Biomedical subjects

A Gemignani

Publications and source records attributed to A Gemignani.

At least 19 recordsLinked to original sources

PubMed2005

Relaxation as a cognitive task.

In the present experiment the instruction to relax was given to awake highly (Highs) and non hypnotizable subjects (Lows), while their heart rate, respirogram and skin resistance were recorded together with electroencephalogram, electroculogram and corrugator electromiogram. At the beginning of the experiment, Highs exhibited no significant difference in heart rate (HR), respiratory frequency (RF) and heart rate variability (HRV) with respect to Lows, but showed a higher EEG alpha and theta1 power. During the session, both groups decreased their heart rate, but changes were significant only in Lows, which increased significantly also the parasympathetic component of their HRV (high frequency, HF). In both groups, EEG showed alpha, beta2 and theta2 power decrements; theta1 activity decreased only in Lows, while gamma power increased in Highs and decreased in Lows. Results suggest that Highs and Lows used different cognitive strategies in the elaboration of the relaxation request and that Highs performed the task through a higher integrative activity.

Adolescent↗

PubMed2005

Slow wave and rem sleep mechanisms are differently altered in hereditary pick disease associated with the TAU G389R mutation.

Sleep disturbances are found in the course of most dementing syndromes. We report a longitudinal polysomnographic and 18FDG-PET study in a 38-year-old male with FTDP17 carrying the Tau gene mutation G389R. All-night sleep EEG and wake cerebral glucose metabolism at rest (eyes/ears covered) of the preceding day were studied twice, eight months (Night 1; PET 1) and sixteen months (Night 2; PET 2) after the initial neurological evaluation. The Night 1 study showed sleep fragmentation associated to a short REM latency and a severe reduction of slow wave sleep, with relatively preserved NREM-REM sleep cycles; daytime PET 1 revealed severe cerebral glucose metabolic reductions in frontal and temporal areas, with relative preservation of remaining cortical regions and subcortical structures. On Night 2, the total sleep time was less than 5 hours, delta sleep and REM latency remained shortened and only two sleep cycles could be identified; daytime PET 2 exam revealed a greater cortical metabolic impairment and an involvement of subcortical brain regions as compared to PET 1. Post-mortem neuropathological data showed severe neuronal loss, spongiosis and gliosis that were mostly marked in cortical layers I, II, V and VI. In vivo, neurometabolic and post-mortem neuropathological data are consistent with and indicative of a severe dysfunction of intra- and trans-hemispheric regional connectivity and of cortico-thalamic circuits. These findings suggest that the decreased cortical and subcortical connectivity may have been the main pathophysiological mechanism responsible for delta sleep reduction and the cognitive decline.

Adult↗

PubMed2004

Influence of mental motor imagery on the execution of a finger-to-thumb opposition task.

The present fMRI study compares regional distribution of the cortical activity during the execution of unilateral hand movements (finger-to-thumb opposition) preceded or not by their motor simulation (S + E and E condition, respectively). The results show that, overall, the number and the spatial distribution of activated voxels are both increased in the S + E with respect to the E condition. The motor performance preceded by mental rehearsal is related to selective increase of the cortical activity. Among the motor areas that are found active during the simple motor execution a significant enhancement of functional activation during the S + E condition ipsilateral primary motor regions (M1). The activity increase may be accounted by a sort of neural recruiting that is made possible by the overlapping of cortical networks involved in both motor output and motor imagery. The beneficial effects of "mental practice" on the physical performance may rely to the close temporal association between motor rehearsal and actual performance.

Adult↗

PubMed2004

Sensory-motor cortex activity modulation by hypnotic susceptibility and hypnosis during finger movement.

