Cognitive decline in adult-onset temporal lobe epilepsy: Insights from aetiology.

PURPOSE: To identify patients with adult-onset temporal lobe epilepsy (TLE) at risk of developing cognitive decline. Detecting which patients, aetiologies, or factors are most closely related with memory decline would allow us to identify patients that would eventually benefit from more specific treatment. METHODS: Single centre, retrospective analysis of a prospectively followed-up cohort study, including all patients with the diagnosis of adult-onset TLE during 2013, with a minimum follow-up of five years. Memory and cognitive decline were analysed at 5 years and at last follow-up. RESULTS: Of 89 initially selected patients, 71 were included. After 5 years, 11/71 (15.5%) patients suffered cognitive decline, of which 1/71 (4%) developed dementia. At last follow-up (range 65-596 m) a total of 34/71 (47.8%) patients were diagnosed with cognitive decline, specifically either memory decline or dementia. Cognitive decline at 5 years was related to: 1. Age at onset: 62.65 years (SD 9.04) in the group with cognitive decline vs 50.33 y. (SD 13.02 in the group without cognitive decline; p=0.004); 2. Onset as status epilepticus (3/6 in patients with memory decline vs 8/65 in patients without cognitive decline; p=0.04); 3. Immune aetiology: 42% compared with unknown (10%) and structural (10%) aetiologies; p=0.036; 4. Hippocampal sclerosis on MRI: 5/11 patients with cognitive decline vs 9/51 patients without cognitive decline; p=0.035. Cognitive decline was not related to seizure frequency, sex, or age (p=0.78; p=0.40; p=0.95, respectively). CONCLUSIONS: Older age at epilepsy onset, onset as status epilepticus, immune aetiology, and hippocampal sclerosis are risk factors for developing cognitive decline in patients with adult-onset temporal lobe epilepsy.

Enfermedad de Parkinson y enfermedad de Alzheimer: factores de riesgo ambientales / Parkinson disease and Alzheimer disease: environmental risk factors

Introducción: Esta revisión pretende actualizar y resumir la evidencia disponible sobre los factores de riesgo ambientales que se han asociado a riesgo de enfermedad de Parkinson (EP) o de Alzheimer (EA) y discutir sus posibles mecanismos. Desarrollo: Hay evidencia consistente de mayor riesgo de EP asociado a pesticidas y de mayor riesgo de EA asociado a pesticidas, hipertensión y colesterol en edad media, hiperhomocisteinemia, tabaco, traumatismo craneoencefálico grave y depresión. Hay evidencia débil de mayor riesgo de EP asociado a consumo elevado de leche en hombres, ingesta alta de hierro, anemia crónica y traumatismo craneoencefálico grave, y de mayor riesgo de EA asociado a ingesta elevada de aluminio en agua potable, alta exposición a redes eléctricas, DM e hiperinsulinemia, obesidad en edad media, consumo excesivo de alcohol y anemia crónica. Hay evidencia consistente de menor riesgo de EP asociado a hiperuricemia, tabaco y café, y de menor riesgo de EA asociado a consumo moderado de alcohol, ejercicio físico, terapia hormonal sustitutiva perimenopáusica y buena reserva cognitiva; hay evidencia débil de menor riesgo de EP asociado a mayor consumo de vitamina E, alcohol, té y AINE y a ejercicio físico vigoroso, y de menor riesgo de EA asociado a dieta mediterránea, café y consumo crónico de AINE. Conclusiones: Diversos factores ambientales contribuyen significativamente al riesgo de EP y EA. Algunos de ellos podrían actuar ya desde etapas tempranas de la vida o interaccionar con otros factores genéticos. Estrategias poblacionales de modificación de estos factores podrían potencialmente evitar algunos casos de EP o de EA

