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Complex partial seizures provoked by photic stimulation
  1. S SEDDIGH,
  2. F THÖMKE,
  3. TH VOGT
  1. Department of Neurology, University of Mainz, Germany
  1. Dr Susann Seddigh, Neurologische Klinik und Poliklinik, Langenbeckstreasse 1, D 55101 Mainz, Germany. Telephone 0049 6131 172226; fax 0049 6131 173271.

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In patients with known or suspected epileptic seizures, non-specific activation methods such as hyperventilation or intermittent photic stimulation (IPS) are used to provoke epileptic potentials, which may prove the epileptic nature and specify epileptic syndromes. A photoconvulsive reaction with generalised spike wave activity may be provoked by IPS and is almost confined to patients with generalised epilepsy. There are, however, some reports on patients with partial epilepsy and photoconvulsive reaction.1 We report on two patients with known photoconvulsive reaction, who developed these with focal epileptic discharges consequent to IPS and discuss possible mechanisms.

Patient 1, a 44 year old woman presented with a 33 year history of complex partial seizures starting with behavioural arrest followed by oroalimentary automatisms, which were sometimes followed by secondary generalisation. She was treated with carbamazepine and reported 1–2 seizures a month. Brain MRI failed to disclose any focal abnormality. Except for mild generalised slowing (7.5/s), probably due to or accentuated by carbamazepine, focal slowing (5–4/s) with intermittent spikes showing phase inversion over F8 was seen in two EEG recordings (average of 1 spike in 7 minutes). During hyperventilation (3 minutes) the number of spikes increased to an average of 1 spike in 1 minute. During IPS (started with 1/s duration), the number of single spikes increased to 6 in 3 minutes or 2 per minute (figure). During the second recording, the spike activity in the anterotemporal region finally became rhythmic with subsequent generalisation. This was accompanied by a complex partial seizure typical for this patient (behavioural arrest followed by oroalimentary automatisms) finally running into a generalised tonic-clonic seizure.

Spike activity during EEG registration in patient 1: (A) without provocation; (B) while IPS.

Patient 2 was a 19 year old woman who had complex partial seizures with secondary generalisation for 2 years. The seizures started with fear (“indiscribable terror”) accompanied by a fearful expression. This was followed by a repetitive ictal speech which was sometimes followed by secondary generalised tonic-clonic seizure. She reported one of these seizures as a consequence of flashing lights in a discotheque and avoided flashing lights since then. She was treated with valproate and reported 4–5 seizures per year. MRI was normal. EEG disclosed focal slowing (4 cps) with phase inversion over T6, which corresponded to decreased perfusion of the right midtemporal and parietotemporal regions established by HMPAO-SPECT. Intermittent photic stimulation (12/s) evoked a photoconvulsive reaction with bifrontal accentuated generalised spike-wave activity associated with myoclonic eyelid jerks. Independent of photoconvulsive reaction, 8 seconds later on single sharp-wave activity with phase inversion over T6occurred consequent to IPS and became rhythmic. This was associated with complex partial seizures starting with fear accompanied by a terrifying fearful expression, which were followed by ictal speech (repition of single words) finally running into a generalised tonic-clonic seizure (documented by a simultaneous EEG/Video recording).

Both patients developed complex partial seizures with secondary generalisation resulting from IPS and one of them reported a complex partial seizure provoked by flashlight in a discotheque. To our knowledge, neither complex partial seizures nor activation of temporal epileptic activity consequent to IPS have previously been reported. Specific stimuli like rubbing, cold wind,2 or tactile stimuli may evoke spike activity in the contralateral cerebral regions and provoke partial seizures. Even patients with myoclonic epilepsy may develop contralateral spikes after electrical peripheral nerve stimulation. In all these patients, spike potentials were evoked in primary cortical representation areas of the respective stimuli. Our patients showed provocation of anterotemporal (F8, patient 1) and posterotemporal (T6, patient 2) epileptic activity resulting from IPS, which may have been adjacent to the visual cortex in patient 2 but was distinctly apart from the primary visual cortex in patient 1. Complex partial seizure symptomatology in the first patient included oroalimentary automatisms, indicating a seizure origin in the amygdalohippocampal complex. Visual hallucinations, which are likely with epileptic discharges in the visual cortex or visual association areas, however, were missed. This indicates that provoked complex partial seizures during IPS in our patients occurred without epileptic activity in the visual cortex. Temporal epileptic activity as a consequence of IPS was probably mediated via occipitotemporal connections such as the fasciculus longitudinalis inferior.

Provocation of sharp waves with phase inversion over F8 and the occurrence of a photoconvulsive reaction in patient 2 raises the question whether both phenomena were interrelated. Similar constellations were previously reported in individual patients with photoconvulsive reaction who had partial epilepsy and occipital epileptic focus.3 Cortical and subcortical recordings in monkeys during IPS showed paroxysmal discharges predominantly in prerolandic areas, which were followed by bursts in the pontine and mesencephalic reticular formation and, finally, by generalised discharges.4 These findings have been interpreted in favour of a cortical origin of the photoconvulsive reaction, which is supported by the studies of Ricci et al 5 using neuromagnetic methods in humans with photoconvulsive reaction to identify the location of the photoconvulsive reaction generator: They found a regional sensitivity involving frontal, occipital, and temporal areas, but the cortical excitability was extremely unstable, which was attributed to a deficient GABA-ergic system. This suggests that photoconvulsive reaction is a generalised phenomenon and not due to polyfocal generation. The occurrence of focal epileptic discharges associated with focal seizures and secondary generalisation in patient 2 does not indicate a relation between focal epileptic discharges and the photoconvulsive reaction as the second appeared in only one of the patients.

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