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Carlo Colosimo

Publications and source records attributed to Carlo Colosimo.

9 recordsLinked to original sources
PubMed2005

Prevalence and clinical features of hedonistic homeostatic dysregulation in Parkinson's disease.

Hedonistic homeostatic dysregulation (HHD) is a neuropsychiatric disorder recently described in Parkinson's disease (PD), which is characterized by self-medication and addiction to dopaminergic drugs. To understand the prevalence of this disorder, we screened 202 PD patients attending our movement disorder unit for HHD. The clinical features of the patients identified as affected by this syndrome were then compared with those of control PD patients in an attempt to ascertain the possible risk factors for HHD. Results showed 7 subjects who fulfilled the HHD criteria. The analysis of a case-control study showed a significant correlation between HHD and a previous history of mood disorders, and the use of dopamine agonists, either in monotherapy or in combination. The prevalence of HHD in our study is similar to the one reported in the United Kingdom by the authors who first described this syndrome in PD. Of interest, our patients showed a somewhat different pattern of the disorder, suggesting that cultural and environmental factors may play a role in the phenomenology of HHD.

Adult↗
PubMed2005

Case-control study of multiple system atrophy.

The epidemiology of multiple system atrophy (MSA) is scarcely known, and risk factors have not been definitely identified. We investigated the effect of family history for neurodegenerative diseases and environmental factors on MSA risk in a multicentric case-control study. A total of 73 MSA patients (42 men, 31 women; age, 64.3 +/- 8.1 years; disease duration, 4.8 +/- 3.9 years), 146 hospital controls (84 men, 62 women; age, 64.9 +/- 8.4 years), and 73 population controls (42 men, 31 women; age, 63.7 +/- 8.9 years) matched for sex, age (+/-3 years), and province of residence were enrolled consecutively at seven neurological centers from 1 January 1994 to 31 July 1998. The following variables were investigated: family history of neurodegenerative diseases, education, smoking habits, hobbies, and occupational history. Occupational history of farming was significantly more frequent among MSA cases than controls (OR adj = 2.52; 95% CI, 1.25 to 5.07, MSA vs. hospital controls; OR adj = 4.53; 95% CI, 1.68 to12.2, MSA cases vs. population controls). A dose-response analysis for years of farming corroborated this association. We recently found that smoking is significantly less frequent among MSA cases than controls (Vanacore et al. [2000] Neurology 54:114-119). Here, we report that the effects of farming and smoking on MSA risk do not interact. Our results suggest that occupational history of farming is a risk factor for MSA. Smoking and farming seem to influence MSA risk independently. Further epidemiological studies might provide clues on the etiopathogenesis of MSA.

Aged↗
PubMed2004

Accuracy of clinical diagnosis of progressive supranuclear palsy.

We assessed the accuracy of clinical diagnosis of progressive supranuclear palsy (PSP, Steele-Richardson-Olszewski disease) and the validity of existing sets of clinical diagnostic criteria for PSP (see Appendix) using neuropathologically examined cases from the Queen Square Brain Bank for Neurological Disorders. Diagnosis of PSP was made by 40 different physicians, and 60 cases clinically diagnosed as PSP when last assessed in life were studied. In 47 cases (78%), the diagnosis of PSP was confirmed pathologically. False-positive diagnoses included Parkinson's disease with significant additional cortical Lewy body (n = 3) or Alzheimer (n = 1) pathology, multiple system atrophy (n = 4), and corticobasal degeneration, Pick's disease, motor neurone disease, cerebrovascular disease, and a sporadic case of frontotemporal dementia and parkinsonism linked to chromosome 17 (1 case each). Most cases of PSP were diagnosed accurately by neurologists at the final assessment. Although application of National Institute of Neurological Disorders and the Society for PSP possible category marginally improved the accuracy of initial clinical diagnosis, none of the existing operational criteria could significantly improve accuracy of the final clinical diagnosis.

Adult↗
PubMed2004

Development and validation of the Unified Multiple System Atrophy Rating Scale (UMSARS).

We aimed to develop and validate a novel rating scale for multiple system atrophy (Unified Multiple System Atrophy Rating Scale-UMSARS). The scale comprises the following components: Part I, historical, 12 items; Part II, motor examination, 14 items; Part III, autonomic examination; and Part IV, global disability scale. For validation purposes, 40 MSA patients were assessed in four centers by 4 raters per center (2 senior and 2 junior raters). The raters applied the UMSARS, as well as a range of other scales, including the Unified Parkinson's Disease Rating Scale (UPDRS) and the International Cooperative Ataxia Rating Scale (ICARS). Internal consistency was high for both UMSARS-I (Crohnbach's alpha = 0.84) and UMSARS-II (Crohnbach's alpha = 0.90) sections. The interrater reliability of most of the UMSARS-I and -II items as well as of total UMSARS-I and -II subscores was substantial (k(w) = 0.6-0.8) to excellent (k(w) > 0.8). UMSARS-II correlated well with UPDRS-III and ICARS (rs > 0.8). Depending on the degree of the patient's disability, completion of the entire UMSARS took 30 to 45 minutes. Based on our findings, the UMSARS appears to be a multidimensional, reliable, and valid scale for semiquantitative clinical assessments of MSA patients.

