101 results on '"Notturno, F."'
Search Results
2. Carotid artery stenting during endovascular thrombectomy for acute ischemic stroke with tandem occlusion: the Italian Registry of Endovascular Treatment in Acute Stroke
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Sallustio, Fabrizio, Pracucci, Giovanni, Cappellari, Manuel, Saia, Valentina, Mascolo, Alfredo Paolo, Marrama, Federico, Gandini, Roberto, Koch, Giacomo, Diomedi, Marina, D’Agostino, Federica, Rocco, Alessandro, Da Ros, Valerio, Wlderk, Andrea, Nezzo, Marco, Argirò, Renato, Morosetti, Daniele, Renieri, Leonardo, Nencini, Patrizia, Vallone, Stefano, Zini, Andrea, Bigliardi, Guido, Pitrone, Antonio, Grillo, Francesco, Bracco, Sandra, Tassi, Rossana, Bergui, Mauro, Naldi, Andrea, Carità, Giuseppe, Casetta, Ilaria, Gasparotti, Roberto, Magoni, Mauro, Simonetti, Luigi, Haznedari, Nicolò, Paolucci, Matteo, Mavilio, Nicola, Malfatto, Laura, Menozzi, Roberto, Genovese, Antonio, Cosottini, Mirco, Orlandi, Giovanni, Comai, Alessio, Franchini, Enrica, Pedicelli, Alessandro, Frisullo, Giovanni, Puglielli, Edoardo, Casalena, Alfonsina, Cester, Giacomo, Baracchini, Claudio, Castellano, Davide, Di Liberto, Alessandra, Ricciardi, Giuseppe Kenneth, Chiumarulo, Luigi, Petruzzellis, Marco, Lafe, Elvis, Persico, Alessandra, Cavasin, Nicola, Critelli, Adriana, Semeraro, Vittorio, Tinelli, Angelica, Giorgianni, Andrea, Carimati, Federico, Auteri, William, Rizzuto, Stefano, Biraschi, Francesco, Nicolini, Ettore, Ferrari, Antonio, Melis, Maurizio, Calia, Stefano, Tassinari, Tiziana, Nuzzi, Nunzio Paolo, Corato, Manuel, Sacco, Simona, Squassina, Guido, Invernizzi, Paolo, Gallesio, Ivan, Ruiz, Luigi, Dui, Giovanni, Carboni, Nicola, Amistà, Pietro, Russo, Monia, Maiore, Mario, Zanda, Bastianina, Craparo, Giuseppe, Mannino, Marina, Inzitari, Domenico, Toni, Danilo, Mangiafico, Salvatore, Gasparotti, R., Inzitari, D., Mangiafico, S., Toni, D., Vallone, S., Zini, A., Bergui, M., Causin, F., Ciccone, A., Nencini, P., Saletti, A., Sallustio, F., Tassi, R., Thyrion, F. Zappoli, Pracucci, G., Saia, V., Gandini, R., Da Ros, V., Greco, L., Morosetti, D., Diomedi, M., Nappini, S., Limbucci, N., Renieri, L., Fainardi, E., Verganti, L., Sacchetti, F., Zelent, G., Bigliardi, G., Dell’Acqua, M. L., Picchetto, L., Vandelli, L., Pentore, R., Maffei, S., Nichelli, P., Longo, M., Pitrone, A., Vinci, S. L., Velo, M., Caragliano, A., Tessitore, A., Bonomo, O., Musolino, R., La Spina, P., Casella, C., Fazio, M. C., Grillo, F., Cotroneo, M., Dell’Aera, C., Francalanza, I., Bracco, S., Cioni, S., Gennari, P., Vallone, I. M., Cerase, A., Martini, G., Stura, G., Daniele, D., Cerrato, P., Naldi, A., Onofrio, M., De Vito, A., Azzini, C., Casetta, I., Mardighian, D., Frigerio, M., Magoni, M., Costa, A., Simonetti, L., Cirillo, L., Taglialatela, F., Isceri, S., Princiotta, C., Dall’Olio, M., Cellerini, M., Gentile, M., Piccolo, L., Migliaccio, L., Brancaleoni, L., Naldi, F., Romoli, M., Zaniboni, A., Ruggiero, M., Sanna, A., Haznedari, N., Commodaro, C., Longoni, M., Biguzzi, S., Cordici, F., Malatesta, E., Castellan, L., Mavilio, N., Salsano, G., Malfatto, L., Finocchi, C., Menozzi, R., Piazza, P., Epifani, E., Andreone, A., Scoditti, U., Castellini, P., Latte, L., Grisendi, I., Cosottini, M., Puglioli, M., Lazzarotti, G., Lauretti, D., Mancuso, M., Giannini, N., Maccarone, M., Orlandi, G., Comai, A., Bonatti, G., Nano, G., Ferro, F., Bonatti, M., Dall’Ora, E., Dossi, R. Currò, Turri, E., Turri, M., Colosimo, C., Pedicelli, A., D’Argento, F., Alexandre, A., Frisullo, G., Di Egidio, V., Puglielli, E. G., Ruggero, L., Assetta, M., Casalena, A., Cester, G., Baracchini, C., Viaro, F., Pieroni, A., Vaudano, G., Comelli, C., Di Maggio, L., Castellano, D., Cavallo, R., Duc, E., Chianale, G., Ciceri, E. F. M., Plebani, M., Augelli, R., Zampieri, P., Grazioli, A., Cappellari, M., Forlivesi, S., Tomelleri, G., Micheletti, N., Chiumarulo, L., Zimatore, D. S., Federico, F., Petruzzelli, M., Zappoli, F., Lafe, E., Sanfilippo, G., Sgreccia, A., Martignoni, A., Cavallini, A., Denaro, F., Persico, A., Cagliari, E., Cavasin, N., Quatrale, R., Critelli, A., Burdi, N., Semeraro, V., Lucarelli, N., Ganimede, M. P., Internò, S., Tinelli, A., Prontera, M. P., Pesare, A., Cotroneo, E., Pampana, E., Ricciardi, F., Gigli, R., Pezzella, F. R., Corsi, F., Giorgianni, A., Baruzzi, F., Pellegrino, C., Terrana, A., Versino, M., Delodovici, M. L., Carimati, F., Cariddi, L. Princiotta, Auteri, W., Di Benedetto, O., Silvagni, U., Perrotta, P., Crispino, E., Petrone, A., Stancati, F., Rizzuto, S., Pugliese, P., Pisani, E., Siniscalchi, A., Gaudiano, C., Pirritano, D., Del Giudice, F., Piano, M., Agostoni, E., Motto, C., Gatti, A., Guccione, A., Tortorella, R., Stecco, A., Guzzardi, G., Del Sette, B., Coppo, L., Baldan, J., Romano, D., Siani, A., Locatelli, G., Saponiero, R., Napolitano, R., De Gregorio, M., Volpe, G., Tenuta, M., Guidetti, G., Biraschi, F., Wulbek, A., Falcou, A., Anzini, A., Mancini, A., De Michele, M., Fausti, S., Di Mascio, M. T., Durastanti, L., Sbardella, E., Mellina, V., Nicolini, E., Comelli, S., Ganau, C., Corraine, S., Fusaro, F., Ferrari, A., Schirru, F., Ledda, V., Secci, S., Melis, M., Piras, V., Moller, J., Padolecchia, R., Allegretti, L., Caldiera, V., Calia, S., Ganci, G., Tassinari, T., Sugo, A., De Nicola, M., Giannoni, M., Bruni, S., Gambelli, E., Provinciali, L., Nuzzi, N. P., Marcheselli, S., Corato, M., Scomazzoni, F., Simionato, F., Roveri, L., Filauri, P., Sacco, S., Orlandi, B., De Santis, F., Tiseo, C., Notturno, F., Ornello, R., Pavia, M., Squassina, G., Cobelli, M., Morassi, M., Magni, E., Invernizzi, P., Pepe, F., Bigni, B., Costa, P., Crabbio, M., Griffini, S., Palmerini, F., Piras, M. P., Gallesio, I., Barbero, S., Ferrandi, D., Dui, G., Fancello, M. C., Zedda, S., Ticca, A., Saddi, M. V., Deiana, G., Rossi, R., Carboni, N., Mela, A., Amistà, P., Russo, M., Iannucci, G., Pinna, V., Di Clemente, L., Santi, M., De Boni, A., De Luca, C., Natrella, M., Fanelli, G., Cristoferi, M., Bottacchi, E., Corso, G., Tosi, P., Sessa, M., Giossi, A., Baietti, Null, Romano, G., Meineri, P., Armentano, A., Versace, P., Arcudi, L., Galvano, G., Petralia, B., Feraco, P., Luppi, G., Giometto, B., Bignamini, V., Piffer, S., Meloni, G. B., Fabio, C., Maiore, M., Pintus, F., Pischedda, A., Manca, A., Mongili, C., Zanda, B., Baule, A., Florio, F., Ciccarese, G., Leone, M., Di Viesti, P., Pappalardo, M. P., Craparo, G., Gallo, C., Monaco, S., Mannino, M., Muto, M., Guarnieri, Gl., Andreone, V., Passalacqua, G., Allegritti, M., Caproni, S., Filizzolo, M., Salmaggi, A., Giordano, A., Marini, C., Frattale, I., Lucente, G., Nozzoli, C., and Lupo, F. A.
