Epilepsy is a symptom of a variety of underlying etiological causes, rather than a specific disease (Engel & Pedley 1997). It is a phenomenon that has been recognised over 4000 years ago. For centuries, patients with epilepsy had a stigma of being possessed by supernatural forces during epileptic seizures. And it was not until as recently as during 1969-1970 that laws concerning marriage and compulsory sterilization of patients with epilepsy were repealed in Finland (Lindberg 1995). Today, according to the Finnish Social Insurance Institution, there are more than 45 000 people receiving antiepileptic medication in Finland (Keränen et al. 1997).
Increasing research work on human genome, and experimental studies on the pathology of epilepsy have opened a new approach to examine different developmental and post-traumatic pathological brain conditions that eventually lead to the development of epileptic seizures. New imaging techniques, especially the magnetic resonance imaging (MRI), have also widened the scope of epilepsy research work, as well as clinical diagnostic and treatment possibilities. The advanced imaging techniques may help in revealing specific pathologies, and in classifying different types of epilepsy (Cascino et al. 1991, Cascino 1997).
Patients have been treated for epilepsy for as long as the seizures have been known. During the last 60 years, major advances have been achieved in the treatment of epilepsy. Advances within antiepileptic drug (AED) treatment and surgical treatment of epilepsy have made it possible to set the goal of epilepsy treatment on seizure-freedom. This goal is achieved in approximately 70%-80% of patients with epilepsy (Cockerell et al. 1995). Unfortunately, approximately 20%-30% of all patients with epilepsy continue to have seizures, despite active treatment (Hauser & Hesdorffer 2001). Particular syndromes, i.e. TLE, may be especially difficult to treat (Engel et al. 1997).
It has been known for long that epilepsy may be associated with disturbances of autonomic nervous system (ANS) function (Schraeder et al. 1989, Frysinger et al. 1993, Devinsky et al. 1994, Massetani et al. 1997, Messenheimer et al. 1997, Tomson et al. 1998, Druschky et al. 2001). During a generalized tonic-clonic seizure, various changes in ANS function can be observed and partial seizures may present themselves as autonomic symptoms (Wannamaker 1985). In addition, epilepsy may be associated with more long-standing forms of ANS dysfunction (Wannamaker 1985).
It is a tribute to the homeostatic safeguards of the organism, that a generalized epileptic seizure is not a fatal event. However, sometimes these safeguards fail, with potentially tragic results. Already at the end of the 19th century, Bacon and his colleagues divided the deaths in an epileptic population into four categories; those due to chronic disease, those due to accidents, those due to status epilepticus and those due to sudden unexpected death in patients with epilepsy (SUDEP) (Bacon et al. 1868). The hypotheses of the basic mechanisms behind SUDEP lie on dysfunction of the cardiovascular autonomic regulatory system that exposes a patient to a fatal arrythmia or central apnea. Although some risk factors of this devastating phenomenon have been identifed, there may be a variety of still unknown risk factors contributing to the risk of SUDEP in an individual patient. (Devinsky et al. 1994, Johnston et al. 1995, Tennis et al. 1995, Johnston et al. 1997, Nashef 1997, Shorvon 1997, Nashef et al. 1998, Nilsson et al. 1999, Sperling et al. 1999, Walczak et al. 2001, Leestma et al. 2002)
The basic mechanisms of the cardiovascular regulation have been known for the past two decades and the most important tehniques used in the investigation of cardiovascular and other ANS functions have been developed and standardized during that time. With these techniques, e.g. BP and HR changes, can be measured during daily activities or after certain stimuli (O´Brien et al. 1986, Goldberger & West 1987, McLeod & Tuck 1987, Saul et al. 1987, Suominen 1987, Bannister & Mathias 1988, Denton et al. 1990, Huikuri et al. 1995, Braune et al. 1996, Goldberger 1996, Task Force 1996, Myllylä et al. 2002). These investigatory methods have not been widely used in evaluating cardiovascular autonomic functions in patients with epilepsy. However, the previous works suggest that epilepsy itself, as well as AEDs, may alter autonomic functions in patients with epilepsy, but the clinical significance of this phenomenon is still incompletely understood (Wannamaker et al. 1985, Schraeder et al. 1989, Frysinger et al. 1993, Devinsky et al. 1994, Massetani et al. 1997, Messenheimer et al. 1997, Tomson et al. 1998, Druschky et al. 2001). Moreover, it is not yet known, whether the type or severity of epilepsy is related to the development of changes in autonomic regulatory functions in patients with epilepsy.
Further information on the value of different methods in studying ANS function in epilepsy patients is needed. It is particularly important to identify the prognostic value of altered cardiovascular regulation associated with epilepsy. Furthermore, deeper understanding of the role of epilepsy itself and the different AEDs in inducing cardiovascular autonomic regulatory dysfunction would be important in diminishing the risks related to epilepsy.
This study was designed to elucidate the possible effects of epilepsy on cardiovascular autonomic function. Its aim is also to evaluate the usefulness of two different methods, cardiovascular reflex test and HRV analysis, in studying autonomic cardiovascular regulation in patients with epilepsy. Finally, this study was designed to assess the possible correlations between the severity of TLE and cardiovascular autonomic functions.