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1. Non-motor symptoms burden, mood, and gait problems are the most significant factors contributing to a poor quality of life in non-demented Parkinson's disease patients: Results from the COPPADIS Study Cohort

Author

Adarmes, A.D., Almeria, M., Alonso Losada, G., Alonso Cánovas, A., Alonso-Frech, F., Arribas, S., Ascunde Vidondo, A., Aquilar, M., Ávila, M.A., Bernardo Lambrich, N., Bejr-Kasem, H., Blázquez Estrada, M., Botí, M., Cabello González, C., Cabo López, I., Caballol, N., Cámara Lorenzo, A., Carrillo, F., Catalán, M.J., Clavero, P., Cortina Fernández, A., Crespo Cuevas, A., de Fábregues-Boixar, O., Díez-Fairen, M., Erro, E., Estelrich Peyret, E., Fernández Guillán, N., Gámez, P., Gallego, M., García Caldentey, J., García Campos, C., García Moreno, J.M., Gastón, I., Gómez Garre, M.P., González Aloy, J., González-Aramburu, I., González Ardura, J., González García, B., González Palmás, M.J., González Toledo, G.R., Golpe Díaz, A., Grau Solá, M., Guardia, G., Hernández-Vara, J., Horta Barba, A., Infante, J., Jesús, S., Kulisevsky, J., Kurtis, M., Labandeira, C., Labrador, M.A., Lacruz, F., Lage Castro, M., Legarda, I., López Ariztegui, N., López Díaz, L.M., López Manzanares, L., López Seoane, B., Martí Andres, G., Martí, M.J., Martínez-Castrillo, J.C., McAfee, D., Meitín, M.T., Menéndez González, M., Méndez del Barrio, C., Miranda Santiago, J., Morales Casado, M.I., Moreno Diéguez, A., Nogueira, V., Novo Amado, A., Novo Ponte, S., Ordás, C., Pagonabarraga, J., Pareés, I., Pascual-Sedano, B., Pastor, P., Pérez Fuertes, A., Pérez Noguera, R., Planellas, Ll, Pol Fuster, J., Prats, M.A., Prieto Jurczynska, C., Puente, V., Redondo Rafales, N., Rodríguez Méndez, L., Roldán, F., Ruíz De Arcos, M., Ruíz Martínez, J., Sánchez Alonso, P., Sánchez-Carpintero, M., Sánchez Díez, G., Sánchez Rodríguez, A., Santacruz, P., Segundo Rodríguez, J.C., Seijo, M., Serarols, A., Sierra Peña, M., Tartari, J.P., Vargas, L., Vázquez Gómez, R., Villanueva, C., Vives, B., Villar, M.D., Santos García, D., de Deus Fonticoba, T., Suárez Castro, E., Borrué, C., Mata, M., Solano Vila, B., Cots Foraster, A., Álvarez Sauco, M., Rodríguez Pérez, A.B., Vela, L., Macías, Y., Escalante, S., Esteve, P., Reverté Villarroya, S., Cubo, E., Casas, E., Arnaiz, S., Carrillo Padilla, F., Pueyo Morlans, M., Mir, P., and Martinez-Martin, P.

Published
2019
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2. Turning a lost reef ecosystem into a national restoration program

Author

McAfee, D, McLeod, IM, Alleway, HK, Bishop, MJ, Branigan, S, Connell, SD, Copeland, C, Crawford, CM, Diggles, BK, Fitzsimons, James, Gilby, BL, Hamer, P, Hancock, B, Pearce, R, Russell, K, Gillies, CL, McAfee, D, McLeod, IM, Alleway, HK, Bishop, MJ, Branigan, S, Connell, SD, Copeland, C, Crawford, CM, Diggles, BK, Fitzsimons, James, Gilby, BL, Hamer, P, Hancock, B, Pearce, R, Russell, K, and Gillies, CL

Published
2022

3. Constipation Predicts Cognitive Decline in Parkinson's Disease: Results from the COPPADIS Cohort at 2-Year Follow-up and Comparison with a Control Group

Author

Santos García D, García Roca L, de Deus Fonticoba T, Cores Bartolomé C, Naya Ríos L, Canfield H, Paz González JM, Martínez Miró C, Jesús S, Aguilar M, Pastor P, Planellas L, Cosgaya M, García Caldentey J, Caballol N, Legarda I, Hernández Vara J, Cabo I, López Manzanares L, González Aramburu I, Ávila Rivera MA, Gómez Mayordomo V, Nogueira V, Puente V, Dotor García-Soto J, Borrué C, Solano Vila B, Álvarez Sauco M, Vela L, Escalante S, Cubo E, Carrillo Padilla F, Martínez Castrillo JC, Sánchez Alonso P, Alonso Losada MG, López Ariztegui N, Gastón I, Kulisevsky J, Blázquez Estrada M, Seijo M, Rúiz Martínez J, Valero C, Kurtis M, de Fábregues O, González Ardura J, Alonso Redondo R, Ordás C, López Díaz L LM, McAfee D, Martinez-Martin P, Mir P, and COPPADIS Study Group

Subjects
impairment, Cognition, Parkinson's disease, constipation, non-motor symptoms
Abstract

Background: Constipation has been linked to cognitive impairment development in Parkinson's disease (PD). Objective: Our aim was to analyze cognitive changes observed in PD patients and controls from a Spanish cohort with regards to the presence or not of constipation. Methods: PD patients and controls recruited from 35 centers of Spain from the COPPADIS cohort from January 2016 to November 2017 were followed-up during 2 years. The change in cognitive status from baseline (V0) to 2-year follow-up was assessed with the PD-CRS (Parkinson's Disease Cognitive Rating Scale). Subjects with a score >= 1 on item 21 of the NMSS (Non-Motor Symptoms Scale) at baseline (V0) were considered as "with constipation". Regression analyses were applied for determining the contribution of constipation in cognitive changes. Results: At V0, 39.7% (198/499) of PD patients presented constipation compared to 11.4% of controls (14/123) (p < 0.0001). No change was observed in cognitive status (PD-CRS total score) neither in controls without constipation (from 100.24 +/- 13.72 to 100.27 +/- 13.68; p = 0.971) and with constipation (from 94.71 +/- 10.96 to 93.93 +/- 13.03; p = 0.615). The PD-CRS total score decreased significantly in PD patients with constipation (from 89.14 +/- 15.36 to 85.97 +/- 18.09; p

Published
2022

4. Diplopia Is Frequent and Associated with Motor and Non-Motor Severity in Parkinson’s Disease: Results from the COPPADIS Cohort at 2-Year Follow-Up

Author

Garcia D, Rios L, Fonticoba T, Bartolome C, Roca L, Painceiras M, Miro C, Canfield H, Jesus S, Aguilar M, Pastor P, Cosgaya M, Caldentey J, Caballol N, Legarda I, Vara J, Cabo I, Manzanares L, Aramburu I, Rivera M, Mayordomo V, Nogueira V, Puente V, Dotor J, Borrue C, Vila B, Sauco M, Vela L, Escalante S, Cubo E, Padilla F, Castrillo J, Alonso P, Losada M, Ariztegui N, Gaston I, Kulisevsky J, Estrada M, Seijo M, Martinez J, Valero C, Kurtis M, de Fabregues O, Ardura J, Redondo R, Ordas C, Diaz L, McAfee D, Martinez-Martin P, Mir P, COPPADIS Study Grp, Instituto de Salud Carlos III, Takeda Pharmaceutical Company, International Parkinson and Movement Disorder Society, AbbVie Pharmaceuticals, Abbott Laboratories, Allergan Foundation, BIAL Foundation, Merz Pharma, UCB Pharma, Zambon, Ministerio de Economía y Competitividad (España), European Commission, Junta de Andalucía, Sociedad Andaluza de Neurología, Jacques and Gloria Gossweiler Foundation, Fundación Alicia Koplowitz, Fundación Mutua Madrileña, Institut Català de la Salut, [Santos-García D, Naya Rios L, Cores Bartolomé C, García Roca L, Feal Painceiras M, Martínez Miró C] Complejo Hospitalario Universitario de A Coruña (CHUAC), A Coruña, Spain. [de Deus Fonticoba T, Canfield H] Complejo Hospitalario Universitario de Ferrol (CHUF), A Coruña, Spain. [Jesús S, Mir P] Unidad de Trastornos del Movimiento, Servicio de Neurología y Neurofisiología Clínica, Instituto de Biomedicina de Sevilla, Hospital Universitario Virgen del Rocío, Universidad de Sevilla, Sevilla, Spain. Centro de Investigación Biomédica en Red Enfermedades Neurodegenerativas (CIBERNED), Madrid, Spain. [Aguilar M, Pastor P] Hospital Universitari Mutua de Terrassa, Terrassa , Spain. [Cosgaya M] Hospital Clínic de Barcelona, Barcelona, Spain. [García-Caldentey J] Centro Neurológico Oms, Palma de Mallorca, Spain. [Caballol N] Consorci Sanitari Integral, Hospital Moisés Broggi, Barcelona, Spain. [Legarda I] Hospital Universitari Son Espases, Palma de Mallorca, Spain. [Hernández-Vara J, de Fábregues O] Vall d'Hebron Hospital Universitari, Barcelona, Spain. [Cabo López I, Seijo M] Complexo Hospitalario Universitario de Pontevedra (CHOP), Pontevedra, Spain. [López Manzanares L] Hospital Universitario La Princesa, Madrid, Spain. [González Aramburu I] Centro de Investigación Biomédica en Red Enfermedades Neurodegenerativas (CIBERNED), Madrid, Spain. Hospital Universitario Marqués de Valdecilla, Santander, Spain. [Ávila Rivera MA] Consorci Sanitari Integral, Hospital General de L'Hospitalet, L'Hospitalet de Llobregat, Spain. [Gómez-Mayordomo V] Hospital Universitario Clínico San Carlos, Madrid, Spain. [Nogueira V] Hospital Da Costa, Burela, Lugo, Spain. [Puente V] Hospital del Mar, Barcelona, Spain. [Dotor J] Hospital Universitario Virgen Macarena, Sevilla, Spain. [Borrué C] Hospital Infanta Sofía, Madrid, Spain. [Solano Vila B] Institut d'Assistència Sanitària (IAS), Institut Català de la Salut (ICS), Salt, Spain. [Álvarez Sauco M] Hospital General Universitario de Elche, Elche, Spain. [Vela-Desojo L] Fundación Hospital de Alcorcón, Madrid, Spain. [Escalante S] Hospital de Tortosa Verge de la Cinta (HTVC), Tortosa, Spain. [Cubo E] Complejo Asistencial Universitario de Burgos, Burgos, Spain. [Carrillo-Padilla F] Hospital Universitario de Canarias, Santa Cruz de Tenerife, Spain. [Martínez Castrillo JC] Hospital Universitario Ramón y Cajal, IRYCIS, Madrid, Spain. [Sánchez Alonso P] Hospital Universitario Puerta de Hierro, Madrid, Spain. [Alonso Losada MG] Hospital Álvaro Cunqueiro, Complexo Hospitalario Universitario de Vigo (CHUVI), Vigo, Spain. [López-Ariztegui N] Complejo Hospitalario de Toledo, Toledo, Spain. [Gastón I] Complejo Hospitalario de Navarra, Pamplona, Spain. [Kulisevsky J] Centro de Investigación Biomédica en Red Enfermedades Neurodegenerativas (CIBERNED), Madrid, Spain. Hospital de Sant Pau, Barcelona, Spain. [Blázquez Estrada M] Hospital Universitario Central de Asturias, Oviedo, Spain. [Ruiz-Martínez J] Hospital Universitario Donostia, San Sebastián, Spain. [Valero C] Hospital Arnau de Vilanova, València, Spain. [Kurtis M] Hospital Ruber Internacional, Madrid, Spain. [González Ardura J] Hospital de Cabueñes, Gijón, Spain. [Alonso Redondo R] Universitario Lucus Augusti (HULA), Lugo, Spain. [Ordás C] Hospital Rey Juan Carlos, Madrid, Spain. [López Díaz LM] Complexo Hospitalario Universitario de Ourense (CHUO), Ourense, Spain. [McAfee D] University of Maryland School of Medicine, Baltimore, USA. [Martinez-Martin P] Centro de Investigación Biomédica en Red Enfermedades Neurodegenerativas (CIBERNED), Madrid, Spain, and Institut d'Assistència Sanitària

