S100B is increased in mood disorders and may be reduced by antidepressive treatment

Previous studies have reported alterations of glial cells and particularly astrocytes in mood disorders. Therefore, serum concentration of the astrocytic marker S100B was ascertained with an immunoluminometric assay in 20 patients with mood disorder and 12 healthy age-matched controls. Serum S100B was elevated in major depression (median after admission 410 ng/l, at discharge < 100 ng/l) and mania (130, 160 ng/l), when compared with controls (< 100 ng/l; rho< 0.01). Antidepressive treatment reduced S100B in conjunction with severity of depressive symptoms ( rho< 0.01). The severity of depression (Hamilton Depression Rating Scale) was positively correlated with S100B (r(s) = 0.51, rho< 0.005). Elevated serum S100B during depressive and manic episodes of mood disorders may indicate alterations of astrocytes, which are reversed by antidepressive treatment.     

Plasma S-100B protein in Chinese patients with schizophrenia: comparison with healthy controls and effect of antipsychotics treatment

PURPOSE: To examine the possibility that structural damage to the brain may play a role in the pathogenesis of schizophrenia by measuring the level of plasma S-100B, a calcium-binding protein found predominantly in the cytosol of glial cells. METHOD: Fifty-seven Chinese psychiatric inpatients who met DSM-IV diagnosis of schizophrenia and 60 healthy controls were enrolled in the study. Patients were assessed with the Positive and Negative Symptoms Scale (PANSS) at admission and at 12 weeks after treatment. Plasma samples were collected from patients and controls and S-100B protein was assayed using ELISA. RESULTS: (1) 29 of 57 patients (50.9%) showed increased S-100B level compared to the mean level of 60 healthy controls (p<0.005) vs. only 1 of 60 (1.67%) controls. The S-100B levels of unmedicated (0.119+/-0.059microg/L) and medicated patients (0.117+/-.0.057microg/L) were significantly higher than controls (0.067+/-0.022microg/L, both p<0.001), and S-100B levels of unmedicated patients were higher than those of medicated patients (p=0.024); (2) at admission, S-100B level was positively correlated with total score of PANSS (r=0.269, p=0.043), especially with negative subscore of PANSS (r=0.306, p=0.021), but the correlation was no longer present after patients were treated by anti-psychotic agents. CONCLUSION: The S-100B levels of patients with schizophrenia are significantly higher than that of healthy controls, and the S-100B level is associated with severity of psychopathology, particularly negative symptoms, indicating that patients with schizophrenia may suffer structural damage to central nervous system. The concentration of S-100B may also be associated with treatment progress.     

Increased serum S100B protein in schizophrenia: a study in medication-free patients

S100B protein, a calcium binding protein produced and released by glial cells, has been used as a sensitive marker of brain damage. Previous studies have found alterations in peripheral S100B levels in schizophrenic patients on medication. We compared serum S100B levels of 20 medication-free DSM-IV schizophrenic patients and 20 age-gender matched healthy controls. Schizophrenic patients presented higher serum S100B levels (mean 0.120 ng/ml+/-S.D. 0.140) compared to controls (mean 0.066 ng/ml+/-S.D. 0.067; P=0.014) and there was a negative correlation with illness duration (r=-0.496, P=0.031). The results of this study indicate that serum S100B levels may be a state marker of a limited neurodegenerative process, particularly in the early course of schizophrenia or, at least, in a subgroup of schizophrenic patients.     

Limbic system abnormalities identified in schizophrenia using positron emission tomography with fluorodeoxyglucose and neocortical alterations with deficit syndrome.

A hypothesis of psychosis localization in schizophrenia was derived from studying metabolic alterations in rat brain in response to phencyclidine hydrochloride administration. Since phencyclidine and its selective agonist dizocilpine maleate (MK801) induced overlapping and long-lasting metabolic alterations predominantly in limbic areas, the hypothesis developed that schizophrenic patients with psychosis would evidence functional abnormalities in limbic circuits compared with normal controls. Accordingly, 12 actively psychotic, drug-free patients with schizophrenia and matched normal controls underwent functional brain scans using positron emission tomography and fluorodeoxyglucose. Regions of interest were identified on five matched axial slices in each patient and control subject, and average metabolic rates were calculated. Patients with schizophrenia showed a significantly lower regional cerebral metabolic rate of glucose in the hippocampus and the anterior cingulate cortex than did normal controls, but not in neocortical areas or in the extrapyramidal system. When the group of schizophrenic patients was divided into deficit and nondeficit types, a preliminary exploratory analysis suggested thalamic, frontal, and parietal cortical hypometabolism in the deficit subgroup, with normal metabolism in the nondeficit patient group in those areas; in contrast, hippocampal and anterior cingulate cortical metabolism was reduced in both deficit and nondeficit subtypes. These results suggest that the limbic system, especially the hippocampus, is functionally involved in schizophrenic psychosis and that different manifestations of schizophrenia may involve different neuronal circuits.     

