Trastornos del sueño en la enfermedad de Parkinson y otros trastornos del movimiento

Neurodegenerative processes with movement disorders is predominant features show a high incidence of sleep alterations at some point in their evolution. The degeneration of structures responsible for maintaining the sleep-wakefulness cycles and the architecture of sleep could be at their root. Other factors like the drugs employed in the treatment of motor problems, the limitations to movement, etc., aggravate the problem. Although, at present, there is no medical therapy able to restore the defects derived from the degeneration of the key structures of sleep, an individual analysis of the coadyuvant factors in each patient could help to improve these problems. In this article we describe the main sleep disorders in Parkinson’s disease and other degenerative diseases such as multi-system atrophies or progressive supranuclear paralysis

Revisión crítica de la estimulación subtalámica en la enfermedad de Parkinson

The authors critically review subthalamic nucleus (STN) stimulation for Parkinson's disease (PD) at long follow-up (3-5 years). Subthalamic stimulation induce a significant improvement during the "off" medication in the assessment motor score UPDRS (Unified Parkinson Disease Rating Scale) 3-5 years after surgery. Results show that the benefits obtained in tremor, rigidity, bradykinesia, dyskinesias induced by medication and levodopa reduction are significantly maintained during long term. The improvement in other clinical signs as gait and postural stability at long follow-up are not maintained comparing with the benefits obtained one year after surgery. A high percentage of patients show a cognitive disturbance during the follow-up period that may be correlated with the disease progression. The conclusion is that bilateral STN stimulation is an effective treatment for PD patients at long term but it should be considered earlier in the course of P

Efecto de los polifenoles sobre la microbiota intestinal en el síndrome metabólico

Durante los últimos años, el estudio de la microbiota intestinal ha surgido como un campo de investigación emergente, ya que se ha demostrado que se ve involucrada en una infinidad de procesos metabólicos que repercuten en la salud del huésped. En concreto, se ha visto que las personas que padecen alguna de las patologías asociadas al síndrome metabólico poseen una microbiota intestinal alterada que provoca un estado patológico denominado “disbiosis intestinal”. Este estado, provocado en parte por el consumo actual de dietas altas en grasa y azúcares y pobres en fibra, se caracteriza por una disminución de la diversidad microbiana y una alteración en su composición, y parece estar fuertemente relacionado con la aparición y desarrollo de las patologías del síndrome metabólico. Entre las distintas estrategias descritas para modificar la microbiota intestinal alterada, se ha observado que la suplementación de la dieta con ciertos tipos de polifenoles, como el resveratrol o las antocianinas, pueden revertir la disbiosis intestinal, ayudando a la proliferación de bacterias beneficiosas para nuestro organismo, como Akkermansia muciniphila, a la vez que disminuyen la cantidad de bacterias nocivas, como las pertenecientes al filo Firmicutes y estimulando así una mayor producción de ácidos grasos de cadena corta, como el butirato. En este trabajo se ha llevado a cabo una revisión de la bibliografía disponible sobre la capacidad de diversos polifenoles (no flavonoides, flavonoles y flavanoles) de contrarrestar el efecto de una dieta occidental sobre la microbiota intestinal, revirtiendo los efectos del síndrome metabólico, así como un estudio de los principales mecanismos implicados en este proceso.In recent years, the study of the intestinal microbiota has emerged as a field of research. Since it has been shown that it is involved in an infinite number of metabolic processes that affect the health of the host. Specifically, people suffering from any of the pathologies associated with the metabolic syndrome have an altered intestinal microbiota that causes a medical state called "intestinal dysbiosis". This state is caused partially due to current consumption of diets high in fat and sugars, and poor in fiber. Consequently, decreasing microbial diversity and altering its composition. Strongly correlating with the appearance and development of metabolic syndrome pathologies. Among the different strategies described to modify the altered intestinal microbiota, it has been observed that dietary supplementation with certain types of polyphenols, such as resveratrol or anthocyanins can reverse intestinal dysbiosis. Therefore, promoting the proliferation of beneficial bacteria for our body, like Akkermansia muciniphila, while reducing the number of harmful bacteria such as those belonging to the Firmicutes phylum. As a result, stimulating a greater production of short chain fatty acids as butyrate. This paper reviews the available literature on various polyphenols (non-flavonoids, flavonols and flavanols) and their ability to counteract the effect of a western diet on the intestinal microbiota. Focusing on reversing the effects of the metabolic syndrome, as well as analyzing the main mechanism involved in this process

Functional correlates of response inhibition in impulse control disorders in Parkinson’s disease

Impulse control disorder is a prevalent side-effect of Parkinson’s disease (PD) medication, with a strong negative impact on the quality of life of those affected. Although impulsivity has classically been associated with response inhibition deficits, previous evidence from PD patients with impulse control disorder (ICD) has not revealed behavioral dysfunction in response inhibition. In this study, 18 PD patients with ICD, 17 PD patients without this complication, and 15 healthy controls performed a version of the conditional Stop Signal Task during functional magnetic resonance imaging. Whole-brain contrasts, regions of interest, and functional connectivity analyses were conducted. Our aim was to investigate the neural underpinnings of two aspects of response inhibition: proactive inhibition, inhibition that has been prepared beforehand, and restrained inhibition, inhibition of an invalid inhibitory tendency. We observed that, in respect to the other two groups, PD patients with ICD exhibited hyperactivation of the stopping network bilaterally while performing proactive inhibition. When engaged in restrained inhibition, they showed hyperactivation of the left inferior frontal gyrus, an area linked to action monitoring. Restrained inhibition also resulted in changes to the functional co-activation between inhibitory regions and left inferior parietal cortex and right supramarginal gyrus. Our findings indicate that PD patients with ICD completed the inhibition task correctly, showing altered engagement of inhibitory and attentional areas. During proactive inhibition they showed bilateral hyperactivation of two inhibitory regions, while during restrained inhibition they showed additional involvement of attentional areas responsible for alerting and orientin

The impact of silent vascular brain burden in cognitive impairment in Parkinson's disease

White matter hyperintensities (WMHs) detected by magnetic resonance imaging (MRI) of the brain are associated with dementia and cognitive impairment in the general population and in Alzheimer's disease. Their effect in cognitive decline and dementia associated with Parkinson's disease (PD) is still unclear. METHODS: We studied the relationship between WMHs and cognitive state in 111 patients with PD classified as cognitively normal (n = 39), with a mild cognitive impairment (MCI) (n = 46) or dementia (n = 26), in a cross-sectional and follow-up study. Cognitive state was evaluated with a comprehensive neuropsychological battery, and WMHs were identified in FLAIR and T2-weighted MRI. The burden of WMHs was rated using the Scheltens scale. RESULTS: No differences in WMHs were found between the three groups in the cross-sectional study. A negative correlation was observed between semantic fluency and the subscore for WMHs in the frontal lobe. Of the 36 non-demented patients re-evaluated after a mean follow-up of 30 months, three patients converted into MCI and 5 into dementia. Progression of periventricular WMHs was associated with an increased conversion to dementia. A marginal association between the increase in total WMHs burden and worsening in the Mini Mental State Examination was encountered. CONCLUSIONS: White matter hyperintensities do not influence the cognitive status of patients with PD. Frontal WMHs have a negative impact on semantic fluency. Brain vascular burden may have an effect on cognitive impairment in patients with PD as WMHs increase overtime might increase the risk of conversion to dementia. This finding needs further confirmation in larger prospective studies