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Biomedical subjects

P F Prior

Publications and source records attributed to P F Prior.

At least 19 recordsLinked to original sources

Quantitative EEG in assessment of anaesthetic depth: comparative study of methodology.

Methodology for assessment of depth of anaesthesia based on analysis of the electroencephalogram (EEG) is controversial. Techniques range from display of single measures, for example median value of the frequency spectrum, to dedicated pattern recognition systems based on measures of several EEG features. We have compared the performance of four techniques using tape-recorded data from 23 patients anaesthetized with either halothane or isoflurane using standardized regimens. The techniques were: (1) median frequency, (2) spectral edge frequency, (3) the cerebral function analysing monitor (CFAM1) and (4) a depth of anaesthesia monitor based on EEG pattern recognition (ADAM). Dose-response curves are presented for stepwise increases in stable end-tidal concentrations of each agent. Results indicated considerable inter-patient variability and the limitations of single EEG measures, particularly with deeper anaesthesia producing a burst suppression pattern in the EEG. Pattern recognition techniques reduced these difficulties and appeared to be promising over a wide range of anaesthetic levels.

Anesthesia, Inhalation

Maturation of electroretinograms and visual evoked potentials in preterm infants.

Electroretinograms (ERGs) and visual evoked potentials (VEPs) to flash stimulation were recorded from 51 infants (gestational age 26 to 42 weeks; post-conceptional age (PCA) 31 to 47 weeks) to give cross-sectional data on the maturation of these responses. Sequential recordings were taken from a separate group of 24 preterm infants (gestational age 28 to 33 weeks) to give longitudinal data. There was a significant decrease in ERG a-wave latency and increase in a-b amplitude with increasing PCA in both groups. For the VEPs there was a significant decrease in latency of the early negative component (N1) and the major positive component (P2). Comparison between recordings made on preterm infants with those from term infants at an equivalent PCA suggested faster maturation of VEPs in the extra-uterine environment, but no difference in maturation of the ERG.

Brain

Serial electroencephalograms in a patient with D-lactic acidosis.

A patient with previous bowel surgery was followed through the course of her recurrent encephalopathy with biochemically demonstrated D-lactic acidosis by detailed serial electroencephalography (EEG). Although the EEG changes were marked and parallelled the clinical and biochemical abnormalities closely, they were essentially non-specific. This diagnosis should be considered in encephalopathic patients with a history of bowel disease particularly after extensive small bowel resection.

Acidosis, Lactic

Electroencephalography.

Notwithstanding recent advances in neuroimaging, EEG remains a major technique for investigation of the brain. Its main applications are in assessment of cerebral function rather than for detecting structural abnormalities. The principal clinical applications are in epilepsy, states of altered consciousness including postanoxic and traumatic coma, the parasomnias, dementias, toxic confusional states, cerebral infections, and various other encephalopathies. Abnormalities in EEG reflect general pathophysiological processes, raised intracranial pressure, cerebral anoxia, or oedema, epileptogenesis etc, and show little specificity for a particular disease. Consequently, they need to be interpreted in a particular clinical context; the use of routine EEG examination for screening purposes is rarely of value. Conversely, the investigation becomes most cost effective when applied to specific problems--for instance, monitoring serial changes in postanoxic coma or during open heart surgery, differential diagnosis (by telemetric ictal recordings) of epileptic and non-epileptic attacks, and providing early prediction of outcome after stroke. High technological standards and an individualised problem solving approach are prerequisites of a cost effective, reliable clinical EEG service. These are most likely to be achieved by a considered, selective referral policy, the use where necessary of prolonged complex procedures such as telemetry, and the avoidance of routine examinations of dubious clinical relevance.

Acquired Immunodeficiency Syndrome

Effect of antecedent glucose control on cerebral function during hypoglycemia.

