Bipolar Manic-depressive Illness Research Articles

A renoprotective role of chitosan against lithium-induced renal toxicity in rats

BackgroundLithium (Li) is considered as the first therapeutic line for treatment of bipolar affective disorders and manic-depressive illness. Renal toxicity can be categorized as the most common undesirable side effect of Li therapy. Therefore, the present study aimed to reveal efficiency of chitosan (CS) as a natural chelator against renal toxicity induced as a result of Li injection. During current experiment, the renal functions (urea, creatinine, blood urea nitrogen (BUN), uric acid and total protein) were determined in serum samples. The urinary excretion of N-acetyl-β-D-glucosaminidase (NAG) was assayed through measuring its level in urine samples. Moreover, markers of the oxidative stress (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), reduced glutathione (GSH) and lipid peroxidation product (LPO)) were assessed in renal tissues. In addition, histopathological and ultrastructural examinations were carried out in that tissue.ResultsIt was found that Li injection caused significant (P < 0.05) elevation in serum urea, creatinin and BUN levels associated with decline in uric acid and T. protein. Moreover, Li increased the urinary excretion of NAG significantly (P < 0.05). Administration of CS orally restored levels of these measurements to normalcy in CS pre-treated group through lowering urea, creatinin, BNU levels and urinary excretion of NAG with enhancing uric acid and T. protein levels.On the other hand, it was found that Li caused significant (P < 0.05) elevation in the LPO level associated with decline in activity of the antioxidant system in the renal tissues. Likewise, it caused severe alterations in the renal levels at histopathological and ultrastructural levels. The treatment with CS reduced the renal LPO associated with stimulating the antioxidant system through increasing levels of SOD, CAT, GPx and GSH in addition to its beneficial role against the histopathological abnormalities.ConclusionsThe CS exhibited promising role in the protection against the oxidative stress and renal toxicity induced as a result of Li injection.

Progress toward discovery of susceptibility genes for bipolar manic-depressive illness and schizophrenia.

The inconsistency in linkage results that has bedeviled psychiatric genetics has been observed to occur regularly in common diseases with complex inheritance. Nonetheless, in two such instances--noninsulin-dependent diabetes mellitus (NIDDM) and inflammatory bowel disease (IBD)--susceptibility genes have been discovered based on the follow-ups of linkage findings. In bipolar illness disorder (BPD) and schizophrenia (SZ), there are some linkage reports with replication of other studies similar to the situation in NIDDM and IBD before the successful positional cloning efforts. Two of the regions with linkage reports, BPD and SZ, on the long arms of chromosomes 13 and 22, show linkage to the same markers in both diseases. This lends some plausibility to the hypothesis of some shared genetic predispositions for both disorders. Cytogenetic evidence offers another positional approach to susceptibility genes. The velocardiofacial syndrome is associated with deletions very close to the linkage region on chromosome 22, and with psychiatric manifestations of both BPD and SZ. Endophenotypes of SZ, previously demonstrated to the be heritable, have been found to have chromosomal linkage in at least one study. These include eye-tracking abnormalities linked to 6p, and an abnormality of the P50 cortical evoked potential linked to chromosome 15. Variants in specific genes have been associated with susceptibility to the psychiatric illnesses. These genetic findings may contribute to etiologic subcategorization of BPD and SZ, and the development of new treatment approaches. A table of genetic terms is included for review

Incorporation of molecular data and redefinition of phenotype: new approaches to genetic epidemiology of bipolar manic depressive illness and schizophrenia