Introduction: The purpose of this review is to update and summarise available evidence on environmental risk factors that have been associated with risk of Parkinson disease (PD) or Alzheimer disease (AD) and discuss their potential mechanisms. Development: Evidence consistently suggests that a higher risk of PD is associated with pesticides and that a higher risk of AD is associated with pesticides, hypertension and high cholesterol levels in middle age, hyperhomocysteinaemia, smoking, traumatic brain injury and depression. There is weak evidence suggesting that higher risk of PD is associated with high milk consumption in men, high iron intake, chronic anaemia and traumatic brain injury. Weak evidence also suggests that a higher risk of AD is associated with high aluminium intake through drinking water, excessive exposure to electromagnetic fields from electrical grids, DM and hyperinsulinaemia, obesity in middle age, excessive alcohol consumption and chronic anaemia. Evidence consistently suggests that a lower risk of PD is associated with hyperuricaemia, tobacco and coffee use, while a lower risk of AD is associated with moderate alcohol consumption, physical exercise, perimenopausal hormone replacement therapy and good cognitive reserve. Weak evidence suggests that lower risk of PD is associated with increased vitamin E intake, alcohol, tea, NSAIDs, and vigorous physical exercise, and that lower risk of AD is associated with the Mediterranean diet, coffee and habitual NSAID consumption. Conclusions: Several environmental factors contribute significantly to risk of PD and AD. Some may already be active in the early stages of life, and some may interact with other genetic factors. Population-based strategies to modify such factors could potentially result in fewer cases of PD or AD

Parkinson disease and Alzheimer disease: environmental risk factors.

INTRODUCTION: The purpose of this review is to update and summarise available evidence on environmental risk factors that have been associated with risk of Parkinson disease (PD) or Alzheimer disease (AD) and discuss their potential mechanisms. DEVELOPMENT: Evidence consistently suggests that a higher risk of PD is associated with pesticides and that a higher risk of AD is associated with pesticides, hypertension and high cholesterol levels in middle age, hyperhomocysteinaemia, smoking, traumatic brain injury and depression. There is weak evidence suggesting that higher risk of PD is associated with high milk consumption in men, high iron intake, chronic anaemia and traumatic brain injury. Weak evidence also suggests that a higher risk of AD is associated with high aluminium intake through drinking water, excessive exposure to electromagnetic fields from electrical grids, DM and hyperinsulinaemia, obesity in middle age, excessive alcohol consumption and chronic anaemia. Evidence consistently suggests that a lower risk of PD is associated with hyperuricaemia, tobacco and coffee use, while a lower risk of AD is associated with moderate alcohol consumption, physical exercise, perimenopausal hormone replacement therapy and good cognitive reserve. Weak evidence suggests that lower risk of PD is associated with increased vitamin E intake, alcohol, tea, NSAIDs, and vigorous physical exercise, and that lower risk of AD is associated with the Mediterranean diet, coffee and habitual NSAID consumption. CONCLUSIONS: Several environmental factors contribute significantly to risk of PD and AD. Some may already be active in the early stages of life, and some may interact with other genetic factors. Population-based strategies to modify such factors could potentially result in fewer cases of PD or AD.

Evidencia sobre el tratamiento de la enfermedad de alzheimer con inhibidores de la acetilcolinesterasa y/o memantina / No disponible

No disponible

Importancia del estudio electromiográfico en el diagnóstico del temblor ortostático. Réplica / Importance of electromyographic studies in the diagnosis of orthostatic tremor. Reply

No disponible

Importancia del estudio electromiográfico en el diagnóstico del temblor ortostático. Réplica / Importance of electromyographic studies in the diagnosis of orthostatic tremor. Reply

No disponible

Encefalopatía de Wernicke en pacientes no alcohólicos: una serie de 8 casos / Wernicke's encephalopathy in non-alcoholic patients: a series of 8 cases

Introduction: Wernicke's encephalopathy (WE) is an underdiagnosed condition, usually associated with alcoholism, and has a worse prognosis if there is a delay in diagnosis. A series of 8 non-alcoholic patients with WE is presented and an assessment is made on whether a delay in diagnosis leads to a worse prognosis. Patients and methods:The clinical records of patients admitted to 2 university hospitals between 2004 and 2009 with the diagnosis of WE, excluding those with a history of alcoholism, were retrospectively reviewed. Results:The study included 4 men and 4 women aged 35-82 of whom 7 had a history of gastrointestinal pathology, and persistent vomiting was the precipitating factor in 7. Encephalopathy was the most frequent onset symptom (4). The classical triad was present in seven patients. Thiamine levels were low in 3/6 and normal in 3/6 cases. MRI was abnormal in seven patients, with high signal intensity in the diencephalon and mammillary bodies (7), periaqueductal grey matter (6), cortex (3) and cerebellum (1). Seven improved with thiamine. Sequelae were mild in 6, and severe in 2 after 6-12 months of follow-up. All patients with a diagnostic delay less than 18 days had mild sequelae.Conclusions: Non-alcoholic WE frequently occurs after gastrointestinal disturbances that could result in lower thiamine absorption. Whereas thiamine levels can be normal in many cases, in almost all cases the MRI shows signal alterations in typical locations. A delay in the diagnosis, and therefore, in treatment leads to a worse prognosis