Subjects
enfermedades del sistema nervioso::enfermedades del sistema nervioso central::enfermedades del sistema nervioso::enfermedades del sistema nervioso central::trastornos del movimiento::trastornos parkinsonianos::enfermedades del sistema nervioso::enfermedad de Parkinson [ENFERMEDADES], Medicine (General), changes, motor, Parkinson’s disease, phenotype, PIGD, Tremor, endocrine system diseases, genetic structures, Parkinson's disease, Clinical Biochemistry, Tremolor, Nervous System Diseases::Central Nervous System Diseases::Nervous System Diseases::Central Nervous System Diseases::Movement Disorders::Parkinsonian Disorders::Nervous System Diseases::Parkinson Disease [DISEASES], enfermedades del sistema nervioso::manifestaciones neurológicas::discinesias::temblor [ENFERMEDADES], Article, eye diseases, Fenotip, R5-920, Genetic Phenomena::Phenotype [PHENOMENA AND PROCESSES], Parkinson, Malaltia de, fenómenos genéticos::fenotipo [FENÓMENOS Y PROCESOS], Pathological Conditions, Signs and Symptoms::Signs and Symptoms::Neurologic Manifestations::Dyskinesias::Tremor [DISEASES]
Abstract

[Background and objective] Diplopia is relatively common in Parkinson’s disease (PD) but is still understudied. Our aim was to analyze the frequency of diplopia in PD patients from a multicenter Spanish cohort, to compare the frequency with a control group, and to identify factors associated with it., [Patients and Methods] PD patients who were recruited from January 2016 to November 2017 (baseline visit; V0) and evaluated again at a 2-year ± 30 days follow-up (V2) from 35 centers of Spain from the COPPADIS cohort were included in this longitudinal prospective study. The patients and controls were classified as “with diplopia” or “without diplopia” according to item 15 of the Non-Motor Symptoms Scale (NMSS) at V0, V1 (1-year ± 15 days), and V2 for the patients and at V0 and V2 for the controls., [Results] The frequency of diplopia in the PD patients was 13.6% (94/691) at V0 (1.9% in controls [4/206]; p < 0.0001), 14.2% (86/604) at V1, and 17.1% (86/502) at V2 (0.8% in controls [1/124]; p < 0.0001), with a period prevalence of 24.9% (120/481). Visual hallucinations at any visit from V0 to V2 (OR = 2.264; 95%CI, 1.269–4.039; p = 0.006), a higher score on the NMSS at V0 (OR = 1.009; 95%CI, 1.012–1.024; p = 0.015), and a greater increase from V0 to V2 on the Unified Parkinson’s Disease Rating Scale–III (OR = 1.039; 95%CI, 1.023–1.083; p < 0.0001) and Neuropsychiatric Inventory (OR = 1.028; 95%CI, 1.001–1.057; p = 0.049) scores were independent factors associated with diplopia (R2 = 0.25; Hosmer and Lemeshow test, p = 0.716)., [Conclusions] Diplopia represents a frequent symptom in PD patients and is associated with motor and non-motor severity., Martínez-Martin P. has received honoraria from National School of Public Health (ISCIII), Editori-al Viguera and Takeda Pharmaceuticals for lecturing in courses, and from the International Parkinson and Movement Disorder Society (MDS) for management of the Program on Rating Scales. Mir P. has received honoraria from AbbVie, Abbott, Allergan, Bial, Merz, UCB, and Zambon and have received grants from the Spanish Ministry of Economy and Competitiveness [PI16/01575], co-founded by ISCIII (Subdirección General de Evaluación y Fomento de la Investigación) and by Fondo Europeo de Desarrollo Regional (FEDER), the Consejería de Economía, Innovación, Ciencia y Empleo de la Junta de Andalucía [CVI-02526, CTS-7685], the Consejería de Salud y Bienestar Social de la Junta de Andalucía [ PI-0437-2012, PI-0471-2013], the Sociedad Andaluza de Neurología, the Jacques and Gloria Gossweiler Foundation, the Fundación Alicia Koplowitz, the Fundación Mutua Madrileña.

Published
2021

5. Predictors of clinically significant quality of life impairment in Parkinson's disease

Author

Garcia D, Fonticoba T, Cores C, Munoz G, Gonzalez J, Miro C, Suarez E, Jesus S, Aguilar M, Pastor P, Planellas L, Cosgaya M, Caldentey J, Caballol N, Legarda I, Vara J, Cabo I, Manzanares L, Aramburu I, Rivera M, Catalan M, Nogueira V, Puente V, de Arcos M, Borrue C, Vila B, Sauco M, Vela L, Escalante S, Cubo E, Padilla F, Castrillo J, Alonso P, Losada M, Ariztegui N, Gaston I, Clavero P, Kulisevsky J, Estrada M, Seijo M, Martinez J, Valero C, Kurtis M, de Fabregues O, Ardura J, Ordas C, Diaz L, McAfee D, Martinez-Martin P, Mir P, and COPPADIS Study Grp

Abstract

Quality of life (QOL) plays an important role in independent living in Parkinson's disease (PD) patients, being crucial to know what factors impact QoL throughout the course of the disease. Here we identified predictors of QoL impairment in PD patients from a Spanish cohort. PD patients recruited from 35 centers of Spain from the COPPADIS cohort from January 2016, to November 2017, were followed up during 2 years. Health-related QoL (HRQoL) and global QoL (GQoL) were assessed with the 39-item Parkinson's disease Questionnaire (PDQ-39) and the EUROHIS-QOL 8-item index (EUROHIS-QOL8), respectively, at baseline (V0) and at 24 months +/- 1 month (V2). Clinically significant QoL impairment was defined as presenting an increase (PDQ-39SI) or decrement (EUROHIS-QOL8) at V2 >= 10% of the score at baseline (V0). A comparison with a control group was conducted for GQoL. GQoL did not change significantly in PD patients (N = 507; p = 0.686) or in the control group (N = 119; p = 0.192). The mean PDQ-39SI was significantly increased in PD patients (62.7 +/- 8.5 years old; 58.8% males; N = 500) by 21.6% (from 16.7 +/- 13 to 20.3 +/- 16.4; p < 0.0001) at V2. Ninety-three patients (18.6%) presented a clinically significant HRQoL impairment at V2. To be younger (OR = 0.896; 95% CI 0.829-0.968; p = 0.006), to be a female (OR = 4.181; 95% CI 1.422-12.290; p = 0.009), and to have a greater increase in BDI-II (Beck Depression Inventory-II) (OR = 1.139; 95% CI 1.053-1.231; p = 0.001) and NMSS (Non-Motor Symptoms Scale) (OR = 1.052; 95% CI 1.027-1.113; p < 0.0001) total scores from V0 to V2 were associated with clinically significant HRQoL impairment at the 2-year follow-up (Hosmer-Lemeshow test, p = 0.665; R-2 = 0.655). An increase in >= 5 and >= 10 points of BDI-II and NMSS total score at V2 multiplied the probability of presenting clinically significant HRQoL impairment by 5 (OR = 5.453; 95% CI 1.663-17.876; p = 0.005) and 8 (OR = 8.217; 95% CI, 2.975-22.696; p = 0.002), respectively. In conclusion, age, gender, mood, and non-motor impairment were associated with clinically significant HRQoL impairment after the 2-year follow-up in PD patients.

