Department of Pathology and Laboratory Medicine (Neuropathology),
Departments of Paediatrics, and Clinical Neurosciences,
University of Calgary Cumming School of Medicine and Alberta Children's Hospital Research Institute, Calgary, Alberta, Canada
Correspondence: Harvey B. Sarnat
Alberta Children's Hospital,
2888 Shaganappi Trail NW,
Calgary, Alberta T3B 6A8, Canada
Olfactory auras (phantosmia) are an infrequent phenomenon in complex focal seizures generated in the mesial temporal lobe. It is generally assumed that all such auras arise from epileptic foci in the entorhinal cortex, amygdala or rostral insula, all of which have major afferent projections from the olfactory bulb or mainly from its relay, the anterior olfactory nucleus. The histological morphology, synaptic circuitry, and foetal development of the olfactory bulb are unique. The olfactory system is the only special sensory system that does not project to the thalamus because its bulb and tract incorporate an intrinsic thalamic equivalent: axonless granular and periglomerular neurons and the anterior olfactory nucleus. The olfactory bulb exhibits continuous synaptic turnover throughout life. Other brain structures with synaptic plasticity (neocortex, hippocampus, and amygdala) are epileptogenic; synaptically stable structures (brainstem, cerebellum, and basal ganglia) are not epileptogenic. Electrophysiological and neuropathological data of the olfactory bulb in epilepsy are sparse. We propose an alternative hypothesis, first hinted in 1954 by Penfield and Jasper, that some epileptic olfactory auras are primarily generated by the olfactory bulb and secondarily mediated by the amygdala and entorhinal cortex.