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Background and Purpose: The Patient-Specific Functional Scale (PSFS) is an individualized patient-reported outcome measure designed to assess the limitations and changes in self-determined functional activities most important to an older patient in the acute care setting. However, its clinimetric properties have not yet been evaluated in these patients. The study aimed to investigate the construct validity, test-retest reliability, sensitivity to change, and feasibility of the PSFS in acutely hospitalized older patients with and without cognitive impairment (CI). Methods: The clinimetric properties of the PSFS were investigated by secondary data analysis from a prospective observational cohort study examining physical activity and mobility in acutely hospitalized older patients. In this analysis, 120 older patients—83.0 (6.4) years—with and without CI (Mini-Mental State Examination [MMSE] score 18-23, n = 52, and MMSE ≥24, n = 68, respectively) receiving early multidisciplinary geriatric rehabilitation in acute care were included. Construct validity was assessed by Spearman correlations (r s) with the Activity-specific Balance Confidence Scale (ABC-6), Short Falls Efficacy Scale-International (Short FES-I), EuroQoL-5 Dimensions (EQ-5D), Short Physical Performance Battery (SPPB), de Morton Mobility Index (DEMMI), and Barthel Index (BI); test-retest reliability within 24 hours by intraclass correlation coefficients (ICCs); sensitivity to change by standardized response means (SRMs) calculated for treatment effects, and feasibility by completion rates/times and floor/ceiling effects. Results: The PSFS showed fair to moderate correlations with all construct variables in patients with CI (r s = 0.31 to 0.53). In patients without CI, correlations were fair for the ABC-6, FES-I, EQ-5D, and BI (r s = |0.27 to 0.36|), but low for the SPPB and DEMMI (r s =−0.04 to 0.14). Test-retest reliability (both: ICC = 0.76) and sensitivity to change (CI: SRM = 1.10, non-CI: SRM = 0.89) were excellent in both subgroups. Excellent feasibility was documented by high completion rates (>94%), brief completion times (<8 min), and no floor/ceiling effects in either subgroup. Conclusions: The PSFS has adequate clinimetric properties for assessing patient-specific functional limitations and changes in acutely hospitalized older patients with and without CI. It might be an appropriate complement to traditional functional scales to enhance patient-centeredness in clinical geriatric assessment. [ABSTRACT FROM AUTHOR]

Background and Purpose: People with dementia show disease-specific sit-to-stand (STS) movement disorders, which relate to deficits of integrating cognitive aspects of motor processes into motor action organization. During STS training in rehabilitation therapy, compensatory STS movement maneuvers are taught aiming to improve patients' STS ability. Previous clinical STS measures do not address these maneuvers or assess cognitive aspects of their motor action organization. The purpose of this study was to develop and validate a motor-cognitive STS assessment instrument for people with dementia (Assessment of Compensatory Sit-to-Stand Maneuvers in People With Dementia, ACSID). Methods: The ACSID covers the recall, initiation, and effective performance of compensatory STS movement maneuvers. The inter- and intrarater reliability, concurrent validity, sensitivity to change, and feasibility were investigated by secondary analysis of data of 97 participants from a randomized controlled trial to improve motor-cognitive performances in people with mild to moderate dementia (mean [standard deviation] age: 82.5 [5.9] years, Mini-Mental Status Examination: 21.9 [2.9] points). Concurrent validity of the individual ACSID items was assessed against reference criteria derived from video-motion analysis. Results: Good to excellent inter- (kappa [κ] = 0.64-0.99; intraclass correlation coefficient [ICC] = 0.74-0.89) and intrarater (κ= 0.77-0.91; ICC = 0.77-0.91), concurrent validity (point-biserial correlation coefficients = |0.56|-|0.84|), and sensitivity to change (standardized response means = 0.61-1.00) were found. Feasibility was excellent with a high completion rate (96.9%), no critical events during assessment, and no floor or ceiling effects. Conclusions: The ACSID represents the first observation-based assessment instrument to document motor and cognitive aspects in the execution of a motor key feature in people with dementia, and has been shown to be reliable, valid, feasible, and sensitive to intervention-induced changes. [ABSTRACT FROM AUTHOR]