The aim of the experiment was to study whether the activity of the primary sensory-motor (S1/M1), supplementary motor (SMA) and pre-motor (PMA) areas during fingers movement is modulated by hypnotic susceptibility and hypnosis. Cortical activity was studied through functional Magnetic Resonance Imaging (fMRI) during a finger-to-thumb opposition task in awake (Highs) and hypnotized highly susceptible (H-Highs) as well as in awake non susceptible subjects (Lows). Results did not show any significant difference in sensory-motor areas activation between Highs and Lows (trait effect) and between Highs and H-Highs (state effect). The activation in 3 subjects among Highs and only 1 among Lows (out of 5) of the caudal S1, receiving the most part of the cutaneous input, appears noteworthy and prompts further investigation on possible hypnotizability-related differences in sensory-motor integration.

Adult↗

PubMed2003

Autonomic and EEG correlates of emotional imagery in subjects with different hypnotic susceptibility.

The autonomic and EEG correlates of the response to a cognitive unpleasant stimulation (US) verbally administered to awake hypnotizable and non hypnotizable subjects were studied. They were compared with the values obtained during a resting condition immediately preceding the stimulus and with those produced by a cognitive neutral stimulation (NS), also administered after a basal resting period. Results showed hypnotic trait effects on skin resistance, heart and respiratory rate as well as on EEG theta, alpha, beta and gamma relative power changes. The autonomic and EEG patterns observed indicated different strategies in the task execution for hypnotizable and non hypnotizable subjects and a discrepancy between the autonomic and EEG changes associated to the US in susceptible subjects. Results support dissociation theories of hypnosis and suggest for hypnotizable persons an active mechanism of protection against cardiac hazard.

Adolescent↗

PubMed2003

Human hypnosis: autonomic and electroencephalographic correlates of a guided multimodal cognitive-emotional imagery.

The effects of a guided neutral and unpleasant imagery involving several sensory modalities were studied in hypnotized subjects. Heart rate (HR), respiratory frequency (RF), tonic skin resistance and different electroencephalographic rhythms were evaluated during a long-lasting hypnotic session including the guided suggestion of a neutral (NS) and an unpleasant (US) imagery, each preceded by a hypnotic relaxation rest period. During NS, the absence of autonomic changes, associated with electroencephalographic gamma power decrement and theta1 power increment, indicated the prevalence of relaxation on the expected task-related modifications. In contrast, US elicited HR and RF increments together with higher electroencephalographic gamma, beta3 and beta2 activities. Thus, hypnotic state appears to prevent the autonomic responses expected during the neutral stimulation, while the emotional valence of the unpleasant imagery overwhelms the hypnosis-related relaxation.

Adolescent↗

PubMed2001

Potentiation of NMDA receptor function through somatostatin release: a possible mechanism for the cognition-enhancing activity of GABA(B) receptor antagonists.

CGP 36742 is a weak GABA(B) receptor antagonist. However, it improves cognitive performances at low doses; it blocks GABA(B) receptors potently and selectively on somatostatinergic terminals; it prevents kynurenate from antagonising NMDA-induced release of noradrenaline from rat brain slices potently. We here investigated whether and how somatostatin plays a role in the CGP 36742 activity. CGP 36742 increased the somatostatin-like immunoreactivity (SRIF-LI) release from hippocampal slices exposed to NMDA. In the kynurenate test with rat hippocampal slices SRIF-14 mimicked the effect of CGP 36742. CGP 36742 lost its activity in rats whose somatostatin content had been depleted with cysteamine. Exogenous SRIF-14 reverted kynurenate antagonism in somatostatin-depleted slices. L362855, an sst(5) receptor agonist, but not the selective sst(1)-sst(4) agonists, L797591, L779976, L796778 and L803087, displayed activity in the kynurenate test. The effects of CGP 36742, SRIF-14 and L362855 were antagonised by the sst(5)-preferring antagonist BIM-23056. The protein kinase C inhibitor GF 109203X prevented the reversal of the kynurenate antagonism by CGP 36742 or SRIF-14. In conclusion, by selectively blocking GABA(B) receptors on somatostatinergic terminals, CGP 36742 may disinhibit somatostatin release; the consequent activation of sst(5) receptors would potentiate the function of NMDA receptors coexisting with sst(5) receptors on noradrenergic neurons.