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Stent ,Acute stroke ,Settore MED/37 - Neuroradiologia ,Acute stroke Internal carotid artery diseases Stent Thrombectomy ,Neurology (clinical) ,General Medicine ,Settore MED/26 ,Internal carotid artery diseases ,Thrombectomy - Abstract
The management of tandem extracranial internal carotid artery and intracranial large vessel occlusion during endovascular thrombectomy (EVT) for acute ischemic stroke (AIS) has been under-investigated. We sought to investigate outcomes of AIS patients with tandem occlusion (TO) treated with carotid artery stenting (CAS) compared to those not treated with CAS (no-CAS) during EVT.We performed a cohort study using data from AIS patients enrolled in the Italian Registry of Endovascular Treatment in Acute Stroke. Outcomes were 3 months' mortality, functional outcome, complete and successful recanalization, any intracranial hemorrhage, parenchymal hematoma and symptomatic intracerebral hemorrhage.Among 466 AIS patients with TO, CAS patients were 122 and no-CAS patients were 226 (118 excluded). After adjustment for unbalanced variables, CAS was associated with a lower rate of 3 months' mortality (OR 0.407, 95% CI 0.171-0.969, p = 0.042). After adjustment for pre-defined variables, CAS was associated with a lower rate of 3 months' mortality (aOR 0.430, 95% CI 0.187-0.989, p = 0.047) and a higher rate of complete recanalization (aOR 1.986, 95% CI 1.121-3.518, p = 0.019), successful recanalization (aOR 2.433, 95% CI 1.263-4.686, p = 0.008) and parenchymal hematoma (aOR 2.876, 95% CI 1.173-7.050, p = 0.021). CAS was associated with lower 3 months mortality (OR 0.373, 95% CI 0.141-0.982, p = 0.046) and higher rates of successful recanalization (OR 2.082, 95% CI 1.099-3.942, p = 0.024) after adjustment for variables associated with 3 months' mortality and successful recanalization, respectively.Among AIS patients with TO, CAS during EVT was associated with a higher rate of successful reperfusion and a lower rate of 3 months' mortality.
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- 2022
3. The effects of prolonged cathodal direct current stimulation on the excitatory and inhibitory circuits of the ipsilateral and contralateral motor cortex
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Di Lazzaro, V., Manganelli, F., Dileone, M., Notturno, F., Esposito, M., Capasso, M., Dubbioso, R., Pace, M., Ranieri, F., Minicuci, G., Santoro, L., and Uncini, A.
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- 2012
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4. Sensory-Motor Cortical Rorganization in Lower Motor Neuron Syndrome
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Pizzella, V, Della Penna, S, Caulo, M, Mollo, G, Marzetti, L, Tamburro, G, Briganti, C, Notturno, F, Uncini, A, and Romani, G L
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- 2009
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5. ANTI-GANGLIOSIDE COMPLEX ANTIBODIES IN GUILLAIN-BARRé SYNDROME
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Notturno, F, Caporale, C M, and Uncini, A
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- 2008
6. Frequency and time to relapse after discontinuing 6-month therapy with IVIg or pulsed methylprednisolone in CIDP
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Nobile orazio, E., Cocito, D., Jann, S., Uncini, A., Messina, P., Antonini, G., Fazio, R., Gallia, F., Schenone, A., Francia, A., Pareyson, D., SANTORO, LUCIO, Tamburin, S., Cavaletti, G., Giannini, F., Sabatelli, M., Beghi, E., Paolasso, I., De Toni Franceschini, L., Notturno, F., Clemenzi, A., Bianchi, F., Fiorina, E., Pontecorvo, S., Piscosquito, G., MANGANELLI, FIORE, Praitano, M. L., Piatti, M., Torzini, A., Luigetti, M., R. Macchia, Nobile Orazio, E, Cocito, D, Jann, S, Uncini, A, Messina, P, Antonini, G, Fazio, R, Gallia, F, Schenone, A, Francia, A, Pareyson, D, Santoro, L, Tamburin, S, Cavaletti, G, Giannini, F, Sabatelli, M, Beghi, E, Nobile orazio, E., Cocito, D., Jann, S., Uncini, A., Messina, P., Antonini, G., Fazio, R., Gallia, F., Schenone, A., Francia, A., Pareyson, D., Santoro, Lucio, Tamburin, S., Cavaletti, G., Giannini, F., Sabatelli, M., Beghi, E., Paolasso, I., De Toni Franceschini, L., Notturno, F., Clemenzi, A., Bianchi, F., Fiorina, E., Pontecorvo, S., Piscosquito, G., Manganelli, Fiore, Praitano, M. L., Piatti, M., Torzini, A., Luigetti, M., and R., Macchia
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medicine.medical_specialty ,Neuromuscular disease ,Time Factors ,NEUROIMMUNOLOGY ,NEUROPATHY ,STEROIDS ,Anti-Inflammatory Agents ,Humans ,Immunoglobulins, Intravenous ,Immunologic Factors ,Methylprednisolone ,Polyradiculoneuropathy, Chronic Inflammatory Demyelinating ,Recurrence ,Retrospective Studies ,Treatment Outcome ,Polyradiculoneuropathy ,Immunoglobulins ,Time to relapse ,Arts and Humanities (miscellaneous) ,Internal medicine ,medicine ,In patient ,Chronic Inflammatory Demyelinating ,neuroimmunology,neuropathy,steroids ,business.industry ,Multiple sclerosis ,Medicine (all) ,Retrospective cohort study ,Neurology (clinical) ,Psychiatry and Mental Health ,Surgery ,medicine.disease ,Discontinuation ,Settore MED/26 - NEUROLOGIA ,business ,Intravenous ,medicine.drug - Abstract
Background: We reported that 6-month therapy with intravenous immunoglobulin (IVIg) was more frequently effective or tolerated than intravenous methylprednisolone (IVMP) in patients with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). We now retrospectively compared the proportion of patients who eventually worsened after discontinuing therapy and the median time to clinical worsening. Methods: By March 2013, data were available from 41 of the 45 patients completing the trial with a median follow-up after therapy discontinuation of 42 months (range 1-60). Three patients withdrew during the original study and one failed to respond to either of the therapies. No patient received a diagnosis alternative to CIDP during the follow-up. Results: Twenty-eight of the 32 patients treated with IVIg (as primary or secondary therapy after failing to respond to IVMP) improved after therapy (87.5%) as compared with 13 of the 24 patients treated with IVMP as primary or secondary therapy (54.2%). After a median follow-up of 42 months (range 1-57), 24 out of 28 patients responsive to IVIg (85.7%) worsened after therapy discontinuation. The same occurred in 10 out of 13 patients (76.9%) responsive to IVMP (p=0.659) after a median follow-up of 43 months (range 7-60). Worsening occurred 1-24 months (median 4.5) after IVIg discontinuation and 1-31 months (median 14) after IVMP discontinuation (p=0.0126). Conclusions: A similarly high proportion of patients treated with IVIg or IVMP eventually relapse after therapy discontinuation but the median time to relapse was significantly longer after IVMP than IVIg. This difference may help to balance the more frequent response to IVIg than to IVMP in patients with CIDP.
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- 2015
7. 83. Hyperreflexia in acute motor sensory axonal neuropathy: A case report
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Tiseo, C., primary, Degan, D., additional, Ornello, R., additional, Carolei, A., additional, and Notturno, F., additional
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- 2017
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8. Glial fibrillary acidic protein in Guillain-Barre syndrome: Methodological issues
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Petzold, A., Rosengren, L., Verbeek, M.M., Notturno, F., Caporale, C.M., Delauretis, A., and Uncini, A.