Background: Prone positioning is often necessary in orthopaedic surgery. The prone position, however, may result in impaired cerebral venous drainage with a subsequent reduction in cerebral perfusion. As a consequence, cerebral hypoxia may occur with the potential for neurological impairment.Objective: We assessed the changes in cerebral oxygen saturation with near-infrared spectroscopy using two different monitors after positioning the patient from supine to prone.Design: Prospective observational study.Setting: Primary Care University Hospital, from May 2010 to February 2011.Participants: Forty patients undergoing general anaesthetic procedures, of which 35 completed the investigation. Similar measurements were done in 35 volunteers, who were studied while awake.Interventions: Near-infrared spectroscopy was measured throughout anaesthesia using INVOS (a trend monitor using two infrared wavelengths) for one hemisphere and FORE-SIGHT (a monitor using four wavelengths of laser light to calculate absolute oxygen saturation) for the other hemisphere in an alternate randomisation pattern.Outcome Measurements: The primary outcome was a change in cerebral oxygen saturation of more than 5% during prone positioning. A comparison with the changes obtained in awake volunteers following similar positioning was also made.Results: Cerebral oxygen saturation increased during prone positioning with INVOS 0.032% per minute (P < 0.01) and with FORE-SIGHT 0.032% per minute (P < 0.01) in anaesthetised patients. Awake volunteers showed an increase of 0.171% per minute (INVOS) and 0.082% per minute (FORE-SIGHT) during prone positioning. Comparison of INVOS with FORE-SIGHT showed a good association, with a gradient of 0.80% per 1% change (P < 0.01).Conclusion: Both monitors detected a small increase in cerebral oxygen saturation of less than 5% in patients undergoing orthopaedic surgery in the prone position and in awake volunteers. This small increase is of limited clinical relevance and prone positioning may be regarded as safe in terms of the maintenance of cerebral oxygen saturation.Trial Registration: clinicaltrials.gov identifier: NCT01275898. [ABSTRACT FROM AUTHOR]

Background: In patients with chronic kidney disease (CKD), atrial fibrillation (AF) is highly prevalent and represents a major risk factor for stroke and death. CKD is associated with atrial proarrhythmic remodeling and activation of the sympathetic nervous system. Whether reduction of the sympathetic nerve activity by renal denervation (RDN) inhibits AF vulnerability in CKD is unknown., Methods: Left atrial (LA) fibrosis was analyzed in samples from patients with AF and concomitant CKD (estimated glomerular filtration rate [eGFR], <60 mL/min per 1.73 m 2 ) using picrosirius red and compared with AF patients without CKD and patients with sinus rhythm with and without CKD. In a translational approach, male Sprague Dawley rats were fed with 0.25% adenine (AD)-containing chow for 16 weeks to induce CKD. At week 5, AD-fed rats underwent RDN or sham operation (AD). Rats on normal chow served as control. After 16 weeks, cardiac function and AF susceptibility were assessed by echocardiography, radiotelemetry, electrophysiological mapping, and burst stimulation, respectively. LA tissue was histologically analyzed for sympathetic innervation using tyrosine hydroxylase staining, and LA fibrosis was determined using picrosirius red., Results: Sirius red staining demonstrated significantly increased LA fibrosis in patients with AF+CKD compared with AF without CKD or sinus rhythm. In rats, AD demonstrated LA structural changes with enhanced sympathetic innervation compared with control. In AD, LA enlargement was associated with prolonged duration of induced AF episodes, impaired LA conduction latency, and increased absolute conduction inhomogeneity. RDN treatment improved LA remodeling and reduced LA diameter compared with sham-operated AD. Furthermore, RDN decreased AF susceptibility and ameliorated LA conduction latency and absolute conduction inhomogeneity, independent of blood pressure reduction and renal function., Conclusions: In an experimental rat model of CKD, RDN inhibited progression of atrial structural and electrophysiological remodeling. Therefore, RDN represents a potential therapeutic tool to reduce the risk of AF in CKD, independent of changes in renal function and blood pressure.