Animals↗

PubMed2001

The temporal relationship between anxiety disorders and (hypo)mania: a retrospective examination of 63 panic, social phobic and obsessive-compulsive patients with comorbid bipolar disorder.

BACKGROUND: The relationship between anxiety and depressive disorders has been conventionally limited to unipolar depression. Recent studies from both clinical and epidemiologic samples have revealed intriguing associations between anxiety and bipolar (mainly bipolar II) disorders. The present report examines the temporal sequence of hypomania to panic (PD), obsessive-compulsive (OCD) and social phobic (SP) disorders. METHODS: Specialty-trained clinicians retrospectively evaluated the foregoing relationships in 63 patients meeting the DSM-III-R diagnosis for PD, OCD and SP with lifetime comorbidity with bipolar disorders (87% bipolar II). Structured interviews were used. RESULTS: In nearly all cases, SP chronologically preceded hypomanic episodes and disappeared when the latter episodes supervened. By contrast, PD and OCD symptomatology, even when preceding hypomanic episodes, often persisted during such episodes; more provocatively, nearly a third of all onsets of panic attacks were during hypomania. LIMITATIONS: Assessing temporal relationships between hypomania and specific anxiety disorders on a retrospective basis is, at best, of unknown reliability. The related difficulty of ascertaining the extent to which past antidepressant treatment of anxiety disorders could explain the anxiety-bipolar II comorbidity represents another major limitation. CONCLUSIONS: Different temporal relationships characterized the occurrence of hypomania in individual anxiety disorder subtypes. Some anxiety disorders (notably SP, and to some extent OCD) seem to lie on a broad affective continuum of inhibitory restraint vs. disinhibited hypomania. By contrast, and more tentatively, PD in the context of bipolar disorder, might be a reflection of a dysphoric manic or mixed hypomanic symptomatology. The foregoing suggestions do not even begin to exhaust the realm of possibilities. The pattern of complex relationships among these disorders would certainly require better designed prospective observations.

Adult↗

PubMed2001

Citalopram in refractory obsessive-compulsive disorder: an open study.

This study aimed to evaluate the effect of citalopram in patients with refractory obsessive-compulsive disorder (OCD) which had not responded to previous antiobsessional treatments. Eighteen patients were selected for this study: they had been suffering from OCD, according to DSM-IV criteria, for at least 2 years and had various comorbid disorders. All had been treated with serotonin reuptake inhibitors at adequate dosages for at least 6 months, but had failed to respond. Consequently, they were shifted to citalopram, titrated up to the dose of 40 mg, within 2 weeks. After 4 months of this regimen, 14 out of the total of 18 patients had shown a reduction in OC symptoms, as assessed by the decrease in the Yale-Brown Obsessive Compulsive Scale total score; no relevant side-effects were reported, except for a mild nausea in four patients within the first few days of treatment, which quickly disappeared. The use of citalopram would appear to be an useful strategy in refractory OCD cases.

Adolescent↗

PubMed2001

No correlation between aggression and platelet (3)H-paroxetine binding in obsessive-compulsive disorder patients.

Different findings suggest that the serotonin (5-HT) system may be involved in both the regulation of aggression and the pathophysiology of obsessive-compulsive disorder (OCD). Our study aimed to evaluate the aggressive features of a group of OCD patients and to explore possible correlations with a serotonergic marker, namely platelet 5-HT transporter. Psychopathological and biological patterns were compared with those of a group of healthy controls and those of patients with major depression. Twenty-one patients affected by OCD, 21 by depression and 21 healthy controls were included in the study. Aggressive features were measured by means of the Buss and Durkee Hostility Inventory (BDHI). The platelet 5-HT transporter was evaluated by means of the (3)H-paroxetine binding parameters (maximum binding capacity, B(max) and dissociation constant, K(d)). The OCD patients showed a total score on the BDHI not significantly different from that of healthy controls and lower than that of depressed patients. The factor profile was similar in the 3 groups, but higher in the depressed patients. The irritability, resentment, guilt, negativism and suspiciousness factors were significantly more pronounced in depressed patients. Some sex-related difference in single factors were also observed. The B(max) of (3)H-paroxetine binding was lower in OCD patients than in depressives or healthy controls. OCD patients were more similar to healthy controls than to depressed patients with regard to aggressive features measured by means of the BDHI. This suggests that aggression in OCD is a complex phenomenon that probably requires specific instruments of evaluation.

