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Mobile Phone Radiation Deflects Brain Energy Homeostasis and Prompts Human Food Ingestion.

Obesity and mobile phone usage have simultaneously spread worldwide. Radio frequency-modulated electromagnetic fields (RF-EMFs) emitted by mobile phones are largely absorbed by the head of the user, influence cerebral glucose metabolism, and modulate neuronal excitability. Body weight adjustment, in turn, is one of the main brain functions as food intake behavior and appetite perception underlie hypothalamic regulation. Against this background, we questioned if mobile phone radiation and food intake may be related. In a single-blind, sham-controlled, randomized crossover comparison, 15 normal-weight young men (23.47 ± 0.68 years) were exposed to 25 min of RF-EMFs emitted by two different mobile phone types vs. sham radiation under fasting conditions. Spontaneous food intake was assessed by an ad libitum standard buffet test and cerebral energy homeostasis was monitored by 31phosphorus-magnetic resonance spectroscopy measurements. Exposure to both mobile phones strikingly increased overall caloric intake by 22-27% compared with the sham condition. Differential analyses of macronutrient ingestion revealed that higher calorie consumption was mainly due to enhanced carbohydrate intake. Measurements of the cerebral energy content, i.e., adenosine triphosphate and phosphocreatine ratios to inorganic phosphate, displayed an increase upon mobile phone radiation. Our results identify RF-EMFs as a potential contributing factor to overeating, which underlies the obesity epidemic. Beyond that, the observed RF-EMFs-induced alterations of the brain energy homeostasis may put our data into a broader context because a balanced brain energy homeostasis is of fundamental importance for all brain functions. Potential disturbances by electromagnetic fields may therefore exert some generalized neurobiological effects, which are not yet foreseeable.

Hypocaloric Dieting Unsettles the Neuroenergetic Homeostasis in Humans.

BACKGROUND: The effects of low-calorie dieting in obesity are disappointing in the long run. The brain's energy homeostasis plays a key role in the regulation of body weight. We hypothesized that the cerebral energy status underlies an adaptation process upon body weight loss due to hypocaloric dieting in humans. OBJECTIVE: We instructed 26 healthy obese participants to reduce body weight via replacement of meals by a commercial diet product for two weeks. The cerebral energy status was assessed by 31 phosphorus magnetic resonance spectroscopy (31 PMRS) before and after low-caloric dieting as well as at follow-up. A standardized test buffet was quantified after body weight loss and at follow-up. Blood glucose metabolism and neurohormonal stress axis activity were monitored. RESULTS: Weight loss induced a decline in blood concentrations of insulin (p = 0.002), C-peptide (p = 0.005), ACTH (p = 0.006), and norepinephrine (p = 0.012). ATP/Pi (p = 0.003) and PCr/Pi ratios (p = 0.012) were increased and NADH levels reduced (p = 0.041) after hypocaloric dieting. At follow-up, weight loss persisted (p < 0.001), while insulin, C-peptide, and ACTH increased (p < 0.005 for all) corresponding to baseline levels again. Despite repealed hormonal alterations, ratios of PCr/Pi remained higher (p = 0.039) and NADH levels lower (p = 0.007) 6 weeks after ending the diet. ATP/Pi ratios returned to baseline levels again (p = 0.168). CONCLUSION: Low-calorie dieting reduces neurohormonal stress axis activity and increases the neuroenergetic status in obesity. This effect was of a transient nature in terms of stress hormonal measures. In contrast, PCr/Pi ratios remained increased after dieting and at follow-up while NADH levels were still reduced, which indicates a persistently unsettled neuroenergetic homeostasis upon diet-induced rapid body weight loss.

Lactate infusion increases brain energy content during euglycemia but not hypoglycemia in healthy men.

