Eating Attitudes Test and culture: a study in northern and southern Italy.

The EAT (Eating Attitudes Test) has been widely used to compare eating morbidity in cultural groups and variations in it have been taken as indicative of cultural differences. This study assumed the existence of cultural differences between the north and the south of Italy. The EAT scores of female students from a northern and a southern Italian high school were compared. They were both higher than in other European studies, though there were no significant differences between the two groups. The result could be due to sampling limitations, but could also indicate that the EAT is not a reliable yardstick of cultural differences.

Psychiatric symptoms do not correlate with cognitive decline, motor symptoms, or CAG repeat length in Huntington's disease.

OBJECTIVES: To investigate the hypothesis that psychiatric disturbances in Huntington's disease are related to degree of cognitive or motor compromise and to determine correlations between CAG repeat length within the gene for Huntington's disease and disease severity. DESIGN: Consecutive series of patients with Huntington's disease. SETTING: Neurological specialty hospital. PATIENTS: Seventeen men and 12 women from 24 families. MAIN OUTCOME MEASURES: The Hamilton Psychiatric and Anxiety Rating Scales and Brief Psychiatric Rating Scale were used to assess psychiatric disturbances; Folstein's Quantified Neurological Examination to evaluate motor status; and the Mini-Mental State Examination, Raven Progressive Matrices), Phonemic Verbal Fluency Test, Short Tale Test, Visual Search Test, and Benton's Visual Orientation Line Test to evaluate cognitive function. The length of the CAG repeat sequence in the Huntington's gene was determined by quantitative polymerase chain reaction. RESULTS: Cognitive test scores correlated significantly with each other; of these, results of the Visual Search and Short Tale tests correlated significantly with the Folstein's Quantified Neurological Examination score (P = .05 and P = .03, respectively). Results of the Folstein's Quantified Neurological Examination also correlated with the illness duration and the length of the CAG repeat. Although psychiatric scores correlated significantly among themselves (P < .01), neither cognitive compromise, motor deterioration, nor CAG length were related to the extent of psychiatric compromise. Patients who were depressed when they were examined tended to have a history of psychiatric disorders. CONCLUSIONS: The lack of correlation between disease severity and psychiatric disturbances indicates that psychiatric disorders progress nonlinearly, possibly because of differential degeneration of the striatal-cortical circuits; the possibility that psychiatric disorders are prevalent in certain families with a member who has Huntington's disease is being further investigated. The lack of correlation between CAG length and cognitive and psychiatric variables needs further investigation.

Neurobiological and psychopharmacological basis in the therapy of bulimia and anorexia.

1. Eating disorders can be found in several psychiatric pathologies: schizophrenia, delusional disorder (somatic type), bipolar disorders, major depressive disorder, borderline personality disorder, generalized anxiety disorder, body dysmorphic disorder, somatization disorder and conversion disorder. 2. Although their clinical features have been defined, relatively little is known about the role of neurobiological patterns in the pathogenesis of these disorders. Several CNS neurotransmitters and neuromodulators are involved in the regulation of eating behavior in animals and have been implicated in symptoms such as depression and anxiety often observed in patients with eating disorders. The authors will review some studies on NA, DA, 5-HT, beta-endorphins, CRH, VP, OT, CCK, NPY and PYY involved in eating disorders. Furthermore, we will highlight some of the studies on drug therapy of eating disorders taking into account the effects of these agents on neurotransmitters and neuromodulators. 3. Antidepressant drugs have long been used for anorexia nervosa and bulimia, these disorders been claimed to be affective equivalent. Antidepressant agents seem to be effective in reducing the frequency of binge-eating episodes, purging behavior and depressive symptomatology. It is notable that antidepressant agents have been proved to be effective in patients with chronic bulimic symptoms, even in cases persisting for many years and in patients who had repeatedly failed courses of alternative therapeutic approaches. In all of the positive studies, antidepressant agents appeared effective even in bulimic subjects who did not display concomitant depression. 4. Few controlled studies on use of medications for anorexia nervosa have been published. Central serotonergic receptor-blocking compounds such as cyproheptadine cause marked increase in appetite and body weight. Zinc supplementation or cisapride could be a therapeutic option in addition to psychological and other approaches in anorexia nervosa. 5. There is no therapy as yet which is fully effective in alimentary disorders. Psychotropic drugs give some relief from symptoms, but they cannot cure the disorders. An integrated approach, either pharmacological or psychological, is still recommendable.