Considerable advances have been made in identifying specific genetic components of bipolar manic depressive illness (BP) and schizophrenia (SZ), despite their complex inheritance. Meta-analysis of all published whole-genome linkage scans reveals overall support for illness genes in several chromosomal regions. In two of these regions, on the lonq arm of chromosome 13 and on the long arm of chromosome 22, the combined studies of BP and SZ are consistent with a common susceptibility locus for the two disorders. This lends some plausibility to the hypothesis of some shared genetic predispositions for BP and SZ. Other linkages are supported by multiple studies of specific chromosomal regions, most notably two regions on chromosome 6 in SZ. The velocardiofacial syndrome is associated with deletions very close to the linkage region on chromosome 22, and with psychiatric manifestations of both BP and SZ. Endophenotypes of SZ, previously demonstrated to be heritable, have been found to have chromosomal linkage in at least one study. These include eye-tracking abnormalities linked to the short arm of chromosome 6, and abnormality of the P50 cortical evoked potential linked to chromosome 15. Variants in specific genes have been associated with susceptibility to illness, and other genes have been associated with susceptibility to side effects of pharmacological treatment. These genetic findings may eventually be part of an integrated genetic, environmental, and interactive-factor epidemiology of the major mental illnesses.

Ten-year outcome: patients with schizoaffective disorders, schizophrenia, affective disorders and mood-incongruent psychotic symptoms.

It is unclear whether outcome in schizoaffective disorders is more similar to schizophrenia or affective disorders. To provide longitudinal data on clinical course and outcome in schizoaffective disorders versus schizophrenia and affective disorders, and determine whether mood-incongruent psychotic symptoms have negative prognostic implications. A total of 210 patients with schizoaffective disorders, schizophrenia, bipolar manic disorders and depression were assessed at hospitalisation and then followed up four times over 10 years. At all four follow-ups, fewer patients with schizoaffective disorders than with schizophrenia showed uniformly poor outcome. Patients with mood-incongruent psychotic symptoms during index hospitalisation showed significantly poorer subsequent outcome (P < 0.05). Schizoaffective outcome was better than schizophrenic outcome and poorer than outcome for psychotic affective disorders. Mood-incongruent psychotic symptoms have negative prognostic implications. The results could fit a symptom dimension view of schizoaffective course.