A special characteristic of the brain is the usage of lactate as alternative fuel instead of glucose to preserve its energy homeostasis. This physiological function is valid for sufficient cerebral glucose supply, as well as presumably during hypoglycemia, given that exogenous lactate infusion suppresses hormonal counterregulation. However, it is not yet clarified whether this effect is mediated by the use of lactate as an alternative cerebral energy substrate or any other mechanism. We hypothesized that under conditions of limited access to glucose (ie, during experimental hypoglycemia) lactate infusion would prevent hypoglycemia-induced neuroenergetic deficits in a neuroprotective way. In a randomized, double-blind, crossover study, lactate vs placebo infusion was compared during hyperinsulinemic-hypoglycemic clamps in 16 healthy young men. We measured the cerebral high-energy phosphate content - ie, adenosine triphosphate (ATP), phosphocreatine (PCr) and inorganic phosphate (Pi) levels - by 31 P-magnetic resonance spectroscopy as well as the neuroendocrine stress response. During euglycemia, lactate infusion increased ATP/Pi as well as PCr/Pi ratios compared with baseline values and placebo infusion. During hypoglycemia, there were no differences between the lactate and the placebo condition in both ratios. Hormonal counterregulation was significantly diminished upon lactate infusion. Our data demonstrate an elevated cerebral high-energy phosphate content upon lactate infusion during euglycemia, whereas there was no such effect during experimental hypoglycemia. Nevertheless, lactate infusion suppressed hypoglycemic hormonal counterregulation. Lactate thus adds to cerebral energy provision during euglycemia and may contribute to an increase in ATP reserves, which in turn protects the brain against neuroglucopenia under recurrent hypopglycemic conditions, eg, in diabetic patients.

Double transcranial direct current stimulation of the brain increases cerebral energy levels and systemic glucose tolerance in men.

Transcranial direct current stimulation (tDCS) is a neuromodulatory method that has been tested experimentally and has already been used as an adjuvant therapeutic option to treat a number of neurological disorders and neuropsychiatric diseases. Beyond its well known local effects within the brain, tDCS also transiently promotes systemic glucose uptake and reduces the activity of the neurohormonal stress axes. We aimed to test whether the effects of a single tDCS application could be replicated upon double stimulation to persistently improve systemic glucose tolerance and stress axes activity in humans. In a single-blinded cross-over study, we examined 15 healthy male volunteers. Anodal tDCS vs sham was applied twice in series. Systemic glucose tolerance was investigated by the standard hyperinsulinaemic-euglycaemic glucose clamp procedure, and parameters of neurohormonal stress axes activity were measured. Because tDCS-induced brain energy consumption has been shown to be part of the mechanism underlying the assumed effects, we monitored the cerebral high-energy phosphates ATP and phosphocreatine by 31 phosphorus magnetic resonance spectroscopy. As hypothesised, analyses revealed that double anodal tDCS persistently increases glucose tolerance compared to sham. Moreover, we observed a significant rise in cerebral high-energy phosphate content upon double tDCS. Accordingly, the activity of the neurohormonal stress axes was reduced upon tDCS compared to sham. Our data demonstrate that double tDCS promotes systemic glucose uptake and reduces stress axes activity in healthy humans. These effects suggest that repetitive tDCS may be a future non-pharmacological option for combating glucose intolerance in type 2 diabetes patients.

Psychosocial stress promotes food intake and enhances the neuroenergetic level in men.

