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Biomedical subjects

B M Frier

Publications and source records attributed to B M Frier.

At least 73 records · Page 4Linked to original sources
PubMed1997

Symptomatic and physiological responses to hypoglycaemia induced by human soluble insulin and the analogue Lispro human insulin.

The aim of this study was to compare the glycaemic threshold for onset of the clinically detectable sympatho-adrenal (autonomic) reaction (defined as 'R') to hypoglycaemia induced by Lispro human insulin, with that induced by human soluble insulin (HS). The hypoglycaemia symptom profile, counterregulatory hormonal responses, and cognitive performance at R were also compared. Sixteen patients with IDDM, aged 32.5 (20-45) (median (range)) years and duration of IDDM 3.0 (0.5-4.5) years participated in a randomized, double-blind study during which intravenous infusions of either Lispro or HS insulin (2.0 mU kg(-1) min(-1)) were used on separate occasions to lower the blood glucose to the level at which R was induced. For both HS and Lispro, significant increments in systolic blood pressure (p<0.05), heart rate (p<0.05), and in autonomic (p<0.05) and neuroglycopenic symptom scores (p<0.05) occurred at R, and a significant deterioration was observed in cognitive performance (p<0.05). In response to hypoglycaemia, a significant increase from baseline occurred in plasma concentrations of all of the counterregulatory hormones (p<0.01) and the magnitude of response and temporal pattern did not differ, nor were any significant differences apparent between HS and Lispro insulins for any of the variables studied. The autonomic reaction occurred at a blood glucose (mean +/- SD) of 2.0 (+/- 0.6) mmol(-1) for Lispro and 1.9 (+/- 0.6) mmol(-1) for HS, which did not differ significantly. Thus, at the autonomic reaction to hypoglycaemia no significant differences were evident in the glycaemic threshold, symptom profile, physiological responses, and counterregulatory hormonal responses between Lispro and human soluble insulin in IDDM patients.

Adult↗
PubMed1997

Auditory information processing during acute insulin-induced hypoglycaemia in non-diabetic human subjects.

Acute insulin-induced hypoglycaemia impairs performance on tests of general mental ability in humans. It is recognized that different brain functions vary in their sensitivity to neuroglycopenia, but little is known about the effects of neuroglycopenia on specific brain processes. The effect of controlled hypoglycaemia on two aspects of auditory information processing (auditory temporal processing and simple auditory processing) was examined in a homogeneous group of 20 healthy non-diabetic human subjects. Auditory temporal processing (temporal order discrimination) and simple auditory processing (pitch discrimination, single-tone duration and single-tone loudness discrimination) tests were part of the Test of Basic Auditory Capabilities (TBAC). Two tests of general cognitive performance (Digit Symbol Substitution and Trail Making B) were included to provide a measure of general brain functioning during hypoglycaemia. Hypoglycaemia lead to a significant deterioration in auditory temporal processing (P < 0.01), and a deterioration in one of three tasks of simple auditory processing (discrimination of single-tone loudness, P < 0.05). Significant disruptions also occurred in both tests of general brain functioning. These results are congruent with other studies in human subjects, showing a disruptive effect of hypoglycaemia on visual information processing when examined under conditions of limited perceptual time, and they provide further evidence of the importance of sensory processing speed in basic perceptual and cognitive functions. The disruptive effect of moderate insulin-induced hypoglycaemia on auditory perception may have implications for insulin-treated diabetic humans exposed to this metabolic stress, because of the importance of hearing in everyday life.

Acoustic Stimulation↗
PubMed1997

Medical assessment for licensing of taxi drivers by Scottish local authorities.

In the UK, licensing of taxi drivers is dealt with by local government authorities. In Scotland, before the recent reorganization of local government, taxi licensing was under the jurisdiction of District Councils, so a telephone survey was conducted of all 52 mainland Scottish District Councils to ascertain the procedures which were being employed in assessing medical fitness to drive a taxi, for which there is no national standard. Medical enquiries relevant to fitness to drive were being made by 41 (79%) of local authorities, but in 38 (73%) this was limited to a single question about health. No enquiry regarding health status was being made by 11 (21%) District Councils (all serving < 100,000 population size). Only three Scottish District Councils conducted a routine medical examination of all applicants. Thirteen of the 15 large (> 100,000 population size), and 20 of the 21 medium-sized (50,000-100,000) Scottish District Councils carried out medical examinations either when a relevant medical disorder was declared by the applicant, or when the applicant was above a defined age (which varied between local authorities). The small local authorities (population < 50,000) examined only those applicants who declared medical disorders. This survey has shown considerable variation and limitations in the approach of the previously existing Scottish District Councils to the assessment of medical fitness to drive of applicants for taxi licences. It is suggested that national standards and guidelines are required for medical fitness to drive in relation to taxi licensing.

