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

The onset of psychotic symptoms later in life requires careful multidisciplinary evaluation, yet may pose significant diagnostic difficulties given current classification schema. Here we describe a patient with new onset of schizophrenia-like symptoms at age 61. Cognitive screening and laboratory tests were within normal limits. However, detailed neuropsychological studies suggested mild to moderate, diffuse cerebral dysfunction, and MR revealed an arachnoid cyst around the right sylvian fissure. Three annual follow-up evaluations demonstrated no additional cognitive deterioration. Neuropsychological findings are discussed along with limitations of current psychiatric nosology and cognitive screening tasks in older patients with new-onset psychosis.
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PMID:Neurobehavioral and neurodiagnostic aspects of late-onset psychosis. 1458 53

Despite clinical evidence of brain dysfunction in schizophrenia, little progress was made for most of the last century in determining its organic parameters. Neuropathology, over the past few decades, has made a substantial contribution to the understanding of cellular and molecular mechanisms of schizophrenia. During the last 10-15 years the concept of schizophrenia as a 'functional' psychosis has changed to the current paradigm of schizophrenia as a neurodevelopmental disorder. Much still has to be unravelled and learnt. This review gives a brief account of the relevant neuroanatomy, viral hypotheses of schizophrenia etiology, pathologic findings reported, concept of neurodevelopmental model and avenues for the future.
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PMID:Neuropathology of schizophrenia--a review. 1502

S100B protein plays a role in promoting the maturation of a variety of neurons in many different CNS regions. Behavioral dysfunction in S100B over-expressed transgenic mice and the chronic elevation of S100B in Down's syndrome and in schizophrenia suggest that S100B over-expression is related to abnormal brain function. Therefore, we believed that the over-expression of S100B protein might be implicated in developmental brain dysfunction. The purpose of this study was to evaluate the serum S100B protein levels in patients with developmental brain dysfunction, such as cerebral palsy and delayed development, and to determine the clinical relevance of serum S100B protein in these patients. The mean values of serum S100B protein were significantly increased in both conditions. Patients with cerebral palsy had a S100B protein level of 3455.8 +/- 5004.6 ng/L and those with delayed development of 2557.0 +/- 2321.0 ng/L, compared with a normal control level of 583.8 +/- 483.0 ng/L (P < 0.05). The over-expression of S100B (defined as the normal mean plus three standard deviations) was found in 47.1% of the total patient group (delayed development (47.5%) and cerebral palsy (47.0%)). The frequency of over-expression was not significantly related to clinical diagnosis, disease severity or to brain MRI findings. However, patients who had periventricular leukomalacia by brain MRI showed a wide range and very high levels of S100B exceeding 10,000 ng/L in some cases. These findings suggest that the pathogenesis implied by the over-expression of S100B protein during brain development may play a role in developmental brain dysfunction.
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PMID:Over-expression of S100B protein in children with cerebral palsy or delayed development. 1503 Sep 8

Neurological soft signs (NSS) are nonspecific indicators of brain dysfunction that are found to be in excess and correlated with cognitive dysfunction and psychopathology in patients with schizophrenia. The aim of the study was to examine whether the severity of NSS determines the efficacy of atypical antipsychotics in schizophrenia. Forty-three patients with schizophrenia were assessed on psychopathology and cognitive domains of executive functioning, memory, attention, and psychomotor speed at baseline and 6 months after they had been switched from typical to atypical antipsychotics. NSS were examined at baseline. The high-NSS group showed more severe psychopathology and greater impaired cognitive function than the low-NSS group at baseline. Following treatment, there were improvements in cognitive functioning and psychopathology with the low-NSS group, which showed significant improvements on measures of verbal fluency, memory, and psychomotor speed and negative symptoms. The high-NSS group also showed improvements on most of these measures, but the improvement was less than that seen in the low-NSS group. The presence of high NSS in schizophrenia patients impedes the improvement in cognitive function with atypical antipsychotics treatment.
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PMID:Neurological soft signs and their relationship to cognitive and clinical efficacy of atypical antipsychotics in schizophrenia. 1527 43

