This chapter discusses the diagnosis, evaluation and management of bradyarrhythmias. Sinus bradycardia occurs in 15-20% of patients with acute myocardial infarction secondary to ischemia of the sinoatrial (SA) node. Syncope may result from primary dysrhythmia or from reduced cardiac output. A 12-lead electrocardiogram (ECG) is essential for the diagnosis of bradycardia and to differentiate between the different types of bradyarrhythmias. History should focus particularly on symptoms of ischemic heart disease, and on medications such as nodal blockers. As the bradycardia worsens, cardiac output decreases as well. This results in hypotension and hypoperfusion that need to be corrected using medications or a pacemaker. In addition, a decrease in cardiac output can result in pulmonary edema. Even with the development of pulmonary edema, the bradycardia is the first thing that needs to be addressed. Treatment of the cardiogenic pulmonary edema can be instituted afterward.

This chapter reviews the spectrum of neuroimaging in Kleine-Levin syndrome (KLS). Although structural neuroimaging in KLS is within the normal range in most cases, the vast majority of studies report hypoperfusion in several brain regions. Cognitive impairment and altered perception occur in all KLS patients during sleep episodes according to the review by Arnulf. It is thus pertinent to investigate the neural concomitants to cognitive function in KLS by functional neuroimaging. N-Acetylasparate (NAA) is a biomarker for neuronal health, associated with either neuronal loss or neuronal dysfunction. Hypothalamic pathology constitutes a main hypothesis for KLS etiology. This hypothesis is based on the important function of the hypothalmus in sleep and appetite regulation as well as regarding sexual activity. The sparsity of neuroimaging findings in the hypothalamus might be a result of the detection limit for functional imaging in this region of the brain.