Activities of Daily Living↗
PubMed2004

Multiple system atrophy.

Multiple system atrophy (MSA) is a sporadic neurodegenerative disorder characterised clinically by any combination of parkinsonian, autonomic, cerebellar, or pyramidal signs and pathologically by cell loss, gliosis, and glial cytoplasmic inclusions in several CNS structures. Owing to the recent advances in its molecular pathogenesis, MSA has been firmly established as an alpha-synucleinopathy along with other neurodegenerative diseases. In parallel, the clinical recognition of MSA has improved and the recent consensus diagnostic criteria have been widely established in the research community as well as movement disorders clinics. Although the diagnosis of this disorder is largely based on clinical expertise, several investigations have been proposed in the past decade to assist in early differential diagnosis. Symptomatic therapeutic strategies are still limited; however, several candidate neuroprotective agents have entered phase II and phase III clinical trials.

Animals↗
PubMed2003

Lack of association between progressive supranuclear palsy and arterial hypertension: a clinicopathological study.

It has been reported that up to 80% of patients clinically diagnosed as having progressive supranuclear palsy (PSP) may have arterial hypertension (HT). Because previous studies were performed on patients with presumed diagnosis of PSP, we tried to replicate these studies in a series of pathologically confirmed patients. Seventy-three patients with a neuropathological diagnosis of PSP autopsied at the Queen Square Brain Bank for Neurological Disorders in London were collected between 1989 and 1999. For the purpose of this study, patients were considered hypertensive if a blood pressure above 140/90 mm Hg was found in the clinical records. The prevalence of HT in PSP patients at the first and at the last visit during their neurological disease was compared with that found in a series of 21 normal controls who donated their brain to the same institution. Overall, 29 of 73 (39.7%) of the patients were recorded as having HT at the first visit during the disease course; this ratio increased to 42 of 73 (57.5%) at the last visit before death. When these figures were compared to the 21 normal controls (11 of 21 with HT, 52.4%), we were unable to find an increased prevalence of HT in PSP (odds ratio, 0.60; 95% confidence interval, 0.20-1.76). Therefore, HT does not represent an important clinical feature of this neurodegenerative disorder, although cerebrovascular disease can masquerade clinically as PSP.

Adult↗
PubMedDate not supplied

Noradrenergic drugs for levodopa-induced dyskinesia.

Dyskinesia frequently mars the long-term therapeutic response to levodopa (LD) in Parkinson's disease (PD). New treatment strategies for levodopa-induced dyskinesia (LID) currently being investigated include some that target the nondopaminergic pathways. Indeed, LID in parkinsonism can be modulated by drugs acting on different neurotransmitters including glutamate, gamma-aminobutyric acid, noradrenaline, acetylcholine, serotonin, adenosine, and cholecystokinin. In many cases, the possibility of using specific compounds to counteract LID was raised by the previously shown efficacy of such compounds in the treatment of other types of dyskinesia. More data are now available on drugs that act on the noradrenergic system. Two studies have recently shown how the alpha-2 adrenoreceptor antagonist idazoxan can significantly reduce LID in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned primate model of parkinsonism and in patients with advanced PD. The experimental paper, which studied the antagonistic action of idazoxan on dyskinesia induced by both LD and apomorphine in marmosets with MPTP-induced parkinsonism, showed that the pharmacologic mechanisms underlying LID and apomorphine-induced dyskinesia in PD are probably distinct. LD, although not apomorphine-induced, dyskinesia was found to be influenced by adrenoreceptor antagonists. Indeed, the action of alpha-2 adrenoreceptor antagonists may involve the blockade of the action of noradrenaline synthesized from LD. The hypothesis is that because dopamine agonists are not metabolized to noradrenaline, alpha-2 adrenoreceptor antagonists do not reduce dyskinesia produced by such agents. This finding is particularly relevant in planning clinical studies in which LD or dopamine agonist challenges are used to assess the potential antidyskinetic properties of new drugs. The clinical study assessed the effects of idazoxan on LID in 18 patients with advanced PD: An improvement in LID, without the reappearance of parkinsonian symptoms, was observed. The practical outcome of this research is that, although the mechanisms underlying the manifestations and the priming process for dyskinesia have yet to be fully elucidated, a nondopaminergic approach to therapy may provide an effective way of preventing, or at least limiting, the expression of involuntary movements in PD.

Adrenergic Agents↗