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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Olanzapine, a serotonin-dopamine-receptor antagonist, is an atypical antipsychotic agent used to treat schizophrenia and other psychotic disorders. It is preferred over older antipsychotics because of its relatively low frequency of sedation, orthostatic hypotension, extrapyramidal symptoms, and anticholinergic side effects. A 45-year-old man with well-controlled type 2 diabetes mellitus experienced an abrupt worsening of his diabetes after 3 years of olanzapine therapy His hemoglobin A1c (HbA1c) level rose from a baseline of 5.9-6.2% to 12.5%. Discontinuation of olanzapine by means of a 3-month taper resulted in a reduction in HbA1c to pretreatment levels. Although cases of olanzapine-induced hyperglycemia have been documented in the literature, this complication has not been reported in a patient maintained on therapy for this duration. Clinicians should be aware of this possible complication in patients receiving long-term olanzapine therapy.
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PMID:Dramatic worsening of type 2 diabetes mellitus due to olanzapine after 3 years of therapy. 1171 19

Cognitive deficits in schizophrenia have been observed with neuropsychological tests of executive function, traditionally considered sensitive to frontal lobe damage. These impairments affect planning abilities, as well as the aptitude to initiate and regulate a goal-directed behaviour. On the other hand, negative symptoms of schizophrenia are widely suspected to reflect a frontal lobe dysfunction. Based on a review of a hundred papers, the present article analyses the anatomical and neuropsychological evidence of disturbed frontal lobe functioning in patients with negative schizophrenic symptoms. The phenomenological similarity of some schizophrenic symptoms to the clinical features of patients with prefrontal injury inspired the hypothesis of damaged frontal lobe in the former disorder. The morphological findings of neuroimaging studies brought inconsistent conclusions, with some researchers noting no differences between patients and control subjects while others observing reduced prefrontal volumes in schizophrenia. The functional neuroimaging demonstrated a reduced frontal blood flow relative to the general cerebral perfusion in patients with schizophrenia. Even though the overall neuroimaging literature provides reliable evidence of frontal impairment in schizophrenia, the average magnitude of the difference between patients and healthy controls is insufficient to defend the hypothesis of frontal lobe dysfunction, as far as brain volume, resting metabolism or blood flow are concerned. The only measure, which clearly distinguishes between the patients' and controls' distributions, is the functional neuroimaging of the frontal lobe while subjects are performing an experimentally controlled task. Schizophrenic patients fail to activate their frontal cortex when the task requires it. Analysing executive abilities in relation to symptom expression leads to recognising the fact that frontal dysfunction is a characteristic of only a sub-syndrome of schizophrenia. The factor analysis of the clinical features consistently reveals three syndromes in schizophrenia, termed disorganisation, positive and negative syndromes. The substantial body of evidence that patients exhibit more than one syndrome indicates these are dimensions within a single illness rather than discrete diseases. Liddle labelled the negative syndrome as "psychomotor poverty" and associated it with malfunction of the neuronal projections from dorsal prefrontal cortex to thalamus via striatum, connections involved in the initiation of mental activity. His hypothesis was supported by the work of other, independent research groups. The patients with negative symptoms, in contrast with the nonnegative symptom group, tend to demonstrate reduced neuronal activation of the frontal cortex during executive task realisation. The nonnegative patients are indistinguishable from the healthy control subjects in this region. Neuropsychological studies reveal that severity of psychomotor poverty is associated with slowing of mental processing and deficits in tasks that require planning abilities. These frontal functions are identified with the selection, the initiation and monitoring of a wide variety of behavioural processes. It was hypothesised that executive dysfunction will appear through different patterns across symptom subtypes, but few studies sought to validate this assumption. Finally, researchers make little effort to develop theoretical conceptualisations of the aetiology of negative schizophrenic symptoms, despite the growing body of evidence on its resemblance to the dorsolateral frontal lobe syndrome. Frith proposes that defects in the initiation of spontaneous action underlie these clinical phenomena, but his definition is not specific enough to be confronted to existing literature, neither has been empirically tested. Disturbed executive functioning has detrimental impact on the quality of daily living in patients with schizophrenia. Indirect observation of the latter accounts for defective long-term adaptation, which has been correlated to severity of negative symptoms and, although not consistently, to executive deficit as assessed by neuropsychological testing. Unfortunately, this area of research lacks ecologically valid studies. Measuring executive dysfunction as it occurs in the natural setting of the patient and validating dissocialbility of frontal deficits with respect to the schizophrenic symptomatology could lead to greater individualization of treatment plans and therefore to more efficient therapy outcome.
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PMID:[Hypofrontality and negative symptoms in schizophrenia: synthesis of anatomic and neuropsychological knowledge and ecological perspectives]. 1176 Jun 90