Karl Kleist, 1879-1960

Back to table of contents Previous article Next article Images In PsychiatryFull AccessKarl Kleist, 1879–1960Andreas Joachim Bartsch, M.D., Klaus-Jürgen Neumärker, M.D., Ernst Franzek, M.D., and Helmut Beckmann, M.D.Andreas Joachim BartschSearch for more papers by this author, M.D., Klaus-Jürgen NeumärkerSearch for more papers by this author, M.D., Ernst FranzekSearch for more papers by this author, M.D., and Helmut BeckmannSearch for more papers by this author, M.D.Published Online:1 May 2000AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail Karl Kleist aspired to take up neuropsychiatry under the most prominent figures of his time. Theodor Ziehen exposed him to Ernst Mach’s empiriocriticism, and Carl Wernicke exposed him to Gustav Theodor Fechner’s psychophysics. Struck by Wernicke’s premature death, Kleist was determined to advance descriptive psychopathology and neuropsychology. His meticulous observations of mental and psychomotor phenomena were framed by Wernicke’s psychic reflex arc, Theodor Meynert’s cerebral connectionism, and associationism. While directing neurological departments at World War I military hospitals, Kleist confirmed similarities between organic mental disorders and endogenous psychoses. Consequently, he identified the latter with less crude manifestations of a related subcortical or cortical pathogenesis. In 1920, Kleist accepted a call to Frankfurt am Main and under his leadership, the Frankfurt School raised sound representatives of psychiatry, neurology, and neurosurgery (e.g., Karl Leonhard, Peter Duus, and Traugott Riechert). Kleist founded the Frankfurt Research Center on Brain Pathology and Psychopathology—an endeavor that illustrated his preference for empirical research and psychophysical body-mind parallelism.Kleist deserves credit for isolating symptomatic (especially influenzal) psychoses, involutional paranoia, episodic twilight states, object- and form-blindness (preceding Derek Denny-Brown’s amorphosynthesis), frontal akinesia and aspontaneity as well as frontal, constructional, limb-kinetic (innervatory), and psychomotor apraxias, e.g., with pure motor negativism (“Gegenhalten”) and automatic motion obedience (“Mitmachen”). Studying cerebral lesions, Kleist refined Wernicke’s typology of aphasias and stratified his structural theory of consciousness. He assembled psychopathological symptoms in semiologic complexes similar to Alfred Erich Hoche’s axis-syndromes. For these syndromes, opposite poles were recognized to facilitate empathic access to a given patient. Furthermore, Kleist combined Wernicke’s syndromatic and Emil Kraepelin’s prognostic principles to classify endogenous psychoses far beyond the genuine Kraepelinian dichotomy. Avoiding hybridization hypotheses, Kleist accommodated bipolar manic-depressive illness, unipolar affective disorders, and marginal (atypical, particularly cycloid) psychoses to phasophrenias. Schizophrenias were restricted to rather guarded long-term catamnestic outcomes (“dementia praecox”). Challenging Bleulerian notions of primary symptoms, Kleist conceptualized schizophrenias as conditions affecting various psychic systems: If specific psychic systems were afflicted in either a simple or combined form (e.g., systems of bestirring and striving in catatonias, affective systems in hebephrenias), schizophrenias were regarded as systematic. Leonhard’s description of unsystematic (extensive) forms of the schizophrenias later completed the Wernicke-Kleist-Leonhard classification of endogenous psychoses. This classification continues to yield seminal insights into both psychopathology and biological psychiatry.Address reprint requests to Dr. Bartsch, Department of Psychiatry and Psychotherapy, University of Würzburg, Fuechsleinstrasse 15, 97080 Würzburg, Germany; [email protected] (e-mail). References and bibliographies for Wernicke, Kleist, and Leonhard are also available from Dr. Bartsch. Photograph courtesy of Karl Kleist's disciple Gerhard Koch. Karl Kleist FiguresReferencesCited byDetailsCited byThe World Journal of Biological Psychiatry, Vol. 5, No. 3Karl Kleist (1879–1960) – A Pioneer of Neuropsychiatry25 July 2016 | History of Psychiatry, Vol. 14, No. 4Recurrent Unipolar Mania in a Psychiatric Hospital Setting in the Fiji Islands18 February 2002 | Psychopathology, Vol. 34, No. 6 Volume 157Issue 5 May 2000Pages 703-703 Metrics PDF download History Published online 1 May 2000 Published in print 1 May 2000

Effect of age, sex steroids, brain region, and genetic strain on brain inositol monophosphatase activity

Inositol monophosphatase (I-M-P'ase), .which catabolizes inositol monophosphate to inositol (Hallcher and Sherman 1980), is a key enzyme in the phosphatidylinositol (PI) cycle that serves as a second messenger system for several brain neurotransmitters (Belmaker et al 1990). Inhibition of inositol monophosphatase by Li (Ki = 0.86 mmol/L) (Moscovich et al 1990) reduces inositol levels by up to 30% (Sherman et ai 1985; Sherman et al 1987). Inositol reduction has been shown to be physiologically important, since replacement by exogenous inositol has been shown to reverse Li's effects in several systems, such as Li-pilocarpine seizures in rats (Kofman et al 1992). Li has powerful therapeutic and prophylactic effects on both phases of bipolar manicdepressive illness (Belmaker 1981). Berridge (1989) proposed that Li's reduction of inositol levels would lead to reduced resynthesis of phosphatidylinositol only in overactive systems, thus leading to their effective dampening. The mechanism of Li's inhibition of inositol monophosphatase is uncompetitive (Nahorski et al 1991). Thus, increasing substrate concentrations to compensate for Li's reduction of the rate of inositol monophosphatase catabolism is particularly ineffective, since elevated substrate concentrations potentiates the inhibition; however, inositol formation will be directly propor-

Maternal inheritance and chromosome 18 allele sharing in unilineal bipolar illness pedigrees

