Biomedical subjects
Publications and source records attributed to W B Lawson.
1. Patterns of fluid intake and urine output was examined in schizophrenia and normal controls. 2. Fluid intake and urine output were significantly higher in schizophrenic patients. 3. Bouts of drinking correlated significantly with fluid intake but did not differ significantly between schizophrenic patients and normal controls. 4. Schizophrenic patients drink more per bout compared to normal controls.
Historically, affective disorders have been underdiagnosed among minorities, while schizophrenia is often overdiagnosed. Cultural differences in symptomatology, such as increased reports of auditory hallucinations, or language differences reportedly contribute to misdiagnoses in Hispanics. Consequently, we performed a thorough evaluation of Hispanic patients with a history of schizophrenia who remained diagnostic enigmas. Evaluation included the use of a Spanish-speaking interpreter, strict adherence to criteria of the Diagnostic and Statistical Manual of Mental Disorders, third edition (revised), and the dexamethasone suppression test. Five patients met criteria for major depression, and all but one were properly classified using the dexamethasone suppression test. Careful evaluation is needed with appropriate cultural and diagnostics support to avoid missing depression in Hispanics. The dexamethasone suppression test may be a useful adjunct in some difficult-to-diagnose patients.
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Clonazepam was added to the neuroleptic regimen of 3 treatment-resistant schizophrenic patients with schizoaffective features. Manic symptoms improved but returned following discontinuation of clonazepam. The drug appears to benefit positive psychotic symptoms but worsens negative symptoms.
We measured red blood cell (RBC) choline and plasma choline concentrations in 27 chronic schizophrenic inpatients and 23 normal controls. Both blood choline measures had a significant test-retest reliability in patients whose neuroleptic status remained unchanged over 1 month. RBC choline concentration was significantly lower in patients medicated with neuroleptics and cogentin. Patients with a low RBC choline and a low RBC/plasma choline ratio were on significantly higher doses of medication and had higher scores on the hostility/suspiciousness subscale of the Brief Psychiatric Rating Scale. RBC choline increased when neuroleptics were discontinued. Blood choline measures were also compared among medication-free schizophrenic patients, inpatients with other diagnoses, and normal controls. No significant differences were seen among these groups for any choline measure, although the schizophrenic patients showed greater variability. Medication-free schizophrenic patients with such clinical factors as tardive dyskinesia and abnormalities on computed tomography contributed to this variability. Age was positively correlated with plasma choline.
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Twenty-seven chronic schizophrenic patients and nine other psychiatric patients closely matched in education were compared on the Halstead-Reitan Battery and the Wechsler Adult Intelligence Scale (WAIS). The schizophrenic patients as a group showed significantly poorer performance on the WAIS (full scale: X +/- SD, 92.9 +/- 2.9 vs. 110.8 +/- 2.1, p less than .002) and the Halstead-Reitan Battery (HRB; Average Impairment Range = 2.1 +/- .2 vs. 1.12 +/- .06, p less than .003). In addition the schizophrenic patients did significantly worse than did nonschizophrenic patients on all WAIS subtests and scored in the impaired range on most HRB subtests. Computed axial tomography scans revealed large ventricles on nine schizophrenic patients and cortical atrophy on three others. Among schizophrenics, the enlarged ventricle group consistently scored the worst. No relationship was seen between neuropsychological test performance and degree of ongoing psychopathology as measured by the Brief Psychiatric Rating Scale. These findings are consistent with previous reports of cognitive impairment in schizophrenia and are discussed in terms of regional localization. They provide additional evidence that the impairment is related to the disease process and that structural abnormalities are associated with the more severe condition.
The mean combined total body excretion of dopamine (DA) and its metabolites, measured by summing the molar excretion of DA and its metabolites in 24-hour urine samples (Sum DA), was reduced in 20 patients with schizophrenia who had not been receiving medication for at least two weeks. These patients were relatively resistant to treatment, as they were unable to live independently outside institutional settings despite conventional neuroleptic therapy. In contrast, sum norepinephrine (Sum NE), measured by summing the molar excretion of NE and its metabolites, was not reduced. These results are highlighted by expressing the data in terms of the ratio of Sum DA/Sum NE. Patients with schizophrenia had a significantly lower ratio. Treatment with haloperidol normalized the low ratio. Urinary excretion of 5-hydroxyindoleacetic acid was normal in the schizophrenic patients. These results suggest that chronic schizophrenia is more likely to be associated with a low rather than a high state of DA activity.
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Although historically research findings about racial and ethnic issues were all too often used to support prevailing concepts of racial inferiority, in recent years racial and ethnic factors have frequently been ignored. However, current findings suggest that racial and ethnic differences exist in the symptom presentations of psychiatric disorders. Significant racial differences have been noted among proposed biological markers for various psychiatric disorders, such as serum creatinine phosphokinase, platelet serotonin, and HLA-A2. Racial and ethnic differences in response to psychotropic medication, such as higher blood levels found among Asians, affect dosage requirements and potential side effects. All of these developments underline the importance of considering ethnic and racial factors in psychiatric research.
