Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Is brain pathology in schizophrenia topographically distinct? If so, are the putative regional changes unique to the disorder? To address these questions, 56 chronic schizophrenic Ss were compared with 16 psychiatric control Ss with mood disorders and with 31 healthy volunteers on multiple-volume measures of regional cerebral atrophy obtained with computed tomography. Generalized cortical and subcortical enlargement of spaces filled with cerebrospinal fluid sparing only the occipitoparietal cortex was found in the schizophrenic Ss compared with normal control Ss. Statistically significant differences in the extent of perisylvian atrophy were noted between schizophrenic Ss and patients with mood disorders: Schizophrenic Ss evidenced greater dilation of perisylvian fissures and sulci. The implications of the results for future research and for recent theories on the etiology of schizophrenia are discussed.
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PMID:Structural cerebral pathology in schizophrenia: regional or diffuse? 840 57

Patients with schizophrenia have larger lateral ventricles, less cerebral substance and smaller mesial temporal lobe structures than groups of normal controls, but it has proved difficult to link these volumetric abnormalities with clinical features of the illness. Such quantitative techniques may overlook qualitative abnormalities of importance. We therefore compared a neuroradiologists' clinical assessment of gross structural abnormalities, generalised 'atrophy' and high intensity signal (HIS) foci, as detected on the first and second echo of a long TR sequence, in 42 patients with schizophrenia (22 treatment responsive, 20 treatment resistant) and 50 normal controls. The schizophrenic group included two (5%) subjects with gross lesions, two (5%) with cerebellar atrophy, 21 (52%) with at least a mild degree of cerebral atrophy, and 15 (38%) with one or more HIS foci; the comparable figures in the controls being 2, 0, 2 and 14%, respectively. Controlling for age, patients with schizophrenia had a substantially elevated rate of cerebral atrophy (odds ratio (OR) = 11.7, p < 0.0001). Treatment-resistant schizophrenics showed a tendency (OR = 2.8, p = 0.06) to greater atrophy than those who were treatment responsive, whereas our previous volumetric study showed no such difference. In contrast, the presence of HIS foci was only related to age. The degree of atrophy was correlated with the number of HIS foci (r = 0.31, p = 0.014). Taken together with previous studies, these findings demonstrate the value of qualitative examination of MRI images in patients with schizophrenia.
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PMID:Qualitative cerebral morphology in schizophrenia: a magnetic resonance imaging study and systematic literature review. 918 15

In forty schizophrenic (or schizophreniform disorder) patients diagnosed according to DSM-IV, the magnetic resonance imaging was performed. The T2 relaxation time was measured in selected brain regions from the dorsolateral prefrontal cortex as well as in amygdala. These results were compared with clinical parameters regarding severity of psychopathology and improvement after neuroleptic treatment. The mean T2 values of grey matter of right inferior frontal gyrus were significantly higher in patients with schizophreniform disorders (those patients were clinically diagnosed as suffering from cycloid psychoses) than in other types of schizophrenia. The T2 values of this region correlated inversely with the severity of negative symptoms before treatment. The T2 values of gray matter of left inferior frontal gyrus correlated positively with the severity of schizophrenic symptoms before treatment. Mean T2 values of left amygdala were significantly higher in patients showing less favorable improvement after neuroleptic treatment in comparison to those who improved better. No correlation was found between the presence of brain atrophy and T2 values in brain regions studied. The results allow to suggest that the measurement of T2 relaxation time might reveal interesting relations between clinical picture and neuroradiologic findings in schizophrenia, however clinical significance of such parameters still requires further elaboration.
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PMID:[Selected parameters of magnetic resonance imaging of the brain, clinical picture and recovery after treatment in schizophrenia. Preliminary report]. 952 53

MR imaging of the head was performed in forty schizophrenics (DSM-IV). Mental status was evaluated before and during 8-weeks of neuroleptic treatment. Cortical atrophy in frontal and temporal regions was found in 40% of subjects. They were older, had longer history of schizophrenia, were less active professionally and were more frequently hospitalized. Patients with and without cortical atrophy in MRI did not differ in the severity of schizophrenic psychopathology at baseline. During neuroleptic treatment negative schizophrenia symptoms were significantly better diminished in patients without cortical atrophy than in subjects with cortical atrophy in MRI; this regarded specially the severity of emotional blunting. Clinical improvement after 8-weeks of neuroleptic administration was less favorable in patients with cortical atrophy.
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PMID:[Cortical atrophy in MRI, mental status and neuroleptic treatment effect in schizophrenia]. 954 81