Patterns of cranial, brain and sulcal CSF volumes in male and female deficit and nondeficit patients with schizophrenia

Recent evidence suggests that schizophrenia reflects a neurodegenerative process. The studies have not compared brain change patterns in male and female patients with schizophrenia or examined the relation of these patterns to patient subgroups defined by specific symptom domains. Maximum Total Brain Volume (TBVmax), total cranial (TCV), total brain (TBV), sulcal CSF (sCSF), and ventricular (VV) volumes were measured in 66 normal controls (32 females, 34 males), and 85 patients with schizophrenia (21 females, 64 males). Sixty-six patients were categorized as nondeficit and 19 as deficit patients. Patients had smaller TBV and larger VV than normal controls. Patients also showed significant excessive brain volume loss after, but not before, TBVmax was achieved compared with normal controls. Although male patients had larger brain volume loss compared with male normal controls than female patients had compared with female normal controls, there were no significant gender x diagnosis interactions. Male patients with the deficit syndrome, but not those without the deficit syndrome, had significantly larger ventricles than normal controls. There were no other significant deficit/nondeficit differences. The present study suggests that brain volume loss in schizophrenia occurs after TBVmax and that male and female patients and deficit and nondeficit patients with schizophrenia do not demonstrate any differences in the time course of their brain volume reductions.     

Three dimensions of clinical symptoms in elderly patients with schizophrenia: prediction of six-year cognitive and functional status

BACKGROUND: A three-syndrome categorization of schizophrenia has been recently proposed [Arndt, S., Alliger R.J., Andreasen, N.C., 1991. The distinction of positive and negative symptoms: the failure of a two-dimensional model. Br. J. Psychiatry 158, 317-322; Miller, D.D., Arndt, S., Andreasen, N.C., 1993. Alogia, attentional impairment, and inappropriate affect: their status in the dimensions of schizophrenia. Comp. Psychiatry 34, 221-226; Gur, R.E., Mozley, D., Resnick, S.M., Levick, S., Erwin, R., Saykin, A.J., Gur, R.C., 1991. Relations among clinical scales in schizophrenia. Am. J. Psychiatry 148, 472-478. Brown, K.W., White, T., 1992. Syndromes of chronic schizophrenia and some clinical correlates. Br. J. Psychiatry 161, pp. 317-322]. METHODS: Chronic, elderly, schizophrenia patients with deficit (N = 111), nondeficit with High reality distortion/Low conceptual disorganization (nondeficit-delusional) (N = 40) and nondeficit with Low reality distortion/High conceptual disorganization (nondeficit-disorganized) (N = 56) were followed-up for 6 years. Assessment included the Positive and Negative Syndrome Scale (PANSS), the Mini-mental Status Examination (MMSE) and the Alzheimer's Disease Assessment-Late Stage Cognitive and Non-Cognitive Subscale (ADAS-L Cog and ADAS-L Self care). RESULTS: At initial assessment, MMSE scores were significantly lower, while the ADAS-L Cog and Negative symptoms were significantly higher in the deficit and nondeficit-disorganized groups compared with the nondeficit-delusional group (all p values <0.05). Positive symptoms were significantly lower in the deficit group than in both nondeficit syndrome groups (p < 0.05). On the ADAS-L Self Care scale the nondeficit-delusional group was the most impaired while the nondeficit-disorganized was the least impaired. There was a significant decline over time in MMSE scores in the deficit and the nondeficit-delusional groups (p < 0.01), but no change in the nondeficit-disorganized group. ADAS-L Cog and ADAS-L Self Care functions worsened over time in all three groups (p < 0.0001). Severity of negative symptoms was stable over time in deficit patients and in nondeficit-disorganized patients but worsened in nondeficit-delusional patients (p < 0.001). There was also a significant worsening of positive symptoms over time in deficit patients (p = 0.04). CONCLUSION: Deficit, nondeficit-delusional and nondeficit-disorganized patients with schizophrenia may represent distinct subgroups discriminated by different courses in negative and positive symptoms and cognitive status.     

