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Biomedical subjects

Francesco Nicoletti

Publications and source records attributed to Francesco Nicoletti.

5 recordsLinked to original sources

Tic disorders: from pathophysiology to treatment.

Tic disorders are stereotypic behaviours,more frequent than once believed, and therefore likely to be encountered by primary care physicians. Tics usually begin in childhood and are the clinical hallmark of Tourette Syndrome (TS), the most common cause of tics. TS is a relatively common neurobehavioural disorder with a spectrum of manifestations that wax and wane during its natural course. The pathophysiology of tics, at molecular and cellular level, is still unknown,whereas structural and functional neuroimaging studies have shown the involvement of the basal ganglia and related cortico-striato-thalamo-cortical circuits, and the dopaminergic neuronal system. Moreover, TS has a strong genetic background. The management of TS is often complicated by the presence of attention-deficit/hyperactivity disorder, obsessive-compulsive disorder, and other behaviour disorders. The correct diagnosis is a fundamental step for a proper management of these disorders, and a multimodal treatment is usually indicated. This approach includes educational and supportive interventions, as well as pharmacological treatments when tics are at their worst.

Humans↗

Evaluation of the prophylactic efficacy of amitriptyline and citalopram, alone or in combination, in patients with comorbidity of depression, migraine, and tension-type headache.

Antidepressants are used to treat chronic daily headache disorders such as migraine and chronic tension-type headache (TTH), which are often associated with depression and anxiety. Here, we studied the efficacy and tolerability of amitriptyline and citalopram, given alone or in combination, in patients with 'triple' comorbidity of depression, TTH, and migraine. Eighty-eight patients were enrolled in the study and randomly divided into two groups. The first group received amitriptyline and the second citalopram for 16 weeks. Patients were assessed at weeks 0, 4, 8, and 16. The two drugs were equally efficacious in relieving depressive symptoms, although amitriptyline was more efficacious than citalopram in reducing migraine and TTH attacks. Patients who did not respond to monotherapy (<30% of improvement in the clinical scores) were treated with a combination of the two drugs for 16 additional weeks. In these selected patients, the combined treatment produced a substantial improvement in depression, migraine and TTH without producing major side effects such as those commonly related to the 'serotonergic' syndrome. The results indicate that a combined therapy with amitriptyline and citalopram may be particularly beneficial for patients with TTH, migraine and comorbid depression that do not respond to monotherapy.

Adult↗

Gerstmann-Sträussler-Scheinker disease with P102L-V129 mutation: a case with psychiatric manifestations at onset.

Gerstmann-Sträussler-Scheinker disease (GSS) is an adult onset, rare, genetically determined autosomal dominant prion disease. Clinically, it is characterized predominantly by slowly progressive spino-cerebellar dysfunction with ataxia, absent reflexes in the legs and cognitive impairment. Onset is usually in the fifth decade and in the early phase, ataxia is predominant. Mutations in the prion protein gene (PRNP) had been identified and the most important of these is at codon 129. A genotype-phenotype relationship with genetic polymorphism at residue 129 between methionine and valine has been supposed. We describe a patient with GSS and P102L-V129 mutation in which the onset with prominent psychiatric features characterized by apathy and depression and not with cerebellar sign and the clinical course with seizures, nor observed in P102L-V129 cases, allow us to confirm observations that the GSS caused by the 102 mutation is influenced by the codon 129 polymorphism with a specific genotype-phenotype influence, but probably other additional factors might be considered as background for phenotypic variability.

Adult↗

The SSRI, citalopram, improves bradykinesia in patients with Parkinson's disease treated with L-dopa.

Idiopathic Parkinson's disease (IPD) is characterized by motor signs such as akinesia, rigidity, and often tremor at rest. In addition to these symptoms, depression is a common finding affecting 40% of patients with IPD. This study evaluates the effect of the selective serotonin reuptake inhibitor, citalopram, on motor and nonmotor symptoms of depressed and nondepressed patients with IPD. Forty-six nondemented patients with IPD (24 men, 22 women; mean age 64 +/- 5.3 years; mean +/- SD disease duration, 6.4 +/- 3.2 years; mean +/- SD Hoehn-Yahr stage, 2.8 +/- 1.2) were included in the study. Patients were divided in two subgroups: depressed (n = 18) and nondepressed (n = 28). Citalopram was added in an unblinded manner, starting with 10 mg/d, and, after a week, increased up to 20 mg/d in the depressed subgroup (n = 18) and in half of the nondepressed subgroup (n = 14). Parkinsonian and depressive symptoms were evaluated before and after 1 and 4 months of treatment. Statistical evaluation was made by analysis of variance for repeated measures. Citalopram did not worsen motor performance in IPD, but improved bradykinesia and finger taps after 1 month and 4 months of treatment both in patients with and without depression (p < 0.05 versus baseline). A clear improvement in mood was also observed in 15 of 16 patients with depression. Although case reports indicate that citalopram can potentially worsen the motor symptoms in patients with PD, to date this effect has not been confirmed. Many of the symptoms, typically associated with depression, can be observed in nondepressed patients with IPD, because signs thought to represent depression can be produced by Parkinson's disease. In this study, we observed that when combined with levodopa, citalopram induces an improvement of motor performance, in particular of subscores 23 and 31 of Unified Parkinson's Disease Rating Scale both in depressed and in nondepressed patients with IPD.

Affect↗