Adolescent↗

PubMed2000

Kindled seizure-evoked somatostatin release in the hippocampus: inhibition by MK-801.

The aim of this study was to evaluate the contribution of ionotropic glutamate receptors to kindled seizure-evoked somatostatin release in the hippocampus, using a microdialysis approach. Basal and amygdala stimulation-evoked somatostatin-like immunoreactivity (-LI) release was significantly greater in kindled compared to naive rats. In naive rats, neither hippocampal perfusion with the selective AMPA/kainate receptor antagonist GYKI 52466 nor with the selective NMDA receptor antagonist MK-801 affected behavior, EEG, or somatostatin-LI release. In kindled rats, GYKI 52466 was still devoid of any effect, while MK-801 significantly decreased stimulus-evoked (but not basal) somatostatin-LI efflux. MK-801 produced identical effects when injected i.p. This study provides the first direct evidence that kindled seizure-evoked somatostatin release in the hippocampus is partly NMDA receptor dependent.

Amygdala↗

PubMed2000

Changes in autonomic and EEG patterns induced by hypnotic imagination of aversive stimuli in man.

Autonomic and electroencephalographic (EEG) responses to aversive stimuli presented by means of hypnotic suggestion have been studied in man.Healthy volunteers with simple phobia were screened for susceptibility to hypnosis. The experimental paradigm included periods of rest during which the hypnotized subjects were asked to produce an emotionally neutral mental image and periods of emotional activation in which they were asked to image a phobic object. Heart rate (HR), respiratory frequency (RF) and EEG were processed to obtain the HR-related indexes of sympatho-vagal balance and the EEG spectral components. The results showed a significant increase in HR and RF with a shift of the sympatho-vagal indexes towards a sympathetic predominance during the hypnotic emotional activation. EEG activity showed a significant increase in the gamma band with a left fronto-central prevalence. There was also a less pronounced increase in the beta band. In conclusion, by means of hypnosis, autonomic and behavioral responses to fear-like stimuli can be induced in man in a reproducible and controlled manner. Such a paradigm could be applied in human neuroimaging studies to identify central nervous structures that modulate stress and fear-related reactions.

Adult↗

PubMed2000

The HIV-1 coat protein gp120 and some of its fragments potently activate native cerebral NMDA receptors mediating neuropeptide release.

The objective of this study was to investigate the effects of the HIV-1 envelope protein gp120 and its peptide fragments on the function of N-methyl-D-aspartate (NMDA) receptors mediating release of cholecystokinin (CCK) and somatostatin (SRIF). These are nonconventional NMDA receptors recently found to be activated by glycine or D-serine 'only'. The release of cholecystokinin-like immunoreactivity (CCK-LI) and of somatostatin-like immunoreactivity (SRIF-LI) elicited by 12 mM K+ from superfused rat neocortex synaptosomes was potently increased by gp120, its cyclic V3 loop and the linear V3 sequence BRU-C-34-A, but not by RP-135 (a central portion of BRU-C-34-A). The EC50 values of gp120 were 0.02 nM (CCK-LI release) and 0.01 nM (SRIF-LI release). The releasing effect of gp120 was prevented by blocking the glycine site or the ion channel of NMDA receptors, but not the glutamate recognition site; in addition, the gp120 effect was strongly inhibited by nanomolar concentrations of Zn2+ ions and by low micromolar concentrations of ifenprodil. It is concluded that gp120 acts as a very potent agonist at the glycine site of NMDA receptors sited on CCK- and SRIF-releasing nerve endings; the protein is able to activate the receptor channel in the absence of glutamate. Gp120 activates the receptors through its V3 loop as peptide fragments related to V3 retain near-maximal activity. The sensitivity of the gp120 effect to both Zn2+ and ifenprodil would not be incompatible with the idea that these NMDA receptors contain the triple subunit combination NR1/NR2A/NR2B.

