Ultrasonically determined thyroid volume and thyroid functions in lithium-naïve and lithium-treated patients with bipolar disorder: a cross-sectional and longitudinal study.

OBJECTIVE: This study investigated thyroid volume, hormone levels and antibodies in long-term lithium-treated and lithium-naïve bipolar patients, some of whom underwent prospective follow-up evaluations. METHODS: Fourteen lithium-naïve patients, 13 long-term lithium-treated patients diagnosed with bipolar disorder and 12 healthy controls were included. Seven lithium-naïve patients were followed-up during their lithium receiving period (range 6-9 months). Thyroid volume and serum levels of thyroid hormones and antibodies were measured once in the long-term lithium-treated patients and controls, and twice in the lithium-naïve patients, i.e. before and after lithium treatment. RESULTS: Mean thyroid volumes in the lithium-naïve patients were significantly higher than those in the controls. Long-term lithium-treated patients had significantly higher total thyroid volume than the lithium-naïve patients and the controls. Total thyroid volume in the patients after the lithium treatment was significantly higher than that before. Serum free thyroxine (fT4) levels in the long-term lithium-treated patients were lower than those in the lithium-naïve patients and the controls. In the lithium-naïve patients, after lithium treatment, free triiodothyronine (fT3) levels were lower, and thyroid stimulating hormone (TSH) levels were higher compared to those before lithium treatment. CONCLUSIONS: The results suggest that thyroid enlargement and some alterations in thyroid hormones in bipolar patients may present even before lithium treatment and increase further with lithium treatment.

[Neurobiology of motherhood]. / Anneligin Nörobiyolojisi.

Motherhood is a physiological status in which certain behavioural patterns are exhibited. Maintenance of the life of the species in mammals is dependent upon the presentation of motherhood services in a certain period that the child is dependent on the mother. Absence of the mother causes some deficiencies in social, behavioural and cognitive abilities, an abnormal development of the stress response system, learning and memory disorders, and later, inadequate motherhood skills of the mature offspring during their own maternity period. Because maternal care is extremely important for the survival of the child and thus, for the species to maintain, nature seems to have provided the development of a healthy mother-child relationship. Therefore, motherhood is programmed by the evolutionary process in the female brain before birth. It is certain that the brain of the mother is very different from the brains of the nulliparous women who are within the same age range, and is very sensitive to her own child's needs. For maternal behaviour to develop in human beings and animals, special neural networks, which are cooperatively developed by genetic, environmental and hormonal factors, are necessary. It also seems likely that non-genetic (epigenetic) transmission responsible for the internalization of maternal behaviours learned from the mother and hormonal exposure of the brain both during the foetal period, throughout the growth, and during the gestation of the woman as well as genetic factors, play an important role in the development of these maternal neural networks and systems. In this paper, which was prepared by obtaining the necessary publications by means of a search for the words related to motherhood in the PubMed search engine, the physical and mental changes that prepare females for motherhood and enable them to tolerate it will be reviewed.

Serum oxytocin levels in patients with depression and the effects of gender and antidepressant treatment.

Abnormalities in the neurohypophyseal system have been reported in depression. This study aimed to investigate serum oxytocin levels in patients with depression and the effects of gender and antidepressant treatment on these levels. Serum oxytocin levels were measured before and after treatment with antidepressant drugs or electroconvulsive therapy (ECT) in 40 inpatients (30 women, 10 men) who met the DSM-IV criteria for major depressive disorder (n=29) or bipolar affective disorder depressive episode (n=11), and in 32 healthy controls (20 women, 12 men). Serum oxytocin levels were decreased both pre-treatment and post-treatment in the patients compared with those in the controls. Serum oxytocin levels were not affected by antidepressant drug treatment or ECT. The female patients had significantly lower oxytocin levels than the control females, whereas no difference was found between the male patients and the male controls. We found no difference in serum levels of oxytocin between the unipolar and bipolar depressive patients. Our result shows reduced oxytocin in depression and a gender difference in oxytocin levels. Furthermore, antidepressant treatments appear to have no effect on serum oxytocin levels.

Hypothalamic-pituitary-adrenal axis activity, dehydroepiandrosterone sulphate and their relationships with aggression in early and late alcohol withdrawal.