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Perception and Action [DCN 1] ,Functional Neurogenomics [DCN 2] - Abstract
Contains fulltext : 80587.pdf (Publisher’s version ) (Closed access)
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- 2009
9. P19.6 Cortical myoclonus responsive to neuromodulation in corticobasal degeneration
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Notturno, F., primary, Zappasodi, F., additional, Maruotti, V., additional, Marzetti, L., additional, Caulo, M., additional, and Uncini, A., additional
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- 2011
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10. P20.11 Cathodal tDCS has a long-lasting inhibitory effect on primary motor cortex excitability
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Profice, P., primary, Ranieri, F., additional, Uncini, A., additional, Santoro, L., additional, Notturno, F., additional, Capasso, M., additional, Pace, M., additional, Manganelli, F., additional, Iodice, R., additional, Pisciotta, C., additional, Dileone, M., additional, and Di Lazzaro, V., additional
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- 2011
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11. P17.4 Pseudocortical and dissociate discriminative sensory dysfunction in a thalamic stroke: a functional magnetic resonance imaging study
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Notturno, F., primary, Sepe, R., additional, Committeri, G., additional, Caulo, M., additional, and Uncini, A., additional
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- 2011
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12. Involvement of sensory fibres in axonal subtypes of Guillain-Barre syndrome
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Capasso, M., primary, Notturno, F., additional, Manzoli, C., additional, and Uncini, A., additional
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- 2011
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13. CD1A and CD1E Gene Polymorphisms are Associated with Susceptibility to Multiple Sclerosis
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Caporale, C.M., primary, Notturno, F., additional, Pace, M., additional, Aureli, A., additional, Di Tommaso, V., additional, De Luca, G., additional, Farina, D., additional, Giovannini, A., additional, and Uncini, A., additional
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- 2011
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14. Pitfalls in electrodiagnosis of Guillain-Barre syndrome subtypes
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Uncini, A., primary, Manzoli, C., additional, Notturno, F., additional, and Capasso, M., additional
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- 2010
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15. ASYMPTOMATIC SPINAL CORD INVOLVEMENT IN POSTERIOR REVERSIBLE ENCEPHALOPATHY SYNDROME
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Briganti, C., primary, Caulo, M., additional, Notturno, F., additional, Tartaro, A., additional, and Uncini, A., additional
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- 2009
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16. T Cell Response in Acute Motor Axonal Neuropathy
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Cencioni, M.T., primary, Notturno, F., additional, Caporale, C.M., additional, Creati, B., additional, Prencipe, V., additional, Battistini, L., additional, and Uncini, A., additional
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- 2009
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17. Antibodies to Ganglioside Complexes in Guillain-Barré Syndrome: Clinical Correlates, Fine Specificity and Complement Activation
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Notturno, F., primary, Luciani, M., additional, Caporale, C.M., additional, Ciarelli, A., additional, and Uncini, A., additional
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- 2009
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18. Non-Alcoholic Partially Reversible Marchiafava-Bignami Disease: Review and Relation with Reversible Splenial Lesions
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Caulo, M., primary, Briganti, C., additional, Notturno, F., additional, Committeri, G., additional, Mattei, P. A., additional, Tartaro, A., additional, Gallucci, M., additional, and Uncini, A., additional
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- 2009
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19. Antiganglioside antibodies are associated with axonal Guillain-Barré syndrome: a Japanese-Italian collaborative study.
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Sekiguchi Y, Uncini A, Yuki N, Misawa S, Notturno F, Nasu S, Kanai K, Noto Y, Fujimaki Y, Shibuya K, Ohmori S, Sato Y, Kuwabara S, Sekiguchi, Yukari, Uncini, Antonino, Yuki, Nobuhiro, Misawa, Sonoko, Notturno, Francesca, Nasu, Saiko, and Kanai, Kazuaki
- Abstract
Background: Whether or not antiganglioside antibodies are related to axonal or demyelinating Guillain-Barré syndrome (GBS) is still a matter of controversy, as detailed in previous studies conducted in Western and Asian countries.Objective: To clarify whether antiganglioside antibodies are associated with axonal dysfunction in Japanese and Italian GBS patient cohorts.Methods: Clinical and electrophysiological profiles were reviewed for 156 GBS patients collected from Japan (n=103) and Italy (n=53). Serum IgG antibodies against GM1, GM1b, GD1a and GalNAc-GD1a were measured by ELISA in the same laboratory. Electrodiagnostic criteria and results of serial electrophysiological studies were used for classification of GBS subtypes: acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN).Results: In both Japanese and Italian cohorts, any of the antibodies were positive in 36% of the patients, and antibody positivity had a significant association with the AMAN electrodiagnosis. Approximately 30% of Japanese and Italian antiganglioside positive patients showed the AIDP pattern at the first examination whereas sequential studies showed that most finally showed the AMAN pattern. Clinically, seropositive patients more frequently had preceding diarrhoea and pure motor neuropathy in both Japanese and Italian cohorts; vibratory sensation was normal in 97% of Japanese and in 94% of Italian seropositive patients.Conclusions: In GBS, clinical and electrophysiological features appear to be determined by antiganglioside antibodies, and the antibodies are associated with motor axonal GBS in both Japan and Italy. Classification of the GBS subtypes as a disease entity should be made, combining the results of antiganglioside assays and serial electrodiagnostic studies. [ABSTRACT FROM AUTHOR]- Published
- 2012
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20. Reversible conduction failure in pharyngeal-cervical-brachial variant of Guillain-Barré syndrome.
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Capasso M, Notturno F, Manzoli C, Yuki N, and Uncini A
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In two patients with the pharyngeal-cervical-brachial variant (PCB) of Guillain-Barré syndrome (GBS), low amplitude distal compound muscle action potentials and partial motor conduction blocks normalized without development of excessive temporal dispersion within 4 weeks. Sensory nerve action potentials significantly improved in amplitude or, when absent, rapidly became recordable at follow-up. Besides axonal degeneration, PCB is characterized by reversible conduction failure in both motor and sensory fibers and is in the continuous spectrum of axonal GBS subtypes. [ABSTRACT FROM AUTHOR]
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- 2010
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21. Glial fibrillary acidic protein: A marker of axonal Guillain-Barrè syndrome and outcome.
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Notturno F, Caporale CM, De Lauretis A, and Uncini A
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Glial fibrillary acid protein (GFAP) is increased in serum and cerebrospinal fluid of patients with dementia, traumatic brain injury, stroke, and multiple sclerosis. To determine whether GFAP is increased in Guillain-Barré syndrome (GBS) we evaluated serum GFAP in 30 controls, 20 patients with acute inflammatory demyelinating neuropathy (AIDP), and 17 with primary axonal GBS. Serum GFAP levels were increased in axonal GBS (median, 0.74) compared with controls (median, 0.41; P < 0.0001) and AIDP (median, 0.58; P = 0.0015). GFAP levels correlated with Hughes grades (serum r = 0.74; P < 0.0001) 6 months after neuropathy onset. Applying the cutoff value in serum of 0.63 to the diagnosis of axonal GBS, we obtained a sensitivity of 76.5% and a specificity of 86%. Thus, serum GFAP levels may be used in GBS as a diagnostic marker of the axonal variant and to predict outcome. Muscle Nerve, 2008. [ABSTRACT FROM AUTHOR]
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- 2008
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22. Non-alcoholic partially reversibile reversible [sic] Marchiafava-Bignami disease: review and relation with reversible splenial lesions. A case report and literature review.
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Caulo M, Briganti C, Notturno F, Committeri G, Mattei PA, Tartaro A, Gallucci M, and Uncini A
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- 2009
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23. Electrophysiological comparison between males and females in HNPP
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Maria Nolano, Raffaele Dubbioso, Fiore Manganelli, Lucio Santoro, Rosa Iodice, Carmine Vitale, Lucia Ruggiero, Valerio Maruotti, Chiara Pisciotta, Francesca Notturno, Antonino Uncini, Manganelli, Fiore, Pisciotta, Chiara, Dubbioso, Raffaele, Maruotti, V, Iodice, Rosa, Notturno, F, Ruggiero, Lucia, Vitale, C, Nolano, M, Uncini, A, Santoro, Lucio, and Nolano, Maria
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Adult ,Male ,medicine.medical_specialty ,Pathology ,Neurology ,Neural Conduction ,Dermatology ,Disease ,Sex Factors ,Internal medicine ,medicine ,Humans ,Occupational activity ,Neuroradiology ,Arthrogryposis ,Palsy ,business.industry ,General Medicine ,Evoked Potentials, Motor ,medicine.disease ,Psychiatry and Mental health ,Electrophysiology ,Peripheral neuropathy ,Female ,Neurology (clinical) ,Neurosurgery ,Hereditary Sensory and Motor Neuropathy ,business - Abstract
Some evidences highlighted a higher clinical expression of hereditary neuropathy with liability to pressure palsy (HNPP) in males, and a higher load of traumatic nerve injuries due to different occupational activity has been invoked to explain this observation. It is unknown whether this increased clinical impairment corresponds to a greater electrophysiological involvement. Thus, we compared clinical and electrophysiological features between men and women in a large cohort of HNPP patients. Nerve palsies and electrophysiological abnormalities were more frequent in men, and electrophysiological findings which differentiated males from females did not show any age-related worsening. In conclusion, our findings showed a higher clinical and electrophysiological involvement in males which does not seem related to different cumulative nerve damage over time. We believe that the higher disease expression may increase the chance to detect the disease in males and, thereby, to underestimate the HNPP diagnosis in females.
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- 2012
24. PDCD10 Gene Mutations in Multiple Cerebral Cavernous Malformations
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Giuseppe De Michele, Andrea Mosca, Maria F ranca Corona, Maria Sole Cigoli, Fausta Ciccocioppo, Francesca Avemaria, Lilia Volpi, Silvana Penco, Margherita Estienne, Leda Bilo, Antonella Antenora, Valeria Capra, Giovanni Baranello, Francesca Notturno, Stefano De Benedetti, Giovanni P. Gesu, Nelia Zamponi, Enrico Alfei, Simona Giovannini, Stefano Parmigiani, Antonietta Tavoni, Daria Riva, Lucio G iordano Accorsi, Cigoli, M, Avemaria, F, De Benedetti, S, Gesu, Gp, Accorsi, Lg, Parmigiani, S, Corona, Mf, Capra, V, Mosca, A, Giovannini, S, Notturno, F, Ciccocioppo, F, Volpi, L, Estienne, M, DE MICHELE, Giuseppe, Antenora, Antonella, Bilo, Leonilda, Tavoni, A, Zamponi, N, Alfei, E, Baranello, G, Riva, D, and Penco, S.
