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Cerebral Function (cerebral + function)
Selected AbstractsCortical control of thermoregulatory sympathetic activationEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 11 2010M. Fechir Abstract Thermoregulation enables adaptation to different ambient temperatures. A complex network of central autonomic centres may be involved. In contrast to the brainstem, the role of the cortex has not been clearly evaluated. This study was therefore designed to address cerebral function during a whole thermoregulatory cycle (cold, neutral and warm stimulation) using 18-fluordeoxyglucose-PET (FDG-PET). Sympathetic activation parameters were co-registered. Ten healthy male volunteers were examined three times on three different days in a water-perfused whole-body suit. After a baseline period (32°C), temperature was either decreased to 7°C (cold), increased to 50°C (warm) or kept constant (32°C, neutral), thereafter the PET examination was performed. Cerebral glucose metabolism was increased in infrapontine brainstem and cerebellar hemispheres during cooling and warming, each compared with neutral temperature. Simultaneously, FDG uptake decreased in the bilateral anterior/mid-cingulate cortex during warming, and in the right insula during cooling and warming. Conjunction analyses revealed that right insular deactivation and brainstem activation appeared both during cold and warm stimulation. Metabolic connectivity analyses revealed positive correlations between the cortical activations, and negative correlations between these cortical areas and brainstem/cerebellar regions. Heart rate changes negatively correlated with glucose metabolism in the anterior cingulate cortex and in the middle frontal gyrus/dorsolateral prefrontal cortex, and changes of sweating with glucose metabolism in the posterior cingulate cortex. In summary, these results suggest that the cerebral cortex exerts an inhibitory control on autonomic centres located in the brainstem or cerebellum. These findings may represent reasonable explanations for sympathetic hyperactivity, which occurs, for example, after hemispheric stroke. [source] The human hippocampus at 7 T,In vivo MRIHIPPOCAMPUS, Issue 1 2009Jens M. Theysohn Abstract The human hippocampus plays a central role in various neuropsychiatric disorders, such as temporal lobe epilepsy (TLE), Alzheimer's dementia, mild cognitive impairment, and schizophrenia. Its volume, morphology, inner structure, and function are of scientific and clinical interest. Magnetic resonance (MR) imaging is a widely employed tool in neuroradiological workup regarding changes in brain anatomy, (sub-) volumes, and cerebral function including the hippocampus. Gain in intrinsic MR signal provided by higher field strength scanners and concomitant improvements in spatial resolution seem highly valuable. An examination protocol permitting complete, high-resolution imaging of the human hippocampus at 7 T was implemented. Coronal proton density, T2, T2*, and fluid-attenuated inversion recovery contrasts were acquired as well as an isotropic 3D magnetization-prepared rapid acquisition gradient-echo (500 ,m isotropic voxel dimension, noninterpolated). Observance of energy deposition restrictions within acceptable scan times remained challenging in the acquisition of thin, spin-echo-based sections. At the higher resolution enabled by 7 T, demarcation of the hippocampus and some internal features including gray/white matter differentiation and depiction of the hippocampal mantle becomes much more viable when compared with 1.5 T; thus, in the future, this imaging technology might help in the diagnosis of subtle hippocampal changes. © 2008 Wiley-Liss, Inc. [source] Predictors of mortality in frontotemporal dementia: a retrospective study of the prognostic influence of pre-diagnostic featuresINTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY, Issue 7 2003A. Gräsbeck Abstract Objectives To find associations between predictors and survival in frontotemporal dementia (FTD). Methods 96 patients with FTD, here defined as Dementia in Pick's disease, were studied. The predictors included psychiatric/behavioural features, language impairment and neurological deficits present up to the time of diagnosis. The influence on mortality was studied by means of Cox regression analyses. Results Most of the behavioural/psychiatric features were associated with longer survival. Among these features, anxiety and suicidal ideation were associated with a statistically significant decreased mortality. Semi-mutism/mutism and neurological deficits were associated with a statistically significant increased mortality. Analyses of the dementia-specific mortality strengthened the already significant results and revealed dysphagia as significantly related to increased mortality. Conclusions Two groups of predictors with different influence on survival were identified in FTD. Most behavioural/psychiatric features were associated with longer survival. These features may indicate a slower disease progress and a better preserved