2-Amino-5-phosphonovalerate↗

PubMed2000

Somatostatin release in the hippocampus in the kindling model of epilepsy: a microdialysis study.

Somatostatin biosynthesis in the hippocampus is activated during and following kindling epileptogenesis. The aim of this study was to investigate whether this phenomenon is associated with enhanced somatostatin release in vivo. Experiments have been run in awake, freely moving rats, implanted with a bipolar electrode in the right amygdala (for kindling stimulation), and with a recording electrode and a microdialysis probe in the left hippocampus. Basal somatostatin-like immunoreactivity (-LI) release was significantly greater in kindled than naive rats. In naive rats, a 2-min perfusion with 100 mM K(+) did not affect behavior and EEG recordings and nonsignificantly increased somatostatin-LI release; a 10-min K(+) perfusion evoked numerous wet dog shakes, electrical seizures (class 0; latency congruent with 8 min, duration congruent with 8 min), and somatostatin-LI release ( congruent with 350% of basal); and a single kindling after-discharge (4 +/- 3-s duration in the hippocampus) also evoked somatostatin-LI release ( congruent with 200% of basal). In kindled rats, a 2-min 100 mM K(+) perfusion evoked hippocampal discharges in three of seven animals (latency congruent with 2 min, mean duration congruent with 1.5 min) and increased somatostatin-LI release ( congruent with 250% of basal); a 10-min K(+) perfusion evoked behavioral seizures (class 1 to 5, latency congruent with 4 min, mean duration congruent with 12 min) with numerous wet dog shakes and robust somatostatin-LI release ( congruent with 350% of basal); and a kindling stimulation evoked generalized seizures (class 4 or 5, 77 +/- 15-s duration in the hippocampus) with remarkable somatostatin-LI release ( congruent with 300% of basal). These data demonstrate that hippocampal somatostatin release is increased in the kindling model in vivo.

Amygdala↗

PubMed2000

Risperidone augmentation in refractory obsessive-compulsive disorder: an open-label study.

Risperidone, an atypical neuroleptic, has been proposed for augmentation strategies in resistant obsessive-compulsive disorder (OCD). We report the results of an open-label trial on the use of the combination of serotonin reuptake inhibitors (SRIs) with risperidone in 20 refractory OCD outpatients. All patients had been suffering from OCD, according to DSM-IV criteria, for at least 2 years and had various comorbid disorders. All had been treated with a SRI at adequate dosages for at least 6 months, but had failed to respond. Therefore, risperidone was added and the dosage titrated up to the mean dose of 3 mg/day over 8 weeks. After 2 months of this regimen, all patients had shown a reduction in obsessive-compulsive symptoms, as assessed by the decrease in the Yale-Brown Obsessive-Compulsive Scale (Y-BOCS) total score, particularly those with a lifetime comorbidity with bipolar disorder; only three patients reported mild sedation and postural hypotension, two mild extrapyramidal side-effects (tremors and akatysia) and two an increased appetite. All these effects were well tolerated and no patient halted the treatment. The addition of risperidone would appear to be a useful strategy for augmenting SRI effectiveness in refractory OCD patients.

Adult↗

PubMed1999

Immunological alterations in adult obsessive-compulsive disorder.

