SEARCH · PubMed Health

Results for “hypoglycaemia”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 181 records · Page 10Linked to original sources

PubMed2002

The effects of glucose fluctuation on cognitive function and QOL: the functional costs of hypoglycaemia and hyperglycaemia among adults with type 1 or type 2 diabetes.

It is traditionally believed that while acute hypoglycaemia has detectable negative consequences, such as unpleasant symptoms and cognitive-motor disruptions, acute hyperglycaemia is not associated with such consequences. However, recent research with adults affected by either type 1 or 2 diabetes mellitus demonstrates that relatively mild hyperglycaemia is associated with unpleasant symptoms and cognitive disruptions. Both hyperglycaemia and hypoglycaemia can be associated with patient experiences of physical, affective, and cognitive symptoms, as well as cognitive-motor disruptions. These effects can lead to impaired functioning and quality of life. Because these effects are different across patients, their significance can be difficult to appreciate. There is ample evidence that acute hypoglycaemia is a problem for both adults with type 1 and those with type 2 diabetes, and that mild and moderate hypoglycaemia reduce one's mental efficiency relative to euglycaemic performance. There is growing evidence that transient hyperglycaemia has similar negative effects. At relatively mild levels of extreme blood glucose--either hypoglycaemia or hyperglycaemia--cognitive efficiency may decay by a third. The impact of this effect will depend on the task the patient is dealing with at the time. If the person is engaging in a relatively dangerous task, such as driving a vehicle, significant consequences could follow. Both hypoglycaemia and hyperglycaemia have been demonstrated to have not only acute, but also chronic effects in patients with type 1 as well as those with type 2 diabetes. Although hypoglycaemia occurs at a lower rate among patients with type 2 diabetes than among those with type 1, the number of patients with type 2 diabetes is so large that even this low rate results in many persons being affected.

Acute Disease↗

PubMed2004

[Reactive hypoglycaemia, a mysterious, insidious but non dangerous critical phenomenon].

Numerous individuals complain of malaise attributed to hypoglycaemia. However, the diagnosis of hypoglycaemia is rarely documented and most often overstated. Reactive hypoglycaemia in the postprandial state is rather exceptional. The diagnosis relies upon the measurement of plasma glucose concentration (< 3 mmol/l or 55 mg/dl) at the time of the malaise. Reactive hypoglycaemia is generally associated with adrenergic symptoms and, less often, with cognitive disturbances. Importantly, a plasma glucose concentration below 3 mmol/l during an oral glucose tolerance test is not sufficient to decide that the patient suffers from reactive hypoglycaemia. Treatment is based on dietary advices including frequent small split meals and limitation of carbohydrates with high glycaemic index. Acarbose, a specific inhibitor of gut alpha-glucosidase enzymes, may be helpful in case of diet failure. As compared with true reactive hypoglycaemia, a postprandial hyperadrenergic reaction without real concomitant hypoglycaemia is much more prevalent. Careful anamnesis may suspect such a diagnosis, but other diagnoses such as panic attack or vasovagal reaction should be excluded. Treatment is purely symptomatic and essentially empiric.

Acarbose↗

PubMed1991

Neurodevelopmental outcome of asymptomatic & symptomatic babies with neonatal hypoglycaemia.

A total of 107 babies with hypoglycaemia were studied over a period of 15 months. Symptomatic hypoglycaemia was found in 43 while it was asymptomatic in the others. Asymptomatic hypoglycaemia occurred at a relatively earlier post-natal age (4.5 +/- 2.2 h), as compared to symptomatic hypoglycemia (18.5 +/- 5.4 h, P less than 0.001). The mean blood glucose in hypoglycaemic babies with seizures was found to be significantly lower (P less than 0.001) when compared to those with other features as well as asymptomatic ones. Hypoglycaemia lasted for a significantly longer duration in symptomatic babies as compared to those without symptoms (P less than 0.001). On neurodevelopment follow up the mental developmental index (MDI) and the psychomotor developmental index (PDI) of symptomatic babies with seizures were significantly lower (P less than 0.001) as compared to those with other features of hypoglycaemia as well as asymptomatic babies. The neurodevelopmental status of babies with symptoms other than seizures was also significantly poorer (P less than 0.001), when compared to asymptomatic hypoglycaemic babies. The duration of hypoglycaemia was directly related to the MDI (r = -0.74, y = 102.5 - 0.69x) and PDI (r = -0.81, y = 105.6 - 0.86x). This study indicates that there is a need to identify babies vulnerable to symptomatic hypoglycaemia more precisely.

