P Gallo

University-Hospital of Padova, Padua, Veneto, Italy

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Publications (110)484.36 Total impact

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    ABSTRACT: We correlated the weighted genetic risk score measured using 107 established susceptibility variants for multiple sclerosis (MS) with the age at onset in bout-onset (BOMS, n=906) and progressive-onset MS Italian patients (PrMS) (n=544). We observed an opposite relationship in the two disease courses: a higher weighted genetic risk score was associated with an earlier age at onset in BOMS (rho= -0.1; p=5 × 10(-3)) and a later age at onset in PrMS cases (rho=0.07; p=0.15) (p of difference of regression=1.4 × 10(-2)). These findings suggest that established MS risk variants anticipate the onset of the inflammatory phase, while they have no impact on, or even delay, the onset of the progressive phase. © The Author(s) 2014.
    Multiple Sclerosis 12/2014; DOI:10.1177/1352458514561910 · 4.86 Impact Factor
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    ABSTRACT: http://www.neurology.org/cgi/content/meeting_abstract/80/1_MeetingAbstracts/P02.115
    XLIV Congresso Società Italiana di Neurologia; 11/2013
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    ABSTRACT: Multiple Sclerosis (MS) is a chronic inflammatory-demyelinating disease that affects both white and gray matter (GM). GM lesions have been demonstrated to play a major role in the physical and cognitive disability and in the disease progression. The diagnosis and monitoring of the disease is mainly based on magnetic resonance imaging (MRI). Lesions identification needs visual detection performed by experienced graders, a process that is always time consuming, error prone and operator dependent.We present a technique to automatically estimate GM lesion load from double inversion recovery (DIR) MRI sequences. We tested the proposed algorithm on DIR sequences acquired from 50 MS patients. Regions corresponding to probable GM lesions were manually labeled to provide a reference. The resulting automatic lesion load estimate provides a correlation of 98.5% with manual lesion number, and of 99.3% with manual lesion volume.
    XIII Mediterranean Conference on Medical and Biological Engineering and Computing 2013, Seville (ES); 09/2013
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    ABSTRACT: Objective Clinical and neuroimaging parameters predictive of the changing clinical course of multiple sclerosis (MS) from relapsing-remitting to secondary progressive have not been clarified yet. We specifically designed a prospective 5-year longitudinal study aimed at assessing demographic, clinical, and magnetic resonance imaging (MRI) parameters that could predict the changing clinical course of MS. Methods At study entry and after 5 years, clinical and MRI (ie, gray matter and white matter lesions, including spinal cord lesions, and global and regional cortical thinning) parameters were assessed in a training set of 334 consecutive relapsing-remitting MS patients and in an independent validation set of 84 relapsing-remitting MS patients. ResultsSixty-six (19.7%) relapsing-remitting MS patients changed their clinical course during the study and entered into the secondary progressive phase. Age (p=0.001, odds ratio [OR]=1.2), cortical lesion volume (p<0.001,OR=1.7), and cerebellar cortical volume (p<0.001, OR=0.2) at study entry were found to predict the changing clinical course. The model including only these 3 variables correctly identified 252 of 268 (94.0%) patients who maintained the relapsing-remitting course and 58 of 66 (87.8%) patients who became secondary progressive (cross-validated error rate=7.2%). When applied on the validation set, the model obtained a similar error rate (8.4%). InterpretationA prediction model based on age, cortical lesion load, and cerebellar cortical volume suitably explains the probability of relapsing-remitting MS patients evolving into the progressive phase. Gray matter damage appears to play a pivotal role in determining the changing clinical course of MS. Ann Neurol 2013;74:76-83
    Annals of Neurology 07/2013; 74(1). DOI:10.1002/ana.23882 · 11.91 Impact Factor
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    ABSTRACT: Background: To what extent the progressive increase in the incidence of multiple sclerosis (MS) observed in the province of Padova over the period 1970-1999 was an expression of a real increased risk of developing MS remained unclear. Objective: The objective of this paper is to update the epidemiological figures of MS and probe whether the risk of having MS has increased in the province of Padova during the decade 2000-2009. Methods: All patients born in Italy and having a diagnosis of MS or possible MS identified through analysis of all available sources of information were included in the study. The incidence and prevalence rates between 2000 and 2009 were obtained and compared with our previously published data. Results: On 31 December 2009, the overall prevalence was 139.5/100,000, 192.0 +/- 9.5 for females and 83.9 +/- 6.3 for males. During the decade 2000-2009, the overall incidence rate of MS was 5.5 +/- 0.5, 7.4 +/- 0.8 for females and 3.5 +/- 0.6 for males. The onset-diagnosis delay, the female/male ratio and the mean age at onset did not significantly change compared to the prior period of observation. Conclusion: Our findings support the hypothesis of a real increased risk of developing MS in the province of Padova. Moreover, the actual prevalence of 1.4/1000 makes our region a high-risk geographical area for MS. The role played by exogenous factors in determining susceptibility to MS needs to be thoroughly investigated.