BACKGROUND: Some recent findings suggest the involvement of autoimmune mechanisms in childhood onset of obsessive-compulsive disorder (OCD), on the basis of a parallel drawn with Sydenham's chorea, a manifestation of rheumatic fever. A monoclonal antibody called D8/D17 characterizing a B-lymphocyte antigen, present in almost all patients with rheumatic fever, has been found also in children affected by OCD, Tourette syndrome, and chronic tics to a greater degree than in healthy control subjects. The few observations of disturbances of some immunologic parameters in adult OCD patients, prompted the authors to investigate and compare subsets of peripheral immunological cells for differences in adult patients with OCD and healthy control subjects. METHODS: Twenty patients suffering from OCD, with no comorbidity for other psychiatric disorders, were compared with a similar group of healthy control subjects. The immune subsets were measured by flow cytometry. RESULTS: The CD8+ lymphocytes were significantly increased and CD4+ lymphocytes significantly decreased in OCD patients, while the other cells did not differ between the two groups. No correlation was found between immunologic and clinical parameters. CONCLUSIONS: These data indicate that patients with adult OCD showed increased CD8+, i.e., suppressor T lymphocytes, and decreased CD4+, which identify helper T lymphocytes, as compared with a similar group of healthy control subjects. The findings appear peculiar to patients with OCD and are suggestive of an immunologic imbalance, which might be related to the stress deriving from the frustrating situation determined by the disorder itself.

Adolescent↗

PubMed1998

Episodic course in obsessive-compulsive disorder.

The course of obsessive-compulsive disorder (OCD) is variable, ranging from episodic to chronic. We hypothesised that the former course is more likely to be related to bipolar mood disorders. With the use of a specially constructed OCD questionnaire, we studied 135 patients fulfilling DSM-III-R criteria for OCD with an illness duration of at least 10 years and divided by course: 27.4% were episodic and 72.6% chronic. We compared clinical and familial characteristics and comorbidity. Univariate analyses showed that episodic OCD had a significantly lower rate of checking rituals and a significantly higher rate of a positive family history for mood disorder. Multivariate stepwise discriminant analysis revealed a positive and significant relationship between episodic course, family history for mood disorders, lifetime comorbidity for panic and bipolar-II disorders, late age at onset and negative correlation with generalized anxiety disorder. These data suggest that the episodic course of OCD has important clinical correlates which are related to cyclic mood disorders. This correlation has implications for treatment and research strategies on the aetiology within a subpopulation of OCD.

Adult↗

PubMed1998

Evidence for functional native NMDA receptors activated by glycine or D-serine alone in the absence of glutamatergic coagonist.

In this study we have examined the effects of N-methyl-D-aspartate (NMDA) receptor activation on the release of cholecystokinin and somatostatin from rat neocortical nerve endings. The release of cholecystokinin-like immunoreactivity (CCK-LI) and of somatostatin-like immunoreactivity (SRIF-LI) elicited by 12 mM K+ from superfused synaptosomes, but not the spontaneous release, was increased by NMDA in a concentration-dependent manner. The effects of NMDA could be prevented by antagonists selective for the glutamate recognition site, the receptor channel and the glycine site of the NMDA receptor. In the absence of NMDA, glycine increased on its own and in a concentration-dependent manner the depolarization-evoked release of both CCK-LI and SRIF-LI. This effect of glycine was strychnine-insensitive and could be mimicked by D-serine, a stereoselective agonist at the NMDA receptor glycine site. Antagonists selective for the glycine site or for the NMDA receptor channel prevented the effects of glycine/D-serine; these effects were, however, insensitive to blockade of the glutamate recognition site of the NMDA receptor, suggesting that glutamate released from synaptosomes or present as contaminant was not involved. The neuropeptide release elicited by D-serine was strongly inhibited by ifenprodil (0.3 microM) and by Zn2+ ions (50 nM), selective ligands at the NR2B and NR2A subunits of NMDA receptors, respectively. It is concluded that nerve terminals of CCK- and SRIF-releasing neurons possess non-conventional NMDA receptors whose channels can be operated by glycine or D-serine without apparent activation of the glutamatergic coagonist site. These receptors may display the triple subunit combination NR1/NR2A/NR2B.

Animals↗