OBJECTIVE: The incidence of both severe and asymptomatic hypoglycemia is increased threefold in intensively treated diabetic patients. To examine whether this reflects cerebral adaptation to low blood glucose levels, we investigated the effect of preceding glycemic experience on hormonal, EEG, and evoked potential responses to experimentally induced hypoglycemia with the slow-fall clamp. RESEARCH DESIGN AND METHODS: Three groups were examined: well-controlled diabetic patients and patients with insulinoma (group 1), poorly controlled diabetic patients (group 2), and nondiabetic subjects (group 3). RESULTS: The glucose threshold for epinephrine release was lower in group 1 (2.3 +/- 0.1 vs. 3.0 +/- 0.3 and 3.1 +/- 0.1 mM, P less than 0.02), and the peak epinephrine response was reduced (1.29 +/- 0.36 vs. 5.48 +/- 1 and 5.62 +/- 1.2 nM, P less than 0.01) compared with groups 2 and 3, whereas symptoms were not perceived until a lower blood glucose level had been reached (2.0 +/- 0.2 vs. 3.3 +/- 0.4 and 2.6 +/- 0.2 mM, P less than 0.01). Other counterregulatory responses were similarly delayed and diminished. In contrast, EEG changes that were compatible with hypoglycemia were detected in all subjects in group 1 (blood glucose 1.9 +/- 0.1 mM) but in only two in group 2 and none in group 3, despite similar blood glucose nadirs. CONCLUSIONS: The glycemic threshold for hormonal responses to hypoglycemia falls in individuals with intensively treated diabetes or insulinomas, but these patients are more likely to develop EEG abnormalities during hypoglycemia. This disparity helps explain the increased vulnerability of intensively treated patients to severe hypoglycemia.

Adult

Quantitative EEG and brainstem auditory evoked potentials: comparison of isoflurane with halothane using the cerebral function analysing monitor.

We studied EEG and brainstem auditory evoked potentials (BAEP) during routine surgery at various concentrations of isoflurane (12 patients) or halothane (11 patients) or during prolonged (mean 2.5 h, range 1.9-3.5 h) administration of 1% isoflurane (five patients). Recording and analysis was performed with the cerebral function analysing monitor (CFAM). At equivalent MAC, the two agents exhibited distinctive neurophysiological profiles. Increasing concentrations of isoflurane produced a clear sequence of EEG changes (decreasing fast and increasing slow components) then burst suppression activity suggesting cortical depression. With halothane, changes in EEG amplitude were less pronounced and those in frequency content less systematic, with no periods of suppression. Simultaneous BAEP showed greater latency increase with halothane than with isoflurane. Prolonged administration of 1% isoflurane was associated with a stable EEG (no periods of suppression) and BAEP.

Adult

Isoflurane prevents EEG depression during trimetaphan-induced hypotension in man.

We have studied the EEG analysed with the cerebral function analysing monitor (CFAM) during trimetaphan (TMP)-induced hypotension to a mean arterial pressure (MAP) of 40 mm Hg in 20 normocapnic patients anaesthetized with either 1% end-tidal isoflurane or 0.5% halothane. During the acute reduction in MAP, the average reduction in mean EEG amplitude with halothane was 14%, two patients showing short periods of EEG suppression; the decline in EEG amplitude correlated with declining MAP in four patients. In contrast, the average reduction in mean EEG amplitude with isoflurane was only 0.3% and there were neither periods of suppression nor any correlation between EEG amplitude and MAP. No significant changes in EEG frequency occurred in either group. Isoflurane prevented EEG amplitude depression during TMP-induced hypotension.

Adult

Minimal neuropsychological sequelae following prophylactic treatment of the central nervous system in adult leukaemia and lymphoma.

The potential long-term toxicity of central nervous system prophylaxis (CNS-P) in adult acute lymphoblastic leukaemia (ALL, n = 17) and non-Hodgkin's lymphoma (NHL, n = 7) was investigated in a multidisciplinary study. At least 4 years had elapsed from CNS-P (mean 11.5 years) for all patients. Neurological history and physical examination were unremarkable; minor signs were commoner in older patients (P less than 0.02). Psychometry yielded normal results, but individual verbal IQ generally exceeded performance IQ, with a trend to more marked differences in younger adults (P = 0.06). EEG was scored and differed significantly from that of controls, with a tendency to more marked (but still minor) abnormalities in younger patients (P = 0.06). Brainstem auditory evoked potentials demonstrated significant but generally minor abnormality in 24% of patients. CT brain scan revealed widening of cerebral hemisphere sulci to greater than 3 mm in 38% of patients; cerebral atrophy was commoner in the older group (P less than 0.02) and those with neurological signs (P less than 0.02). MRI brain scans were normal in all patients tested. Thus, following standard CNS-P for ALL at this hospital, there is a 5% primary CNS relapse rate, and only minimal, mainly subclinical, long-term neuropsychological toxicity.

Adult

Continuous EEG and ICP monitoring as a guide to the administration of althesin sedation in severe head injury.