cerebral function. By contrast, semi-mutism/mutism, neurological deficits and dysphagia were associated with shorter survival, indicating an aggressive, degenerative process. Copyright © 2003 John Wiley & Sons, Ltd. [source] Synthesis and transport of creatine in the CNS: importance for cerebral functionsJOURNAL OF NEUROCHEMISTRY, Issue 2 2010Elidie Béard J. Neurochem. (2010) 115, 297,313. Abstract Apart of its well known function of ,energetic buffer' through the creatine/phosphocreatine/creatine kinase system allowing the regeneration of ATP, creatine has been recently suggested as a potential neuromodulator of even true neurotransmitter. Moreover, the recent discovery of primary creatine deficiency syndromes, due to deficiencies in l -arginine : glycine amidinotransferase or guanidinoacetate methyltransferase (the two enzymes allowing creatine synthesis) or in the creatine transporter, has shed new light on creatine synthesis, metabolism and transport, in particular in CNS which appears as the main tissue affected by these creatine deficiencies. Recent data suggest that creatine can cross blood-brain barrier but only with a poor efficiency, and that the brain must ensure parts of its needs in creatine by its own endogenous synthesis. Finally, the recent years have demonstrated the interest to use creatine as a neuroprotective agent in a growing number of neurodegenerative diseases, including Parkinson's and Huntington's diseases. This article aims at reviewing the latest data on creatine metabolism and transport in the brain, in relation to creatine deficiencies and to the potential use of creatine as neuroprotective molecule. Emphasis is also given to the importance of creatine for cerebral function. [source] Definition and management of anemia in patients infected with hepatitis C virusLIVER INTERNATIONAL, Issue 4 2006John G. McHutchison Abstract: Chronic infection with hepatitis C virus (HCV) can progress to cirrhosis, hepatocellular carcinoma, and end-stage liver disease. The current best treatment for HCV infection is combination therapy with pegylated interferon and ribavirin. Although this regimen produces sustained virologic responses (SVRs) in approximately 50% of patients, it can be associated with a potentially dose-limiting hemolytic anemia. Hemoglobin concentrations decrease mainly as a result of ribavirin-induced hemolysis, and this anemia can be problematic in patients with HCV infection, especially those who have comorbid renal or cardiovascular disorders. In general, anemia can increase the risk of morbidity and mortality, and may have negative effects on cerebral function and quality of life. Although ribavirin-associated anemia can be reversed by dose reduction or discontinuation, this approach compromises outcomes by significantly decreasing SVR rates. Recombinant human erythropoietin has been used to manage ribavirin-associated anemia but has other potential disadvantages. Viramidine, a liver-targeting prodrug of ribavirin, has the potential to maintain the virologic efficacy of ribavirin while decreasing the risk of hemolytic anemia in patients with chronic hepatitis C. [source] Role of circulating neurotoxins in the pathogenesis of hepatic encephalopathy: potential for improvement following their removal by liver assist devicesLIVER INTERNATIONAL, Issue 2003Roger F. Butterworth Abstract Both acute and chronic liver failure result in impaired cerebral function known as hepatic encephalopathy (HE). Evidence suggests that HE is the consequence of the accumulation in brain of neurotoxic and/or neuroactive substance including ammonia, manganese, aromatic amino acids, mercaptans, phenols, short-chain fatty acids, bilirubin and a variety of neuroactive medications prescribed as sedatives to patients with liver failure. Brain ammonia concentrations may attain levels in excess of 2 mm, concentrations which are known to adversely affect both excitatory and inhibitory neurotransmission as well as brain energy metabolism. Manganese exerts toxic effects on dopaminergic neurones. Prevention and treatment of HE continues to rely heavily on the reduction of circulating ammonia either by reduction of gut production using lactulose or antibiotics or by increasing its metabolism using l -ornithine- l -aspartate. No specific therapies have so far been designed to reduce circulating concentrations of other toxins. Liver assist devices offer a potential new approach to the reduction of circulating neurotoxins generated in liver failure. In this regard, the Molecular Absorbents Recirculating System (MARS) appears to offer distinct advantages over hepatocyte-based systems. [source] Hemispheric brain volume replacement with free latissimus dorsi flap as first step in skull reconstructionMICROSURGERY, Issue 4 2005Anton H. Schwabegger M.D. Large skull defects lead to progressive depression deformities, with resulting neurological deficits. Thus, cranioplasty with various materials is considered the first choice in therapy to restore cerebral function. A 31-year-old female presented with a massive left-sided hemispheric