“Temporal plus” epilepsy (TPE) is a term that is used when the epileptogenic zone (EZ) extends beyond the boundaries of the temporal lobe. Stereotactic electroencephalography (SEEG) has been essential to identify additional EZs in adjacent structures that might be part of the temporal lobe/limbic network.

We present a small case series of temporal plus cases successfully identified by SEEG who were seizure-free after resective surgery.

We conducted a retrospective analysis of 156 patients who underwent SEEG in 5 years. Six cases had TPE and underwent anterior temporal lobectomy (ATL) with additional extra-temporal resections.

Five cases had a focus on the right hemisphere and one on the left. Three cases were non-lesional and three were lesional. Mean follow-up time since surgery was 2.9 years (SD ± 1.8). Three patients had subdural electrodes investigation prior or in addition to SEEG. All patients underwent standard ATL and additional extra-temporal resections during the same procedure or at a later date. All patients were seizure-free at their last follow-up appointment (Engel Ia = 3; Engel Ib = 2; Engel Ic = 1). Pathology was nonspecific/gliosis for all six cases.

TPE might explain some of the failures in temporal lobe epilepsy surgery. We present a small case series of six patients in whom SEEG successfully identified this phenomenon and surgery proved effective.

Six/second spike waves, 14 and 6/second positive spikes and small sharp spikes are apiculate paroxysmal rhythms in the electroencephalogram, thought to be of no diagnostic importance. The cortical origin of these discharges is documented in this report.

These waveforms were assessed in recordings from the surface of the cerebral cortex using implanted subdural electrodes in 61 patients monitored for possible epilepsy surgery.

Eight patients had 6/second spike wave, four had 14 and 6/second positive spikes and 3 had small sharp spikes. The 6/second spike waves were localised to the posterior cingulate gyrus, a more restricted region than would be predicted from scalp recordings and the 14 and 6/second spikes to the posterior mesial temporal cortex. Small sharp spikes were more widely distributed but also predominated in the posterior mesial temporal area. None of the discharges were congruent with the focus of seizure origin and no interaction with other interictal spikes was found.

These benign paroxysmal rhythms can appear incidentally in the electrocorticograms of patients with focal epilepsy and should not be confused with focal pathological spike activity or considered to be of any value in localizing the seizure focus.

A seizure is the most common cause of loss of driving privileges for medical reasons but there is variability in how physicians and the authorities who regulate driving approach this issue.

A questionnaire regarding epilepsy and driving was sent to all adult neurologists in Canada (n = 494).

Of 289 (59%) neurologists responding, 50% usually report patients with seizures to the department of motor vehicles compared to only 4% for stroke/TIA, 26% for dementia and 8% for other neurologic disorders (p < 0.0001). In the five provinces with mandatory reporting laws, seizures were reported most of the time by 84% compared to only 19% in the five provinces with discretionary reporting (p < 0.0001). Nationwide, 44% agreed with mandatory reporting but this also differed in provinces with and without mandatory reporting legislation (63% vs. 37%, p < 0.0001). Only 49% agreed with the current recommendation of at least one year seizure free interval before resuming driving.

Seizures are disproportionately reported compared to other neurological conditions. Many neurologists disagree with the recommended Canadian standards for duration of driving restriction after seizures. Variability in the attitude and practice of neurologists in regard to reporting of seizures is confirmed.

Stimulation of the central cholinergic system results in generalized epileptic seizures. The goal of this study was to map the epileptogenic effects of the cholinergic agonist, carbachol injected into different sites of the basal forebrain and diencephalon of the rat brain.

Carbachol was injected directly into the brain in a dose of 1 or 3 (jg. Seizures were assessed behaviourally on a five-stage scale with electroencephalographic controls. Seizures at stage 1 were the least severe and those at stage 5 the most severe.

Injections of high dose carbachol (3 (jg) induced seizures from 40% of all injected brain sites. Injections of low dose carbachol (1 ug) or isotonic saline into the same brain sites did not cause any behavioural or electrographic seizures. The majority of sites (84%) producing generalized seizures (stage 5) were concentrated in or around the zona incerta.

Within the anatomical limits of the study, the zona incerta is the area most sensitive to carbachol-induced generalized seizures.

Escalating focal sensorimotor seizures, progressive neurologic deficit and cognitive decline with associated typical magnetic resonance imaging (MRI) findings or pathological confirmation constitute the syndrome of Rasmussen's encephalitis.

Three patients with this clinical scenario had long-term follow-up after being given the antiviral drug ganciclovir 10 mg/kg/day IV for ten days within one to three months of disease onset.

Seizures occurred at least hourly and were localized to the Rolandic region. The MRIs were normal in one patient and in two showed changes consistent with ongoing seizures. Two patients, one whose short-term outcome was reported previously, had immediate and sustained cessation of seizures and resolution of their neurologic deficit. One patient with seizures from both hemispheres did not respond and went on to hemispherectomy that confirmed chronic encephalitis. Seizures continued in five other patients treated 6 to 72 months after disease onset.

The sustained seizure control after ganciclovir in two of three patients suggests this drug may be effective when given early in the course of this subacute intractable focal epilepsy syndrome.