Psychosocial stress may lead to increased food consumption and overweight. In turn, obesity is related to reduced brain energy content. We hypothesized that psychosocial stress influencing food intake may alter the neuroenergetic status in the human brain. We tested 14 healthy normal weight men in a randomized crossover design. A modified version of the Trier Social Stress Test (TSST) was carried out to induce psychosocial stress vs. control in a neuroimaging setting. Cerebral energy content, i.e. high energy phosphates adenosine triphosphate (ATP) and phosphocreatine (PCr), was measured by 31phosphorus magnetic resonance spectroscopy. Food intake was quantified by an ad libitum buffet test. Stress hormonal response and alterations in glucose metabolism were monitored by blood sampling. Before data collection, we mainly expected a stress-induced reduction in cerebral high energy phosphates, followed by higher food intake. Psychosocial stress increased serum cortisol concentrations (p = .003) and fat intake of all participants by 25% (p = .043), as well as food intake of "stress-eaters" by 41.1% (p = .003) compared with controls. Blood glucose and insulin concentrations were not affected (p > .174 for both). Cerebral ATP and PCr levels generally increased upon stress-induction (p > = .022 and p = .037, respectively). Our data confirm that psychosocial stress may enhance food intake. Contrary to our expectations, stress induces a distinct increase in the neuroenergetic status. This insight suggests that the underlying central nervous mechanisms of stress-induced overeating may involve the regulation of the brain energy homeostasis.

Impaired brain energy gain upon a glucose load in obesity.

BACKGROUND: There is evidence that the brain's energy status is lowered in obesity despite of chronic hypercaloric nutrition. The underlying mechanisms are unknown. We hypothesized that the brain of obese people does not appropriately generate energy in response to a hypercaloric supply. METHODS: Glucose was intravenously infused in 17 normal weights and 13 obese participants until blood glucose concentrations reached the postprandial levels of 7 mmol/L and 10 mmol/L. Changes in cerebral adenosine triphosphate (ATP) and phosphocreatine (PCr) content were measured by 31phosphorus magnetic resonance spectroscopy and stress hormonal measures regulating glucose homeostasis were monitored. Because vitamin C is crucial for a proper neuronal energy synthesis we determined circulating concentrations during the experimental testing. RESULTS: Cerebral high-energy phosphates were increased at blood glucose levels of 7 mmol/L in normal weights, which was completely missing in the obese. Brain energy content moderately raised only at blood glucose levels of 10 mmol/L in obese participants. Vitamin C concentrations generally correlated with the brain energy content at blood glucose concentrations of 7 mmol/L. CONCLUSIONS: Our data demonstrate an inefficient cerebral energy gain upon a glucose load in obese men, which may result from a dysfunctional glucose transport across the blood-brain barrier or a downregulated energy synthesis in mitochondrial oxidation processes. Our finding offers an explanation for the chronic neuroenergetic deficiency and respectively missing satiety perception in obesity.

Persistent blood glucose reduction upon repeated transcranial electric stimulation in men.

BACKGROUND: Transcranial direct current stimulation (tDCS) of the human brain increases systemic glucose tolerance. OBJECTIVE/HYPOTHESIS: To investigate whether this effect persists after one week of repeated stimulation. Because systemic glucose uptake relates to brain energy homeostasis, we concomitantly measured cerebral high-energy phosphate metabolites. METHODS: In a sham-controlled crossover design, 14 healthy men were tested under daily anodal tDCS vs. sham for 8 days. Systemic glucose metabolism was examined by concentrations of circulating glucose and insulin. Cerebral energy metabolism - i.e. adenosine triphosphate (ATP) and phosphocreatine (PCr) levels - was assessed by 31phosphorous magnetic resonance spectroscopy. RESULTS: Blood glucose concentrations were distinctly lower upon tDCS compared with sham stimulation on day 1. This effect persisted on day 8, while serum insulin levels remained persistently unchanged. Transcranial stimulation increased mean levels of ATP and PCr compared with sham on day 1 only. Blood glucose concentrations negatively correlated with PCr content after repeated daily stimulation. CONCLUSIONS: Our data confirm that tDCS reduces blood glucose through an insulin-independent mechanism. This effect persists after 8 days of repeated stimulation and relates to brain energy metabolism. Therefore, transcranial electric stimulation may be a promising non-pharmacological adjuvant option to treat systemic disorders such as glucose intolerance or type 2 diabetes mellitus with a low side-effect profile.

Risk assessment of magnetic resonance imaging in chronically implanted paddle electrodes for cortical stimulation.

