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)

Clinical electroencephalography is a relatively simple and inexpensive diagnostic tool with a high sensitivity for diffuse organic encephalopathy of various aetiologies but with a rather low specificity for the type of diagnosis. The highest sensitivity is shown in DAT and Parkinson dementia, and in these conditions the degree of EEG abnormality is correlated with the disease severity. Quantification of EEG makes these correlations more reliable and provides a method for monitoring therapeutic effects. Dementias with predominantly frontal pathology show much less EEG abnormality, and in these conditions the EEG is often normal despite obvious clinical dementia. Also, alcohol dementias often show normal EEG patterns. At an early stage of clinical evaluation, EEG may be useful in the discrimination of organic dementia from pseudodementia, because EEG is usually normal in depression, confusion, agitation and other psychiatric conditions. In pseudodementia due to intoxication with sedatives the EEG is usually dominated by diffuse beta activity. At the stage of differential diagnosis of an organic brain disorder, EEG cannot reliably discriminate between encephalopathies secondary to hydrocephalus, AIDS, cerebrovascular disease, B12 deficiency and primary degenerative diseases such as DAT. More specific EEG patterns are seen in acute cerebrovascular lesions, metabolic encephalopathies, i.e. of hepatic origin, Creutzfeldt-Jakob disease, herpes encephalitis, and nonconvulsive status epilepticus as possible causes of a rapidly deteriorating mental and neurological condition. Repeated EEG recordings over time would add significantly to the diagnostic information. New techniques such as topographical brain mapping, analysis of the EEG during REM sleep, coherence analysis of the EEG activity, and the combination of quantified EEG techniques with evoked potentials and event-related potentials will presumably add to the sensitivity as well as the specificity of the electrophysiological methods in the diagnosis of dementia.
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PMID:Electroencephalography as a diagnostic tool in dementia. 906 24

Following pilocarpine-induced status epilepticus, rats become chronically epileptic showing 2-3 spontaneous recurrent seizures per week. The aim of this work was to verify the characteristics of spreading depression (SD) in these chronic epileptic rats (n = 16). SD was evoked in one point of the frontal cortex by topical application of KCl solution at 20 min intervals, and recordings were made in two points over the parietal cortex (a 'near' point and a 'remote' one, about 3 and 8 mm posterior to the stimulating region, respectively). In all control animals (n = 10), KCl stimulation elicited SD which in 100% of the cases propagated regularly to the two recording points. In the chronic epileptic rats only about 50% of the KCl applications were effective in eliciting SD, detected at the 'near' recording point. Of these, only 3% propagated to the 'remote' recording point. In eight of the above epileptic rats, diazepam (5-10 mg/kg, i.v.) was injected after 1-2 h of recording, when SD incidence in response to KCl stimulation has been established. After diazepam, the incidence of SDs propagating regularly to the 'near' and to the 'remote' recording points increased significantly, (132 and 53 SDs, respectively, out of 139 KCl stimulations), as compared with the incidence in the pretreatment period (33 and 1, respectively, out of 63 stimulations; P < 0.005). These data indicate an impairment in the susceptibility to cortical SD in chronic epileptic rats suggesting modifications in cortical excitability in the pilocarpine model of epilepsy. They also indicate a facilitatory effect of diazepam on SD, confirming previous observations in non-epileptic rats.
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PMID:Blockade of spreading depression in chronic epileptic rats: reversion by diazepam. 916 89

Midazolam is a familiar agent commonly used in the emergency department to provide sedation prior to procedures such as laceration repair and reduction of dislocations. Midazolam is also effective in the treatment of generalized seizures, status epilepticus, and behavioral emergencies, particularly when intravenous access is not available. Midazolam is often employed as an induction agent for rapid sequence endotracheal intubation. Midazolam has a rapid onset of action following intravenous, intramuscular, oral, nasal, and rectal administration. Only 50% of an orally administered dose reaches the systemic circulation due to extensive first-pass metabolism. Midazolam is metabolized by the cytochrome P450 enzyme system to several metabolites including an active metabolite, alpha-hydroxymidazolam. Cytochrome P450 inhibitors such as cimetidine can profoundly reduce the metabolism of midazolam. Midazolam has a half-life of approximately 1 h, but this half-life may be prolonged in patients with renal or hepatic dysfunction. Midazolam has been associated with respiratory depression and cardiac arrest when used in combination with an opioid, particularly in the elderly, although all ages are at risk for respiratory depression. Midazolam is relatively free of side effects when used alone and offers several advantages over traditional pharmacological agents such as chloral hydrate and the combination of meperidine, chlorpromazine, and promethazine. Hiccups, cough, nausea, and vomiting are the most commonly reported adverse effects. Many of the adverse effects associated with midazolam can be reversed rapidly by the administration of flumazenil, a competitive benzodiazepine receptor antagonist. Midazolam is a safe and effective agent for providing sedation in the emergency department.
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PMID:Midazolam: a review of therapeutic uses and toxicity. 925 87