    Multiple Sclerosis 04/2013; 19(5):601-604. DOI:10.1177/1352458512461970 · 4.86 Impact Factor
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    ABSTRACT: BACKGROUND: Patients with multiple sclerosis (MS) are more frequently born in spring when compared to autumn. Fluctuation of UV-light has been hypothesized to drive this phenomenon. AIM: To assess the correlation between fluctuation of sunlight and birth season in persons with MS. METHODS: For this record-linkage study, we collected from the international MSBase and the Italian MS iMed-web databases the dates of birth of 11,415 patients with MS from 36 centres from 15 countries worldwide and compared these to dates of live-births from national registries. From all participating sites, we collected data on UV-light fluctuation and assessed its correlation with seasonal fluctuation in MS births. RESULTS: Compared with the reference cohort, an increased proportion of persons with MS were born in spring and a decreased proportion in autumn (odds ratio (OR) to be born in spring versus autumn = 1.158, χ(2 ) = 36.347, P < 0.001). There was no significantly increased fluctuation of MS births with increased quartile of ambient UV-light fluctuation (P(trend ) = 0.086). CONCLUSION: Seasonal fluctuation of MS births as found in this worldwide cohort of patients with MS did not correlate with variation in seasonal fluctuation of UV-light. Most likely, it results from a complex interplay between fluctuation of sunlight, behavioural factors, other environmental factors and (epi)genetic factors.
    Acta Neurologica Scandinavica 03/2013; 127(5):301-8. DOI:10.1111/ane.12007 · 2.44 Impact Factor
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    ABSTRACT: Clinical and/or neuroimaging evidence of disease reactivation has been described in multiple sclerosis (MS) patients after a break from natalizumab. Whether fingolimod might be a therapeutic option following natalizumab needs to be evaluated. Twenty-two relapsing remitting MS patients having JC virus antibodies (JCVAb+) in serum were shifted from natalizumab to fingolimod after a three-month washout period. Neurological evaluation with the Expanded Disability Status Scale (EDSS) was performed monthly for a mean follow-up period of nine months. In 20/22 patients, brain magnetic resonance imaging (MRI) was obtained within one month after therapy initiation. Disease reactivation was observed in 11/22 (50%) patients: clinical relapses in six patients (four patients within the first month of therapy) and MRI activity in a further five patients (three patients within the first month of therapy). Clinical and/or MRI signs suggestive of disease rebound were observed in three patients. Our data indicate that fingolimod does not exert clinical activity quickly enough to stop MS reactivation after a break from natalizumab.
