Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The rapid-cycling variant of bipolar disorder constitutes about 15%-20% of all bipolar patients, and 72%-82% of these patients exhibit less than adequate response to lithium therapy. Valproate's spectrum of efficacy was examined in 78 patients with rapid-cycling bipolar disorder in a prospective, open, 15.8-month trial. Thirty patients received valproate monotherapy and 48 received combination therapy. Treatment assignment was nonrandomized and based on prior treatment history. A marked acute response was seen in 54% of the patients with mania, 87% of those with mixed states, and 19% of those with depression. Marked prophylactic responses were seen in 72% of manic patients, 94% of mixed states patients, and 33% of depressed patients. In addition, moderate acute antimanic responses were observed in another 31% of the patients, prophylactic antimanic responses in 17%, acute antimixed state responses in 0%, prophylactic antimixed state responses in 0%, acute antidepressant responses in 25%, and prophylactic antidepressant responses in mixed states in 34%. Pattern analysis was conducted to examine the spectrum of efficacy of valproate in various cells (e.g., the cohort of patients who had an acute antimanic response to the drug). Pattern analysis showed that 40% of the patients with a marked prophylactic antimanic response had a marked antidepressant response to valproate. However, among the patients with a marked antidepressant response to valproate, 91% had a marked antimanic response. The most common side effects of valproate in our study, as in earlier studies, were gastrointestinal problems (nausea, stomach cramps, diarrhea), tremors, lethargy, and hair thinning.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Spectrum of efficacy of valproate in 78 rapid-cycling bipolar patients. 154 18

The familial transmission risk of developing bipolar disorder for first=degree relatives of the patient is 1.5-10.2%, however, the risk of any affective primary disorder is 15-20% in such relatives. Pregnancy places additional stress on patients, and physiological changes are particularly acute during postpartum. The risk of abnormalities and teratogenicity from psychotropic drugs is significant: taking of phenothiazines, tricyclic antidepressants, monoamine oxidase inhibitors, benzodiazepines, lithium, valproate, and clonazepam require extreme caution. In 225 pregnancies exposed to lithium in the 1st trimester congenital malformations occurred in 11%. Premature birth and macrosomia may also increase, thus halting lithium well before planned conception with weekly serum monitoring is advised. Recurrence of the illness can be managed by electroconvulsive therapy. About 40% of patients can experience postpartum mania or depression. Taking drugs up to delivery can result in behavioral teratogenesis in the neonate even in the absence of physical malformations. Lithium toxicity causes lethargy, hypotonia, tachycardia, coma, cyanosis, and chronic twitching in the newborn. Breast feeding is discouraged in women taking lithium because of the high rate of transmission to the infant. The stress of parenting can also trigger relapses of the disease. The deleterious effect of a manic or depressive mother on the child's development is manifested in criticism and stressing achievement often leads to low self-esteem. It behooves the psychiatrist to frankly reveal the risks of pregnancy to couples who wish to have a child or to advise about the pregnancy to term so they can make an informed decision.
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PMID:Family planning for women with bipolar disorder. 158 11

The author reviews European studies on the effect of the anticonvulsant agent valproate in the treatment of bipolar affective disorder. Since mania is associated with depletion of inhibitory transmitters in the central nervous system and gamma-aminobutyric acid (GABA) is one of the most important inhibitory transmitters, the GABAergic effects of valproate provide a theoretical basis for its use in affective disorders. The European studies, which have been both open and controlled, showed beneficial effects of valproate in acute and prophylactic treatment of bipolar illness, with particularly good results in mania. Side effects reported most often were mild and transient, and included gastrointestinal upset, lethargy, increased levels of hepatic transaminases, and mild alopecia.
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PMID:Valproate use in acute mania and bipolar disorder: an international perspective. 249 52

A 14-year-old boy with mild mental retardation and behavioral features suggestive of the so called Asperger's syndrome is described. From the age of 8 years he has had recurrent episodes of lethargy. At the onset of puberty these episodes took on a more dramatic form and became more reminiscent of cycloid/manic-depressive psychosis. There is a family history of manic-depressive disorder. Neurobiological links with and differences from the syndrome of infantile autism were found. It is suggested that there is still too little evidence clearly to single out the entity of Asperger's syndrome from the spectrum of autistic syndromes.
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PMID:Asperger's syndrome and recurrent psychosis--a case study. 407 13

'Spike-wave stupor' was observed in a 58-year-old male patient with manic-depressive psychosis. Almost continuous atypical spike-wave activity was seen in conjunction with a stuporous episode with stereotyped automatism. Intravenous diazepam ended both the electroencephalographic epileptiform discharges and the clinical stupor. Before and during this episode the patient was treated with an average-dose amitriptyline monotherapy. There was no family history of epileptic seizures. The patient had had electroconvulsive therapy. The history suggests that the analeptic property of amitriptyline induced the 'spike-wave stupor' in this patient.
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PMID:Unusual 'spike-wave stupor' in a patient with manic-depressive psychosis treated with amitriptyline. 618 83