A 33-year-old male patient began to develop schizophrenia-like symptoms and slowly progressive cerebellar ataxia. He was 170 cm tall and he had mild frontal baldness. Psychiatrically he was aconative, only willing to do nothing all day long after admission. He had neither hallucinations nor delusions, and his mental acuity was normal. Neurological examination revealed positive cerebellar signs including clumsiness in F-N-T and K-H-T and dysdiadochokinesis. He could neither stand up nor walk because of ataxia. The brain MRI showed severe cerebellar atrophy with normal basal ganglia. His EEG and the value of NCV were within normal range, whereas electroretinography showed a notable abnormality, pointing to the extremely small b-wave, resulting in a negative shape of the ERG. Although he was eating sufficiently, the level of serum iron and ferritin remained constantly low. The serum copper level was within normal range, whereas the serum ceruloplasmin level was mildly decreased. A hepatic biopsy indicated no accumulation of copper or iron. This case suggests the importance of the investigation of the serum iron and ceruloplasmin levels in patients who have cerebellar degeneration with psychosis.
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PMID:[A case of cerebellar degeneration with schizophrenia-like psychosis, severe iron deficiency, hypoceruloplasminemia and abnormal electroretinography: a new syndrome?]. 1188 36

Within 1 year of severe trauma to the left anterior temporal lobe and minor injury to the frontal lobes, a 35-year-old individual developed classic positive and negative symptoms of schizophrenia. His antipsychotic drug-induced parkinsonism was greater on the left side, suggesting increased left striatal dopaminergic transmission. The authors propose that even in adulthood, significant and selective disruption of fronto-temporal connectivity is sufficient to produce a phenocopy of schizophrenia.
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PMID:Limbic cortical injury sustained during adulthood leads to schizophrenia-like syndrome. 1240 60

We introduce a multimodular, psychological outpatient, intervention program for the treatment of the early prodromal stage which includes individual and group psychotherapy, cognitive training, and family support. The conceptual framework is comprised of the vulnerability and stress-coping concept for schizophrenia. We use cognitive-behavioural strategies which are derived from first-episode and relapse prevention in the treatment of schizophrenia and from the treatment of anxiety disorders and depression. We report the case of a 25-year-old college student in the early prodromal state who was treated by the program. His self-experienced neuropsychological deficits improved, depressive and anxiety symptoms decreased, and positive self-concept was stabilised. During the treatment period of 1 year, social deterioration and prepsychotic and psychotic symptoms were prevented.
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PMID:[A psychological early intervention program for the prepsychotic prodromal state. A case report]. 1296 18

Sam Greenhouse began his involvement in mental disorders research in 1954 when appointed chief of the Theoretical Statistics and Mathematics section at the National Institute of Mental Health. He remained with the NIMH until 1966. Despite moving on to several other positions at the NIH and at the university during the ensuing years, he continued as a consultant to NIMH investigators. He also participated actively as an advisor and co-investigator on a number of important collaborative research programmes launched by the Institute in the 1970s and 1980s. His contributions to the design and methodology of the first clinical trials of drugs for the treatment of schizophrenia, to research aimed at revising the national and international classification systems for the mental disorders, and his participation in the planning of the first attempt to use the collaborative research model to test hypotheses about the genesis of a specific mental disorder (depression), are described. Finally, the signal importance of the 'profile analysis of variance' method that he and Seymour Geisser developed, to research on personality and mental disorders, is examined in detail. The authors describe applications of the method in their own research on the classification of the mental disorders, predicting response to drug treatment and the variations in the expression of mental illness across different cultures. Sam worked in mental health during an era of revolutionary changes in the diagnosis and treatment of mental disorders. The field was acutely aware of his many contributions to the progress of research and his colleagues are very grateful to have had the opportunity to work with him.
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PMID:The contributions of Sam Greenhouse to research on psychiatric diagnosis and psychopharmacology. 1456 13

Chromosome anomalies are responsible for a significant proportion of patients with mental retardation, and congenital anomalies. Development of new molecular cytogenetic techniques has provided a powerful tool for detection of patients with subtle chromosome abnormalities. Particularly, investigation of the gene-rich subtelomeric regions has generated interest regarding the implications and prevalence of cryptic chromosomal rearrangements. Here we describe an adult with a submicroscopic deletion of 18pter, detected by subtelomeric FISH probe. The patient is a 42-year-old man with a history of developmental delay, moderate mental retardation, and symptoms of paranoid schizophrenia since adolescence. His physical examination is remarkable for only a few dysmorphic findings typically seen in 18p- syndrome (round face, hypertelorism, down-slanted palpebral fissures, temporal narrowing, small hands and feet). He lacks significant short stature, skin changes, and associated anomalies involving internal organs. All known patients with deletions of the short arm of chromosome 18 have either loss of large parts of 18p or of the entire p-arm, or have complex chromosomal rearrangement involving other chromosomes. To our knowledge, this is the first description of a cryptic subtelomeric deletion of 18p and the first case of such a chromosomal anomaly in a patient with schizophrenia. Small subtelomeric chromosomal deletions would be missed by standard G-banded karyotyping. Therefore, FISH analysis using subtelomeric probes should be considered for diagnostic evaluation of patients with psychiatric symptoms and mental retardation in whom the karyotype is normal.
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PMID:Subtelomeric deletion of 18p in an adult with paranoid schizophrenia and mental retardation. 1470 8

