Cerebral Small Vessel Disease: A Review Focusing on Pathophysiology, Biomarkers, and Machine Learning Strategies.

Cerebral small vessel disease (cSVD) has a crucial role in lacunar stroke and brain hemorrhages and is a leading cause of cognitive decline and functional loss in elderly patients. Based on underlying pathophysiology, cSVD can be subdivided into amyloidal and non-amyloidal subtypes. Genetic factors of cSVD play a pivotal role in terms of unraveling molecular mechanism. An important pathophysiological mechanism of cSVD is blood-brain barrier leakage and endothelium dysfunction which gives a clue in identification of the disease through circulating biological markers. Detection of cSVD is routinely carried out by key neuroimaging markers including white matter hyperintensities, lacunes, small subcortical infarcts, perivascular spaces, cerebral microbleeds, and brain atrophy. Application of neural networking, machine learning and deep learning in image processing have increased significantly for correct severity of cSVD. A linkage between cSVD and other neurological disorder, such as Alzheimer's and Parkinson's disease and non-cerebral disease, has also been investigated recently. This review draws a broad picture of cSVD, aiming to inculcate new insights into its pathogenesis and biomarkers. It also focuses on the role of deep machine strategies and other dimensions of cSVD by linking it with several cerebral and non-cerebral diseases as well as recent advances in the field to achieve sensitive detection, effective prevention and disease management.

[Protocol for neurophysiological studies of the pelvic floor to appraise anorectal dysfunction in patients with multiple sclerosis]. / Protocolo de estudios neurofisiológicos del suelo pélvico para la valoración de la disfunción anorrectal en pacientes con esclerosis múltiple.

INTRODUCTION: Patients with multiple sclerosis (MS) frequently develop anorectal dysfunction. The neuromuscular structures of the pelvic floor and the mechanisms of voluntary control over defecation can be compromised by the patchy lesions of MS or secondary to the patient's disability. The involvement of multiple factors limits understanding of the pathophysiology of anorectal dysfunction in MS. Specific neurophysiological tests assess the functionality of the elements of the central and peripheral nervous system involved in anorectal dysfunction. AIM: To propose a diagnostic protocol of standardised neurophysiological studies of the pelvic floor in order to characterise the pathophysiology of anorectal dysfunction in patients with MS. PATIENTS AND METHODS: The following studies were conducted on 16 patients with defined MS and who met criteria for constipation or faecal incontinence: external anal sphincter electromyography (EAS-EMG), somatosensory evoked potentials (SSEP) of the internal pudendal nerve, recording of ano-sacral reflexes and pudendal nerve neurography. RESULTS: The clinical and neurophysiological characteristics were heterogeneous. Nine patients presented constipation; two had isolated faecal incontinence; and five, a combination of both. Abolition or delay in the latency of the SSEP was the most frequent finding (n = 12), followed by the detection of paradoxical contraction (n = 11) and deficient recruitment (n = 8) in the EAS-EMG. CONCLUSIONS: The correct interpretation of each available neurophysiological test and the correlation of the findings as a whole enable us to understand the pathophysiology of anorectal dysfunction. The implementation of a protocol for neuro-physiological studies of the pelvic floor makes it possible to adjust the diagnosis by identifying the central or peripheral nervous lesion determining anorectal dysfunction in patients with MS.