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Pathology ,medicine.medical_specialty ,lcsh:Medicine ,Gene mutation ,Biology ,medicine.disease_cause ,Vascular Medicine ,Genotype-phenotype distinction ,Diagnostic Medicine ,Gene duplication ,medicine ,Genetics ,Medicine and Health Sciences ,Multiplex ligation-dependent probe amplification ,lcsh:Science ,Clinical Genetics ,Mutation ,Multidisciplinary ,Population Biology ,lcsh:R ,Biology and Life Sciences ,Phenotype ,Penetrance ,Neurology ,lcsh:Q ,Age of onset ,Research Article ,Neuroscience - Abstract
Cerebral cavernous malformations (CCMs) are vascular abnormalities that may cause seizures, intracerebral haemorrhages, and focal neurological deficits. Familial form shows an autosomal dominant pattern of inheritance with incomplete penetrance and variable clinical expression. Three genes have been identified causing familial CCM: KRIT1/CCM1, MGC4607/ CCM2, and PDCD10/CCM3. Aim of this study is to report additional PDCD10/CCM3 families poorly described so far which account for 10-15% of hereditary cerebral cavernous malformations. Our group investigated 87 consecutive Italian affected individuals (i.e. positive Magnetic Resonance Imaging) with multiple/familial CCM through direct sequencing and Multiplex Ligation-Dependent Probe Amplification (MLPA) analysis. We identified mutations in over 97.7% of cases, and PDCD10/ CCM3 accounts for 13.1%. PDCD10/CCM3 molecular screening revealed four already known mutations and four novel ones. The mutated patients show an earlier onset of clinical manifestations as compared to CCM1/CCM2 mutated patients. The study of further families carrying mutations in PDCD10/CCM3 may help define a possible correlation between genotype and phenotype; an accurate clinical follow up of the subjects would help define more precisely whether mutations in PDCD10/ CCM3 lead to a characteristic phenotype.
- Published
- 2014
25. The effects of prolonged cathodal direct current stimulation on the excitatory and inhibitory circuits of the ipsilateral and contralateral motor cortex
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Lucio Santoro, Marcello Esposito, Federico Ranieri, Francesca Notturno, V. Di Lazzaro, Fiore Manganelli, Marta Pace, Michele Dileone, Antonino Uncini, G. Minicuci, Raffaele Dubbioso, Margherita Capasso, Di Lazzaro, V, Manganelli, Fiore, Dileone, M, Notturno, F, Esposito, Marcello, Capasso, M, Dubbioso, Raffaele, Pace, M, Ranieri, F, Minicuci, G, Santoro, Lucio, and Uncini, A.
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Adult ,Male ,medicine.medical_specialty ,Neurology ,Genotype ,medicine.medical_treatment ,Stimulation ,Inhibitory postsynaptic potential ,Functional Laterality ,Time ,Neurotrophic factors ,motor cortex ,medicine ,Humans ,transcranial direct current stimulation, motor cortex, motor evoked potentials, plasticity, BDNF ,Biological Psychiatry ,Transcranial direct-current stimulation ,Brain-Derived Neurotrophic Factor ,Evoked Potentials, Motor ,Transcranial Magnetic Stimulation ,Transcranial magnetic stimulation ,Psychiatry and Mental health ,medicine.anatomical_structure ,BDNF ,plasticity ,Excitatory postsynaptic potential ,Female ,Neurology (clinical) ,transcranial direct current stimulation ,motor evoked potentials ,Psychology ,Neuroscience ,Motor cortex - Abstract
Weak cathodal transcranial direct current stimulation (tDCS) of the human hand area modulates corticospinal excitability with a suppression of motor-evoked potentials (MEPs) evoked by transcranial magnetic stimulation (TMS). The changes in excitability persist beyond the time of stimulation if tDCS is given for several minutes and can remain stable for an hour or more. The aim of present study was to evaluate whether a long-lasting suppression of cortical excitability could be induced by prolonged cathodal tDCS (20 min of stimulation). We also explored the impact of brain-derived neurotrophic factor (BDNF) gene polymorphisms, on tDCS after-effects. Cortical excitability to single and paired-pulse TMS was evaluated both for the stimulated and contralateral hemisphere, before and up to 24 h after 20 min of cathodal tDCS. We evaluated threshold and amplitude of MEPs, short interval intracortical inhibition (SICI), and intracortical facilitation (ICF). tDCS produced a pronounced suppression of MEP amplitude that was still significant at 3 h after the end of stimulation. The BDNF genotype had not influence on tDCS after-effects. Thresholds for MEPs, SICI and ICF were not affected. No significant effect was observed in the contralateral hemisphere. Twenty minutes of cathodal tDCS is capable of inducing a long-lasting suppression of the excitability of the human motor cortex.
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- 2012
26. Impact of 2021 European Academy of Neurology/Peripheral Nerve Society diagnostic criteria on diagnosis and therapy of chronic inflammatory demyelinating polyradiculoneuropathy variants.
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De Lorenzo A, Liberatore G, Doneddu PE, Manganelli F, Cocito D, Briani C, Fazio R, Mazzeo A, Schenone A, Di Stefano V, Cosentino G, Marfia GA, Benedetti L, Carpo M, Filosto M, Antonini G, Clerici AM, Luigetti M, Matà S, Rosso T, Lucchetta M, Siciliano G, Lauria Pinter G, Cavaletti G, Inghilleri M, Cantisani T, Notturno F, Ricciardi D, Habetswallner F, Spina E, Peci E, Salvalaggio A, Falzone Y, Strano C, Gentile L, Vegezzi E, Mataluni G, Cotti Piccinelli S, Leonardi L, Romano A, and Nobile-Orazio E
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- Humans, Peripheral Nerves, Neural Conduction physiology, Databases, Factual, Polyradiculoneuropathy, Chronic Inflammatory Demyelinating diagnosis
- Abstract
Background and Purpose: There are different criteria for the diagnosis of different variants of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). The 2021 European Academy of Neurology/Peripheral Nerve Society (EAN/PNS) guidelines provide specific clinical criteria for each CIDP variant even if their therapeutical impact has not been investigated., Methods: We applied the clinical criteria for CIDP variants of the 2021 EAN/PNS guidelines to 369 patients included in the Italian CIDP database who fulfilled the 2021 EAN/PNS electrodiagnostic criteria for CIDP., Results: According to the 2021 EAN/PNS clinical criteria, 245 patients achieved a clinical diagnosis of typical CIDP or CIDP variant (66%). We identified 106 patients with typical CIDP (29%), 62 distal CIDP (17%), 28 multifocal or focal CIDP (7%), four sensory CIDP (1%), 27 sensory-predominant CIDP (7%), 10 motor CIDP (3%), and eight motor-predominant CIDP (2%). Patients with multifocal, distal, and sensory CIDP had milder impairment and symptoms. Patients with multifocal CIDP had less frequently reduced conduction velocity and prolonged F-wave latency and had lower levels of cerebrospinal fluid protein. Patients with distal CIDP more frequently had reduced distal compound muscle action potentials. Patients with motor CIDP did not improve after steroid therapy, whereas those with motor-predominant CIDP did. None of the patients with sensory CIDP responded to steroids, whereas most of those with sensory-predominant CIDP did., Conclusions: The 2021 EAN/PNS criteria for CIDP allow a better characterization of CIDP variants, permitting their distinction from typical CIDP and more appropriate treatment for patients., (© 2023 The Authors. European Journal of Neurology published by John Wiley & Sons Ltd on behalf of European Academy of Neurology.)
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- 2024
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27. Prevalence of Fabry disease and GLA variants in young patients with acute stroke: The challenge to widen the screening. The Fabry-Stroke Italian Registry.
