Delayed onset catatonia after COVID-19.

COVID-19 has many complications that are associated with this infection. Neuropsychiatric symptoms are common and can present with symptoms documented both during acute COVID-19 infection and developing after the resolution of respiratory symptoms. Patients have presented with a variety of symptoms such as anosmia, seizures, cognitive and attention deficits, new or progression of existing anxiety, depression, psychosis, and rarely catatonia. Although rare, catatonia and each of its subtypes have now been reported as complications of COVID-19 and therefore, should be considered known to occur in both during the acute and postinfectious states. Diagnosis of catatonia in the context of COVID-19 should be considered when work-up for more common medical causes of encephalopathy are negative. There have been cases documented in the literature of patients presenting to the hospital with catatonia during COVID-19 infection. However, we present a case of akinetic catatonia in setting of COVID-19 infection and premorbid serious mental illness that was diagnosed and treated on an outpatient basis with close collaboration between primary care and psychiatry.

Inflammation of atrium after cardiac surgery is associated with inhomogeneity of atrial conduction and atrial fibrillation.

BACKGROUND: Atrial fibrillation (AF) is common after cardiac surgery. Abnormal conduction is an important substrate for AF. We hypothesized that atrial inflammation alters atrial conduction properties. METHODS AND RESULTS: Normal mongrel canines (n=24) were divided into 4 groups consisting of anesthesia alone (control group); pericardiotomy (pericardiotomy group); lateral right atriotomy (atriotomy group); and lateral right atriotomy with antiinflammatory therapy (methylprednisolone 2 mg/kg per day) (antiinflammatory group). Right atrial activation was examined 3 days after surgery. Inhomogeneity of conduction was quantified by the variation of maximum local activation phase difference. To initiate AF, burst pacing was performed. Myeloperoxidase activity and neutrophil cell infiltration in the atrial myocardium were measured to quantify the degree of inflammation. The inhomogeneity of atrial conduction of the atriotomy and pericardiotomy groups was higher than that of the control group (2.02+/-0.10, 1.51+/-0.03 versus 0.96+/-0.08, respectively; P<0.005). Antiinflammatory therapy decreased the inhomogeneity of atrial conduction after atriotomy (1.16+/-0.10; P<0.001). AF duration was longer in the atriotomy and pericardiotomy groups than in the control and antiinflammatory groups (P=0.012). There also were significant differences in myeloperoxidase activity between the atriotomy and pericardiotomy groups and the control group (0.72+/-0.09, 0.41+/-0.08 versus 0.18+/-0.03 DeltaOD/min per milligram protein, respectively; P<0.001). Myeloperoxidase activity of the antiinflammatory group was lower than that of the atriotomy group (0.17+/-0.02; P<0.001). Inhomogeneity of conduction correlated with myeloperoxidase activity (r=0.851, P<0.001). CONCLUSIONS: The degree of atrial inflammation was associated with a proportional increase in the inhomogeneity of atrial conduction and AF duration. This may be a factor in the pathogenesis of early postoperative AF. Antiinflammatory therapy has the potential to decrease the incidence of AF after cardiac surgery.

Liver-directed neonatal gene therapy prevents cardiac, bone, ear, and eye disease in mucopolysaccharidosis I mice.

Mucopolysaccharidosis I (MPS I) due to deficient alpha-L-iduronidase (IDUA) activity results in accumulation of glycosaminoglycans in many cells. Gene therapy could program liver to secrete enzyme with mannose 6-phosphate (M6P), and enzyme in blood could be taken up by other cells via the M6P receptor. Newborn MPS I mice were injected with 10(9) (high dose) or 10(8) (low dose) transducing units/kg of a retroviral vector (RV) expressing canine IDUA. Most animals achieved stable expression of IDUA in serum at 1240 +/- 147 and 110 +/- 31 units/ml, respectively. At 8 months, untreated MPS I mice had aortic insufficiency, increased bone mineral density (BMD), and reduced responses to sound and light. In contrast, MPS I mice that received high-dose RV had normal echocardiograms, BMD, auditory-evoked brain-stem responses, and electroretinograms. This is the first report of complete correction of these clinical manifestations in any model of mucopolysaccharidosis. Biochemical and pathologic evaluation confirmed that storage was reduced in these organs. Mice that received low-dose RV and achieved 30 units/ml of serum IDUA activity had no or only partial improvement. We conclude that high-dose neonatal gene therapy with an RV reduces some major clinical manifestations of MPS I in mice, but low dose is less effective.