The study aims at investigating the relationship between hypothalamic-pituitary-adrenal (HPA) axis alterations and aggression level in alcoholic patients during early and late alcohol withdrawal. Serum levels of basal cortisol and dehydroepiandrosterone sulphate (DHEAS) were measured three times, and cortisol and DHEAS response to dexamethasone twice during the early and late withdrawal periods in alcohol dependent males (n=30) and once in healthy control males (n=20). Abnormal cortisol non-suppression response to dexamethasone in dexamethasone suppression test (DST) was observed in some proportion of the patients in early withdrawal, which normalized in late withdrawal. The study revealed reduced basal DHEAS levels and reduced DHEAS response to dexamethasone in late withdrawal. When the patients were assessed in two separate groups as high- and low-aggressives, in the high-aggression group abnormality in DST was observed during both early and late withdrawal periods, in the low-aggression group it was observed only in early withdrawal. While basal DHEAS levels were low in the high-aggression group only in early withdrawal, it was reduced in the low-aggression group during late withdrawal period. Some alterations of the HPA axis during alcohol withdrawal might be associated not only with alcohol use per se but also with aggressivity tendency of alcoholic patients.

The effects of electroconvulsive therapy on GABAergic function in major depressive patients.

OBJECTIVES: It has been proposed that major depression is associated with a dysfunction of the gamma-aminobutyric acid (GABA) system. This study was planned to investigate whether there are any alterations in GABAergic activities in major depressive patients and, if there are, whether electroconvulsive therapy (ECT) has any effect on these changes. METHODS: Twenty-five depressed inpatients who responded to a course of ECT and 23 healthy subjects were included in the study. Serum GABA levels were measured 2 days before and 10 minutes after the first ECT and 3 days after the last ECT, and a baclofen challenge test was performed 2 days before the first ECT and 3 days after the last ECT in the patients. The same tests were carried out only once in the control group. RESULTS: Depressive patients had lower serum GABA levels compared with healthy individuals, and ECT caused a significant increase in these levels. The acute effect of the one-ECT procedure was a huge increase in the baseline GABA levels. Although there was no difference in the maximum alteration in growth hormone with baclofen between the patients and controls before the therapeutic ECT course, it became significantly higher in the depressive patients than in the controls after the treatment. CONCLUSIONS: The findings of this study support the GABA deficit hypothesis of major depression because major depressive patients have lower levels of serum GABA that are increased by a completed ECT course. ECT seems to increase brain GABA levels as well as GABAB activity, and these effects may contribute to its mechanism of therapeutic effect.

[Acute and chronic effects of electroconvulsive therapy on neuroactive steroids in patients with major depressive disorder]. / Major depresif bozuklugu olan hastalarda elektrokonvulsif tedavinin nöroaktif steroidler üzerine akut ve uzun süreli etkisi.

OBJECTIVE: Baseline serum levels of neuroactive steroids such as dehydroepiandrosterone sulfate (DHEAS), 17-hydroxyprogesterone (17-OHP), testosterone, and cortisol were measured, and the acute and long-term effects of electroconvulsive therapy (ECT) on these hormones and the effect of gender on alterations in steroid hormones were investigated in patients with major depressive disorder (MDD). METHODS: The study included 25 inpatients (11 male, 14 female) diagnosed with MDD that responded to ECT, and 37 healthy controls (17 male, 20 female). Serum levels of cortisol, DHEAS, 17-OHP, and testosterone were measured 2 days before and 10 min after the first ECT, and 3 days after the last ECT in the patients. These measurements were obtained only once in the controls. RESULTS: Basal DHEAS increased, testosterone and 17-OHP decreased, and cortisol levels remained unchanged in MDD patients as compared to the controls. After completion of the therapeutic course of ECT, DHEAS levels in the patients were higher than they were before the treatment. After ECT treatment, cortisol and 17-OHP levels in the patients were lower than those in the controls; however, testosterone levels did not differ between the groups. In the MDD patients, increases in DHEAS and decreases in testosterone were only observed in men, while decreases in 17-OHP were only seen in women. CONCLUSIONS: Alterations were observed in some neuroactive steroids in MDD patients and it appears that ECT affected these hormones. It is not clear whether the observed alterations in neuroactive steroids are associated with the pathophysiology of depression or whether they play a role in the therapeutic effects of ECT.

Suggested Biomarkers for Major Depressive Disorder.