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Romani I, Sarti C, Nencini P, Pracucci G, Zedde M, Cianci V, Nucera A, Moller J, Orsucci D, Toni D, Palumbo P, Casella C, Pinto V, Barbarini L, Bella R, Scoditti U, Ragno M, Mezzapesa DM, Tassi R, Volpi G, Diomedi M, Bigliardi G, Cavallini AM, Chiti A, Ricci S, Cecconi E, Linoli G, Sacco S, Rasura M, Giordano A, Bonetti B, Melis M, Cariddi LP, Dossi RC, Grisendi I, Aguglia U, Di Ruzza MR, Melis M, Sbardella E, Vista M, Valenti R, Musolino RF, Passarella B, Direnzo V, Pennisi G, Genovese A, Di Marzio F, Sgobio R, Acampa M, Nannucci S, Dagostino F, Dell'Acqua ML, Cuzzoni MG, Picchioni A, Calchetti B, Notturno F, Di Lisi F, Forlivesi S, Delodovici ML, Buechner SC, Biagini S, Accavone D, Manna R, Morrone A, and Inzitari D
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- Female, Humans, Male, Italy epidemiology, Mutation, Prevalence, Prospective Studies, Adolescent, Young Adult, Adult, Middle Aged, alpha-Galactosidase genetics, Fabry Disease diagnosis, Fabry Disease epidemiology, Fabry Disease genetics, Ischemic Attack, Transient diagnosis, Ischemic Attack, Transient epidemiology, Ischemic Stroke diagnosis, Ischemic Stroke epidemiology, Ischemic Stroke genetics
- Abstract
Background: Fabry disease (FD) is a treatable X-linked lysosomal storage disorder caused by GLA gene variants leading to alpha-galactosidase A deficiency. FD is a rare cause of stroke, and it is still controversial whether in stroke patients FD should be searched from the beginning or at the end of the diagnostic workup (in cryptogenic strokes)., Methods: Fabry-Stroke Italian Registry is a prospective, multicentric screening involving 33 stroke units. FD was sought by measuring α-galactosidase A activity (males) and by genetic tests (males with reduced enzyme activity and females) in patients aged 18-60 years hospitalized for TIA, ischemic stroke, or intracerebral hemorrhage. We diagnosed FD in patients with 1) already known pathogenic GLA variants; 2) novel GLA variants if additional clinical, laboratory, or family-derived criteria were present., Results: Out of 1906 patients, we found a GLA variant in 15 (0.79%; 95%CI 0.44-1.29) with a certain FD diagnosis in 3 (0.16%; 95%CI 0.03-0.46) patients, none of whom had hemorrhage. We identified 1 novel pathogenic GLA variant. Ischemic stroke etiologies in carriers of GLA variants were: cardioaortic embolism (33%), small artery occlusion (27%), other causes (20%), and undetermined (20%). Mild severity, recurrence, previous TIA, acroparesthesias, hearing loss, and small artery occlusion were predictors of GLA variant., Conclusion: In this large multicenter cohort the frequency of FD and GLA variants was consistent with previous reports. Limiting the screening for GLA variants to patients with cryptogenic stroke may miss up to 80% of diagnoses. Some easily recognizable clinical features could help select patients for FD screening., Competing Interests: Declaration of competing interest IR received travel grants and speaker's honoraria from Takeda, Sanofi, and Amicus; PN received speaker's honoraria from Takeda, Sanofi, and Amicus; MZ received fees as consultant and advisory board member from Takeda, Sanofi, and Amicus; SS received personal fees as speaker or advisor (Abbott, Allergan-Abbvie, AstraZeneca, Eli Lilly, Lundbeck, Novartis, NovoNordisk, Pfizer, Teva), research grants (Allergan, Novartis, Uriach), and fees for CME/education (Medscape, Neurodiem Ology Medical Education); UA received speaker's fees and honoraria from EISAI; AM received speaker's honoraria and travel grants from Takeda, Sanofi, and Amicus; DI received speaker's honoraria from Takeda. Other authors declared that they have no competing interests for FSIR study., (Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.)
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- 2024
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28. Risk of disease relapse, safety and tolerability of SARS-CoV-2 vaccination in patients with chronic inflammatory neuropathies.
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Doneddu PE, Briani C, Cocito D, Manganelli F, Fabrizi GM, Matà S, Mazzeo A, Fazio R, Benedetti L, Luigetti M, Inghilleri M, Ruiu E, Siciliano G, Cosentino G, Marfia GA, Carpo M, Filosto M, Antonini G, Notturno F, Sotgiu S, Cucurachi L, Dell'Aquila C, Bianchi E, Rosso T, Giordano A, Fernandes M, Campagnolo M, Peci E, Spina E, Tagliapietra M, Sperti M, Gentile L, Strano C, Germano F, Romozzi M, Moret F, Zarbo IR, Viola DV, Vegezzi E, Mataluni G, Cotti-Piccinelli S, Leonardi L, Carta A, and Nobile-Orazio E
- Subjects
- Humans, COVID-19 Vaccines adverse effects, SARS-CoV-2, Cross-Over Studies, Vaccination adverse effects, Recurrence, Polyradiculoneuropathy, Chronic Inflammatory Demyelinating diagnosis, COVID-19 prevention & control, Polyneuropathies
- Abstract
Background and Purpose: The aim was to evaluate the risk of relapse after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccination, and its safety and tolerability, in patients with chronic inflammatory neuropathies., Methods: In this multicenter, cohort and case-crossover study, the risk of relapse associated with SARS-CoV-2 vaccination was assessed by comparing the frequency of relapse in chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) and multifocal motor neuropathy (MMN) patients who underwent or did not undergo vaccination. Frequency of relapse in the 3 months prior to and after vaccination, and safety and tolerability of SARS-CoV-2 vaccination, were also assessed., Results: In all, 336 patients were included (278 CIDP, 58 MMN). Three hundred and seven (91%) patients underwent SARS-CoV-2 vaccination. Twenty-nine patients (9%) did not undergo vaccination. Mild and transient relapses were observed in 16 (5%) patients (13 CIDP, 3 MMN) after SARS-CoV-2 vaccination and in none of the patients who did not undergo vaccination (relative risk [RR] 3.21, 95% confidence interval [CI] 0.19-52.25). There was no increase in the specific risk of relapse associated with type of vaccine or diagnosis. Comparison with the 3-month control period preceding vaccination revealed an increased risk of relapse after vaccination (RR 4.00, 95% CI 1.35-11.82), which was restricted to CIDP patients (RR 3.25, 95% CI 1.07-9.84). The safety profile of SARS-CoV-2 vaccination was characterized by short-term, mild-to-moderate local and systemic adverse events., Conclusions: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccination in CIDP and MMN patients does not seem to be associated with an increased risk of relapse at the primary end-point, although a slightly increased risk in CIDP patients was found compared to the 3 months before vaccination., (© 2023 European Academy of Neurology.)
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- 2023
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29. Yield of EEG features as markers of disease severity in amyotrophic lateral sclerosis: a pilot study.
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Notturno F, Croce P, Ornello R, Sacco S, and Zappasodi F
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- Humans, Pilot Projects, Electroencephalography, Patient Acuity, Brain Mapping methods, Brain, Amyotrophic Lateral Sclerosis diagnosis
- Abstract
Objective: To clarify the role of electroencephalography (EEG) as a promising marker of severity in amyotrophic lateral sclerosis (ALS). We characterized the brain spatio-temporal patterns activity at rest by means of both spectral band powers and EEG microstates and correlated these features with clinical scores., Methods: Eyes closed EEG was acquired in 15 patients with ALS and spectral band power was calculated in frequency bands, defined on the basis of individual alpha frequency (IAF): delta-theta band (1-7 Hz); low alpha (IAF - 2 Hz - IAF); high alpha (IAF - IAF + 2 Hz); beta (13 - 25 Hz). EEG microstate metrics (duration, occurrence, and coverage) were also evaluated. Spectral band powers and microstate metrics were correlated with several clinical scores of disabilities and disease progression. As a control group, 15 healthy volunteers were enrolled., Results: The beta-band power in motor/frontal regions was higher in patients with higher disease burden, negatively correlated with clinical severity scores and positively correlated with disease progression. Overall microstate duration was longer and microstate occurrence was lower in patients than in controls. Longer duration was correlated with a worse clinical status., Conclusions: Our results showed that beta-band power and microstate metrics may be good candidates of disease severity in ALS. Increased beta and longer microstate duration in clinically worse patients suggest a possible impairment of both motor and non-motor network activities to fast modify their status. This can be interpreted as an attempt in ALS patients to compensate the disability but resulting in an ineffective and probably maladaptive behavior.
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- 2023
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30. Acute psychotic onset in LGI1-related limbic encephalitis.
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Notturno F and Uncini A
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- Aged, Autoantibodies, Female, Humans, Intracellular Signaling Peptides and Proteins, Proteins genetics, Limbic Encephalitis complications, Limbic Encephalitis diagnosis
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- 2021
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31. Association of rhabdomyolysis with nebivolol.
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Notturno F and Uncini A
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- Creatine Kinase blood, Female, Humans, Middle Aged, Myoglobin blood, Nebivolol adverse effects, Pleurodynia, Epidemic complications, Rhabdomyolysis diagnosis, Nebivolol pharmacology, Rhabdomyolysis drug therapy, Rhabdomyolysis etiology
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- 2021
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32. Erenumab Plus Subcutaneous Immunoglobulin in a Patient With Comorbid Chronic Migraine and Myasthenia Gravis.
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Ornello R, Frattale I, Pistoia F, Sacco S, and Notturno F
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- Adult, Antibodies, Monoclonal, Humanized administration & dosage, Calcitonin Gene-Related Peptide Receptor Antagonists administration & dosage, Chronic Disease, Female, Humans, Immunoglobulins administration & dosage, Immunologic Factors administration & dosage, Injections, Subcutaneous, Antibodies, Monoclonal, Humanized pharmacology, Calcitonin Gene-Related Peptide Receptor Antagonists pharmacology, Immunoglobulins pharmacology, Immunologic Factors pharmacology, Migraine without Aura drug therapy, Myasthenia Gravis drug therapy
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- 2020
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33. Hyper-reflexia in Guillain-Barré syndrome: systematic review.
