Toxoplasma gondii is an obligate intracellular parasite considered one of the most successful pathogens in the world, owing to its ability to produce long-lasting infections and to persist in the central nervous system (CNS) in most warm-blooded animals, including humans. This parasite has a preference to invade neurons and affect the functioning of glial cells. This could lead to neurological and behavioral changes associated with cognitive impairment. Although several studies in humans and animal models have reported controversial results about the relationship between toxoplasmosis and the onset of dementia as a causal factor, two recent meta-analyses have shown a relative association with Alzheimer’s disease (AD). AD is characterized by amyloid-β (Aβ) peptide accumulation, neurofibrillary tangles, and neuroinflammation. Different authors have found that toxoplasmosis may affect Aβ production in brain areas linked with memory functioning, and can induce a central immune response and neurotransmitter imbalance, which in turn, affect the nervous system microenvironment. In contrast, other studies have revealed a reduction of Aβ plaques and hyperphosphorylated tau protein formation in animal models, which might cause some protective effects. The aim of this article is to summarize and review the newest data in regard to different pathophysiological mechanisms of cerebral toxoplasmosis and their relationship with the development of AD and cognitive impairment. All these associations should be investigated further through clinical and experimental studies.

False lateralization of ictal onset by scalp electroencephalogram (EEG) is an infrequent entity that has been reported in patients with mesial temporal lobe epilepsy associated with hippocampal sclerosis (HS). In these cases, a tendency for rapid seizures that spread through the frontal-limbic system and hippocampal commissural pathways to the contralateral hemisphere has been proposed. Cerebral cavernous malformations (CCMs), which constitute a collection of abnormally configured small blood vessels with irregular structures, is a well-defined epilepsy-associated pathology. Their primary association with seizures might be explained either as a result of physiological changes affecting the cerebral cortex immediately surrounding the CCM (an epileptogenic mechanism that is relevant for both, temporal and extratemporal lesions) or as a result of promoting epileptogenicity in remote but anatomo-functionally connected brain regions, a mechanism that is particularly relevant for temporal lobe lesions. To date, there have been only two publications on falsely lateralizing ictal onsets by EEG in temporal cavernoma, but not in other regions. Here, we report a rare case of apparent false lateralization of ictal onset by scalp EEG in a patient with a left medial frontal gyrus cavernoma (supplementary motor area), and discuss some relevant pathophysiological mechanisms of false lateralization.