Currently, the diagnosis of major depressive disorder (MDD) mainly relies on clinical examination and subjective evaluation of depressive symptoms. There is no non-invasive, quantitative test available today for the diagnosis of MDD. In MDD, exploration of biomarkers will be helpful in diagnosing the disorder as well as in choosing a treatment, and predicting the treatment response. In this article, it is aimed to review the findings of suggested biomarkers such as growth factors, cytokines and other inflammatory markers, oxidative stress markers, endocrine markers, energy balance hormones, genetic and epigenetic features, and neuroimaging in MDD and to evaluate how these findings contribute to the pathophysiology of MDD, the prediction of treatment response, severity of the disorder, and identification of subtypes. Among these, the findings related to the brain-derived neurotrophic factor, the hypothalamo-pituitary-adrenal axis, cytokines, and neuroimaging may be strong candidates for being biomarkers MDD, and may provide critical information in understanding biological etiology of depression. Although the findings are not sufficient yet, we think that the results of epigenetic studies will also provide very important contributions to the biomarker research in MDD. The availability of biomarkers in MDD will be an advancement that will facilitate the diagnosis of the disorder, treatment choices in the early stages, and prediction of the course of the disorder.

Growth hormone response to the GABA-B agonist baclofen in 3-week abstinent alcoholics.

Gamma-aminobutyric acid (GABA) dysfunction is a known feature of alcoholism. We investigated GABA-B receptor activity in 3-week abstinent alcoholics using the growth hormone (GH) response to baclofen, a GABA-B receptor agonist. The study aimed to investigate the relationship between GABA-B receptor activity and alcohol withdrawal. GH response to baclofen was measured in alcohol-dependent males without depression (n = 22) who were on day 21 of alcohol abstinence and in healthy control male subjects (n = 23). After 20mg baclofen was given orally to the subjects, blood samples for GH assay were obtained every 30 min for the subsequent 150 min. The patients were divided into two subgroups (continuing withdrawal and recovered withdrawal subgroups) according to their withdrawal symptom severity scores on day 21 of alcohol cessation. Baclofen administration significantly altered GH secretion in the controls, but not in the patients. When GH response to baclofen was assessed as DeltaGH, it was lower in the patients with continuing withdrawal symptoms than in the controls and in the recovered withdrawal group. Impaired GH response to baclofen in all patients mainly pertained to the patients whose withdrawal symptoms partly continued. Our results suggest that reduced GABA-B receptor activity might be associated with longer-term alcohol withdrawal symptoms in alcoholic patients.

[Neurobiology of Alcohol Dependence and Implications on Treatment]. / Alkol Bagimliliginin Nörobiyolojisi ve Tedaviye Yansimalari.

The process of alcohol dependence has been conceptualized as a progress from controlled alcohol intake to compulsive alcohol consumption or a shift from alcohol intake for pleasure to compulsory alcohol seeking behavior. Hereditary and physical factors and the interaction of individuals with their environment, as well as permanent changes in the neurotransmitter and neurohormonal systems in the brain due to alcohol use, play the most important role in the etiology of alcohol dependence. The effects of ethanol on the neurotransmitter, neuropeptide and neuroendocrine systems not only account for its acute physiological and euphoric/reinforcing effects but also seem to be responsible for the development of dependence. While the motivation for alcohol use is mainly positive reinforcement in the earlier phases of alcohol consumption, both positive and negative reinforcements are involved in the process once dependence has developed. This event is caused by neuroadaptive process due to chronic alcohol consumption and also called as "allostasis". It seems that the most important neuroadaptive changes in progression from occasional alcohol intake to dependence are the down-regulation of the dopamine and gamma aminobutyric acid systems, permanent upregulation in the glutamate system and dysregulation in the stress systems (corticotropin-releasing hormone and serotonin) of the brain. In this paper, we will review the adaptive changes caused by chronic alcohol consumption which are important in the development of dependence and address the potential therapeutic contributions of interventions to these changes in alcohol dependence.

Relationship between orexin A and childhood maltreatment in female patients with depression and anxiety.