Schizophrenia resistant to treatments with D(2) antagonists is thought to have the changes of extradopaminergic systems. In addition, histamine has been suggested to be a neurotransmitter in the mammalian brain that regulates many brain functions. We have recently found evidence of the role of brain histamine in schizophrenia in basic and clinical studies. Methamphetamine-induced behavioral sensitization, which has been well established as the animal model of schizophrenia, induced the enhanced histamine release, and histamine agonists inhibited the development of behavioral sensitization. As another animal model of schizophrenia, phencyclidine also increased the histamine release. In clinical studies, the levels of N-tele-methylhistamine, a major brain histamine metabolite, were elevated in the cerebrospinal fluid of schizophrenics. Moreover, H(1) receptor binding sites decreased in schizophrenics. Many atypical antipsychotics also increased histamine turnovers. Therefore, the dysfunction of the histamine neuron system may participate in the extradopaminergic brain dysfunction of schizophrenia, and histamine agents may improve the refractory schizophrenia.
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PMID:The role of the central histaminergic system on schizophrenia. 1533 89

Recent research shows that categorizing patients with schizophrenia based on frontal-striatal and frontal-temporal memory profiles may yield neurobiologically meaningful disease subtypes. We hypothesize that parents of patients exhibit similar memory profiles. Both parents of 36 patients with schizophrenia (N = 72) and 26 healthy married control couples (N = 52) participated in this study. All subjects were physically healthy and had no history of neurological illness or alcohol/drug abuse. The presence of a psychiatric and/or personality disorder was assessed with the Comprehensive Assessment of Symptoms and History (CASH) interview, the Schedule for Affective Disorders and Schizophrenia-lifetime (SADS-L) interview and the Structured Interview for DSM-IV Personality Disorders (SIDP-IV), respectively. Cluster analysis of selected measures from the Dutch version of the California Verbal Learning Test (CVLT) delineated parents into two subgroups with distinct memory deficits and a third subgroup without impairments. Specific frontal-striatal and frontal-temporal subgroups, however, were not found. In addition, our results indicated that mothers seem to be more protected against the negative effects of genetic liability to schizophrenia than fathers. Furthermore, relatives with a higher level of intelligence may have more cognitive reserve to compensate for the negative impact of implied brain dysfunction on verbal memory than relatives with a low level of intelligence. Although the parents of patients with schizophrenia could be delineated into subgroups with primary memory deficits, frontal-striatal and frontal-temporal subgroups could not be unambiguously identified. The association that emerged between level of intelligence, gender and severity of memory impairment deserves further exploration.
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PMID:Memory profiles in parents of patients with schizophrenia. 1545 Sep 12

Neurological soft signs (NSS) are characterized by abnormalities in motor, sensory, and integrative functions. NSS have been regarded as a result of neurodevelopmental dysfunction, and as evidence of a central nervous system defect, resulting in considerable sociopsychological dysfunction. During the last decade there has been growing evidence of brain dysfunction in severe aggressive behavior. As a symptom, aggression overlaps a number of psychiatric disorders, but it is commonly associated with antisocial personality disorder. The aim of the present study was to examine NSS in an adult criminal population using the scale by Rossi et al. [29]. Subjects comprised 14 homicidal men with antisocial personality disorder recruited from a forensic psychiatric examination. Ten age- and gender-matched healthy volunteers as well as eight patients with schizophrenia, but no history of physical aggression, served as controls. The NSS scores of antisocial offenders were significantly increased compared with those of the healthy controls, whereas no significant differences were observed between the scores of offenders and those of patients with schizophrenia. It can be speculated that NSS indicate a nonspecific vulnerability factor in several psychiatric syndromes, which are further influenced by a variety of genetic and environmental components. One of these syndromes may be antisocial personality disorder with severe aggression.
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PMID:Neurological soft signs in homicidal men with antisocial personality disorder. 1550 51

Mutations in the gene encoding the cell adhesion molecule L1 or its close homologue, CHL1 (close homologue of L1), cause brain dysfunction in both humans and mice. Here we report that prepulse inhibition (PPI) of the acoustic startle response is impaired in mice deficient in either L1 or CHL1. This newly identified feature may provide a basis for using these mice as models for sensorimotor gating impairment found in some neuropsychiatric disorders such as schizophrenia.
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PMID:Impairment of sensorimotor gating in mice deficient in the cell adhesion molecule L1 or its close homologue, CHL1. 1553 25

