It has been shown that the acoustic startle reflex is inhibited by weak auditory prepulses presented 30-500 ms prior to the startling stimulus and that this prepulse inhibition (PPI) is modulated by ventral striato-pallidal circuitry. However, dorsal striatal modulation of PPI has not been examined. Cell-specific lesions and intracerebral drug infusions were used to elucidate striatal modulation of PPI. Quinolinic acid lesions of the ventral and caudodorsal striatum significantly decreased PPI, whereas lesions of the rostrodorsal and middorsal striatum did not significantly alter PPI. Infusion of the GABA-A antagonist picrotoxin into the ventral and caudal dorsal pallidum also significantly reduced PPI, whereas rostral pallidal picrotoxin infusion had no significant effect. Thus, PPI in the rat seems to be modulated by both ventral and caudodorsal striato-pallidal circuitry, but not by rostrodorsal or middorsal striato-pallidal projections.
Background
The coronavirus disease 2019 (COVID‐19) pandemic has affected millions of people worldwide resulting in significant morbidity and mortality. Arrhythmias are prevalent and reportedly, the second most common complication. Several mechanistic pathways are proposed to explain the pro‐arrhythmic effects of severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection. A number of treatment approaches have been trialled, each with its inherent unique challenges. This rapid systematic review aimed to examine the current incidence and available treatment of arrhythmias in COVID‐19, as well as barriers to implementation.
Methods
Our search of scientific databases identified relevant published studies from 1 January 2000 until 1 June 2020. We also searched Google Scholar for grey literature. We identified 1729 publications of which 1704 were excluded.
Results
The incidence and nature of arrhythmias in the setting of COVID‐19 were poorly documented across studies. The cumulative incidence of arrhythmia across studies of hospitalised patients was 6.9%. Drug‐induced long QT syndrome secondary to antimalarial and antimicrobial therapy was a significant contributor to arrhythmia formation, with an incidence of 14.15%. Torsades de pointes (TdP) and sudden cardiac death (SCD) were reported. Treatment strategies aim to minimise this through risk stratification and regular monitoring of corrected QT interval (QTc).
Conclusion
Patients with SARS‐CoV‐2 are at an increased risk of arrhythmias. Drug therapy is pro‐arrhythmogenic and may result in TdP and SCD in these patients. Risk assessment and regular QTc monitoring are imperative for safety during the treatment course. Further studies are needed to guide future decision‐making.
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