substance defect involving bone and brain tissue. Computed tomography showed a substantial convex defect involving the absence of calvarial bone as well as more than half of the left hemisphere of the brain, with a profound midline shift and a compression of the ventricular system. There was a severe problem due to multiple deep-skin ulcerations at the depression margin, prone to skin perforation with a probability of intracranial infection. In a first step, a free myocutaneous latissimus dorsi flap was transplanted for volume replacement of the hemispheric brain defect, and 4 months later, artificial bone substitute was implanted in order to prevent progressive vault depression deformity. Healing was uneventful, and the patient showed definite neurological improvement postoperatively. Free tissue transfer can be a valuable option in addition to cranioplasty in the treatment of large bony defects of the skull. Besides providing stable coverage for the reconstructed bone or its substitute, it can also serve as a volume replacement. © 2005 Wiley-Liss, Inc. Microsurgery 25:325,328, 2005. [source] Acute hyperglycemia produces transient improvement in glucose transporter type 1 deficiencyANNALS OF NEUROLOGY, Issue 1 2010Cigdem I. Akman MD Objective Glucose transporter type 1 deficiency syndrome (Glut1-DS) is characterized clinically by acquired microcephaly, infantile-onset seizures, psychomotor retardation, choreoathetosis, dystonia, and ataxia. The laboratory signature is hypoglycorrhachia. The 5-hour oral glucose tolerance test (OGTT) was performed to assess cerebral function and systemic carbohydrate homeostasis during acute hyperglycemia, in the knowledge that GLUT1 is constitutively expressed ubiquitously and upregulated in the brain. Methods Thirteen Glut1-DS patients completed a 5-hour OGTT. Six patients had prolonged electroencephalographic (EEG)/video monitoring, 10 patients had plasma glucose and serum insulin measurements, and 5 patients had repeated measures of attention, memory, fine motor coordination, and well-being. All patients had a full neuropsychological battery prior to OGTT. Results The glycemic profile and insulin response during the OGTT were normal. Following the glucose load, transient improvement of clinical seizures and EEG findings were observed, with the most significant improvement beginning within the first 30 minutes and continuing for 180 minutes. Thereafter, clinical seizures returned, and EEG findings worsened. Additionally, transient improvement in attention, fine motor coordination, and reported well-being were observed without any change in memory performance. Interpretation This study documents transient neurological improvement in Glut1-DS patients following acute hyperglycemia, associated with improved fine motor coordination and attention. Also, systemic carbohydrate homeostasis was normal, despite GLUT1 haploinsufficiency, confirming the specific role of GLUT1 as the transporter of metabolic fuel across the blood-brain barrier. The transient improvement in brain function underscores the rate-limiting role of glucose transport and the critical minute-to-minute dependence of cerebral function on fuel availability for energy metabolism. ANN NEUROL 2010;67:31,40 [source] Does indomethacin for closure of patent ductus arteriosus affect cerebral function?ACTA PAEDIATRICA, Issue 10 2010A Flisberg Objective:, To study whether indomethacin used in conventional dose for closure of patent ductus arteriosus affects cerebral function measured by Electroencephalograms (EEG) evaluated by quantitative measures. Study design:, Seven premature neonates with haemodynamically significant persistent ductus arteriosus were recruited. EEG were recorded before, during and after an intravenous infusion of 0.2 mg/kg indomethacin over 10 min. The EEG was analysed by two methods with different degrees of complexity for the amount of low-activity periods (LAP, "suppressions") as an indicator of affection of cerebral function. Results:, Neither of the two methods identified any change in the amount of LAPs in the EEG as compared to before the indomethacin infusion. Conclusion:, Indomethacin in conventional dose for closure of patent ductus arteriosus does not affect cerebral function as evaluated by quantitative EEG. [source] A case of near-drowning: a case for routine cerebral monitoringACTA PAEDIATRICA, Issue 3 2010V Ponnusamy Abstract A 6-week-old infant presenting with near-drowning was medically paralysed and ventilated on admission. Status epilepticus was found on cerebral function monitoring, without which the diagnosis would have been missed or delayed for many hours. This case illustrates the value of cerebral function monitoring for patients in intensive care, where clinical signs of seizure activity are frequently masked by paralysis and sedation. Conclusion:, Limited availability of electroencephalogram (EEG) and cerebral function monitoring (CFM) in paediatric intensive care may inadvertently delay diagnosis and appropriate treatments and so adversely affect outcomes. We propose that round-the-clock