The development of emotion and empathy skills after childhood brain injury

Lasting socio-emotional behaviour difficulties are common among children who have suffered brain injuries. A proportion of difficulties may be attributed to impaired cognitive and/or executive skills after injury. A recent and rapidly accruing body of literature indicates that deficits in recognizing and responding to the emotions of others are also common. Little is known about the development of these skills after brain injury. In this paper we summarize emotion-processing systems, and review the development of these systems across the span of childhood and adolescence. We describe critical phases in the development of emotion recognition skills and the potential for delayed effects after brain injury in earlier childhood. We argue that it is important to identify the specific nature of deficits in reading and responding to emotions after brain injury, so that assessments and early intervention strategies can be devised.     

Determinants of Pace-Terminable Ventricular Tachycardia: Implications for Implantable Antitachycardia Devices

The next generation of implantable antitachycardia devices incorporate anti-tachycardia pacing for the treatment of ventricular tachycardia. To evaluate the potential determinants of pace terminability, we analyzed 62 episodes of induced monomorphic ventricular tachycardia. We found that the tachycardia cycle length and cycle length variability are the major determinants of pace terminability. These findings should be considered in the designing of ventricular tachycardia detection and termination algorithms.     

Long-Term Clinical Performance of a Central Venous Oxygen Saturation Sensor for Rate Adaptive Cardiac Pacing

Rate adaptive ventricular pacemakers using central venous oxygen saturation (O₂Sat) to control the pacing rate have been implanted in 14 patients (mean age 71 years), with a mean follow-up period of 44 months (range 2–63 months). In eight patients the pacemakers were replaced due to signs of battery depletion after an implant duration of 39–58 months. During bicycle exercise testing the O₂Sat decreased on average from 61%± 4% at rest to 36%± 4% (P < 0,0001) at peak exercise, and the maximum pacing rate was 122 ± 5 beats/min. The time delay until the O₂Sat bad dropped 10%, 65%, and 90% of the total reduction during exercise was 4.8 ± 0.9 seconds, 39.8 ± 3.8 seconds, and 71.3 ± 7.5 seconds, respectively. The O₂Sat decreased 9.4%± 2% (P <0.005) from resting supine to resting sitting. Oxygen breathing increased the telemetered O₂Sat from the pacemaker by 8.4 %± 1 % (P < 0.001). During follow-up the O₂Sats were relatively stable in 50% of the patients, but demonstrated significant fluctuations in the others. At 1-year invasive follow-up O₂Sat measured by the pacemaker decreased 22%± 2%, and in blood samples from the right ventricle 22%± 2% from rest to 3 minutes exercise at 25 watts. There was a significant correlation between O₂Sat measured by the pacemaker and in blood samples from right ventricle (n = 105; r = 0.73; P < 0.001). In two patients the O₂Sat dropped significantly during pneumonia. In another patient episodes of angina pectoris was associated with low O₂Sat and a concomitant fast pacing rate.     

Early Mortality in the Megaloblastic Anaemias

Review of 108 cases of severe megaloblastic anaemia (P.C.V.< 25 per cent) admitted to one Glasgow hospital revealeda 14 per cent mortality rate while in a similar group of 63patients with severe iron-deficiency anaemia the rate was only1·6 per cent. A computer search of the records of 2686cases of megaloblastic anaemia discharged from hospital in westernScotland disclosed that 126 (4·3 per cent) had died andthat 10 (7·7 per cent) of these were less than 60 yearsold. In both surveys the deaths were predominantly due to cardiovascularcauses and pulmonary oedema was particularly frequent, evenin patients who had not received transfusions. A prospectiveinvestigation of 34 cases of severe megaloblastic anaemia revealedthat prior to therapy the red-blood-cell potassium tended tobe low. Following specific replacement therapy, there was afall in serum potassium which, in the majority of cases, occurredat the onset of the reticulocyte response. Subsequently boththe serum potassium and the red-blood-cell potassium graduallyrose to normal levels. Hypokalaemia was more common in patientswith severe anaemia and thrombocytopenia. Following treatment,in seven patients (20·8 per cent) thrombocytosis developed. It is suggested that in severe megaloblastic anaemia, polyuriaand diarrhoea may lead to depletion of whole-body potassiumand that with replacement therapy the sudden cellular demandcauses a rapid fall in extracellular potassium. As most of thesepatients already have marked atheroma and are severely hypoxic,a precipitate drop in serum potassium levels may further embarrassmyocardial function. We therefore suggest that the serum potassiumbe closely monitored in the early stages of treatment and thatpotassium supplements are given where necessary. This and themore frequent use of exchange transfusion may reduce the unexpectedlyhigh mortality of the megaloblastic anaemias.     