Objective: The beneficial effects of hypertonic saline on neuronal survival and on cerebral blood flow have been shown in several animal models of global and focal brain ischemia. Because of the potential benefits of hypertonic solutions, it is hypothesized that hydroxyethyl starch enhances cerebral blood flow and improves long-term outcome after cardiac arrest and cardiopulmonary resuscitation in an animal model., Design: Laboratory animal study., Setting: University animal research laboratory., Subjects: Fifty-nine male Sprague-Dawley rats., Interventions: Rats were randomized to receive either 7.2% saline/6% hypertonic saline hydroxyethyl starch (4 mL/kg) or vehicle (NaCl 0.9 %) after 9 mins of asphyxic cardiac arrest and cardiopulmonary resuscitation. Local cerebral blood flow and physiologic parameters were evaluated during arrest and early restoration of spontaneous circulation. Survival and neurologic assessment were evaluated over a 7-day observation period. Animals received 5-bromo-2-deoxyuridine for 6 days. Neuronal injury and neurogeneration (5-bromo-2-deoxyuridine positive neurons) were quantified on day 7 after cardiac arrest and cardiopulmonary resuscitation., Measurements and Main Results: Hypertonic saline hydroxyethyl starch treatment resulted in an accentuated local cerebral blood flow during early reperfusion, compared to the vehicle group. Animal survival and neurologic outcome were not altered between groups. Neurohistopathological injury was present in hippocampal CA1 and neocortex with no effects of hypertonic saline hydroxyethyl starch on neuronal survival. Increased neurogeneration was found in the dentate gyrus after cardiac arrest/cardiopulmonary resuscitation, which was not influenced by hypertonic saline hydroxyethyl starch administration., Conclusions: Despite promising results in other models of brain injury, hypertonic saline hydroxyethyl starch failed to improve the outcome when administered after asphyxic cardiac arrest/cardiopulmonary resuscitation in rats. One major difference between the cardiac arrest/cardiopulmonary resuscitation model and other models of brain ischemia is that the effects of asphyxic cardiac arrest involve the whole organism (post-cardiac arrest syndrome) and not exclusively the brain leading to a more severe injury. This might explain why hypertonic saline hydroxyethyl starch has failed to improve outcome in the present model.

Background: Autologous blood transfusion (ABT), for example, by means of cell saver equipment, is used to reduce the need for allogenic blood transfusion in patients with high perioperative blood loss. This study investigated the effect of blood/extracorporal surface interaction during withdrawal and retransfusion of shed autologous blood on cerebral inflammation in rats. Rats subjected to hypotension with cerebral ischemia served as positive controls., Methods: Eighty-eight male Sprague-Dawley rats were anesthetized with sevoflurane, instrumented, and randomly assigned to the following groups: sham-operation (SHAM), autologous blood withdrawal/transfusion only (ABT), or bilateral carotid artery occlusion and autologous blood withdrawal/transfusion (BCAO/ABT). Inflammatory gene expression was investigated with real-time RT-polymerase chain reaction at 6, 12, and 24 hours after SHAM, ABT, or BCAO/ABT in brain hippocampal tissue. Naive rats were investigated as reference., Results: ABT alone had no impact on hippocampal inflammatory gene expression, whereas after BCAO/ABT tumor necrosis factor-alpha (10.7 fold at 24 h), interleukin-1β (2.1 fold at 6 h), interleukin-6 (35.7 fold at 24 h), COX-2 (9.3 fold at 6 h), and inducible nitric oxide synthase (3.4 fold at 24 h) increased compared with SHAM., Conclusions: ABT by itself did not provoke an inflammatory reaction in the healthy brain. However, in combination with cerebral ischemia the induction of a broad spectrum of inflammatory parameters indicates an inflammatory reaction of the hippocampus beginning after 6 hours and being most pronounced after 24 hours. Therefore, this study shows that cerebral inflammation is not induced by ABT after contact with extracorporal surfaces in rats.