OBJECTIVE: Childhood maltreatment leads to neuroendocrine changes, which may be associated with an increased vulnerability for psychopathology, such as depression and anxiety in later life. This study aimed to investigate the relationship between childhood maltreatment and orexin A levels in patients with depression and anxiety. The study consisted of 27 female outpatients who presented with depressive and/or anxiety symptoms, and 27 healthy female controls. Childhood trauma history was assessed using the childhood trauma questionnaire (CTQ-28) in patients and controls. Serum levels of orexin and cortisol were measured in all subjects. There were positive correlations between serum orexin levels and CTQ total score and between orexin levels and some CTQ subscale scores, such as physical and emotional neglect, in patients. Orexin levels in patients with a positive history of physical and emotional neglect were higher than those in patients with a negative history of them. In the controls, there was a positive correlation between emotional neglect score and serum orexin level. There were no differences in serum levels of orexin and cortisol between patients and controls. Orexin levels may be associated with childhood maltreatment per se, rather than psychopathology, such as depression or anxiety.

Cerebellar syndrome in a patient with pneumonia under lithium treatment: A case report.

We report the case of a 31-year-old man with bipolar disorder who was on a combination therapy of lithium, lamotrigine and escitalopram. Serum lithium level was within therapeutic range. Cerebellar symptoms such as dysarthria, ataxia, and dyskinesia developed in the patient following the pneumonia. Cerebellar syndrome was most likely due to lithium neurotoxicity, which was associated with additional factors such as acute febrile pneumonia, fever and hyponatremia. The reported case suggests that infections may increase the risk of cerebellar toxicity of lithium, even in the therapeutic doses.

[Neurobiology of alcohol withdrawal inhibitory and excitatory neurotransmitters]. / Alkol Yoksunlugunun Nörobiyolojisi: Baskilayici ve Uyarici Nörotransmiterler.

Alcohol withdrawal is a syndrome that is the result of adaptive changes in the brain secondary to chronic alcohol use and is associated with changes in many neurotransmitter, neuropeptide, and hormonal systems. Long-term exposure to ethanol leads to an imbalance in different excitatory (especially glutamate, a major excitatory amino acid), and inhibitory neurotransmitter (especially GABA, a major inhibitory amino acid) systems. When alcohol consumption is reduced or completely ceases, these imbalances are behaviorally expressed in the form of alcohol withdrawal. Symptoms of alcohol withdrawal are mainly associated with the hypofunction of GABA receptors and enhanced function of NMDA receptors. The imbalance between receptors may be exacerbated by repeated withdrawal. Some of these alterations may last for months following alcohol cessation and cause symptoms of protracted alcohol withdrawal, which may contribute to the continuation of the cycle of alcohol addiction relapses. The search for biological alterations during alcohol withdrawal may not only render some important insights into the pathophysiology of alcohol dependence, but might also identify new targets for the treatment of alcohol withdrawal symptoms and for preventing relapses following withdrawal. Therapists specializing in the treatment of addiction should be cognizant of the underlying biological mechanisms of alcohol withdrawal in order to more adequately understand the physiopathology of substance dependence in general. In this paper, we will review the changes in the inhibitory and excitatory neurotransmitter systems involved in alcohol withdrawal, and we will discuss their roles in the development of alcohol dependence.

Effects of antidepressant treatment and of gender on serum leptin levels in patients with major depression.

Leptin is a product of the obese gene and plays an important role in the regulation of body weight and food intake. Weight and appetite are frequently altered in depression. So far, inconsistent results have been reported in terms of leptin levels in depression. Therefore, the authors investigated serum leptin levels in patients with depression and in healthy controls, and whether there was any alteration throughout antidepressant treatment. Female patients showed significantly higher leptin levels than those of the control females both before and after the response to antidepressant treatment, whereas no difference was found between the male patients and the male controls. The improvement from depression with antidepressant treatment caused a further elevation on the leptin levels, in both female and male patients. These findings confirm an increase in leptin levels in depressive patients and presence of a sexual dimorphism. Moreover, clinical response to antidepressant treatment seems to have an additional increasing effect on leptin levels.

[Is there any alteration in bone mineral density in patients with depression?]. / Depresyonlu Hastalarda Kemik Mineral Yogunlugunda Degisiklik Var mi?