Beta-endorphin, vasoactive intestinal peptide and cholecystokinin in peripheral blood mononuclear cells from healthy subjects and from drug-free and haloperidol-treated schizophrenic patients.

Beta-endorphin, cholecystokinin and vasoactive intestinal peptide were measured in peripheral blood mononuclear cells of healthy controls, and schizophrenic patients at the first diagnosis before any treatment and after 2 or 15 d of treatment with haloperidol. Beta-endorphin concentrations were similar in controls and untreated patients, and increased with treatment. Cholecystokinin concentrations were higher in patients than in controls, and decreased during treatment. Vasoactive intestinal peptide was lower in patients and did not change with treatment. These observations are consistent with measurements of the same peptides in autopsy samples or cerebrospinal fluid. Peripheral blood mononuclear cells might be an useful tool for the study of some neuropeptides in brain.

Alexithymia and obesity. Study of the impaired symbolic function by the Rorschach test.

Many authors consider alexithymia a predisposing factor to psychosomatic and somatopsychic pathologies. In this study we investigated the presence of alexithymic characteristics in a group of 106 massive obese patients who requested a surgical intervention. 6 Rorschach alexithymia variables in the protocols of patients and a non-patient reference group (n = 600) were studied. Findings supported the presence of a striking alexithymic element among severely obese patients in comparison with their lean counterparts.

Bromocriptine therapy in chronic schizophrenia: effects on symptomatology, sleep patterns, and prolactin response to stimulation.

Ten chronic schizophrenic patients were given bromocriptine in doses increasing from 1.25 to 5 mg over 6 days (the low-dose therapy) and then up to 40 mg over 15 days (the high-dose therapy). Psychopathological status was assessed using the Brief Psychiatric Rating Scale, twice daily the first 6 days, and every 2 days thereafter. The prolactin (PRL) response to haloperidol stimulation (1 mg i.v.) was measured in five cases before and 3 days after the end of high-dose therapy, and in one patient before and 3 days after the end of low-dose therapy. Electroencephalographic sleep studies were carried out before therapy and every 2 nights during low-dose therapy in five patients, and in two cases during high-dose therapy. Bromocriptine therapy modified neither clinical symptomatology nor sleep patterns. The PRL response to haloperidol after therapy was markedly lower than that before therapy in the five patients treated with high doses, and markedly higher in the single patient tested who was treated only with low-dose therapy.

Failure of pyridoxine to effect neuroleptic-induced hyperprolactinemia in psychotic patients.

The effects of acute and repeated administration of pyridoxine on serum prolactin levels were studied in 18 chronic schizophrenics, 10 women and 8 men, in whom hyperprolactinemia had been induced by long-term treatment with phenothiazines, haloperidol, sulpiride or clopentixol. The patients were divided into 5 groups: group 1 received 300 mg of the vitamin per os in a single dose; group 2 received 300 mg of the vitamin per os for 7 days; group 3 received 300 mg of the vitamin iv as a single bolus; group 4 received 600 mg of the vitamin iv as a single bolus; group 5 received 1200 mg of the vitamin per os in a single dose. Prolactin levels were examined before and 15, 30, 60, 90, 120 and 150 min after the single administration of pyridoxine, either iv or per os, and on days 3,5, 7 of the chronic administration. There was no decrease in prolactin levels either after oral or iv administration of the drug, given in single or repeated doses. Therefore, this treatment is not useful for the suppression of hyperprolactinemia induced by neuroleptics.