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Uncini A, Notturno F, and Kuwabara S
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- Guillain-Barre Syndrome physiopathology, Humans, Male, Middle Aged, Guillain-Barre Syndrome complications, Guillain-Barre Syndrome diagnosis, Reflex, Abnormal
- Abstract
Areflexia or hyporeflexia is a mandatory clinical criterion for the diagnosis of Guillain-Barré syndrome (GBS). A systematic review of the literature from 1 January 1993 to 30 August 2019 revealed 44 sufficiently detailed patients with GBS and hyper-reflexia, along with one we describe. 73.3% of patients were from Japan, 6.7% from the USA, 6.7% from India, 4.4% from Italy, 4.4% from Turkey, 2.2% from Switzerland and 2.2% from Slovenia, suggesting a considerable geographical variation. Hyper-reflexia was more frequently associated with antecedent diarrhoea (56%) than upper respiratory tract infection (22.2%) and the electrodiagnosis of acute motor axonal neuropathy (56%) than acute inflammatory demyelinating polyneuropathy (4.4%). Antiganglioside antibodies were positive in 89.7% of patients. Hyper-reflexia was generalised in 90.7% of patients and associated with reflex spread in half; it was present from the early progressive phase in 86.7% and disappeared in a few weeks or persisted until 18 months. Ankle clonus or Babinski signs were rarely reported (6.7%); spasticity never developed. 53.3% of patients could walk unaided at nadir, none needed mechanical ventilation or died. 92.9% of patients with limb weakness were able to walk unaided within 6 months. Electrophysiological studies showed high soleus maximal H-reflex amplitude to maximal compound muscle action potential amplitude ratio, suggestive of spinal motoneuron hyperexcitability, and increased central conduction time, suggestive of corticospinal tract involvement, although a structural damage was never demonstrated by MRI. Hyper-reflexia is not inconsistent with the GBS diagnosis and should not delay treatment. All GBS variants and subtypes can present with hyper-reflexia, and this eventuality should be mentioned in future diagnostic criteria for GBS., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2020. No commercial re-use. See rights and permissions. Published by BMJ.)
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- 2020
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34. Acute motor axonal neuropathy and transverse myelitis overlap: the importance of history taking.
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Degan D, Tiseo C, Ornello R, and Notturno F
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- Adult, Diagnosis, Differential, Female, Gait Ataxia etiology, Humans, Magnetic Resonance Imaging methods, Medical History Taking methods, Muscle Weakness etiology, Urination Disorders etiology, Medical History Taking standards, Myelitis, Transverse diagnosis, Nervous System Diseases diagnosis
- Abstract
In young adults, acute motor axonal neuropathy and transverse myelitis rarely occur as associated conditions. Clinical reasoning, symptoms, laboratory and ancillary investigations (electroneurographic and radiological findings), should properly address the physician to the correct diagnosis.
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- 2018
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35. Not all intermittent shakings are epilepsy.
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Tiseo C, Ornello R, Degan D, and Notturno F
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- Aged, Blood Flow Velocity, Breath Holding, Diagnosis, Differential, Diagnostic Imaging, Hemodynamics, Humans, Ischemic Attack, Transient therapy, Male, Syndrome, Ischemic Attack, Transient complications, Ischemic Attack, Transient diagnosis, Tremor etiology
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- 2017
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36. Demyelinating Guillain-Barré syndrome recurs more frequently than axonal subtypes.
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Notturno F, Kokubun N, Sekiguki Y, Nagashima T, De Lauretis A, Yuki N, Kuwabara S, and Uncini A
- Subjects
- Adolescent, Adult, Aged, Antibodies metabolism, Campylobacter Infections epidemiology, Campylobacter Infections immunology, Child, Electric Stimulation, Female, Gangliosides immunology, Humans, Italy epidemiology, Japan epidemiology, Longitudinal Studies, Male, Middle Aged, Miller Fisher Syndrome physiopathology, Recurrence, Retrospective Studies, Statistics, Nonparametric, Young Adult, Guillain-Barre Syndrome epidemiology, Guillain-Barre Syndrome physiopathology, Miller Fisher Syndrome epidemiology, Neural Conduction physiology
- Abstract
Guillain-Barré syndrome (GBS) is considered a monophasic disorder yet recurrences occur in up to 6% of patients. We retrospectively studied an Italian-Japanese population of 236 GBS and 73 Miller Fisher syndrome (MFS) patients and searched for factors which may be associated with recurrence. A recurrent patient was defined as having at least two episodes that fulfilled the diagnostic criteria for GBS and MFS with an identifiable recovery after each episode and a minimum of 2months between episodes. Preceding Campylobacter jejuni (C. jejuni) infection and antiganglioside antibodies were also assessed. Seven (3%) recurrent GBS and one (1.4%) recurrent MFS patients were identified. In the individual patient the clinical features during episodes were usually similar varying in severity whereas the preceding infection differed. None of the patients had GBS in one episode and MFS in the recurrence or vice versa. Recurrent GBS patients, compared with monophasic GBS, did not have preceding diarrhea at the first episode and considering the electrophysiological subtypes, acute inflammatory demyelinating polyneuropathies recurred more frequently than axonal GBS (6.5% vs 0.9%, p=0.04). In conclusion in a GBS population with a balanced number of demyelinating and axonal subtypes less frequent diarrhea and demyelination at electrophysiology were associated with recurrence., (Copyright © 2016. Published by Elsevier B.V.)
- Published
- 2016
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37. Electrodiagnosis of GBS subtypes by a single study: not yet the squaring of the circle.
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Uncini A, Zappasodi F, and Notturno F
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- Humans, Electrodiagnosis methods, Guillain-Barre Syndrome diagnosis, Guillain-Barre Syndrome physiopathology
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- 2015
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38. Autoantibodies to neurofascin-186 and gliomedin in multifocal motor neuropathy.
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Notturno F, Di Febo T, Yuki N, Fernandez Rodriguez BM, Corti D, Nobile-Orazio E, Carpo M, De Lauretis A, and Uncini A
- Subjects
- Animals, Cell Adhesion Molecules genetics, Computational Biology, Enzyme-Linked Immunosorbent Assay, Female, G(M1) Ganglioside genetics, G(M1) Ganglioside immunology, Humans, Male, Membrane Proteins genetics, Motor Neuron Disease complications, Nerve Growth Factors genetics, Nerve Tissue Proteins genetics, Polyneuropathies complications, Protein Isoforms immunology, Rats, Transfection, Autoantibodies blood, Cell Adhesion Molecules immunology, Membrane Proteins immunology, Motor Neuron Disease blood, Nerve Growth Factors immunology, Nerve Tissue Proteins immunology, Polyneuropathies blood
- Abstract
We tested autoantibodies to neurofascin-186 (NF186) and gliomedin in sera from patients with multifocal motor neuropathy (MMN, n=53) and chronic inflammatory demyelinating polyneuropathy (CIDP, n=95) by ELISA. IgG antibodies to NF186 or gliomedin were found in 62% of MMN and 1% of CIDP sera, and IgM antibodies to the same antigens in 12% of MMN and 1% of CIDP sera. These autoantibodies activated complement. Ten percent of the MMN sera without IgM anti-GM1 reactivity had anti-NF186 antibodies. Because NF186 and gliomedin play a crucial role for salutatory conduction, the autoantibodies may contribute to produce motor nerve conduction block and muscle weakness in MMN., (Copyright © 2014 Elsevier B.V. All rights reserved.)
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- 2014
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39. PDCD10 gene mutations in multiple cerebral cavernous malformations.
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Cigoli MS, Avemaria F, De Benedetti S, Gesu GP, Accorsi LG, Parmigiani S, Corona MF, Capra V, Mosca A, Giovannini S, Notturno F, Ciccocioppo F, Volpi L, Estienne M, De Michele G, Antenora A, Bilo L, Tavoni A, Zamponi N, Alfei E, Baranello G, Riva D, and Penco S
- Subjects
- Adolescent, Adult, Age of Onset, Aged, Child, Preschool, DNA Mutational Analysis, Female, Hemangioma, Cavernous, Central Nervous System pathology, Humans, Italy, Male, Middle Aged, Pedigree, Apoptosis Regulatory Proteins genetics, Hemangioma, Cavernous, Central Nervous System genetics, Membrane Proteins genetics, Mutation, Proto-Oncogene Proteins genetics
- Abstract
Cerebral cavernous malformations (CCMs) are vascular abnormalities that may cause seizures, intracerebral haemorrhages, and focal neurological deficits. Familial form shows an autosomal dominant pattern of inheritance with incomplete penetrance and variable clinical expression. Three genes have been identified causing familial CCM: KRIT1/CCM1, MGC4607/CCM2, and PDCD10/CCM3. Aim of this study is to report additional PDCD10/CCM3 families poorly described so far which account for 10-15% of hereditary cerebral cavernous malformations. Our group investigated 87 consecutive Italian affected individuals (i.e. positive Magnetic Resonance Imaging) with multiple/familial CCM through direct sequencing and Multiplex Ligation-Dependent Probe Amplification (MLPA) analysis. We identified mutations in over 97.7% of cases, and PDCD10/CCM3 accounts for 13.1%. PDCD10/CCM3 molecular screening revealed four already known mutations and four novel ones. The mutated patients show an earlier onset of clinical manifestations as compared to CCM1/CCM2 mutated patients. The study of further families carrying mutations in PDCD10/CCM3 may help define a possible correlation between genotype and phenotype; an accurate clinical follow up of the subjects would help define more precisely whether mutations in PDCD10/CCM3 lead to a characteristic phenotype.
- Published
- 2014
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40. Neuroprotective effect of cathodal transcranial direct current stimulation in a rat stroke model.