Humans↗

PubMed1990

Hypoglycaemia in insulin dependent diabetic patients attending an outpatients' clinic.

One hundred and fifty-eight patients with insulin dependent diabetes mellitus attending two Auckland outpatient clinics answered a questionnaire about hypoglycaemia. Almost all (98%) had experienced hypoglycaemic episodes and for 30% these were a major problem. Seventy-seven percent reported nocturnal hypoglycaemia, 39% of whom required external assistance during episodes. Forty-three percent had experienced coma, or convulsions during hypoglycaemia and a small group, 7%, had recurrent severe episodes. Twenty percent carried no diabetic identification and 13% did not routinely carry a glucose supply. Only 38% of patients kept glucagon at home. Forty percent of patients driving vehicles had experienced hypoglycaemia while driving and 13% reported traffic accidents attributed to hypoglycaemia. Hypoglycaemia is a major problem for many patients taking insulin. Improved education, wider availability of glucagon and more liberal glycaemic control of patients with problematic hypoglycaemia may be advisable.

Adolescent↗

PubMed1981

Unsuspected hypoglycaemia, haemoglobin A1 and diabetic control.

Control of diabetes in a group of 82 insulin-treated diabetics was assessed by in-patient 24-hour plasma glucose profiles and haemoglobin A1 (HbA1) estimation. Thirty-two of these patients (39 per cent) had hypoglycaemia (plasma glucose less than or equal to 2 mmol/l) which was rarely associated with symptoms. Twenty-seven (61 per cent) of 44 patients who took a series of out-patient pre-prandial capillary blood samples over a three-day period had hypoglycaemia. Conventional measurements of diabetic control including fasting plasma glucose and HbA1, were lower in patients with hypoglycaemia than in those without. Rebound hyperglycaemia following hypoglycaemia was not seen and its absence was not due to diabetic autonomic neuropathy. Cortisol/creatinine ratios in early morning urine samples were similar in patients with and without nocturnal hypoglycaemia, consistent with the absence or rebound hyperglycaemia. Diabetic retinopathy was less prevalent in patients with hypoglycaemia, possibly reflecting better long-term diabetic control in this group. HbA1 concentration reflects overall blood glucose control in diabetes but near-normal levels must be interpreted with caution since they may be associated with recurrent hypoglycaemia.

Adult↗

PubMed1994

Hypoglycaemia unawareness.

Hypoglycaemia is a severe complication of insulin-dependent diabetes mellitus, especially when it is not preceded by warning signs. A patient unaware of a low blood glucose concentration may not take any remedial action, becomes severely hypoglycaemic and may lapse into a potentially fatal coma. Hypoglycaemic unawareness is associated particularly with good glycaemic control. Hypoglycaemia unawareness was first related to diabetic autonomic neuropathy. Subsequently it emerged that well controlled diabetic patients suffered from hypoglycaemia unawareness more often than poorly controlled patients. Next to autonomic neuropathy and good glycaemic control, the transfer of more slowly resorbed beef and porcine insulin to more rapidly resorbed human insulin has been incriminated as causing an increased incidence of hypoglycaemia unawareness. Reviewing the scientific literature concerning the connection between hypoglycaemia unawareness and the use of human insulin, there is no rationale for supporting the hypothesis that human insulin leads to hypoglycaemia unawareness any longer. While the pathophysiology of hypoglycemia unawareness remains unclear in patients with insulin-dependent diabetes mellitus of long duration, it may well be related to impaired adrenaline secretion. The cause of this impaired adrenaline secretion during hypoglycaemia is unknown and it does not seem to be a result of diabetic autonomic neuropathy.