Autopsy reports of patients with mitochondrial encephalopathy with lactic acidosis and strokelike episode (MELAS) are rare. This report documents the clinical and autopsy findings of a 47-year-old woman with MELAS syndrome. The diagnosis was corroborated by documenting a mitochondrial DNA mutation tRNA-Leu (UUR) at position 3243. The patient's clinical history was marked by schizophrenia, peptic ulcer disease, constipation requiring hemicolectomy, migraine headaches, deafness, and a left temporal lobe infarct. At autopsy, a muscle biopsy demonstrated numerous ragged red fibers and a partial cytochrome C oxidase deficiency. By electron microscopy, increased numbers of slightly hypertrophic mitochondria were observed focally within myocytes and vessel walls; paracrystalline mitochondrial inclusions were not seen. The brain at autopsy showed mild cerebral atrophy and diffuse cortical gliosis. Prominent bilateral basal ganglia calcifications and vascular sclerosis were present, and a small remote left temporal lobe infarct was seen.
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PMID:Mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes (MELAS) syndrome: an autopsy report. 982 26

Recent evidence from controlled CT and MRI longitudinal studies suggests that some cerebral ventricular enlargement and hemispheric volumetric reductions (e.g. cerebral atrophy) may have a progressive component in patients with schizophrenia. These studies vary in cohort composition, stage of illness examined, duration of follow-up interval, imaging techniques used, and specific brain regions with findings. They also conflict with earlier evidence suggesting that schizophrenia is a neurodevelopmental disorder with brain pathological deviance occurring prior to the illness onset. The newer brain imaging reports may be detecting subtle brain plasticity that results from a continuing cortical disruptive process, may be epi-phenomena caused by scanning and image analysis artifacts or may possibly reflect systemic physiological fluctuations. Future longitudinal studies of subjects at all stages of illness using a variety of new technologies are needed to clarify these findings.
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PMID:Defining the course of brain structural change and plasticity in schizophrenia. 1068 56

The administration of the omega-3 fatty acid eicosapentaenoic acid (EPA) to a drug-naive patient with schizophrenia, untreated with conventional antipsychotic medication, led to a dramatic and sustained clinical improvement in both positive and negative symptoms. This was accompanied by a correction in erythrocyte membranes of abnormalities in both n-3 and n-6 highly unsaturated fatty acids and with reduced neuronal membrane phospholipid turnover, as evidenced by serial 31-phosphorus cerebral magnetic resonance spectroscopy. Using recently developed techniques of image segmentation, subvoxel registration and quantitation, analysis of serial high-resolution 3D cerebral MRI scans showed that, in the year before EPA treatment, cerebral atrophy was taking place and that this atrophy was reversed by six months of EPA treatment. These results demonstrate that EPA can reverse both the phospholipid abnormalities previously described in schizophrenia and cerebral atrophy. They provide strong further evidence in support of the membrane phospholipid model of schizophrenia.
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PMID:Eicosapentaenoic acid treatment in schizophrenia associated with symptom remission, normalisation of blood fatty acids, reduced neuronal membrane phospholipid turnover and structural brain changes. 1075 Feb 63

Recent reports from serial brain scans suggest that the rate of ventricular expansion and/or brain atrophy may be accelerated in at least some schizophrenics. The authors assessed the effect of state changes upon such findings.Within-subject 3D MRIs were assessed for ventricular and brain volumes during periods of [partial] remission and of exacerbation of psychosis. Additional scans at comparable within-subject SAPS were used to assess rates of change in volumes that were independent of SAPS changes. Correlations of changes of ventricle and brain volumes vs. change of SAPS cores between scans revealed that ventricle volumes decreased during a period of psychotic exacerbation and increased at a time of [partial] remission (r(p)=-0.666; P<0.0005); conversely, brain volumes increased during psychotic exacerbation and decreased at [partial] remission (r(p)=+0.448; P=0.032). Scans at comparable SAPS scores suggested that the majority of patients had rates of ventricular expansion comparable to controls (0.9+/-0.6 cc/year), though two patients appeared to have rates of ventricular increase of 4.5+/-2. 1 cc/year (Lilliefores P=0.036; K-means clustering F=17.75). Exacerbation of psychosis in schizophrenia is accompanied by evidence of brain swelling, especially of periventricular brain, with encroachment of brain substance upon ventricular volumes. Controlled for state changes, the majority of schizophrenics show rates of ventricular expansion or brain atrophy indistinguishable from controls.
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PMID:Brain and ventricle instability during psychotic episodes of the schizophrenias. 1086 8

