Figure 11.1 A and B
A spike and a sharp wave differ only in duration
The chapter is explicit that this morphological distinction is clinically less relevant than separating epileptiform activity from artefact.
Figure 11.1 C and D
Multiple spikes, and the spike-and-wave complex
Two or more spikes at more than 10 Hz form a multiple spike complex; a spike followed by a slow wave of more than 200 ms forms a spike-and-wave complex.
Figure 11.2 A
A gyral source produces a radial dipole
Discharges are surface-negative with a distant positive field. When spikes arise from the surface of a cortical gyrus, the negative field projects to the cortical surface and the positive field projects deeper into the brain.
Figure 11.2 B
A sulcal source produces a tangential dipole — and inverts the polarity
This single geometric fact explains several counter-intuitive localisations in the chapter, including the paradoxical lateralisation of mesial frontal foci.
Why it matters
- A source in the wall of a sulcus faces across the head, so its positivity and negativity appear on opposite sides of the source, not above it.
- A midline mesial frontal focus can therefore be recorded with maximal amplitude over the contralateral frontal electrode — paradoxical lateralisation (Figure 11.13).
- It is also why the maximum electronegativity of a temporal spike sits anterior and inferior to the standard 10–20 positions.
- Practical rule: never infer the depth or the side of a generator from scalp voltage alone.
Figure 11.3
Basal temporal electrodes sit in the plane of their superior counterpart
Reading the figure
- The coronal head section shows how far the basal temporal surface sits from any standard 10–20 electrode.
- Adding a basal chain is the cheapest way to sample that surface without an invasive procedure.
- It is also why the chapter defers to Chapter 9 for polarity principles: on basal electrodes, which way a discharge points is not obvious.
Figure 11.4
T1: the Silverman anterior temporal electrode
Placement rule
- Sited 1 cm above the junction of the anterior two-thirds and posterior one-third of the line connecting the outer canthus of the eye to the external auditory meatus.
- Non-invasive, inexpensive, and safe — which is why it survives into modern practice while sphenoidal electrodes have largely receded.
- The 2024–2026 literature puts the incremental detection of temporal discharges at roughly 10–20% when T1/T2 is added to a routine montage.
Figure 11.5
Type 1 spikes phase reverse at the anterior temporal electrodes
In a longitudinal bipolar montage, mesial temporal spikes show phase reversal at F7/F8, with maximum negativity at the anterior temporal and sphenoidal electrodes and a widespread positive field over the contralateral centro-parietal region.
Figure 11.6
Type 1 is focal and steep; Type 2 spreads without a positive field
Type 1 · mesial
How to tell them apart
- Type 1: sharp contoured, steep gradient, maximum negativity anteriorly, and a positive field over the contralateral centro-parietal region.
- Type 2: a broad negative field extending beyond the temporal region, with no positive field — the signature of a lateral temporal generator.
- Field mapping places the maximum electronegativity of a temporal spike anterior and inferior to the standard 10–20 positions.
- Predominant mid-temporal (T3/T4 → T7/T8) discharges may indicate a larger extra-mesial generator.
Figure 11.7 A and B
Bilateral discharges are common — and the 75% rule decides their weight
About one third of patients with unilateral mesial temporal epilepsy have bilateral independent temporal discharges.
To carry lateralising significance in the presence of bilateral independent temporal IEDs, at least three-quarters of discharges should localise to one temporal region. Here the combination of a significantly lateralised interictal EEG and a concordant ictal pattern provided sufficient non-invasive data to hypothesise the epileptogenic zone and proceed to right temporal resective surgery.
Figure 11.7 C
The recorded seizure: evolving rhythmic beta to theta
Ictal patterns are sustained rhythmic discharges that evolve in frequency, morphology and distribution — the evolution is the localising signal, not any single frame of it.
Why evolution matters
- Frequency change over seconds is what separates an ictal rhythm from an interictal run or a state-dependent rhythm.
- The earliest, most restricted expression is the most localising; later spread is not.
- A start–stop–start pattern can occur, and the initial start has a more restricted field than the restart.