    Multiple Sclerosis 11/2012; 18(11):1640-3. DOI:10.1177/1352458512464282 · 4.86 Impact Factor
  • Claudio Baracchini, Paolo Gallo
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    ABSTRACT: Multiple sclerosis (MS) is a chronic inflammatory and neurodegenerative disease of the central nervous system (CNS). Its autoimmune origin has been recently challenged by a substantially different mechanism termed chronic cerebrospinal venous insufficiency (CCSVI), which has attracted worldwide attention in the scientific community, in the media and among MS patients. According to this hypothesis, a congestion of cerebrovenous outflow induces an increased intracranial pressure and a disintegration of the blood–brain barrier in perivenular regions promoting local iron deposition and activation of pro-inflammatory factors, ultimately leading to MS. After the initial report of a perfect association between CCSVI and MS, different independent groups were not able to replicate these results, casting doubts on the credibility of the CCSVI concept in MS. In spite of this, interventional procedures like venous angioplasty named the “liberation” treatment have been claimed as a cure of MS or at least as a major improvement of MS symptoms. As a result, an increasing number of MS patients are undergoing endovascular treatment, in spite of a lack of an evidenced-based benefit and recent reports of serious adverse events. This review represents a critical appraisal of the CCSVI hypothesis, discusses its basis, the diagnostic criteria and its relationship with MS.
    09/2012; 1(1-12):371-374. DOI:10.1016/j.permed.2012.01.005
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    ABSTRACT: The risk of progressive multifocal leukoencephalopathy (PML) in patients treated with natalizumab for multiple sclerosis (MS) is a serious concern. The presence of anti-JC virus antibodies is a risk factor for PML development, but 2.5 % of the patients result falsely-negative, while the prognostic relevance of testing JCV-DNA in biological fluids of treated patients is debated. Aim of this work was to evaluate the utility of testing JCV-DNA, together with anti-JCV antibodies, in biological samples of treated patients as a tool for PML risk stratification. 126 subjects from 5 MS Centers in Italy were included in the study. We performed a cross-sectional study in 63 patients testing JCV-DNA in blood, peripheral blood cells and urine. We longitudinally assessed the presence of JCV-DNA in a cohort of 33 subjects, one of which developed PML. We could test retrospectively serum samples from another PML case occurred during natalizumab therapy. Anti-JCV antibodies and urinary JCV-DNA were both tested in 73 patients. No changes in JCV-DNA status occurred during natalizumab treatment. The subject who developed PML in the longitudinal cohort had detectable JCV-DNA in urine at all time-points while serum or blood from both PML patients were always negative before the onset of disease and, in one case, after. Four subjects with JCV-DNA in urine and undetectable anti-JCV antibodies were retested for anti-JCV antibodies and three out of four resulted positive. In conclusion, testing JCV-DNA in urine is complementary to testing anti-JCV antibodies in identifying patients at risk of PML.
    Journal of Neuroimmune Pharmacology 05/2012; 7(3):665-72. DOI:10.1007/s11481-012-9366-z · 3.17 Impact Factor
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    ABSTRACT: Background: Since cortical pathology has been indicated to play a relevant role in the physical and cognitive disability of multiple sclerosis (MS) patients, this study aims to analyze the efficacy of natalizumab in slowing down its progression.Methods: A total of 120 relapsing-remitting MS patients completed a 2-year prospective study: 35 received natalizumab, 50 received interferon beta-1a or glatiramer acetate (immunomodulatory agents - IMA) and 35 remained untreated. Forty healthy subjects constituted the reference population. Clinical and magnetic resonance imaging (MRI) evaluations (including cortical lesions and atrophy) were performed at baseline and after 2 years.Results: Natalizumab significantly reduced accumulation of new cortical lesions (0.2±0.6,range 0-3) compared to immunomodulatory agents (1.3±1.1 togli spazio, range 1-6, p=0.001) and no treatment (2.9±1.5, range 1-8, p<0.001). The percentage of patients with new cortical lesions was also lower in natalizumab-treated patients (20%) compared to IMA-treated and untreated patients (68.0% and 74.2%; p<0.001 for both comparisons). Furthermore, the progression of cortical atrophy was significantly reduced by natalizumab (% change=1.7%) compared to IMA (3.7%, p=0.003) and no therapy (4.6%, p<0.001). Finally, a greater percentage (51.4%) of natalizumab-treated patients remained disease-free (no clinical or MRI evidence of disease activity or progression) compared to IMA-treated (18%, p=0.001) and untreated patients (5.7%, p<0.001).Conclusions: Natalizumab treatment significantly decreases cortical lesion accumulation and cortical atrophy progression in severe relapsing-remitting MS. While supporting the inflammatory origin of cortical lesions, our results highlight the significant impact of natalizumab on cortical pathology.