Published
2021

6. Predictors of clinically significant quality of life impairment in Parkinson's disease

Author

Santos García, Diego, de Deus Fonticoba, Teresa, Cores Bartolomé, Carlos, Muñoz, G., Paz González, J. M., Martínez Miró, C., Suárez, E., Jesús, S., Aguilar Barberà, Miquel, Pastor, P., Planellas, L., Cosgaya, Marina, García Caldentey, J., Caballol, Nuria, Legarda, I., Hernández-Vara, Jorge, Cabo-Lopez, Iria, López Manzanares, L., González Aramburu, I., Ávila, Asunción, Catalán, M. J., Nogueira, V., Puente, V., Ruíz de Arcos, M., Borrué, Carmen, Solano Vila, B., Álvarez Sauco, M., Vela, Lydia, Escalante, Sonia, Cubo, Esther, Carrillo Padilla, Francisco, Martínez-Castrillo, Juan Carlos, Sánchez Alonso, P., Alonso Losada, M. G., López Ariztegui, N, Gastón, I., Clavero, P., Kulisevsky, Jaime, Blázquez Estrada, Marta, Seijo, M., Rúiz Martínez, J., Valero, C., Kurtis, M., Fàbregues-Boixar i Nebot, Oriol de, González-Ardura, J, Ordás, C., López Díaz, L. M., McAfee, D., Martinez-Martin, P., Mir, P., Adarmes, D. A., Almeria, Marta, Alonso-Cánovas, Araceli, Alonso Frech, Fernando, Alonso Redondo, Rubén, Álvarez, I., Aneiros Díaz, Á., Arnáiz, S., Arribas, S., Ascunce Vidondo, A., Bernardo Lambrich, N., Bejr-Kasem Marco, Helena, Botí, M. Ángeles, Buongiorno, M. T., Cabello González, C., Cámara, Ana, Canfield Medina, H., Carrillo, F., Casas, E., Cortina Fernández, A., Cots-Foraster, Anna, Crespo Cuevas, Ane Miren, Díez-Fairen, M., Dotor García-Soto, J., Erro, E., Estelrich Peyret, E., Fernández Guillán, N., Gámez, Pedro, Gallego, Miguel, García Campos, C., García Moreno, José Manuel, Gómez Garre, M. P., Gómez Mayordomo, V., González Aloy, J., González García, B., González Palmás, M. J., Toledo, G., Gabriel, R., Golpe Díaz, A., Grau Solá, M., Guardia, G., Horta, Andrea, Idoate Calderón, D., Infante, J., Labandeira, C., Labrador-Espinosa, Miguel A, Lacruz, F., Lage Castro, M., Lastres Gómez, S., López Seoane, B., Lucas del Pozo, S., Macías, Y., Mata, M., Martí Andres, G., Martí, M. J., Meitín, M. T., Menéndez González, M., Méndez del Barrio, C., Miranda Santiago, J., Casado, M., María, I., Moreno Diéguez, A., Novo Amado, A., Novo Ponte, S., Pagonabarraga Mora, Javier, Pareés, I., Pascual-Sedano, Berta María, Pérez Fuertes, A., Pérez Noguera, R., Planas-Ballvé, A., Prats, M. A., Prieto Jurczynska, C., Pueyo Morlans, M., Puig-Davi, Arnau, Redondo Rafales, N., Rodríguez Méndez, L., Rodríguez Pérez, A. B., Roldán, F., Sánchez-Carpintero, M., Sánchez Díez, G., Sánchez Rodríguez, A., Santacruz, P., Segundo Rodríguez, J. C., Sierra Peña, M., Tartari, J. P., Vargas, L., Villanueva, C., Vives-Pastor, B, Villar, M. D., Institut Català de la Salut, [Santos García D, Cores C, Muñoz G, Paz González JM, Martínez Miró C] CHUAC, Complejo Hospitalario Universitario de A Coruña, A Coruña, Spain. [de Deus Fonticoba T] CHUF, Complejo Hospitalario Universitario de Ferrol, A Coruña, Spain. [Hernández Vara J, de Fábregues O] Vall d’Hebron Hospital Universitari, Barcelona, Spain, Vall d'Hebron Barcelona Hospital Campus, Universidad de Cantabria, AbbVie Pharmaceuticals, Abbott Laboratories, Allergan Foundation, BIAL Foundation, Merz Pharma, UCB Pharma, Zambon, Ministerio de Economía y Competitividad (España), Instituto de Salud Carlos III, European Commission, Junta de Andalucía, Sociedad Andaluza de Neurología, Jacques and Gloria Gossweiler Foundation, Fundación Alicia Koplowitz, and Fundación Mutua Madrileña

Subjects
Quality of life, Qualitat de vida--Avaluació, Parkinson's disease, Parkinson, Malaltia de - Prognosi, Nervous System Diseases::Nervous System Diseases::Nervous System Diseases::Neurodegenerative Diseases::Parkinson Disease [DISEASES], Article, humanities, Environment and Public Health::Public Health::Epidemiologic Measurements::Demography::Health Status::Quality of Life [HEALTH CARE], Cellular and Molecular Neuroscience, enfermedades del sistema nervioso::enfermedades del sistema nervioso::enfermedades del sistema nervioso::enfermedades neurodegenerativas::enfermedad de Parkinson [ENFERMEDADES], Neurology, Pathological Conditions, Signs and Symptoms::Pathologic Processes::Disease Attributes::Disease Progression::Clinical Deterioration [DISEASES], Neurology. Diseases of the nervous system, Neurology (clinical), Parkinson, Malaltia de, RC346-429, afecciones patológicas, signos y síntomas::procesos patológicos::atributos de la enfermedad::progresión de la enfermedad::deterioro clínico [ENFERMEDADES], Qualitat de vida - Avaluació, ambiente y salud pública::salud pública::medidas epidemiológicas::demografía::estado de salud::calidad de vida [ATENCIÓN DE SALUD]
Abstract

COPPADIS Study Group., Quality of life (QOL) plays an important role in independent living in Parkinson’s disease (PD) patients, being crucial to know what factors impact QoL throughout the course of the disease. Here we identified predictors of QoL impairment in PD patients from a Spanish cohort. PD patients recruited from 35 centers of Spain from the COPPADIS cohort from January 2016, to November 2017, were followed up during 2 years. Health-related QoL (HRQoL) and global QoL (GQoL) were assessed with the 39-item Parkinson’s disease Questionnaire (PDQ-39) and the EUROHIS-QOL 8-item index (EUROHIS-QOL8), respectively, at baseline (V0) and at 24 months ± 1 month (V2). Clinically significant QoL impairment was defined as presenting an increase (PDQ-39SI) or decrement (EUROHIS-QOL8) at V2 ≥ 10% of the score at baseline (V0). A comparison with a control group was conducted for GQoL. GQoL did not change significantly in PD patients (N = 507; p = 0.686) or in the control group (N = 119; p = 0.192). The mean PDQ-39SI was significantly increased in PD patients (62.7 ± 8.5 years old; 58.8% males; N = 500) by 21.6% (from 16.7 ± 13 to 20.3 ± 16.4; p, Mir P. has received honoraria from AbbVie, Abbott, Allergan, Bial, Merz, UCB and Zambon and have received grants from the Spanish Ministry of Economy and Competitiveness [PI16/01575] co-founded by ISCIII (Subdirección General de Evaluación y Fomento de la Investigación) and by Fondo Europeo de Desarrollo Regional (FEDER), the Consejería de Economía, Innovación, Ciencia y Empleo de la Junta de Andalucía [CVI-02526, CTS-7685], the Consejería de Salud y Bienestar Social de la Junta de Andalucía [PI-0437-2012, PI-0471-2013], the Sociedad Andaluza de Neurología, the Jacques and Gloria Gossweiler Foundation, the Fundación Alicia Koplowitz, the Fundación Mutua Madrileña.

Published
2021

7. Mood in Parkinson's disease: From early- to late-stage disease

Author

Santos-Garcia D, De Deus F, Cores B, Valdes A, Suarez C, Aneiros A, Jesus S, Aguilar M, Pastor P, Planellas L, Cosgaya M, Garcia C, Caballol N, Legarda I, Hernandez V, Cabo I, Lopez M, Gonzalez A, Avila R, Jose C, Nogueira V, Puente V, Garcia M, Borrue C, Solano V, Alvarez S, Vela L, Escalante S, Cubo E, Carrillo P, Martinez C, Sanchez A, Alonso L, Lopez A, Gaston I, Kulisevsky J, Blazquez E, Seijo M, Ruiz M, Valero C, Kurtis M, de Fabregues-Boixar O, Prieto J, Lopez D, McAfee D, Mir P, and COPPADIS Study Grp

Subjects
s disease, quality of life, mood, depression, disease duration, Parkinson&apos, Parkinson's disease
Abstract

BACKGROUND: Although depression is known to be frequent in Parkinson's disease (PD), it is unclear how mood can change and/or impact on patient's quality of life (QoL) over time. Our aim was to analyze the frequency of depression, mood related factors and the contribution of mood to a patient's QoL perception in regard to disease duration. METHODS: PD patients recruited from the COPPADIS cohort from January 2016 to November 2017 were included in this cross-sectional study. Three groups were defined

Published
2021

10. High ultrasensitive serum C-reactive protein may be related to freezing of gait in Parkinson's disease patients

Author

Santos-Garcia, D, Fonticoba, TD, Castro, ES, Diaz, AA, Gonzalez, JMP, Panceiras, MJF, Sancho, CG, Jesus, S, Mir, P, Aguilar, M, Pastor, P, Vara, JH, de Fabregues-Boixar, O, Puente, V, Cuevas, AC, Gonzalez-Aramburu, I, Infante, J, Padilla, FC, Pueyo, M, Escalante, S, Bernardo, N, Solano, B, Foraster, AC, Martinez-Martin, P, Astrid, DA, Almeria, M, Losada, MGA, Canovas, AA, Frech, FA, Sauco, MA, Arnaiz, S, Arribas, S, Vidondo, AA, Avila, MA, Bejr-Kasem, H, Estrada, MB, Boti, M, Borrue, C, Gonzalez, CC, Lopez, IC, Caballol, N, Lorenzo, AC, Carrillo, F, Casas, E, Catalan, MJ, Clavero, P, Fernandez, AC, Cubo, E, Diez-Fairen, M, Erro, E, Peyret, EE, Guillan, NF, Gamez, P, Gallego, M, Caldentey, JG, Campos, CG, Moreno, JMG, Gaston, I, Garre, MPG, Aloy, JG, Ardura, JG, Garcia, BG, Palmas, MJG, Toledo, GRG, Diaz, AG, Sola, MG, Guardia, G, Horta-Barba, A, Kulisevsky, J, Kurtis, M, Labandeira, C, Labrador, MA, Lacruz, F, Castro, ML, Legarda, I, Ariztegui, NL, Diaz, LML, Manzanares, LL, Seoane, BL, Macias, Y, Mata, M, Andres, GM, Marti, MJ, Castrillo, JCM, McAfee, D, Meitin, MT, Gonzalez, MM, del Barrio, CM, Santiago, JM, Casado, MIM, Dieguez, AM, Nogueira, V, Amado, AN, Ponte, SN, Ordas, C, Pagonabarraga, J, Parees, I, Pascual-Sedano, B, Fuertes, AP, Noguera, RP, Planellas, L, Prats, MA, Jurczynska, CP, Rafales, NR, Mendez, LR, Perez, ABR, Roldan, F, De Arcos, MR, Martinez, JR, Alonso, PS, Sanchez-Carpintero, M, Diez, GS, Rodriguez, AS, Santacruz, P, Rodriguez, JCS, Seijo, M, Serarols, A, Pena, MS, Tartari, JP, Valero, C, Vargas, L, Gomez, RV, Vela, L, Villanueva, C, Vives, B, and Villar, MD