Introducción: La encefalopatía de Wernicke (EW) es una entidad infradiagnosticada, generalmente asociada a alcoholismo, que tiene peor pronóstico si existe retraso diagnóstico. Se presenta una serie de 8 pacientes no alcohólicos con EW y se evalúa si el retraso en el diagnóstico implica un peor pronóstico. Pacientes y métodos:Revisión retrospectiva de las historias clínicas de pacientes ingresados en dos hospitales universitarios entre 2004 y 2009 con diagnóstico de EW, excluidos aquéllos con historia de alcoholismo.Resultados: Se incluyó a 4 varones y 4 mujeres, con edades comprendidas entre los 35 y los 82 años; 7 tenían antecedentes patológicos gastrointestinales y los vómitos persistentes fueron el desencadenante en 7 casos. La encefalopatía fue la forma de inicio más frecuente (4 casos). La tríada clásica llegó a estar presente en 7 pacientes. Los niveles de tiamina fueron bajos en 3/6 y normales en 3/6 pacientes. La RM fue patológica en 7 pacientes, con hiperintensidad en diencéfalo y cuerpos mamilares (7), sustancia gris periacueductal (6), corteza (3) y cerebelo (1). Siete pacientes mejoraron tras el tratamiento con tiamina. Las secuelas fueron leves en 5 casos y graves en 3 pacientes. Todos los pacientes con un retraso diagnóstico inferior a 18 días tuvieron secuelas leves.Conclusiones: En la EW no alcohólica son frecuentes los antecedentes gastrointestinales que podrían condicionar una menor absorción de tiamina. Mientras que los niveles de tiamina pueden ser normales en muchos casos, la RM casi siempre muestra alteración de señal en localizaciones típicas. El retraso en el diagnóstico y, por tanto, en el tratamiento podría implicar un peor pronóstico (AU)

[Wernicke's encephalopathy in non-alcoholic patients: a series of 8 cases]. / Encefalopatía de Wernicke en pacientes no alcohólicos: una serie de 8 casos.

INTRODUCTION: Wernicke's encephalopathy (WE) is an underdiagnosed condition, usually associated with alcoholism, and has a worse prognosis if there is a delay in diagnosis. A series of 8 non-alcoholic patients with WE is presented and an assessment is made on whether a delay in diagnosis leads to a worse prognosis. PATIENTS AND METHODS: The clinical records of patients admitted to 2 university hospitals between 2004 and 2009 with the diagnosis of WE, excluding those with a history of alcoholism, were retrospectively reviewed. RESULTS: The study included 4 men and 4 women aged 35-82 of whom 7 had a history of gastrointestinal pathology, and persistent vomiting was the precipitating factor in 7. Encephalopathy was the most frequent onset symptom (4). The classical triad was present in seven patients. Thiamine levels were low in 3/6 and normal in 3/6 cases. MRI was abnormal in seven patients, with high signal intensity in the diencephalon and mammillary bodies (7), periaqueductal grey matter (6), cortex (3) and cerebellum (1). Seven improved with thiamine. Sequelae were mild in 6, and severe in 2 after 6-12 months of follow-up. All patients with a diagnostic delay less than 18 days had mild sequelae. CONCLUSIONS: Non-alcoholic WE frequently occurs after gastrointestinal disturbances that could result in lower thiamine absorption. Whereas thiamine levels can be normal in many cases, in almost all cases the MRI shows signal alterations in typical locations. A delay in the diagnosis, and therefore, in treatment leads to a worse prognosis.

Importancia del estudio electromiográfico en el diagnóstico del temblor ortostático / Importance of electromyographic studies in the diagnosis of orthostatic tremor

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Pelvic dyskinesia with an outstanding response to tetrabenazine.

We report on a patient who presented an invalidating progressive pelvic dyskinesia while receiving different kinds of neuroleptic drugs for a psychiatric disorder. The clinical features and different drug-induced movement scales showed an outstanding improvement after tetrabenazine was started. To the best of our knowledge, this is the first case report of pelvic dyskinesia with good evolution and control of dyskinesias after treatment with tetrabenazine.

Familial Creutzfeldt-Jakob disease with E200K mutation presenting with neurosensorial hypoacusis.

