazepoxide for managing ethanol withdrawal should be based on criteria other than efficacy of control. Potential antidepressant effects and drug kinetics were suggested as the basis for rational decision-making.
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PMID:Double-blind trial of alprazolam and chlordiazepoxide in the management of the acute ethanol withdrawal syndrome. 388 64

The coagulation and fibrinolytic mechanisms were investigated in a group of patients with severe pre-eclampsia and eclampsia and the findings were compared with those of healthy women in late pregnancy. In patients with pre-eclampsia the following significant differences were found: (1) greater depression of plasma fibrinolytic activity (euglobulin lysis time) than in normal pregnancy, (2) a higher level of inhibitor to urokinaseinduced lysis, (3) increased levels of serum fibrin degradation products, and (4) reduced platelet counts.In patients with eclampsia a progressive increase of the level of serum fibrin degradation products was found over the three days following eclamptic seizures. No such increase occurred after grand mal seizures in late pregnancy. The findings in this study support the view that intravascular clotting is taking place in pre-eclampsia and that this disturbance of the balance between coagulation and fibrinolysis may be localized to certain areas of the vascular compartment, particularly the placental and renal circulations. Fibrin deposition in the maternal vessels supplying the placenta would impair the placental blood flow, which may explain the placental insufficiency which occurs in pre-eclampsia. Likewise fibrin deposition in the renal vasculature will result in glomerular damage and proteinuria. Hypertension may be related to the renal ischaemic changes or a compensatory response to the presence of fibrin deposition in the vascular compartment. This evidence of intravascular fibrin deposition raises the question of the possible therapeutic value of antithrombotic agents to inhibit the clotting process. On a theoretical basis such treatment might be expected to improve blood flow to the placenta and thereby fetal growth.
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PMID:Coagulation and fibrinolytic systems in pre-eclampsia and eclampsia. 499 19

From March 1976 until March 1979, 28 patients with disabling emotional symptoms were studied in the Psychiatry and Neurosurgery Departments at Tulane University, and pre-selected for cerebellar electrode implantation and subsequent cerebellar stimulation. This series include 12 patients with different types of schizophrenia; 7 epileptic patients with Grand Mal and/or psychomotor attacks, and concomitant psychiatric symptoms; 5 patients with intractable depression; and 4 patients with miscellaneous psychiatric symptoms. Follow-up results are graded as excellent, good, fair and poor. The authors conclude that significant improvement were observed in many patients, and the results, although preliminary and incomplete, are encouraging.
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PMID:Chronic cerebellar stimulation in the modulation of behavior. 680 46

A transient functional depression of thalamic activity (TFDTA) was induced in acute experiments in cats by the microinjection of 25% KCl into the thalamus. Spontaneous and evoked thalamic electrical activity was markedly depressed at the site of KCl microinjection. Spread of this depression to other thalamic areas often occurred, mainly when KCl was injected into the midline thalamus. In normal cats both spontaneous and evoked cortical spindle bursts as well as other evoked thalamocortical responses were reduced or abolished during the KCl-induced TFDTA. The generalized spike-and-wave discharges of feline generalized epilepsy were also suppressed for the duration of TFDTA, while incidental focal cortical interictal and ictal epileptic discharges, as well as generalized tonic-clonic seizure discharge, remained unaffected. The same effects were observed in animals with lesions of the mesencephalic reticular formation, indicating that the suppression of spindles and spike-and-wave discharges cannot be attributed to a release of the activity of the reticular formation by the TFDTA. An unexplained occurrence of generalized tonic-clonic EEG seizure was observed in most cases late after thalamic KCl microinjection, usually after the spike-and-wave discharges had recovered. These data are consistent with the hypothesis that the spontaneous bilaterally synchronous epileptic bursts of feline generalized penicillin epilepsy are not only closely related to spindles but are crucially dependent on thalamic inputs to the cerebral cortex.
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PMID:The effects of transient functional depression of the thalamus on spindles and on bilateral synchronous epileptic discharges of feline generalized penicillin epilepsy. 726 50


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