We have replicated the observation of McMahon et al. [1995] that there is excess maternal transmission of illness in a series of previously described unilineal Bipolar manic-depressive illness extended pedigrees [Berrettini et al., 1991]. ("Transmission" is defined for any ill person in a pedigree when father or mother has a personal or immediate family history of major affective disorder.) We divided our pedigrees into exclusively maternal transmission (Mat) and mixed maternal-paternal transmission (in different pedigree branches) (Pat). Using affected sib-pair-analysis, linkage to a series of markers on chromosome 18p-cen was observed in the Pat but not the Mat pedigrees, with significantly greater identity by descent (IBD) at these markers in the Pat pedigrees. As compared with the pedigree series as a whole, the proportion of alleles IBD in the linkage region is much increased in the Pat pedigrees. As shown by Kruglyak and Lander [1995], as the sharing proportion of alleles in affected relative pairs increases, the number of such pairs needed to resolve the linkage region to a 1 cM interval becomes smaller. Genetic subdivision of an illness by clinical or pedigree configuration criteria may thus play an important role in discovery of disease susceptibility mutations.

Prophylactic lithium treatment of unipolar and bipolar manic-depressive illness.

Prophylactic lithium treatment of unipolar and bipolar manic-depressive illness.

Doppler blood flow measurements of umbilical artery of the in vitro perfused human placenta

Lymphoblastoid cell lines established from patients suffering from bipolar manic depression have been used to study the possible involvement of cation transport in the aetiology of this illness. No significant difference was found in the K+ fluxes mediated by the ouabain-sensitive sodium pump, the diuretic-sensitive cotransport system and the passive leak pathway of cell lines established from either control or bipolar subjects. The mean value for the specific binding of 3H-ouabain (sodium pump site number) was significantly higher in the bipolar group (approximately 30%) than in the control group.

Marker genotyping errors in old data on X-linkage in bipolar illness

Investigations of linkage markers of the X-chromosome colorblindness region in bipolar manic-depressive illness (BP) have yielded inconsistent results, with linkage accepted in some and rejected in other studies. Although genetic heterogeneity has been proposed as the reason for differences, other possibilities exist, including systematic procedural errors. Statistical evidence for linkage between the markers, Xg and colorblindness, is present in a series of papers on bipolar illness reported in 1972–1975. The linkage implied by this reanalysis is spurious, since the two markers are at opposite ends of the X chromosome. The presumptive reason for this spurious linkage is that it is a result of systematic genotyping errors. The support provided by these data to the X-linkage hypothesis in BP illness is thus diminished. That is, the linkage to illness may depend on systematic errors in marker genotyping. In general, the possible causes of inconsistency between linkage reports may be divided into statistical and systematic causes. Statistical causes would generally consist of chance differences in sampling, such as might occur under genetic heterogeneity. If this occurs, the reports rejecting linkage may be false negatives, or the reports detecting linkage may be false-positive results. Systematic causes of differences among reports could include systematic errors (or variations) in procedures, including ascertainment, diagnosis, genotyping, or analysis. Consistency of the marker map in a particular study with the known marker map is one test for systematic erros in genotyping.

Extremely Slow Metabolism of Amitriptyline but Normal Metabolism of Imipramine and Desipramine in an Extensive Metabolizer of Sparteine, Debrisoquine, and Mephenytoin