TITLE: Protocolo de estudios neurofisiologicos del suelo pelvico para la valoracion de la disfuncion anorrectal en pacientes con esclerosis multiple.Introduccion. Los pacientes con esclerosis multiple (EM) frecuentemente desarrollan disfuncion anorrectal. Las estructuras neuromusculares del suelo pelvico y los mecanismos de control voluntario de la defecacion pueden afectarse por las lesiones parcheadas de la EM o secundarias a la discapacidad del paciente. La implicacion multifactorial limita la comprension de la fisiopatologia de la disfuncion anorrectal en la EM. Tests neurofisiologicos especificos valoran la funcionalidad de los elementos del sistema nervioso central y periferico implicados en las disfunciones anorrectales. Objetivo. Proponer un protocolo diagnostico de estudios neurofisiologicos estandarizados del suelo pelvico para caracterizar la fisiopatologia de la disfuncion anorrectal en los pacientes con EM. Pacientes y metodos. Se realizaron estudios de electromiografia de esfinter anal externo, potenciales evocados somatosensoriales desde el nervio pudendo interno, registro de reflejos sacros anales y neurografia del nervio pudendo a 16 pacientes con EM definida y criterios de estreñimiento o incontinencia fecal. Resultados. Las caracteristicas clinicas y neurofisiologicas fueron heterogeneas. Nueve pacientes presentaron estreñimiento; dos, incontinencia fecal aislada; y cinco, combinacion de ambos. La abolicion o el retraso de la latencia de los potenciales evocados somatosensoriales fue el hallazgo mas frecuente (n = 12), seguido de la deteccion de contraccion paradojica (n = 11) y de reclutamiento deficitario (n = 8) en la electromiografia de esfinter anal externo. Conclusiones. La correcta interpretacion de cada test neurofisiologico disponible y la correlacion de los hallazgos en conjunto permiten comprender la fisiopatologia de la disfuncion anorrectal. La protocolizacion de estudios neurofisiologicos del suelo pelvico permite ajustar el diagnostico al identificar la lesion nerviosa, central o periferica, determinante de disfuncion anorrectal en los pacientes con EM.

CHA(2)DS(2)-VASc score and prognosis in ischemic strokes with atrial fibrillation.

The CHA(2)DS(2)-VASc score was developed to improve stroke risk stratification in atrial fibrillation (AF) patients. We sought to analyze the distribution and prognostic value of the CHA(2)DS(2)-VASc score in a cohort of ischemic stroke patients with AF. In total, 439 consecutive stroke patients with AF were studied. The CHA(2)DS(2)-VASc score was calculated according to clinical status before stroke onset. Poor outcome was defined as a modified Rankin score of 3 to 6 at 3 months. Association between CHA(2)DS(2)-VASc score and poor outcome was analyzed using logistic regression analysis. In 95.6% of patients, CHA(2)DS(2)-VASc was >1 and only 41.8% of those with previously diagnosed AF were using oral anticoagulation at the time of the stroke. Poor outcome was found in 53.1% of the patients. In univariate analysis age, female sex, current smoking, previous stroke, CHA(2)DS(2)-VASc score, and stroke severity were associated with outcome. In multivariate analysis, CHA(2)DS(2)-VASc score was independently associated with poor outcome [OR 1.36 (95% CI: 1.14-1.62), P = 0.001] as well as NIHSS [OR 1.22 (95% CI: 1.17-1.26), P < 0.001]. After removing stroke severity, therapeutic anticoagulation was also associated with stroke prognosis [OR 0.45 (95% CI: 0.23-0.86), P = 0.016]. Most patients with ischemic stroke and AF have a high CHA(2)DS(2)-VASc score. Independent of stroke severity, CHA(2)DS(2)-VASc score is associated with 3-month outcome. Despite all the available information and guidelines, our AF patients are clearly undertreated.

[Review of the model of vertical gaze control]. / Revisión del modelo del control de la mirada vertical.

INTRODUCTION: The main structures involved in the control of vertical gaze, both saccades, smooth pursuit and oculovestibular reflexes, are the rostral interstitial nucleus of medial longitudinal fasciculus, posterior commissure, interstitial nucleus of Cajal, oculomotor complex and trochlear nerve nucleus. Despite knowing the functions of these nuclei, and their main interconnections, afferents and efferents, there is no definitive and contrasted model of vertical gaze control in humans. AIM: Through the description of three cases, and as described in scientific literature, our aim is to review the models described to date. DEVELOPMENT: The control of vertical saccades generates in the rostral interstitial nucleus of medial longitudinal fasciculus, projecting to the pertinent oculomotor nuclei ipsilaterally for the inferior gaze, and bilaterally for the superior gaze. CONCLUSIONS: The double cross-innervation of the nuclei responsible for superior gaze, implies that unilateral lesions predominantly affect the inferior gaze.