Blood Glucose↗

PubMed1998

Severe hypoglycaemia in children and adolescents during multiple-dose insulin therapy.

Episodes of severe hypoglycaemia, resulting in coma and/or convulsions, were documented in an unselected, population-based group of 376 children and adolescents with Type 1 diabetes mellitus (Type 1 DM) treated at the Aurora Hospital, City of Helsinki. A prospective study in 1994-95 yielded 493 patient-years and a retrospective study in 1990-93, 904 patient-years of data. Of these patients, 77-85% received insulin in three or more daily doses. During 1990-95, 43 patients had a total of 48 severe hypoglycaemic episodes. For each episode (n = 48), one control Type 1 DM patient who had never experienced any severe hypoglycaemia, matched by age, diabetes duration and puberty, was sought from the study population. Incidence of severe hypoglycaemia was 3.1/100 patients years prospectively and 3.6/100 retrospectively. At the time of the episode, median age was 13.3 (range 2.2-21) years, and median diabetes duration 6.1 (0.5-14.6) years. Rates were similar in different age groups (< 6, 6-12.9 and > or = 13 years). A potential explanation for the hypoglycaemia was found in 79% of the episodes. Insulin dose was higher (p = 0.04) and HbA1c lower (p = 0.005) in patients with severe hypoglycaemia than in controls. In conclusion, multiple-dose insulin therapy in young patients with Type 1 DM can be associated with a low rate of severe hypoglycaemia. The majority of such episodes seem to be preventable.

Adolescent↗

PubMed1995

Dysfunction in the beta 2-adrenergic signal pathway in patients with insulin dependent diabetes mellitus (IDDM) and unawareness of hypoglycaemia.

The majority of the impaired symptoms in hypoglycaemia unawareness, such as palpitations, tachycardia and tremor, are caused by increased release of adrenaline (ADR) and noradrenaline (NA), and induced by stimulation of beta-adrenergic receptors. Binding of ADR or NA to the beta-adrenergic receptor generates a signal, transmitted via a guanine nucleotide binding protein complex (G-protein), which in turn activates adenylate cyclase with increased production of cAMP. The aim of this study was to show whether IDDM-patients with hypoglycaemia unawareness had deficient coupling between beta2-adrenergic receptors and G-proteins compared to IDDM-patients with hypoglycaemia unawareness and healthy controls. The IDDM-patients were subgrouped as hypoglycaemia aware or unaware based on questionnaire answers, clinical information and the results of isoprenaline sensitivity tests. Mononuclear leukocytes (MNL) were isolated from venous blood. By saturation binding experiments, using [125I]-(-)-iodopindolol ((-)-IPIN), total receptor number (Bmax) and affinity (Kd) were determined. By displacement experiments the relative number of low- and high-affinity receptors for the beta-adrenergic agonist (-)-isoprenaline ((-)-ISO) were determined. We found no difference in Bmax- or Kd-values. for (-)-IPIN between the subgroups. However, there was a reduced capability to form high-affinity binding complexes with (-)-ISO in MNL from IDDM-patients with hypoglycaemia unawareness. It was concluded that hypoglycaemia unawareness in IDDM was associated with dysfunction of the proximal beta2-adrenergic signal pathway.

Adrenergic beta-Agonists↗

PubMed1987

Prolonged insulin resistance following insulin-induced hypoglycaemia.

