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)

Previous work has indicated that abnormal methylation processes may be associated with schizophrenia. In this study, leukocytes from patients with schizophrenia were incubated with methyl-14C-L-methionine and the evolved 14CO2 measured. With increasing concentration of methionine, the evolved 14CO2 was lower in the patients than in normal control subjects. The incorporation of 14C into protein was the same in both groups, and when carboxyl-14C-L-methionine was used the evolved 14CO2 was the same in both groups, thus excluding the possibility that altered incorporation into protein or oxidation of the methionine molecule as a whole were responsible. The observed differences in methionine-methyl metabolism suggest that an abnormality in transmethylation processes or in oxidation of the methyl group to CO2 is associated with schizophrenia. That this occurs in a peripheral tissue indicates that the abnormality is not restricted to the central nervous system.
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PMID:Altered metabolism of the methionine methyl group in the leukocytes of patients with schizophrenia. 73 53

55 patients with schizophrenia were divided into three groups according to the clinical symptoms: (1) productive schizophrenias, i.e. patients with hallucinations, catatonic excitation and stupor; (2) paranoia and schizophrenia simplex, and (3) non-productive schizophrenias, i.e. patients with schizophrenic defects and hebephrenia. Total cerebral blood flow (CBF) and the rates of cerebral oxygen, carbon dioxide, glucose and lactate metabolism were investigated. Patients with productive schizophrenias displayed a significant increase in CBF (to an average of 101.4 ml/100 g min), CMR oxygen (to an average of 6.26 ml/100 g min) and CMR glucose (to an average of 12.11 mg/100 g min), i.e. CBF and CMR oxygen nearly doubled and CMR glucose more than doubled in comparison with normal findings. In patients with paranoia and schizophrenia simplex CBF and oxidative metabolism did not vary much and were within the normal range. Non-productive schizophrenias showed a significant decrease in CBF (to an average of 36.7 ml/100 g min), CMR oxygen (to an average of 2.20 ml/100 g min) and CMR glucose (to an average of 3.86 mg/100 g min) in comparison with both other groups of schizophrenias and the group of healthy young men. The results demonstrated variations in CBF and oxidative metabolism of the brain in patients with distinct types of schizophrenia. It was possible to find a correlation between the mental state of the psychosis on the one hand and CBF and metabolism on the other. The high CBF and metabolic rates of the brain in productive schizophrenias might be due to disturbances in the cerebral metabolism of biogenic amines.
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PMID:Blood flow and oxidative metabolism of the brain in patients with schizophrenia. 123 37

The original transmethylation hypothesis of schizophrenia has evolved with time and experiment to the present concept that a defect in the methyl-carbon metabolic pathway may be causative in this illness. Various researchers have proposed that specific steps in the methyl-carbon pathway may be defective, and have presented evidence to support these possibilities. We have tested the general concept of the hypothesis by administering methionine labeled with 11C or 14C in the S-methyl carbon to patients with schizophrenia and to controls and measured the expiration of 11CO2 and 14CO2. We found that the rate and total expiration of labeled CO2 were three times less in the patients than in the controls, with no overlap of data points in the two groups. Specific steps in the methylcarbon pathway that might be defective and produce the results seen here are discussed in light of this and other researchers' findings.
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PMID:Tracer kinetic evidence for abnormal methyl metabolism in schizophrenia. 147 88

Carbon dioxide (CO2) is a potent cerebrovasodilator; even mild changes in CO2 are associated with marked changes in cerebral blood flow (CBF). We measured CBF before and after 5% CO2 inhalation in 19 medicated patients with schizophrenia and 16 normal volunteers. Another group of 16 volunteers had 2 CBF measurements under resting conditions. Although both patients and controls showed marked CBF increase during CO2 inhalation, the CBF response was significantly less in the patients. Change in CBF per mm of CO2 was lower in the patients. The second group of controls did not show significant differences between the 2 resting CBF measurements.
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PMID:Cerebral blood flow responses to inhaled carbon dioxide in schizophrenia. 211 76

Regional cerebral blood flow (CBF) was measured with the 133xenon inhalation technique in 27 patients with schizophrenia of less than 5 years' duration and in 27 patients with schizophrenia of more than 12 years' duration, under resting conditions. Similar measurements were also performed in 54 normal control subjects matched for age and sex. Patients with schizophrenia of long duration had lower anteroposterior gradients of CBF than patients with schizophrenia of short duration and matched control subjects. Covarying out age and end-tidal levels of CO2 did not alter the results.
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PMID:Chronicity and a low anteroposterior gradient of cerebral blood flow in schizophrenia. 230 62

