Imaging of acute cerebellitis in children. Report of 4 cases

Acute cerebellitis is one of the main causes of acute cerebellar dysfunction in children. It is either infectious, usually viral, post-infectious or post vaccinal in etiology. Diagnosing acute cerebellitis may be difficult in patients with only subtle cerebellar signs and when cerebro-spinal fluid examination is normal. MRI is the most adequate imaging technique to demonstrate cerebellar involvement. The authors report the clinical and neuro-imaging findings in 4 paediatric cases. Patient's age varied from 2 to 7 years and predominant clinical symptoms were fever, headache and vomiting; ataxia was noted only in 2 cases. Viral serologic tests were negative in 3 cases and demonstrated Epstein-Barr virus in 1. Initial MRI examination (2 cases) demonstrated increased intensity on T2W and Flair sequences of the cerebellar gray matter with pial enhancement. Clinical outcome was good with complete resolution of symptoms in 3 cases and persistent mild right upper limb paresis in one. The resolution of the signal abnormality was well demonstrated on MRI in one case, suggesting an inflammatory etiology with moderate residual cerebellar atrophy.     

Pyruvate/dichloroacetate supply during reperfusion accelerates recovery of cardiac energetics and improves mechanical function following cardioplegic arrest

Objectives: Cardioplegic arrest during cardiac surgery induces severe abnormalities of the pyruvate metabolism, which may affect functional recovery of the heart. We aimed to evaluate the effect of pyruvate and dichloroacetate administration during reperfusion on recovery of mechanical function and energy metabolism in the heart subjected to prolonged cardioplegic arrest. Methods: Four groups of rat hearts perfused in working mode were subjected to cardioplegic arrest (St. Thomas’ No. 1), 4 h of ischaemia at 8°C and reperfusion with either Krebs buffer alone (C) or with 2.8 mM pyruvate (P), with 1 mM dichloroacetate (D), or with a combination of both (PD). Mechanical function was recorded before cardioplegic arrest and at the end of experiments. In groups C and PD, additional experiments were performed using ³¹P nuclear magnetic resonance spectroscopy in non-working Langendorff mode to evaluate cardiac high-energy phosphate concentration changes throughout the experiment. Results: Improved recovery of cardiac output (% of the preischaemic value±SEM, n=9–12) was observed in all three treated groups (65.7±4.3, 59.5±5.2 and 59.5±5.3% in PD, P and D, respectively) as compared with C (42.2±4.6%; P<0.05). Recovery of coronary flow was improved from 66.4±3.8 in C to 94.9±8.6% in PD (P<0.05). The phosphocreatine recovery rate in the first minutes of reperfusion was increased from 9.9±1.5 in C to 31.5±4.3 μmol/min per g dry wt in PD (P<0.001). No differences were observed in ATP or phosphocreatine concentrations at the end of experiment. Conclusions: The administration of pyruvate and dichloroacetate improves the recovery of mechanical function following hypothermic ischaemia. Accelerated restoration of the energy equilibrium in the initial phase of reperfusion may underlie the metabolic mechanism of this effect.     

Bridge to transplantation with a left ventricular assist device for systemic ventricular failure after Mustard procedure

In recent years the conservative techniques to treat degenerative mitral valve insufficiency have developed to such an extent mainly due to a better understanding of the physiology and pathology of the mitral valve and to the possibility to get predictable and satisfactory results. Still a challenge persists for the cardiac surgeon when he has to deal with complex reconstructions. The technique described seems to offer an even better surgical option for patients with complex lesions involving the posterior mitral leaflet, especially as far as the hemodynamic performance is concerned.     

Uptake of porcine rubulavirus (LPMV) by PK-15 cells

BACKGROUND: The porcine virus denominated La Piedad Michoacan Virus (LPMV) is a member of the family Paramyxoviridae and is the cause of a disease in pigs present only in Mexico. The disease is characterized by meningoencephalitis and respiratory distress in young pigs, epididymitis and orchitis in boars, and reproductive failure and abortion in sows. METHODS: The cytopathology, morphology, and distribution of the hemagglutination neuraminidase (HN) and nucleoprotein (NP) proteins of LPMV were investigated following inoculation into PK-15 cells. The cytopathic effect was characterized by cytoplasmic vacuolation and the formation of syncytia and cytoplasmic inclusion bodies. RESULTS: In immunofluorescence assays using a monoclonal antibody (MAb) against the HN protein at 5-60 min post-infection (early infection), a diffuse immunofluorescence was observed near the cell membrane and adjacent to the nuclear membrane. At 24 h post-infection (late infection), a dust-like immunofluorescence was observed throughout the cytoplasm. LPMV-infected cells incubated with the MAb against the NP protein showed punctate cytoplasmic fluorescence during the early stages of infection. At the late infection stage, these fluorescent particles became larger and were seen predominantly in the cytoplasm of syncytia. This pattern was also apparent by immunohistochemical labeling and immunogold electron microscopy. The latter technique revealed that HN protein was diffusely distributed throughout the cytoplasm. When using the MAb against the NP protein, nucleocapsid organization was the most prominent feature and resulted in the formation of cytoplasmic inclusion bodies visible by light and electron microscopy. Immunogold labeling of purified nucleocapsids was shown by electron microscopy. Virus particles and nucleocapsids were morphologically similar to members of the Paramyxoviridae family. CONCLUSIONS: The morphologic characteristics of the virions and the distribution patterns of the HN and NP proteins in PK-15 infected cells indicate that the mechanisms of LPMV replication are generally similar to those of the members of the Paramyxoviridae family.     

Surgical treatment of coronary artery anomalies

In this paper, we review literature from June 1990 through May 1991. We discuss normal anatomy and physiology of the proximal coronary arteries, anomalous origin of the coronary arteries from an inappropriate aortic sinus, and anomalous origin of the left coronary artery from the pulmonary artery. Other topics reviewed include coronary arteriovenous fistulas, coronary anomalies in left-sided heart syndrome and pulmonary atresia with intact interventricular septum, coronary arterial abnormalities in transposition of the great arteries, and iatrogenic coronary anomalies.     

Cardiac rhythm and conduction after two-stage anatomic correction of simple transposition of the great arteries

To assess postoperative arrhythmias and AV-conduction defects associated with anatomic correction of simple transposition of the great arteries, 207 standard 12-lead surface and 43 24-hour electrocardiograms of all 17 patients followed after anatomic correction for up to 6.5 years were reviewed. No dysrhythmias or AV-conduction delays definitely attributable to anatomic correction were observed. One patient with a severe complex supraventricular tachyarrhythmia after a Blalock-Hanlon procedure has improved markedly, exhibiting respiratory AV-dissociation and 5 premature atrial complexes/minute 5 years after anatomic correction.     

Neonatal anatomical correction of transposition of the great arteries: non-invasive assessment of haemodynamic function up to four years after operation

Intracardiac and great artery blood flow velocities were recorded by pulsed and continuous wave Doppler ultrasound in 18 children aged between eight months and four years (mean 25 months) who had undergone anatomical correction of transposition of the great arteries in the first month of life. Postoperative peak flow velocities across the mitral valve and in the ascending aorta were not significantly different from those in an age matched control population, but tricuspid flow velocities were higher than normal. Aortic regurgitation was detected in only one of the eighteen patients, a markedly lower frequency than that reported after two stage anatomical correction. Peak velocities in the pulmonary artery were higher than normal, and in most cases there was some degree of stenosis of the pulmonary artery at the site of anastomosis.