BACKGROUND: Cortical epidural stimulation is used for the treatment of different neuropsychiatric disorders such as chronic neuropathic pain, tinnitus, movement disorders, and psychiatric diseases. While preoperative magnetic resonance imaging (MRI) is considered the imaging tool of choice for planning the approach and electrode placement, postoperative MRI is still a contraindication with implanted paddle leads due to the risk of thermal damage or current induction creating seizures or neurological deficits. OBJECTIVES: In this feasibility in vitro study the temperature changes and induction were determined as well as the artifacts caused by 2 parallel paddle leads (Resume II, Model 3587 A; Medtronic, Minneapolis, Minn., USA), commonly used in clinical practice with and without a pulse generator (Prime Advanced, Model 7489; Medtronic). METHODS: An ultrasound gel-filled head phantom with 2 paddle leads mimicking the surgical scenario was used to evaluate temperature changes as well as induced currents in a 1.5- and 3-tesla MR scanner. In addition, 1 patient underwent a 3-tesla MRI with an implanted subdural paddle lead. RESULTS: Negligible temperature changes were detected with turbo spin echo sequences in the 1.5- and 3-tesla scanner using a head and body coil. Induced voltages up to 6 V were measured. The imaging artifacts in the phantom were well tolerable. The patient's imaging was uneventful under the settings which are accepted for deep brain stimulation imaging. CONCLUSION: MRI under the conditions described here seems to be safe with the implants used in this study. In particular, the induced temperature is much lower with paddle compared to conventional leads due to the different electrode design. The induced voltage does not carry any risks. However, these findings cannot automatically be transferred to other implants or other scanning conditions, and further studies are needed. The biomedical companies should be encouraged to develop MR-conditional paddle leads. Also, further research is necessary to study the mechanism of action of cortical stimulation in the future.

Blunted brain energy consumption relates to insula atrophy and impaired glucose tolerance in obesity.

Brain energy consumption induced by electrical stimulation increases systemic glucose tolerance in normal-weight men. In obesity, fundamental reductions in brain energy levels, gray matter density, and cortical metabolism, as well as chronically impaired glucose tolerance, suggest that disturbed neuroenergetic regulation may be involved in the development of overweight and obesity. Here, we induced neuronal excitation by anodal transcranial direct current stimulation versus sham, examined cerebral energy consumption with (31)P magnetic resonance spectroscopy, and determined systemic glucose uptake by euglycemic-hyperinsulinemic glucose clamp in 15 normal-weight and 15 obese participants. We demonstrate blunted brain energy consumption and impaired systemic glucose uptake in obese compared with normal-weight volunteers, indicating neuroenergetic dysregulation in obese humans. Broadening our understanding of reduced multifocal gray matter volumes in obesity, our findings show that reduced appetite- and taste-processing area morphometry is associated with decreased brain energy levels. Specifically, gray matter volumes of the insula relate to brain energy content in obese participants. Overall, our results imply that a diminished cerebral energy supply may underlie the decline in brain areas assigned to food intake regulation and therefore the development of obesity.

Intranasal insulin suppresses food intake via enhancement of brain energy levels in humans.

Cerebral insulin exerts anorexic effects in humans and animals. The underlying mechanisms, however, are not clear. Because insulin physiologically facilitates glucose uptake by most tissues of the body and thereby fosters intracellular energy supply, we hypothesized that intranasal insulin reduces food consumption via enhancement of the neuroenergetic level. In a double-blind, placebo-controlled, within-subject comparison, 15 healthy men (BMI 22.2 ± 0.37 kg/m(2)) aged 22-28 years were intranasally administered insulin (40 IU) or placebo after an overnight fast. Cerebral energy metabolism was assessed by (31)P magnetic resonance spectroscopy. At 100 min after spray administration, participants consumed ad libitum from a test buffet. Our data show that intranasal insulin increases brain energy (i.e., adenosine triphosphate and phosphocreatine levels). Cerebral energy content correlates inversely with subsequent calorie intake in the control condition. Moreover, the neuroenergetic rise upon insulin administration correlates with the consecutive reduction in free-choice calorie consumption. Brain energy levels may therefore constitute a predictive value for food intake. Given that the brain synchronizes food intake behavior in dependence of its current energetic status, a future challenge in obesity treatment may be to therapeutically influence cerebral energy homeostasis. Intranasal insulin, after optimizing its application schema, seems a promising option in this regard.