Creutzfeldt-Jakob disease (CJD) is characterised by rapidly progressive dementia, myoclonus, ataxia, visual disturbances and motor dysfunction. Most of the cases are sporadic. Only 10% to 15% are familial, and the most frequent point mutation is E200K. A 53-year-old man presented with subacute progressive bilateral hypoacusis, with tinnitus in the left ear. During the following months, his hypoacusis worsened and he progressively developed bilateral stocking-type paresthaesia and gait instability. An audiometric examination showed bilateral neurosensorial hypoacusis and nerve conduction studies showed a mixed axonal polyneuropathy. A CT scan and MRI of the brain were normal and the electroencephalography (EEG) showed non-specific changes. He died of respiratory infection 10 months after onset of symptoms. Neuropathological examination showed neuronal loss, punctate, synaptic-like deposits of protease-resistant prionic protein (PrP(RES)) in the cerebral and cerebellar cortices and auditory nuclei. This is a rare case of sporadic CJD presenting with hearing loss.

Degeneración lobular frontotemporal: estudio descriptivo de 42 pacientes / Frontotemporal lobar degeneration: a descriptive study of 42 patients

Introducción. La degeneración lobular frontotemporal(DLFT) se considera la segunda causa de demencia presenil.A pesar del gran interés que ha generado en los últimosaños existen pocos estudios publicados en España.Métodos. Estudio descriptivo retrospectivo de 42 pacientescon DLFT evaluados en nuestra unidad durante elperíodo 1996-2006.Resultados. Treinta y un pacientes presentaban la variantefrontal de DLFT (DFT), ocho afasia progresiva no fluentey tres demencia semántica. La edad media de inicio fue 56años, el retraso diagnóstico 3,5 años y la supervivencia media6,8 años. El 35 % tenían historia familiar indicativa de demencia.En los pacientes con DFT la expresión clínica fue unacombinación de trastorno de conducta y personalidad juntocon alteración del lenguaje. La resonancia magnética mostróatrofia frontal y/o temporal en el 62% de los casos y la SPECThipoperfusión frontal y/o temporal en el 75%. En cuatro pacientes(dos de ellos hermanos) se detectó la mutación P301Lde tau y en otro la mutación A303AfsX57 de progranulina(PGRN). Se realizó necropsia a cinco pacientes, encontrándoseDLFT con inclusiones ubiquitina-inmunorreactivas (DLFT-U) yenfermedad de motoneurona en dos casos, DLFT-U con inclusionesintranucleares lanceoladas en el caso con mutación dePGRN y taupatía generalizada con predominio de isoformas4R en los otros dos, ambos con la mutación P301L.Conclusiones. Nuestros resultados son similares a losde las grandes series europeas. Debe sospecharse DLFT enpacientes preseniles con trastorno predominante y precozde la conducta y/o del lenguaje. La neuroimagen apoya eldiagnóstico en la mayoría de los casos. El gran impacto sociofamiliarde la DLFT, el inicio presenil, la alta frecuencia de antecedentesfamiliares de demencia y la posibilidad de realizarestudio y consejo genético realzan su importancia clínica (AU)

Introduction. Frontotemporal lobar degeneration (FTLD)is considered to be the second cause of presenile dementia.In spite of the great interest it has generated over the lastfew years, few studies have been published in our country.Methods. A descriptive retrospective study of 42 patientswith FTLD evaluated in our unit during the period1996-2006 was performed.Results. Thirty one patients presented with frontalvariant FTLD (FTD), eigth with non-fluent progressiveaphasia and three with semantic dementia. Mean age atonset was 56 years, diagnostic delay 3.5 years and meansurvival 6.8 years. 35% had a family history suggestiveof dementia. In patients with FTD the clinical expressionwas a combination of behavioral and personality disorderstogether with language impairment. Magnetic resonanceimaging showed frontal and/or temporal atrophy in62% of cases and SPECT showed frontal and/or temporalhypoperfusion in 75%. The P301L tau mutation was detectedin four patients (two of them siblings) and theA303AfsX57 progranulin mutation in one. Necropsy wasperformed in five patients, revealing FTLD with ubiquitininmunoreactiveinclusions (FTLD-U) and motor neuron diseasein two cases, FTLD-U with «cat’s-eye» shaped intranuclearinclusions in the case with the progranulinmutation and FTLD tauopathy with predominance of 4Rtau in the remaining two, both with the P301L mutation.Conclusions. Our results are similar to those of thegreat European series. FTLD must be suspected in presenilepatients with prominent behavioral and/or languagedisorders. Neuroimaging supports the diagnosis in themajority of cases. The huge sociofamiliar impact ofFTLD, presenile onset, high frequency of familial historyof dementia and possibility of genetic study and counse-69 ling highlight its clinical relevance (AU)

[Frontotemporal lobar degeneration: a descriptive study of 42 patients]. / Degeneración lobular frontotemporal: estudio descriptivo de 42 pacientes.