Subjects
Inflammation, genetic structures, Parkinson's disease, Freezing, C-Reactive protein, Gait
Abstract

C-reactive protein (CRP) is a biomarker of systemic inflammation that has been linked to accelerated decline in walking speed in older adults. The aim of the present study was to compare the CRP levels of PD patients with vs patients without freezing of gait (FOG). Patients and controls participating in the COPPADIS-2015 study that performed blood extraction for determining molecular serum biomarkers were included. Patients with FOG were identified as those with a score of 1 or greater on item-3 of the Freezing of Gait Questionnaire (FOG-Q). Immunoassay was used for determining ultrasensitive CRP (US-CRP) level (mg/dL). In the PD group (n = 225; 61.8 +/- 9.5 years old, 61.8% males), 32% of the patients presented FOG but none in the control group (n = 65; 60.3 +/- 6.1 years old, 56.9% males) (p < 0.0001). Differences in US-CRP level were significant in patients with FOG vs patients without FOG and vs controls (0.31 +/- 0.52 vs 0.16 +/- 0.21 vs 0.21 +/- 0.22; p = 0.04). Significant differences were also observed between patients with vs without FOG (p = 0.001) but not between patients and controls (p = 0.163). US-CRP level was related to FOG (OR = 4.369; 95% CI 1.105-17.275; p = 0.036) along with H&Y (OR = 2.974; 95% CI 1.113-7.943; p = 0.030) and non-motor symptoms burden (NMSS total score; OR = 1.017; 95% CI 1.005-1.029; p = 0.006) after adjusting for age, gender, disease duration, equivalent daily levodopa dose, number of non-antiparkinsonian drugs per day, motor fluctuations, cognition, motor phenotype, and chronic use of anti-inflammatory drugs. The present study suggests that serum US-CRP level is related to FOG in PD patients. Inflammation could be linked to FOG development.

Published
2019

11. COPPADIS-2015 (COhort of Patients with PArkinson's DIsease in Spain, 2015): an ongoing global Parkinson's disease project about disease progression with more than 1000 subjects included. Results from the baseline evaluation

Author

Garcia, DS, Jesus, S, Aguilar, M, Planellas, LL, Caldentey, JG, Caballol, N, Legarda, I, Vara, JH, Cabo, I, Manzanares, LL, Aramburu, IG, Rivera, MAA, Catalan, MJ, Diaz, LL, Puente, V, Moreno, JMG, Borrue, C, Vila, BS, Sauco, MA, Vela, L, Escalante, S, Cubo, E, Padilla, FC, Castrillo, JCM, Alonso, PS, Losada, MGA, Ariztegui, NL, Gaston, I, Kulisevsky, J, Gonzalez, MM, Seijo, M, Martinez, JR, Valero, C, Kurtis, M, de Fabregues-Boixar, O, Ardura, JG, Jurczynska, CP, Martinez-Martin, P, Mir, P, Astrid, DA, Almeria, M, Canovas, AA, Frech, FA, Diaz, AA, Arnaiz, S, Arribas, S, Vidondo, AA, Lambrich, NB, Bejr-Kasem, H, Estrada, MB, Boti, M, Gonzalez, CC, Lorenzo, AC, Carrillo, F, Casas, E, Clavero, P, Fernandez, AC, Foraster, AC, Cuevas, AC, Fonticoba, TD, Diez-Fairen, M, Erro, E, Peyret, EE, Guillan, NF, Gamez, P, Gallego, M, Campos, CG, Garre, MPG, Aloy, JG, Garcia, BG, Palmas, MJG, Toledo, GRG, Diaz, AG, Sola, MG, Guardia, G, Horta-Barba, A, Infante, J, Labandeira, C, Labrador, MA, Lacruz, F, Castro, ML, Seoane, BL, Macias, Y, Mata, M, Andres, GM, Marti, MJ, McAfee, D, Meitin, MT, del Barrio, CM, Santiago, JM, Casado, MIM, Dieguez, AM, Nogueira, V, Amado, AN, Ponte, SN, Ordas, C, Pagonabarraga, J, Parees, I, Pascual-Sedano, B, Pastor, P, Fuertes, AP, Noguera, RP, Prats, MA, Morlans, MP, Rafales, NR, Mendez, LR, Perez, ABR, Roldan, F, De Arcos, MR, Sanchez-Carpintero, M, Diez, GS, Rodriguez, AS, Santacruz, P, Rodriguez, JCS, Serarols, A, Pena, MS, Castro, ES, Tartari, JP, Vargas, L, Gomez, RV, Villanueva, C, Vives, B, and Villar, MD

Subjects
motor fluctuations, quality of life, mood, Parkinson's disease, gait, non-motor symptoms
Abstract

Background and purpose In Parkinson's disease (PD), the course of the disorder is highly variable between patients. Well-designed, prospective studies for identifying PD progression biomarkers are necessary. Our aim was to show the results of baseline evaluations of an ongoing global PD project, COPPADIS-2015 (Cohort of Patients with PArkinson's DIsease in Spain, 2015). Methods This was an observational, descriptive, nationwide study (Spain). The recruitment period ended in October 2017. Baseline evaluation included more than 15 validated scales and complementary studies in a subgroup of participants. Results In total, 1174 subjects from 35 centres were considered valid for baseline analysis: 694 patients (62.6 +/- 8.9 years old, 60.3% males), 273 caregivers (58.5 +/- 11.9 years old, 31.8% males) and 207 controls (61 +/- 8.3 years old, 49.5% males). The mean disease duration was 5.5 +/- 4.4 years. Hoehn and Yahr stage was 1 or 2 in 90.7% of the patients whilst 33.9% and 18.1% of them presented motor fluctuations and dyskinesias, respectively. The mean Non-Motor Symptoms Scale total score was 45.4 +/- 38.1, and 30.4% of the patients presented cognitive impairment, 16.1% major depression, 12.7% impulse control disorder, 7.2% compulsive behaviour, 57.2% pain and 13.2% falls. Compared to the control group, PD patients presented a significantly higher burden of non-motor symptoms and a worse quality of life. More than 300 subjects conducted complementary studies (serum biomarkers, genetic and neuroimaging). Conclusions Parkinson's disease is a complex disorder and different non-motor symptoms are frequently present and are more prevalent than in controls. In real clinical practice it is important to ask for them.

Published
2019

12. Non-motor symptoms burden, mood, and gait problems are the most significant factors contributing to a poor quality of life in non-demented Parkinson's disease patients: Results from the COPPADIS Study Cohort

Author

Garcia, D, Fonticoba, T, Castro, E, Borrue, C, Mata, M, Vila, B, Foraster, A, Sauco, M, Perez, A, Vela, L, Macias, Y, Escalante, S, Esteve, P, Villarroya, S, Cubo, E, Casas, E, Arnaiz, S, Padilla, F, Morlans, M, Mir, P, Martinez-Martin, P, Adarmes, A, Almeria, M, Losada, G, Canovas, A, Alonso-Frech, F, Arribas, S, Vidondo, A, Aguilar, M, Avila, M, Lambrich, N, Bejr-Kasem, H, Estrada, M, Boti, M, Gonzalez, C, Lopez, I, Caballol, N, Lorenzo, A, Carrillo, F, Catalan, M, Clavero, P, Fernandez, A, Cuevas, A, de Fabregues-Boixar, O, Diez-Fairen, M, Erro, E, Peyret, E, Guinan, N, Gamez, P, Gallego, M, Caldentey, J, Campos, C, Moreno, J, Gaston, I, Garre, M, Aloy, J, Gonzalez-Aramburu, I, Ardura, J, Garcia, B, Palmas, M, Toledo, G, Diaz, A, Sola, M, Guardia, G, Hernandez-Vara, J, Barba, A, Infante, J, Jesus, S, Kulisevsky, J, Kurtis, M, Labandeira, C, Labrador, M, Lacruz, F, Castro, M, Legarda, I, Ariztegui, N, Diaz, L, Manzanares, L, Seoane, B, Andres, G, Marti, M, Martinez-Castrillo, J, McAfee, D, Meitin, M, Gonzalez, M, del Barrio, C, Santiago, J, Casado, M, Dieguez, A, Nogueira, V, Amado, A, Ponte, S, Ordas, C, Pagonabarraga, J, Parees, I, Pascual-Sedano, B, Pastor, P, Fuertes, A, Noguera, R, Planellas, L, Fuster, J, Prats, M, Jurczynska, C, Puente, V, Rafales, N, Mendez, L, Roldan, F, De Arcos, M, Martinez, J, Alonso, P, Sanchez-Carpintero, M, Diez, G, Rodriguez, A, Santacruz, P, Rodriguez, J, Seijo, M, Serarols, A, Pena, M, Tartari, J, Vargas, L, Gomez, R, Villanueva, C, Vives, B, Villar, M, and Coppadis Study Grp

Subjects
Quality of life, Parkinson's disease, Mood, Non-motor symptoms, Gait, humanities, Motor fluctuations
Abstract