Methamphetamine (MAP), the most frequently abused substance in Japan, causes severe drug dependence and psychosis, similar to schizophrenia. It is suggested that long-term alterations in gene expression is related to MAP-induced brain dysfunction, including dependence and psychosis. DNA (cytosine-5) methyltransferase (Dnmt), a methylating enzyme of cytosine residues on CpG-dinucleotides, plays an important role in X chromosome inactivation, genomic imprinting, and gene expression. Reelin is an extracellular matrix protein secreted by GABAergic interneurons. Heterozygous reeler mice that exhibit a 50% downregulation of reelin expression replicate the dendritic spine and GABAergic defects described in schizophrenia. DNA methylation plays an important role in the epigenetic modification of reelin expression. We previously found that MAP could alter expression of Dnmt1 mRNA in the rat brain. In this study, we examined the brain mRNA for Dnmt2 and reelin in MAP-treated Wistar rats. Acute MAP (4 mg/kg) treatment significantly decreased Dnmt2 mRNA by 27% to 39% in hippocampus dentate gyrus, CA1, and CA3 24 h after treatment, and significantly decreased reelin mRNA by 28% in frontal cortex 3 h after treatment. These results suggest that (1) MAP can alter DNA methylation as well as expression of genes in these brain regions, and (2) decrease in reelin mRNA in the frontal cortex is similar to heterozygous reeler mice, which might be related to schizophrenia-like psychotic symptoms of MAP psychosis.
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PMID:Psychostimulant alters expression of DNA methyltransferase mRNA in the rat brain. 1554 6

With optimal pregnancy conditions (natural, enriched diet which includes fish) African (Digo) infants are 3-4 weeks ahead of European/American infants in sensorimotor terms at birth, and during the first year. Infants of semi-aquatic sea-gypsies swim before they walk, and have superior visual acuity compared with us. With adverse pregnancy behaviour (fear of fat, a trend to dieting), neglecting the need for brain fat to secure normal brain development and function, we run a risk of dysfunction--death. Sudden Infant Death Syndrome victims have depressed birth weight, lower levels of marine fat in brainstem than controls, and >80 suffer multiple hypoxic episodes prior to death. Depressed birth weight (more than 10% below mean) is seen in learning and behaviour disorders, and a trend towards weights of less than 3kg is increasing, which supports a rise in antenatal sub optimality. Given marine fat deficiency in pregnancy and infancy, neurons starved for fuel could delay myelination and maturation in the latest developed Frontal Lobes. The phylogenetic oldest Lateral Frontal Lobe System (feed-back mechanism etc.) derived from olfactory bulb-amygdala, which crosses in Anterior Commisure is probably spared, while the Medial Frontal Lobe System derived from Hippocampus-Cingulum and crosses in Corpus Callosum (delayed response task) is most likely affected. The rise in infantile autism (intact vision and hearing) with deficit in delayed response task only, could suggest a deficit in the Medial Frontal Lobe System. The human species is unique; 70% of total energy to the foetus goes to development of the brain, which mainly consists of marine fat. It undergoes pervasive regressive events, before birth, in infancy and at puberty. Minimal retraction of neuronal arborisation is advantageous. Attributable to adverse pregnancy childrearing practice, excessive retraction is likely prenatally and in infancy. Pubertal age affects the fundamental property of nervous tissue, excitability: excessive excitatory drive is seen in early, and a deficiency in late puberty. It is postulated that with adequate marine fat, there is probably no risk of psychopathology at the extremes, whereas a deficiency could lead to paroxysmal (subcortical) dysfunction in early puberty, and breakdown of cortical circuitry and cognitive dysfunctions in late puberty. The post-pubertal psychoses, schizophrenia and manic-depressive psychosis at the extremes of the pubertal age continuum, with contrasting excitability and biological treatment, are probably the result of continuous dietary deficiency, which has inactivated the expression of genes for myelin development and oligodendrocyte-related genes in their production of myelin. The beneficial effect of marine fat in both disorders, in other CNS disorders as well as in developmental dyslexia (DD) and ADHD among others, supports our usual diet is persistently deficient. We have neglected the similarity of our great brain to other mammals, and our marine heritage. Given the amount of marine fat needed to secure normal brain development and function is not known, nor the present dietary level, it seems unduly conjectural to postulate that a dietary deficiency in marine fat is causing brain dysfunction and death. However, all observations point in the same direction: our diet focusing on protein mainly, is deficient, the deficiency is most pronounced in maternal nutrition and in infancy.
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PMID:From superior adaptation and function to brain dysfunction--the neglect of epigenetic factors. 1561 23


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