INTRODUCTION: Frontotemporal lobar degeneration (FTLD) is considered to be the second cause of presenile dementia. In spite of the great interest it has generated over the last few years, few studies have been published in our country. METHODS: A descriptive retrospective study of 42 patients with FTLD evaluated in our unit during the period 1996-2006 was performed. RESULTS: Thirty one patients presented with frontal variant FTLD (FTD), eigth with non-fluent progressive aphasia and three with semantic dementia. Mean age at onset was 56 years, diagnostic delay 3.5 years and mean survival 6.8 years. 35% had a family history suggestive of dementia. In patients with FTD the clinical expression was a combination of behavioral and personality disorders together with language impairment. Magnetic resonance imaging showed frontal and/or temporal atrophy in 62% of cases and SPECT showed frontal and/or temporal hypoperfusion in 75%. The P301L tau mutation was detected in four patients (two of them siblings) and the A303AfsX57 progranulin mutation in one. Necropsy was performed in five patients, revealing FTLD with ubiquitininmunoreactive inclusions (FTLD-U) and motor neuron disease in two cases, FTLD-U with <> shaped intranuclear inclusions in the case with the progranulin mutation and FTLD tauopathy with predominance of 4R tau in the remaining two, both with the P301L mutation. CONCLUSIONS: Our results are similar to those of the great European series. FTLD must be suspected in presenile patients with prominent behavioral and/or language disorders. Neuroimaging supports the diagnosis in the majority of cases. The huge sociofamiliar impact of FTLD, presenile onset, high frequency of familial history of dementia and possibility of genetic study and counseling highlight its clinical relevance.

Increased cerebral activity in Parkinson's disease patients carrying the DRD2 TaqIA A1 allele during a demanding motor task: a compensatory mechanism?

Previous studies suggest that neuroimaging techniques are useful for detecting the effects of functional genetic polymorphisms on brain function in healthy subjects or in patients presenting with psychiatric or neurodegenerative conditions. Former evidence showed that individuals carrying risk alleles displayed broader patterns of brain activity during behavioural and cognitive tasks, despite being clinically comparable to non-carriers. This suggests the presence of compensatory brain mechanisms. In the present study, we investigated this effect in Parkinson's disease (PD) patients carrying the DRD2 TaqIA A1 allelic variant. This variant may confer an increased risk of developing the disease and/or influence the clinical presentation. During a complex sequential motor task, we evidenced by functional magnetic resonance imaging that A1 allele carriers activated a larger network of bilateral cerebral areas than non-carriers, including cerebellar and premotor regions. Both groups had similar clinical and demographic measures. In addition, their motor performance during the functional magnetic resonance experiment was comparable. Therefore, our conclusions, pending replication in a larger sample, seem to reflect the recruitment of compensatory cerebral resources during motor processing in PD patients carrying the A1 allele.

[A pilot study on a specific measure for sleep disorders in Parkinson's disease: SCOPA-Sleep]. / Estudio piloto sobre una medida especifica para los trastornos del sueno de la enfermedad de Parkinson: SCOPA-sueño.

INTRODUCTION: There is a high prevalence of sleep disorders in Parkinson's disease (PD). AIMS. To assess some basic metric attributes of the SCOPA-Sleep scale, a measure for PD patients; secondary objective: to check the impact caused by the sleep disorder on the health-related quality of life (HRQoL) of patients and their caregivers. SUBJECTS AND METHODS: 68 PD patients and their main caregivers; measures: Hoehn and Yahr staging, SCOPA-Motor, Clinical Impression of Severity Index (CISI-PD), PDSS, Hospital Anxiety and Depression Scale, SCOPA-Psychosocial, and EuroQoL. Carers filled in a PDSS questionnaire about patient sleep and HRQoL measures (SF-36, EuroQoL). SCOPA-Sleep acceptability, scaling assumptions, internal consistency, construct validity and precision were determined. RESULTS: SCOPA-Sleep acceptability and scaling assumptions resulted satisfactory, although the nocturnal sleep subescale (SC-Ns) showed a mild ceiling effect (22.1%) and a defective convergent validity was found for daytime sleepiness (SC-Ds) item 6. Internal consistency also was satisfactory for both scales (alpha = 0.84 and 0.75, respectively). The correlation between SC-Ns and PDSS was high (rs = -0.70), as it was between SC-Ns and PDSS questionnaire by caregiver (rs = -0.53). The corresponding coefficients with the SC-Ds gained lower values (rs = -0.41 y -0.50). Standard error of measurement was 1.45 for the SC-Ns and 1.76 for the SC-Ds. Both, patient and caregiver HRQoL showed a loose association with the sleep measures. CONCLUSION: SCOPA-Sleep is a feasible, consistent, and useful scale for assessment of sleep disorder in PD patients. A weak association between sleep disorder and HRQoL was found.