OBJECTIVE: Depression is associated with some alterations in behavior and hypothalamic-pituitary-adrenal axis function that may be risk factors for decreased bone mineral density (BMD). There is considerable inconsistency as to whether depressed patients really have decreased BMD or not. Decreased BMD has been reported in patients suffering from major depression in some studies, but not in some others. Moreover, few studies have investigated BMD in male depressed patients. The aim of this study was to investigate BMD in patients with major depression, including male ones. METHOD: BMD was investigated in forty-two inpatients that fully met the DSM-IV criteria for major depressive disorder (21 women, 21 men; mean age+/-SD: 37.57+/-8.70) and compared with that in twenty-three healthy controls (12 women, 11 men; mean age+/-SD: 33.73+/-7.16). The severity of clinical symptomatology was assessed by the Montgomery-Asberg Depression Rating Scale (MADRS). BMDs of lumbar vertebrae (L1-L4) and femur neck were measured using dual energy X-ray absorptiometry. RESULTS: We found no difference in the values of BMDs of lumbar vertebra (L1-L4) and femur neck between depressive patients and controls among women or men. However, BMDs of the males in the control group were higher than those of the healthy females for both regions investigated; this gender difference was not observed in the depressive patients. CONCLUSION: Major depression is not associated with any alteration in BMD either in women or in men.

Effects of antidepressant treatment on thyrotropin-releasing hormone stimulation, growth hormone response to L-DOPA, and dexamethasone suppression tests in major depressive patients.

Dexamethasone suppression (DST), thyroid-stimulating hormone (TSH) and prolactin (PRL) responses to thyrotropin-releasing hormone (TRH) and growth hormone (GH) response to L-DOPA tests were evaluated in 19 depressed inpatients before the commencement of the antidepressant treatment and after the clinical response to examine: (i) the functional relationships among the hypothalamic-pituitary-adrenal (HPA) and hypothalamic-pituitary-thyroid (HPT) axis and dopaminergic system in depression, (ii) any alterations in these hormonal functions with the antidepressant treatment. TSH responses to TRH showed a tendency to increase from pre- to posttreatment period, while TRH-induced PRL and L-DOPA-induced GH responses did not change with treatment in depressed patients who responded to the treatment. Females showed significantly higher TSH and PRL responses to TRH compared to males. No interconnections were found among the responses in DST, TRH stimulation test and L-DOPA-induced GH test in the patients. The results do not support the interrelations between the abnormalities in the HPT and HPA axes and central dopaminergic activity in depression.

Effects of electroconvulsive therapy on hypothalamic-pituitary-thyroid axis activity in depressed patients.

In this study, the authors aimed to test the hypothesis that electroconvulsive therapy (ECT) may cause some alterations in hypothalamic-pituitary-thyroid (HPT) axis hormones and these responses may change throughout respective ECT sessions. Nineteen depressed inpatients (8 males, 11 females; mean age+/-S.D.: 44.77+/-10.59 years) considered suitable for ECT were included in the study. Each patient was exposed to 7 ECT sessions with general anaesthesia. The blood samples for measurements of thyroid-stimulating hormone (TSH), free thyroiodothyronine (fT3) and free thyroxine (fT4) were drawn before (baseline) and after propofol, immediately after ECT, and 30 and 60 min after ECT during the first and last (seventh) ECTs. In both the first and seventh ECTs, there was a significant increase in TSH levels 30 min after ECT compared to the pre-ECT values. Additionally, a significant decrease in post-ECT fT4 values compared to the baseline values was found only during the seventh ECT. No difference was detected in the TSH, fT3 and fT4 responses to ECT between males and females, and between bipolar and unipolar depressive patients. These results show that ECT may have some effects on the HPT system. However, whether there is a relationship between these neuroendocrine responses and the therapeutic effect of ECT is not clear.

Effects of short- and long-term lithium treatment on kidney functioning in patients with bipolar mood disorder.

