Every medical condition has its mimics, borderland, and chameleons (Smith, 2012). But for epilepsy, where the diagnosis is largely clinical and the consequences of misdiagnosis are so serious, conditions that simulate or overlap with epilepsy assume great importance. The mimics of epilepsy—principally syncope and psychogenic attacks—are well known to epileptologists, and their clinical distinguishing features are well rehearsed. Within the list of mimics are those conditions at the borderland of epilepsy, truly overlapping and often responding to antiepileptic medications. The best examples are the startle syndromes, parasomnias, and migralepsy, but also perhaps cataplexy, tonic spasms of multiple sclerosis, central pain syndromes, and even panic disorder. Finally, there are the “chameleons”--disorders in disguise—which for epilepsy includes situations such as frontal lobe seizures mimicking nonepileptic attacks or transient epileptic amnesia, first mislabeled as its “global” cousin.

Sir William Gowers, in his celebrated treatise, “The Border-land of Epilepsy,” was first to distinguish this group. Gowers’ scholarly work has largely stood the test of time (excepting perhaps his inclusion of vertigo), even though he worked without technology to appreciate better the etiologies of those conditions “in the border-land of epilepsy—near it but not of it” (Gowers, 1907; Crompton & Berkovic, 2009). This supplement assembles texts from the Chairs’ symposium of the 10th European Congress on Epileptology, London, September 2012, where Gowers’ text was the foundation upon which to develop the theme of the Borderland of Epilepsy.

The startle syndromes (Dreissen & Tijssen, 2012) clearly do overlap with epilepsy, hyperekplexia being the exemplar. They have a central (although subcortical) mechanism, and include symptoms that mimic epilepsy, although with retained consciousness; typically they respond to clonazepam. Pediatric epileptologists will be well aware of their importance in the differential diagnosis of suspected neonatal or infantile seizures. Parasomnias present to both adult and pediatric epilepsy services and often prove a diagnostic challenge. Again, there are clear overlaps with epilepsy, both in the clinical features and their response to antiepileptic medication. Paolo Tinuper (Tinuper et al., 2012) explores their mechanisms, manifestations, and management and illustrates this with case examples. Migralepsy—the apparent overlap between migraine and epilepsy—occasionally crops up in clinical practice. Dorothee Kasteleijn-Nolst Trenité brings her experience of this syndrome to focus on both the patient context and its scientific basis, perhaps surprisingly concluding that migralepsy as an entity may not exist (Kasteleijn-Nolst Trenité & Parisi, 2012).

The overlapping treatment response of these borderland conditions helps us better to understand their mechanisms, presenting a new marketing opportunity for industry. Meir Bialer (2012) explores how our evolving understanding of the mechanisms of actions of antiepileptic medications may be applied to improve the management of conditions at the borderland of epilepsy. Finally there is syncope, which Gowers included among his borderland list, and certainly we recognize some overlap (with ictal bradycardia for example). However, our better appreciation of cardiovascular mechanisms now would remove syncope from the epilepsy borderland. But whether listed or not, patients with cardiac syncope most definitely do present to epilepsy clinics, typically with a label of “first seizure.” Only careful attention to history detail and close scrutiny of 12-lead electrocardiography (ECG) will prevent their next “seizure” from being fatal. Peter O’Callaghan (Anderson & O’Callaghan, 2012) helps to clarify our clinical thinking on cardiac syncope for the epileptologist and advises us on how risk stratification can prevent the clinical disaster of sudden cardiac death.

The contributors to this supplement have built upon Gowers’ prescient foundation and now present a view of the borderland of epilepsy for the twenty-first century.


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  2. Disclosure
  3. References

We have no conflicts of interest to disclose. We confirm that we have read the Journal’s position on issues involved in ethical publication and affirm that this report is consistent with those guidelines.


  1. Top of page
  2. Disclosure
  3. References
  • Anderson J, O’Callaghan P. (2012) Cardiac syncope. Epilepsia 53(Suppl. 7):3542.
  • Bialer M. (2012) Why are antiepileptic drugs used for nonepileptic conditions? Epilepsia 53(Suppl. 7):2633.
  • Crompton DE, Berkovic SF. (2009) The borderland of epilepsy: clinical and molecular features of phenomena that mimic epileptic seizures. Lancet Neurol 8:370381.
  • Dreissen YEM, Tijssen MAJ. (2012) The startle syndromes: Physiology and treatment. Epilepsia 53(Suppl. 7):311.
  • Gowers WR. (1907) The border-land of epilepsy: faints, vagal attacks, vertigo, migraine, sleep symptoms and their treatment. Churchill, London.
  • Kasteleijn-Nolst Trenité D, Parisi P. (2012) Migraine in the borderland of epilepsy: “Migralepsy”: an overlapping syndrome of children and adults? Epilepsia 53(Suppl. 7):2025.
  • Smith PE. (2012) Epilepsy: mimics, borderland and chameleons. Pract Neurol 12:299307.
  • Tinuper P, Bisulli F, Provini F. (2012) The parasomnias: Mechanisms and treatment. Epilepsia 53(Suppl. 7):1219.