Nineteen normal male volunteers underwent a 10-h glucose clamp study to examine the duration and mechanism of insulin resistance after hypoglycaemia. Dextrose delivery by the Biostator to maintain the target blood glucose level fell below baseline 2 h after induction of hypoglycaemia and remained suppressed for at least 7 h after insulin hypoglycaemia. Insulin secretion as manifested by C-peptide levels remained suppressed for 3-4 h after insulin hypoglycaemia despite return of blood glucose to baseline by 90 min. Glucose kinetic data (3-3H-glucose) performed in six of the subjects indicated that the prolonged insulin resistance was due to significantly increased hepatic glucose production and to suppressed glucose utilisation, persisting for at least 4 h after counterregulatory hormone levels had returned to normal. Post-hypoglycaemic insulin resistance as determined by dextrose delivery was markedly attenuated and the rise in hepatic glucose output totally eliminated in five hypopituitary subjects without growth hormone or cortisol responses to hypoglycaemia. We conclude that post-hypoglycaemic insulin resistance occurs in non-diabetic subjects and persists for at least 7 h following hypoglycaemia. This prolonged insulin resistance is largely related to release of growth hormone and cortisol.

Adult↗

PubMed1994

Regional cerebral blood flow in IDDM patients: effects of diabetes and of recurrent severe hypoglycaemia.

Chronic hyperglycaemia and recurrent severe hypoglycaemia have both been implicated as causing cerebral damage in patients with diabetes. Although cognitive dysfunction and intellectual impairment have been demonstrated in patients with recurrent severe hypoglycaemia, structural correlates have not been described, and it is not known whether specific functional changes occur in the brains of affected patients. Regional cerebral blood flow was estimated by SPECT with 99mTechnetium Exametazime in 20 patients with IDDM. Ten patients had never experienced severe hypoglycaemia and 10 had a history of recurrent severe hypoglycaemia. Patient results were compared with 20 age- and sex-matched healthy volunteers. We observed differences between the two patient groups and the control group. Tracer uptake was greater in diabetic patients in the superior pre-frontal cortex. This effect was particularly pronounced in the group who had a history of previous severe hypoglycaemia. Patients with a history of recurrent hypoglycaemia also had a relative reduction in tracer uptake to the calcarine cortex. This suggests an alteration in the pattern of baseline regional cerebral blood flow in diabetic patients with frontal excess and relative posterior reduction in cerebral blood flow.

Adult↗

PubMed1993

Symmetry of cerebral blood flow and cognitive responses to hypoglycaemia in humans.

A low blood glucose level is associated with impairment of higher cerebral function and an increase in cerebral blood flow. This study examined whether there are differences in the physiological responses to hypoglycaemia between the cerebral hemispheres. Eight healthy men participated in two hyperinsulinaemic glucose clamp studies: after 60 min at 4.5 mmol/l, blood glucose was either lowered to 2.0 mmol/l and "clamped" there for 60 min (hypoglycaemia) or continuously maintained at 4.5 mmol/l (euglycaemia). Cardiac output, middle cerebral artery velocity (transcranial Doppler) and cerebral blood flow (133-xenon inhalation) were measured during the studies. Neuropsychological tests were used to determine whether hypoglycaemia caused differential impairment of hemispheric cognitive function. Hypoglycaemia was associated with symmetrical impairment of cognitive function in both cerebral hemispheres and a rise in cardiac output (from 5.5 [0.2] to 8.7 [0.2] l.min-1, p < 0.0001, mean [standard error]), middle cerebral artery velocity (from 55 [2.6] to 64 [2.8] cm.s-1, p < 0.002), and global cerebral blood flow (from 56 [2.6] to 69 [2.9] ml.100 g-1.min-1, p < 0.005 compared to pre-insulin values). There were no differences in the blood flow response during hypoglycaemia between hemispheres and the increase in blood flow did not correlate with either the change in cardiac output or rise in plasma catecholamine levels. After 120 min of hyperinsulinaemic, euglycaemia, global cerebral blood flow rose significantly above baseline (from 58 [2.4] to 63 [2.2] ml.100 g-1.min-1, p < 0.05). In conclusion, using the techniques described, the physiological and cognitive responses of each cerebral hemisphere to hypoglycaemia were symmetrical.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1992

Cognitive function in type 1 (insulin-dependent) diabetic patients after nocturnal hypoglycaemia.

