Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of mild insulin-induced hypoglycaemia on symptoms, physiological changes, and adrenaline responses was assessed in 10 normal subjects and 15 insulin-dependent diabetic patients (5 with reduced awareness of hypoglycaemic symptoms). When blood glucose was maintained at 3.2 mmol/l, reaction time was prolonged in both normal and diabetic subjects and plasma adrenaline levels increased in the normals and some diabetics; there were no other physiological responses. 2 normals and 1 diabetic were aware that their blood glucose was low. When blood glucose was maintained at 2.5 mmol/l for 30 min, 9/10 normals but only 4/15 diabetics recognised hypoglycaemia. Increases in hypoglycaemic symptom score, tremor, and sweating, and falls in diastolic blood pressure were significant only in the normal subjects and the 4 "aware" patients. Adrenaline levels increased in all cases, but were more pronounced in the normals and aware diabetics. Reaction time remained prolonged in all groups. All measurements returned to baseline when blood glucose was raised to 4.5 mmol/l. Impairments in adrenaline response may be common, even in diabetic patients without autonomic neuropathy and in those who do not complain of hypoglycaemic unawareness; consequent failure to recognise a falling blood glucose may predispose to a risk of severe hypoglycaemia.
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PMID:Influence of sympathetic nervous system on hypoglycaemic warning symptoms. 288 22

The case-histories of 3 patients with insulin-dependent diabetes mellitus (IDDM) suggested that, after a switch from beef/porcine to human insulin, a given level of hypoglycaemia may cause less pronounced sympathoadrenal symptoms (tremor, sweating, &c), so that there is less warning of impending unconsciousness. This possibility was investigated by questioning of 176 IDDM patients who had switched from beef/porcine to human insulin with negligible change in dosage 1-48 months earlier. 66 (36%) said that their symptoms of hypoglycaemia had changed from those of sympathoadrenal activation to those of neuroglycopenia. This disadvantage of human insulin is an argument for continued availability of beef/porcine insulin.
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PMID:Hypoglycaemia unawareness in diabetics transferred from beef/porcine insulin to human insulin. 288 33

The response of neonatal tremor to a suckling stimulation test was investigated in 102 healthy neonates born at full term. In 84 the tremor resolved immediately; none had hypocalcaemia and only one had mild hypoglycemia. Eighteen in whom the tremor continued had either hypocalcaemia (n = 13) or hypoglycaemia (n = 5).
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PMID:Suckling stimulation test for neonatal tremor. 292 85

Study of ACTH responsiveness to oral metyrapone and insulin hypoglycemia in children with repetitive nervous system manifestations (convulsions, coma, mental confusion apathy, tremor) has led to diagnosis of isolated ACTH deficiency in nine children within a three year period. Hypoglycemia was ascertained in five children; in four cases no hypoglycemia was proved, possibly because of promptly disappearance or because of other mechanisms accounting for clinical symptoms (occurrence of intracellular overhydratation associated with corticol deficiency is considered). The incidence of isolated ACTH deficiency in children is possibly undervalued. Reappraisal of isolated ACTH deficiency in childhood as to be considered in idiopathic spontaneous hypoglycemia and perhaps in some paroxysmal neurologic and/or digestive manifestations without proved hypoglycemia and so far poorly defined or held for epileptic fits. In order to disclose further additional tropic hormone deficiencies, and to differentiate permanent from transient impairment of ACTH responsiveness which often seems to be related to emotional deprivation syndrome, more protracted follow up studies are needed.
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PMID:[Lack of ACTH responsiveness in children and paroxysmal central nervous system manifestations. (Study of nine cases of isolated ACTH deficiency) (author's transl)]. 625 61

Suspected postprandial (reactive or idiopathic) hypoglycemia is characterized by predominantly adrenergic symptoms appearing after meals rich in carbohydrates and by their rare association with low blood glucose level (< 2.77 mmol/L). We studied heart rate, blood pressure, plasma insulin, C-peptide, and catecholamine responses during a 5-h oral glucose tolerance test in eight patients with suspected postprandial hypoglycemia and eight age-, sex-, and body mass index-matched healthy controls. We also evaluated beta-adrenergic sensitivity by using the isoproterenol sensitivity test. Psychological profile was assessed by the Symptom Checklist (SCL-90R) self-report symptom inventory. Patients with suspected postprandial hypoglycemia had higher beta-adrenergic sensitivity (defined as the dose of isoproterenol required to increase the resting heart rate by 25 beats/min) than controls (mean +/- SEM, 0.8 +/- 0.13 vs. 1.86 +/- 0.25 microgram isoproterenol; P = 0.002). After administration of glucose (75 g) blood glucose, plasma C-peptide, plasma epinephrine, and plasma norepinephrine responses were identical in the two groups, but plasma insulin was higher in the patients (group effect, P = 0.02; group by time interaction, P = 0.0001). Both heart rate and systolic blood pressure were significantly higher (but remained in the normal range) after glucose administration in patients with suspected postprandial hypoglycemia than in controls (group by time interactions, P = 0.004 and 0.0007, respectively). After glucose intake, seven patients had symptoms (palpitations, headache, tremor, generalized sweating, hunger, dizziness, sweating of the palms, flush, nausea, and fatigue), whereas in the control group, one subject reported flush and another palpitations, tremor, and hunger. Analysis of the SCL-90R questionnaire revealed that patients had emotional distress and significantly higher anxiety, somatization, depression, and obsessive-compulsive scores than controls. We may conclude that patients with suspected postprandial hypoglycemia have normal glucose tolerance, increased beta-adrenergic sensitivity, and emotional distress.
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PMID:Suspected postprandial hypoglycemia is associated with beta-adrenergic hypersensitivity and emotional distress. 796 39

