Quejas cognitivas subjetivas: hacia una identificación precoz de la enfermedad de Alzheimer / Subjective cognitive impairment: Towards early identification of Alzheimer disease

Introducción: La neurodegeneración en enfermedad de Alzheimer (EA) empieza décadas antes que la demencia y algunos pacientes con deterioro cognitivo leve presentan una importante carga lesional. La ausencia de información sobre la fisiopatología temprana de la enfermedad dificulta la búsqueda de estrategias terapéuticas. La queja cognitiva subjetiva (QCS) agrupa a sujetos con quejas mnésicas sin déficits significativos en test neuropsicológicos. Es un síndrome heterogéneo sobre el que no existe consenso, pero algunos de estos pacientes podrían representar el estadio más precoz de EA. Método: Realizamos una revisión bibliográfica para resumir el estado del conocimiento actual sobre quejas cognitivas subjetivas. Resultados: Aunque a nivel individual no presenten enfermedad objetivable, a nivel de grupo los pacientes con QCS rinden peor en test neuropsicológicos que la población general y tienen mayor incidencia de declive cognitivo futuro. La depresión y la comorbilidad psiquiátrica desempeñan un papel pero no son la única causa de quejas cognitivas. Estudios con resonancia magnética muestran un patrón de atrofia hipocampal similar al del deterioro cognitivo leve amnésico y en resonancia funcional hay aumento de activación en tareas cognitivas que podrían representar una compensación ante pérdida de función. Los pacientes con QCS presentan un patrón tipo EA de marcadores betaamiloide (A 42) y tau con mayor frecuencia que la población general. Conclusiones: Las quejas mnésicas son un síntoma relevante y podrían predecir EA. La heterogeneidad de los pacientes y de los ensayos clínicos ha dificultado la definición del síndrome. En el futuro, una definición estandarizada y estudios longitudinales con un seguimiento suficiente, y centrados en variables cuantificables, podrían clarificar aspectos tempranos de la EA

Introduction: Neurodegeneration in Alzheimer disease (AD) begins decades before dementia and patients with mild cognitive impairment (MCI) already demonstrate significant lesion loads. Lack of information about the early pathophysiology in AD complicates the search for therapeutic strategies. Subjective cognitive impairment is the description given to subjects who have memory-related complaints without pathological results on neuropsychological tests. There is no consensus regarding this heterogeneous syndrome, but at least some of these patients may represent the earliest stage in AD. Method: We reviewed available literature in order to summarise current knowledge on subjective cognitive impairment. Results: Although they may not present detectable signs of disease, SCI patients as a group score lower on neuropsychological tests than the general population does, and they also have a higher incidence of future cognitive decline. Depression and psychiatric co-morbidity play a role but cannot account for all cognitive complaints. Magnetic resonance imaging studies in these patients reveal a pattern of hippocampal atrophy similar to that of amnestic mild cognitive impairment and functional MRI shows increased activation during cognitive tasks which might indicate compensation for loss of function. Prevalence of an AD-like pattern of beta-amyloid (A 42) and tau proteins in cerebrospinal fluid is higher in SCI patients than in the general population. Conclusions: Memory complaints are relevant symptoms and may predict AD. Interpatient variability and methodological differences between clinical studies make it difficult to assign a definition to this syndrome. In the future, having a standard definition and longitudinal studies with sufficient follow-up times and an emphasis on quantifiable variables may clarify aspects of early AD

Subjective cognitive impairment: Towards early identification of Alzheimer disease. / Quejas cognitivas subjetivas: hacia una identificación precoz de la enfermedad de Alzheimer.

INTRODUCTION: Neurodegeneration in Alzheimer disease (AD) begins decades before dementia and patients with mild cognitive impairment (MCI) already demonstrate significant lesion loads. Lack of information about the early pathophysiology in AD complicates the search for therapeutic strategies.Subjective cognitive impairment is the description given to subjects who have memory-related complaints without pathological results on neuropsychological tests. There is no consensus regarding this heterogeneous syndrome, but at least some of these patients may represent the earliest stage in AD. METHOD: We reviewed available literature in order to summarise current knowledge on subjective cognitive impairment. RESULTS: Although they may not present detectable signs of disease, SCI patients as a group score lower on neuropsychological tests than the general population does, and they also have a higher incidence of future cognitive decline. Depression and psychiatric co-morbidity play a role but cannot account for all cognitive complaints. Magnetic resonance imaging studies in these patients reveal a pattern of hippocampal atrophy similar to that of amnestic mild cognitive impairment and functional MRI shows increased activation during cognitive tasks which might indicate compensation for loss of function. Prevalence of an AD-like pattern of beta-amyloid (Aß42) and tau proteins in cerebrospinal fluid is higher in SCI patients than in the general population. CONCLUSIONS: Memory complaints are relevant symptoms and may predict AD. Interpatient variability and methodological differences between clinical studies make it difficult to assign a definition to this syndrome. In the future, having a standard definition and longitudinal studies with sufficient follow-up times and an emphasis on quantifiable variables may clarify aspects of early AD.