UNLABELLED: Eight Type 1 (insulin-dependent) diabetic patients with no diabetic complications were studied on two consecutive and one subsequent overnight occasions. The aim was to evaluate the influence of nocturnal hypoglycaemia on neuropsychological and reaction time tests the following morning. Hypoglycaemia was induced by i.v. insulin infusion, blood glucose nadir was 1.5 +/- 0.3 mmol/l. Duration of hypoglycaemia (blood glucose less than 3 mmol/l) was 101 +/- 38 min. Whole night sleep statistics for all patients showed no statistical differences between the normoglycaemic and hypoglycaemic nights, however, there was a tendency of prolongation of the second sleep cycle in the nights with hypoglycaemia. Each patient was used as his own control and periods with blood glucose concentration less than 3 mmol/l were compared to exactly the same periods in nights with blood glucose level over 5 mmol/l. During hypoglycaemia the amount of deep sleep was reduced and replaced by superficial sleep and arousals of short duration. Further, the reduction in deep sleep was replaced later at night. Neuropsychological test scores and reaction time measurements in the morning showed no differences between the normoglycaemic and hypoglycaemic nights. IN CONCLUSION: despite sleep disturbances, nocturnal hypoglycaemia did not impair cognitive function the following morning in Type 1 (insulin-dependent) diabetic patients.

Adult↗

PubMed1995

Lack of preservation of higher brain function during hypoglycaemia in patients with intensively-treated IDDM.

Severe hypoglycaemia with cognitive dysfunction is 3 times more common in intensively, rather than conventionally, treated insulin-dependent diabetes mellitus (IDDM). To investigate the effect of diabetes control on higher brain function during acute hypoglycaemia, we studied one of the earliest detectable changes in cognitive function, i.e. the four-choice reaction time, and symptomatic and hormonal responses during euglycaemic and hypoglycaemic clamping in human subjects. There were no changes in symptoms or counterregulatory hormones and four-choice reaction time was stable during 220 min of euglycaemic insulin clamping in five men with IDDM, with a coefficient of variation of less than 2.2% (1% for accuracy) for the cognitive function test. During stepped hypoglycaemic clamping however, hormonal responses and subjective awareness of hypoglycaemia occurred in all groups but started at much lower blood glucose concentrations in eight intensively-treated diabetic subjects (Group 1) than in ten conventionally-treated (Group 2) or in eight non-diabetic subjects (Group 3). For example, for adrenaline, plasma glucose thresholds were 2.7 +/- 0.2 vs 3.4 +/- 0.2 and 3.2 +/- 0.1 mmol/l, respectively, p < 0.05, Group 1 vs Groups 2 or 3 and for subjective awareness of hypoglycaemia 2.3 +/- 0.2 vs 3.0 +/- 0.1 and 3.2 +/- 0.1 mmol/l, p < or = 0.003), as in previous studies. In contrast, deterioration in reaction time occurred at 3.2 +/- 0.3, 3.2 +/- 0.2 and 3.0 +/- 0.2 mmol/l, respectively (p = NS), thus occurring at higher glucose levels than subjective awareness in the intensively-treated subjects only. The altered hierarchy of responses to hypoglycaemia in well-controlled intensively-treated diabetes explains the increased risk of severe hypoglycaemia without warning seen in such patients.

Adult↗

PubMed1996

Inhibition of muscle glycogen synthase activity and non-oxidative glucose disposal during hypoglycaemia in normal man.