Objective: To identify factors related to a poor health-related and global quality of life (QoL) in a cohort of nondemented Parkinson's disease (PD) patients and compare to a control group. Methods: The data correspond to the baseline evaluation of the COPPADIS-2015 Study, an observational, 5-year follow-up, multicenter, evaluation study. Three instruments were used to assess QoL: (1) the 39-item Parkinson's disease Questionnaire (PDQ-39), (2) a subjective rating of global QoL (PQ-10), and (3) the EUROHIS-QOL 8-item index (EUROHIS-QOL8). Multiple linear regression methods were used to evaluate the direct impact of different variables on these QoL measures. Results: QoL was worse in PD patients (n = 692; 62.6 +/- 8.9 years old, 60.3% males) than controls (n = 206; 61 +/- 8.3 years old, 49.5% males): PDQ-39, 17.1 +/- 13.5 vs 4.4 +/- 6.3 (p < 0.0001); PQ-10, 7.3 +/- 1.6 vs 8.1 +/- 1.2 (p < 0.0001); EUROHIS-Q0L8, 3.8 +/- 0.6 vs 4.2 +/- 0.5 (p < 0.0001). A high correlation was observed between PDQ-39 and Non-Motor Symptoms Scale (NMSS) (r = 0.72; p < 0.0001), and PDQ-39 and Beck Depression Inventory-II (BDI-II) (r = 0.65; p < 0.0001). For health-related QoL (PDQ-39), non-motor symptoms burden (NMSS), mood (BDI-II), and gait problems (Freezing Of Gait Questionnaire [FOGQ]) provided the highest contribution to the model (beta = 0.32, 0.28, and 0.27, respectively; p < 0.0001); whereas mood and gait pro- blems contributed the most to global QoL (PQ-10, beta = -0.46 and -0.21, respectively; EUROHIS-QOL8, beta = - 0.44 and - 0.23, respectively). Conclusions: QoL is worse in PD patients than in controls. Mood, non-motor symptoms burden, and gait problems seem to be the most relevant factors affecting health-related and global perceived QoL in non-demented PD patients.

Published
2019

13. Non-motor symptoms burden, mood, and gait problems are the most significant factors contributing to a poor quality of life in non-demented Parkinson's disease patients: Results from the COPPADIS Study Cohort

Author

Santos García, D., primary, de Deus Fonticoba, T., additional, Suárez Castro, E., additional, Borrué, C., additional, Mata, M., additional, Solano Vila, B., additional, Cots Foraster, A., additional, Álvarez Sauco, M., additional, Rodríguez Pérez, A.B., additional, Vela, L., additional, Macías, Y., additional, Escalante, S., additional, Esteve, P., additional, Reverté Villarroya, S., additional, Cubo, E., additional, Casas, E., additional, Arnaiz, S., additional, Carrillo Padilla, F., additional, Pueyo Morlans, M., additional, Mir, P., additional, Martinez-Martin, P., additional, Adarmes, A.D., additional, Almeria, M., additional, Alonso Losada, G., additional, Alonso Cánovas, A., additional, Alonso-Frech, F., additional, Arribas, S., additional, Ascunde Vidondo, A., additional, Aquilar, M., additional, Ávila, M.A., additional, Bernardo Lambrich, N., additional, Bejr-Kasem, H., additional, Blázquez Estrada, M., additional, Botí, M., additional, Cabello González, C., additional, Cabo López, I., additional, Caballol, N., additional, Cámara Lorenzo, A., additional, Carrillo, F., additional, Catalán, M.J., additional, Clavero, P., additional, Cortina Fernández, A., additional, Crespo Cuevas, A., additional, de Fábregues-Boixar, O., additional, Díez-Fairen, M., additional, Erro, E., additional, Estelrich Peyret, E., additional, Fernández Guillán, N., additional, Gámez, P., additional, Gallego, M., additional, García Caldentey, J., additional, García Campos, C., additional, García Moreno, J.M., additional, Gastón, I., additional, Gómez Garre, M.P., additional, González Aloy, J., additional, González-Aramburu, I., additional, González Ardura, J., additional, González García, B., additional, González Palmás, M.J., additional, González Toledo, G.R., additional, Golpe Díaz, A., additional, Grau Solá, M., additional, Guardia, G., additional, Hernández-Vara, J., additional, Horta Barba, A., additional, Infante, J., additional, Jesús, S., additional, Kulisevsky, J., additional, Kurtis, M., additional, Labandeira, C., additional, Labrador, M.A., additional, Lacruz, F., additional, Lage Castro, M., additional, Legarda, I., additional, López Ariztegui, N., additional, López Díaz, L.M., additional, López Manzanares, L., additional, López Seoane, B., additional, Martí Andres, G., additional, Martí, M.J., additional, Martínez-Castrillo, J.C., additional, McAfee, D., additional, Meitín, M.T., additional, Menéndez González, M., additional, Méndez del Barrio, C., additional, Miranda Santiago, J., additional, Morales Casado, M.I., additional, Moreno Diéguez, A., additional, Nogueira, V., additional, Novo Amado, A., additional, Novo Ponte, S., additional, Ordás, C., additional, Pagonabarraga, J., additional, Pareés, I., additional, Pascual-Sedano, B., additional, Pastor, P., additional, Pérez Fuertes, A., additional, Pérez Noguera, R., additional, Planellas, Ll, additional, Pol Fuster, J., additional, Prats, M.A., additional, Prieto Jurczynska, C., additional, Puente, V., additional, Redondo Rafales, N., additional, Rodríguez Méndez, L., additional, Roldán, F., additional, Ruíz De Arcos, M., additional, Ruíz Martínez, J., additional, Sánchez Alonso, P., additional, Sánchez-Carpintero, M., additional, Sánchez Díez, G., additional, Sánchez Rodríguez, A., additional, Santacruz, P., additional, Segundo Rodríguez, J.C., additional, Seijo, M., additional, Serarols, A., additional, Sierra Peña, M., additional, Tartari, J.P., additional, Vargas, L., additional, Vázquez Gómez, R., additional, Villanueva, C., additional, Vives, B., additional, and Villar, M.D., additional

Published
2019
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14. Non‐motor symptom burden is strongly correlated to motor complications in patients with Parkinson's disease.

Author

Santos‐García, D., Deus Fonticoba, T., Suárez Castro, E., Aneiros Díaz, A., McAfee, D., Catalán, M. J., Alonso‐Frech, F., Villanueva, C., Jesús, S., Mir, P., Aguilar, M., Pastor, P., García Caldentey, J., Esltelrich Peyret, E., Planellas, L. L., Martí, M. J., Caballol, N., Hernández Vara, J., Martí Andrés, G., and Cabo, I.

Subjects
PARKINSON'S disease, DISEASE duration, LOGISTIC regression analysis, ODDS ratio, REGRESSION analysis
Abstract

Background and purpose: The objective of this study was to analyze the relationship between motor complications and non‐motor symptom (NMS) burden in a population of patients with Parkinson's disease (PD) and also in a subgroup of patients with early PD. Methods: Patients with PD from the COPPADIS cohort were included in this cross‐sectional study. NMS burden was defined according to the Non‐Motor Symptoms Scale (NMSS) total score. Unified Parkinson's Disease Rating Scale (UPDRS) part IV was used to establish motor complication types and their severity. Patients with ≤5 years of symptoms from onset were included as patients with early PD. Results: Of 690 patients with PD (62.6 ± 8.9 years old, 60.1% males), 33.9% and 18.1% presented motor fluctuations and dyskinesia, respectively. The NMS total score was higher in patients with motor fluctuations (59.2 ± 43.1 vs. 38.3 ± 33.1; P < 0.0001) and dyskinesia (63.5 ± 40.7 vs. 41.4 ± 36.3; P < 0.0001). In a multiple linear regression model and after adjustment for age, sex, disease duration, Hoehn & Yahr stage, UPDRS‐III score and levodopa equivalent daily dose, UPDRS‐IV score was significantly related to a higher NMSS total score (β = 0.27; 95% confidence intervals, 2.81–5.61; P < 0.0001), as it was in a logistic regression model on dichotomous NMSS total score (≤40, mild or moderate vs. >40, severe or very severe) (odds ratio, 1.31; 95% confidence intervals, 1.17–1.47; P < 0.0001). In the subgroup of patients with early PD (n = 396; mean disease duration 2.7 ± 1.5 years), motor fluctuations were frequent (18.1%) and similar results were obtained. Conclusions: Motor complications were frequent and were associated with a greater NMS burden in patients with PD even during the first 5 years of disease duration. [ABSTRACT FROM AUTHOR]

Published
2020
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21. Radio frequency coaxial high pass filter Patent

Author

Bailey, J. W and Mcafee, D. F

Subjects
Electronic Equipment
Abstract

Radio frequency coaxial filter to provide dc isolation and low frequency signal rejection in audio range

Published
1968

26. The ionic basis of adenosine receptor actions on post‐ganglionic neurones in the rat.

Author

Henon, B K and McAfee, D A

Abstract

Adenosine inhibited three Ca2+‐dependent potentials recorded intracellularly from post‐ganglionic neurones of the rat superior cervical ganglion. A shoulder on the falling phase of the action potential elicited in normal Locke solution, a hyperpolarizing after‐potential (h.a.p.) that follows the spike, and a regenerative Ca2+ spike elicited in Locke solution containing TTX and TEA were all reversibly inhibited by adenosine analogues in a dose‐dependent fashion. The maximum rate of rise of the Ca2+ spike (dV/dt) was markedly reduced suggesting that the underlying mechanism of adenosine action is inhibition of the Ca2+ conductance mechanism and thus, the voltage‐sensitive Ca2+ current. I/V curves in low Ca2+, high Mg2+, TTX, TEA, and Co2+ to block the Ca2+ current show no change in resistance in the presence of 2‐chloroadenosine. The actions of adenosine were nearly eliminated in the presence of 1 mM‐theophylline, an adenosine receptor antagonist. The order of agonist potency on the inhibition of the h.a.p. was: N‐6‐[L‐phenylisopropyl] adenosine (L‐PIA) greater than 2‐chloroadenosine greater than adenosine greater than cyclic AMP = 5' AMP. The concentration of L‐PIA which produced a half‐maximal effect (EC50) was 0.5 microM and that for cyclic AMP was 100 microM. Dipyridamole, an adenosine uptake blocker, potentiated the effects of low concentrations of adenosine and shifted the dose‐response curve for adenosine towards that of 2‐chloroadenosine (EC50 = 1 microM). These results are consistent with the concept of an external adenosine receptor, but we are unable to assign a receptor subtype. Cyclic AMP mimicked the effects of adenosine, but these effects were eliminated by adenosine deaminase. Our results suggest that the electrogenic effects of bath‐applied cyclic AMP may result from the metabolism of cyclic AMP to adenosine by ganglionic tissue. We conclude that adenosine activates a receptor on the neuronal cell surface to inhibit the voltage‐dependent Ca2+ current.

