Crossed aphasia following cerebral infarction in a right-handed patient with atypical cerebral language dominance.

OBJECTIVE: Crossed aphasia (CA), usually referred to as an acquired language disturbance, is caused by a lesion in the cerebral hemisphere ipsilateral to the dominant hand, and the exact mechanism is not clear. The development of handedness is influenced by education and training and the impact of habitualization, while language is more susceptible to the impact of speech habits, and it is not absolutely accurate to judge cerebral language dominance by the degree of hand preference. METHODS: We describe a case of CA after right hemispheric stroke in a right-handed patient with atypical language dominance and attempt to analyze the mechanism of CA based on functional imaging methods, including arterial spin labeling (ASL) and positron emission tomography/magnetic resonance imaging (PET-MRI). RESULTS: Brain MRI at 24 h after admission showed a large cerebral infarction in the right cerebral hemisphere, including the posteroinferior part of Broca's area in the right frontal lobe, the right temporal lobe, and the right occipital lobe. The patient exhibited a non-fluent aphasia on a standard language test (the Aphasia Battery of Chinese [ABC]) performed on the 7th day after onset. Thus, atypical language dominance was suspected. One week after admission, ASL imaging showed high perfusion in the infarct core zone and low perfusion in the left cerebellar hemisphere. Two months later, PET/MRI demonstrated low metabolism in the posterior frontal lobe, temporal lobe, temporal occipital junction area, and the right basal ganglia. CONCLUSION: The findings suggest that the patient has right-sided cerebral language dominance, or that both hemispheres have linguistic functions. Not all patients show linguistic capabilities on the side opposite hand preference. The language dominance should be predicted by a combination of clinical manifestations and functional imaging techniques.

Pycnogenol Attenuates the Release of Proinflammatory Cytokines and Expression of Perilipin 2 in Lipopolysaccharide-Stimulated Microglia in Part via Inhibition of NF-κB and AP-1 Activation.

Over activation of microglia results in the production of proinflammatory agents that have been implicated in various brain diseases. Pycnogenol is a patented extract from French maritime pine bark (Pinus pinaster Aiton) with strong antioxidant and anti-inflammatory potency. The present study investigated whether pycnogenol may be associated with the production of proinflammatory mediators in lipopolysaccharide-stimulated BV2 (mouse-derived) microglia. It was found that pycnogenol treatment was dose-dependently associated with significantly less release of nitricoxide (NO), TNF-α, IL-6 and IL-1ß, and lower levels of intercellular adhesion molecule1 (ICAM-1) and perilipin 2 (PLIN2). Furthermore, this effect was replicated in primary brain microglia. Levels of inducible NO synthase mRNA and protein were attenuated, whereas there was no change in the production of the anti-inflammatory cytokine IL-10. Further evidence indicated that pycnogenol treatment led to the suppression of NF-κB activation through inhibition of p65 translocation into the nucleus and inhibited DNA binding of AP-1, suggesting that these proinflammatory factors are associated with NF-κB and AP-1. We conclude that pycnogenol exerts anti-inflammatory effects through inhibition of the NF-κB and AP-1pathway, and may be useful as a therapeutic agent in the prevention of diseases caused by over activation of microglia.