To determine efficacy of continuous diazepam infusion in the treatment of refractory status epilepticus in a retrospective study, we analyzed data of 62 children admitted consecutively to our Pediatric Intensive Care Unit with a diagnosis of refractory status epilepticus. The unit followed a standard treatment protocol for diazepam infusion; if it failed, thiopental infusion was used. The mean age of patients was 2.80 years (range, 1.5 to 11.5 yr). Thirty-six patients (60%) had acute infections of the central nervous system and 10 (16%) had idiopathic epilepsy. Diazepam infusion was used in 57 patients. This treatment controlled seizures in 86% of patients (49/57), on average within 40 minutes (median, 30 min; range, 10-120 min), at a mean infusion rate of 0.017 mg/kg/min (range, 0.01-0.03 mg/kg/min). The mean total duration of infusion was 68 hours (range, 12-220 hr). Diazepam infusion was associated with hypotension in one patient, respiratory depression requiring ventilatory support in 12% of patients (6/49), and death in 14% of patients (7/49). Thiopental infusion was used in nine patients, including eight in whom diazepam infusion had failed. Thiopental infusion controlled seizures in all nine patients, but all of them needed mechanical ventilation, and seven needed vasopressor support for hypotension; four patients (44%) died. We conclude that continuous diazepam infusion is a reasonably effective modality to control refractory status epilepticus in children and is associated with reduced need for ventilatory and vasopressor support.
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PMID:Refractory status epilepticus in children: role of continuous diazepam infusion. 947 44

All children who presented in a convulsion, including convulsive status epilepticus, to the accident and emergency department over a 12-month period and who required treatment, were reviewed retrospectively to identify the effectiveness and safety of a specific treatment protocol. This protocol recommends the initial use of one, or if necessary, two doses of rectal or intravenous diazepam (0.4 mg/kg) followed by the simultaneous administration of phenytoin (18 mg/kg) and rectal paraldehyde (0.4 mL/kg), with instructions for maximum doses and timings of administration. Eighty-one evaluable children (52 male) were audited. The mean age of the study population was 4.1 (range 0.1 to 14.9) years. Overall, the presenting convulsion was successfully terminated in 76 children (94%) within the accident and emergency department. In 69 children (85% of the entire study population) this was after a single dose of diazepam (rectal in 41 and intravenous in 28). In only an additional two children did the presenting convulsion stop after a second dose of diazepam. In five of the 10 children (50%) who received paraldehyde and phenytoin as a combination, the convulsion stopped. Nine patients (11%) required admission to the intensive-care unit, five because of persisting convulsive activity, and four because of respiratory depression. The results of this retrospective audit suggest that the current treatment protocol appears to be effective and relatively safe in treating acute convulsions, including convulsive status epilepticus. The audit is to be repeated prospectively to either confirm or refute these findings before recommending any changes to the protocol.
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PMID:Children presenting with convulsions (including status epilepticus) to a paediatric accident and emergency department: an audit of a treatment protocol. 1006 49

Information on GH in relation to epilepsy is sparse, and to our knowledge there is no information on GH levels during status epilepticus in man. We studied GH in serum in six patients during status epilepticus, and in a control group of six seizure-free patients with epilepsy, before and after injection of TRH. The baseline GH values before TRH administration were within the normal range in all patients. After injection of TRH all patients with status epilepticus showed a paradoxical peak-shaped increase of GH to at least twice their baseline levels within 45 min after the injection (median basal GH value 1.5 mU/l and median peak GH value 6. 5 mU/l, mean increase 330%). No uniform reaction to TRH was observed in the control group (median basal GH value 2.7 U/l and median of the highest value within 45 min 5.2mU/l). A paradoxical peak reaction of GH to TRH was significantly more frequent in the status epilepticus group compared with the control group (P=0.008, Fisher exact probability test). TRH is not considered a GH-releasing hormone in humans during normal conditions, but a paradoxical response of GH to TRH, similar to that observed during status epilepticus, has been reported in various other pathological conditions, such as acromegaly, liver cirrhosis, mental depression and hypothyroidism. Our results of GH release after TRH administration in patients with status epilepticus suggest an altered regulation of GH as a result of the long-standing epileptic activity.
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PMID:Paradoxical GH response to TRH during status epilepticus in man. 1009 49