Lithium (Li) carbonate has been reported to be able to cause some reversible functional changes in the kidney. In this study, the authors aimed to investigate whether the duration of Li treatment is the primary determinant of the changes in renal functioning due to the Li treatment. For this purpose, 10 Li-naïve (mean age+/-S.D.: 34.50+/-4.85), 10 short-term (mean age+/-S.D.: 31.77+/-7.61) and 10 long-term (mean age+/-S.D.: 36.60+/-10.15) Li-treated bipolar patients were included in the study. Serum blood urea nitrogen (BUN) and creatinine, urine creatinine levels, creatinine clearance, urine osmolality before and after 8-h water deprivation and urine osmolality after desmopressin injection were measured in all patients. Serum BUN and creatinine levels were within the normal limits and not statistically different among the groups. Creatinine clearance of the long-term Li-treated group was significantly lower than both that of the Li-naïve group and that of the short-term Li-treated group. After 8-h water deprivation and also after desmopressin injection, no difference was found among the groups in terms of urine osmolality. However, when each patient was evaluated individually in terms of their renal concentrating ability, partial nephrogenic diabetes insipidus was diagnosed in four patients on long-term and in two patients on short-term Li treatment. To our surprise, hypothalamic diabetes insipidus was also diagnosed in other two patients on long-term Li treatment. These results demonstrate that long-term Li treatment may cause impairment in renal concentrating ability, some of which may originate from the effects of Li on vasopressin on hypothalamic level, and a decrease in glomerular filtration rate (GFR). In the light of these data, we can conclude that long-term administration of Li may be a risk factor for Li-induced renal impairment, which is a progressive effect in nature.

Auditory event-related potentials in panic and generalised anxiety disorders.

In this study, we aimed to investigate event-related potential (ERP) changes in panic disorder (PD) and generalised anxiety disorder (GAD) and to determine whether two disorders are different from each other in terms of endogenous potentials. A total of 35 outpatients who fully met DSM-III-R criteria for PD (8 males and 27 females) were included in this study as the PD group. The GAD group consisted of 30 subjects (5 males and 25 females) who met DSM-III-R GAD criteria. The control group consisted of 29 healthy age and sex-matched volunteers (5 males and 24 females) having no history of psychiatric or neurological illness. ERPs were recorded by using auditory "odd-ball two-tone discrimination task" method. It was found that there was significant prolongation in P3 latency in the PD group compared to the GAD and control groups. Our study suggests that there are some disturbances in early information processing in patients with PD but not with GAD.

P300 changes in major depressive disorders with and without psychotic features.

BACKGROUND: Although there are many P300 studies in depressive patients, only a few studies have focused on the effects of psychotic features in depression and of response to antidepressant treatment on P300. This study was designed to investigate possible differences in the P300 component of event-related potentials in depressed patients with and without psychotic features and if any, to see whether these changes altered with treatment of depression. METHODS: Thirty-six patients with major depressive disorder diagnosed according to DSM-IV, and 20 healthy control subjects were involved in the study. Sixteen of the patients had psychotic features. Auditory P300 was recorded before treatment and after remission. RESULTS: Pretreatment P300 latencies were significantly prolonged both in patients with and without psychotic features compared to controls. Pretreatment P300 amplitudes were significantly decreased only in the patients with psychotic features. After treatment of depression, delayed P300 latencies in both patient groups and decreased P300 amplitude in the patient group with psychotic features were normalized. LIMITATIONS: The medication status of the patient was heterogeneous. CONCLUSION: Since the impairment seems to be improved by drug treatment, prolonged P300 latency might be a state marker for a major depressive episode, and decreased P300 amplitude which is correlated with paranoid ideation might be more associated with psychotic subtype.

A Tc-99m HMPAO SPECT study of regional cerebral blood flow in drug-free schizophrenic patients with deficit and non-deficit syndrome.

Twenty-nine patients with DSM-IV diagnoses of schizophrenia were categorized into deficit syndrome (n=14) and non-deficit syndrome (n=15) subgroups on the basis of the Schedule for the Deficit Syndrome. The patients, who had all been free of antipsychotic medication for at least 3 weeks, and 17 sex- and age-matched normal controls were studied with single-photon emission computed tomography with Tc-99m HMPAO. Age at onset, Brief Psychiatric Rating Scale (BPRS) total scores, BPRS positive symptom subscores and duration of illness were similar between the two schizophrenic subgroups. As expected, the deficit patients had more negative symptoms than the non-deficit patients. There were no statistically significant correlations between clinical parameters and regional cerebral blood flow (rCBF) values. The deficit syndrome subgroup showed diminished rCBF in the frontal regions bilaterally, right parietal regions and right superior temporal region compared with the control groups. Deficit patients showed significantly lower rCBF perfusion ratios in the right superior and inferior frontal cortex than did the non-deficit patients. No differences were detected between the controls and the non-deficit schizophrenic patients in terms of rCBF perfusion indices. The results of the present study confirm previous reports of different patterns of rCBF in deficit vs. non-deficit schizophrenic subgroups.