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Background. Neuropsychiatric symptoms (NPS) are a common and potentially serious manifestation of Parkinson’s disease (PD) but are frequently overlooked in favor of a focus on motor symptomatology. Here, we conducted a literature review of the prevalence and type of NPS experienced by PD patients with a clinically defined course of their illness. Methods. We identified reports of NPS in patients with PD and mean disease duration over 3 years. Three databases—PubMed, Scopus, and Dialnet—were searched for relevant literature published between 2010 and 2020. Predefined exclusion criteria were applied prior to a descriptive analysis of the literature base. Results. In all, 87 unique reports were identified and 30 met inclusion and exclusion criteria. These included 7142 patients with PD (male: 67.3%; mean age: 66.2 years; mean disease duration: 6.7 years). The most frequent NPS were mood disorders (apathy, depression, and anxiety), psychosis, and impulse control disorders (ICD). Treatment with dopamine agonists was identified as an important risk factor for ICD. Co-occurrence of NPS and cognitive dysfunction was also evidenced in a number of studies. Patients with more significant cognitive deficits and higher levels of NPS appeared to be of older age with a longer disease duration and to have more severe motor symptoms. Conclusions. NPS, most commonly mood disorders (apathy, depression, and anxiety), psychosis, and ICDs are frequent manifestations of PD. The results of this review reflect the need to develop unified validated assessment protocols for NPS in PD, as well as to improve their management in clinical practice.

BackgroundExcessive oscillations at beta frequencies (13–35 Hz) in the subthalamic nucleus (STN) represent a pathophysiological hallmark of Parkinson's disease (PD), which correlates well with parkinsonian symptoms and is reduced in response to standard disease treatments. However, the association of disease-specific regional gray matter (GM) atrophy or cortical thickness (CT) with the presence of STN beta oscillatory activity has been poorly investigated but is of relevance given the potential of these variables for extracting information about PD pathophysiology. This exploratory study investigated the involvement of regional GM volume and CT in the basal ganglia-cortical network and its potential association with the presence of STN beta oscillatory activity in PD.MethodsWe acquired preoperative GM densities on T1-weighted magnetic resonance imaging scans and we carried out regional estimation of GM volume and CT. LFP activities from the STN were recorded post-operatively in 7 cognitively preserved PD patients off dopaminergic medication undergoing deep-brain stimulation surgery. Oscillatory beta power was determined by power spectral density of 4-min resting state STN LFP activity. Spearman partial correlations and regression analysis were used to screen the presence of STN beta power for their relationship with GM volume and CT measurements.ResultsAfter controlling for the effects of age, educational level, and disease duration, and after correcting for multiple testing, enhanced STN beta power showed significant and negative correlations between, first, volume of the right putamen and left caudate nucleus, and second, smaller CT in frontal regions involving the left rostral middle frontal gyrus (MFG) and left medial orbitofrontal gyrus. A lower volume in the right putamen and a lower CT in the left MFG demonstrated the strongest associations with increased STN beta power.ConclusionsThese tentative results seem to suggest that STN LFP beta frequencies may be mainly linked to different but ongoing parallel neurodegenerative processes, on the one hand, to GM volume reduction in dorsal striatum, and on the other hand, to CT reduction of prefrontal-“associative” regions. These findings could further delineate the brain structural interactions underpinning the exaggerated STN beta activity commonly observed in PD patients.

El estudio y comprensión del deterioro cognitivo en los pacientes de esclerosis múltiple (EM) resulta esencial para entender esta enfermedad. El uso de las técnicas de neuroimagen puede aportar datos a la comprensión de la naturaleza de dichos déficits, así como a su evolución. Durante los últimos años, se ha producido un marcado incremento de trabajos que evalúan la relación entre el deterioro cognitivo de esta población clínica y diversas variables patológicas ob- tenidas mediante técnicas de neuroimagen clásicas, así como mediante el uso de otros procedimientos de desarrollo más reciente. Los resultados de los estudios que usan técnicas de neuroimagen estructural han revelado la importancia de procesos atróficos en el deterioro cognitivo de la EM. Sin embargo, esta información debe complementarse con la aporta- da por otros procedimientos más novedosos acerca de alteraciones en la sustancia blanca y en la sustancia gris de ‘apariencia normal’. Por otra parte, los estudios que han empleado técnicas de resonancia magnética funcional han mostrado la existencia de distintos procesos de neuroplasticidad que pueden enmascarar la relación entre los índices morfológicos de daño cerebral y el rendimiento cognitivo de los pacientes con EM. Estos procesos no deben ignorarse, en tanto que pueden compensar las alteraciones cognitivas de esta población clínica. El presente trabajo de revisión intenta aportar una visión crítica e integradora de los estudios dedicados a evaluar la relación entre el deterioro cognitivo de la EM y diferentes tipos de información aportados por las técnicas de neuroimagen. Studying the cognitive impairment of multiple sclerosis (MS) patients is fundamental for a global understanding of this disease. Neuroimaging techniques might provide crucial data about the nature of this deficit and their progression. Accordingly to this idea, over the last years there has been a marked increase in the number of studies devoted to explore the possible relationship between the cognitive alterations of this clinical population and different sorts of neuropathological indexes provided by both, classical as well as by more recently developed techniques. The results of the studies using structural information provided by structural techniques, have revealed the important role of atrophic processes in the aethiology of cognitive decline in MS patients. However, this information needs to be complemented with newer indexes of neuropathological alterations in ‘apparently normal’ gray and white matter. On the other hand, functional magnetic resonance imaging studies have provided clear evidence of the existence and functional significance of neuroplastic processes that can mask the relationship between morphological markers of tissue damage and cognitive performance of MS patients. Those neuroplastic processes need to be taken into account as they might compensate the cognitive decline of this clinical population. In summary, the present review tries to provide a critic and integrative view of different studies assessing the relationship between cognitive impairment in MS patients and different kinds of information provided by neuroimaging techniques.