ABSTRACT
Alzheimer's and Parkinson's diseases are the most prevalent neurodegenerative disorders. Their etiologies are idiopathic, and treatments are symptomatic and orientated towards cognitive or motor deficits. Neuropathologically, both are proteinopathies with pathological aggregates (plaques of amyloid-ß peptide and neurofibrillary tangles of tau protein in Alzheimer's disease, and Lewy bodies mostly composed of α-synuclein in Parkinson's disease). These deposits appear in the nervous system in a predictable and accumulative sequence with six neuropathological stages. Both disorders present a long prodromal period, characterized by preclinical signs including hyposmia. Interestingly, the olfactory system, particularly the anterior olfactory nucleus, is initially and preferentially affected by the pathology. Cerebral atrophy revealed by magnetic resonance imaging must be complemented by histological analyses to ascertain whether neuronal and/or glial loss or neuropil remodeling are responsible for volumetric changes. It has been proposed that these proteinopathies could act in a prion-like manner in which a misfolded protein would be able to force native proteins into pathogenic folding (seeding), which then propagates through neurons and glia (spreading). Existing data have been examined to establish why some neuronal populations are vulnerable while others are resistant to pathology and to what extent glia prevent and/or facilitate proteinopathy spreading. Connectomic approaches reveal a number of hubs in the olfactory system (anterior olfactory nucleus, olfactory entorhinal cortex and cortical amygdala) that are key interconnectors with the main hubs (the entorhinal-hippocampal-cortical and amygdala-dorsal motor vagal nucleus) of network dysfunction in Alzheimer's and Parkinson's diseases.
Subject(s)
Alzheimer Disease/diagnostic imaging , Olfactory Pathways/diagnostic imaging , Parkinson Disease/diagnostic imaging , Smell/physiology , Alzheimer Disease/complications , Alzheimer Disease/physiopathology , Humans , Olfaction Disorders/complications , Olfaction Disorders/physiopathology , Olfactory Bulb/diagnostic imaging , Olfactory Bulb/physiopathology , Olfactory Pathways/physiopathology , Parkinson Disease/complications , Parkinson Disease/physiopathologyABSTRACT
Originally discovered in elasmobranchs by Fritsh in 1878, the nervus terminalis has been found in virtually all species, including humans. After more than one-century debate on its nomenclature, it is nowadays recognized as cranial pair zero. The nerve mostly originates in the olfactory placode, although neural crest contribution has been also proposed. Developmentally, the nervus terminalis is clearly observed in human embryos; subsequently, during the fetal period loses some of its ganglion cells, and it is less recognizable in adults. Fibers originating in the nasal cavity passes into the cranium through the middle area of the cribiform plate of the ethmoid bone. Intracranially, fibers joint the telencephalon at several sites including the olfactory trigone and the primordium of the hippocampus to reach preoptic and precommissural regions. The nervus terminalis shows ganglion cells, that sometimes form clusters, normally one or two located at the base of the crista galli, the so-called ganglion of the nervus terminalis. Its function is uncertain. It has been described that its fibers facilitates migration of luteinizing hormone-releasing hormone cells to the hypothalamus thus participating in the development of the hypothalamic-gonadal axis, which alteration may provoke Kallmann's syndrome in humans. This review summarizes current knowledge on this structure, incorporating original illustrations of the nerve at different developmental stages, and focuses on its anatomical and clinical relevance. Anat Rec, 302:394-404, 2019. © 2018 Wiley Periodicals, Inc.
Subject(s)
Cranial Nerves/anatomy & histology , Kallmann Syndrome/pathology , Nasal Mucosa/anatomy & histology , Nerve Endings/chemistry , Animals , Cranial Nerves/metabolism , Humans , Kallmann Syndrome/metabolism , Luteinizing Hormone/metabolism , Nasal Mucosa/metabolism , Nerve Endings/metabolismABSTRACT
El trastorno de conversión (término que describe lo que anteriormente se llamaba histeria) se refiere a los síntomas motores, sensitivos o ambos, que se asemejan a una enfermedad neurológica, pero que no tienen origen en una enfermedad física conocida, ni se pueden explicar por ella, dándose la particularidad de que el enfermo no es consciente de lo que le ocurre. La incapacidad funcional para los pacientes a veces es mayor que la observada en los casos en los que, con una semiología similar, hay un sustrato orgánico. Material y método: Presentamos 16 pacientes, valorados en consulta externa de neurología, con un trastorno motor o sensitivo, sin evidencia de enfermedad orgánica subyacente, con al menos un año de seguimiento. Discusión: Se comentan las características semiológicas. La fisiopatología de los síndromes conversivos está todavía en discusión. Las técnicas de neuroimágenes funcionales parecen mostrar alteraciones que nos permiten acercarnos a la fisiopatología de estos trastornos. Es importante señalar que aunque la fisiopatología de los síndromes conversivos está todavía en discusión, lo cierto es que se trata de pacientes de diagnóstico difícil, pero posible; es responsabilidad del médico intentar entender el sustrato neurológico de un problema que implica una gran incapacidad funcional e instaurar un tratamiento adecuado, buscando, si es necesario, la colaboración de un psiquiatra con experiencia en el abordaje de estos trastornos...
Subject(s)
Humans , Disease , Neurology , Patients , Dyskinesias , PsychiatryABSTRACT
OBJECTIVES: To make an analysis of the usefulness of urodynamic tests and what can be obtained from them. METHODS: We also perform and analytical deduction of those parameters that define detrusor behavior, such as the constant defining bladder compliance, the bladder elastic constant, in its tensile properties, and we found the expression of resistances and calculate the abdominal pressure formula; therefore we don't need to introduce a rectal catheter to know the value of those parameters that define bladder dynamics. RESULTS: Although they are provisional, they allow foreseeing a promising future for this application of a well-known device. CONCLUSIONS: Currently, we can only define the bladder behaviour, its resistances, the detrusor drive and compliance with the only discomfort of a perineal Doppler ultrasound. Time will open new possibilities.
Subject(s)
Urodynamics , Humans , Mathematics , Ultrasonography, DopplerABSTRACT
OBJETIVOS: En este trabajo, hacemos un análisis somero de las utilidades de las pruebas urodinámicas y de lo que de ellas podemos obtener. MÉTODOS: También hacemos una deducción analítica de los parámetros que definen el comportamiento del detrusor, como son la constante que define la acomodación vesical, la constante elástica de la vejiga, en lo que de tensor tiene y hallamos la expresión de las resistencias, y calculamos la fórmula de la presión abdominal; por lo que no necesitamos colocar sonda transrectal para conocer el valor de los parámetros que definen la dinámica vesical. RESULTADOS: Aun siendo provisionales, dejan preveer un futuro prometedor, para esta aplicación de un dispositivo ya conocida por todos. CONCLUSIONES: De momento hemos de conformarnos con definir el comportamiento vesical, sus resistencias, empuje del detrusor y acomodación del mismo; sin mas molestias que la eco-doppler perineal. El tiempo nos irá abriendo posibilidades (AU)