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A robust two-way analysis of variance technique was applied to determine simultaneously the effects of method and thromboplastin on prothrombin time. A new approach to outlier detection for two-way analysis of variance was used. Focusing on the underlying error structure improved the uniformity of the grading procedure in the hematology proficiency testing program of the New York State Department of Health. The logarithm-transformed scale produced constancy of error variance and resulted in uniformity of the acceptable spread of data. The common variance was lower than that obtained by previous methods and allowed for a narrower acceptable range of reported prothrombin times by reducing the inflated standard deviation, thus improving the efficiency of the grading procedure. For proficiency testing, no advantage was found in the use of either a common thromboplastin or freeze-dried, coumadinized patient plasmas rather than artificially depleted commercial plasmas, except for special purposes.
Polydipsia and polyuria have a long association with schizophrenia. To assess the prevalence of polydipsia and polyuria in schizophrenia, urine volume was examined in medication-free chronic schizophrenic patients, normal controls, and nonschizophrenic patients. Mean urine volume was significantly higher in the schizophrenic patients (2319 +/- SD 2052 ml/24 hours) than in the other two groups (1054 +/- SD 471 ml/24 hours for nonschizophrenic patients and 1265 +/- SD 613 ml/24 hours for normals). Seven of 35 patients with schizophrenia but 0/7 nonschizophrenics had urine volumes greater than any normal control. Polyuria was associated with a good premorbid history and a positive neuroleptic response. Among polyuric patients, those with hyponatremia may represent a different, distinct subgroup. Neuroleptic treatment was associated with a further, significant increase in urine volume. Hence, polydipsia and polyuria appear to be relatively common in schizophrenia.
The interactions of human thrombin and bovine trypsin with 4-amidinophenylpyruvate (p-APPA), 3-amidinophenylpyruvate (m-APPA) and benzamidine were studied by equilibrium binding and by stopped-flow kinetics with proflavin displacement. The excellent inhibitory properties of p-APPA with both enzymes are explained by a two-step transition-state mechanism in which the initial Michaelis complex E.I reacts rapidly to form a fairly stable, chemically bonded complex E-I, in which the keto group of p-APPA forms a hemiketal with the gamma-O-atom of Ser195 at the active site. The hemiketal complex of thrombin and p-APPA may be further stabilized by a hydrogen bond between a carboxylate oxygen of p-APPA and the N tau-atom (= N epsilon 2) of His57, as was previously shown for the trypsin-p-APPA complex by X-ray crystal structure analysis by J. Walter and W. Bode. m-APPA is apparently sterically incapable of forming a hemiketal with Ser195 O gamma; it does not bind to thrombin or trypsin in a time-dependent manner, and it displays KI values with both enzymes close to those obtained for benzamidine itself. In the p-APPA-thrombin reaction the overall binding constant KI (E-I) is 1.3 microM, while the initial binding displays a KM (E.I) estimated at least 100-fold higher (700 microM). The half-time for the formation of E-I is about 0.6 s at a p-APPA concentration of 1 microM.
The occasional presence of polydipsia in psychiatric patients, at times progressing to hyponatremia with severe medical complications, has been previously noted. The clinical history and laboratory data from eight chronically hyponatremic psychiatric inpatients were examined. Common characteristics were a diagnosis of chronic undifferentiated schizophrenia, an early age of onset of their illness, extended hospitalizations with minimal response to neuroleptic medications, heavy tobacco use, and a relatively high frequency of tardive dyskinesia and brain scan abnormalities. Water loading in three patients showed responses consistent with inappropriate secretion of antidiuretic hormone. Potential pathophysiologic mechanisms and treatment considerations are discussed.
The effects of blood plasma and some plasma constituents on several types of thrombin inhibitors were quite varied. Two active esters were rapidly destroyed by serum albumin; one of these reacted initially with Lys-199, the residue that is also acylated by aspirin. Of two sulfonyl fluorides one was unaffected by albumin, and the other bound reversibly to albumin; this binding was greater with albumin acetylated at Tyr-411 near the binding site for medium-chain fatty acids. The effects of a chloromethyl ketone were inhibited, apparently reversibly, by albumin but were practically abolished by glutathione. Of two potent reversible inhibitors one was unaffected by plasma constituents, while the other was over 10-fold less potent in plasma than in fibrinogen. The effect of plasma could be partially explained by binding to albumin and lipoproteins.
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In order to determine whether a generalized defect in glucose recognition exists in diabetes, taste detection and preference were measured in adult onset diabetics (AOD), juvenile onset diabetics (JOD), and healthy first-degree relatives of diabetics (NR). Controls (C) were age and sex matched nondiabetics without first-degree diabetic relatives. The AOD and NR gorups showed significantly higher glucose thresholds than their controls. In contrast, glucose threshold in JOD was not different from C. The AOD group also demonstrated a higher sucrose threshold than C. This difference was not present for JOD or NR groups. No difference in salt detection was seen in any of the groups. Taste preference was assessed by two choice situations and ratings of test solutions of varying concentrations. No significant difference in glucose or sucrose preference were noted, but both the AOD and NR groups preferred lower salt concentrations than C. These findings indicate that thery may be a widespread impariment of cellular glucose recognition in AOD and their relatives, while JOD have a specific beta cell defect.