[Transient ischemic attack: the only presenting syndrome of dural sinus thrombosis]. / Ataque isquémico transitorio como expresión de trombosis de senos venosos durales.

INTRODUCTION: Intracranial hypertension (ICHT) is the most frequent presenting syndrome of dural vein sinus thrombosis (CVT). A transient ischemic attack as an acute mode of onset is exceptional. CASE REPORT: A right handed, forty years old man with a medical history of recurrent headaches, microcephalia and calcifications in his brain, presenting to the emergency department with left paresis that lasted a few minutes and with a complete recovery. The cerebral and neck magnetic resonance (MR) including MR angiography showed superior sagittal sinus, both transverse sinuses and right sigmoid sinus thrombosis with an increase in size of superficial cerebral venous that drained to the left sigmoid sinus. There was no evidence of intracranial dural malformations. The cerebral MR did not show any abnormal parenchymal enhancement (edema, arterial or venous infarctions, hemorrhage) including diffusion-weighted IMR. The digital subtraction angiography (ADC) confirmed the same findings as the MR angiography. The diagnosis was a chronic CVT. We studied stroke in a young adult and we did not find other irregularities. The neurological examination was normal when the patient left the hospital with an antiplatelet drug. CONCLUSIONS: Focal neurological deficit is an exceptional event of a chronic vein sinus thrombosis during follow-up. Isolated cases regarding an acute time course have been described. The interest of this case lies in the fact that venous sinus thrombosis rarely has transitory focal deficit in its course and we found no such description as onset symptoms.

[Neurotransmitters in Alzheimer's disease]. / Neurotransmisores en la enfermedad de Alzheimer.

AIM: To review the current state of the art in neurotransmission in Alzheimer's disease (AD) and its involvement in the pathophysiology of the disease. INTRODUCTION: AD is a neurodegenerative disorder that is estimated to affect 15 million people around the world. Since the cholinergic hypothesis of AD was put forward 20 years ago, numerous studies have been conducted in an attempt to determine the role that neurotransmitters play in AD. Among other things, this has made it possible to develop drugs based on the inhibition of acetylcholinesterase. DEVELOPMENT: The monoaminergic neurotransmission systems are examined, with special attention given to the cholinergic system, and their anatomical distribution, function, receptors, activity and degradation systems are also described. Peptidergic neurotransmission systems are only briefly discussed, since they are not the main objective of this report. We also review the cholinergic hypothesis and the possible interrelations between cholinergic neurotransmission and beta-amyloid metabolism, as well as the potential involvement of acetylcholinesterase inhibitor drugs in more fundamental pathophysiological mechanisms, which act with a neuroprotective component.

Ataque isquémico transitorio como expresión de trombosis de senos venosos durales / Transient ischemic attack: the only presenting syndrome of dural sinus thrombosis

Introducción. La forma más frecuente de expresión de la trombosis de senos venosos (TSV) durales es la hipertensión intracraneal (HTIC). Excepcionalmente puede manifestarse clínicamentre como déficit neurológico focal. Caso clínico. Paciente varón de 40 años, con antecedentes personales de cefaleas recurrentes, microcefalia y calcificaciones cerebrales que consultó por dos episodios de hemiparesia izquierda de minutos de duración con recuperación completa. La resonancia magnética (RM) craneal y cervical, incluyendo secuencias de angio-RM most´ró trombosis del seno sagital superior, ambos senos transversos y seno sigmoide derecho con marcado aumento del tamaño de venas cerebrales superficiales que drenaban en el seno sigmoide izquierdo, sin existencia de malformaciones durales intracraneales. No presentó alteración del parénquima cerebral en forma de edema, infartos, hemorragia ni infartos venosos en ninguna de las secuencias (incluida la difusión). La angiografía por sustracción digital (ADC) confirmó los hallazgos de angio-RM. Se interpretó como TSV de curso crónico, procediendo al estudio de ictus en paciente joven, no encontrando otras alteraciones significativas. La exploración neurológica a alta fue normal, pautándose tratamiento antiagregante. Conclusiones. La sintomatología focal transitoria como manifestación clínica de una TSV de curso crónico es excepcional. Se han descrito casos aislados con referencia a un curso temporal agudo. El interés del caso reside en que la trombosis de senos venosos rara vez presenta clínica focal transitoria deficitaria en su evolución y no hemos encontrado tal descripción como sintomatología de inicio

