![]() It is acknowledged that the presence of ECG changes, for example T wave inversion, ST segment elevation and a prolonged QT interval, in patients with intracranial pathology, such as subarachnoid haemorrhage, are a manifestation of massive catecholamine release and autonomic dysregulation resulting in ventricular wall motion abnormalities, vasospasm and subsequent cardiac contraction band necrosis. 6 In addition to an isolated cardiologic or epileptic basis for an episode of collapse, there exists the phenomenon of cerebrogenic cardiac arrhythmias, which further confounds the diagnostic process ( figure 1). 4,5 For example, when 74 patients previously diagnosed with epilepsy were investigated with tilt-table testing, prolonged electrocardiogram (ECG) monitoring, blood pressure and ECG-monitored carotid sinus massage, an alternative cardiologic diagnosis was found in 31 (41.9%) of patients, including 13 taking anti-epileptic medication. Misdiagnosis is common and possibly affects up to 20 to 30% of adults with a diagnosis of epilepsy. Patients with episodes of collapse are frequently referred to either cardiologic or neurologic services and the correct diagnosis is often elusive. There has always been a degree of clinical overlap between cardiology and neurology, and, more specifically, epileptology. It is important to note, however, that although small series observational studies are helpful in raising awareness of this poorly understood entity, unfortunately, they have little capacity to inform the debate about possible mechanisms, risk factors and preventative measures. The study by Chaila and colleagues lends support to the now fairly well-established thesis that disturbed cerebral electrical activity during an epileptic seizure may cause transient cardiac arrhythmias (see pages 245–8). This has been driven by the publication of a number of important studies that have documented the frequent occurrence of cardiac rhythm changes during epileptic seizures, 2,3 and the lack of a clear pathophysiological mechanism for sudden unexpected death in epilepsy (SUDEP), an unexplained cause of death for over 500 patients with epilepsy in the UK each year. Cardiac arrhythmias and ST segment changes have been observed with acute intracerebral events such as sub-arachnoid haemorrhage or cerebrovascular accidents 1 and, more recently, the interaction of the heart and brain in patients with epilepsy has been the subject of intense scrutiny. ![]() IntroductionĪnatomical and functional connections between the brain and heart in both health and disease have long been established. A key aim is to stratify the risk of SUDEP for an individual patient and, ideally, identify potential therapeutic targets. ![]() Future work should include the evaluation of inter-ictal and ictal electrophysiological, cardiorespiratory and metabolic variables in a large population of patients, including in specific syndromes, to further establish the pathophysiological mechanisms of SUDEP. Patients with epilepsy may be predisposed to developing arrhythmias due to a number of factors including chronic autonomic dysfunction, effects of anti-epileptic medication and a common genetic susceptibility. Cardiac dysrhythmias are a potential cause of SUDEP. Sudden unexpected death in epilepsy (SUDEP) is a major cause of mortality in patients with epilepsy. ![]() Cerebrogenic control of cardiac function is well recognised and acute neurological events, including epileptic seizures, may cause a disturbance of cardiac function even in the absence of significant cardiac structural or electrophysiological abnormalities. ![]()
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