Automobile Driving↗
PubMed1997

Is type II diabetes associated with an increased risk of cognitive dysfunction? A critical review of published studies.

Type II (non-insulin-dependent) diabetes may be associated with impaired cognitive function. A detailed search of the literature has identified 19 controlled studies in which cognitive function in type II diabetes has been examined. The studies vary widely with respect to the nature of the diabetic populations studied and the psychological tests used. Thirteen studies demonstrated that the diabetic individuals performed more poorly in at least one aspect of cognitive function. The most commonly affected cognitive ability was verbal memory. Psychomotor ability and frontal lobe function were affected less consistently. The remaining six studies showed no differences in cognitive ability between subjects with type II diabetes and nondiabetic control subjects, but none had adequate statistical power to detect a between-group difference in cognitive ability of 0.5 of a standard deviation (a medium effect size). These findings are consistent with type II diabetes being associated with an increased risk of cognitive dysfunction. However, the widespread differences in methodology between the studies should lead to a cautious interpretation of their conclusions. The etiology of any cognitive decrement in type II diabetes is likely to result from an interaction between metabolic abnormalities intrinsic to diabetes, diabetes-specific complications, and other diabetes-related disorders.

Cognition Disorders↗
PubMed1997

Brain abnormalities demonstrated by magnetic resonance imaging in adult IDDM patients with and without a history of recurrent severe hypoglycemia.

OBJECTIVE: Previous studies of a cohort of 100 patients with IDDM have shown that a history of recurrent severe hypoglycemia is associated with a modest impairment of cognitive function. The aim of the present study was to determine whether IDDM patients with and without a history of severe hypoglycemia have lesions in the brain that are identifiable by magnetic resonance imaging (MRI) and magnetic resonance spectroscopy (MRS) and to investigate the putative relationship of any structural brain abnormalities with cognitive function. RESEARCH DESIGN AND METHODS: MRI and MRS of the brain were performed in 22 patients from the original cohort. Eleven IDDM patients with no history of severe hypoglycemia (group A) were compared with 11 IDDM patients who had a history of five or more episodes of severe hypoglycemia (group B). RESULTS: Nine patients (41%) had abnormal scans. Two types of abnormalities were observed: high-intensity rounded lesions, > 3 mm in diameters, distributed in the periventricular white matter (leukoaraiosis) in four patients; and cortical atrophy in five patients. Five patients in group B had cortical atrophy, whereas no patient in group A demonstrated this feature (P < 0.05). MRS of the frontal and parietal lobes showed no differences in the N-acetyl aspartate/creatine or N-acetyl aspartate/choline ratios between groups A and B. Patients with cortical atrophy showed a nonsignificant trend toward reduced performance on Rapid Visual Information Processing. CONCLUSIONS: Brain abnormalities demonstrated by MRI are common in patients with IDDM of long duration and are suggestive of premature aging of the brain. IDDM per se may be an important pathogenic factor, but a significant association was observed between a history of recurrent severe hypoglycemia and cortical atrophy, which may be related to the modest impairment of cognitive function that has been reported previously.

Adult↗
PubMed1996

A comparative study of responses to acute hypoglycaemia induced by human and porcine insulins in patients with Type 1 diabetes.

The effects of human and porcine insulins on the symptomatic, physiological, and counterregulatory hormonal responses to acute hypoglycaemia were compared in 40 patients with Type 1 diabetes, 20 of whom were newly diagnosed while 20 had been treated for between 5 and 20 years. In a double-blind, cross-over trial all patients were treated with human or porcine insulin, in random order, for two consecutive 3-month periods. At the end of each treatment period they were subjected to an acute episode of experimental hypoglycaemia induced by a continuous intravenous infusion (2.0 mU kg(-1)min(-1)) of the same insulin species. Haemodynamic, sweating, and tremor responses were measured during both studies, symptom scores were recorded and the arterialized plasma glucose thresholds for autonomic activation and the onset of subjective symptoms were identified. In all patients the glycaemic thresholds for the initiation of the autonomic physiological responses to hypoglycaemia and the onset of the symptomatic response were concurrent and did not differ with insulin species (plasma glucose 1.94 vs 1.96 mmol I(-1), human vs porcine studies). The onset, temporal pattern, nature, and magnitude of the physiological responses (sweating, heart rate, blood pressure, and tremor) during acute experimental hypoglycaemia were also identical with each insulin species. The magnitude and temporal pattern of the response of counterregulatory hormones (adrenaline, noradrenaline, glucagon, ACTH, and GH) to hypoglycaemia as induced by human and porcine insulins were indistinguishable, as were the total and individual scores of autonomic and neuroglycopenic symptoms. In conclusion, in patients who had newly diagnosed and intermediate duration (5-20 years) of diabetes, the symptomatic, physiological, and counterregulatory hormonal responses to acute insulin-induced hypoglycaemia did not differ between human and porcine insulins, and the plasma glucose thresholds at which the symptomatic and autonomic responses were initiated were identical with both insulin species. This study does not support the hypothesis that treatment with human insulin modifies the symptomatic, physiological, and counterregulatory hormonal responses to acute hypoglycaemia.

