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Lorraine Mackenzie

Publications and source records attributed to Lorraine Mackenzie.

3 recordsLinked to original sources

Physiological and pathological spindling phenomena have similar regional EEG power distributions.

Sleep spindles in human and in rat are known to have a thalamocortical substrate. It has also been suggested that absence epilepsy spike and wave discharges may be generated by a similar mechanism. In addition, we have previously reported a possible thalamocortical origin of the EEG spindling rhythmic discharges associated with myoclonic jerks in the picrotoxin rat model of primary generalised epilepsy. To investigate whether pathological and physiological brain rhythms have common mechanisms of generation, we analysed four electroencephalographic (EEG) spindling activities in the rat. These were the non-convulsive spindle discharges induced by picrotoxin (picrotoxin spindles), naturally occurring absence epilepsy spike and wave discharges (absence spindles), spindle discharges during natural sleep (sleep spindles) and spindling activity that occurs under barbiturate anaesthesia (barbiturate spindles). We used power spectral analysis to define and compare the strength and brain distribution of EEG power during the spindling activities in 12 forebrain and 7 brainstem regions. There were brain-wide differences in power for each of the different spindle types with the pathological rhythms of the epilepsies containing more power than the physiological rhythms. There were also similar differences in the expression of spindles related to the region examined and no thalamic emphasis. These results provide evidence for a similar regional EEG power distribution for all four types of spindling activity and thus for the different spindles being expressions of a single phenomenon.

Analysis of Variance↗

Fluorocitrate-mediated astroglial dysfunction causes seizures.

A role for astroglia in epileptogenesis has been hypothesised but is not established. Low doses of fluorocitrate specifically and reversibly disrupt astroglial metabolism by blocking aconitase, an enzyme integral to the tricarboxylic acid cycle. We used cerebral cortex injections of fluorocitrate, at a dose that we demonstrated to inhibit astroglial metabolism selectively, to determine whether astroglial disturbances lead to seizures. Rats were halothane-anesthetized, and 0.8 nmol of sodium fluorocitrate was injected into the cerebral cortex. Extradural electroencephalogram (EEG) electrodes were implanted, after which the anesthesia was ceased and the animals were observed. In all experiments, 14 of 15 fluorocitrate-treated animals exhibited epileptiform EEG discharges, with some animals exhibiting convulsive seizures. Discharges commenced as early as 30 min postfluorocitrate injection. Intraperitoneal octanol, but not halothane by inhalation, given to test the possible participation of gap junctions in EEG discharge generation, blocked or delayed the occurrence of discharges after fluorocitrate. These results indicate that focal cerebrocortical astroglial dysfunction leads to focal epileptiform discharges and sometimes to convulsive seizures and that the process possibly depends on effects mediated by gap junctions.

Animals↗

Mental tasks induce gamma EEG with reduced responsiveness in primary generalized epilepsies.

PURPOSE: We previously revealed an interictal increase in intensity of EEG rhythms during quiescent mental activity in the 30- to 100-Hz frequency (gamma) range in primary generalized epilepsy (PGE). We have evidence that there is induction of gamma EEG in normal subjects in response to controlled mental activity. Here we test whether mental tasks further augment interictal gamma oscillations in people with PGE. METHODS: We recorded interictal EEG from patients with PGE and partial epilepsy and compared EEG power spectral responses (increases over resting) during mental tasks. RESULTS: In partial epilepsy, mental tasks (except for alternating checkerboard visual stimulation) induced 1.5- to 2.5-fold increases in power of gamma EEG. In generalized epilepsy, generalized increases of 1.5-fold in gamma EEG were induced by only two mental tasks (reading and subtraction), and enhancement of 1- to 1.5-fold in the remaining six (checkerboard, expectancy, music, learning, recalling, and a video). CONCLUSIONS: Gamma EEG is less responsive to mental activation in PGE than in partial epilepsy, confirming an abnormality in gamma mechanisms in PGE. Our findings also provide a possible mechanistic link between mental activity and seizures in reading- and arithmetic-induced seizures.

Adult↗