RESUMEN
PURPOSE: transient ischemic attack (TIA) is defined as a transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia, with clinical symptoms typically lasting less than one hour, and without evidence of acute infarction. In this type of ischemic event, there are no data about a possible cardiac injury tested with troponin. After a stroke, it is well established the cardiac involvement due to a neuro-inflammatory response (recently defined as Stroke Heart Syndrome). The aim of this study is to compare the troponin elevation after a stroke with TIA. MATERIALS AND METHODS: this is a retrospective, single center study on 565 patients (73 TIAs, 492 stroke). We collected demographic characteristics, cardiovascular risk factors, cardiac data such as troponin, NT-proBNP, left atrial dilatation, etiology of the ischemic event (TOAST classification). RESULTS: we compare IS and TIA for each TOAST subtype. In all groups no substantial differences were found in demographic and past medical history (p>0.05). However, the maximum troponin level reached were significantly lower in TIAs than IS (p<0.05), except in lacunar etiology were troponin elevation was low also in IS group. We found a trend in favor to IS in the rise and fall troponin elevation over 30% in all the TOAST subgroups, but only in the cryptogenic etiology the difference was significant. About the others cardiac markers of injury, a significant higher rate of elevated NT-proBNP was found in the IS cohort. CONCLUSIONS: troponin level after TIAs is significantly lower than after IS. Troponin elevation after an ischemic event may be more relevant in patients with higher NT-proBNP levels and older age. More studies are needed to better understand the patho-physiology of this phenomenon after an ischemic event.
RESUMEN
Although deep brain stimulation of the subthalamic nucleus is an effective surgical treatment for Parkinson's disease, it may expose patients to non-motor side effects such as increased impulsivity and changes in decision-making behavior. Even if several studies have shown that stimulation of the subthalamic nucleus increases the incentive salience of food rewards in both humans and animals, temporal discounting for food rewards has never been investigated in patients who underwent STN-DBS. In this study, we measured inter-temporal choice after STN-DBS, using both primary and secondary rewards. In particular, PD patients who underwent STN-DBS (in ON medication/ON stimulation), PD patients without STN-DBS (in ON medication) and healthy matched controls (C) performed three temporal discounting tasks with food (primary reward), money and discount vouchers (secondary rewards). Participants performed also neuropsychological tests assessing memory and executive functions. Our results show that STN-DBS patients and PD without DBS behave as healthy controls. Even PD patients who after DBS experienced weight gain and/or eating alterations did not show an increased temporal discounting for food rewards. Interestingly, patients taking a higher dosage of dopaminergic medications, fewer years from DBS surgery and, unexpectedly, with better episodic memory were also those who discounted rewards more. In conclusion, this study shows that STN-DBS does not affect temporal discounting of primary and secondary rewards. Furthermore, by revealing interesting correlations between clinical measures and temporal discounting, it also shed light on the clinical outcomes that follow STN-DBS in patients with PD.