Summer birth and deficit schizophrenia: a pooled analysis from 6 countries

BACKGROUND: In some reports, summer birth has been associated with deficit schizophrenia. Deficit schizophrenia and nondeficit schizophrenia also differ in several other ways. OBJECTIVE: To conduct a combined analysis of the published and unpublished data sets from the northern hemisphere that relate deficit and nondeficit schizophrenia to month of birth. DATA SOURCES: Studies of season of birth in which it was possible to make a deficit/nondeficit categorization. STUDY SELECTION: Published studies with samples of convenience and all known population-based studies with the deficit/nondeficit categorization were included. The studies came from 6 countries. DATA EXTRACTION: Three published studies of samples of convenience, 2 population-based prevalence studies, and 5 population-based studies that approximated incident samples were included. Month of birth was compared for deficit and nondeficit schizophrenia, using meta-analytic fixed-effects models. DATA SYNTHESIS: A group x month goodness-of-fit chi2 showed a significant difference between deficit and nondeficit subjects in season of birth (P < .001) in the studies that approximated incidence. This difference was largely due to an increase in deficit schizophrenia births in June and July (odds ratio, 1.9; 95% confidence interval, 1.3-2.9). Similar results were found in the prevalence studies. A similar pattern was found in 2 of the 3 samples of convenience, but when combined, these 3 samples did not show a significant deficit/nondeficit difference. CONCLUSIONS: Deficit schizophrenia has a season of birth pattern that differs from that of nondeficit schizophrenia. This analysis supports the notion of a separate disease within schizophrenia.     

The P50 auditory evoked potential in violent and non-violent patients with schizophrenia

BACKGROUND: Emotionally driven violence is facilitated by increased arousal. It may be a consequence of an information-processing deficit and the cognitive attributions for the stimuli given by the subject. The aim of this study was to compare the P50 evoked potential responses of violent patients with schizophrenia with non-violent patients with schizophrenia and healthy controls. METHOD: Patients were classified into violent and non-violent in accordance to the Overt Aggression Scale. P50 auditory evoked potentials of 32 unmedicated patients with schizophrenia (violent=14, non-violent=18) and 17 healthy controls were recorded during five runs of 30 click pairs. RESULTS: Healthy controls exhibited a lower S2/S1 ratio when compared to violent (p<0.001) and non-violent (p=0.04) patients. Using a cutoff point of 0.50 for S2/S1 ratio to define abnormal gating a significant proportion of violent patients did not show P50 suppression (71.4%) in comparison to non-violent patients (38.9%) and healthy controls (23.5%) (p=0.02). CONCLUSIONS: Violent behavior in patients with schizophrenia could be associated with a disturbed information sensory gating. Violence in patients with schizophrenia may be facilitated by an increased arousal which may in turn be the result of an information-processing deficit.     

Neurocognitive, social, and emotional dysfunction in deficit syndrome schizophrenia

The deficit syndrome is a promising distinction within schizophrenia that requires further validation. This study examined the replicability of differences in clinical symptoms, neurocognitive functioning, affect perception, and social functioning previously reported among deficit (n=15) and nondeficit syndrome (n=30) schizophrenia patients classified according to the Schedule for the Deficit Syndrome (SDS; Psychiatry Res. 30 (1989) 119) and nonpatient controls (n=41). Additionally, participants completed self-report affective trait measures of positive affectivity, negative affectivity, and social anhedonia to examine the deficit syndrome concept of diminished emotional range. We were able to replicate symptom profiles and neurocognitive and social functioning impairments in deficit vs. nondeficit patients, but did not find more severe affect perception impairment in deficit vs. nondeficit patients as previously reported. Regarding range of subjectively experienced emotion, deficit patients reported lower trait positive affectivity and marginally higher social anhedonia than nondeficit patients and controls, but also reported elevations in negative affectivity that were similar to nondeficit patients as compared to controls. While replication of patterns of impairment across multiple domains of functioning supports the validity of the deficit syndrome, results also suggest that SDS-defined deficit patients may be characterized by a relative reduction in the tendency or ability to experience positive emotions, rather than a pervasive diminution in the range of emotional experience.     