Kenneth Leslie Artiss (1913-2001) was an Army psychiatrist who did significant investigative work in schizophrenia and milieu therapy and whose broad scholarship led to decisively important and enduring contributions to operational psychiatry. After retirement from military service, he developed a bold approach for teaching psychodynamic theory and its applications, and he led seminars for psychiatry residents and other physicians for over four decades. He was among the first to apply psychodynamic ideas to improve oncology practice. His death in 2001 motivated a group of his military students to memorialize his life and contributions and to demonstrate why they merit continuing consideration.
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PMID:The contributions of Kenneth Leslie Artiss, M.D. 1471 33

Karl Kleist (1879-1960) was instrumental in pioneering German neuropsychiatry and neuropsychology, including the description of frontal, constructional, limb-kinetic (innervatory) and psychomotor apraxias, frontal akinesia and aspontaneity, as well as object and form blindness. Besides isolating episodic twilight states, involutional paranoia and symptomatic (especially influenza) psychoses, he was particularly involved in applying Wernicke's syndromatic and Kraepelin's prognostic and aetiological principles to classify "neurogenous" psychoses by refuting the assumption of mixed entities whenever possible. Thus, has phasophrenias denoted manic-depressive illness, unipolar affective disorders and marginal, i.e., atypical psychoses. The rather benign cycloid psychoses form the most prominent examples of the latter. Schizophrenias, on the other hand, were limited to poor long-term catamnestic outcomes. Kleist conceptualized the core group of schizophrenic illness as psychic system diseases-hence the origin of the term "systematic schizophrenias" within the Wernicke-Kleist-Leonhard School. Kleist was mainly influenced by Wernicke and his psychic reflex arc, but Ernst Mach's empiriocriticism, Theodor Meynert's cerebral connectionism, and associationism also shaped his outlook. Kleist's localization of cerebral functions by lesion analyses was indeed the best available at the time and continues to reveal insights to the interested reader. From his Frankfurt School, which may have been the last of a completely unified neuropsychiatry, came sound representatives of psychiatry, neurology and neurosurgery. His technical mastery and achievements seem indisputable, but his balancing acts during the Third Reich may today be questioned. Despite joining the National Socialist German Workers' Party (NSDAP) and the local Court of Genealogical Health (Erbgesundheitsgericht), Kleist was, however, one of the few German physicians who continued to treat Jewish patients, to employ Jewish colleagues and to voice evident criticism of the policies of "eugenics" and "euthanasia". This paper attempts to illuminate Kleist's biography and life's work in the relevant historical context.
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PMID:Karl Kleist (1879-1960)- a pioneer of neuropsychiatry. 1474 Jun 33

A 44-year-old male patient was hospitalised with paranoid schizophrenia in 1985. Depot neuroleptic treatment was started which successfully prevented further psychotic relapses for the next ten years. His myasthenia gravis started with bulbar signs in 1997 and the symptoms soon became generalized. The diagnosis of myasthenia gravis was confirmed by electromyography, by positive anticholinesterase test and by the detection of anti-acetylcholine receptor antibodies in the serum. Mediastinal CT examination showed enlarged hilar lymph nodes on the left but no thymic pathology was observed. Mediastinoscopy was performed and biopsies were obtained from the affected nodes. Histology revealed sarcoidosis. The patient suffered respiratory crisis following the thoracic intervention (in September 1998). Combined oral corticosteroid (64 mg methylprednisolone/e.o.d.) and azathioprine (150 mg/day) treatment regimen was initiated and complete remission took place in both the myasthenic symptoms and the sarcoidosis. The follow-up CT scans showed no mediastinal pathology (January 2000). During steroid treatment a transient psychotic relapse occurred which was successfully managed by supplemental haloperidol medication added to his regular depot neuroleptics. The patient currently takes 150 mg/day azathioprine and receives 40 mg/month flupentixol depot i.m. His physical and mental status are stable and he has been completely symptom free in the last 24 months. The association of myasthenia gravis and sarcoidosis is very rare. To our best knowledge no case has been reported of a patient suffering from myasthenia gravis, sarcoidosis, and schizophrenia at the same time.
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PMID:Myasthenia in a patient with sarcoidosis and schizophrenia. 1533 Mar 99


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