Evaluación del estado nutricional en la enfermedad de Alzheimer y su influencia en la progresión tras el diagnóstico / Nutritional status assessment in Alzheimer disease and its influence on disease progression

Introducción: Las deficiencias nutricionales son frecuentes en la enfermedad de Alzheimer (EA), incluso en fases iniciales. El deterioro nutricional (DN) puede asociarse con una progresión más rápida de la enfermedad. El objetivo fue describir la frecuencia y los factores de riesgo asociados a DN en el momento del diagnóstico y analizar su influencia en la evolución posterior.MétodosEstudio observacional, multicéntrico, prospectivo. Se incluyeron sujetos recién diagnosticados de EA prodrómica (EAp) o demencia por EA (EAd). Se realizaron dos evaluaciones en un periodo de 18 meses. Para estimar el estado nutricional se empleó el Mini Nutritional Assessment Test (MNA, rango 0-30; DN: MNA < 24). El criterio de progresión fue un incremento en la Clinical Dementia Rating-sum of boxes ≥ 3.ResultadosSe incluyeron 50 sujetos con EAp (edad 76,1 ± 5,3 años; 68% mujeres) y 127 con EAd (edad 80 ± 5,9 años; 72,4% mujeres); 141 (79,7%) completaron las dos evaluaciones. La prevalencia de DN fue del 28,2% (EAp 24%, EAd 29,9%; p = 0,43), la mayoría (92%) en riesgo de desnutrición. El DN se asoció con el sexo femenino (OR: 4,2; IC 95%: 1,7-10,5; p < 0,001) y mayor afectación conductual (OR: 5,8; IC 95%: 2,6-12,7; p < 0,001). Se observó mayor proporción de sujetos con progresión entre los que tenían un DN respecto a estado nutricional normal (50% vs 28,7%, p < 0,05; EAd 53,6% vs 31,8%, p < 0,05; EAp 41,7% vs 22,9%; p = 0,21). Una mayor afectación cognitiva (OR: 2,1; IC 95%: 1,03-4,4; p < 0,05) y un DN (OR: 2,4; IC 95%: 1,1-5,1; p < 0,05) fueron factores de riesgo independientes de progresión.ConclusionesLa prevalencia de DN en la EA es elevada. La evaluación del estado nutricional en el momento del diagnóstico puede permitir identificar pacientes con mayor riesgo de progresión de la enfermedad. (AU)

Introduction: Nutritional deficiencies are frequent in Alzheimer disease (AD), even in early stages. Nutritional impairment (NI) may be associated with faster disease progression. The objective of this study was to describe the frequency of NI and the associated risk factors at the time of diagnosis and to analyse its influence on subsequent progression.MethodsWe performed a prospective, multicentre, observational study of patients recently diagnosed with prodromal AD (pAD) or dementia due to AD (ADd). Two clinical assessments were conducted over a period of 18 months. The Mini Nutritional Assessment test (MNA; score range, 0-30; cut-off point for NI, < 24) was used to estimate nutritional status. Progression was defined as an increase of ≥ 3 points on the Clinical Dementia Rating-sum of boxes test.ResultsThe sample included 50 patients with pAD (mean [standard deviation] age, 76.1 [5.3] years; 68% women), and 127 with ADd (80 [5.9] years; 72.4% women). A total of 141 (79.7%) completed both evaluations. The prevalence of NI was 28.2% (24% for pAD, 29.9% for ADd; P = .43), with the majority (92%) at risk of malnutrition. NI was associated with female sex (odds ratio [OR]: 4.2; 95% confidence interval [CI]: 1.7-10.5; P < .001) and greater behavioural involvement (OR: 5.8; 95% CI: 2.6-12.7; P < .001). A larger proportion of patients with progression was observed among those with NI than among those with normal nutritional status (50% vs 28.7%, P < .05; ADd: 53.6% vs 31.8%, P < .05; pAD: 41.7% vs 22.9%, P = .21). Greater cognitive impairment (OR: 2.1; 95% CI: 1.03-4.4; P < .05) and NI (OR: 2.4; 95% CI: 1.1-5.1; P < .05) were independent risk factors for disease progression.ConclusionsNI is highly prevalent in patients with AD. Assessing nutritional status at the time of diagnosis may enable identification of patients at greater risk of disease progression. (AU)

Nutritional status assessment in Alzheimer disease and its influence on disease progression.