Interstitial cells of the white matter in the inferior parietal cortex in schizophrenia: An unbiased cell‐counting study

Previous studies have found an increased density of the interstitial cells of the white matter (ICWMs) in the frontal and temporal cortex in schizophrenia. Some data suggested this abnormality was restricted to a subgroup of patients, whose clinical features were consistent with the presence of the deficit syndrome. Clinical studies suggest deficit features are due to an abnormality in a cortical‐subcortical circuit that includes dorsolateral prefrontal and inferior parietal cortex. We compared the density of ICWMs labeled for MAP2 immunoreactivity in Brodmann area 39 (inferior parietal cortex) from nine schizophrenia subjects (three deficit and six nondeficit) and nine matched controls using an unbiased cell‐counting technique. The density of ICWMs was significantly greater in the deficit syndrome subjects compared to the nondeficit schizophrenia group (respective means ± SEM, 0.22 ± 0.04, and 0.13 ± 0.02; P < 0.05). The density of ICWMs in the deficit group was also significantly greater (P < 0.05) than that of the control group (0.09 ± 0.02), but the nondeficit and control groups were not significantly different. These findings 1) confirm that an abnormal placement of neurons in the white matter is found in schizophrenia, 2) provide evidence for a microscopic anatomical abnormality in the inferior parietal cortex, and 3) suggest the ICWM abnormality may be confined to deficit patients. Synapse 34:95–102, 1999. © 1999 Wiley‐Liss, Inc.     

Neuropsychology of the deficit syndrome: new data and meta-analysis of findings to date

The deficit syndrome is thought to characterize a pathophysiologically distinct subgroup of patients with schizophrenia. Supporting this notion, prior research examining the neuropsychological correlates of the deficit syndrome has suggested the presence of a differential impairment in frontal and parietal functions. This article reports findings from 2 studies attempting to replicate and extend previous reports of a differential neuropsychological impairment in deficit schizophrenia. In the first study, we administered a comprehensive neuropsychological battery to 20 deficit and 25 nondeficit patients with schizophrenia and 25 normal healthy controls. In the second study, a meta-analysis was conducted of 13 separate studies examining the neuropsychology of the deficit syndrome. There was little evidence from either of the present studies that the deficit syndrome is associated with a selective impairment in frontal and parietal lobe functions. The first study failed to find significant differences in frontal or parietal abilities for deficit vs nondeficit patients. The meta-analytic findings revealed that deficit patients were globally more neuropsychologically impaired than nondeficit patients (effect size [ES] = 0.41). Relative to nondeficit patients, deficit patients performed poorest on tests of olfaction (ES = 1.11), social cognition (ES = 0.56), global cognition (ES = 0.52), and language (ES = 0.51). The neuropsychological impairments associated with the deficit form of schizophrenia do not follow an obvious anatomically defined pattern of impairment. The question of whether deficit patients exhibit a unique cognitive impairment profile will require a more sophisticated and rigorous examination of the neuropsychology of the deficit syndrome.     

Relationship between performance on the Stroop test and N-acetylaspartate in the medial prefrontal cortex in deficit and nondeficit schizophrenia: preliminary results

The aim of this research was to investigate the relationship between performance on the Stroop test and N-acetylaspartate/creatine assessed using proton magnetic resonance spectroscopy in the medial prefrontal cortex (MPFC) of schizophrenia patients. The Schedule for the Deficit Syndrome was used to subdivide the schizophrenia patients into deficit (n=5) and nondeficit (n=17) subtypes. Twenty-one control subjects served as a comparison group. A strong correlation between right-sided N-acetylaspartate/creatine levels and Stroop scores was found in the deficit patients but not in the nondeficit patients and the controls. This result suggests a relationship between a dysfunction of the right medial prefrontal cortex and a deficit in selective attention in schizophrenia patients with the deficit syndrome.     

