OBJECTIVE: To review the classification, clinical characteristics, and epidemiology of bipolar disorders in old age with a special focus on neurologic comorbidity, high mortality, and management. QUALITY OF EVIDENCE: Most available data is gleaned from retrospective chart reviews and cohort studies. Treatment recommendations are based on evidence from younger populations and a few anecdotal case reports and series involving elderly people. MAIN MESSAGE: While relatively rare in the community setting, mania in old age frequently leads to hospitalization. It is associated with late-onset neurologic disorders (especially cerebrovascular disease) involving the right hemisphere and orbitofrontal cortex. Prognosis is relatively poor; morbidity and mortality rates are high. Management of bipolarity includes cautious use of mood stabilizers, especially lithium and divalproex. CONCLUSIONS: Mania in old age should trigger a careful assessment of underlying neurologic disease, especially cerebrovascular disease. Close clinical follow up is essential. (+info)
Depression duration but not age predicts hippocampal volume loss in medically healthy women with recurrent major depression.
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This study takes advantage of continuing advances in the precision of magnetic resonance imaging (MRI) to quantify hippocampal volumes in a series of human subjects with a history of depression compared with controls. We sought to test the hypothesis that both age and duration of past depression would be inversely and independently correlated with hippocampal volume. A sample of 24 women ranging in age from 23 to 86 years with a history of recurrent major depression, but no medical comorbidity, and 24 case-matched controls underwent MRI scanning. Subjects with a history of depression (post-depressed) had smaller hippocampal volumes bilaterally than controls. Post-depressives also had smaller amygdala core nuclei volumes, and these volumes correlated with hippocampal volumes. In addition, post-depressives scored lower in verbal memory, a neuropsychological measure of hippocampal function, suggesting that the volume loss was related to an aspect of cognitive functioning. In contrast, there was no difference in overall brain size or general intellectual performance. Contrary to our initial hypothesis, there was no significant correlation between hippocampal volume and age in either post-depressive or control subjects, whereas there was a significant correlation with total lifetime duration of depression. This suggests that repeated stress during recurrent depressive episodes may result in cumulative hippocampal injury as reflected in volume loss. (+info)
Naloxone in the prevention of the adverse cognitive effects of ECT: a within-subject, placebo controlled study.
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Electroconvulsive therapy (ECT) is a highly effective treatment for major depression, but is also associated with characteristic cognitive side effects. Several reports document that endogenous opioids and their receptors are activated by electroconvulsive shock (ECS) and that naloxone in doses sufficient to block endogenous opioid receptors may reverse ECS-induced retrograde amnesia. This placebo-controlled, randomized, within-patient study was conducted to examine the potential of naloxone, given in doses sufficient to block opioid receptors (high dose), to ameliorate acute anterograde and retrograde memory impairments following ECT. Compared to placebo and low dose naloxone, high dose naloxone administered immediately before ECT resulted in significant reductions in anterograde amnesia, and better performance on an attention task. Both low and high dose naloxone improved verbal fluency. There were no beneficial effects of high dose naloxone on retrograde amnesia, and an indication that high dose naloxone may have worsened retrograde amnesia for shape stimuli. There were no effects of high dose naloxone on seizure duration, vital signs, and subjective side effects. The study is consistent with prior research in which change in behavioral and physiological measures was produced principally by naloxone doses sufficient to block endogenous opioid receptors and offers evidence of the potential for ameliorating some adverse cognitive effects associated with ECT. (+info)
Mechanism underlying the therapeutic effects of electroconvulsive therapy (ECT) on depression.
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Electroconvulsive therapy (ECT) is used to treat drug-resistant depressive disorders. The results of studies on the mechanism underlying the effectiveness of ECT on depression are still controversial. ECT stimulus is usually larger than the threshold of induction of seizures and activation of whole-brain is believed to be necessary to produce therapeutic effects. A single ECT session induces alterations of the electroencephalogram (EEG) including initial epileptic discharges, then slow waves, and finally flattened EEG. Repeated ECT results in an increasing number of slower waves in the EEG for as long as a month. ECT-induced changes in various neurotransmitter systems have also been reported. Serotonin (5-hydroxytryptamine, 5-HT) is one of the most important neurotransmitters involved in depressive illness, and ECT alters several 5-HT-receptor subtypes in the central nervous system. 5-HT1A receptors in post-synaptic neurons are sensitized by repeated ECT, but those in pre-synaptic neurons (auto-receptors) are not changed. In addition, our electrophysiological studies have shown that ECT increases sensitivity to 5-HT of 5-HT3 receptors in the hippocampus, resulting in an increase in release of neurotransmitters such as glutamate and gamma-aminobutyric acid. In contrast, ECT decreases the auto-receptor functions in noradrenergic and dopaminergic neurons in the locus coeruleus and substantia nigra, respectively, resulting in an increase in release of noradrenaline and dopamine. In conclusion, 5-HT1A-receptor sensitization may be important for explaining the effectiveness of ECT, as this change induces a decrease in the number of 5-HT2A receptors that are elevated in depressive patients. Facilitation of neurotransmitter releases due to 5-HT3-receptor sensitization by ECT may also play an important role in effective treatment of depressive patients refractory to therapeutic drugs. (+info)
Repeated propofol anesthesia for a patient with a history of neuroleptic malignant syndrome.