INTRODUCTION: Nutritional deficiencies are frequent in Alzheimer disease (AD), even in early stages. Nutritional impairment (NI) may be associated with faster disease progression. The objective of this study was to describe the frequency of NI and the associated risk factors at the time of diagnosis and to analyse its influence on subsequent progression. METHODS: We performed a prospective, multicentre, observational study of patients recently diagnosed with prodromal AD (pAD) or dementia due to AD (ADd). Two clinical assessments were conducted over a period of 18 months. The Mini Nutritional Assessment test (MNA; score range, 0-30; cut-off point for NI, < 24) was used to estimate nutritional status. Progression was defined as an increase of ≥ 3 points on the Clinical Dementia Rating-sum of boxes test. RESULTS: The sample included 50 patients with pAD (mean [standard deviation] age, 76.1 [5.3] years; 68% women), and 127 with ADd (80 [5.9] years; 72.4% women). A total of 141 (79.7%) completed both evaluations. The prevalence of NI was 28.2% (24% for pAD, 29.9% for ADd; P = .43), with the majority (92%) at risk of malnutrition. NI was associated with female sex (odds ratio [OR]: 4.2; 95% confidence interval [CI]: 1.7-10.5; P < .001) and greater behavioural involvement (OR: 5.8; 95% CI: 2.6-12.7; P < .001). A larger proportion of patients with progression was observed among those with NI than among those with normal nutritional status (50% vs 28.7%, P < .05; ADd: 53.6% vs 31.8%, P < .05; pAD: 41.7% vs 22.9%, P = .21). Greater cognitive impairment (OR: 2.1; 95% CI: 1.03-4.4; P < .05) and NI (OR: 2.4; 95% CI: 1.1-5.1; P < .05) were independent risk factors for disease progression. CONCLUSIONS: NI is highly prevalent in patients with AD. Assessing nutritional status at the time of diagnosis may enable identification of patients at greater risk of disease progression.

Nutritional status assessment in Alzheimer disease and its influence on disease progression. / Evaluación del estado nutricional en la enfermedad de Alzheimer y su influencia en la progresión tras el diagnóstico.

INTRODUCTION: Nutritional deficiencies are frequent in Alzheimer disease (AD), even in early stages. Nutritional impairment (NI) may be associated with faster disease progression. The objective of this study was to describe the frequency of NI and the associated risk factors at the time of diagnosis and to analyse its influence on subsequent progression. METHODS: We performed a prospective, multicentre, observational study of patients recently diagnosed with prodromal AD (pAD) or dementia due to AD (ADd). Two clinical assessments were conducted over a period of 18months. The Mini Nutritional Assessment test (MNA; score range, 0-30; cut-off point for NI, <24) was used to estimate nutritional status. Progression was defined as an increase of ≥3points on the Clinical Dementia Rating-sum of boxes test. RESULTS: The sample included 50 patients with pAD (mean [standard deviation] age, 76.1 [5.3] years; 68% women), and 127 with ADd (80 [5.9] years; 72.4% women). A total of 141 (79.7%) completed both evaluations. The prevalence of NI was 28.2% (24% for pAD, 29.9% for ADd; P=.43), with the majority (92%) at risk of malnutrition. NI was associated with female sex (odds ratio [OR]: 4.2; 95% confidence interval [CI]: 1.7-10.5; P<.001) and greater behavioural involvement (OR: 5.8; 95%CI: 2.6-12.7; P<.001). A larger proportion of patients with progression was observed among those with NI than among those with normal nutritional status (50% vs 28.7%, P<.05; ADd: 53.6% vs 31.8%, P<.05; pAD: 41.7% vs 22.9%, P=.21). Greater cognitive impairment (OR: 2.1; 95%CI: 1.03-4.4; P<.05) and NI (OR: 2.4; 95%CI: 1.1-5.1; P<.05) were independent risk factors for disease progression. CONCLUSIONS: NI is highly prevalent in patients with AD. Assessing nutritional status at the time of diagnosis may enable identification of patients at greater risk of disease progression.

[Metronidazole-induced encephalopathy: description of a case with radiological and anatomopathological findings]. / Encefalopatia inducida por metronidazol: descripcion de un caso con hallazgos radiologicos y anatomopatologicos.