Psychopathology and neuropsychological impairments in deficit and nondeficit schizophrenia of Chinese origin

Deficit schizophrenia is a relatively homogeneous subtype of patients which is considered helpful to explore the pathogenesis of schizophrenia. The aim of the present study was to reexamine the clinical characteristics of deficit (n=30) and nondeficit schizophrenia (n=93) in a Chinese sample and investigate the differences of neurocognitive function among the two subtypes of schizophrenia and the normal controls (n=103). Schizophrenia patients completed the Brief Psychiatric Rating Scale (BPRS), Scale for the Assessment of Negative Symptoms (SANS) and Scale for the Assessment of Positive Symptoms (SAPS). Additionally, all participants completed an abbreviated version of the Wechsler Adult Intelligence Scale (WAIS-RC) and a neuropsychological test battery examining the executive functions, visuospatial abilities and explicit memory related to the frontal, parietal, and temporal lobe functions. The deficit group received higher scores than the nondeficit group on the BPRS anergia factor and SANS affective flattening, alogia, avolition-apathy, anhedonia-asociality subscales, but not on the SAPS. Both two schizophrenia subgroups performed more poorly on the WAIS-RC and neuropsychological tests than the normal controls. Moreover, deficit patients performed worse than nondeficit patients on the prorated IQ, the Trail Making Test, Wisconsin Card Sorting test and Block Design test. The present study replicated symptom profiles in deficit vs. nondeficit schizophrenia in the Chinese sample. Furthermore, this study suggested that deficit schizophrenia is associated with frontal and parietal lobe impairment, and that temporal lobe dysfunction may be a common basis for cognitive impairment in schizophrenia as a whole.     

S100B and NSE serum levels in obstructive sleep apnea syndrome

BACKGROUND AND PURPOSE: Obstructive sleep apnea syndrome (OSAS) is a chronic disease ranging from innocuous to life-threatening and causes brain alterations manifested by neuropsychiatric symptoms. Neuron-specific enolase (NSE) and the astrocytic protein S100B are established sensitive peripheral biochemical markers of brain injury. In the present work we measured the serum levels of S100B and NSE in order to evaluate the deleterious effects of OSAS to the brain. PATIENTS AND METHODS: We studied 29 male patients with OSAS and 17 male asymptomatic control subjects with an apnea-hypopnea index (AHI) less than five events per hour. Patients and control subjects were evaluated by full-night polysomnography (PSG) and by Mini International Neuropsychiatric Interview (MINI) for the presence of neuropsychiatric symptoms. In the morning following the PSG, blood was collected and serum levels of S100B and NSE were measured using standard techniques. RESULTS: The AHI in the OSAS group was (mean+/-SD) 27+/-25 AH/h, ranging from 5 to 99 AH/h. S100B was higher in OSAS (0.15+/-0.09 microg/l) than in the control group (0.08+/-0.06 microg/l; P<0.01). Serum NSE was similar in both groups (17.5+/-12.2 vs. 15.8+/-6.8ng/ml). CONCLUSIONS: We report elevated serum S100B levels in OSAS patients in this study.     

Deficit schizophrenia: association with serum antibodies to cytomegalovirus

BACKGROUND: Patients with deficit schizophrenia differ from nondeficit patients with schizophrenia relative to several neurobiological correlates and relative to the risk factors of family history and season of birth. Exposure to human herpesviruses is a possible risk factor for schizophrenia. We hypothesized that there would be deficit/nondeficit difference in the prevalence of serum antibodies to human herpesviruses. METHODS: In deficit (N = 88) and nondeficit (N = 235) schizophrenia patients, we measured IgG class antibodies to the 6 known human herpesviruses: herpes simplex virus type 1, herpes simplex virus type 2, cytomegalovirus, Epstein-Barr virus, human herpes virus 6, and varicella-zoster virus. RESULTS: Deficit categorization was associated with the presence of serum antibodies to cytomegalovirus (odds ratio = 2.01, p = .006). This association remained significant after covarying for positive psychotic symptoms and demographic features known to be associated with cytomegalovirus seropositivity and after correcting for multiple comparisons. An association between herpes simplex virus type 1 and deficit status was not significant after covarying for potentially confounding variables. No other human herpesvirus was significantly associated with deficit versus nondeficit categorization. CONCLUSIONS: The association between deficit schizophrenia and cytomegalovirus antibody seropositivity provides further evidence for differences in etiopathophysiology between deficit and nondeficit schizophrenia.     