Acute Disease↗
PubMed1996

An audit of waiting times in the diabetic outpatient clinic: role of patients' punctuality and level of medical staffing.

A survey of patients' waiting times was performed in the follow-up clinics of a large hospital outpatient diabetic department (approximately 6500 patients). Over a period of 1 week, 138 patients attended 5 review outpatient clinics. The overall patient:doctor ratio was 11.1:1. Only 18.8% of patients were seen by the doctor, and 86% by the nurse within 30 min of their appointment time. A policy of strict adherence to the formal appointment times was implemented but had no effect on the waiting time (20% of patients were seen by the doctor, and 82.2% by the nurse within 30 min of their appointment time). The combined effects of adherence to actual appointment times and increasing the number of doctors (lowering the patient:doctor ratio to 7.7:1), reduced the total waiting times, and increased the proportion of patients seen by the doctor or nurse within 30 min of their appointment time, to 31% and 100%, respectively. Strict adherence to appointment times was difficult to implement and ineffective but the patient:doctor ratio was important in determining waiting times in the diabetic clinic. Inadequate medical staffing of diabetic outpatient clinics is a major cause of prolonged waiting time for patients. This approach may be useful in assessing and improving the organizational efficiency of a diabetes service.

Ambulatory Care Facilities↗
PubMed1996

The effects of acute hypoglycemia on relative cerebral blood flow distribution in patients with type I (insulin-dependent) diabetes and impaired hypoglycemia awareness.

To examine the hypothesis that in diabetic patients with impaired hypoglycemia awareness the relative regional distribution of cerebral blood flow (rCBF) would be abnormal in a specific area, namely the frontal lobes, rCBF was examined in 20 type I diabetic patients, of whom 10 had a normal awareness of hypoglycemia and 10 had a history of impaired hypoglycemia awareness. rCBF was determined sequentially using single photon emission computed tomography (SPECT) during (1) normoglycemia (arterialized blood glucose 4.5 mmol. L-1) and (2) hypoglycemia (blood glucose 2.5 mmol.L-1) induced by a hyperinsulinemic glucose clamp technique. Distribution of the isotope, 99mTc-Exametazime, was detected using a single-slice multi-detector head scanner. A split-dose technique was used, with 250 MBq being injected during steady-state normoglycemia and 250 MBq during subsequent hypoglycemia. rCBF was estimated in 30 regions of interest, derived from a standard neuroanatomical atlas on two parallel slices at 40 and 60 mm above the orbitomeatal line (OML). No between-group differences in the pattern of overall rCBF or changes in regional tracer uptake were demonstrated. In comparison to the rCBF during normoglycemia, both patient groups exhibited significant changes in the pattern of rCBF during hypoglycemia, with increments of rCBF to both superior frontal cortices and the right thalamus and reduced rCBF to the right posterior cingulate cortex and the right putamen. This pattern of relative redistribution of rCBF during hypoglycemia was preserved in patients who had impaired hypoglycemia awareness.

Acute Disease↗
PubMed1996

Visual information processing during controlled hypoglycaemia in humans.

A general impairment of cognitive performance occurs during acute insulin-induced hypoglycaemia, but little objective evidence is available for disruption of more specific cognitive processes. The effect of controlled hypoglycaemia on the early stages of visual information processing and contrast sensitivity was examined in a homogeneous group of 20 nondiabetic human subjects. Hypoglycaemia caused a significant disruption in general cognitive performance as assessed by a digit symbol task (P < 0.001) and the trail making B task (P < 0.05). Hypoglycaemia also produced a highly significant deterioration in performance on all of the visual information processing tasks, namely inspection time (IT) (P = 0.01), visual change detection (VCD) (P < 0.005) and visual movement detection (VMD) (P < 0.005). A significant deterioration in contrast sensitivity was observed during hypoglycaemia (P < 0.005). In contrast, no significant effect of hypoglycaemia was demonstrated on standard clinical measures of visual acuity or stereoscopic vision. Thus, although hypoglycaemia caused no detectable deterioration in visual acuity as measured by Snellen-type tests, a marked deterioration occurred in the speed of visual information processing and in contrast sensitivity. As many decisions are made under conditions of limited perceptual time and low visual contrast (e.g. when driving), the disruptive effect of moderate insulin-induced hypoglycaemia on visual perception will have important practical implications in diabetic humans exposed to this metabolic stress. The present results are congruent with other evidence which shows that the early stages of visual information processing are susceptible to deterioration by general cerebral insults.