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Notturno F, Pace M, Zappasodi F, Cam E, Bassetti CL, and Uncini A
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- Animals, Cerebral Infarction pathology, Cerebral Infarction physiopathology, Cortical Spreading Depression physiology, Disease Models, Animal, Male, Rats, Time Factors, Transcranial Direct Current Stimulation adverse effects, Brain pathology, Brain physiopathology, Cerebral Infarction therapy, Cytoprotection, Transcranial Direct Current Stimulation methods
- Abstract
Experimental focal brain ischemia generates in the penumbra recurrent depolarizations which spread across the injured cortex inducing infarct growth. Transcranial direct current stimulation can induce a lasting, polarity-specific, modulation of cortical excitability. To verify whether cathodal transcranial direct current stimulation could reduce the infarct size and the number of depolarizations, focal ischemia was induced in the rat by the 3 vessels occlusion technique. In the first experiment 12 ischemic rats received cathodal stimulation (alternating 15 min on and 15 min off) starting 45 min after middle cerebral artery occlusion and lasting 4 h. In the second experiment 12 ischemic rats received cathodal transcranial direct current stimulation with the same protocol but starting soon after middle cerebral artery occlusion and lasting 6 h. In both experiments controls were 12 ischemic rats not receiving stimulation. Cathodal stimulation reduced the infarct volume in the first experiment by 20% (p=0.002) and in the second by 30% (p=0.003). The area of cerebral infarction was smaller in animals receiving cathodal stimulation in both experiments (p=0.005). Cathodal stimulation reduced the number of depolarizations (p=0.023) and infarct volume correlated with the number of depolarizations (p=0.048). Our findings indicate that cathodal transcranial direct current stimulation exert a neuroprotective effect in the acute phase of stroke possibly decreasing the number of spreading depolarizations. These findings may have translational relevance and open a new avenue in neuroprotection of stroke in humans., (Copyright © 2014. Published by Elsevier B.V.)
- Published
- 2014
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41. Local and remote effects of transcranial direct current stimulation on the electrical activity of the motor cortical network.
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Notturno F, Marzetti L, Pizzella V, Uncini A, and Zappasodi F
- Subjects
- Adult, Analysis of Variance, Electroencephalography, Fourier Analysis, Functional Laterality, Humans, Male, Psychomotor Performance, Transcranial Direct Current Stimulation, Brain Mapping, Evoked Potentials, Motor physiology, Motor Cortex physiology, Movement physiology, Neural Pathways physiology
- Abstract
We systematically investigated the effects of cathodal and anodal Transcranial Direct Current Stimulation (CtDCS, AtDCS) on the electric activity of primary motor cortex during a motor task. High-density electroencephalography was used to define the spatial diffusion of tDCS after effects. Ten healthy subjects performed a finger tapping task with the right hand before and after three separate sessions of 20 minutes of Sham, AtDCS or CtDCS over left primary motor cortex (M1). During movement, we found an increment of low alpha band Event-Related Desynchronization (ERD) in bilateral central, frontal areas and in the left inferior parietal region, as well as an increment of beta ERD in fronto-central and parieto-occipital regions, after AtDCs compared to Sham and CtDCS. In the rest pre-movement period, after Sham as well as AtDCS, we documented an increment of low alpha band power over the course of pre- and post-stimulation recording sessions, localized in the sensorimotor and parieto-occipital regions. On the contrary, after CtDCS no increment of low alpha power was found. Finally beta band coherence among signals from left sensorimotor cortex and activity of bilateral parietal, occipital and right frontal regions was higher after AtDCS compared with Sham condition. Similarly, theta coherence with parietal and frontal regions was enhanced after AtDCS. We hypothesize that the local modulation of membrane polarization, as well as long-lasting synaptic modification induced by tDCS over M1, could result in changes of both local band power and functional architecture of the motor network., (Copyright © 2013 Wiley Periodicals, Inc.)
- Published
- 2014
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42. Natura non facit saltus in anti-ganglioside antibody-mediated neuropathies.
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Uncini A, Notturno F, and Capasso M
- Subjects
- Antigen-Antibody Reactions immunology, Humans, Oligosaccharides immunology, Polyneuropathies classification, Autoantibodies adverse effects, Gangliosides immunology, Polyneuropathies immunology
- Abstract
Natura non facit saltus (Latin for "nature does not make jumps") is a maxim expressing the idea that natural things and properties change gradually, in a continuum, rather than suddenly. In biomedical sciences, for taxonomic purposes, we make jumps that emphasize differences more than similarities. Among the dysimmune neuropathies, 2 disorders, characterized by the presence of antibodies to gangliosides GM1 and GD1a and a peculiar, exclusive motor involvement, have been identified: acute motor axonal neuropathy (AMAN) and multifocal motor neuropathy (MMN). However, anti-GM1 or -GD1a antibodies are also associated with acute motor and sensory axonal motor neuropathy (AMSAN). We review the results of recent clinical and experimental studies showing that AMAN and MMN are not exclusively motor. We discuss the possible explanations for the greater resistance of sensory fibers to antibody attack to finally suggest that AMAN, AMSAN, and MMN belong to a continuous spectrum with a common pathophysiological mechanism., (Copyright © 2013 Wiley Periodicals, Inc.)
- Published
- 2013
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43. Electrophysiological comparison between males and females in HNPP.
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Manganelli F, Pisciotta C, Dubbioso R, Maruotti V, Iodice R, Notturno F, Ruggiero L, Vitale C, Nolano M, Uncini A, and Santoro L
- Subjects
- Adult, Arthrogryposis diagnosis, Female, Hereditary Sensory and Motor Neuropathy diagnosis, Humans, Male, Sex Factors, Arthrogryposis physiopathology, Evoked Potentials, Motor, Hereditary Sensory and Motor Neuropathy physiopathology, Neural Conduction
- Abstract
Some evidences highlighted a higher clinical expression of hereditary neuropathy with liability to pressure palsy (HNPP) in males, and a higher load of traumatic nerve injuries due to different occupational activity has been invoked to explain this observation. It is unknown whether this increased clinical impairment corresponds to a greater electrophysiological involvement. Thus, we compared clinical and electrophysiological features between men and women in a large cohort of HNPP patients. Nerve palsies and electrophysiological abnormalities were more frequent in men, and electrophysiological findings which differentiated males from females did not show any age-related worsening. In conclusion, our findings showed a higher clinical and electrophysiological involvement in males which does not seem related to different cumulative nerve damage over time. We believe that the higher disease expression may increase the chance to detect the disease in males and, thereby, to underestimate the HNPP diagnosis in females.
- Published
- 2013
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44. Pseudocortical and dissociate discriminative sensory dysfunction in a thalamic stroke.
- Author
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Notturno F, Sepe R, Caulo M, Uncini A, and Committeri G
- Subjects
- Adult, Agnosia etiology, Humans, Male, Somatosensory Cortex physiopathology, Stroke complications, Agnosia physiopathology, Stroke physiopathology, Thalamus physiopathology, Touch physiology, Touch Perception physiology
- Abstract
In thalamic lesions a pseudocortical syndrome has been occasionally described but the effect of the lesion on the cortical network of tactile recognition has never been studied. We report a patient who developed tactile agnosia in the left hand after right thalamic stroke, configuring a pseudocortical sensory syndrome. The discriminative sensory dysfunction was dissociate because only tactile agnosia and mild pseudoathetosis were present. A functional magnetic resonance imaging (fMRI) study showed that tactile recognition with the unaffected hand recruited a bilateral fronto-parietal network. During recognition with the left hand the activation was restricted and lateralized to the ipsilateral hemisphere. In this patient with pseudocortical discriminative sensory dysfunction the lack of activation of the whole cortical network, implicated in tactile recognition, demonstrates that pseudocortical is functionally equivalent to cortical tactile agnosia., (Copyright © 2012 Elsevier Ltd. All rights reserved.)
- Published
- 2013
- Full Text
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45. Guillain-Barré syndrome associated with normal or exaggerated tendon reflexes.
- Author
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Yuki N, Kokubun N, Kuwabara S, Sekiguchi Y, Ito M, Odaka M, Hirata K, Notturno F, and Uncini A
- Subjects
- Adolescent, Adult, Aged, Aged, 80 and over, Child, Child, Preschool, Cohort Studies, Female, Follow-Up Studies, Humans, Male, Middle Aged, Young Adult, Guillain-Barre Syndrome diagnosis, Guillain-Barre Syndrome physiopathology, Reflex, Abnormal physiology, Reflex, Stretch physiology
- Abstract
Areflexia is part one of the clinical criteria required to make a diagnosis of Guillain-Barré syndrome (GBS). The diagnostic criteria were stringently developed to exclude non-GBS cases but there have been reports of patients with GBS following Campylobacter jejuni enteritis with normal and exaggerated deep tendon reflexes (DTRs). The aim of this study is to expand the existing diagnostic criteria to preserved DTRs. From the cohort of patients referred for anti-ganglioside antibody testing from hospitals throughout Japan, 48 GBS patients presented with preserved DTR at admission. Thirty-two patients had normal or exaggerated DTR throughout the course of illness whereas in 16 patients the DTR became absent or diminished during the course of the illness. IgG antibodies against GM1, GM1b, GD1a, or GalNAc-GD1a were frequently present in either group (84 vs. 94%), suggesting a close relationship between the two groups. We then investigated the clinical and laboratory findings of 213 GBS patients from three hospital cohorts. In 23 patients, eight presented with normal tendon reflexes throughout the clinical course of the illness. Twelve showed hyperreflexia, with at least one of the jerks experienced even at nadir, and exaggerated reflexes returning to normal at recovery. The other three had hyperreflexia throughout the disease course. Compared to 190 GBS patients with reduced or absent DTR, the 23 DTR-preserved patients more frequently presented with pure motor limb weakness (87 vs. 47%, p = 0.00026), could walk 5 m independently at the nadir (70 vs. 33%, p = 0.0012), more frequently had antibodies against GM1, GM1b, GD1a, or GalNAc-GD1a (74 vs. 47%, p = 0.014) and were more commonly diagnosed with acute motor axonal neuropathy (65 vs. 34%, p = 0.0075) than with acute inflammatory demyelinating polyneuropathy (13 vs. 43%, p = 0.0011). This study demonstrated that DTRs could be normal or hyperexcitable during the entire clinical course in approximately 10% of GBS patients. This possibility should be added in the diagnostic criteria for GBS to avoid delays in diagnosis and effective treatment to these patients.
