Influencia de la infección SARS-CoV-2 sobre enfermedades neurodegenerativas y neuropsiquiátricas: ¿una pandemia demorada?

Abstract

INTRODUCCIÓN: La infección por el coronavirus SARS-CoV2 originada en Diciembre de 2019 en la región china de Wuhan ha adquirido proporciones pandémicas. A día de hoy ha ocasionado de Impact of SARS-CoV-2 infection on neurodegenerative and neuropsychiatric diseases: a delayed pandemic?ABSTRACT Introduction: SARS-CoV-2 was first detected in December 2019 in the Chinese city of Wuhan and has since spread across the world. At present, the virus has infected over 1.7 million people and caused over 100 000 deaths worldwide. Research is currently focused on understanding the acute infection and developing effective treatment strategies. In view of the magnitude of the epidemic, we conducted a speculative review of possible medium-and long-term neurological consequences of SARS-CoV-2 infection, with particular emphasis on neurodegenerative and neuropsychiatric diseases of neuroinflammatory origin, based on the available evidence on neurological symptoms of acute SARS-CoV-2 infection. Development:We systematically reviewed the available evidence about the pathogenic mechanisms of SARS-CoV-2 infection, the immediate and lasting effects of the cytokine storm on the central nervous system, and the consequences of neuroinflammation for the central nervous system.Conclusions: SARS-CoV-2 is a neuroinvasive virus capable of triggering a cytokine storm, with persistent effects in specific populations. Although our hypothesis is highly speculative, the impact of SARS-CoV-2 infection on the onset and progression of neurodegenerative and neuropsychiatric diseases of neuroinflammatory origin should be regarded as the potential cause of a delayed pandemic that may have a major public health impact in the medium to long term. Cognitive and neuropsychological function should be closely monitored in COVID-19 survivors.

The psychiatric and neuropsychiatric repercussions associated with severe infections of COVID-19 and other coronaviruses

“…Although the main clinical signs are related to respiratory function, SARS-CoV-2 is also capable of infecting cells of the Nervous System, intestinal mucosa, kidneys and lymphoid system, for example, culminating in nausea, diarrhea, vomiting, among other symptoms whose severity depends on tissue sensibility ( Serrano-Castro et al, 2020 ; Li et al, 2020 ). For possible associations between SARS-CoV-2 tropism and neurological symptoms, it is necessary to understand its characteristics and its similarity to SARS-CoV.…”

18F-FDG brain PET metabolism in post-SARS-CoV-2 infection: substrate for persistent/delayed disorders?

“…Accordingly, a cortical FLAIR-MRI hyperintensity was visually identi ed in the right gyrus rectus and olfactory bulbs of a patient with SARS-CoV-2 anosmia [6]. By trans-synaptic transfer, again already reported for other virus [7], this propagation from the olfactory bulb could spread to other limbic structures, such as the amygdala, the hippocampus, and the cingulate cortex which are well-known to be involved in cognition and emotion [8], and pathologically in neurodegenerative and neuropsychiatric diseases [2]. SARS-CoV-2 may also target deeper parts of the brain including the thalamus and the brainstem, and then potentially contributes to the respiratory impairment [7], and also to painful symptoms.…”

“…Post-viral cohort studies are required to specify the exact relationship between limbic/brainstem hypometabolisms and the possible persistent disorders, especially involving cognitive or emotion disturbances, residual respiratory symptoms or painful complaints. These metabolic features could be also correlated to other brain PET biomarkers of neuroin ammation and infection, such as TSPO and CXCR4 expressions [10], to address the possible relationship with the hypothesized association to neuropsychiatric and neurodegenerative diseases of neuroin ammatory origin [2]. Figure 1 Brain 18F-FDG PET hypometabolism of the rst patient.…”

“…Several brain complications of SARS-CoV-2 infection have been already reported including acute cerebrovascular disorders, encephalopathy, encephalitis, and Guillain-Barré syndromes [1]. It has been moreover speculated that SARS-CoV-2 neurotropism could potentially cause a delayed outbreak with onset and progression of neuropsychiatric and neurodegenerative diseases of neuroin ammatory origin [2]. A recent systematic review and meta-analysis of other coronavirus infections con rms confusion, depressed mood, anxiety, impaired memory or insomnia in 27.9 to 41.9% of patients in the acute illness, while in the post-illness stage, the prevalence of post-traumatic stress disorder was of 32.2%, and almost 15% for depression and anxiety disorders [3], with also a clinical overlap with bromyalgia and chronic fatigue syndrome [4].…”

¿Va a cambiar la neurología tras la pandemia de COVID-19 en los próximos 5 años? Estudio de enfoque mediante informadores clave

“…El confinamiento (1) y la situación muchas veces de colapso en los hospitales de nuestro país está provocando un nuevo escenario de atención médica, al que también se ven expuestos los servicios de Neurología (2 ) . Aunque la presencia de clínica neurológica en los pacientes primeros pacientes afectados por Covid-19 fue aparentemente baja según lo que se muestra en las primera series publicadas (3,4,5,6,7,8,9) , así como la descripción de casos neurológicos empieza a ser más frecuente (10,11,12 ) , las consecuencias en el sistema nervioso central a medio y largo plazo de la pandemia (13,14,15,16,17) o el impacto sobre las enfermedades neurológicas (18) . Una de las amenazas que presenta la pandemia de COVID-19 es lo que grupos de oncología han denominado como "el efecto de distracción" (19) , que supone que al desviar la atención preferente a los pacientes infectados por Covid-19 se disminuye o se deja al descubierto la atención al resto de las enfermedades, especialmente como consecuencia de la asignación de recursos a un problema urgente y que se percibe como decisivo, ello podría ocurrir también en el enfermo neurológico.…”