Estudio piloto sobre una medida específica para los trastornos del sueño de la enfermedad de Parkinson: SCOPA-sueño / A pilot study on a specific measure for sleep disorders in parkinson's disease: scopa-sleep

Introducción. En la enfermedad de Parkinson (EP) existe una alta prevalencia de trastornos del sueño. Objetivos. Comprobar los atributos métricos básicos de la escala SCOPA-sueño para pacientes con EP; objetivo secundario: analizar el impacto del trastorno del sueño en la calidad de vida relacionada con la salud(CVRS) del paciente y de su cuidador principal. Sujetos y métodos. 68 pacientes con EP y sus cuidadores principales. Se aplicaron: Hoehn y Yahr, SCOPA-motor, impresión clínica de gravedad (CISIPD),escala PDSS, Hospital Anxiety and Depression Scale, SCOPA-psicosocial y EuroQoL. El cuidador cumplimentó un cuestionario PDSS sobre el sueño del paciente y las medidas de la CVRS(SF-36, EuroQoL). Se analizaron la aceptabilidad, las asunciones escalares, la consistencia interna, la validez de constructo y la precisión de la SCOPA-sueño. Resultados. La SCOPA-sueño mostró aceptabilidad satisfactoria y asunciones escalares. La subescala sueño nocturno (SC-Sn) presentó leve efecto techo (22,1%), y la subescala somnolencia diurna (SC-Sd), defectuosa validez convergente del ítem 6; la consistencia interna de ambas resultó satisfactoria(alfa = 0,84 y 0,75, respectivamente). SC-Sn correlacionó significativamente con la PDSS (rS= –0,70) y con el cuestionario PDSS cumplimentado por el cuidador (rS= –0,53), y fueron menores los valores respectivos para la SC-Sd (rS= –0,41 y –0,50). Error estándar de la medida: SC-Sn, 1,45; SC-Sd, 1,76. La CVRS del pacientey la del cuidador mostraron una escasa correlación con las medidas de sueño. Conclusiones. La escala SCOPA-sueño es viable, consistente y útil para evaluar el trastorno del sueño en pacientescon EP. La relación entre la CVRS y la alteración del sueño fue débil

Introduction. There is a high prevalence of sleep disorders in Parkinson’s disease (PD). Aims. To assess some basicmetric attributes of the SCOPA-Sleep scale, a measure for PD patients; secondary objective: to check the impact caused by thesleep disorder on the health-related quality of life (HRQoL) of patients and their caregivers. Subjects and methods. 68 PDpatients and their main caregivers; measures: Hoehn and Yahr staging, SCOPA-Motor, Clinical Impression of Severity Index(CISI-PD), PDSS, Hospital Anxiety and Depression Scale, SCOPA-Psychosocial, and EuroQoL. Carers filled in a PDSSquestionnaire about patient sleep and HRQoL measures (SF-36, EuroQoL). SCOPA-Sleep acceptability, scaling assumptions,internal consistency, construct validity and precision were determined. Results. SCOPA-Sleep acceptability and scalingassumptions resulted satisfactory, although the nocturnal sleep subescale (SC-Ns) showed a mild ceiling effect (22.1%) and adefective convergent validity was found for daytime sleepiness (SC-Ds) item 6. Internal consistency also was satisfactory forboth scales (alpha = 0.84 and 0.75, respectively). The correlation between SC-Ns and PDSS was high (rS = –0.70), as it wasbetween SC-Ns and PDSS questionnaire by caregiver (rS = –0.53). The corresponding coefficients with the SC-Ds gainedlower values (rS = –0.41 y –0.50). Standard error of measurement was 1.45 for the SC-Ns and 1.76 for the SC-Ds. Both,patient and caregiver HRQoL showed a loose association with the sleep measures. Conclusion. SCOPA-Sleep is a feasible,consistent, and useful scale for assessment of sleep disorder in PD patients. A weak association between sleep disorder andHRQoL was found