Although the psychotic symptoms in schizophrenia can be alleviated by treatment with dopaminergic receptor antagonists, the etiology and underlying neurochemical pathology remains obscure. Both neuropathological and magnetic resonance imaging studies have found evidence for neuronal loss and atrophy in the thalamus in schizophrenia, implicating this key structure for gating information to cortical areas in the pathophysiology. Recent studies have also found evidence of synaptic loss in the thalamus in schizophrenia. To further examine possible synaptic disturbances, we studied the synaptic related protein rab3a as a marker for synaptic density, using both quantitative Western blotting and immunohistochemistry. The material consisted of brains from 22 schizophrenic patients (mean age 79.3 years), and 24 control subjects (74.8 years). Reduced rab3a protein levels were found in the left thalamus in schizophrenia (0.47 +/- 0.17 vs. 1.00 +/- 0.18; p < 0.0001), while a less marked decrease was found also in the right thalamus (0.75 +/- 0.13 vs. 1.00 +/- 0.09; p < 0.0001). Immunohistochemistry, performed on two schizophrenic and two control brains, revealed that rab3a immunoreactivity was most reduced in the left anterior and mediodorsal thalamic nuclei. Therefore, we extended the study to brain regions connected these thalamic nuclei. Reduced rab3a protein levels were found schizophrenia also in the frontal cortex, hippocampus, gyrus cinguli, and parietal cortex, while no significant differences were found in the temporal cortex, or in cerebellum. The reduction in rab3a was not found to be secondary to confounding factors such as age-differences, post-mortem delay time, generalized brain atrophy, or antipsychotic medication. Therefore, the reduction of rab3a probably reflects synaptic disturbances, possibly synaptic loss, in the limbic system and neocortical areas, in schizophrenia. This part of the brain is known to be involved in behavioral and emotional control, and thus to be crucial for higher mental functions, suggesting that synaptic disturbances in the limbic system may be of importance in the development of psychotic symptoms in schizophrenia.
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PMID:Reduction of the synaptic protein rab3a in the thalamus and connecting brain regions in post-mortem schizophrenic brains. 1104 Dec 84

We report a young adult female case of Wilson's disease presenting with mental disorder and frontal lobe signs. The patient was admitted to our neurological unit on October 4, 1999 because of schizophrenia-like symptom, dysphagia, dysarthria and gait disturbance. She showed slowly progressive rigidity and dystonia. Her parents were the second cousins. Neurological examination revealed bilateral pyramidal and extrapyramidal signs, frontal lobe signs (include the imitation behavior). Tendon reflexes were slightly exaggerated in all extremities. Bilateral Babinski, Chaddock and Hoffmann signs were positive. Her verbal IQ on the Wechsler Adult Intelligence Scale-revised was 49. Biochemical examination revealed low plasma copper and ceruloplasmin concentration. Cerebrospinal fluid was normal. Cranial MRI demonstrated diffuse brain atrophy and enlargement of the lateral ventricles. T2-weighted images of the MRI demonstrated hyperintense signal in both thalamus and basal ganglia. SPECT showed hypoperfusion in the left frontal lobe, both thalamus and basal ganglia. EEG revealed diffuse theta wave. The diagnosis of Wilson's disease was made and the treatment of D-penicillamine 900 mg per day was started. This hypoperfusion of SPECT and EEG findings improved after 2 months under D-penicillamine therapy. Neurological findings showed slight improvement. A few Wilson's disease patients presenting with mental disorder have been reported. Wilson's disease should always be considered in differential diagnosis of mental disorders. We emphasize the importance of early diagnosis and treatment of Wilson's disease.
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PMID:[A young adult female case of Wilson's disease presenting with mental disorder and frontal lobe signs]. 1108 96


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