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- 2012
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46. Cortical origin of myoclonus in early stages of corticobasal degeneration.
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Notturno F, Zappasodi F, Maruotti V, Marzetti L, Caulo M, and Uncini A
- Subjects
- Aged, Electric Stimulation, Electroencephalography, Electromyography, Evoked Potentials, Somatosensory physiology, Female, Humans, Magnetic Resonance Imaging, Muscle, Skeletal physiopathology, Myoclonus diagnosis, Reaction Time, Basal Ganglia physiopathology, Cerebral Cortex physiopathology, Myoclonus etiology, Neurodegenerative Diseases complications, Neurodegenerative Diseases pathology
- Published
- 2011
- Full Text
- View/download PDF
47. Polymorphism of CD1 and SH2D2A genes in inflammatory neuropathies.
- Author
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Uncini A, Notturno F, Pace M, and Caporale CM
- Subjects
- Genotype, Humans, Adaptor Proteins, Signal Transducing genetics, Antigens, CD1 genetics, Genetic Predisposition to Disease genetics, Guillain-Barre Syndrome genetics, Polymorphism, Genetic, Polyradiculoneuropathy, Chronic Inflammatory Demyelinating genetics
- Abstract
In the quest for susceptibility factors of inflammatory neuropathies, many genes implicated in the pathogenesis of autoimmune diseases have been investigated with negative or conflicting results. We studied, with a gene candidate approach, the CD1 system specialized in capturing and presenting glycolipids to antigen-specific T cells, and the SH2D2A gene encoding for a T-cell-specific adapter protein implicated in control of early T-cell activation. In Guillain-Barré syndrome, an initially positive association study with polymorphism of CD1A and CD1E genes was not confirmed. In chronic inflammatory demyelinating polyneuropathy, we did not find an association with CD1 genes, but we found an association with a homozygous genotype for a low repeat number of tandem GA in the SH2D2A gene. This genotype could result in defective control and elimination of autoreactive T cells. All the studies were performed on relatively small size populations. Confirmation in larger sized studies is required both for CD1 and SH2D2A genes. Considering the relative rarity of patients with inflammatory neuropathies, this can only be accomplished by international collaboration., (© 2011 Peripheral Nerve Society.)
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- 2011
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48. Motor and sensory conduction failure in overlap of Guillain-Barré and Miller Fisher syndrome: two simultaneous cases.
- Author
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Rajabally YA, Hassan-Smith G, Notturno F, Eames PJ, Hayton T, Capasso M, and Uncini A
- Subjects
- Action Potentials physiology, Adult, Autoantibodies immunology, Axons pathology, Electric Stimulation, Electrophysiological Phenomena, Female, Gangliosides immunology, Guillain-Barre Syndrome complications, Humans, Miller Fisher Syndrome complications, Muscle Weakness etiology, Neurologic Examination, Paresthesia etiology, Respiratory Tract Infections complications, Speech Disorders etiology, Guillain-Barre Syndrome physiopathology, Miller Fisher Syndrome physiopathology, Motor Neurons physiology, Neural Conduction physiology, Sensory Receptor Cells physiology
- Abstract
We report 2 patients diagnosed simultaneously with an overlap of Guillain-Barré syndrome (GBS) and Miller Fisher syndrome (MFS), who had anti-GT1a, anti-GQ1b, anti-GD1a and anti-GD1b antibodies. There was no identifiable specific preceding infection. Both patients presented with upper and lower limb paresthesias and severe weakness, bulbar and facial weakness, ophthalmoparesis and areflexia. In one, electrophysiology demonstrated multifocal conduction blocks (CBs) and mild motor conduction velocity slowing in intermediate segments and absent sensory nerve action potentials (SNAPs). The patient improved rapidly and fully recovered within 18 days from onset. CBs resolved, distal compound muscle action potential (CMAP) amplitudes increased and SNAPs normalized on subsequent testing. In the other patient, initial studies showed low/normal CMAPs, with absent SNAPs, without demyelinating features. This patient fully recovered within 21 days from onset. CMAPs markedly increased, SNAPs improved marginally. These 2 patients exhibited features indicative of the pathophysiological mechanism of conduction failure in motor and sensory fibers. This phenomenon relates to rapidly resolving CBs possibly induced by the transitory and limited attack of antiganglioside antibodies at the axolemma of the nodes of Ranvier not progressing to axonal degeneration. These cases widen the range of GBS subtypes in which reversible conduction failure has been described, to include overlap syndromes with MFS. The factors determining the electrophysiology, as well as the rate, degree and quality of recovery in GBS subtypes remain uncertain at the present time., (Copyright © 2011 Elsevier B.V. All rights reserved.)
- Published
- 2011
- Full Text
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49. Monospecific high-affinity and complement activating anti-GM1 antibodies are determinants in experimental axonal neuropathy.
- Author
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Notturno F, Del Boccio P, Luciani M, Caporale CM, Pieragostino D, Prencipe V, Sacchetta P, and Uncini A
- Subjects
- Animals, Autoantibodies, Binding Sites, Antibody immunology, Campylobacter Infections complications, Campylobacter jejuni pathogenicity, Disease Models, Animal, Enzyme-Linked Immunosorbent Assay methods, Guillain-Barre Syndrome etiology, Guillain-Barre Syndrome pathology, Humans, Immunoglobulin G immunology, Rabbits, Antibodies, Anti-Idiotypic immunology, Axons pathology, Complement System Proteins immunology, Gangliosidosis, GM1 immunology, Guillain-Barre Syndrome immunology
- Abstract
It has been difficult to replicate consistently the experimental model of axonal Guillain-Barré syndrome (GBS). We immunized rabbits with two lipo-oligosaccharides (LOS1 and LOS2) derived from the same C. jejuni strain and purified in a slightly different way. LOS1 did not contain proteins whereas several proteins were present in LOS2. In spite of a robust anti-GM1 antibody response in all animals the neuropathy developed only in rabbits immunized with LOS1. To explain this discrepancy we investigated fine specificity, affinity and ability to activate the complement of anti-GM1 antibodies. Only rabbits immunized with LOS1 showed monospecific high-affinity antibodies which activated more effectively the complement. Although it is not well understood how monospecific high-affinity antibodies are induced these are crucial for the induction of experimental axonal neuropathy. Only a strict adherence to the protocols demonstrated to be successful may guarantee the reproducibility and increase the confidence in the animal model as a reliable tool for the study of the human axonal GBS., (Copyright 2010 Elsevier B.V. All rights reserved.)
- Published
- 2010
- Full Text
- View/download PDF
50. Capsular warning syndrome mimicking a jacksonian sensory march.
- Author
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Caporale CM, Notturno F, Caulo M, and Uncini A
- Subjects
- Anticonvulsants therapeutic use, Brain drug effects, Brain pathology, Brain physiopathology, Brain Infarction drug therapy, Brain Infarction pathology, Diagnosis, Differential, Electroencephalography, Epilepsy diagnosis, Epilepsy drug therapy, Epilepsy pathology, Humans, Male, Middle Aged, Recurrence, Seizures drug therapy, Seizures pathology, Stroke drug therapy, Stroke pathology, Syndrome, Treatment Outcome, Brain Infarction diagnosis, Seizures diagnosis, Stroke diagnosis
- Abstract
A 57-year-old man, operated eight years before for a left frontal falx meningioma, presented with short lasting, stereotyped episodes of paresthesias ascending from the right foot to the hand. A diagnosis of somatosensory seizures with jacksonian march was made. The patient was given antiepilectics but 5 days later, a few hours after another paresthesic episodes, he developed right hemiplegia, hemianesthesia and dysartria due to an infarct of left capsular posterior limb. We deem that in this patient the paresthesic episodes were more likely an expression of a capsular warning syndrome than of parietal epilepsy because of the frontal localization of the surgical lesion, the absence of motor components in all episodes, the negativity of repeated EEG, and the lack of recurrences after stroke. In capsular warning syndrome sensory symptoms mimicking a jacksonian march can be due to ischemic depolarization progressively recruiting the somatotopically arranged sensory fibers in the posterior capsular limb.
- Published
- 2009
- Full Text
- View/download PDF
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