INTRODUCTION: Metronidazole is a widely known and used antibiotic. In exceptional cases, an encephalopathy with characteristic lesions on magnetic resonance imaging (MRI), usually located in the cerebellum and splenium of the corpus callosum, may be an adverse effect. The incidence and pathogenesis are unknown. The suspension of the treatment usually resolves the symptoms and normalizes the MRI in a few weeks. Due to the usual good prognosis, the anatomopathological findings are exceptional. We present a clinical case with the radiological findings suggestive of metronidazole-induced encephalopathy and, exceptionally, we provide the anatomopathological findings. CASE REPORT: A 72 years-old woman with severe Crohn's disease who, months after starting treatment with metronidazole, presented a slowly progressing bradypsychia and difficulty walking until she came to coma. In MRI it showed hyperintense images in T2 in the corpus callosum, red and dentate nuclei. He improved by stopping metronidazole but later developed sepsis and died. At autopsy, softening of the red nucleus was observed and, microscopically, cell necrosis and demyelination. CONCLUSION: With the publication of the clinical, radiological and anatomopathological information of our case we intend to promote the knowledge of this infrequent treatable cause of subacute encephalopathy and provide data that help to clarify its pathogenesis.

TITLE: Encefalopatia inducida por metronidazol: descripcion de un caso con hallazgos radiologicos y anatomopatologicos.Introduccion. El metronidazol es un antibiotico ampliamente conocido y utilizado. En casos excepcionales puede producir como efecto adverso un cuadro de encefalopatia con unas lesiones caracteristicas en la resonancia magnetica, localizadas generalmente en el cerebelo y el esplenio del cuerpo calloso. La incidencia y la patogenia se desconocen. La suspension del tratamiento habitualmente resuelve los sintomas y normaliza la resonancia magnetica en pocas semanas. Debido al habitual buen pronostico, los hallazgos anatomopatologicos son excepcionales. Se presenta un caso clinico con los hallazgos radiologicos sugestivos de la encefalopatia inducida por metronidazol y, de forma excepcional, se aportan los hallazgos anatomopatologicos. Caso clinico. Mujer de 72 años, con enfermedad de Crohn grave, que meses mas tarde de iniciar tratamiento con metronidazol presento de forma lentamente progresiva bradipsiquia y dificultad para caminar hasta llegar al coma. En la resonancia magnetica mostraba caracteristicas imagenes hiperintensas en T2 en el cuerpo calloso, y los nucleos rojos y dentados. Mejoro al suspender el metronidazol, pero posteriormente desarrollo una sepsis y fallecio. En la autopsia se observo reblandecimiento del nucleo rojo y, microscopicamente, necrosis celular y desmielinizacion. Conclusion. Con la publicacion de la informacion clinica, radiologica y anatomopatologica de este caso se pretende fomentar el conocimiento de esta infrecuente causa tratable de encefalopatia subaguda y aportar datos que ayuden a aclarar su patogenia.

Anosognosia in Alzheimer disease: Prevalence, associated factors, and influence on disease progression. / Anosognosia en la enfermedad de Alzheimer: prevalencia, factores asociados e influencia en la evolución de la enfermedad.

INTRODUCTION: Anosognosia is a frequent symptom in Alzheimer disease (AD). The objective of this article is to describe prevalence of this condition at time of diagnosis and analyse any predisposing factors and their influence on disease progression. METHODS: Observational, prospective, and analytical multi-centre study in an outpatient setting. Patients recently diagnosed with AD (NINCDS-ADRDA criteria) were included. Each patient underwent two cognitive, functional, and neuropsychiatric assessments separated by an interval of 18 months. The Clinical Insight Rating Scale was employed as a measure of anosognosia (CIR, scored 0-8). Progression was defined as an increase in the Clinical Dementia Rating Scale-sum of boxes of more than 2.5 points. The predictor variables were analysed using binary logistic regression. RESULTS: The study included 127 patients, and 94 completed both assessments. Of the total, 31.5% displayed severe anosognosia (CIR 7-8); 39.4%, altered level of consciousness (CIR 3-6); and 29.1%, normal awareness (CIR 0-2). The median baseline CIR in this cohort was 4 (Q1-Q3: 1-7), and at 18 months, 6 (Q1-Q3: 3-8), P<.001. Advanced age (odds ratio (OR) 2.43; CI 95%:1.14-5.19), lower educational level (OR 2.15; CI 95%:1.01-4.58), and more marked neuropsychiatric symptoms (OR 2.66; CI 95%:1.23-5.74) were predictor variables of anosognosia. Baseline CIR was similar in the groups with and without significant clinical progression. CONCLUSIONS: The large majority of patients with AD at the time of diagnosis showed significant anosognosia, and this condition was associated with advanced age, lower educational level, and more marked behavioural symptoms. Our results did not show that anosognosia had an effect on the initial clinical progression of AD after diagnosis.