Twenty percent of a cohort of 206 outpatient depressives with no past bipolar history switched during prospective observation. These 41 probands developed manic periods on the average of 6.4 years (median 4, range 1-25) after their first depressive episode. The change in polarity occurred throughout the life span, but was most common in adolescence and early adulthood. The following variables were found useful in predicting this outcome: onset less than or equal to 25 years, bipolar family history, loaded pedigrees, precipitation by childbirth, hypersomnic-retarded phenomenology, and pharmacologically-mobilized hypomania. Although the respective sensitivities of these findings were relatively low (32-71%), their specificities ranged from 69% to 100% for bipolar outcome; the diagnostic specificity of any 3 of these variables when combined was 98%. When compared with nonbipolar depression, bipolar disorder was seldom chronologically secondary to nonaffective psychiatric disorders. These findings suggest that many young depressives with lethargy and oversleeping are not manifesting a "neurotic" disorder, but rather a precursor of primary bipolar affective disorder. Finally, a psychotically depressed adolescent or young adult with positive bipolar family history should be observed for eventual bipolar outcome, especially when the clinical presentation is that of stupor.
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PMID:Bipolar outcome in the course of depressive illness. Phenomenologic, familial, and pharmacologic predictors. 622 91

The purpose of this study is to determine the stability of symptoms of hypomania and depression across repeated affective episodes in patients with rapid-cycling bipolar disorder. Nine patients had a total of 30 depressive episodes and 31 hypomanic episodes during the period of observation. Standardized observer ratings indicated that the three symptoms most consistently reported during depressive episodes were fatiguability, decreased work activities and hypersomnia. These results as well as those from the standardized observer ratings of hypomania indicate that depression in this population consists of a lethargic, hypoactive state while hypomania may be a heightened state of activation. The clinical and theoretical implications of these findings are discussed.
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PMID:The reproducibility of depressive and hypomanic symptoms across repeated episodes in patients with rapid-cycling bipolar disorder. 775 65

Lithium carbonate is a widely used pharmacologic agent for acute bipolar disorder, long term prophylaxis of mania in a bipolar patient, and prevention of "manic overshoot" with an antidepressant in acute depression in a bipolar patient. Although clinical neurological associations with lithium overdose have been-established, there has been a dearth of reports of pathologic changes related to lithium toxicity. We report a case of a 52-year-old Black female with bipolar disorder who had been treated with lithium for over 5 years and who expired 24 days after presenting in a stuporous state with an elevated lithium level of 3.2 mEq/l. Postmortem neuropathologic examination revealed severe cerebellar atrophy of the internal granule and Purkinje cell layers with attendant Bergmann gliosis presumably resulting from chronic lithium use and toxicity. There was also Alzheimer type II cell change in the thalamus and lentiform nuclei possibly due to terminal uremia. In summary, this is a unique case which appears to illustrate cerebellar atrophic changes related to lithium therapy and acute lithium intoxication.
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PMID:Pathologic assessment of cerebellar atrophy following acute lithium intoxication. 902 Mar 92

Lithium carbonate is used for the treatment of bipolar disorder. Because of its widespread use, many women of childbearing age are taking lithium carbonate, which belongs to the US FDA Category D. Administration during pregnancy can result in fetal toxicity. A 17-y-old female with pre-eclampsia and a history of manic depression gave birth to an infant at 37-w gestational age. Several hours prior to delivery, the mother had a lithium level of 2.6 mEq/L. The infant's initial lithium level after birth was 2.1 mEq/L. A subsequent lithium level on the 3rd d of the child's life was 1.4 mEq/L; the half-life in the infant was > 24 h. During the first 4 d of life, the infant was lethargic and exhibited poor suck-swallow coordination that required supplemental enteral feeding. By the 7th d of life, the infant was alert and tolerating all oral feedings. Lithium carbonate readily crosses the placental barrier and can produce teratogenic effects and toxicity. Neonates exposed in utero should be carefully monitored for symptoms of toxicity. In this case only minor toxic effects occurred.
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PMID:Neonatal lithium toxicity as a result of maternal toxicity. 908 Jun 35

Many important aspects of our life are regulated by the free cytosolic Ca2+ concentration. The intracellular Ca2+ signal is regulated both in space, frequency and amplitude. Each cell chooses a unique set of Ca2+ signals to control its function. Ca2+ signal transduction is based on rises in free cytosolic Ca2+ concentration. Ca2+ can come from the extracellular space or be released from intracellular stores. Extracellular Ca2+ enters the cell through various types of plasma-membrane Ca2+ channels and leaves the cell using Ca2+ pumps and Na+/Ca(2+)-exchangers. Ca2+ is accumulated in intracellular stores by means of Ca2+ pumps and is released via inositol 1,4,5-trisphosphate (IP3) and ryanodine receptors. Mutations or abnormalities in one of the above mentioned Ca(2+)-transporting proteins can lead to disease. Skeletal-muscle pathology can be caused by abnormal ryanodine receptors (malignant hyperthermia, porcine stress syndrome, central core disease), plasma-membrane Ca2+ channels (hypokalemic periodic paralysis, muscular dysgenesis mice, paraneoplastic Lambert-Eaton myasthenia syndrome) or Ca2+ pumps (Brody disease). Neurologic disorders can be related to altered function of plasma-membrane Ca2+ channels (episodic ataxia type 2, spinocerebellar ataxia type 6, familial hemiplegic migraine, glutamate excitotoxicity, tottering, leaner, lethargic and stargazer mice), IP3 receptors (Lowe's oculocerebrorenal syndrome, manic depression, Alzheimer's disease, opisthotonos mice) and Ca2+ pumps (deafwaddler mouse and wriggle mouse sagami). Two skin diseases are caused by Ca(2+)-pump mutations (Darier disease and Hailey-Hailey disease). Incomplete X-linked congenital stationary night blindness is caused by a mutation in the plasma-membrane Ca2+ channels in rods and cones.
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PMID:[Intracellular calcium: physiology and physiopathology]. 1119 78


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