A 34-year-old man with bipolar manic depressive illness suffered from severe adverse effects during treatment with amitriptyline, 50 mg/day. It was subsequently shown that the patient was a slow metabolizer of amitriptyline. However, he tolerated a dose of 200 mg of imipramine/day, which was necessary in order to reach a therapeutic level of about 900 nM for imipramine plus desipramine. Since both antidepressants are subject to the genetic sparteine/debrisoquine oxidation polymorphism, the patient was phenotyped with sparteine. The test performed during paroxetine treatment indicated that the patient was a poor metabolizer. Subsequent tests performed during a drug-free period, however, showed the patient to be an extensive metabolizer, with a sparteine metabolic ratio (MR) of 1.7 and 2.8 and debrisoquine MR of 2.3. It was subsequently shown that paroxetine is a potent, competitive inhibitor of 1'-hydroxybufuralol formation in a human liver microsome preparation (K1 approximately 800 nM). This patient thus illustrates two problems: (a) the erroneous phenotyping due to concurrent medication, and (b) the existence of a very slow amitriptyline elimination apparently not related to the sparteine/debrisoquine oxidation polymorphism.

Cation transport in lymphoblastoid cell lines established from bipolar manic-depressive patients

Lymphoblastoid cell lines established from patients suffering from bipolar manic depression have been used to study the possible involvement of cation transport in the aetiology of this illness. No significant difference was found in the K + fluxes mediated by the ouabain-sensitive sodium pump, the diuretic-sensitive cotransport system and the passive leak pathway of cell lines established from either control or bipolar subjects. The mean value for the specific binding of 3 H-ouabain (sodium pump site number) was significantly higher in the bipolar group (approximately 30%) than in the control group.

Disturbance of water and sodium in a manic-depressive illness.

Specific questioning and frequent observation of a 69 year-old woman with cyclic bipolar manic-depressive illness showed that she had disturbances of thirst, appetite, bowel and bladder function and dramatic changes in body weight, in association with different phases of her mental illness. Examination of one manic phase under constant diet and inpatient control showed cardiovascular changes, sodium retention, body weight gain, with raised aldosterone secretion but steady vasopressin. There appears to be a sub-group of manic-depressive patients with evidence of disturbed hypothalamic functions as part of their mental illness, as shown particularly by changes in water and electrolyte metabolism.

Effect of Corticosteroids on Renal Excretion of Lithium

Lithium salts are being used increasingly to treat patient with affective disorders, especially acute mania, or bipolar manic-depressive illness. For therapeutic effect the lithium content must be maintained at or above a particular level. Lithium poisoning due to overdosage may be seen occasionally, and its course is determined primarily by the rate of renal lithium elimination. A search is therefore indicated for procedures that could raise the lithium clearance. In a number of reports renal lithium excretion has been studied in relation to the excretion of water, sodium, potassium and hydrogen, but effects of sodium or water on the lithium excretion has not yet been clarified. Hence the present study was undertaken to investigate the effects of corticosteroid on the excretion of lithium ion. The female rat(Sprague-Dowley), weighing from 200 to 300g, was injected with 50mg/kg of lithium chloride intraperitoneally, and then injected with graded dosage of fludrocortisone and dexamethasone in each group. During the injected rats were incubated in metabolic cage, 24 hour urine of rats were collected. At 24 hours after injection, the rats were sacrificed with guillotin, the blood were collected. And then the concentratios of , , of collected urine and serum were checked by Flame photometer. The results are summarized as follows; 1. Fludrocortisone decreased the serum concentration of lithium and increased the urinary excretion of lithium. 2. In the group treated with low dose of dexamethasone(0.1mg/kg), the serum concentration of lithium was decreased and high dose of dexamethasone (1mg/kg) increased the urinary excretion of lithium. 3. Fludrocortisone increased the urinary in serum and decreased in urine, but opposite effects were occurred in dexamethasone. By above results, it may be concluded that corticosteroid increased the urinary excretion of lithium and decreased the serum concentration of lithium, but it seems to be there is no relationship between these effects of corticosteroid and of the renal or transport.

A Study of State-Dependent Reversal of Tardive Dyskinesia

A longitudinal study of a case report in which bipolar manic-depression was complicated by tardive dyskinesia indicates an antithetical relationship between the severity of tardive dyskinesia and that of depression as well as mania. Reversal of tardive dyskinesia in depression was compatible with the current neurochemical postulates of these disorders. The scarce reports of state-dependent dyskinesias are reviewed in the hope that this can be a useful probe in human studies. Finally, the "undopamine" hypothesis of tardive dyskinesia as a hypernoradrenergic state is discussed and the need for phenomenological-neurochemical characterization of tardive dyskinesia is emphasized.