The purpose of the present study was to evaluate the role of muscle glycogen synthase activity in the reduction of glucose uptake during hypoglycaemia. Six healthy young men were examined twice; during 120 min of hyperinsulinaemic (1.5 mU.kg-1. min-1) euglycaemia followed by: 1)240 min of graded hypoglycaemia (plasma glucose nadir 2.8 mmol/l) or 2) 240 min of euglycaemia. At 350-360 min a muscle biopsy was taken and indirect calorimetry was performed at 210-240 and 330-350 min. Hypoglycaemia was associated with markedly increased levels of adrenaline, growth hormone and glucagon and also with less hyperinsulinaemia. During hypoglycaemia the fractional velocity for glycogen synthase was markedly reduced; from 29.8 +/- 2.3 to 6.4 +/- 0.9%, p < 0.05. Total glucose disposal was decreased during hypoglycaemia (5.58 +/- 0.55 vs 11.01 +/- 0.75 mg.kg-1. min-1 (euglycaemia); p < 0.05); this was primarily due to a reduction of non-oxidative glucose disposal (2.43 +/- 0.41 vs 7.15 +/- 0.7 mg.kg-1 .min-1 (euglycaemia); p < 0.05), whereas oxidative glucose disposal was only suppressed to a minor degree. In conclusion hypoglycaemia virtually abolishes the effect of insulin on muscle glycogen synthase activity. This is in keeping with the finding of a marked reduction of non-oxidative glucose metabolism.

Adult↗

PubMed1991

Cumulative cognitive impairment following recurrent severe hypoglycaemia in adult patients with insulin-treated diabetes mellitus.

To examine the hypothesis that episodes of severe hypoglycaemia may cause cumulative cognitive impairment. 100 Type 1 (insulin-dependent) diabetic patients were examined. Their age range was 25-52 years, and the onset of diabetes had occurred after the age of 19 years. Patients with evidence of organic brain disease, including cerebrovascular disease, were excluded. A questionnaire was used to assess the number, frequency and severity of hypoglycaemic episodes experienced during treatment with insulin and the accuracy of this retrospective information was verified from general practice and hospital case-notes. A detailed neuropsychological assessment was undertaken, including tests of pre-morbid and present IQ (Wechsler-Revised), memory and information-processing speed. Significant correlations were observed between the frequency of severe hypoglycaemia and the magnitude of intellectual decline, Performance IQ, inspection time and reaction time (patients with the more frequent hypoglycaemia had poorer performance). Two sub-groups of patients were identified on the basis of their experience of severe hypoglycaemia, and were balanced for pre-morbid IQ, age and duration of diabetes. One sub-group (n = 23) had never experienced severe hypoglycaemia (Group A), whilst the other sub-group (n = 24) had suffered at least five episodes of severe hypoglycaemia (Group B). Group B had greater intellectual impairment than Group A, and Group B also had a significantly slower mean reaction time and higher reaction time variance when compared with Group A.

Adult↗

PubMed2005

Glycaemic control and severe hypoglycaemia following training in flexible, intensive insulin therapy to enable dietary freedom in people with type 1 diabetes: a prospective implementation study.

AIMS/HYPOTHESIS: The aim of this study was to evaluate the implementation of a course teaching flexible, intensive insulin therapy on glycaemic control and severe hypoglycaemia in routine care. METHODS: This is a continuous quality-assurance project involving hospital diabetes centres. Every third year each centre re-examines 50 consecutive patients (evaluation sample) 1 year after participation in the course. Ninety-six diabetes centres in Germany participated and 9,583 patients with type 1 diabetes (190 evaluation samples) were re-examined between 1992 and 2004. The intervention was a 5-day inpatient course for groups of up to ten patients with a fixed curriculum of education and training for dietary flexibility and insulin adjustment. The main outcome measures were HbA1c and severe hypoglycaemia. RESULTS: Mean baseline HbA1c was 8.1%, and had decreased to 7.3% at follow-up; incidence of severe hypoglycaemia was 0.37 events per patient per year prior to intervention and 0.14 after intervention. In mixed-effects models adjusted for effects of centres, age and diabetes duration, the mean difference was -0.7% (95% CI -0.9 to -0.6%, p<0.0001) for HbA1c and -0.21 events per patient per year (95% CI -0.32 to -0.11, p=0.0001) for severe hypoglycaemia, with similar results for evaluation samples, with a maximum of 10% of patients lost to follow-up. Before intervention, the incidence of severe hypoglycaemia was three-fold higher in the lowest quartile than in the highest quartile of HbA1c, whereas the risk was comparable across the range of HbA1c values after intervention. CONCLUSIONS/INTERPRETATION: Implemented as part of a continuous quality-assurance programme the self-management programme is effective and safe in routine care. Improvement of glycaemic control can be achieved without increasing the risk of severe hypoglycaemia.

