Elsevier

Clinical Neurophysiology

Volume 124, Issue 2, February 2013, Pages 221-227
Clinical Neurophysiology

Invited Review
Fixation-off sensitivity

https://doi.org/10.1016/j.clinph.2012.07.017Get rights and content

Abstract

Fixation-off sensitivity (FOS) is a phenomenon induced by elimination of central vision/fixation, and may either manifest clinically with seizures or only represent an EEG abnormality. FOS is characterized by posterior or generalized epileptiform discharges that consistently occur after closing of the eyes and last as long as the eyes are closed. It is most commonly encountered in patients with idiopathic childhood occipital epilepsies, but may also be observed in cases of symptomatic or cryptogenic focal and generalized epilepsies, as well as in asymptomatic non-epileptic individuals. FOS should be differentiated from pure forms of scotosensitivity, in which EEG discharges or epileptic seizures are elicited by darkness, and from epileptiform discharges triggered by eye closure, which refer to eye closure sensitivity. Although FOS is probably associated with occipital hyperexcitability its intrinsic epileptogenic potential is presumed to be low.

Highlights

► Fixation-off sensitivity (FOS) is characterized by the appearance of epileptiform discharges occurring after eyes-closure and lasting as long as the eyes are closed. ► FOS is induced by elimination of central vision/fixation. ► FOS is probably associated with occipital hyperexcitability but its intrinsic epileptogenic potential seems to be low.

Introduction

Fixation-off sensitivity (FOS) is a phenomenon induced by elimination of central vision/fixation (Panayiotopoulos, 1981). This term refers to a condition that may either manifest clinically with seizures or only represent an EEG abnormality. FOS is characterized by posterior or generalized epileptiform discharges that consistently occur after closing of the eyes and last as long as the eyes are closed (Panayiotopoulos, 1998). FOS may be easily demonstrated using methods that eliminate fixation (e.g. Frenzel lenses) without preventing light from reaching the retina, thus distinguishing FOS from pure scotosensitivity (Panayiotopoulos, 1998).

We review most important studies dealing with the clinical, neurophysiological and pathophysiological aspects of this fascinating but still obscure phenomenon.

Section snippets

Historic background

The term FOS was coined by Panayiotopoulos (1987). This phenomenon was first observed in four children with occipital paroxysms (two of them had Panayiotopoulos syndrome, one had idiopathic childhood occipital epilepsy of Gastaut and one symptomatic occipital epilepsy) (Panayiotopoulos, 1981). Panayiotopoulos was the first to describe the characteristic occurrence of this pattern after eye closure and elimination of central vision/fixation. In those same years also Gastaut (1982) and Newton and

EEG description and diagnostic aspects

FOS is characterized by continuous epileptiform discharges (spikes, spike wave or sharp wave focal, regional or generalized) that consistently occur within 1–3 s of eye closure (although sometimes they may be delayed for a few additional seconds), persist throughout the eye-closed state (i.e., when central vision and fixation are blocked or compromised) and disappear immediately with eye opening (Fig. 1, Fig. 2, Fig. 3). Other means of eliminating central fixation also lead to the reoccurrence

Differential diagnosis

Testing for actual fixation-off is required to differentiate FOS from pure forms of scotosensitivity (Pazzaglia et al., 1970), in which EEG discharges or epileptic seizures are elicited by darkness. Scotosensitive epilepsy is defined as seizures and EEG abnormalities induced by the complete elimination of retinal light stimulation (Panayiotopoulos, 1998). However, patients with pure scotosentivity do not exhibit EEG abnormalities when fixation is hampered by the use of translucent spherical

Related conditions

Overall, FOS is a rare phenomenon. It is most commonly encountered in patients with idiopathic childhood epilepsies with occipital paroxysms (Gastaut type), and Panayiotopoulos syndrome when occipital paroxysms occur (Panayiotopoulos, 1981, Panayiotopoulos, 1998, Panayiotopoulos, 2007), and represents about 0.2% of epilepsies (Koutroumanidis et al., 2009). FOS may also be observed in symptomatic or cryptogenic focal (Panayiotopoulos, 1981, Maher et al., 1995, Kurth et al., 2001, Iannetti et

Epileptogenicity potential

FOS-related seizures have been described as myoclonic (Garcia Silva et al., 1987), absences (Koutroumanidis et al., 2009), and absence status epilepticus (Ming and Kaplan, 1998). However, the overall intrinsic epileptogenic potential of FOS is presumed to be low, and the FOS-related occipital discharges that occur in idiopathic occipital lobe epilepsy and most of the generalized FOS discharges in idiopathic generalized epilepsies do not seem to be associated with overt clinical manifestations (

FOS and photosensitivity

FOS has EEG features that are the opposite of those observed during photosensitivity. Despite the conflicting corresponding mechanisms underlying these two phenomena (Panayiotopoulos, 1998), both FOS and photosensitivity can occur in the same patient, and one phenomenon may evolve into the other (Panayiotopoulos, 1979, Koutroumanidis et al., 2009). Eye-closed discharges of FOS are elicited by darkness, and are inhibited by fixation and central vision. Conversely, eye-closure abnormalities

Pathophysiology

The rarity of FOS prevents large group studies, so that the underlying pathophysiology of this condition remains not fully understood. However, several studies adopting different methodologies have been conducted so far to better investigate the pathogenesis of this intriguing phenomenon.

Conclusion

FOS is an intriguing phenomenon, its uniqueness being represented by the fact that elimination of central vision/fixation is a specific precipitating stimulus that induces epileptiform discharges even in presence of light. Despite the fact that the results of several studies suggested the involvement of occipital hyperexcitability, the exact mechanism underlying FOS remains somewhat obscure. Therefore, further research is required to investigate this condition, and shed light on the

Conflict of interest

None declared.

References (37)

  • G.L. Gigli et al.

    Eye closure sensitivity without photosensitivity in juvenile myoclonic epilepsy: polysomnographic study of electroencephalographic epileptiform discharge rates

    Epilepsia

    (1991)
  • J.B. Green

    Seizures on closing the eyes. Electroencephalographic studies

    Neurology

    (1968)
  • F.J. Herranz Tanarro et al.

    La pointe onde occipitale avec et sans epilepsie benigne chez l’enfant

    Rev Electroencephalogr Neurophysiol Clin

    (1984)
  • G.D. Iannetti et al.

    FMRI/EEG in paroxysmal activity elicited by elimination of central vision and fixation

    Neurology

    (2002)
  • M. Koutroumanidis et al.

    Fixation-off sensitivity in epilepsies other than the idiopathic epilepsies of childhood with occipital paroxysms: a 12-year clinical-video EEG study

    Epileptic Disord

    (2009)
  • C. Kurth et al.

    Fixation-off sensitivity in an adult with symptomatic occipital epilepsy

    Epilepsia

    (2001)
  • A. Labate et al.

    Silent celiac disease in patients with childhood localization-related epilepsies

    Epilepsia

    (2001)
  • J.A. Lewis

    Eye closure as a motor trigger for seizures

    Neurology

    (1972)
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