Brain energy consumption induced by electrical stimulation promotes systemic glucose uptake.

BACKGROUND: Controlled transcranial stimulation of the brain is part of clinical treatment strategies in neuropsychiatric diseases such as depression, stroke, or Parkinson's disease. Manipulating brain activity by transcranial stimulation, however, inevitably influences other control centers of various neuronal and neurohormonal feedback loops and therefore may concomitantly affect systemic metabolic regulation. Because hypothalamic adenosine triphosphate-sensitive potassium channels, which function as local energy sensors, are centrally involved in the regulation of glucose homeostasis, we tested whether transcranial direct current stimulation (tDCS) causes an excitation-induced transient neuronal energy depletion and thus influences systemic glucose homeostasis and related neuroendocrine mediators. METHODS: In a crossover design testing 15 healthy male volunteers, we increased neuronal excitation by anodal tDCS versus sham and examined cerebral energy consumption with ³¹phosphorus magnetic resonance spectroscopy. Systemic glucose uptake was determined by euglycemic-hyperinsulinemic glucose clamp, and neurohormonal measurements comprised the parameters of the stress systems. RESULTS: We found that anodic tDCS-induced neuronal excitation causes an energetic depletion, as quantified by ³¹phosphorus magnetic resonance spectroscopy. Moreover, tDCS-induced cerebral energy consumption promotes systemic glucose tolerance in a standardized euglycemic-hyperinsulinemic glucose clamp procedure and reduces neurohormonal stress axes activity. CONCLUSIONS: Our data demonstrate that transcranial brain stimulation not only evokes alterations in local neuronal processes but also clearly influences downstream metabolic systems regulated by the brain. The beneficial effects of tDCS on metabolic features may thus qualify brain stimulation as a promising nonpharmacologic therapy option for drug-induced or comorbid metabolic disturbances in various neuropsychiatric diseases.

Evidence for a relationship between body mass and energy metabolism in the human brain.

Cerebral energy metabolism has been suggested to have an important function in body weight regulation. We therefore examined whether there is a relationship between body mass and adenosine triphosphate (ATP) metabolism in the human brain. On the basis of our earlier findings indicating a neuroprotective preferential energy supply of the brain, as compared with peripheral muscle on experimentally induced hypoglycemia, we examined whether this physiological response is preserved also in low-weight and obese participants. We included 45 healthy male subjects with a body mass index (BMI) ranging from 17 to 44 kg/m(2). Each participant underwent a hypoglycemic glucose-clamp intervention, and the ATP metabolism, that is, the content of high-energy phosphates phosphocreatine (PCr) and ATP, was measured repeatedly by (31)phosphor magnetic resonance spectroscopy ((31)P-MRS) in the cerebral cortex and skeletal muscle. Results show an inverse correlation between BMI and high-energy phosphate content in the brain (P<0.01), whereas there was no such relationship found between skeletal muscle and BMI. The hypoglycemic clamp intervention did not affect the ATP metabolism in both tissues. Our data show an inverse correlation between BMI and cerebral high-energy phosphate content in healthy humans, suggesting a close relationship between energetic supply of the brain and body weight regulation.

Divergent effects of hyper- and hypoglycemia on circulating vascular endothelial growth factor in humans.