Published
1983
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27. Neurophysiology and pharmacology of long‐term potentiation in the rat sympathetic ganglion.

Author

Briggs, C A, Brown, T H, and McAfee, D A

Abstract

Brief tetanic stimulation of the preganglionic nerve induced a persistent potentiation of nicotinic synaptic transmission in the rat superior cervical sympathetic ganglion. Quantitative measurements of the post‐tetanic increase in synaptic efficacy revealed two distinct time courses. The early, rapidly decaying component, termed post‐tetanic potentiation (p.t.p.), had a decay time constant of 2‐3 min, as reported elsewhere. The duration of the more persistent component, called long‐term potentiation (l.t.p.), was extremely temperature dependent, lasting much longer at 32 degrees C than at 22 degrees C. In half of the experiments performed at 32 degrees C, l.t.p. showed no detectable decay over the course of 1 h or more after a brief tetanic stimulation. Other experiments were conducted at 22 degrees C. The induction of l.t.p. was dependent on the extracellular [Ca2+]. Transient elevation of the extracellular [K+] also produced a long‐term enhancement of synaptic efficacy, and this effect was also Ca2+ dependent. The tetani that were effective in inducing l.t.p. (5‐20 Hz for 5‐20 s) were well within the physiological range of preganglionic activity. The magnitude and time course were related to frequency and duration of stimulation. The occurrence of l.t.p. was restricted to those preganglionic fibres that were tetanically stimulated. This lack of heterosynaptic or generalized effects was demonstrated by splitting the preganglionic nerve into two branches that could be independently tested and conditioned. Physiological activation of muscarinic or nicotinic receptors apparently does not play an essential role in causing ganglionic l.t.p., which is expressed as an enhancement of nicotinic transmission. A muscarinic antagonist (2 microM‐atropine) did not block l.t.p. Preganglionic stimulation induced l.t.p. even when a high concentration of a nicotinic antagonist (3 mM‐hexamethonium) was present during the tetanic stimulation. Furthermore, bath application of a cholinergic agonist (100‐1000 microM‐carbachol) could not substitute for tetanic stimulation in provoking l.t.p. Activation of adrenergic receptors also appeared not to play an essential role. Neither a beta‐adrenergic antagonist (10 microM‐sotolol or 1 microM‐propranolol) nor an alpha‐adrenergic antagonist (1 microM‐phentolamine) had any significant effect on the magnitude or duration of l.t.p. The results indicate that ganglionic l.t.p. is a Ca2+‐ and temperature‐dependent process that can be created independently of the activation of nicotinic, muscarinic or adrenergic receptors.

Published
1985
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28. Long‐term potentiation of synaptic acetylcholine release in the superior cervical ganglion of the rat.

Author

Briggs, C A, McAfee, D A, and McCaman, R E

Abstract

The release of endogenous acetylcholine (ACh) from the in vitro rat superior cervical ganglion was measured by assaying the bathing medium. Simultaneously, synaptic transmission in the ganglion was assessed by recording post‐ganglionic compound action potentials. A brief period of tetanic preganglionic stimulation (20 Hz for 20 s) induced a long‐term potentiation of the post‐ganglionic compound action potential. The same tetanic stimulation also consistently induced a long‐term potentiation of stimulated ACh release. Spontaneous (non‐stimulated) ACh release was not enhanced after tetanic stimulation. The content of ACh in the ganglion was not measurably increased after tetanic stimulation. These results suggest that the long‐term increase in synaptic efficacy is due, at least in part, to an increase in the amount of ACh released by the afferent impulse.

Published
1985
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29. Modulation of cyclic nucleotide levels in peripheral nerve without effect on resting or compound action potentials.

Author

Horn, J P and McAfee, D A

Abstract

1. Cyclic nucleotide levels and compound action potential magnitudes were measured in frog sciatic nerves following exposure to carbachol, isoprenaline and cyclic nucleotide related substances. 2. The resting cyclic AMP level was 2‐4 p‐mole/mg protein and the cyclic GMP level was 0‐27 p‐mole/mg protein in desheathed nerves. 3. Isoprenaline (100 micrometer) caused a twofold increase in cyclic AMP without affecting cyclic GMP levels. Carbachol (100 micrometer) caused a twofold increase in cyclic GMP without affecting cyclic AMP levels. 4. The phosphodiesterase inhibitor theophylline (5 mM) augmented both cyclic AMP and cyclic GMP. 5. The magnitude of the resting or compound action potential was not affected by isoprenaline, carbachol, or phosphodiesterase inhibitors. 6. The cyclic nucleotides and their butyryl derivatives did not affect the magnitude of the resting or compound action potential, either when applied alone or in the presence of a phosphodiesterase inhibitor. 7. In contrast to sympatic tissue we conclude that hormone mediated cyclic nucleotide metabolism in peripheral nerve is unrelated to control of axonal excitability.

Published
1977
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30. Calcium‐dependent potentials in the mammalian sympathetic neurone.

Author

McAfee, D A and Yarowsky, P J

Abstract

1. Intracellular recordings from post‐ganglionic neurones of the rat superior cervical ganglion revealed two non‐synaptic potentials dependent upon Ca2+, a hyperpolarizing afterpotential (h.a.p.) and a tetrodotoxin (TTX)‐insensitive spike. 2. The h.a.p. followed regeneration discharge of the membrane potential in normal and TTX‐containing Locke solution. 3. The h.a.p. appeared to arise from an increased K+ conductance because it was associated with a decrease in input resistance, reversed at ‐90 mV, and was proportional in magnitude to the extracellular K+ concentration. 4. Tetraethylammonium (TEA) and 4‐aminopyridine (4‐AP) apparently antagonized a voltage‐sensitive K+ conductance because they broadened the action potential. However, these substances reduced only slightly the peak amplitude and earliest phases of the h.a.p. 5. The TTX‐insensitive spike was most apparent when TEA was present and was invariably followed by an h.a.p. with a magnitude proportional to that of the spike. 6. The magnitude of the h.a.p. and the TTX‐insensitive spike was directly proportional to the external Ca2+ concentration and was antagonized by Co2+ and Mn2+ in a dose‐dependent fashion. 7. In normal Locke solution, Ba2+ antagonized the h.a.p. and allowed the neurone to sustain discharge during prolonged depolarization. In Locke solution containing TTX and TEA, Ba2+ reduced the magnitude of the h.a.p. but greatly increased the duration of the TTX‐insensitive spike. 8. The h.a.p. was not significantly affected by altering external Cl‐ concentration and the TTX‐insensitive spike was not reduced by altering external Na+ concentration. 9. It is concluded that the post‐ganglionic neurone supports a regenerative Ca2+ conductance mechanism which in turn triggers an increased K+ conductance. The h.a.p. appears to result from outward K+ current in both a Ca2+ and voltage‐dependent fashion.

Published
1979
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31. Alpha‐drenergic inhibition of calcium‐dependent potentials in rat sympathetic neurones.

Author

Horn, J P and McAfee, D A

Abstract

1. Post‐ganglionic neurones of the rat superior cervical ganglion were studied in vitro (21‐26 degrees C) using single intracellular micro‐electrode methods. 2. Three Ca2+‐dependent potentials were studied: the shoulder on the normal action potential, the hyperpolarizing afterpotential (h.a.p.), and th Ca2+ spike. 3. Bath‐applied noradrenaline reversibly inhibited these Ca2+‐dependent potentials. The EC50 for inhibition of peak h.a.p. amplitude was about 1 microM. The order of catetholamine potency was: L‐adrenaline > L‐noradrenaline > D‐noradrenaline congruent to dopamine > DL‐isoprenaline. Phentolamine (10 microM), an alpha‐blocker, but not MJ‐1999 (10 microM), a beta‐blocker, antagonized the action of noradrenaline. 4. Noradrenaline (10 microM) hyperpolarized most neurones (1‐6 mV) studied, with no detectable change in resting membrane conductance. 5. Superfusion with low external Ca2+ and high Mg2+ mimicked the effect of noradrenaline. Either procedure alone antagonized the h.a.p. conductance increase but did not alter the h.a.p. reversal potential. However, in the presence of low Ca2+, high Mg2+, the remaining action potential and h.a.p. were not further reduced by noradrenaline. 6. The Ca2+‐dependent shoulder of the action potential did not appear dependent upon GK. Noradrenaline and low Ca2+ antagonized the shoulder when enhanced by TEA+ or Ba2+. 7. Both the rate of rise and amplitude of the Ca2+ spike were antagonized by noradrenaline. 8. We propose that activation of an alpha‐adrenoceptor inhibits a voltage‐sensitive Ca2+ conductance (GCa(V)), thereby reducing the inward Ca2+ current which may generate the noraml action potential shoulder and the rising phase of the Ca2+ spike. Reduction of Ca2+ current would also reduce the Ca2+‐dependent portion of outward K+ current underlying the h.a.p.

Published
1980
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32. Long‐term potentiation at nicotinic synapses in the rat superior cervical ganglion.

Author

Briggs, C A and McAfee, D A

Abstract

1. Nicotinic fast excitatory postsynaptic potentials (fast EPSPs) were recorded intracellularly from postganglionic neurones in the isolated rat superior cervical ganglion. 2. An hours‐long potentiation of the fast EPSP could be induced by brief tetanic stimulation of the preganglionic nerve (5 Hz for 5 s to 20 Hz for 20 s). While long‐term potentiation (LTP) can be detected in every ganglion by extracellular techniques, LTP was induced in only two‐thirds of the nicotinic synaptic responses. 3. Muscarinic blockade with atropine did not prevent LTP of the fast EPSP. 4. LTP of the fast EPSP did not correlate with changes in input resistance nor cell potential, as recorded in the soma. 5. The formation of nicotinic LTP appeared to depend upon stimulation of the nerve terminals. Non‐synaptic tetanic depolarization of the postganglionic neurone, effected by injecting depolarizing current pulses through the intracellular microelectrode, was not sufficient. LTP could be induced by synaptic tetani in two‐thirds of the same neurones. 6. The response to exogenous 1,1‐dimethyl‐4‐phenylpiperazinium (DMPP), a selective nicotinic agonist, was not increased during nicotinic synaptic LTP. This was true whether DMPP was applied by pressure‐ejection from an extracellular micropipette during intracellular recording, or by brief superfusion during sucrose‐gap recording of postganglionic responses. 7. Responses to exogenous acetylcholine and carbachol were increased during nicotinic LTP when these non‐selective cholinergic agonists were applied by pressure‐ejection during intracellular recording. However, the potentiation of the fast EPSP was always at least twofold greater than the potentiation of the response to these exogenous agonists. 8. Potentiation of the responses to acetylcholine and carbachol may have been due to long‐term enhancement of muscarinic responses. Thus, no postsynaptic basis for nicotinic LTP was uncovered in these studies.