    Multiple Sclerosis 05/2012; 18(12). DOI:10.1177/1352458512447704 · 4.86 Impact Factor
  • Journal of Neuroimmune Pharmacology 05/2012; · 3.17 Impact Factor
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    ABSTRACT: http://www.neurology.org/cgi/content/meeting_abstract/78/1_MeetingAbstracts/P04.112
    Neurology 04/2012; DOI:10.1212/WNL.78.1_MeetingAbstracts.P04.112 · 8.30 Impact Factor
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    ABSTRACT: GM pathology is considered a major determinant of disability in MS, but the comprehension of its origin and progression rate is limited by the uncertainty of dating the biologic disease onset. Thus, we planned a longitudinal study aimed at analyzing and comparing cortical pathology in pediatric and adult MS patients at clinical onset. Within 12 months from clinical onset, 35 patients with cMS and 57 with aMS were included in a longitudinal study. At T0, GMf and CL number and volume were analyzed. Percentages of Δ-GMf and number of new CLs were assessed every year for 3 years (T1-T3). Twenty-eight age- and sex-matched NCs constituted the reference population. At T0, GMf did not differ between cMS and NC (P = .18), while it was lower in patients with aMS compared with both NCs (P < .001) and patients with cMS (P < .001). The number of patients with CLs, as well as CL number and volume, were higher in patients with aMS than in those with cMS (P < .001). At T3, Δ-GMf was higher in both patients with cMS (1.6% ± 0.5%; range 0.7%-3.4%; P < .001) and aMS (1.6% ± 0.6%; range 0.6%-3.4%; P < .001) compared with NCs (0.7% ± 0.2%; range 0.4%-1.1%), whereas no difference was observed between patients with cMS and aMS (P = .93). Δ-GMf significantly correlated with increased CL volume (cMS: r = 0.46; aMS: r = 0.48) and with the appearance of new CLs (cMS: r = 0.51; aMS: r = 0.49). Our findings suggest that focal (CLs) and diffuse (atrophy) GM damage are strictly associated with the biologic onset of MS, and proceed linearly and partly independently of WM pathology.
    American Journal of Neuroradiology 03/2012; 33(8):1507-11. DOI:10.3174/ajnr.A3011 · 3.68 Impact Factor
  • Parkinsonism & Related Disorders 01/2012; 18:S98-S99. DOI:10.1016/S1353-8020(11)70463-1 · 4.13 Impact Factor
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    ABSTRACT: To evaluate the incidence and dose-dependency of mitoxantrone (MTX)-associated acute myelocytic leukemia (AML) in the network of Italian multiple sclerosis (MS) clinics. We performed a multicenter retrospective cohort study of patients treated with MTX in MS centers under the Italian national health care system between 1998 and 2008. Demographic, disease, treatment, and follow-up information were collected using hospital records. Data were available for 3,220 patients (63% women) from 40 Italian centers. Follow-up (mean ± SD) was 49 ± 29 months (range 12-140 months). We observed 30 cases of AML (incidence 0.93% [95% confidence interval 0.60%-1.26%]). The mean cumulative dose was higher in patients with AML (78 vs 65 mg/m(2), p = 0.028). The median interval from the start of therapy to AML diagnosis was longer than expected at 33 months (range 13-84 months); 8 patients (27%) developed AML 4 years or more after the first MTX infusion. The rate of mortality associated with AML was 37%. This higher than expected risk of AML and related mortality requires that treatment decisions must be made jointly between clinicians and patients who understand their prognosis, treatment options, and treatment-related risks. The now large exposed MS population must be monitored for hematologic abnormalities for at least 6 years from the end of therapy, to ensure the rapid actions needed for early diagnosis and treatment of AML.
