Introduction. Cardiac magnetic resonance imaging (CMR) is considered the reference diagnostic method for quantifying right ventricular size and function, and pulmonary regurgitation in patients with tetralogy of Fallot surgery. The aim of this paper is to confirm the importance of magnetic resonance continuous postoperative monitoring of right and left heart function parameters as a diagnostic method that provides the most precise and accurate assessment. Methods. The prospective observational study included subjects with TOF surgery who were diagnosed with residual morphological and/or functional disorders on control postoperative echocardiographic examinations. All subjects underwent magnetic resonance imaging of the heart on a 1.5 T scanner with dedicated coils for the heart surface according to the standard protocol for a period of one year from the beginning of the study. Criteria for exclusion from the study were: significant residual pulmonary stenosis, condition after pulmonary valve replacement, existence of residual shunt lesions, contraindications for cardiac magnetic resonance imaging (pacemaker, ICD, claustrophobia). Depending on the time elapsed since the tetralogy of Fallot surgery, the subjects were divided into groups: more than 15 years, 11-15 years, 6-10 years, less than 5 years. Results. The study included 131 subjects with an average age of 24.18 ± 11.57 years with complete correction of TOF. Intergroup differences in values of right ventricular end-diastolic volume, right ventricular ejection fraction, and left ventricular ejection fraction were demonstrated, but there was no statistically significant intergroup difference in values of pulmonary regurgitation fraction. The negative interaction of the right and left ventricles intensifies during the years of follow-up of patients after TOF surgery, which is especially true fifteen years after surgery. Conclusion. CMR has the most significant role in research efforts aimed at improving the outcomes of operated patients with tetralogy of Fallot.

Cancer-related cognitive dysfunction is an important clinical problem that can interfere with the daily functioning, work productivity, childcare, and other responsibilities of women with a history of breast cancer. Risks of cancer-related cognitive impairment include cancer and cancer treatment, as well as patient-related vulnerabilities. There is no established standard of neuroprotective care or treatment for breast cancer-related cognitive impairment.

BACKGROUND Patients with Huntington disease (HD) develop diabetes mellitus more often than do matched healthy controls. Recent studies in neurodegenerative diseases suggested that insulin resistance constitutes a metabolic stressor that interacts with a preexisting neurobiological template to induce a given disorder. OBJECTIVE To investigate possible changes in insulin sensitivity and secretion, major determinants of glucose homeostasis, in a group of consecutive normoglycemic patients with HD. DESIGN Metabolic investigations. PARTICIPANTS Twenty-nine untreated, nondiabetic patients with HD and 22 control participants matched by age, sex, and socioeconomic background. MAIN OUTCOME MEASURES Glucose tolerance, assessed by means of the glucose curve during oral glucose challenge; insulin sensitivity, assessed using homeostasis model assessment and minimal model analysis based on frequent sampling of plasma glucose and plasma insulin during the intravenous glucose tolerance test; and insulin secretion, determined by means of the acute insulin response and the insulinogenic index. RESULTS The evaluation of insulin sensitivity using homeostasis model assessment demonstrated higher homeostasis model assessment insulin resistance indices, and a lower sensitivity index when the minimal model approach was used, in patients with HD compared with controls (P = .03 and P = .003, respectively). In the assessment of early-phase insulin secretion, the acute insulin response and the insulinogenic index were lower in patients with HD compared with controls (P = .02). The number of CAG repeats correlated significantly only with acute insulin response (P = .003). CONCLUSIONS Besides impairment in insulin secretion capacity, a simultaneous decrease in insulin sensitivity, with an increase in the insulin resistance level, was found in normoglycemic patients with HD compared with controls. These data imply that progression of the insulin secretion defect in HD may lead to a failure to compensate for insulin resistance.

It is known that cerebellum influences the action of the motor system. The cerebellum may exert a facilitatory influence in the motor cortex, and should be involved in temporal computations in movement performance. The inability to compute time differences would affect time-related tasks. However, the cerebellar role to control precise movement performance is contradictory. Furthermore, facilitatory effect of cerebellum might be decreased in cerebellar degeneration. The aim of the study was to investigate the performance of the rapid movements in patients with “pure” cerebellar ataxia. Movement performance was compared in 13 patients and 8 healthy subjects. Movements were performed from the initial to the target position, with the movement length of 40 deg in the elbow flexion. Motor threshold (MT) of the motor cortex was determined and TMS was then applied right of the inion, in two conditions: With the strength of 5% below the MT, at the moment of command to start the flexion movement, and with the same strength 20 ms before the movement start. Two additional conditions were also tested: TM stimulus was applied with the strength of 30% above the MT at the moment of movement start, and at 20 ms before movement start. Patients perform significantly longer movements then healthy subjects, and accuracy of the movements deteriorates. Length of the movements was also prolonged in the conditions where stronger stimulus was applied. Accuracy of the movements in patients was not different when the stimulus was applied in the phase of the movement preparation, compared in moment 0 and -20 ms. Same was true for healthy subjects in both conditions - stimulus below and above MT. Results that differences in disturbance timing and strength have no clear effects might speak for preprogrammed characteristics of rapid movements in both healthy subjects and ataxia patients, where sensory input is not of primary importance. Deficits in cerebellar ataxia for the movement length may be attributable to improper processing of motor command and/or sensory information.

Autosomal dominant cerebellar ataxias are characterized by their underlying genetic defect and are referred to as spinocerebellar ataxias (SCAs 1-23). The clinical classification of the SCA has been difficult owing to variations and overlapping of the clinical signs. The aim of this study was to compare cortical motor evoked potential (MEP), central motor conduction time (CMCT) and cortical silent period (CSP) duration in SCA patients in Serbia, namely in genetically homogenous groups of ataxia patients with type 1, type 2 and IDCA (idiopathic sporadic cerebellar ataxia). We examined 29 patients, 16 with the diagnosis of SCA 1, 6 SCA 2 and 7 IDCA patients. Eight healthy control subjects were gender and age matched. Transcranial magnetic stimulation (TMS) was used to investigate parameters of cortical excitability such as: motor threshold (MT) and MEP, CSP and CMCT. MT was established at rest, MEP was calculated as the area in the rectified EMG recording. CSP was evoked by 30% suprathreshold stimulation while subjects activated FDI muscle with contraction of 30% of their MVC. CMCT was calculated as a difference between the shortest MEP latency after cortical and after cervical stimulation (in the region of C5-C6). Results show that MT was increased in all ataxia patient groups, compared to control subjects. CMCT has significant increase in SCA 1 patients. CSP in IDCA patients is significantly longer then in SCA 1, SCA 2 and control subjects, while no difference was found between SCA 1, SCA 2 and control. MEP duration was significantly increased in all ataxia groups compared to control in relaxed muscle. Due to the cerebellar influence on the cortico-spinal system through control of inhibitory cortical interneurons, could be assumed that different categories of ataxia patients have disturbed cerebellar inhibitory influence to the various degrees. It might be possible that SCA 1 prominent abnormalities in cortical excitability originate from expansion of damage from cerebellum to some other cerebellar and brain structures.