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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Stress, which can precipitate and exacerbate depression, causes atrophy and in severe cases death of hippocampal neurons. Atrophy of the hippocampus has also been observed in patients suffering from recurrent major depression. The present study examines the influence of electroconvulsive seizures, one of the most effective treatments for depression, on the morphology and survival of hippocampal neurons. The results demonstrate that chronic administration of electroconvulsive seizures induces sprouting of the granule cell mossy fiber pathway in the hippocampus. This sprouting is dependent on repeated administration of electroconvulsive seizures, reaches a maximum 12 days after the last treatment and is long lasting (i.e. up to six months). Electroconvulsive seizure-induced sprouting occurs in the absence of neuronal loss, indicating that sprouting is not a compensatory response to cell death. This is different from the sprouting induced by kindling or excitotoxin treatment, which induce cell death along with recurrent seizures. Electroconvulsive seizure-induced sprouting is significantly diminished in brain-derived neurotrophic factor heterozygote knockout mice, indicating that this neurotrophic factor contributes to mossy fiber sprouting. However, infusion of brain-derived neurotrophic factor into the hippocampus does not induce sprouting of the mossy fiber pathway. The results demonstrate that chronic administration of electroconvulsive seizures induces mossy fiber sprouting and suggest that increased expression of brain-derived neurotrophic factor is necessary, but not sufficient for the induction of this sprouting. Although the functional consequences remain unclear, sprouting of the mossy fiber pathway would appear to oppose the actions of stress and could thereby contribute to the therapeutic actions of electroconvulsive seizure therapy.
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PMID:Hippocampal mossy fiber sprouting induced by chronic electroconvulsive seizures. 1005 Dec 25

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.
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PMID:Naloxone in the prevention of the adverse cognitive effects of ECT: a within-subject, placebo controlled study. 1043 76

Gabapentin, a novel antiepileptic drug, is effective in the treatment of partial seizures with and without secondary generalization. Evidence suggests that it may have mood-stabilizing and possibly antidepressant properties in bipolar depression. We report on a 48-year-old woman who had recurrent major depressive disorder. Following inguinal herniorrhaphy, she developed severe stabbing pain in the lower abdomen and inguinal area that progressed to constant pain in her whole body. She was depressive, hopeless, and had given up her social activities. A diagnosis of major depressive disorder and somatoform pain disorder was made. Antidepressants and carbamazepine were ineffective, and she had attempted suicide. Gabapentin resulted in remission of both the pain and the depressive mood at a dose of 1.800 mg/day.
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PMID:Gabapentin leads to remission of somatoform pain disorder with major depression. 1059 36

Electroconvulsive therapy (ECT) is considered to be one of the most effective treatments for patients with major depression and persistent psychosis. Seizure characteristics probably determine the therapeutic effect of ECT; as a consequence, short seizures are accepted as one of the factors of poor outcome. During most ECT courses seizure threshold increases and seizure duration decreases. Methylxanthine preparations, caffeine, and theophylline have been used to prolong seizure duration. The use of aminophylline, more readily available than caffeine, has not been well documented. The objective of this study was to test the effects of aminophylline on seizure length. Fourteen drug-free patients with diagnoses of affective disorder or psychotic episode receiving ECT participated in this study. Seizure length was assessed clinically and per EEG. Statistical comparisons were done using paired t tests. A significant increase (p < 0.04) in seizure length was achieved and maintained on three subsequent treatments with aminophylline. No adverse events were noted from the addition of aminophylline.
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PMID:Aminophylline increases seizure length during electroconvulsive therapy. 1061 31