[Neurological complications of cardiac catheterization]. / Complicaciones neurológicas del cateterismo cardíaco.

AIMS: To describe the neurological complications of cardiac catheterization, together with its risk factors and pathogenic mechanisms. METHOD: Over the past few years there has been a marked increase in the number of interventions involving cardiac catheterizations. For this very reason, we can expect a proportional rise in the number of complications. The incidence of neurological pathologies secondary to heart interventions oscillates between 0.01 and 0.4% of procedures performed. The most frequent clinical pictures are cerebrovascular disease, neuro ophthalmological syndromes and peripheral neuropathies, due to damage done to the median, femoral and lateral femoral cutaneous nerves, and to the lumbar plexus. The most usual mechanisms are cerebral ischemia originated by embolisms and direct compression of the peripheral nerves. Factors increasing the likelihood of complications are old age, the presence of classic vascular risk factors and, probably, the patient s being female. More risk is involved in mitral and aortic valvuloplasties and non elective revascularization procedures. The personal experience of the operator and the overall activity of the department of haemodynamics where the physician works are factors that are very closely linked to the incidence of complications. CONCLUSIONS: Knowledge about neurological illness secondary to cardiac catheterization and its mechanisms of production may allow us to identify higher risk patients, to develop protocols to prevent it and to apply early therapeutic measures.

Complicaciones neurológicas del cateterismo cardíaco / Neurological complications of cardiac catheterization

Objetivos. Describir las complicaciones neurológicas del cateterismo cardíaco (CC), así como sus factores de riesgo y mecanismos patogénicos. Desarrollo. En los últimos años, se ha incrementado notablemente el número de CC. Por este motivo se espera un aumento proporcional de sus complicaciones. La incidencia de patología neurológica secundaria al intervencionismo cardíaco oscila entre el 0,01 y el 0,4 por ciento de los procedimientos. Los cuadros clínicos más frecuentes son la enfermedad cerebrovascular, los síndromes neurooftalmológicos y las neuropatías pariféricas, por afectación de los nervios mediano, femoral, femorocutáneo y del plexo lumbar. Los mecanismos más habituales son la isquemia cerebral de origen embólico y la compresión directa de los nervios periféricos. La edad avanzada, la presencia de factores clásicos de riesgo vascular y, probablemente, el sexo femenino se asocian con una mayor incidencia de complicaciones. Las valvulopatías mitral y aórtica y los procedimientos de revascularización no electivos conllevan mayor riesgo. La experiencia personal del operador y la actividad global de la unidad de hemodinámica donde trabaja, son factores muy relacionados con la incidencia de complicaciones. Conclusiones. El conocimiento de la patología neurológica secundaria al CC y sus mecanismos de producción puede permitir identificar a los pacientes de mayor riesgo, establecer protocolos para su prevención y aplicar medidas terapéuticas de forma precoz (AU)

Síndrome de Guillain-Barré asociado a adenocarcinoma gástrico. ¿Origen para neoplásicoo coincidencia? / Guillain-Barré syndrome associated with gastric adenocarcinoma. Paraneoplastic origin or coincidence?

No disponible

[Horner's syndrome secondary to ophthalmic herpes zoster]. / Síndrome de Horner secundario a herpes zoster oftálmico.

INTRODUCTION: Ophthalmoparesias is a frequent complication of ophthalmic herpes zoster. It occurs in 31% of all cases. However, the presence of Horner's syndrome during viral reactivation is a rarity which has only been previously described on two occasions, and never associated with cranial nerve involvement. CLINICAL CASE: We describe a patient with the first case of Horner's syndrome secondary to ophthalmic herpes zoster, with simultaneous, homolateral lesions of the third and sixth cranial nerves. Clinical evaluation, the course of the disorder, negative magnetic resonance studies and tests with cocaine and foledrin eye drops confirmed the presence of a post-ganglionar sympathetic lesion, probably situated in the ipsilateral cavernous sinus. CONCLUSIONS: Ophthalmoparesias as a complication of ophthalmic herpes zoster may have various origins. Diffusion of viral particles from the Gasserian ganglion and branches of the trigeminal nerve to adjacent structures, muscles, nerves and vessels, is the mechanism often mentioned. Presence of a simultaneous sympathetic lesion is very rare and of unknown pathology. However, it is probable that the origin of the lesion of the vegetative fibres is the same as that of the sensory or motor fibres, and adjacent inflammatory process caused by the virus extending. We analyze the factors involved in the low incidence of this association.