Published
1988
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33. Facilitation, augmentation, and potentiation of synaptic transmission at the superior cervical ganglion of the rabbit.

Author

Zengel, J E, Magleby, K L, Horn, J P, McAfee, D A, and Yarowsky, P J

Abstract

The effect of repetitive stimulation on synaptic transmission was studied in the isolated superior cervical ganglion of the rabbit under conditions of reduced quantal content. Excitatory postsynaptic potentials (EPSP) were recorded with the sucrose gap technique to obtain estimates of transmitter release. Four components of increased transmitter release, with time constants of decay similar to those observed at the frog neuromuscular junction at 20 degrees C, were found in the ganglion at 34 degrees C: a first component of facilitation, which decayed with a time constant of 59 +/- 14 ms (mean +/- SD); a second component of facilitation, which decayed with a time constant of 388 +/- 97 ms; augmentation, which decayed with a time constant of 7.2 +/- 1 s; and potentiation, which decayed with a time constant of 88 +/- 25 s. The addition of 0.1-0.2 mM Ba2+ to the Locke solution increased the magnitude but not the time constant of decay of augmentation. Ba2+ had little effect on potentiation. The addition of 0.2-0.8 mM Sr2+ to the Locke solution appeared to increase the magnitude of the second component of facilitation. Sr2+ had little effect on augmentation or potentiation. These selective effects of Ba2+ and Sr2+ on the components of increased transmitter release in the rabbit ganglion are similar to the effects of these ions at the frog neuromuscular junction. Although the effects of Ba2+ and Sr2+ are similar in the two preparations, the magnitudes of augmentation and the second component of facilitation after a single impulse were about 6-10 times greater in the rabbit ganglion than at the frog neuromuscular junction. These results suggest that the underlying mechanisms in the nerve terminal that give rise to the components of increased transmitter release in the rabbit ganglion and frog neuromuscular junction are similar but not identical.

Published
1980
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36. Motor Fluctuations development is associated with non-motor symptoms burden progression in Parkinson's disease patients: A 2-year follow-up study

Author

Santos, D., Deus, T., Cores, C., Feal Painceiras, M., Suarez Castro, E., Martinez, C., Jesus, S., Aguilar, M., Pastor, P., Planellas, L., Cosgaya, M., Garcia Caldentey, J., Caballol, N., Legarda, I., Hernandez Vara, J., Cabo, I., Lopez Manzanares, L., Gonzalez Aramburu, I., Avila, M., Gomez Mayordomo, V., Nogueira, V., Puente, V., Dotor, J., Borrue, C., Solano, B., Alvarez Sauco, M., Vela, L., Escalante, S., Cubo, E., Carrillo, F., Martinez Castrillo, J., Sanchez Alonso, P., Alonso Losada, M., Lopez Ariztegui, N., Gaston, I., Jaime Kulisevsky, Blazquez, M., Seijo, M., Ruiz Martinez, J., Valero, C., Kurtis, M., Fabregues, O., Gonzalez, J., Alonso Redondo, R., Ordas, C., Lopez Diaz, L., Mcafee, D., Martinez Martin, P., Mir, P., and Coppadis, C.

Subjects
motor fluctuations, Parkinson's disease, follow-up, non-motor symptoms, burden
Abstract

Objective: The aim of the present study was to analyze the progression of non-motor symptoms (NMS) burden in Parkinson's disease (PD) patients regarding the development of motor fluctuations (MF). Methods: PD patients without MF at baseline, who were recruited from January 2016 to November 2017 (V0) and evaluated again at a 2-year follow-up (V2) from 35 centers of Spain from the COPPADIS cohort, were included in this analysis. MF development at V2 was defined as a score >= 1 in the item-39 of the UPDRS-Part IV, whereas NMS burden was defined according to the Non-motor Symptoms Scale (NMSS) total score. Results: Three hundred and thirty PD patients (62.67 +/- 8.7 years old; 58.8% males) were included. From V0 to V2, 27.6% of the patients developed MF. The mean NMSS total score at baseline was higher in those patients who developed MF after the 2-year follow-up (46.34 +/- 36.48 vs. 34.3 +/- 29.07; p = 0.001). A greater increase in the NMSS total score from V0 to V2 was observed in patients who developed MF (+16.07 +/- 37.37) compared to those who did not develop MF (+6.2 +/- 25.8) (p = 0.021). Development of MF after a 2-year follow-up was associated with an increase in the NMSS total score (beta = 0.128; p = 0.046) after adjustment to age, gender, years from symptoms onset, levodopa equivalent daily dose (LEDD) and the NMSS total score at baseline, and the change in LEDD from V0 to V2. Conclusions: In PD patients, the development of MF is associated with a greater increase in the NMS burden after a 2-year follow-up.

44. Modeling seizure networks in neuron-glia cultures using microelectrode arrays.

Author

Boddeti U, Langbein J, McAfee D, Altshuler M, Bachani M, Zaveri HP, Spencer D, Zaghloul KA, and Ksendzovsky A

Abstract

Epilepsy is a common neurological disorder, affecting over 65 million people worldwide. Unfortunately, despite resective surgery, over 30 % of patients with drug-resistant epilepsy continue to experience seizures. Retrospective studies considering connectivity using intracranial electrocorticography (ECoG) obtained during neuromonitoring have shown that treatment failure is likely driven by failure to consider critical components of the seizure network, an idea first formally introduced in 2002. However, current studies only capture snapshots in time, precluding the ability to consider seizure network development. Over the past few years, multiwell microelectrode arrays have been increasingly used to study neuronal networks in vitro . As such, we sought to develop a novel in vitro MEA seizure model to allow for study of seizure networks. Specifically, we used 4-aminopyridine (4-AP) to capture hyperexcitable activity, and then show increased network changes after 2 days of chronic treatment. We characterize network changes using functional connectivity measures and a novel technique using dimensionality reduction. We find that 4-AP successfully captures persistently elevated mean firing rate and significant changes in underlying connectivity patterns. We believe this affords a robust in vitro seizure model from which longitudinal network changes can be studied, laying groundwork for future studies exploring seizure network development., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Boddeti, Langbein, McAfee, Altshuler, Bachani, Zaveri, Spencer, Zaghloul and Ksendzovsky.)

Published
2024
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45. Anthropogenic noise disrupts acoustic cues for recruitment.

Author

Williams BR, McAfee D, and Connell SD

Subjects
Animals, Larva physiology, Larva growth & development, Acoustics, Crassostrea physiology, Behavior, Animal, Noise, Cues
Abstract

Anthropogenic noise is rising and may interfere with natural acoustic cues used by organisms to recruit. Newly developed acoustic technology provides enriched settlement cues to boost recruitment of target organisms navigating to restoration sites, but can it boost recruitment in noise-polluted sites? To address this dilemma, we coupled replicated aquarium experiments with field experiments. Under controlled and replicated laboratory conditions, acoustic enrichment boosted recruitment by 2.57 times in the absence of anthropogenic noise, but yielded comparable recruitment in its presence (i.e. no boosting effect). Using the same technique, we then tested the replicability of these responses in real-world settings where independently replicated 'sites' are unfeasible owing to the inherent differences in soundscapes. Again, acoustic enrichment increased recruitment where anthropogenic noise was low (by 3.33 times), but had no effect at a site of noise pollution. Together, these coupled laboratory-to-field outcomes indicate that anthropogenic noise can mask the signal of acoustic enrichment. While noise pollution may reduce the effectiveness of acoustic enrichment, some of our reported observations suggest that anthropogenic noise per se might also provide an attractive cue for oyster larvae to recruit. These findings underscore the complexity of larval behavioural responses to acoustic stimuli during recruitment processes.

Published
2024
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46. Levodopa-Induced Dyskinesias are Frequent and Impact Quality of Life in Parkinson's Disease: A 5-Year Follow-Up Study.

Author

Santos-García D, de Deus T, Cores C, Feal Painceiras MJ, Íñiguez Alvarado MC, Samaniego LB, López Maside A, Jesús S, Cosgaya M, García Caldentey J, Caballol N, Legarda I, Hernández-Vara J, Cabo López I, López Manzanares L, González-Aramburu I, Ávila A, Gómez-Mayordomo V, Nogueira V, Dotor García-Soto J, Borrué-Fernández C, Solano B, Álvarez Sauco M, Vela L, Escalante S, Cubo E, Mendoza Z, Pareés I, Sánchez Alonso P, Alonso Losada MG, López-Ariztegui N, Gastón I, Kulisevsky J, Seijo M, Valero C, Alonso Redondo R, Buongiorno MT, Ordás C, Menéndez-González M, McAfee D, Martinez-Martin P, and Mir P

Subjects
Humans, Male, Female, Middle Aged, Aged, Follow-Up Studies, Severity of Illness Index, Levodopa adverse effects, Parkinson Disease drug therapy, Quality of Life, Dyskinesia, Drug-Induced epidemiology, Dyskinesia, Drug-Induced etiology, Antiparkinson Agents adverse effects
Abstract

Background: Levodopa-induced dyskinesias (LID) are frequent in Parkinson's disease (PD)., Objective: To analyze the change in the frequency of LID over time, identify LID related factors, and characterize how LID impact on patients' quality of life (QoL)., Patients and Methods: PD patients from the 5-year follow-up COPPADIS cohort were included. LID were defined as a non-zero score in the item "Time spent with dyskinesia" of the Unified Parkinson's Disease Rating Scale-part IV (UPDRS-IV). The UPDRS-IV was applied at baseline (V0) and annually for 5 years. The 39-item Parkinson's disease Questionnaire Summary Index (PQ-39SI) was used to asses QoL., Results: The frequency of LID at V0 in 672 PD patients (62.4 ± 8.9 years old; 60.1% males) with a mean disease duration of 5.5 ± 4.3 years was 18.9% (127/672) and increased progressively to 42.6% (185/434) at 5-year follow-up (V5). The frequency of disabling LID, painful LID, and morning dystonia increased from 6.9%, 3.3%, and 10.6% at V0 to 17.3%, 5.5%, and 24% at V5, respectively. Significant independent factors associated with LID (P < 0.05) were a longer disease duration and time under levodopa treatment, a higher dose of levodopa, a lower weight and dose of dopamine agonist, pain severity and the presence of motor fluctuations. LID at V0 (β = 0.073; P = 0.027; R 2  = 0.62) and to develop disabling LID at V5 (β = 0.088; P = 0.009; R 2  = 0.73) were independently associated with a higher score on the PDQ-39SI., Conclusion: LID are frequent in PD patients. A higher dose of levodopa and lower weight were factors associated to LID. LID significantly impact QoL., (© 2024 International Parkinson and Movement Disorder Society.)

