Biomedical subjects

J W Elting

Publications and source records attributed to J W Elting.

6 recordsLinked to original sources

PubMed2003

P300 component identification using source analysis techniques: reduced latency variability.

P300 latency variability in normal subjects is a complicating factor in clinical event-related potential studies because it limits diagnostic applicability. The current study was conducted to determine whether identification of P300 (P3A and P3B) components using source analysis techniques can reduce variability in P300 parameters. Data were recorded with a 128-channel EEG system in 18 healthy subjects. The authors used a standard, auditory two-tone oddball paradigm with targets of 2000 Hz and standards of 1000 Hz. Two simple source analysis models with one or two rotating dipoles were applied to grand average data and individual data. Dipole time courses were combined with mapping results to extract P3A and P3B component latencies. Latencies obtained with conventional P300 analysis were compared with source analysis results. The source analysis method identified both P3A and P3B components in a substantially larger percentage of subjects (88% vs. 33%) than the conventional method. The source analysis method yielded a later mean P3B latency (357 msec vs. 323 msec, P < 0,001) with a smaller standard deviation (9 msec vs. 23 msec, P = 0,003) than the conventional P300 method. The relative contribution of the temporally separate P3A and P3B components to the P300 complex amplitude is highly variable. This explains the larger latency standard deviation in conventional P300 analysis. The source analysis method was able to identify P300 components in a large percentage of the cases. The result is a considerable reduction of P300 latency variability in normal subjects. This could have important consequences for clinical event-related potential research, because diagnostic sensitivity and specificity of P300 latency may improve with this method.

Adult↗

PubMed2000

Comparison of serum S-100 protein levels following stroke and traumatic brain injury.

Temporal changes in serum S-100 protein levels were compared between patients with ischemic stroke, transient ischemic attack (TIA) and traumatic brain injury (TBI). In addition, S-100 levels were correlated with clinical severity and outcome. Measurements were done with a LIA-mat((R)) Sangtec((R)) 100 using an automated immunoluminometric assay. Serum S-100 was measured in 21 stroke patients, 18 TIA patients and ten TBI patients on days 1 (0-24 h), 2, 3, 4, 5 or 6 and 8 or 9. In a control group of 28 healthy volunteers one measurement was done. For the stroke and TIA patients, National Institutes of Health Stroke Scale (NIHSS) scores were obtained on admission and on day 10. For the TBI patients, Glasgow Coma Scale (GCS) scores were obtained on admission and Glasgow Outcome Scale (GOS) scores were obtained after 6 months. Changes in serum S-100 levels over the first 3 days were significantly different between stroke and TBI patients (P=0.014) and between stroke and TIA patients (P=0.006). Peak concentrations of S-100 were most often observed on day 3 or 4 after stroke and on day 1 or 2 after TBI. In the stroke patients individual S-100 peak levels correlated well with the NIHSS score on admission (r=0.58 P=0.014) and the change in NIHSS score between day 10 and day 1 (r=0.65, P=0. 005). In the TBI patients a good correlation between individual peak levels of S-100 and the GCS score on admission (r=-0.81, P=0.010) and the GOS score 6 months after the trauma was found (r=-0.87, P=0. 004). We conclude that there is a significant difference in temporal changes of S-100 levels between ischemic stroke and TBI patients. This suggests different pathophysiological mechanisms. The results of this study further confirm that peak levels of serum S-100 correlate with neurological deficit resulting from either stroke or TBI.

Adult↗

PubMed2000

Continuous pulse oximetry in acute hemiparetic stroke.

BACKGROUND AND PURPOSE: Hypoxemia can adversely affect ischemic brain tissue in laboratory animals. The aim of this study was to assess the value of early continuous monitoring with pulse oximetry in detecting arterial oxygen desaturations in patients with acute hemiparetic stroke, and the effects of oxygen administration. METHODS: Over a period of 6 months 49 consecutive patients with acute hemiparetic stroke of </=12 h duration were monitored for the first 48 h with pulse oximetry. Patients in whom arterial oxygen saturation (SaO(2)) fell beneath 96% for a period longer than 5 min were treated with oxygen administered via nasal prongs or oxygen mask. RESULTS: Thirty-one patients (63.3%) developed arterial oxygen desaturations. Of these patients 28 could effectively be treated with oxygen up to a flow-rate of 5 l/min. Only 3 patients required higher oxygen concentrations from 6 to 10 l/min. No acute adverse effects of oxygen treatment were observed. All patients with a history of cardiac and pulmonary disease developed drops in SaO(2). The occurrence of arterial oxygen desaturations was related to stroke severity (P=0.024), the presence of dysphagia (P=0.047), and older age (P=0.037). CONCLUSION: Patients with acute hemiparetic stroke frequently develop arterial oxygen desaturations. Continuous monitoring with pulse oximetry in this group of patients is a simple and useful method to detect drops in SaO(2) and to titrate oxygen administration.

Acute Disease↗

PubMed2000

Predicting outcome from coma: man-in-the-barrel syndrome as potential pitfall.

The Glasgow coma scale motor score is often used in predicting outcome after hypoxic-ischemic coma. Judicious care should be exerted when using this variable in predicting outcome in patients with coma following hypotension since borderzone infarction can obscure the clinical picture. We describe a patient who underwent skull base surgery for a schwannoma of the left facial nerve. The operation, which lasted for 10 h, was conducted under controlled hypotension. After the intervention the patient remained comatose with absent arm movements upon painful stimuli. An absent motor score usually carries a poor prognosis. However, magnetic resonance inversion recovery imaging of the brain showed bilateral hyperintense lesions in the arm-hand area indicative of borderzone ischemic damage. The patient received optimal supportive care and after 17 days he regained consciousness with 'man-in-the-barrel syndrome', which also further improved over time.

Coma↗

PubMed1999

Management of acute ischaemic stroke.

Over the past few years there have been enormous changes in the management of stroke patients. General practitioners, ambulance personnel/paramedics and the general public need to be well informed that stroke is a medical emergency. Prevention of secondary brain damage by normalising vital parameters and combating fever should already start at the scene or in the ambulance. Early recognition of stroke symptoms, immediate transfer to a suitable treatment facility, and rapid in hospital triage protocols should bring thrombolysis to a larger number of stroke victims. Admission to a unit that is dedicated to the care of stroke patients helps to reduce mortality and morbidity.

Brain Ischemia↗

PubMed1998

Increased serum neuron specific enolase concentrations in patients with hyperglycemic cortical ischemic stroke.

A detrimental effect of hyperglycemia in ischemic brain has been demonstrated in laboratory experiments and it has been found that hyperglycemia in ischemic stroke is a predictor of poor outcome. We determined serum neuron specific enolase (NSE) concentrations in 41 consecutive patients with a cerebral hemispheric stroke between 12 and 24 h after stroke onset. In cortical ischemic strokes complicated by hyperglycemia (blood glucose concentration > 7 mmol/l) we found significantly higher NSE levels than in normoglycemic patients. In lacunar ischemic strokes NSE levels were not significantly different between normoglycemic and hyperglycemic patients. Our findings support the concept that hyperglycemia during acute cortical ischemic stroke is associated with enhanced neuronal cell death.

Aged↗