ABSTRACT
La neuropatía diabética se presenta hasta en el 60 % de los pacientes diabéticos. La neuropatía diabética periférica es la causa más común de neuropatía en el mundo. La fisiopatología de la neuropatía diabética involucra daño periférico nervioso por acumulación de productos tóxicos derivados de la hiperglicemia. El sistema nervioso central se ve posteriormente involucrado a través de sensibilización, disminución de la función del sistema inhibitorio y aumento en la excitabilidad del sistema de facilitación. La clínica más común se manifiesta de manera simétrica afectando fibras sensitivas pequeñas y grandes, aunque se han encontrado formas atípicas de presentación. Las pruebas diagnósticas confirmatorias se reservan para la duda diagnóstica, casos de síntomas atípicos o investigación. El consenso en cuanto a tratamiento es el uso de gabapentinoides, antidepresivos tricíclicos e inhibidores de recaptura de serotonina y noradrenalina. Estas tres familias se consideran como primera línea de tratamiento.
Diabetic neuropathy occurs in up to 60% of diabetic patients. Diabetic peripheral neuropathy is the most common cause of neuropathy in the world. The pathophysiology of diabetic neuropathy involves peripheral nerve damage due to the accumulation of toxic products derived from hyperglycemia. The central nervous system is subsequently involved through sensitization, decreased function of the inhibitory system, and increased excitability of the facilitative system. The most common symptoms manifest symmetrically, affecting small and large sensory fibers, although atypical forms of presentation have been found. Confirmatory diagnostic tests are reserved for diagnostic doubt, atypical symptoms, or research. The consensus regarding treatment is the prescription of gabapentinoids, tricyclic antidepressants, and serotonin and norepinephrine reuptake inhibitors. These three families are considered the first line.
ABSTRACT
INTRODUCTION: Cognitive impairment is common in Parkinson's disease and represents a risk for dementia. Identifying associated factors will help implement early interventions and study its progression. OBJECTIVE: To identify factors associated with cognitive impairment. METHOD: Cross-sectional study of 306 subjects with Parkinson's disease who were assessed for 12 months. Demographics and clinical variables were analyzed as explanatory variables, and cognitive impairment as outcome variable. Significant variables were used to construct a cognitive impairment predictive model. RESULTS: Cognitive impairment was reported in 43.8%. Female gender (p = 0.001, odds ratio [OR] = 1.77), age at diagnosis (p < 0.001, mean deviation [MD] = 5.7), level of education (p < 0.001, MD = -2.9), disease duration (p = 0.003, MD = 1.7), MDS-UPDRS part III score (p < 0.001, MD = 9.7), presence of anxiety (p = 0.007, OR = 2.11), hallucinations (p = 0.029, OR = 2.27) and freezing of gait (p = 0.048, OR = 1.91) were predictors for cognitive impairment. The use of type B monoamine oxidase inhibitors was associated with less cognitive impairment (p = 0.001). CONCLUSIONS: Predictive factors that were consistent with those previously reported were identified. Prospective studies are required in order to clarify the effect of type B monoamine oxidase inhibitors on cognition.
INTRODUCCIÓN: El deterioro cognitivo en Parkinson es común y representa un riesgo para demencia. Identificar los factores asociados ayudará a implementar intervenciones tempranas y estudiar la progresión del deterioro cognitivo. OBJETIVO: Identificar factores asociados con deterioro cognitivo. MÉTODO: Estudio transversal de 306 sujetos con Parkinson evaluados durante los últimos 12 meses. Se estudiaron variables demográficas y clínicas como explicativas y el deterioro cognitivo como desenlace. Las variables significativas se utilizaron para construir un modelo predictor de deterioro cognitivo. RESULTADOS: El 43.8 % reportó deterioro cognitivo. El sexo femenino (p = 0.001, RM = 1.77), edad al diagnóstico (p < 0.001, desviación media [DM] 5.7), escolaridad (p < 0.001, DM −2.9), duración de enfermedad (p = 0.003, DM 1.7), puntuación en MDS-UPDRS parte III (p < 0.001, DM 9.7), presencia de ansiedad (p = 0.007, RM = 2.11), de alucinaciones (p = 0.029, RM = 2.27) y congelamientos de la marcha (p = 0.048, RM = 1.91) fueron predictores para deterioro cognitivo. El uso de inhibidores monoamina-oxidasa tipo B se asoció con menor deterioro cognitivo (p = 0.001). CONCLUSIONES: Se identificaron factores predictores consistentes con lo reportado previamente. Se requieren estudios prospectivos para aclarar el efecto de los inhibidores monoamina-oxidasa tipo B en la cognición.
Subject(s)
Cognitive Dysfunction/etiology , Monoamine Oxidase Inhibitors/administration & dosage , Parkinson Disease/complications , Age Factors , Aged , Aged, 80 and over , Cognitive Dysfunction/epidemiology , Cross-Sectional Studies , Disease Progression , Female , Humans , Male , Mexico , Middle Aged , Monoamine Oxidase Inhibitors/pharmacology , Parkinson Disease/physiopathology , Risk Factors , Sex Factors , Time FactorsABSTRACT
BACKGROUND: Recent studies have shown that cerebral vascularity may be impaired in Alzheimer's disease. Cerebral vasomotor reactivity could be an important biomarker for this pathology. AIMS: The aim of this study was to investigate the alterations in cerebral vascular motor reactivity in Alzheimer's disease subjects and to associate these changes with their cognitive scores. METHODS: We recruited subjects with a diagnosis of Alzheimer's disease and healthy controls. Demographic, clinical, imaging, and cognitive test were obtained. Then all participants performed a cerebral vascular motor reactivity test with 7% CO2 and cerebral blood flow velocities (CBFV) were recorded with transcranial doppler ultrasound before and after the test. RESULTS: We recruited 45 subjects, 26 (21 female) Alzheimer's disease participants and 19 (15 female) healthy controls. There were no differences in baseline cerebral blood flow velocities between the groups. After the cerebral vasomotor reactivity test, absolute mean difference in mean CBFV (ΔCBFV-m) was 8.70±4.14 versus 4.81±6.96 (p<0.01), respectively. Calculated percentage of change (%CVMR) was lower in the AD group 7.45±18.25 versus 23.29±17.48, and there was a positive but weak correlation with mini-mental scores (ρ=0.337, p=0.023). CONCLUSIONS: In this study, Alzheimer's disease subjects showed significant changes in all absolute cerebral blood flow velocities after the cerebral vasomotor reactivity test with CO2, but only diastolic phase responses were statistically significant. There was a positive but weak correlation between cerebral vasomotor reactivity and cognitive scores. Further studies are needed to investigate these effects in larger Latin-American samples.
ABSTRACT
The relationship between frailty and cognitive impairment has been recognized for decades, but it was not until a few years ago that the interest in this relationship increased and is now being understood. Epidemiological evidence suggests that physical frailty may be linked to cognitive impairment since both conditions share pathophysiological mechanisms at the cellular and systemic levels. Aging itself promotes multiple vascular changes, making the brain susceptible to cognitive decline through mechanisms such as thinning of blood vessels, increased collagen accumulation, rupture of the blood-brain barrier, inflammation, and oxidative damage. The prevalence of frailty and cognitive decline increases as individuals become older, and cognitive impairment attributable to cerebrovascular disease has become a major public health problem since vascular dementia is now the second most common subtype of dementia. However, full understanding of the mechanisms underlying the relationship between frailty and vascular cognitive impairment remains fragmented. This review examines the link between frailty and vascular cognitive decline and also explores the role of vascular changes in the genesis of both conditions.