Figure 11.8
TIRDA — short runs of rhythmic temporal delta
Defined as short runs of rhythmic, saw-toothed or sinusoidal 1–4 Hz delta activity of 50–100 µV and ≥ 10 seconds, occurring predominantly over the anterior temporal regions.
Clinical reading
- The presence of TIRDA has a high correlation with mesial temporal epilepsy with hippocampal sclerosis.
- It generally occurs unilaterally; during drowsiness and sleep bilateral and asynchronous TIRDA may appear.
- TIPDA — the polymorphic variant — is instead more frequent in lateral temporal epilepsy and in temporal epilepsy due to lesions such as low-grade neoplasms.
- Independently reported in 20–40% of temporal lobe epilepsy cohorts, with high specificity and moderate sensitivity; bilateral TIRDA suggests bitemporal or more diffuse involvement.
Figure 11.9 A
Type I A in practice: rhythmic 5 Hz sharp-contoured theta
Figure 11.9 B and C
Type II A and Type II C: polymorphic delta before rhythmic fast activity
Figure 11.10 A and B
Temporal plus epilepsy: a network, not a lobe
Temporal plus epilepsies involve complex epileptogenic networks encompassing the temporal lobe and neighbouring structures — orbito-frontal cortex, insula, frontal and parietal operculum, and the temporo-parieto-occipital junction.
Interictal discharges in temporal plus epilepsy are often bilateral or pre-central, and the ictal EEG may show early involvement of frontal, temporo-parietal or central regions. Distinguishing temporal, temporal-plus and pseudotemporal syndromes often requires invasive monitoring.
Figure 11.10 C and D
The same patient: evolving bradycardia and sinus arrest
This patient also illustrates the importance of recording and carefully reviewing the ECG during seizures. The EEG change here is a consequence of the cardiac arrest, not a seizure pattern.
Figure 11.11
Burned-out hippocampal syndrome: scalp EEG lateralised to the wrong side
A 32-year-old woman with drug-resistant seizures of temporal lobe semiology. MRI showed atrophy of the left hemisphere with marked left hippocampal atrophy; IEDs were seen exclusively over the right temporal region.
Figure 11.12 A and B
Nocturnal hypermotor seizures: spikes reversing at C4/Cz
A 24-year-old woman with a history of drug-resistant nocturnal hypermotor seizures. Frequent runs of spikes phase reverse across C4/Cz.
Figure 11.12 C and D
The spikes potentiate into a seizure, and MRI shows the dysplasia
Figure 11.14
Ciganek’s midline theta versus genuine midline spikes
A 29-year-old woman referred with a diagnosis of non-epileptic spells. The drowsy record initially looked like the benign midline theta rhythm of Ciganek — until sleep recording revealed spikes at the central region.
The two could be distinguished by the spikes’ sharp configuration, the presence of aftercoming slow waves, and their lack of expression over C3 and C4. The case is the chapter’s argument for obtaining a sleep recording before calling a midline rhythm benign.
Figure 11.13
Paradoxical lateralisation with a midline frontal lesion
A patient with a mesial frontal lobe lesion whose interictal discharges phase reverse at Cz and F4 — midline and right.
This is the practical payoff of tangential dipole geometry: a sulcal or midline source projects its positive and negative fields to opposite sides, so the maximal scalp amplitude can sit contralateral to the generator.
Figure 11.15 A and B
A parietal dysplasia: periodic multiple spike complexes
A 29-year-old woman with seizures characterised by a painful sensation followed by dystonic posturing of the right upper limb since the age of 7.
Figure 11.15 C and D
The same seizure progresses to 9 seconds of asystole
The patient underwent urgent cardiac pacing, and later resection of the focal cortical dysplasia. Note that this is a parietal focus producing a cardiac arrest — ictal asystole is not confined to the temporal lobe.
Figure 11.16
Bilateral parieto-occipital gliosis and ulegyria
A 25-year-old man with poor vision and drug-resistant epilepsy from early childhood.
Figure 11.17
Post-encephalitic occipital epilepsy: delta that acquires a spike
A 17-year-old girl with post-encephalitic drug-resistant epilepsy.
