Biomedical subjects
Publications and source records attributed to F Brambilla.
In a double blind, random, cross-over design, 10 patients and seven controls inhaled one vital capacity of 35% CO2-65% O2 during their early-follicular and midluteal phases. Anxiety after CO2 intake was significantly stronger in the early-follicular phase than in the midluteal phase for patients. Controls had no anxiety reactions.
Baseline levels of GH and somatomedin C (SmC) and GH responses to GHRH (1 microgram/kg b.w.) and to clonidine (150 micrograms) were measured in 10 outpatients with panic disorder before and after 30 days of 2-2.5 mg of alprazolam therapy, and in 10 psychophysically healthy controls. Basal levels of GH were normal in the patients and those of SmC significantly elevated, both before and after therapy. Basal GH responses to GHRH stimulation were normal and did not change change after alprazolam treatment. Basal GH responses to clonidine stimulation were blunted in the patients and improved after therapy, in parallel with an amelioration of the psychopathology. Our data suggest that adrenoceptor sensitivity, investigated by the clonidine test, is reduced in panic disorder.
The cortisol responses to acute administration of saline and of clonidine (Clon), 150 micrograms IV, were examined in 12 patients with panic disorder and agoraphobia, before and after 32 days of alprazolam therapy (2.5 mg/day), and in 12 normal controls. The responses in the Clon test corrected for the responses to saline differed in the two groups, and in patients were not changed by the therapy even though significant symptomatological improvement was achieved. The results suggest that presynaptic alpha 2- or postsynaptic alpha 1-beta-adrenoceptor sensitivity is impaired in panic disorder.
Twenty-two female patients with anorexia nervosa, restricted type, 14-35 years old, were treated with a 4-month course of combined cognitive-behavioral therapy, nutritional counselling and antidepressant drugs (nortriptyline for 7, fluoxetine for 15). Patients were monitored for body mass index (BMI), for eating disorder symptoms by the Eating Disorder Inventory (EDI) and the Bulimic Investigation Test (BITE) and for depression and anxiety by the Hamilton Rating Scales for Depression and for Anxiety (HRS-D and -A). The scores were determined before and after 1, 2 and 4 months of therapy. BMI, depression, anxiety and EDI scores improved significantly and equally in both groups during the 4 months of therapy, while BITE scores did not change.
Thirteen women with anorexia nervosa, binge-eating/purging type (AN-BP), 17-43 years old, were treated with a 4-month course of combined cognitive-behavioral, nutritional and antidepressant therapy (7 with amineptine and 6 with fluoxetine). Patients were monitored before and after 1, 2 and 4 months of treatment for body mass index (BMI), for eating disorder symptoms by the Eating Disorder Inventory (EDI) and the Bulimic Investigation Test (BITE) and for depression and anxiety by the Hamilton Rating Scales for Depression and for Anxiety. BMI, EDI scores, depression and anxiety improved significantly and equally in the two groups during the 4 months of therapy, while BITE scores did not change.
Fifteen women with bulimia nervosa were treated with a 4-month course of combined cognitive-behavioral, nutritional and antidepressant therapy (5 with amineptine and 10 with fluvoxamine). Patients were monitored before and after 1, 2 and 4 months of therapy for body mass index (BMI), for eating disorder symptoms by the Eating Disorder Inventory (EDI) and the Bulimic Investigation Test (BITE), and for depression and anxiety by the Hamilton Rating Scale for Depression and for Anxiety (HRS-D and -A). BITE symptoms and gravity improved significantly and equally in the two groups during the 4 months of therapy. Global EDI scores, depression and anxiety decreased but not significantly. BMI was normal before therapy and did not change during treatment.
The responses of growth hormone (GH) to administration of growth hormone-releasing hormone (GHRH-1 micrograms/kg b.w.) and of clonidine (clon-2.5 micrograms/kg b.w.) and basal levels of somatomedin C (SmC) were measured in nine peripubertal patients with Major Depressive Disorder (MDD) and in 9 age- and gender-matched controls. Basal GH and SmC levels, and GH response to GHRH did not differ in patients and controls, whereas responses to clonidine were significantly higher in some and lower in other patients than in controls.
Plasma interleukin-1 beta (IL-1 beta) concentrations were measured in 10 outpatients with panic disorder before and on days 30 and 32 of treatment with alprazolam (2-2.5 mg/day). IL-1 beta concentrations were found to be significantly higher in patients than in control subjects both before and during therapy. Thus, IL-1 beta levels may be a marker of panic disorder that is not related to the current level of symptomatology.
Growth hormone (GH) and prolactin (PRL) responses to the acute administration of clonidine (150 micrograms) and apomorphine (0.5 mg) were investigated in parallel in 20 drug-free subchronic and chronic schizophrenic patients and in nine control subjects. Neither basal levels of the two hormones nor their mean responses to both stimuli differed significantly between the two groups. However, eight patients had blunted GH responses to clonidine and seven to apomorphine; only two patients showed blunted GH responses to both stimuli. The blunted GH response to apomorphine correlated with the chronicity of the disorder. A greater than normal GH response to clonidine stimulation was observed in paranoid patients. Significant correlations were observed between negative symptoms and GH responses to clonidine (negative), between negative symptoms and PRL responses to apomorphine (positive), and between positive symptoms and PRL responses to apomorphine (negative).