The effects of 142 intravenous boluses of althesin (0.05 ml/kg) on cerebral perfusion pressure (CPP) were studied in twelve head injured comatose patients. The data were divided into those where the mean pre-bolus intracranial pressure (ICP) was above or below 20 mmHg and then subdivided into those where the minimum pre-bolus voltage of the cerebral function monitor (CFM) was above or below 5 microV (representing marked reduction in cortical electrical activity). The pre-bolus ICP influenced the extent of the fall in ICP and thus the direction of the resulting change in CPP. A mean reduction in CPP was observed in both groups in which ICP was below 20 mmHg irrespective of the CFM voltage. In the subgroups with high ICP, CPP increased when CFM was not depressed and fell when CFM was below 5 microV. The effects of individual boluses varied within and between the subgroups and, occasionally, severe and unpredictable hypotension occurred. If althesin administration had been restricted to the high CFM and high ICP group, 90% of the episodes of reduced CPP would have been avoided. In fact, when cortical electrical activity is already severely depressed, further administration of hypnotic anaesthetic agents produces only small reductions in ICP and usually a fall in CPP. These findings suggest that the minimum voltage of the CFM trace is a clinically useful guide to the administration of intravenous anaesthetic agents and offers a relevant prediction of their effects on CPP.

Adolescent

Polygraphic monitoring in prevention of ischaemic brain damage during surgery and intensive care.

The investigations described show: Firstly, the EEG concomitants of cerebral ischaemia are quantitatively related to the extent of subsequent infarction. Secondly, their time sequence can be characterised by relatively simple measures such as continuous display of amplitude variability (including clear indication of even very brief periods of electrocerebral silence) of the EEG filtered to emphasize the alpha and beta frequency bands. Addition of information about frequency distribution helps differentiate between effects of ischaemia and of anaesthesia. Thirdly, there is considerable potential value in the routine clinical use of such techniques to prevent ischaemic brain damage. The arguments for routine clinical monitoring are based on the cited correlative studies between EEG and clinical or neuropathological outcome and on follow-up studies as to the effect of intervention based on neurophysiological warning signs on clinical outcome (e.g., Kriticou and Branthwaite 1977).

Brain

Electrical activity of the cerebral cortex during induced hypotension in man. A comparison of sodium nitroprusside and trimetaphan.

During the routine use of controlled hypotension the electroencephalogram (EEG) and mean arterial pressure (MAP) were monitored in 20 normotensive patients (younger than 70 years-of-age) receiving either trimetaphan (TMP) or sodium nitroprusside (SNP). The reduction in MAP was quicker and greater with SNP. Significant differences in EEG voltage between the two agents were seen in the range 55-40 mm Hg, electrical activity being better maintained with SNP. However, all patients showed some decline in EEG voltage with hypotension and half of these showed significant correlations with MAP. These pressure-dependent cerebral effects were not predictable in terms of age, preoperative arterial pressure or hypotensive agent. Our work supports previous experimental evidence that, during more profound hypotension, cerebral electrical activity is better maintained with SNP than with TMP. A simple measure of total EEG power, or filtered EEG voltage envelope (CFM) was shown to be a more useful monitor of cerebral electrical activity during controlled hypotension than measurements of power distribution in different frequency bands.

Adult

Cerebral electrical activity influences the effects of etomidate on cerebral perfusion pressure in traumatic coma.

The effects of 124 boluses of etomidate 0.2 mg kg-1 i.v. on intracranial pressure (ICP), mean arterial pressure (MAP) and cerebral perfusion pressure (CPP) were studied in eight patients with severe head injury (Glasgow coma score less than 8). The data were divided into two groups based on the minimum voltage of the cerebral function monitor (CFM) recording before the bolus. In group A this was less than 5 microV (representing profound cortical electrical depression), while in group B the minimum voltage was greater than 5 microV. The mean decrease in ICP following etomidate was significantly greater in group B (mean +/- SEM: -8.6 +/- 0.7 mm Hg) than in group A (-3.8 +/- 0.6 mm Hg) (P less than 0.0001). The decrease in arterial pressure was similar in both groups. Consequently, there was a small mean increase in CPP in group B (2.2 +/- 0.9 mm Hg), whereas in group A CPP decreased (-4.7 +/- 1.5 mm Hg) (P less than 0.001). There was a strong correlation between the decreases in ICP and MAP in group A (r = 0.70, P less than 0.01), but not in group B (r = 0.05). Thus, when cortical electrical activity was already maximally suppressed, further administration of an i.v. anaesthetic agent produced only relatively small decreases in ICP, largely as a passive response to decreases in MAP. CPP was therefore usually reduced. Conversely, in the absence of such depression larger decreases in ICP, unrelated to hypotension, occurred and these were usually associated with increases in CPP. However, even under these circumstances, potentially dangerous decreases in CPP may be seen.

Adolescent