MANIC DEPRESSIVE ILLNESS

Psychodynamic features of families with multigenerational bipolar manic-depressive illness are described. Repetitive maladaptive patterns, including avoidance of affect, unrealistic standards of conformity, absence of intimate relationships apart from family, displaced parental low self-esteem, and fears related to illness heritability, may influence the maintenance of family pathology.

Reduced cholecystokinin immunoreactivity in the cerebrospinal fluid of patients with psychiatric disorders

The close relationship of cholecystokinin peptides with some of the dopamine pathways and the limbic system suggests a putative role for these peptides in the pathophysiology of neuropsychiatric disorders such as Parkinson's disease, manic-depression and schizophrenia. By use of radio-immunoassay, we report a significant decrease in cholecystokinin-immunoreactivity in the cerebrospinal fluid of patients with bipolar manic-depression and untreated schizophrenia in comparison to control subjects.

Behavioral Toxicity to Medications in a Six-Year-Old Boy: A Genetic Marker?

The case of a 6-year-old boy is presented who developed a stereotyped behavioral response to a wide range of sympathomimetics and minor central nervous system stimulants. The behavioral changes closely resembled the existing descriptions of mania in childhood. Since the boy's mother suffers from bipolar manic-depression, and some of her manic episodes have been secondary to sympathomimetics, we hypothesize that her son is showing a similar profile of behavioral reactivity and that in him, it is a behavioral marker of the genetic predisposition to bipolar manic-depression. The relevant literature is reviewed and certain ethical issues are highlighted.

Serum dopamine-beta-hydroxylase activity and family history of patients with bipolar manic-depressive illness.

Acta Psychiatrica ScandinavicaVolume 68, Issue 2 p. 140-141 Serum dopamine-beta-hydroxylase activity and family history of patients with bipolar manic-depressive illness Zoltán Rihmer M.D., Zoltán Rihmer M.D. National Institute for Nervous and Mental Diseases Budapest 27, Pf. 1, 1281 HungarySearch for more papers by this authorGyörgy Bagdy Ph.D., György Bagdy Ph.D. National Institute for Nervous and Mental Diseases Budapest 27, Pf. 1, 1281 HungarySearch for more papers by this authorMihály Arará M.D., Ph.D., Mihály Arará M.D., Ph.D. National Institute for Nervous and Mental Diseases Budapest 27, Pf. 1, 1281 HungarySearch for more papers by this author Zoltán Rihmer M.D., Zoltán Rihmer M.D. National Institute for Nervous and Mental Diseases Budapest 27, Pf. 1, 1281 HungarySearch for more papers by this authorGyörgy Bagdy Ph.D., György Bagdy Ph.D. National Institute for Nervous and Mental Diseases Budapest 27, Pf. 1, 1281 HungarySearch for more papers by this authorMihály Arará M.D., Ph.D., Mihály Arará M.D., Ph.D. National Institute for Nervous and Mental Diseases Budapest 27, Pf. 1, 1281 HungarySearch for more papers by this author First published: August 1983 https://doi.org/10.1111/j.1600-0447.1983.tb06992.xCitations: 1AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume68, Issue2August 1983Pages 140-141 RelatedInformation

The phenomenology of bipolar I manic-depressive illness.

There have been several advances in the knowledge of the phenomenology of Bipolar Manic-Depressive Illness in the past decade. Studies of groups of carefully diagnosed bipolar patients have characterized features of the course of illness, the presence and prognostic influence of psychotic features, the influence of stressful life events, features of social adjustment and aspects of personality and long-term functioning. Similar studies of bipolar illness in non-western cultures would be of interest.