Angeletti G.,Mental Health and Sensory Organs |
D'Onofrio M.,Mental Health and Sensory Organs |
Lai C.,University of Rome La Sapienza |
Tambelli R.,University of Rome La Sapienza |
And 2 more authors.
European Review for Medical and Pharmacological Sciences | Year: 2014
BACKGROUND: Evidence has shown that psychotherapy is effective for depression, whereas the outcome for suicide risk is unclear. AIM: It was to investigate whether possible pre-treatment predictors of suicide risk (SR) decrease after a brief psychodynamic psychotherapy treatment and at follow-up. PATIENTS AND METHODS: Forty-one patients were assessed at: baseline (T0) for clinical history, clinical family history, physical diseases, type of suffered abuse; after the treatment (T1); and, at six-month follow-up (T2) for mood ratings, temperamental features, and SR levels. RESULTS: The levels of depression and cyclothymia decreased at T1 and T2 compared toT0; however, the distribution of the patients with high SR level was similar between T0 and T1, and at T2 it increased. T1-T0 SR (δ1SR) was correlated with suicidal-ity in the last month and with depression levels at T0; T2-T0 SR (δ2SR) was correlated with many historical, clinical, and temperamental variables; T2-T1 SR (δ3SR) was correlated with the presence of previous psychotherapy, abuse, and anxiety. Linear regression models revealed that δ1SR was predicted by the suicidality in the last month; δ2SR was not significantly predicted by any variable; and, δ3SR was predicted by anxiety. CONCLUSIONS: The treatment was able to decrease the depression but not the SR. Findings confirm the difficulty of affecting SR and the importance of carefully considering the anxiety and the previous experiences of abuse in order to manage the interruption of the psychotherapy. Source
Serafini G.,University of Genoa |
Pompili M.,Mental Health and Sensory Organs |
Belvederi Murri M.,University of Genoa |
Respino M.,University of Genoa |
And 4 more authors.
Neuropsychobiology | Year: 2015
Major depressive disorder (MDD) is a disabling illness associated with significant functional and psychosocial impairment. Although many psychopharmacological agents are currently available for its treatment, many MDD patients suffer from treatment-resistant depression (TRD). Methods: A systematic review of the current literature (Pubmed/Medline, Scopus and ScienceDirect search) has been conducted with the primary aim to investigate the role of repetitive transcranial magnetic stimulation (rTMS) in improving neurocognition in patients with TRD. Studies were included according to the following criteria: (a) being an original paper in a peer-reviewed journal and (b) having analyzed the effect of rTMS on neurocognitive functioning in TRD. Results: The combined search strategy yielded a total of 91 articles, of which, after a complete analysis, 22 fulfilled our inclusion criteria. Based on the main findings, most of the selected studies suggested the existence of a trend towards improvements in the neurocognitive profile using rTMS. Negative findings have also been reported. However, most studies were limited by their small sample size or included mixed samples, or the adopted single-blind designs potentially biased the blinding of the study design. Conclusion: rTMS is a noninvasive brain stimulation that may be considered a valuable and promising technique for cognitive enhancement in TRD. © 2015 S. Karger AG, Basel. Source
Notartomaso S.,I.R.C.C.S Neuromed |
Zappulla C.,I.R.C.C.S Neuromed |
Biagioni F.,I.R.C.C.S Neuromed |
Cannella M.,I.R.C.C.S Neuromed |
And 14 more authors.