Adult↗
PubMed1996

Altered taste sensation in newly-diagnosed NIDDM.

OBJECTIVE: To assess gustatory appreciation in newly diagnosed NIDDM patients and to determine whether it altered with the improvement of glycemic control after treatment with diet and oral hypoglycemic drugs. RESEARCH DESIGN AND METHODS: Assessments of taste, peripheral and autonomic neural function, diet, and oral microbiological flora were performed in 20 patients before and after treatment of hyperglycemia, 20 matched nondiabetic control subjects, and 11 patients with long duration of diabetes and advanced peripheral neuropathy. RESULTS: Median total HbA1 fell from 12.6 to 8.8% in new diabetic patients after 3-5 months of treatment. Electrical taste thresholds, detection threshold for glucose, and recognition threshold for glucose and salt were increased in newly-diagnosed NIDDM patients compared with the control subjects. The dose-response curve to glucose (using a visual analogue scale [VAS]) of newly-diagnosed NIDDM patients was significantly impaired and improved after treatment. By contrast, newly-diagnosed NIDDM patients had normal VAS taste responses to fructose, salt, and urea. Measurements of somatic and autonomic nerve function did not correlate with electrical or chemical taste function. CONCLUSIONS: Newly-diagnosed NIDDM patients have a blunted taste response, which displays a degree of specificity to glucose, is partially reversed after correction of hyperglycemia, and is independent of somatic or autonomic nerve function. This taste abnormality may influence the premorbid choice of nutrients, with a preference for sweet-tasting foods, thereby exacerbating hyperglycemia.

Autonomic Nervous System Diseases↗
PubMed1995

Cognitive function during insulin-induced hypoglycemia in humans: short-term cerebral adaptation does not occur.

It has been suggested that cerebral adaptation may occur in response to short-term hypoglycemia. This was examined in the present study by measuring serial changes in cognitive function and symptoms after 60 min of continuous hypoglycemia. Hypoglycemia was induced with a hyperinsulinemic glucose clamp on two separate occasions in 24 non-diabetic human subjects. Cognitive function was assessed using the following cognitive test battery: Paced Auditory Serial Addition Test (PASAT), Rapid Visual Information Processing (RVIP), Trail-Making B (TMB), Digit Symbol Substitution Test (DSST) and Four Choice Reaction Time (CRT). In condition A the blood glucose was maintained at 4.5 mmol/l throughout. On two separate occasions (condition B and condition C) the blood glucose was stabilised at 4.5 mmol/l for 30 min, lowered to 2.5 mmol/l for 60 min and restored to 4.5 mmol/l for 30 min. In each condition the cognitive test battery was performed immediately after stabilisation of blood glucose at 4.5 mmol/l and the subsequent battery was repeated at different time intervals: condition A--after a further 40 min of euglycemia; condition B--after 5 min of hypoglycemia; condition C--after 40 min of hypoglycemia. Acute hypoglycemia induced a significant deterioration in cognitive function which was manifest in all tests except TMB (P < 0.05), but performance ability did not differ between conditions B and C. Symptom scores, assessed by a scaled questionnaire, increased significantly during hypoglycemia (P < 0.001) but no differences were detected between the scores at 30 min and 60 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Hypoglycemia-induced cognitive dysfunction in diabetes mellitus: effect of hypoglycemia unawareness.

Hypoglycemia results in cognitive dysfunction. The aim of this study was to assess and compare the degree of cognitive dysfunction experienced by insulin-dependent diabetic patients (IDDM) with hypoglycemia unawareness with patients with normal awareness of hypoglycemia. Cognitive function was examined in 10 patients who had normal awareness of the onset of hypoglycemia and 10 patients who had a history of impaired awareness of hypoglycemia. A hyperinsulinemic glucose clamp was used to manipulate blood glucose concentrations. Cognitive function was assessed using Rapid Visual Information Processing (RVIP), Trial Making B (TMB), Paced Auditory Serial Addition Test (PASAT) and Digit Symbol Substitution Test (DSST). Multivariate analysis of variance demonstrated a significant effect of hypoglycemia on cognitive function (p < 0.01). A trend was observed towards an overall effect of awareness on performance (p = 0.08). There were trends in the effects of awareness on RVIP correct responses across time (p = 0.07) and the interaction of awareness by study by TMB (p = 0.08). During hypoglycemia subjects with impaired awareness were less cautious in their responses (RVIP misses p = 0.03) and on recovery from hypoglycemia, their cognitive function remained abnormal (TMB p = 0.04, RVIP correct responses p = 0.02, RVIP misses p = 0.04). Thus, IDDM patients with hypoglycemia unawareness exhibited more profound cognitive dysfunction during acute hypoglycemia which persisted for longer following blood glucose recovery.

Adult↗