The paper gives a brief review of human molybdenum metabolism and toxicity and presents the first known case of acute clinical poisoning with molybdenum from the dietary molybdenum (Mo) supplement in a male patient in late thirties. In over 18 days, the patient had consumed a cumulative dose of 13.5 mg Mo (300-800 micrograms Mo/day). Followed the development of acute psychosis with visual and auditory hallucinations, a series of petit mal seizures, and one life threatening grand mal attack. The symptoms remitted several hours after the start of chelation therapy with calcium ethylene diamine tetraacetic acid (CaEDTA). A battery of neuropsychological tests and Spectral Emission Computer Tomography demonstrated evident frontal cortical damage of the brain. One year after the Mo poisoning, the patient was diagnosed toxic encephalopathy with executive deficiencies, learning disability, major depression, and post-traumatic stress disorder. The paper strongly advocates issuance of and strict adherence to written warnings on the instruction labels not to mix potentially harmful neurotoxic substances, such as molybdenum, with other nutriceuticals and to instructions stating maximal single and cumulative doses. Molybdenum is a new and unwelcome member of the "metal madness" family.
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PMID:A case report of acute human molybdenum toxicity from a dietary molybdenum supplement--a new member of the "Lucor metallicum" family. 1064 45

We tested the hypothesis that major depression meeting DSM-III-R criteria or medical therapies for depression increase the risk for unprovoked seizures. Major depression was associated with a sixfold increased risk for unprovoked seizures (95% CI, 1.56-22). The risk remained increased even when controlling for age, sex, length of medical follow-up, and medical therapies for depression. In the absence of known prior neurological insult, major depression is associated with an increased risk for unprovoked seizures.
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PMID:Major depression is a risk factor for seizures in older adults. 1066 98

Animal studies have shown that a course of electroconvulsive shock (ECS) leads to a significant reduction in glucose metabolism in rat brains 1 day after the last ECS. In humans, of the two positron emission tomography (PET) studies that assessed the effects of a course of electroconvulsive therapy (ECT) on brain glucose metabolism in depressed patients, one reported no change while the other found a trend for reduction in glucose metabolism in frontal cortical region 24 hours after last ECT. The changes in glucose metabolism detected 24 hours after the last ECS/ECT treatment might simply be due to subacute effects of a seizure. We hypothesized that the changes in brain metabolism that persist 1 week after a course of ECT are more likely to underlie the therapeutic effects of ECT. We, therefore, investigated the effects of a course of ECT on brain glucose metabolism 1 week after last ECT by using PET and [18F]fluorodeoxyglucose (FDG). Six patients who met DSM-IV criteria for a diagnosis of major depressive disorder (unipolar), and were referred for ECT as the clinically indicated treatment were recruited. They underwent two PET scans, one prior to first ECT and the second a week after last ECT. The number of ECT treatments subjects received ranged from 8 to 12 with a mean of 11. Five out of six patients responded to the ECT treatment. Cerebral metabolic rates for glucose were slightly lower in most regions post treatment compared with pretreatment but the differences were not statistically significant. Similarly, there was no significant correlation between changes in regional cerebral metabolic rates for glucose (rCMRglc) and changes in Hamilton Depression Rating Scale (HAM-D 21-item) scores. Our results might suggest that rCMRglc rates are not altered 1 week after a therapeutic course of ECT in depressed patients. Further studies using new generation PET scanners, which have a higher resolution, in larger numbers of depressed patients, are clearly needed before firm conclusions can be drawn.
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PMID:A preliminary study of the effects of electroconvulsive therapy on regional brain glucose metabolism in patients with major depression. 1086 26