    Neurology 11/2011; 77(21):1887-95. DOI:10.1212/WNL.0b013e318238ee00 · 8.30 Impact Factor
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    ABSTRACT: OBJECTIVES: To evaluate the incidence and dose-dependency of mitoxantrone (MTX)-associated acute myelocytic leukemia (AML) in the network of Italian multiple sclerosis (MS) clinics. METHODS: We performed a multicenter retrospective cohort study of patients treated with MTX in MS centers under the Italian national health care system between 1998 and 2008. Demographic, disease, treatment, and follow-up information were collected using hospital records. RESULTS: Data were available for 3,220 patients (63% women) from 40 Italian centers. Follow-up (mean ± SD) was 49 ± 29 months (range 12-140 months). We observed 30 cases of AML (incidence 0.93% [95% confidence interval 0.60%-1.26%]). The mean cumulative dose was higher in patients with AML (78 vs 65 mg/m(2), p = 0.028). The median interval from the start of therapy to AML diagnosis was longer than expected at 33 months (range 13-84 months); 8 patients (27%) developed AML 4 years or more after the first MTX infusion. The rate of mortality associated with AML was 37%. CONCLUSIONS: This higher than expected risk of AML and related mortality requires that treatment decisions must be made jointly between clinicians and patients who understand their prognosis, treatment options, and treatment-related risks. The now large exposed MS population must be monitored for hematologic abnormalities for at least 6 years from the end of therapy, to ensure the rapid actions needed for early diagnosis and treatment of AML
    Neurology 11/2011; 77(21-77):1887-95.. · 8.30 Impact Factor
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    ABSTRACT: The cause of epilepsy in multiple sclerosis (MS) has not yet been elucidated. The relevance of cortical pathology (cortical lesions and thickness) in MS patients with and without epilepsy was evaluated in a longitudinal study. 32 relapsing-remitting MS patients with epilepsy (RRMS/E) and 60 matched RRMS patients without epilepsy were included in a 3 year longitudinal study. The following clinical and MR parameters were analysed: Expanded Disability Status Scale (EDSS), cognitive score (CS), cortical lesion (CL) number and volume, grey matter fraction (GMf), global cortical thickness (CTh), T2 white matter lesion volume (T2WMLV), new CLs and new WM lesions. At baseline (T0), CLs were observed in 27/32 (84.4%) RRMS/E and in 26/60 (43.3%) RRMS (p<0.001) patients, and the RRMS/E group had a higher number (10.2 ± 8.9 vs 4.5 ± 2.4; p<0.001) and total volume (2.0 ± 1.3 vs 0.7 ± 0.8 cm(3); p<0.001) of CLs compared with the RRMS group. No significant difference in T2WMLV was observed. Global CTh was lower in RRMS/E (2.12 ± 0.19 vs 2.35 ± 0.14 mm; p<0.001), and this group also showed a decline in cognition (CS 10.9 ± 6.3 vs 6.2 ± 3.5; p<0.001). After 3 years (T1), the RRMS/E group had a higher accumulation of new CLs (3.4 ± 3.2 vs 1.2 ± 1.1; p<0.001) and faster reduction of GMf (p=0.022) while the two groups did not differ in the number of new WM and new Gad+ lesions. RRMS/E had a more severe and rapidly evolving cortical pathology (CLs and atrophy) compared with RRMS without epilepsy. The RRMS/E group was also characterised by more pronounced cognitive decline, higher EDSS and higher prevalence of men.