Learning capacities during sleep: a preliminary study in a group of schizophrenic inpatients.

The relationship between sleep and learning processes is analysed in a sample of schizophrenic patients, starting from more recent hypotheses about the function of REM sleep in learning and memory processes. This is done by means of two experiments: in the first AA. evaluate the possibility to elicit a simple motor conditional reflex acquired during daytime in different sleep stages. With the second experiment daytime learning performances are evaluated with and without a reinforcement administered during REM sleep. Results for the first experiment underline a qualitative difference between REM and nREM sleep in a reflexological perspective. In nREM sleep the conditional response is better maintained than in REM sleep. The second experiment confirms the possibility to improve daytime learning performances after an additional presentation of learning material in REM. The joint study of sleep abnormalities and learning and cognitive impairment in schizophrenic patients is finally suggested.

Neurophysiological aspects and learning processes in schizophrenic patients.

Two groups of schizophrenic patients (acute and chronic subjects) were observed in order to study possible differences in neuropsychological performances and their relationship with symptomatology. 16 acute and 16 chronic patients, aged 18 to 35 years were tested with a battery of neuropsychological tests (Word Association Test, Serial Verbal Learning, Weigl's test, Simple Reaction Times, Choice Continuous Reaction Time). Clinical profiles were evaluated by means of MMPI and WAIS (Wechsler Adult Intelligence Scale). Findings concerning cognitive processes show no significant differences between the two groups. Results suggest a correlation between clinical profiles and performances in acute patients, whereas in chronic subjects this correlation seems markedly reduced. Finally, chronicity (i.e. the length of illness) does not seem so be an important factor in determining consistent defects in neuropsychological performances.

Sleep, psychophysiological functioning and learning processes in schizophrenia.

Sleep research has underlined how sleep is a specific functional moment inserted in the more complex system of circadian psychobiological rhythms. Many experimental data have evidenced that in particular REM sleep is involved in information processing and cognitive processes. The authors examine correlations between daytime cognitive performances and sleep patterns in a group of 11 schizophrenic patients, and in a control group made of 11 non-schizophrenic (borderline, depressed, character disorders) patients. Results show that there exists a relationship between REM sleep and cognitive activities, beyond nosographic partitions. They on the other side suggest caution in using sleep as a means of discrimination between schizophrenic and non-schizophrenic patients.

Cobalt-induced experimental epilepsy in cats pharmacologically immunodepressed. An EEG and histological study.

The authors made 11 adult cats epileptic by implanting cobalt powder on the left sensorimotor cortex. Some of the animals were treated with the immunodepressant drug, cyclophosphamide (Endoxan), before and after surgery, and others were not. Then the two groups of animals were compared in terms of EEG and histopathological findings. The treatedanimals showed a definite reduction of focal electrical activity both primary and secondary, and a much milder perifocal parvicellular infiltration and cerebral edema. In view of these findings, the authors suggest that in addition to other well-known factors, the pathogenesis of cobalt-induced experimental epilepsy involves immunological mechanisms triggered by the release of nerve tissue antigens as a result of tissue injury caused by cobalt. This would result in the formation of antibodies directed against several brain constituents. Last, the authors submit that a similar autoimmune mechanism may be at play also in the pathogenesis of some forms of focal epilepsy of traumatic origin.

A study of the EEG sleep patterns and the sleep and dream experience of a group of schizophrenic patients treated with sulpiride.

The modifications of spontaneous sleep in schizophrenic patients following N-ethyl-2(2-methoxy-5-sulfamido-benzamidomethyl)-pyrrolidine (sulpiride, Dobren) administration are reported in this study. No significant modifications in the quantitative distribution of the various sleep phases (LST, SWS, REM) were observed, while a significant percent increase of SWS was noted, together with a significant decrease in the number of awakenings during the night and an increase of the sleep onset time. The patients' own difficulty to fall asleep, however, decreased significantly, and also a significant increase of dream recall could be observed.