Behavioural dysregulation of decision-making in deficit but not nondeficit schizophrenia patients

This study aimed to determine whether deficit but not nondeficit schizophrenia showed dysregulation of decision-making. In a two-choice prediction task, the subject is asked to predict whether a stimulus appears on the left or right side of a computer screen. Schizophrenia patients were divided into 12 patients with and 12 patients without deficit syndrome and compared to 12 healthy control subjects. Dynamical entropy and mutual information analyses were used to determine underlying strategies and the degree to which sequences of responses are nonrandom. When compared to controls, deficit but not nondeficit schizophrenia patients showed a dysregulation of decision-making characterized by an increased oscillation between highly predictable and highly unpredictable response sequences. Moreover, in deficit patients, the previous choice was more predictive of the current response. Therefore, the two-choice prediction task may be useful in differentiating between deficit and nondeficit schizophrenia.     

Over-expression of S100B protein in children with cerebral palsy or delayed development

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.     

Sibling correlation of deficit syndrome in the Irish study of high-density schizophrenia families

OBJECTIVE: The deficit syndrome is a subtype of schizophrenia characterized by primary and enduring negative features of psychopathology. It appears to reflect a distinct subtype within the syndrome of schizophrenia. Little is known about the familial or genetic aspects of the deficit syndrome. The purpose of this study was to determine whether deficit versus nondeficit subtypes are correlated in sibling pairs affected with schizophrenia. METHOD: The present study was based on the Irish Study of High-Density Schizophrenia Families. From the earlier study the authors selected a subset of patients who were members of sibling pairs in which both siblings had been diagnosed with "core" schizophrenia, which included schizophrenia, simple schizophrenia, and schizoaffective disorder with poor outcome. The Schedule for the Deficit Syndrome was used to make deficit versus nondeficit diagnoses, which were based on chart examinations by reviewers blind to sibling status. This method resulted in 65 patients being diagnosed with the deficit syndrome and 401 patients diagnosed as nondeficit (prevalence=13.9%). This group included 347 full sibling pairs, which were analyzed for resemblance with respect to deficit versus nondeficit subtype by means of logistic regression. RESULTS: Deficit versus nondeficit subtypes were significantly correlated in sibling pairs concordant for core schizophrenia. CONCLUSIONS: Familial factors contribute significantly to whether a person has the deficit subtype of schizophrenia. This familial contribution could be genetic or environmental.     

Evaluation of the secretory pattern of plasma arginine vasopressin in stroke patients

Arginine vasopressin (AVP) may play a role in the development of ischemic brain edema and/or cerebral vasospasm. Data available on AVP plasma levels in ischemic stroke are few and discordant. In order to ascertain whether changes in AVP plasma levels occur in ischemic stroke, plasma AVP levels, plasma osmolality and mean arterial pressure were determined in 24 patients with unprecedented ischemic cerebral infarction and in 15 controls over a 24-hour period. In stroke patients, mean 24-hour plasma AVP levels (7.2 +/- 0.8 ng/l) were higher (p < 0.05) than in control subjects (2.4 +/- 0.3 ng/l), and correlated with the severity score of the neurologic deficit and the mean size of the lesion. In patients with a more severe neurologic deficit, the mean 24-hour plasma AVP levels (8.7 +/- 1.0 ng/l) were higher than in patients with a less severe neurologic deficit (5.2 +/- 0.8 ng/l). Data indicate that in ischemic stroke an increased AVP secretion occurs independently of osmotic or baroreceptorial mechanisms. The possibility that AVP may play a role in neuronal cell damage following cerebral ischemia warrants further attention.     

Interstitial cells of the white matter in the dorsolateral prefrontal cortex in deficit and nondeficit schizophrenia

An increased density of neurons in the white matter of the neocortex has been found in schizophrenia, and the original reports suggested this abnormality was restricted to a subgroup of patients. In a study of the inferior parietal cortex, we found that deficit schizophrenia subjects, but not nondeficit subjects, had an increased density of ICWMs. We extended that finding by comparing the density of microtubule-associated protein 2-immunoreactive ICWMs in deficit schizophrenia (N = 3), nondeficit schizophrenia (N = 4), and control (N = 5) subjects, using postmortem tissue from the dorsolateral prefrontal cortex (Brodmann area 46). The deficit group differed significantly from the other two groups; the respective mean (SD) density values for the deficit, nondeficit, and control groups were 1.27 (.10),.53 (.39), and.76 (.20) cells per 10-6 cubic microns. These group differences provide further evidence that deficit and nondeficit schizophrenia differ in their pathophysiology.