    Journal of neurology, neurosurgery, and psychiatry 09/2011; 83(1):49-54. DOI:10.1136/jnnp-2011-300414 · 5.58 Impact Factor
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    ABSTRACT: Chronic cerebrospinal venous insufficiency (CCSVI) had been suggested to play a major pathogenetic role in multiple sclerosis (MS), but recent data on early stages of MS have not confirmed this theory. Nonetheless, CCSVI could represent a late phenomenon of MS or be associated with progression of disability. Thus, we studied CCSVI prevalence in primary progressive (PP) and secondary progressive (SP) MS, to clarify whether CCSVI characterizes the progressive forms of this disease. A total of 35 patients with SPMS, 25 patients with PPMS, and 60 age- and gender-matched normal controls (NC) were enrolled into a cross-sectional study. Extracranial and transcranial high-resolution venous echo color Doppler sonography (ECDS-TCDS) was performed in all patients and NC. Those patients having any abnormal ultrasound finding were asked to undergo selective venography (VGF). Patients with PPMS (11 women, 14 men; mean age 47 ± 11 years) had a disease duration of 11 ± 7 years and Expanded Disability Status Scale (EDSS) score of 6.0 ± 0.5. Patients with SPMS (22 women, 13 men; mean age 45 ± 14.5 years) had a disease duration of 18 ± 14 years and EDSS score of 6.0 ± 0.8. TCDS was normal in all patients. ECDS showed one or more abnormal findings in 9/60 (15.0%) patients (7/35 [20.0%] SPMS, 2/25 [8.0%] PPMS) and in 14/60 (23.3%) NC (p not significant for all comparisons). CCSVI criteria were fulfilled in 0 NC and 4 (6.7%) patients with MS: 3 SPMS and 1 PPMS. VGF, performed in 6/9 patients, was abnormal only in one case who had bilateral internal jugular vein stenosis. Our findings indicate that CCSVI is not a late secondary phenomenon of MS and is not associated with disability.
    Neurology 08/2011; 77(9):844-50. DOI:10.1212/WNL.0b013e31822c6208 · 8.30 Impact Factor
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    ABSTRACT: Although gray matter (GM) atrophy is recognized as a common feature of multiple sclerosis (MS), conflicting results have been obtained in patients with clinically isolated syndromes (CIS). Methodologic and clinical constraints may take account for literature discrepancies. A total of 105 patients presenting with CIS and 42 normal controls (NC) were studied. At baseline, 65/105 patients with CIS met the criterion of dissemination in space of lesions (DIS+). All patients were clinically assessed by means of the Expanded Disability Status Scale every 6 months and underwent MRI evaluation at study entry and then annually for 4 years. Global and regional cortical thickness and deep GM atrophy were assessed using Freesurfer. No significant reduction in GM atrophy was observed between the entire CIS group and the NC, excepting for the cerebellum cortical volume. When the 59 patients with CIS (46 DIS+, 13 DIS-) who converted to MS during the follow-up were compared to the NC, a significant atrophy in the precentral gyrus, superior frontal gyrus, thalamus, and putamen was observed (p ranging from 0.05 to 0.001). The multivariate analysis identified the atrophy of superior frontal gyrus, thalamus, and cerebellum as independent predictors of conversion to MS. CIS with atrophy of such areas had a double risk of conversion compared to DIS+ (odds ratio 9.6 vs 5.0). Selective GM atrophy is relevant in patients with CIS who convert early to MS. The inclusion of GM analysis in the MS diagnostic workup is worthy of further investigation.
    Neurology 05/2011; 77(3):257-63. DOI:10.1212/WNL.0b013e318220abd4 · 8.30 Impact Factor

Publication Stats

3k Citations
484.36 Total Impact Points

Institutions

  • 1988–2014
    • University-Hospital of Padova
      Padua, Veneto, Italy
  • 1983–2012
    • University of Padova
      • • Department of Neurosciences
      • • Department of Medicine DIMED
      Padua, Veneto, Italy
  • 1988–1998
    • It-Robotics
      Vicenza, Veneto, Italy
  • 1992
    • Istituto Superiore di Sanità
      Roma, Latium, Italy
  • 1990
    • Interuniversity Research Centre on Bioactive Peptides
      Napoli, Campania, Italy
  • 1988–1989
    • University of Zurich
      • Internal Medicine Unit
      Zürich, Zurich, Switzerland