cerebral function and/or EEG monitoring should be available in all centres that provide paediatric intensive care. [source] Cerebrospinal fluid drainage in posthaemorrhagic ventricular dilatation leads to improvement in amplitude-integrated electroencephalographic activityACTA PAEDIATRICA, Issue 6 2009Monika Olischar Abstract Aim: Progressive posthaemorrhagic ventricular dilatation (PHVD) may induce abnormal amplitude-integrated electroencephalographic (aEEG) activity prior to clinical deterioration or significant cerebral ultrasound changes. These abnormalities might be ameliorated with cerebrospinal fluid (CSF) drainage. The aims of this study were to investigate the occurrence of aEEG-abnormalities with progressive PHVD in relation to clinical and cerebral ultrasound changes and to evaluate whether CSF drainage results in aEEG improvement. Methods: aEEG and cerebral ultrasound scans were performed in 12 infants with PHVD, before and after CSF drainage, until normalization of aEEG occurred. Results: aEEG was abnormal with progressive PHVD in all patients. Concurrently, 60% of the patients were clinically stable without deterioration in ultrasonographic cerebral abnormalities. Post drainage, continuous pattern was restored in all but one patient, whereas the frequency of discontinuous pattern decreased in nine patients and burst-suppression pattern decreased in all but one patient. Low-voltage pattern was only observed in one patient who suffered severe grade IV IVH and died one week after EVD placement. Sleep-wake cycling matured in 75%. Conclusion: These findings demonstrate the impact of CSF drainage on compromised aEEG-activity associated with PHVD. aEEG changes indicative of impaired cerebral function were apparent before clinical deterioration or major ultrasound changes. These changes were reversible with CSF drainage. aEEG should therefore be used in addition to clinical observation and ultrasound when monitoring PHVD. [source] Neuropsychiatric dysfunction in patients with chronic hepatitis and liver cirrhosisHEPATOLOGY RESEARCH, Issue 11 2008Kojiro Michitaka Aim:, The aim of this study is to clarify the cerebral functions in patients with chronic hepatitis (CH) as well as those with liver cirrhosis (LC). Methods:, We studied 58 patients with CH (20 in fibrosis stage F1, 20 in F2, 18 in F3), 77 with LC (46 rated as Child,Pugh class A, 24 as B, 7 as C), and 20 healthy volunteers (HV). Computer-aided quantitative neuropsychiatric function test systems, including eight neuropsychiatric tests were performed. Results:, Subjects with results over the cut-off value for healthy subjects ranged from 11.1,28.6% in CH and 19.5,36.4% in LC. The percentages with abnormality in at least one test in CH and LC were 72.4% and 80.6%, respectively, which were significantly higher than that in the HV group (35.0%) (P = 0.003, P = 0.0003, respectively). Among CH subjects, those with three or more abnormal results in the F1, F2 and F3 subgroups were 15.0%, 20.0% and 38.9%, respectively. Among LC subjects, those with three or more abnormal results in the Child,Pugh class A, B and C subgroups comprised 30.4%, 50.0% and 57.1%, respectively. The rate in the CH F3 subgroup (P = 0.011) and in all three LC subgroups (P = 0.023, P = 0.001, P = 0.002, respectively) were significantly higher than that in the HV group. Conclusion:, The percentage of patients with neuropsychiatric function impairment was high in both LC and CH, especially in stage F3. Neuropsychiatric dysfunction may initiate in CH in a considerable number of patients. [source] Synthesis and transport of creatine in the CNS: importance for cerebral functionsJOURNAL OF NEUROCHEMISTRY, Issue 2 2010Elidie Béard J. Neurochem. (2010) 115, 297,313. Abstract Apart of its well known function of ,energetic buffer' through the creatine/phosphocreatine/creatine kinase system allowing the regeneration of ATP, creatine has been recently suggested as a potential neuromodulator of even true neurotransmitter. Moreover, the recent discovery of primary creatine deficiency syndromes, due to deficiencies in l -arginine : glycine amidinotransferase or guanidinoacetate methyltransferase (the two enzymes allowing creatine synthesis) or in the creatine transporter, has shed new light on creatine synthesis, metabolism and transport, in particular in CNS which appears as the main tissue affected by these creatine deficiencies. Recent data suggest that creatine can cross blood-brain barrier but only with a poor efficiency, and that the brain must ensure parts of its needs in creatine by its own endogenous synthesis. Finally, the recent years have demonstrated the interest to use creatine as a neuroprotective agent in a growing number of neurodegenerative diseases, including Parkinson's and Huntington's diseases. This article aims at reviewing the latest data on creatine metabolism and transport in the brain, in relation to creatine deficiencies and to the potential use of creatine as neuroprotective molecule. Emphasis is also given to the importance of creatine for cerebral function. [source] | |||||||||||||