Molecular Brain | Year: 2013
Background: Spinocerebellar ataxia type 1 (SCA1) is a genetic disorder characterized by severe ataxia associated with progressive loss of cerebellar Purkinje cells. The mGlu1 metabotropic glutamate receptor plays a key role in mechanisms of activity-dependent synaptic plasticity in the cerebellum, and its dysfunction is linked to the pathophysiology of motor symptoms associated with SCA1. We used SCA1 heterozygous transgenic mice (Q154/Q2) as a model for testing the hypothesis that drugs that enhance mGlu1 receptor function may be good candidates for the medical treatment of SCA1. Results: Symptomatic 30-week old SCA1 mice showed reduced mGlu1 receptor mRNA and protein levels in the cerebellum. Interestingly, these mice also showed an intense expression of mGlu5 receptors in cerebellar Purkinje cells, which normally lack these receptors. Systemic treatment of SCA1 mice with the mGlu1 receptor positive allosteric modulator (PAM), Ro0711401 (10 mg/kg, s.c.), caused a prolonged improvement of motor performance on the rotarod and the paw-print tests. A single injection of Ro0711401 improved motor symptoms for several days, and no tolerance developed to the drug. In contrast, the mGlu5 receptor PAM, VU0360172 (10 mg/kg, s.c.), caused only a short-lasting improvement of motor symptoms, whereas the mGlu1 receptor antagonist, JNJ16259685 (2.5 mg/kg, i.p.), further impaired motor performance in SCA1 mice. The prolonged symptomatic benefit caused by Ro0711401 outlasted the time of drug clearance from the cerebellum, and was associated with neuroadaptive changes in the cerebellum, such as a striking reduction of the ectopically expressed mGlu5 receptors in Purkinje cells, increases in levels of total and Ser880-phosphorylated GluA2 subunit of AMPA receptors, and changes in the length of spines in the distal dendrites of Purkinje cells. Conclusions: These data demonstrate that pharmacological enhancement of mGlu1 receptors causes a robust and sustained motor improvement in SCA1 mice, and lay the groundwork for the development of mGlu1 receptor PAMs as novel "cerebellum-specific", effective, and safe symptomatic drugs for the treatment of SCA1 in humans. © 2013 Notartomaso et al.; licensee BioMed Central Ltd. Source
Pompili M.,Mental Health and Sensory Organs |
Pompili M.,Harvard University |
Serafini G.,Mental Health and Sensory Organs |
Innamorati M.,European University at Rome |
And 4 more authors.
Schizophrenia Research | Year: 2011
Many studies have confirmed that the risk of suicide in patients with first-episode psychosis (FEP) is high, and high rates of premature mortality, particularly from suicide, may occur in the early phases of schizophrenia. However, suicide rates are difficult to measure in FEP patients, even in carefully defined samples, and there is relatively little specific information about the risk of suicide at illness onset or retrospectively concerning the untreated psychotic period. This selected review of the literature investigates suicidal behaviour with particular regard to severe suicidality (plans and attempts) and risk factors associated with suicide in FEP patients. A search was performed to identify all papers and book chapters during the period 1965-2010, and approximately 100 studies met the inclusion criteria. Most of evidence suggests that risk of suicidal behaviour is relatively high in FEP patients. The research reports highlight the need for universal, comprehensive, public mental health interventions aimed, not only toward early detection, but also toward the rapid engagement in treatment of people with psychoses. These interventions should include an adequate assessment of suicidal behaviour in patients with FEP, and an examination of the efficacy of specific components of the interventions. © 2011 Elsevier B.V. Source
Marrocco J.,IRCCS Centro Neurolesi Bonino Pulejo |
Mairesse J.,North University of Lille |
Bucci D.,I.R.C.C.S Neuromed |
Lionetto L.,Mental Health and Sensory Organs |
And 8 more authors.
Molecular Pharmacology | Year: 2013
The use of classic antipsychotic drugs is limited by the occurrence of extrapyramidal motor symptoms, which are caused by dopamine (DA) receptor blockade in the neostriatum. We examined the impact of early-life stress on haloperidol-induced catalepsy using the rat model of prenatal restraint stress (PRS). Adult "PRS rats," i.e., the offspring of mothers exposed to restraint stress during pregnancy, were resistant to catalepsy induced by haloperidol (0.5-5 mg/kg i.p.) or raclopride (2 mg/kg s.c.). Resistance to catalepsy in PRS rats did not depend on reductions in blood or striatal levels, as compared with unstressed control rats. PRS rats also showed a greater behavioral response to the DA receptor agonist, apomorphine, suggesting that PRS causes enduring neuroplastic changes in the basal ganglia motor circuit. To examine the activity of this circuit, we performed a stereological counting of c-Fos+ neurons in the external and internal globus pallidus, subthalamic nucleus, and ventral motor thalamic nuclei. Remarkably, the number of c-Fos+ neurons in ventral motor thalamic nuclei was higher in PRS rats than in unstressed controls, both under basal conditions and in response to single or repeated injections with haloperidol. Ventral motor thalamic nuclei contain exclusively excitatory projection neurons that convey the basal ganglia motor programming to the cerebral cortex. Hence, an increased activity of ventral motor thalamic nuclei nicely explains the refractoriness of PRS rats to haloperidol-induced catalepsy. Our data raise the interesting possibility that early-life stress is protective against extrapyramidal motor effects of antipsychotic drugs in the adult life. Copyright © 2013 by The American Society for Pharmacology and Experimental Therapeutics. Source