Published
2024
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47. Disparities in Epilepsy Diagnosis and Management in High-Income Countries: A Review of the Literature.

Author

Miller JS, Oladele F, McAfee D, Adereti CO, Theodore WH, and Akinsoji EO

Abstract

Purpose of Review: Currently, an estimated 3.4 million people in the United States live with epilepsy. Previous studies have identified health disparities associated with race/ethnicity, socioeconomic status (SES), sex, insurance status, and age in this population. However, there has been a dearth of research addressing these disparities. We performed a literature review of articles published between 2010 and 2020 pertaining to health disparities in people with epilepsy (PWE), identified key factors that contribute to gaps in their care, and discussed possible solutions., Recent Findings: Health disparities in prevalence, treatment access, time to diagnosis, health care delivery and engagement, and clinical outcomes were identified among individuals who were either of low SES, rural-based, uninsured/underinsured, older patients, patients of color, or female sex., Summary: Disparities in care for PWE continue to persist. Greater priority should be placed on addressing these gaps intricately tied to sociodemographic factors. Reforms to mitigate health disparities in PWE are necessary for timely diagnosis, effective treatment, and positive long-term outcomes., Competing Interests: The authors report no relevant disclosures. Full disclosure form information provided by the authors is available with the full text of this article at Neurology.org/cp., (Written work prepared by employees of the Federal Government as part of their official duties is, under the U.S. Copyright Act, a “work of the United States Government” for which copyright protection under Title 17 of the United States Code is not available. As such, copyright does not extend to the contributions of employees of the Federal Government.)

Published
2024
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48. Staging Parkinson's disease according to the MNCD classification correlates with caregiver burden.

Author

Santos-García D, de Deus Fonticoba T, Cores Bartolomé C, Feal Painceiras MJ, García Díaz I, Alvarado MCÍ, Paz JM, Jesús S, Cosgaya M, Caldentey JG, Caballol N, Legarda I, Hernández Vara J, Cabo I, López Manzanares L, González Aramburu I, Ávila Rivera MA, Gómez Mayordomo V, Nogueira V, Dotor García-Soto J, Borrué C, Solano Vila B, Álvarez Sauco M, Vela L, Escalante S, Cubo E, Mendoza Z, Martínez Castrillo JC, Sánchez Alonso P, Alonso Losada MG, López Ariztegui N, Gastón I, Kulisevsky J, Seijo M, Valero C, Alonso Redondo R, Buongiorno MT, Ordás C, Menéndez-González M, McAfee D, Martinez-Martin P, and Mir P

Subjects
Male, Female, Humans, Middle Aged, Aged, Quality of Life, Caregiver Burden, Cross-Sectional Studies, Caregivers, Parkinson Disease
Abstract

Background and Objective: Recently, we demonstrated that staging Parkinson's disease (PD) with a novel simple classification called MNCD, based on four axes (motor, non-motor, cognition, and dependency) and five stages, correlated with disease severity and patients' quality of life. Here, we analyzed the correlation of MNCD staging with PD caregiver's status., Patients and Methods: Data from the baseline visit of PD patients and their principal caregiver recruited from 35 centers in Spain from the COPPADIS cohort from January 2016 to November 2017 were used to apply the MNCD total score (from 0 to 12) and MNCD stages (from 1 to 5) in this cross-sectional analysis. Caregivers completed the Zarit Caregiver Burden Inventory (ZCBI), Caregiver Strain Index (CSI), Beck Depression Inventory-II (BDI-II), PQ-10, and EUROHIS-QOL 8-item index (EUROHIS-QOL8)., Results: Two hundred and twenty-four PD patients (63 ± 9.6 years old; 61.2% males) and their caregivers (58.5 ± 12.1 years old; 67.9% females) were included. The frequency of MNCD stages was 1, 7.6%; 2, 58.9%; 3, 31.3%; and 4-5, 2.2%. A more advanced MNCD stage was associated with a higher score on the ZCBI (p < .0001) and CSI (p < .0001), and a lower score on the PQ-10 (p = .001), but no significant differences were observed in the BDI-II (p = .310) and EUROHIS-QOL8 (p = .133). Moderate correlations were observed between the MNCD total score and the ZCBI (r = .496; p < .0001), CSI (r = .433; p < .0001), and BDI-II (r = .306; p < .0001) in caregivers., Conclusion: Staging PD according to the MNCD classification is correlated with caregivers' strain and burden., (© 2023 The Authors. Brain and Behavior published by Wiley Periodicals LLC.)

Published
2023
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49. Cognitive impairment and dementia in young onset Parkinson's disease.

Author

Santos-García D, de Deus Fonticoba T, Cores Bartolomé C, Feal Painceiras MJ, García Díaz I, Íñiguez Alvarado MC, Paz JM, Jesús S, Cosgaya M, García Caldentey J, Caballol N, Legarda I, Hernández Vara J, Cabo I, López Manzanares L, González Aramburu I, Ávila Rivera MA, Gómez Mayordomo V, Nogueira V, Dotor García-Soto J, Borrué C, Solano Vila B, Álvarez Sauco M, Vela L, Escalante S, Cubo E, Mendoza Z, Martínez Castrillo JC, Sánchez Alonso P, Alonso Losada MG, López Ariztegui N, Gastón I, Kulisevsky J, Seijo M, Valero C, Alonso Redondo R, Buongiorno MT, Ordás C, Menéndez-González M, McAfee D, Martinez-Martin P, and Mir P

Subjects
Male, Humans, Middle Aged, Female, Cognition, Sleep, Neuropsychological Tests, Parkinson Disease complications, Parkinson Disease epidemiology, Parkinson Disease diagnosis, Cognitive Dysfunction epidemiology, Cognitive Dysfunction etiology, Dementia epidemiology, Dementia etiology
Abstract

Background and Objective: Patients with young-onset Parkinson's disease (YOPD) have a slower progression. Our aim was to analyze the change in cognitive function in YOPD compared to patients with a later onset and controls., Patients and Methods: Patients with Parkinson's disease (PD) and controls from the COPPADIS cohort were included. Cognitive function was assessed with the Parkinson's Disease Cognitive Rating Scale (PD-CRS) at baseline (V0), 2-year ± 1 month (V2y), and 4-year ± 3 months follow-up (V4y). Regarding age from symptoms onset, patients were classified as YOPD (< 50 years) or non-YOPD (≥ 50). A score in the PD-CRS < 81 was defined as cognitive impairment (CI): ≤ 64 dementia; 65-80 mild cognitive impairment (MCI)., Results: One-hundred and twenty-four YOPD (50.7 ± 7.9 years; 66.1% males), 234 non-YOPD (67.8 ± 7.8 years; 59.3% males) patients, and 205 controls (61 ± 8.3 years; 49.5% males) were included. The score on the PD-CRS and its subscore domains was higher at all visits in YOPD compared to non-YOPD patients and to controls (p < 0.0001 in all analysis), but no differences were detected between YOPD patients and controls. Only non-YOPD patients had significant impairment in their cognitive function from V0 to V4y (p < 0.0001). At V4y, the frequency of dementia and MCI was 5% and 10% in YOPD compared to 25.2% and 22.3% in non-YOPD patients (p < 0.0001). A lower score on the Parkinson's Disease Sleep Scale at baseline was a predictor of CI at V4y in YOPD patients (Adjusted R 2  = 0.61; OR = 0.965; p = 0.029)., Conclusion: Cognitive dysfunction progressed more slowly in YOPD than in non-YOPD patients., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany.)

Published
2023
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50. Differential metabolic alterations in IDH1 mutant vs. wildtype glioma cells promote epileptogenesis through distinctive mechanisms.

Author

McAfee D, Moyer M, Queen J, Mortazavi A, Boddeti U, Bachani M, Zaghloul K, and Ksendzovsky A

Abstract

Glioma-related epilepsy (GRE) is a hallmark clinical presentation of gliomas with significant impacts on patient quality of life. The current standard of care for seizure management is comprised of anti-seizure medications (ASMs) and surgical resection. Seizures in glioma patients are often drug-resistant and can often recur after surgery despite total tumor resection. Therefore, current research is focused on the pro-epileptic pathological changes occurring in tumor cells and the peritumoral environment. One important contribution to seizures in GRE patients is metabolic reprogramming in tumor and surrounding cells. This is most evident by the significantly heightened seizure rate in patients with isocitrate dehydrogenase mutated (IDH mut ) tumors compared to patients with IDH wildtype (IDH wt ) gliomas. To gain further insight into glioma metabolism in epileptogenesis, this review compares the metabolic changes inherent to IDH mut vs. IDH wt tumors and describes the pro-epileptic effects these changes have on both the tumor cells and the peritumoral environment. Understanding alterations in glioma metabolism can help to uncover novel therapeutic interventions for seizure management in GRE patients., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 McAfee, Moyer, Queen, Mortazavi, Boddeti, Bachani, Zaghloul and Ksendzovsky.)

Published
2023
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