Status epilepticus (SE), i.e. ongoing seizures of more than 30 min duration, gives rise to bilateral pan-necrotic lesions of the substantia nigra, pars reticulata (SNPR). These are known to be preceded by an initial increase, followed by a depression of metabolic rate, and by failure of the bioenergetic state, suggesting mitochondrial dysfunction. We have previously shown that the spin trap alpha-phenyl-N-tert-butyl nitrone (PBN) prevents the lesions caused by 45 min of SE from occurring, in spite of ongoing seizure activity. In this article, we demonstrate that PBN, given 30 min before seizure induction, reduces or prevents the decrease in ATP concentration and adenylate energy charge, without significantly reducing the amount of lactate accumulated, or the decrease in intracellular pH (pHi). The results suggest that the spin trap nitrone preserves the structural and functional integrity of SNPR neurons by protecting the mitochondria against oxidative damage.
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PMID:The effect of alpha-phenyl-N-tert-butyl nitrone on bioenergetic state in substantia nigra following flurothyl-induced status epilepticus in rats. 1035 42

Nonconvulsive status epilepticus (NCSE) is characterized by behavioral or cognitive change from baseline for at least 30 minutes with EEG evidence of seizures. Categorized into complex partial status epilepticus (with lateralized seizures), and generalized nonconvulsive status epilepticus (bilateral diffuse synchronous seizures), there is debate regarding the diagnosis and morbidity of NCSE. Because EEG is needed for diagnosis, only a high index of suspicion leads to a request for the study, whereas EEG is often unavailable after hours or on weekends. Furthermore, the cognitive changes during NCSE are often incorrectly ascribed to a postictal state, intoxication, psychogenic or psychotic states, and mental retardation. Regarding categorization, present classifications address EEG features but fail to distinguish among depths of coma. Deeply comatose patients (with coma etiologies that themselves carry poor prognoses) are mixed with lightly obtunded patients with no morbidity, confusing the prognosis. Thus, a classification that subsumes depth of coma, and possibly etiology, is sorely warranted. Regarding treatment, comatose NCSE patients treated with benzodiazepines may worsen, whereas generalized nonconvulsive status epilepticus patients may suffer iatrogenically from aggressive treatment (hypotension and respiratory depression) necessitating balancing the potential neurologic morbidity of NCSE against the possible morbidity of IV antiepileptic drugs. A high index of suspicion is needed to initiate EEG studies. Better stratification of level of consciousness will be needed to distinguish among morbidity due to underlying conditions, treatment, and the effects of status epilepticus, proper.
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PMID:Assessing the outcomes in patients with nonconvulsive status epilepticus: nonconvulsive status epilepticus is underdiagnosed, potentially overtreated, and confounded by comorbidity. 1047 7

Generalized convulsive status epilepticus (GCSE) is a medical emergency requiring prompt resolution. Acute treatment is often delayed by difficulty in obtaining intravenous (i.v.) access. Refractory GCSE is often difficult to treat, and traditional therapy with barbiturates induces hypotension and respiratory depression and prolongs recovery. Midazolam is particularly useful for treating acute GCSE because it has an imidazole ring that is open at low pH, allowing it to be dissolved in aqueous solution for intramuscular injection, but closed at physiologic pH, increasing lipophilicity and rendering good intramuscular absorption, brain penetration, and fast onset of action. When given intramuscularly as a 0.2 mg/kg bolus, it has efficacy at least equal to that of i.v. diazepam, is well tolerated, induces little respiratory compromise, and has a shorter latency to onset of action. Therefore, it should be considered for the treatment of acute GCSE when i.v. access is problematic. For refractory GCSE, continuous i.v. midazolam infusion at 0.1-0.6 mg/kg/hr after a 0.2 mg/kg i.v. bolus is effective and has advantages over traditional therapies because it induces less hypotension and cardiorespiratory depression and can be easily titrated. Further prospective studies are needed to define the role of continuous i.v. midazolam compared to other contemporary therapies.
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PMID:Midazolam treatment of acute and refractory status epilepticus. 1051 75

We report the unusual features of a female patient who had MELAS-specific A3243G mutation in mitochondrial DNA (mtDNA) and diabetes mellitus (DM). The patient showed mitochondrial myopathy, encephalopathy, lactic acidosis, and deafness but lacked the stroke-like episode. Acute hyperglycemia was noted after one attack of status epilepticus. Molecular genetic analysis demonstrated a heteroplasmic A3243G point mutation in the mtDNAs of muscle, blood cells and hair follicles. Glucagon stimulation test exhibited marked depression of pancreatic beta-cell function. However, in a further study neither this mutation, nor MELAS syndrome or DM, was found in all of her maternal relatives. A series of follow-up studies for beta-cell function also showed gradual improvement. The pedigree study led us to believe that this A3243G mutation arose from the germ line cells or occurred later in somatic tissues of the patient. We also suggest that the A3243G mutation of mtDNA may elicit the pathogenesis of a subtype of DM. Nevertheless, environmental stress may be another important factor for provocation of the disease.
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PMID:Absence of maternal A3243G mtDNA mutation and reversible hyperglycemia in a patient with MELAS syndrome. 1066 Jan 56


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