Noradrenergic receptor sensitivity of 16 healthy male siblings of heroin addicts and of 8 age and sex-matched controls was examined by administering a clonidine stimulation test and by measuring the resulting growth hormone (GH) (alpha-2-adrenoceptors) and beta-endorphin (beta-endorphin) (alpha-1-adrenoceptors) responses. Siblings were divided into two groups: A = siblings of heroin addicts with personality disorders and high aggressivity and B = siblings of heroin addicts without mental disorders. The GH and beta-endorphin responses to clonidine were blunted in group A subjects compared with controls and normal in group B.
Growth hormone (GH) and beta-endorphin (beta-EP) responses to clonidine stimulation were examined in 18 male heroin addicts, 9 with and 9 without previous histories of attention deficit disorder with hyperactivity (ADD-H) and conduct disorder (CD). Ten psychophysically healthy volunteers were used as controls. ADD-H/CD addicts had blunted GH and beta-EP responses as compared to controls while those of non-ADD-H/CD addicts were normal. This suggests that postsynaptic adrenoceptor sensitivity is decreased and, possibly, that presynaptic noradrenaline secretion is increased in ADD-H/CD patients with heroin addiction.
Plasma noradrenaline (NE), adrenocorticotrophic hormone (ACTH), growth hormone (GH), prolactin (PRL) and luteinizing hormone (LH) concentrations were examined in basal conditions and after stimulation by the step test in two groups of psychophysically healthy adolescent girls, 18 from divorced families and 16 from non-divorced families. Basal NE, ACTH, GH, PRL values did not differ in the two groups, whereas those of LH were significantly lower in the adolescents from divorced parents than in those from non-divorced families. Responses of NE and ACTH to the stimulus were normal, of GH and PRL were weaker, and of LH slightly weaker in children of divorced parents. An impaired catecholaminergic and serotoninergic tonus in children of disrupted families might underly the hormonal alterations.
Immunological and neuroendocrine parameters were examined in 11 women with anorexia nervosa, 6 restricted and 5 bulimic-anorectics, 17-43 years old with 2-15 years duration of the disease, and in 11 age- and sex-matched psychophysically healthy controls. The T lymphocyte proliferative response to phytohemagglutinin (PHA), plasma adrenocorticotropic hormone (ACTH), cortisol and beta-endorphin (beta-EP) levels was examined in basal conditions and after corticotropin-releasing hormone (CRH) stimulation. Cortisol inhibition by dexamethasone (DST), and basal growth hormone (GH) and prolactin (PRL) levels were also examined. The immune study did not reveal significant differences between patients and controls. ACTH and cortisol basal levels were significantly higher in anorectics, while beta-EP, GH and PRL concentrations did not differ in the two groups. ACTH, beta-EP and cortisol responses to CRH were blunted in anorectics and the DST impaired in 55% of the patients. No correlations were observed between neuroendocrine impairments and the T lymphocyte response to PHA, or between the immunological neuroendocrine parameters and the body mass index of either patients or controls.
Seventy physically healthy 14-year-old adolescents, 40 boys and 30 girls, were evaluated psychologically and endocrinologically. After the psychological tests (Anxiety Score Test for Adolescents, Rosenzweig, Pictures Frustration Test for Children), subjects were divided into group A, with low anxiety/sense of guilt and high self-esteem/tolerance to frustration and group B with the opposite. In both groups, we measured basal plasma levels of noradrenaline (NE), growth hormone (GH), prolactin (PRL), melatonin (MT) and luteinizing hormone (LH) and their response to physical exercise (the Harvard step test). Basal levels of the hormones and of NE were not different in the two groups. After the physical stimulus, NE levels rose significantly more in B girls than in A and significantly less in B than in A boys. GH and PRL levels increased only in A girls and MT in B boys, while LH levels decreased in A boys and girls but not in B subjects.
The responses of cortisol to acute administration of saline and of clonidine (2.5 micrograms/kg B.W.) were examined in 10 children and adolescents with major depressive disorder and in 10 age- and sex-matched controls. Clonidine administration did not inhibit cortisol secretion in controls or in patients, contrary to what has been observed in depressed adults. In controls, but not in patients, clonidine administration induced a transitory increase of the steroid.
Since cholecystokinin (CCK) is known to be anxiogenic in experimental animals and to induce panic attacks in humans, lymphocyte CCK-8 concentrations were measured in 15 patients with panic disorder and 15 age- and sex-matched healthy subjects. The patients' levels were measured again after a 30-day course of alprazolam therapy, 1.5 mg/day. The CCK-8 concentrations were significantly lower in the patients than in the control subjects and did not change after alprazolam therapy. There was no correlation between the peptide values and levels of anxiety or frequency and severity of panic attacks.
Psychological impairments can occur during the course of major endocrine diseases. These impairments range from mild affective-cognitive-behavioral disturbances to frank psychoses. The former are rather specific for each hormonal disorder and disappear with the hormonal correction. The latter, instead, seem to be quite nonspecific and include depression, mania, schizophrenia-like and organic brain syndromes which appear at random in each endocrinopathy, not always regressing with hormonal recovery, and apparently correlating more with the severity than with the nosographic classification of the metabolic disturbances. It is suggested that age-related physiological changes of hormonal and psychological patterns mimic those occurring in neuroendocrine diseases and that, possibly, common brain biochemical changes may underlie the two phenomena.
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