Introduction. Intracranial hypertension (ICHT) is the most frequent presentig syndrome of dural vein sinus thrombosis (CVT). A transient ischemic attack as an acute mode of onset is exceptional. Case report. A right handed, forty years old man with a medical history of recurrent headaches, microcephalia and calcifications in his brain, presenting to the emergency department with left paresis that lasted a few minutes and with a complete recovery. The cerebral and neck magnetic resonance (MR) including MR angiography showed superior sagital sinus, both transverse sinuses and right sigmoid sinus thrombosis with and increase in size of superficial cerebral venous that drained to the left sigmoid sinus. There was no evidence of intracranial dural malformations. the cerebral MR did not show any abnormal parenchymal enhancement (edema, arterial or venous infarctions, hemorrhage) including diffusion-weighted IMR. The digital subtration angiography (ADC) confirmed the same findings as the MR angiography. the diagnosis was a chronic CVT. We studied stroke in a young adult and we did not find other irregularities . the neurological examination was normal when the patients left the hospìtal with and antiplatelet drug. conclusions. focal neurological deficit is an exception event of a chronic vein sinus thrombosis during follow-up. Isolated cases regarding an acute time course have been described. The interest of this case lies in the fact that venous sinus thrombosis rarely has transitory focal deficit in its course and we found no such description as onset symptoms

Neurotransmisores en la enfermedad de Alzheimer / Neurotransmitters in Alzheimer’s disease

Objetivo. Revisar el estado actual de los conocimientos sobre la neurotransmisión en la enfermedad de Alzheimer (EA) y su implicación en la fisiopatología de la enfermedad. Introducción. La EA es un trastorno neurodegenerativo que se estima que afecta a 15 millones de personas en todo el mundo. Desde que se postuló hace 20 años la hipótesis colinérgica de la EA, se han realizado múltiples estudios para intentar conocer el papel que desempeñan los neurotransmisores en la EA. Entre otras cosas, esto ha permitido el desarrollo de fármacos basados en la inhibición de la acetilcolinesterasa. Desarrollo. Se revisan los sistemas de neurotransmisión monoaminérgicos, con especial atención en el sistema colinérgico, describiendo su distribución anatómica, función, receptores, actividad y sistemas de degradación. Se citan brevemente, ya que no es el objetivo primario de esta revisión, los sistemas de neurotransmisión peptidérgicos y se revisan la hipótesis colinérgica y las posibles interrelaciones entre la neurotransmisión colinérgica y el metabolismo del b-amiloide, así como la posible implicación de los fármacos inhibidores de la acetilcolinesterasa en mecanismos fisiopatológicos más básicos, con un componente neuroprotector (AU)

Aim. To review the current state of the art in neurotransmission in Alzheimer’s disease (AD) and its involvement in the pathophysiology of the disease. Introduction. AD is a neurodegenerative disorder that is estimated to affect 15 million people around the world. Since the cholinergic hypothesis of AD was put forward 20 years ago, numerous studies have been conducted in an attempt to determine the role that neurotransmitters play in AD. Among other things, this has made it possible to develop drugs based on the inhibition of acetylcholinesterase. Development. The monoaminergic neurotransmission systems are examined, with special attention given to the cholinergic system, and their anatomical distribution, function, receptors, activity and degradation systems are also described. Peptidergic neurotransmission systems are only briefly discussed, since they are not the main objective of this report. We also review the cholinergic hypothesis and the possible interrelations between cholinergic neurotransmission and β-amyloid metabolism, as well as the potential involvement of acetylcholinesterase inhibitor drugs in more fundamental pathophysiological mechanisms, which act with a neuroprotective component (AU)

Síndrome de encefalopatía posterior reversible / Posterior reversible encephalopathy syndrome

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