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• Seizures and movement disorders : cortico-subcortical networks
  Aileen McGonigal
  Published on: 1 March 2019

• Published on: 1 March 2019

  Seizures and movement disorders : cortico-subcortical networks

  • Aileen McGonigal, Consultant Epileptologist Aix Marseille Univ, Inserm, INS, Institut de Neurosciences des Systèmes, Marseille, France

  Seizures and movement disorders : cortico-subcortical networks

  Dr Aileen McGonigal

  Aix Marseille Univ, Inserm, INS, Institut de Neurosciences des Systèmes, Marseille, France
  APHM, Timone Hospital, Clinical Neurophysiology, Marseille, France

  Corresponding author: Dr Aileen McGonigal, Service de Neurophysiologie Clinique, CHU Timone, AP-HM, Marseille, France
  Email : aileen.mcgonigal@univ-amu.fr
  Tel: 00 33 491384995
  Fax:00 33 491385826

  To the Editors

  I was interested to read the recent review by Dr Freitas and colleagues1. This interesting article highlights diagnostic challenges, clinical overlap and possible shared pathophysiological processes in epileptic seizures and movement disorders. I would like to add a couple of points that seem important to acknowledge.
  Firstly, in terms of clinical expression, the authors rightly mention that automatic movements occurring during focal epileptic seizures can sometimes resemble those seen in certain movement disorders, and they give the examples of orofacial automatisms (most often seen in temporal lobe seizures), as well as hyperkinetic behaviors. While the authors highlight sleep-related epilepsy as the main cause of hyperkinetic behavior, in fact hyperkinetic behavior may be seen in seizures from various cortical origins both in wakefulness and in sleep. It should be recognized that especially (though not exclusivel...

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  Seizures and movement disorders : cortico-subcortical networks

  Dr Aileen McGonigal

  Aix Marseille Univ, Inserm, INS, Institut de Neurosciences des Systèmes, Marseille, France
  APHM, Timone Hospital, Clinical Neurophysiology, Marseille, France

  Corresponding author: Dr Aileen McGonigal, Service de Neurophysiologie Clinique, CHU Timone, AP-HM, Marseille, France
  Email : aileen.mcgonigal@univ-amu.fr
  Tel: 00 33 491384995
  Fax:00 33 491385826

  To the Editors

  I was interested to read the recent review by Dr Freitas and colleagues1. This interesting article highlights diagnostic challenges, clinical overlap and possible shared pathophysiological processes in epileptic seizures and movement disorders. I would like to add a couple of points that seem important to acknowledge.
  Firstly, in terms of clinical expression, the authors rightly mention that automatic movements occurring during focal epileptic seizures can sometimes resemble those seen in certain movement disorders, and they give the examples of orofacial automatisms (most often seen in temporal lobe seizures), as well as hyperkinetic behaviors. While the authors highlight sleep-related epilepsy as the main cause of hyperkinetic behavior, in fact hyperkinetic behavior may be seen in seizures from various cortical origins both in wakefulness and in sleep. It should be recognized that especially (though not exclusively) in prefrontal seizures2, more elaborate automatic behaviors may include complex and often repetitive movements that tend to occur in a context of altered consciousness, including naturalistic movements such as hand tapping, rocking or leg movements. These may be associated with vocalization including verbal stereotypies, laughing or singing, and sometimes emotional signs. The seizure semiological pattern is typically similar for a given patient from one seizure to the next. These excessively repetitive movements occurring within a limited behavioral repertoire could indeed be characterised as stereotypies, according to the definition of this term3.
  In cases of focal pharmacoresistant epilepsy, presurgical evaluation may require intracerebral electroencephalography (EEG). This offers a rich source of data for correlating clinical seizure expression with intracerebral electrical activity measured with millisecond resolution. The depth electrode methodology of stereoelectroencephalography (SEEG) allows sampling of widely distributed structures, through which signal analysis studies have helped to establish the network basis of epilepsy4.
  In a series of frontal seizures recorded with SEEG, the clinical expression of ictal stereotyped movements was shown to correlate with a rostrocaudal gradient of seizure organisation within frontal cortex, notably whether movements involved predominantly proximal or distal body segments: more distal stereotypies were associated with more anterior prefrontal regions 5. Thus, while both cortical and subcortical structures seem likely to be involved in such complex seizure-related behavior4 6, it can be suspected that cortico-subcortical circuits are topographically organised in a way that directly influences clinical expression.
  While most SEEG recording is from cortical structures, aimed at identifying a pathological zone for surgical resection, deeper subcortical structures including thalamus and caudate nucleus are sometimes also explored. In the context of Freitas and colleagues’ discussion of pathophysiology, it is of interest to note that in SEEG exploration of frontal lobe epilepsy, the caudate nucleus has been shown to be involved in generation of both spontaneous and stimulation-triggered seizures7. An SEEG study of temporal lobe seizures demonstrated an association between greater impairment of awareness and increased long-distance connectivity between thalamus and associative cortical structures 8. Lastly, in a separate and recent study of patients with temporal lobe epilepsy recorded with SEEG, direct stimulation of pulvinar during hippocampal seizures produced electroclinical change, with clinically less severe seizures9.
  Thus, an exciting role of SEEG exploration of epilepsy is not only in defining a potential surgical excision for each patient, but also using the recorded data to pursue better understanding of organisation of pathophysiological networks, including in terms of interactions between their cortical and subcortical components. As well as the strong neuroscientific interest of such data, this could potentially advance therapeutic approaches, for example facilitating development of tailored deep brain stimulation methods according to anatomical and electrophysiological specificities of different cases. This is of direct clinical relevance to management of epilepsy but could eventually also open up therapeutic possibilities for some movement disorders.

  1. Freitas ME, Ruiz-Lopez M, Dalmau J, et al. Seizures and movement disorders: phenomenology, diagnostic challenges and therapeutic approaches. 2019:jnnp-2018-320039.
  2. Bonini F, McGonigal A, Trébuchon A, et al. Frontal lobe seizures: From clinical semiology to localization. Epilepsia 2014;55.2 264-77.
  3. Edwards MJ, Lang AE, Bhatia KP. Stereotypies: a critical appraisal and suggestion of a clinically useful definition. Mov Disord 2012;27(2):179-85. doi: 10.1002/mds.23994
  4. Bartolomei F, Lagarde S, Wendling F, et al. Defining epileptogenic networks: Contribution of SEEG and signal analysis. Epilepsia 2017
  5. McGonigal A, Chauvel P. Prefrontal seizures manifesting as motor stereotypies. Movement Disorders 2013 doi: doi: 10.1002/mds.25718
  6. Chauvel P, McGonigal A. Emergence of semiology in epileptic seizures. Epilepsy & Behavior 2014
  7. Aupy J, Kheder A, Bulacio J, et al. Is the caudate nucleus capable of generating seizures? Evidence from direct intracerebral recordings. Clinical Neurophysiology 2018
  8. Arthuis M, Valton L, Régis J, et al. Impaired consciousness during temporal lobe seizures is related to increased long-distance cortical-subcortical synchronization. Brain 2009;132(Pt 8):2091-101. doi: 10.1093/brain/awp086
  9. Filipescu C, Lagarde S, Lambert I, et al. The effect of medial pulvinar stimulation on temporal lobe seizures. Epilepsia 2019

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  Conflict of Interest:
  None declared.

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