Carlo Pozzilli

Prof. Carlo Pozzilli

orcid

Research Focus & Metrics

Academic Career Length

34Years (1993-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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14 January 2003 in European Journal of Neurology
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Journal Article
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CPCarlo Pozzilli
Carlo Pozzilli
VTV. Tomassini
V. Tomassini
FMF. Marinelli
F. Marinelli
APA. Paolillo
A. Paolillo
CGC. Gasperini
C. Gasperini
SBStefano Bastianello
Stefano Bastianello

1 February 2005 in Journal of Neurology, Neurosurgery & Psychiatry
Verified
Journal Article
Open access
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VTV Tomassini
V Tomassini
EOE Onesti
E Onesti
CMC Mainero
C Mainero
EGE Giugni
E Giugni
APA Paolillo
A Paolillo
CPCarlo Pozzilli
Carlo Pozzilli
Background: Sex related differences in the course and severity of multiple sclerosis (MS) could be mediated by the sex hormones. Objective: To investigate the relation between serum sex hormone concentrations and characteristics of tissue damage on conventional magnetic resonance imaging (MRI) in men and women suffering from relapsing-remitting MS. Results: Serum testosterone was significantly lower in women with MS than in controls. The lowest levels were found in women with a greater number of gadolinium enhancing lesions. A positive correlation was observed between testosterone concentrations and both tissue damage on MRI and clinical disability. In men, there was a positive correlation between oestradiol concentrations and brain damage. Conclusions: The hormone related modulation of pathological changes supports the hypothesis that sex hormones play a role in the inflammation, damage, and repair mechanisms typical of MS.

15 October 2009 in European Journal of Neurology
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Journal Article
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LPLuca Prosperini
Luca Prosperini
Valentina GalloValentina Gallo
Valentina Gallo
NPN. Petsas
N. Petsas
GBG. Borriello
G. Borriello
CPCarlo Pozzilli
Carlo Pozzilli

1 January 2021 in Therapeutic Advances in Neurological Disorders
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Journal Article
Open access
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PIPietro Iaffaldano
Pietro Iaffaldano
GLGiuseppe Lucisano
Giuseppe Lucisano
FCFrancesca Caputo
Francesca Caputo
Damiano PaolicelliDamiano Paolicelli
Damiano Paolicelli
FPFrancesco Patti
Francesco Patti
MTMaria Trojano
Maria Trojano
No consensus exists on how aggressively to treat relapsing–remitting multiple sclerosis (RRMS) nor on the timing of the treatment. The objective of this study was to evaluate disability trajectories in RRMS patients treated with an early intensive treatment (EIT) or with a moderate-efficacy treatment followed by escalation to higher-efficacy disease modifying therapy (ESC). RRMS patients with ⩾5-year follow-up and ⩾3 visits after disease modifying therapy (DMT) start were selected from the Italian MS Registry. EIT group included patients who received as first DMT fingolimod, natalizumab, mitoxantrone, alemtuzumab, ocrelizumab, cladribine. ESC group patients received the high efficacy DMT after ⩾1 year of glatiramer acetate, interferons, azathioprine, teriflunomide or dimethylfumarate treatment. Patients were 1:1 propensity score (PS) matched for characteristics at the first DMT. The disability trajectories were evaluated by applying a longitudinal model for repeated measures. The effect of early versus late start of high-efficacy DMT was assessed by the mean annual Expanded Disability Status Scale (EDSS) changes compared with baseline values (delta-EDSS) in EIT and ESC groups. The study cohort included 2702 RRMS patients. The PS matching procedure produced 363 pairs, followed for a median (interquartile range) of 8.5 (6.5–11.7) years. Mean annual delta-EDSS values were all significantly (p < 0.02) higher in the ESC group compared with the EIT group. In particular, the mean delta-EDSS differences between the two groups tended to increase from 0.1 (0.01–0.19, p = 0.03) at 1 year to 0.30 (0.07–0.53, p = 0.009) at 5 years and to 0.67 (0.31–1.03, p = 0.0003) at 10 years. Our results indicate that EIT strategy is more effective than ESC strategy in controlling disability progression over time.

14 September 2005 in Journal of Neurology
Verified
Journal Article
Closed access
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VTV. Tomassini
V. Tomassini
APA. Paolillo
A. Paolillo
GPGiorgio Palù
Giorgio Palù
EGE. Giugni
E. Giugni
LPLuca Prosperini
Luca Prosperini
CPCarlo Pozzilli
Carlo Pozzilli

1 April 2007 in Clinical Rehabilitation
Verified
Journal Article
Closed access
MGM. Giovannelli
M. Giovannelli
GBG. Borriello
G. Borriello
PCP. Castri
P. Castri
LPLuca Prosperini
Luca Prosperini
CPCarlo Pozzilli
Carlo Pozzilli
Objective : To determine whether additional physiotherapy increases botulinum toxin type A effects in reducing spasticity in patients with multiple sclerosis. Design : A single-blind, randomized, controlled pilot trial with a 12-week study period. Subjects : Thirty-eight patients with progressive multiple sclerosis affected by focal spasticity and who were observed at the Multiple Sclerosis Centre operating in the S. Andrea Hospital in Rome. Interventions : For intervention all patients received botulinum toxin type A; the treatment group also received additional physiotherapy to optimize management through passive or active exercise and stretching regimens. Main measures : To measure objective and subjective level of spasticity, patients were assessed at baseline, 2, 4 and 12 weeks post treatment by Modified Ashworth Scale and visual analogue scale. Results : When compared with the control group, we found a significant decrease of spasticity by Modified Ashworth Scale (P < 0.01 by t-test) in the treatment group at week 2 (2.73 versus 3.22), week 4 (2.64 versus 3.33) and week 12 (2.68 versus 3.33). The mean (%) difference in Modified Ashworth Scale score between baseline and the end of follow-up was —0.95 (26.1) in the treatment group and —0.28 (7.7) in the control group (P < 0.01). The combined treatment proved also to be more effective by visual analogue scale (P < 0.01) at week 4 (6.95 versus 5.50) and at week 12 (7.86 versus 6.56) but not at week 2 (5.18 versus 5.50; P = 0.41). Conclusions : Our data suggest that physiotherapy in combination with botulinum toxin type A injection can improve overall response to botulinum toxin.