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Efthimios Dardiotis, Kostas N. Fountas, Maria Dardioti, Georgia Xiromerisiou, Eftychia Kapsalaki, Anastasia Tasiou and Georgios M. Hadjigeorgiou

Traumatic brain injury (TBI) constitutes a major cause of mortality and disability worldwide, especially among young individuals. It is estimated that despite all the recent advances in the management of TBI, approximately half of the patients suffering head injuries still have unfavorable outcomes, which represents a substantial health care, social, and economic burden to societies.

Considerable variability exists in the clinical outcome after TBI, which is only partially explained by known factors. Accumulating evidence has implicated various genetic elements in the pathophysiology of brain trauma. The extent of brain injury after TBI seems to be modulated to some degree by genetic variants.

The authors' current review focuses on the up-to-date state of knowledge regarding genetic association studies in patients sustaining TBI, with particular emphasis on the mechanisms underlying the implication of genes in the pathophysiology of TBI.

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Kostas N. Fountas, Eftychia Kapsalaki and Georgios Hadjigeorgiou


The wide application of deep brain stimulation in the management of movement as well as other degenerative neurological and psychiatric disorders has renewed the interest in using deep brain stimulation in the management of medically intractable epilepsy. Various stimulation targets have been used with significantly varying results in aborting seizure activity. Electrical cerebellar stimulation (CS) has been used for more than 50 years in the management of epilepsy, with conflicting results. In the current study, the authors review the pertinent literature to outline the role of CS in the management of medically refractory epilepsy.


The PubMed medical database was systematically searched for the following terms: “cerebellar,” “epilepsy,” “stimulation,” and “treatment,” and all their combinations. Case reports were excluded from this study.


The pertinent articles were categorized into 2 large groups: animal experimental and human clinical studies. Particular emphasis on the following aspects was given when reviewing the human clinical studies: their methodological characteristics, the number of participants, their seizure types, the implantation technique and its associated complications, the exact stimulation target, the stimulation technique, the seizure outcome, and the patients' psychological and social poststimulation status. Three clinical double-blind studies were found, with similar implantation surgical technique, stimulation target, and stimulation parameters, but quite contradictory results. Two of these studies failed to demonstrate any significant seizure reduction, whereas the third one showed a significant poststimulation decrease in seizure frequency. All possible factors responsible for these differences in the findings are analyzed in the present study.


Cerebellar stimulation seems to remain a stimulation target worth exploring for defining its potential in the treatment of medically intractable epilepsy, although the data from the double-blind clinical studies that were performed failed to establish a clear benefit in regard to seizure frequency. A large-scale, double-blind clinical study is required for accurately defining the efficacy of CS in epilepsy treatment.

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Georgia Xiromerisiou, Efthimios Dardiotis, Vaïa Tsimourtou, Persa Maria Kountra, Konstantinos N. Paterakis, Eftychia Z. Kapsalaki, Kostas N. Fountas and Georgios M. Hadjigeorgiou

Over the past few years, considerable progress has been made in understanding the molecular mechanisms of Parkinson disease (PD). Mutations in certain genes are found to cause monogenic forms of the disorder, with autosomal dominant or autosomal recessive inheritance. These genes include alpha-synuclein, parkin, PINK1, DJ-1, LRRK2, and ATP13A2. The monogenic variants are important tools in identifying cellular pathways that shed light on the pathogenesis of this disease. Certain common genetic variants are also likely to modulate the risk of PD. International collaborative studies and meta-analyses have identified common variants as genetic susceptibility risk/protective factors for sporadic PD.