Lights, Camera, Seizure? Factors to consider during photic stimulation
Loretta Stefanopoulos
Neurophysiology Scientist - Alfred Hospital, Peninsula Health - Frankston
As a neurophysiology scientist, one of my favourite parts about the role is the conversation we have with patients during the setup process. In the outpatient setting, I have a usual battery of questions to understand why the patient has been sent for an EEG, which I find helpful especially when the referral states nothing more than “? seizure”. Identifying provoking or precipitating factors in seizures relies on the recognition and insight from the patient themselves, family and friends as witnesses, as well as the treating neurologist (Kasteleijn-Nolst Trenité & Andermann, 2015). Occasionally, the patient reaches us without making any connection between these factors and their lifestyle, especially if they have yet to have their neurology consultation.
The conversation during setup therefore allows for a reflection of potential factors contributing to seizures. Seizures can occur spontaneously, with or without an identifiable precipitating factor such as sleep deprivation, physical exercise, fever, drug/alcohol withdrawal, menstruation, or stress. Spontaneous seizures differ to reflex seizures, which are elicited consistently and objectively due to exposure to specific external or internal stimuli. External stimuli include flashing lights, patterns or other visual stimuli, a startle, monotone, or other auditory stimuli just to name a few. Internal stimuli include mental processes such as thinking, calculating or reading (see Kaelasha’s blog post on reading epilepsy). Reflex seizures are classified by seizure type (focal or generalised) and aetiology (Kasteleijn-Nolst Trenité & Andermann, 2015; Okudan & Ozkara, 2018).
Performing intermittent photic stimulation, an assessment of photosensitivity, is a standard procedure during outpatient EEG. Photosensitivity is the abnormal neurological response to visual stimuli. Visual stimuli provoke the majority of reflex seizures (~80%), especially flashing lights from TV or video games (Fisher, et al., 2022; Okudan & Ozkara, 2018). Photosensitivity is common amongst particular epilepsy types, especially genetic generalised epilepsies (GGE; juvenile myoclonic epilepsy; childhood absence epilepsy; juvenile absence epilepsy; and generalised tonic-clonic seizures alone). We expect to see myoclonic, absence or generalised tonic-clonic seizures (GCTS) more often than focal seizures in photosensitive individuals (Fisher, et al., 2022). During EEG, we are looking for a photoparoxysmal response (PPR), which is the abnormal EEG response to sources of light. Specifically, we can group the types of EEG discharges captured during photic stimulation: type 1 (occipital spikes); type 2 (parieto-occipital spikes with biphasic slow wave); type 3 (type 2 with frontal spread) or type 4 (generalised spike-wave) (Waltz, Christen, & Doose, 1992). An in-depth discussion of these discharges and the mechanisms of photosensitivity would require a whole blog post in itself! I will simply note that PPRs can occur in the normal population, especially children, and Type 4 responses have the highest association with epilepsy. (Fisher, et al., 2022; Rathore, Prakash, & Makwana, 2020). These are important considerations, as our awareness of the patient’s epilepsy history and seizure type should elicit a heightened suspicion for a seizure and/or PPR during photic stimulation.
Upon discussion of the photic stimulation process, I have encountered many patients who dislike or avoid sources of light in everyday life, such as concerts, video games or driving at sunset or night. When I probe them further about this, some explain they feel unwell or uncomfortable, some are convinced they will have a seizure, others have a preconceived notion that flashing lights are simply bad for epilepsy in general. I have had patients with a long-standing diagnosis of epilepsy who have not been reviewed by or in touch with a neurologist for many years. They have commented that they have never been affected by or tested for photosensitivity, but assumed or told they should simply avoid flashing lights. If you do an internet search of “epilepsy myths”, sure enough you will find many websites stating something along the lines of “Myth: all people with epilepsy should avoid flashing lights”. It’s easy to forget when you are so immersed in the world of neuroscience that many of our patients lack our same level of epilepsy-literacy. They are usually shocked when I inform them that it’s quite a low percentage (approximately 5%) of people with epilepsy who actually experience photosensitive seizures (Rathore, Prakash, & Makwana, 2020). Upon concluding my setup, I am often suspicious and expect to capture a PPR from the history given by the patient. However, I am often met with a clinically and electrographically normal EEG. This has prompted me to revisit some of the photic stimulation recording basics, and consider any other explanations to normal findings, to ensure I am maximising the yield of my recording.
During the setup process, I consider the following factors prior to performing the photic stimulation specifically:
§ Any diagnosis/history of epilepsy, which may increase the likelihood of a PPR, such as the aforementioned GGE’s
§ History of photosensitivity, and the corresponding provoking visual stimuli
§ Age and gender
o Photosensitivity occurs most often in women, and adolescents aged between 10-20
§ Current anti-epileptic medications (AED), and, whether the patient is sleep-deprived
o Adequate sleep and AEDs both reduce the risk of provoking a GTCS
§ History of migraines triggered by bright lights, as patients may elect to skip photic stimulation to prevent a migraine
§ Pregnancy, as this is a contraindication
When I have established that the patient is an appropriate candidate for photic stimulation, I ensure the following stimulation parameters are adhered to:
§ Baseline EEG with eye opening and eye closure is recorded
o To capture posterior dominant rhythm
o Witness spontaneous discharges
§ Conduct photic stimulation at least 3 minutes before hyperventilation
o Photic stimulation can be anxiety-provoking, where hyperventilation might be more relaxing and promote drowsiness
§ Room is dimly lit and the patient is seated upright
o Allows for the observation of subtle clinical signs, such as eyelid myoclonus or limb jerks
o Contrast of dark room with bright light increases chance of an abnormal response
§ Place the lamp centrally, 30cms from the nasion, and ensure the patient looks at the centre
o Binocular and central stimulation is more effective than monocular and peripheral stimulation
§ Use flash frequencies 1–2–8–10–15–18–20–25–40–50–60Hz
o Pay special attention to 10-20Hz which is where we are most likely to capture a PPR
o Stop stimulation when a generalised discharge is seen, and begin working backwards from 60Hz to determine upper and lower photosensitivity thresholds
o We do not want to provoke a GTCS!