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Neuroleptic malignant syndrome (NMS) is the most serious side effect produced by the administration of antipsychotic drugs. NMS shares many clinical similarities with malignant hyperthermia (MH), but the etiology of NMS and the relation between NMS and MH remain unknown. Anesthetic regimens for patients with NMS are not well established. We gave repeated anesthesia to a patient with a history of NMS undergoing electroconvulsive therapy for the treatment of depression. Propofol and vecuronium were used in twelve consecutive ECT sessions without complications. In this case report, we describe the safe and satisfactory repeated use of propofol in a patient with a history of NMS, and outline NMS and its questionable relation to MH. (+info)
Low-dose esmolol bolus reduces seizure duration during electroconvulsive therapy: a double-blind, placebo-controlled study.
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We have measured the effect of a bolus dose of esmolol 80 mg i.v. on heart rate, and systolic (SAP), diastolic (DAP) and mean (MAP) arterial pressures during electroconvulsive therapy (ECT). We also assessed seizure duration using both the cuff method and two-lead EEG. We studied 20 patients in a double-blind, placebo-controlled, within-patient blocked randomized study. No patient was receiving psychotherapeutic drugs or had cardiovascular disease. Esmolol significantly reduced heart rate, SAP and MAP before the stimulus, and also significantly reduced the increases in these variables during the convulsion, compared with placebo. However, seizure duration was also significantly reduced, possibly making ECT less effective. The reduction in seizure duration was 5.83 s when monitored clinically and 9.9 s when measured by the EEG. Because of the reduction in seizure duration, routine administration of esmolol is not advisable because it may interfere with the efficacy of ECT, but administration of esmolol during ECT could be useful to reduce tachycardia and hypertension in high-risk patients. (+info)
Differential changes in the expression of cyclic nucleotide phosphodiesterase isoforms in rat brains by chronic treatment with electroconvulsive shock.
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Electroconvulsive shock (ECS) has been suggested to affect cAMP signaling pathways to exert therapeutic effects. ECS was recently reported to increase the expression of PDE4 isoforms in rat brain, however, these studies were limited to PDE4 family in the cerebral cortex and hippocampus. Thus, for comprehensive understanding of how ECS regulates PDE activity, the present study was performed to determine whether chronic ECS treatment induces differential changes in the expression of all the PDE isoforms in rat brains. We analyzed the mRNA expression of PDE isoforms in the rat hippocampus and striatum using reverse transcription polymerase chain reaction. We found chronic ECS treatment induced differential changes in the expression of PDE isoform 1, 2, 3, 4, 5 and 7 at the rat hippocampus and striatum. In the hippocampus, the expression of PDE1A/B (694%), PDE4A (158%), PDE4B (323 %), and PDE4D (181%) isoforms was increased from the controls, but the expression of PDE2 (62.8%) and PDE7 (37.8%) decreased by chronic ECS treatment. In the striatum, the expression of PDE1A/B (179%), PDE4A (223%), PDE4B (171%), and PDE4D (327%) was increased by chronic ECS treatment with the concomitant decrease in the expression of PDE2 (78.4%) and PDE3A (67.1%). In conclusion, chronic ECS treatment induces differential changes in the expression of most PDE isoforms including PDE1, PDE2, PDE3, PDE4, PDE5, and PDE7 in the rat hippocampus and striatum in an isoform- and brain region-specific manner. Such differential change is suggested to play an important role in regulation of the activity of PDE and cAMP system by ECS. (+info)
Effects of implantable cardioverter defibrillator implantation and shock application on biochemical markers of myocardial damage.
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BACKGROUND: Implantable cardioverter defibrillator (ICD) implantation is a common approach in patients at high risk of sudden cardiac death. To check for normal function, it is necessary to test the ICD. For this purpose, repetitive induction and termination of ventricular fibrillation by direct current shocks is required. This may lead to minor myocardial damage. Cardiac troponin T (cTnT) and I (cTnI) are specific markers for the detection of myocardial injury. Because these proteins usually are undetectable in healthy individuals, they are excellent markers for detecting minimal myocardial damage. The objective of this study was to evaluate the effect of defibrillation of induced ventricular fibrillation on markers of myocardial damage. METHODS: This study included 14 patients who underwent ICD implantation and intraoperative testing. We measured cTnT, cTnI, creatine kinase MB (CK-MB) mass, CK activity, and myoglobin before and at definite times after intraoperative shock application. RESULTS: Depending on the effectiveness of shocks and the energy applied, the cardiac-specific markers cTnT and cTnI, as well as CK-MB mass, showed a significant increase compared with the baseline value before testing and peaked for the most part 4 h after shock application. In contrast, the increases in CK activity and myoglobin were predominantly detectable in patients who received additional external shocks. CONCLUSIONS: ICD implantation and testing leads to a short release of cardiac markers into the circulation. This release seems to be of cytoplasmic origin and depends on the number and effectiveness of the shocks applied. (+info)