Vascular endothelial growth factor (VEGF) is known to be up-regulated by hypoxia, hyperglycemia, and hypoglycemia in vitro. In contrast, it has been found in healthy humans that plasma concentrations of VEGF decrease upon hypoxia under in vivo conditions, indicating that systemic VEGF concentration may be differently regulated than cellular expression. To test the effect of blood glucose levels on VEGF concentrations in vivo, we examined plasma VEGF changes upon brief hyper- and hypoglycemia in healthy male subjects. We rapidly induced in a crossover design hypoglycemia by insulin bolus application of 0.1 U/kg or hyperglycemia by dextrose infusion in 24 healthy young men. Plasma VEGF concentrations were measured at baseline, at the target glucose concentration of <2.2 mmol/L or >10 mmol/L, and after further 5 and 10 minutes. Plasma VEGF concentrations decreased upon hyperglycemia as compared with euglycemic baseline (P = .027), whereas during hypoglycemic condition, there was a trend for an increase (P = .091). Analysis for repeated measurements including both conditions revealed a differential regulation of plasma VEGF levels upon glycemic condition (P = .035). Our results are consistent with the hypothesis that systemic VEGF concentration may be differentially regulated than expression on cellular basis. Because VEGF is a candidate hormone for regulating glucose passage across the blood-brain barrier under critical conditions, it possibly acts as a neuroprotective controller for constant cerebral glucose supply. This may be of relevance for the understanding of VEGF alterations in different pathological states such as diabetes mellitus.

Differential energetic response of brain vs. skeletal muscle upon glycemic variations in healthy humans.

The brain regulates all metabolic processes within the organism, and therefore, its energy supply is preserved even during fasting. However, the underlying mechanism is unknown. Here, it is shown, using (31)P-magnetic resonance spectroscopy that during short periods of hypoglycemia and hyperglycemia, the brain can rapidly increase its high-energy phosphate content, whereas there is no change in skeletal muscle. We investigated the key metabolites of high-energy phosphate metabolism as rapidly available energy stores by (31)P MRS in brain and skeletal muscle of 17 healthy men. Measurements were performed at baseline and during dextrose or insulin-induced hyperglycemia and hypoglycemia. During hyperglycemia, phosphocreatine (PCr) concentrations increased significantly in the brain (P = 0.013), while there was a similar trend in the hypopglycemic condition (P = 0.055). Skeletal muscle content remained constant in both conditions (P > 0.1). ANOVA analyses comparing changes from baseline to the respective glycemic plateau in brain (up to +15%) vs. muscle (up to -4%) revealed clear divergent effects in both conditions (P < 0.05). These effects were reflected by PCr/Pi ratio (P < 0.05). Total ATP concentrations revealed the observed divergency only during hyperglycemia (P = 0.018). These data suggest that the brain, in contrast to peripheral organs, can activate some specific mechanisms to modulate its energy status during variations in glucose supply. A disturbance of these mechanisms may have far-reaching implications for metabolic dysregulation associated with obesity or diabetes mellitus.

Motor memory consolidation in sleep shapes more effective neuronal representations.

Learning a motor skill involves a latent process of consolidation that develops after training to enhance the skill in the absence of any practice and crucially depends on sleep. Here, we show that this latent consolidation during sleep changes the brain representation of the motor skill by reducing overall the neocortical contributions to the representation. Functional magnetic resonance brain imaging was performed during initial training and 48 h later, at retesting, on a sequential finger movement task with training followed by either a night of regular sleep or sleep deprivation. An additional night of sleep for all subjects served to rule out unspecific effects of sleep loss at retrieval testing. Posttraining sleep, but not sleep deprivation, led to improved motor skill performance at retrieval. This sleep-dependent improvement was linked to greatly reduced brain activation in prefrontal, premotor, and primary motor cortical areas, along with a stronger involvement of left parietal cortical regions. Our findings indicate that storing a motor skill during sleep reorganizes its brain representation toward enhanced efficacy.

Radiation dose to the radiologist's hand during continuous CT fluoroscopy-guided interventions.