§ Record 5 seconds of each flash frequency during eye closure, eyes closed, and eyes open, or, eye closure for 7 seconds per frequency if time-limited
o Important to test all eye conditions
§ Eye closure is the most provocative state, where the eyelids diffuse light across the retina
(Kasteleijn-Nolst Trenité & Andermann, 2015; Kasteleijn-Nolst Trenité, et al., 2012; Martins da Silva & Leal, 2017; Okudan & Ozkara, 2018; Peltola, et al., 2023)
In following these processes, I arrive at the same conclusion: normal EEG with no clinical changes. I consider any other possible explanations:
§ Epilepsy syndrome and treatment status
The type of epilepsy diagnosed as well as status of antiepileptic treatment, if any, both play a large role in the presence of a PPR. We expect to see a PPR in those with untreated GGE far more than treated GGE or focal epilepsy. Although a “drug-naïve” state provides a more diagnostically informative EEG, this is often not appropriate in the routine outpatient setting. The risk provoking a GTCS from suddenly ceasing or reducing AEDs for the purposes of an outpatient EEG far outweighs the benefit of capturing a PPR (Kasteleijn-Nolst Trenité, et al., 2012; Rathore, Prakash, & Makwana, 2020). Perhaps an elective video EEG monitoring admission is more appropriate in such cases where the patient can be safely managed on the ward.
§ Seizures provoked by another specific visual stimulus
We have now established the most potent visual stimulus is bright, flashing lights. Although far less likely, we should consider other specific stimuli such as contrasting or geometric patterns, coloured flashes, strobe lights (nightclub), the reflective effect of sunlight off water or flickering of sunlight through trees (Kasteleijn-Nolst Trenité & Andermann, 2015; Fisher, et al., 2022).
§ Differential diagnoses
Prior seizures may have occurred coincidentally in the presence of a light source, or, in conjunction with other precipitating factors known to change the photosensitive threshold, such as sleep deprivation, alertness, attention or emotion. Perhaps they have occurred completely spontaneously in the past, and the patient has simply avoided testing the theory out of fear. A dislike for bright lights might bear no relation to epilepsy at all, and be attributed to ocular discomfort, photophobia, headache or migraine. Visual auras may precede migraines in a similar way to seizures, and patients who may suffer from both adds a layer of complexity to diagnosis (Fisher, et al., 2022; Okudan & Ozkara, 2018),
As I reflect on my EEG practice, I remind myself that I have done all I can to maximise the quality and utility of my recording. Whilst the current literature into the mechanisms of photosensitivity are fascinating, complex, and without consensus, I hope this general overview has been a valuable refresher for my fellow neurophysiology scientists.
References
Fisher, R. S., Acharya, J. N., Baumer, F. M., French, J. A., Parisi, P., Solodar, J. H., . . . Kasteleijn-Nolst Trenité, D. (2022). Visually sensitive seizures: An updated review by the Epilepsy Foundation. Epilepsia, 63(4), 739-768.
Kasteleijn-Nolst Trenité, D., Rubboli, G., Hirsch, E., Martins da Silva, A., Seri, S., Wilkins, A., . . . Harding, G. (2012). Methodology of photic stimulation revisited: Updated European algorithm for visual stimulation in the EEG laboratory. Epilepsia, 51(1), 16-24.
Kasteleijn-Nolst Trenité, D., & Andermann, F. (2015). Epilepsy with reflex seizures. Wyllie's treatment of epilepsy: Principles and practice: Sixth edition.
Martins da Silva, A., & Leal, B. (2017). Photosensitivity and epilepsy: Current concepts and perspectives—A narrative review. Seizure, 50(1), 209-218.
Okudan, Z. V., & Ozkara, C. (2018). Reflex epilepsy: triggers and management strategies. Neuropsychiatr Dis Treat, 14, 327-337.
Peltola, M. E., Leitinger, M., Halford, J. J., Vinayan, K. P., Kobayashi, K., Pressler, R. M., . . . Beniczky, S. (2023). Routine and sleep EEG: Minimum recording standards of the International Federation of Clinical Neurophysiology and the International League Against Epilepsy. Epilepsia, 64(3), 602-618.
Rathore, C., Prakash, S., & Makwana, P. (2020). Prevalence of photoparoxysmal response in patients with epilepsy: Effect of the underlying syndrome and treatment status. Seizure, 82, 39-43.
Waltz, S., Christen, H. J., & Doose, H. (1992). The different patterns of the photoparoxysmal response--a genetic study. Electroencephalogr Clin Neurophysiol, 83(2), 138-145.