Electroconvulsive therapy, which is used to treat refractory major depression in humans increases seizure threshold and decreases seizure duration. Moreover, the expression of brain derived neurotrophic factor induced by electroshocks (ECS) might protect hippocampal cells from death in patients suffering from depression. As temporal lobe epilepsy is linked to neuronal damage in the hippocampus, we tested the effect of repeated ECS on subsequent status epilepticus (SE) induced by lithium-pilocarpine and leading to cell death and temporal epilepsy in the rat. Eleven maximal ECS were applied via ear-clips to adult rats. The last one was applied 2 days before the induction of SE by lithium-pilocarpine. The rats were electroencephalographically recorded to study the SE characteristics. The rats treated with ECS before pilocarpine (ECS-pilo) developed partial limbic (score 2) and propagated seizures (score 5) with a longer latency than the rats that underwent SE alone (sham-pilo). Despite this delay in the initiation and propagation of the seizures, the same number of ECS- and sham-pilo rats developed SE with a similar characteristic pattern. The expression of c-Fos protein was down-regulated by repeated ECS in the amygdala and the cortex. In ECS-pilo rats, c-Fos expression was decreased in the piriform and entorhinal cortex and increased in the hilus of the dentate gyrus. Neuronal damage was identical in the forebrain areas of both groups, while it was worsened by ECS treatment in the substantia nigra pars reticulata, entorhinal and perirhinal cortices compared to sham-pilo rats. Finally, while 11 out of the 12 sham-pilo rats developed spontaneous recurrent seizures after a silent period of 40+/-27 days, only two out of the 10 ECS-pilo rats became epileptic, but after a prolonged latency of 106 and 151 days. One ECS-pilo rat developed electrographic infraclinical seizures and seven did not exhibit any seizures. Thus, the extensive neuronal damage occurring in the entorhinal and perirhinal cortices of the ECS-pilo rats seems to prevent the establishment of the hyperexcitable epileptic circuit.
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PMID:Electroshocks delay seizures and subsequent epileptogenesis but do not prevent neuronal damage in the lithium-pilocarpine model of epilepsy. 1099 2

A 44-yr-old woman presented with major depression. She was scheduled to receive electroconvulsive therapy under anesthetic care because of drug-induced leukopenia. Her significant past medical history was myasthenia gravis. She had been treated with thymectomy and pyridostigmine. She showed no evidence of muscle weakness while receiving the medication. After preanesthetic assessment, pyridostigmine was continued and routine anesthetics were chosen. Under 100% oxygen inhalation, thiamylal and suxamethonium were administered intravenously. Alternate current was delivered for 5 seconds, which induced seizure satisfactorily. However, asystole lasted for 10 seconds during the procedure. Spontaneous beating appeared followed by tachycardia and bigemina. Normal sinus rhythm returned four minutes later. She recovered smoothly, and showed no evidence of confusion nor muscle weakness. We speculated that pyridostigmine potentiated the ECT-induced vagal reflex and provoked asystole. In the following session, we pretreated her with intravenous atropine prior to thiamylal and suxamethonium. Although the current delivery increased RR-interval up to 1.2 seconds, neither asystole nor serious tachyarrhythmia occurred. Seven sessions of ECT relieved her psychiatric symptoms uneventfully. We presented a case of depression for which ECT was applied. Asystole with ECT seems associated with administration of pyridostigmine for the treatment of myasthenia gravis. Pretreatment with atropine can prevent asystole without inducing hazardous tachyarrhythmia.
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PMID:[Asystole during electroconvulsive therapy in a patient with depression and myasthenia gravis]. 1099 85

Depression in epilepsy patients is not only extremely common, but is often poorly recognized and inadequately treated. Depression can have significant consequences including increased medical utilization, poor quality of life, social disability, and mortality. Etiology of depression is multifaceted with prominent psychosocial determinants. Salient medical issues include iatrogenic causes, especially side effects of antiepileptic drugs (AEDs). In addition, seizures with increased frequency and with "forced normalization" can be associated with mood disturbance. After a thorough search for correctable causes, treatment should not be delayed, and should include both psychotherapy and pharmacologic therapies. Antidepressants remain the mainstay of pharmacologic intervention with the selective serotonin reuptake inhibitors (SSRIs) considered first-line treatment. Venlafaxine, nefazadone, and tricyclic antidepressants (TCAs) can also be used, but with some important caveats. Decreasing the seizure threshold is a common side effect of all antidepressants, but the risk can be minimized and should not prevent vigorous treatment of the depressive state. Other side effects present with varying frequency from the common (eg, sexual dysfunction as seen with SSRIs) to uncommon withdrawal reactions and rare complications of serotonin syndrome. Depression must also be considered a recurring disease, and when a successful regimen is ascertained, adequate continuation of treatment is a necessity. Care must be taken to treat the patient until complete resolution is achieved. Many patients with a major depressive disorder (MDD) will improve with inadequate treatment, but remain encumbered by a smoldering, low-level dysthymia that, in itself, can severely restrict the patient's quality of life.
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PMID:Depression in Individuals with Epilepsy. 1109 81


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