A Clinical and Laboratory Study of Benign Multiple Sclerosis

In a hospital-based study of 400 patients with multiple sclerosis(MS), 42 per cent of patients who had had MS for 10 years ormore had benign disease. Early age of onset and a long firstremission were significantly associated with a good prognosis.There was a suggestion that initial presentation with paraesthesiaeand possibly optic neuritis were associated with a benign prognosis,but the only significant finding was the association betweenlimb weakness and a poor outcome (p<0.05). Fewer patientswith benign disease had a progressive element to their diseasethan those in the more disabled group (p<0.001). The only laboratory test which was associated with a benignprognosis was the absence of CSF myelin basic protein in remission.Abnormalities of visual evoked responses, CSF IgG and peripheralblood T lymphocytes appeared to have no value in assessing prognosisin the patients studied.     

Central haemodynamics in acute myocardial infarction in relation to mortality and peak enzyme activity

The relation of central haemodynamic changes to subsequent mortalityand peak enzyme activity was investigated in 190 patients withacute myocardial infarction. The mean delay time from onsetof symptoms to the haemodynamic study was 7.2 hours. Major exclusioncriteria were heart rate < 65beats min^–1, systolicblood pressure < 105 mmHg and lung rales to a distance of> 10 cm above the lung bases. Nine patients (4.7%) died within15 days and 16 patients (8.4%) within 90 days after the infarction.Compared to survivors, non-survivors were characterized by baselinedepression of cardiac index, stroke volume index and left ventricularstroke work index, while pulmonary capillary wedge pressureand peripheral resistance were increased. However, a wide overlapbetween survivors and non-survivors makes the predictive valuelow in the individual patient. Peak serum aspartate aminotransferase (S-ASAT) activity wasweakly related to baseline pulmonary capillary wedge pressure(r = 0.28; P< 0.001) and stroke volume index (r = –0.22;P7lt;0.01). The correlation to pulmonary capillary wedge pressurewas only found in anterior (r = 0.34) infarcts. Peak serum lactatedehydrogenase (LD¹) was not correlated with baseline haemodynamics.     

Epicardial repolarization mapping in man

A simple method was developed for recording epicardial monophasicaction potentials intraoperatively in man. Potentials were recordedrapidly and reliably from multiple epicardial sites using ahand-held probe. The feasibility of repolarization mapping wasassessed in 30 patients. It was possible to record technicallyadequate signals from most left ventricular and posterior rightventricular sites (success rates 72% and 61%, respectively),but it was more difficult to achieve satisfactory recordingsover the free wall of the right ventricle (success rate 36%).The onset of cardiopulmonary bypass resulted in a transientrise in action potential duration of approximately 30–40ms in the first minutes of bypass. An approximate steady statewas achieved thereafter. Reproducibility of the method was assessedby mapping a small number of sites repeatedly. The 95% confidencelimits for an estimate of repolarization time, based on a singlepotential, were ±21 ms. With 4 probe applications ateach site, the confidence limits of the estimated site meanwere reduced to ±8 ms. Based on this approach, statisticallysignificant differences between sites were demonstrated in 9of 10 patients, confirming that the method is sensitive enoughto provide information on regional differences in repolarization. Intraoperative epicardial repolarization mapping has been shownto be a practical possibility. The technique holds promise asa means of assessing the role of dispersion of repolarizationin arrhythmogenesis in man.