Unlabelled: Pain after craniotomy may be underdiagnosed, despite the fact that it can increase postoperative complications for example arterial hypertension and postoperative hemorrhage. This study investigates the incidence and intensity of pain after craniotomy and characterizes the influencing parameters. During a 1-year period 256 patients undergoing elective craniotomy were prospectively included in the study. Intensity of pain was evaluated 1, 4, and 24 hours after extubation using a verbal numerical rating scale (NRS) ranging from 0 (no pain) to 10 (maximal pain). Routine perioperative pain management was not influenced by the investigators. Parameters including patient-related factors, drug administration, and surgical factors were correlated with incidence and intensity of postcraniotomy pain., Statistical Analysis: logistic regression and chi using SPSS program (Windows, version 12.0). During the first 24 hours 87% of the patients experienced pain (NRS 1 to 3: 32%, NRS 4 to 7: 44%, NRS 8 to 10: 11%). For postoperative analgesia, the opioid piritramide (a mu-receptor agonist) was administered to 70% and nonopiod analgesics to 73% of the patients. The probability of experiencing postcraniotomy pain was reduced by 3% for each year of life. Maintenance of anesthesia with sevoflurane increased the probability of suffering from postcraniotomy pain by 147% and the absence of corticosteroids by 119%. Other investigated parameters did not influence pain after craniotomy. This study shows that pain is experienced by the majority of patients after craniotomy, despite conventional pain management, emphasizing the necessity for improved and individualized pain management in this special group of patients.

Background: The present study assesses the utility of a novel invasive device (O2C-, oxygen-to-see-device) for intraoperative measurement of the cerebral microcirculation. CO2 vasoreactivity during 2 different propofol concentrations was used to investigate changes of capillary venous cerebral blood flow (rvCBF), oxygen saturation (srvO2), and hemoglobin concentration (rvHb) during craniotomy., Methods: Thirty-four patients were randomly assigned to a low propofol (4 mg/kg/h) versus a high propofol (6 mg/kg/h) group. A fiberoptic probe was applied on the cortex next to the surgical site. Measurements were performed during lower (35 mm Hg) and higher (45 mm Hg) levels of partial pressure of carbon dioxide (paCO2). Arterio-venous difference in oxygen concentration (avDO2) and approximated cerebral metabolic rate of oxygen (aCMRO2) were calculated for each paCO2 state. Linear models were fitted to test changes of end points in response to paCO2 and propofol concentration., Results: In comparison to the lower levels of paCO2, higher levels of paCO2 increased rvCBF (P<0.001), and srvO2 (P=0.002). RvHb remained unchanged during measurements (P=0.325). Calculated avDO2 decreased with increasing paCO2 (P<0.001), whereas aCMRO2 did not change during the study (P=0.999). Propofol concentration had no effect on measured or calculated end points., Conclusions: Increase of rvCBF by paCO2 indicates a preserved CO2 reactivity independent of propofol anesthesia. The consecutive rise in srvO2 implies enhanced oxygen availability due to vasodilatation. Unchanged rvHb represents constant venous hemoglobin concentration. As expected, calculated avDO2 decreases with increased paCO2, whereas aCMRO2 remains unchanged. Despite the promising technical approach, the technology needs validation and further investigation for usage during neurosurgery.

Background: We investigated the effects of 4 h of posttraumatic hyperventilation on neurocognitive performance, motor function, and coordination as well as lesion volume in rats subjected to focal traumatic brain injury., Methods: After a 14-day training period with various neurocognitive tests including hole-board, beam walk, and beam balance, 21 male Sprague-Dawley rats (369 +/- 15 g) were anesthetized with halothane, tracheally intubated, their lungs mechanically ventilated, and subjected to controlled cortical impact (1.75 mm depth, diameter 5 mm, 4 m/s). They were then randomized to either normoventilation (n = 10; PaCO(2) = 38-42 mm Hg) or hyperventilation (n = 11; PaCO(2) = 28-32 mm Hg) and ventilated for 4 h, respectively. Posttraumatic performance in the behavioral and motor tests was evaluated for 20 days. Rats were then decapitated under deep anesthesia, and their brains frozen and sliced to evaluate lesion volume., Results: Hyperventilated animals performed significantly worse in explicit memory tests compared with normoventilated rats over time. Both groups showed deficits in advanced motor function and coordination (evaluated by beam walk and beam balance) initially, with a significantly worse performance of hyperventilated compared with normoventilated animals. However, there was no difference between groups by the end of the study. On Day 20 after injury, lesion volume was significantly larger with hyperventilated (69.7 +/- 13.0 mm(3)) compared with normoventilated animals (48.3 +/- 15.6 mm(3))., Conclusions: Although hyperventilation enhanced histologic damage, there was no long-term adverse neurocognitive effect from 4 h of posttraumatic hyperventilation (PaCO(2) = 28-32 mm Hg) in rats.