Computed tomography fluoroscopy (CT fluoroscopy) enables real-time image control over the entire body with high geometric accuracy and, for the most part, without significant interfering artifacts, resulting in increased target accuracy, reduced intervention times, and improved biopsy specimens [1--4]. Depending on the procedure being used, higher radiation doses than in conventional CT-supported interventions might occur. Because the radiologist is present in the CT room during the intervention, he is exposed to additional radiation, which is an important aspect. Initial experience with CT fluoroscopically guided interventions is from the work of Katada et al. in 1994 [5] and only relatively few reports on radiation aspects in CT fluoroscopy are found in the literature [1, 2, 6--11]. To date, there are no reported injuries to patients and radiologists occurring with CT fluoroscopy. The time interval since the wide use of CT fluoroscopy is too short to have data on late effects to the operator using CT fluoroscopy on a daily basis. In addition, the spectrum of CT fluoroscopically guided interventional procedures will expand and more sophisticated procedures requiring longer fluoroscopy times will be performed. Thus, effective exposure reduction is very important. The purpose of our study was to assess the radiation dose to the operator's hand by using data from phantom measurements. In addition, we investigated the effect of a lead drape on the phantom surface adjacent to the scanning plane, the use of thin radiation protective gloves, and the use of different needle holders.

[Procedures, spectrum and radiation exposure in CT-fluoroscopy]. / Verfahren, Spektrum und Strahlenexposition der CT-Fluoroskopie.

PURPOSE: To assess the techniques, indications and radiation exposures incurred with CT fluoroscopy. MATERIAL AND METHODS: A 1-year period of use of CT fluoroscopy to guide diagnostic and therapeutic interventional procedures was analyzed. The spectrum of indications, different CT fluoroscopic methods and radiation exposures for the radiologist were assessed. Scatter exposures were measured with and without placement of a lead drape on the patient, with and without use of thin rubber radiation protection gloves. In addition, scattered radiation was determined for a combination of lead drape and radiation protection gloves. RESULTS: There is a wide variety for the use of CT fluoroscopy ranging from diagnostic biopsy procedures to therapeutic interventions such as radiofrequency ablation of liver metastases and CT fluoroscopy-guided osteosynthesis of fractures. Scatter exposure rates to the radiologists hand ranged from 1-320 microSv/case without use of a lead drape and without radiation protection gloves. The lead drape reduced the scattered exposure for the radiologists hand by 72%. Radiation protection gloves reduced scatter radiation by 49%. The combination of both radiation protection devices was most effective in decreasing the dose by 97%. CONCLUSIONS: CT fluoroscopy is a useful targeting method with a wide variety for interventional procedures. However, significant radiation exposures may occur. Therefore, the radiologists should be aware of different techniques of CT fluoroscopy guidance and the methods to reduce scatter radiation.

Modulation of cerebellar activation by predictive and non-predictive sequential finger movements.

We investigated the modulation of cerebellar activation by predictive and non-predictive sequential finger movements. It is hypothesized that the prediction of desired movement sequences and adaptation to new movement parameters is mediated by the cerebellum. Using functional MRI at 1.5 T, seven normal subjects performed sequential finger to thumb opposition movements, either in predictive (repeatedly 2,3,4,5) or non-predictive (randomized) fashion at a constant frequency of 1 Hz. Performance and error rates were monitored by simultaneous recording of the finger movements. Predictive sequential finger opposition movements activated a cerebellar network including the lobuli IV-VI ipsilateral to the movements, the contralateral lobuli IV-VI, the vermis, and lobuli VIIB-VIII ipsilaterally. Non-predictive compared to predictive finger opposition movements activated a broader area within the ipsi- and contralateral anterior cerebellum, lobuli IV-VI, the vermis, and the ipsilateral lobuli VIIB-VIII. Additional activation foci were found in the contralateral lobuli VIIA and VIIB-VIII. Our study demonstrates a modulated information processing within the cerebellar network dependent on the predictability of movement sequences.