Changes in regional cerebral blood flow and behavioral and physiological indices were monitored after intravenous administration of d-amphetamine sulfate and placebo in groups of patients with schizophrenia and normal volunteers. Amphetamine administration was associated with decreased anxiety, emotional withdrawal, depressed mood, blunted affect and increased excitement in the patients. Subjects who received amphetamine showed significant increases in systolic and diastolic blood pressure and reduction in end-tidal carbon dioxide. Post-amphetamine cerebral blood flow was decreased equally in both patients and controls. The blood flow change, however, did not show any regional variations.
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PMID:Changes in cerebral blood flow and mental state after amphetamine challenge in schizophrenic patients. 261 28

Respiratory sensitivity was evaluated in 10 patients with schizophrenia and 10 normal control subjects utilizing a rebreathing system and measurements of the changes in the mouth occlusion pressure in 100 ms and ventilation in response to the increase in end-tidal PCO2 (PetCO2). Although ventilation response was similar in both groups, we noted that the occlusion pressure response was more variable (coefficient of variability, CV = 17.5%) and the correlation coefficient (r = 0.75 +/- 0.13) lower in the patients with schizophrenia compared to controls (CV = 4.6%; r = 0.90 +/- 0.04). Apnea threshold was also lower in patients with schizophrenia (29.03 +/- 12.73 Torr, mean +/- SD) compared to controls (39.5 +/- 4.5 Torr). Furthermore, schizophrenia patients showed a significant positive and negative correlation between occlusion pressure response and age (r = 0.73; p less than 0.001) and estimated duration of schizophrenia (r = 0.65; p less than 0.05). We conclude that the apnea threshold is lower and the respiratory sensitivity to CO2 is more variable in patients with schizophrenia compared to normal subjects.
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PMID:Respiratory sensitivity to carbon dioxide in schizophrenia. 311 27

Ten patients with schizophrenia participated in 120-min free-smoking sessions when actively psychotic and free of antipsychotic medications, and again after the initiation of haloperidol treatment. During these free-smoking sessions they had access to cigarettes ad libitum. Their expired air carbon monoxide (CO) and plasma nicotine and cotinine levels were measured at the end of the 120-min free-smoking sessions. These patients smoked more after starting haloperidol treatment, relative to their baseline rate of smoking when free of antipsychotic medications, as evidenced by significantly higher expired CO and plasma nicotine levels.
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PMID:Haloperidol increases smoking in patients with schizophrenia. 767 43

Nicotine use is a major public health problem that increases medical morbidity and mortality. Nicotine's action and the pathobiology of schizophrenic disorders have common neurobiological substrates. Tobacco smoking alters medication blood levels and effectiveness, modifies psychiatric symptoms, and is a clue for other substance abuse. This article presents an evaluation of a smoking cessation program for 24 smokers with schizophrenia. Fifty percent completed the program, 40 percent decreased use by 50 percent, and 13 percent remained abstinent (carbon monoxide verified) for 6 months. Nicotine replacement, motivational enhancement therapy, and relapse prevention behavioral therapy were important components of treatment. Pharmacotherapy strategies of a higher-dose nicotine patch, combining nicotine gum and a patch, and augmentation medication to nicotine replacement should be evaluated in future studies in this population.
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PMID:Schizophrenia and nicotine use: report of a pilot smoking cessation program and review of neurobiological and clinical issues. 916 35

Klein's (1993: Arch Gen Psychiatry 50:306-317) "false suffocation alarm" theory of spontaneous panic attacks posits that central receptors compare CO2, O2, and lactate levels and trigger panic when an impending "false" state of suffocation is detected. Several investigators have found abnormalities of respiratory physiology in subjects with panic disorder. Twin and family studies have suggested that both panic disorder and tidal volume response to CO2 are inherited. We hypothesized that, if smothering symptoms are a marker for a hypersensitive suffocation detector and if this hypersensitivity is familial, then relatives of panic subjects with smothering symptoms would have higher rates of panic with smothering than relatives of panic subjects without smothering. We conducted a family study involving 104 panic disorder probands and 247 of their interviewed first-degree relatives. Probands and their relatives were interviewed using the Schedule for Affective Disorders and Schizophrenia--Lifetime Version for Anxiety Disorders to determine their panic disorder and smothering symptom status. Relatives of panic probands with smothering symptoms had an almost threefold higher risk for panic and an almost sixfold higher risk for panic with smothering symptoms when compared with relatives of panic probands without smothering. We conclude that panic disorder with smothering symptoms may be a subtype of panic disorder associated with increased familial risk and may be a group of interest to genetic investigators. These findings provide the first empiric evidence from a family study in support of Klein's false suffocation alarm theory of spontaneous panics.
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PMID:Panic disorder with smothering symptoms: evidence for increased risk in first-degree relatives. 955 84


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