Background: Postischemic improvement of functional outcome by therapeutic hypothermia may be related to cerebral regeneration by postischemic neurogenesis. We investigated whether mild peri-ischemic hypothermia leads to a long-term increase in postischemic neurogenesis., Methods: Seventy male sevoflurane-anesthetized Sprague Dawley rats were randomly assigned to the following treatment groups: normothermic ischemia, intraischemic hypothermia, and postischemic hypothermia with corresponding sham-operated controls. Fifteen naïve rats were investigated as reference for natural neurogenesis. Forebrain ischemia was induced by bilateral common carotid artery occlusion and hemorrhagic hypotension. In normothermic groups, the pericranial temperature was maintained at 37.5 degrees C. Animals in the hypothermic groups were cooled to a pericranial temperature of 33 degrees C for 45 min. All animals received 5-bromo-2-deoxyuridine for 7 days. Histopathological damage and 5-bromo-2-deoxyuridine-positive neurons of the hippocampus were analyzed after 28 days., Results: Hypothermia had no impact on natural neurogenesis. Cerebral ischemia increased the number of new neurons regardless of pericranial temperature. Forty-five minutes of hypothermia beginning before ischemia diminished hippocampal injury to <10% in the CA1 and CA3 regions, whereas 45 min of postischemic hypothermia beginning after reperfusion did not reduce neuronal injury compared with normothermia., Conclusions: Neither intraischemic nor postischemic hypothermia affected the ischemia-induced increase in endogenous neurogenesis. Intraischemic hypothermia reduced hippocampal damage, whereas postischemic hypothermia as applied here did not prevent formation of histopathological injury. This indicates that, 28 days after cerebral ischemia, postischemic neurogenesis is not significantly increased by mild peri-ischemic hypothermia and not affected by the severity of histopathological damage.

Background: Intraoperative routine monitoring of cerebral blood flow and oxygenation remains a technological challenge. Using the physiological principle of carbon dioxide reactivity of cerebral vasculature, we investigated a recently developed neuromonitoring device (oxygen-to-see, O2C device) for simultaneous measurements of regional cerebral blood flow (rvCBF), blood flow velocity (rvVelo), oxygen saturation (srvO2), and hemoglobin amount (rvHb) at the capillary venous level in patients subjected to craniotomy., Methods: Twenty-six neurosurgical patients were randomly assigned to anesthesia with 1.4% or 2.0% sevoflurane end-tidal concentration. After craniotomy, a fiberoptic probe was applied on a macroscopically healthy surface of cerebral tissue next to the site of surgery. Simultaneous measurements in 2 and 8 mm cerebral depth were performed in each patient during lower (35 mm Hg) and higher (45 mm Hg) levels (random order) of arterial carbon dioxide partial pressure (PaCO2). The principle of these measurements relies on the combination of laser-Doppler flowmetry (rvCBF, rvVelo) and photo-spectrometry (srvO2, rvHb). Linear models were fitted to test changes of end points (rvCBF, rvVelo, srvO2, rvHb) in response to lower and higher levels of PaCO2, 1.4% and 2.0% sevoflurane end-tidal concentration, and 2 and 8 mm cerebral depth., Results: RvCBF and rvVelo were elevated by PaCO2 independent of sevoflurane concentration in 2 and 8 mm depth of cerebral tissue (P < 0.001). Higher PaCO2 induced an increase in mean srvO2 from 50% to 68% (P < 0.001). RvVelo (P < 0.001) and srvO2 (P = 0.007) were higher in 8 compared with 2 mm cerebral depth. RvHb was not influenced by alterations in PaCO2 but positively correlated to sevoflurane concentration (P = 0.005)., Conclusions: Increases in rvCBF and rvVelo by PaCO2 suggest preserved hypercapnic vasodilation under anesthesia with sevoflurane 1.4% and 2.0% end-tidal concentration. A consecutive increase in srvO2 implies that cerebral arteriovenous difference in oxygen was decreased by elevated PaCO2. Unchanged levels of rvHb signify that there was no blood loss during measurements. Data suggest that the device allows detection of local changes in blood flow and oxygen saturation in response to different PaCO2 levels in predominant venous cerebral microvessels.