Adult↗

PubMed1999

Brain substrate utilisation during acute hypoglycaemia.

AIMS/HYPOTHESIS: Our study was undertaken to examine directly the utilisation of glucose and alternative substrates, in particular amino acids, during hypoglycaemia. METHODS: Catheters were positioned in the jugular venous bulb and an artery in six healthy subjects in the overnight fasted state. Arterio-venous differences for glucose, amino acids, lactate and pyruvate were measured in the basal state, during hyperinsulinaemic euglycaemia and during hyperinsulinaemic hypoglycaemia. The subjects were studied on two different occasions, once during intravenous infusion of amino acids and once during infusion of saline. RESULTS: In the basal state the fractional extraction of glucose across the brain was 10 +/- 2%, glucose uptake accounted for 106 +/- 5% of the brain's oxidative metabolism. There was a small release of lactate and pyruvate. During hyperinsulinaemia glucose uptake continued to account for the entire fuel requirement of the brain. Hyperaminoacidaemia did not result in net amino acid uptake by the brain. During hypoglycaemia (2.4 +/- 0.2 mmol/l) fractional extraction of glucose by the brain increased (p < 0.01) and glucose uptake accounted for 90 +/- 15% of the brain's oxidative metabolism. Uptake of amino acids, lactate or pyruvate could not be detected. CONCLUSION/INTERPRETATION: 1) Brain fractional extraction of glucose increases during hypoglycaemia, 2) hyperinsulinaemia does not change fractional extraction of glucose by the brain, 3) augmented availability of amino acids does not result in brain amino acid uptake during euglycaemia or hypoglycaemia and 4) under the present study conditions glucose remains the major substrate for cerebral metabolism during hypoglycaemia; lactate or pyruvate uptake by the brain can not be detected.

Acute Disease↗

PubMed1999

Cranial MRI of neurologically impaired children suffering from neonatal hypoglycaemia.

BACKGROUND: Metabolic disturbances such as anoxia and hypoglycaemia are important in causing maldevelopment of the neonatal brain. While there have been some pathology studies of the effects of neonatal hypoglycaemia on brain development, reports of MRI findings in such infants have been rare. OBJECTIVES: To describe the MRI findings in neurologically handicapped children who had suffered from neonatal hypoglycaemia and to evaluate the relationship between the neurological impairment and neonatal hypoglycaemia. MATERIALS AND METHODS: We retrospectively evaluated the MRI findings in eight full-term infants with neonatal symptomatic hypoglycaemia who later exhibited neurological handicap. The age at which the MRI scans were obtained ranged from 9 months to 8 years 10 months (mean 4 years 1 month, median 4 years). RESULTS: The most striking findings were prolonged T1 weighting and T2 weighting in the parieto-occipital periventricular deep white matter in six patients, suggesting abnormal or delayed myelination. Dilatation of the lateral ventricles, especially of the trigones, was observed in five patients in whom the distance between the posterior horns of the lateral ventricles and the adjacent sulci was reduced. The volume of white matter relative to grey matter was reduced in two patients. In addition, four patients exhibited cerebral cortical atrophy, mainly in the occipital lobe. CONCLUSIONS: These findings suggest that neonatal hypoglycaemia may cause delayed or abnormal myelination, especially in the parieto-occipital, periventricular, deep white matter, and may cause cerebral cortical atrophy, especially in the occipital lobe.

Brain↗