Hypoglycaemia is the most frequent acute complication of insulin-dependent diabetes mellitus. The clinical symptoms of insulin-induced hypoglycaemia can be grouped into those attributable to the sympathetic and adrenergic responses, e.g. tremor, pallor, palpitation, sweating, mydriasis ('hypoglycaemia awareness'), and those attributable to brain dysfunction, ranging from headache to convulsions and coma. Hypoglycaemia in diabetic children can occur at any time of the day, but nocturnal hypoglycaemia is a particular fear and worry. The frequency of mild hypoglycaemia is almost impossible to ascertain and the incidence of severe hypoglycaemia varies between 0.07 and 3.6 episodes per patient-year, though most authors report a range of 0.1-0.2 episode per patient-year. The most frequent causes of hypoglycaemia in diabetic children are deviations from treatment routine such as strenuous exercise, omission of snacks or skipped meals, and gross deviations from the prescribed times of insulin injections and recommended doses of insulin. Other predisposing factors include intensified insulin treatment, improved glycaemic control, young age, longer duration of diabetes and defective counterregulation. The available paediatric studies do not seem to support the suggestion that human insulin impairs the perception of hypoglycaemic symptoms ('hypoglycaemia unawareness') and increases the frequency of hypoglycaemic episodes, but further conclusive studies are needed. Prolonged and recurrent severe hypoglycaemia, particularly in younger children, can cause permanent neuropsychological dysfunction (e.g. learning disabilities) and permanent electroencephalographic abnormalities. Mild hypoglycaemia has also been documented to affect cognitive function, and the performance of neuropsychological tasks can remain decreased for some time (up to several hours) after full clinical recovery from hypoglycaemia. An impending hypoglycaemic attack can usually be averted by the ingestion of 20 g of rapidly absorbed carbohydrate. A severe episode can be effectively treated outside hospital with subcutaneous or intramuscular glucagon (0.5-1.0 mg) or in the hospital by an intravenous bolus of 0.2-0.5 g/kg glucose followed by a continuous glucose infusion. Patient and parent education and vigilant application of diabetes self-care principles are perhaps the most effective means of prevention, but in very young children a less strict metabolic control (higher glycosylated haemoglobin levels) may be necessary.
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PMID:Hypoglycaemia in the diabetic child. 837 14

The allocation of hypoglycaemic symptoms to autonomic or neuroglycopenic groups tends to occur on an a priori basis. In view of the practical need for clear symptom markers of hypoglycaemia more scientific approaches must be pursued. Substantial evidence is presented from two large scale studies we performed which support a three factor model of hypoglycaemic symptomatology, based on the statistical associations discovered among symptoms reported by diabetic patients. Study 1 involved 295 insulin-treated out-patients and found that 11 key hypoglycaemic symptoms segregated into three clear factors: autonomic (sweating, palpitation, shaking and hunger) neuroglycopenic (confusion, drowsiness, odd behaviour, speech difficulty and incoordination), and malaise (nausea and headache). The three factors were validated on a separate group of 303 insulin-treated diabetic out-patients. Confirmatory factor analyses showed that the three factor model was the optimal model for explaining symptom covariance in each group. A multi-sample confirmatory factor analysis tested the rigorous assumptions that the relative loadings of symptoms on factors across groups were equal, and that the residual variance for each symptom was identical across groups. These assumptions were successful, indicating that the three factor model was replicated in detail across these two large samples. It is suggested that the results indicate valid groupings of symptoms that may be used in future research and in clinical practice.
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PMID:Partitioning the symptoms of hypoglycaemia using multi-sample confirmatory factor analysis. 840 46

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.
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PMID:Dysfunction in the beta 2-adrenergic signal pathway in patients with insulin dependent diabetes mellitus (IDDM) and unawareness of hypoglycaemia. 864 18

Recent studies have reported reduced endocrine and symptomatic responses to hypoglycaemia 18-24 h after antecedent hypoglycaemia in both non-diabetic subjects and those with insulin-dependent diabetes mellitus. We examined these and peripheral physiological responses in eight non-diabetic subjects aged 23-35 years in the week following antecedent hypoglycaemia. Blood glucose levels were held at plateaus of 5 mmol/l and 2.5 mmol/l for 30 min during hyperinsulinaemic (60 mU x m-2x min-1) morning clamps on days 1, 3 and 8 of two study periods separated by at least 4 weeks. Measurements were made at time 0, 15 and 30 min of each plateau on each day. One the afternoon of Day 1 we also induced either euglycaemia with a blood glucose level of 5 mmol/l (control week) or hypoglycaemia of 2.9 mmol/l (hypo week) for 2 h in random order. The adrenaline response to morning hypoglycaemia (p<0.001 on all days) was attenuated on Day 3 (p<0.05) and Day 8 (p<0.05) compared to Day 1 of hypo week only. Sweating was also attenuated on Day 3 (p<0.05) and Day 8 (p<0.02) of hypo week only. Noradrenaline levels and tremor increased during hypoglycaemia on each study day (p<0.05) but did not differ between days in either week. During hypo week only, the total symptom score response to hypoglycaemia was attenuated on Day 3 (p<0.03) but not Day 8 (p=0.10). Autonomic symptoms were similarly affected. In summary, the physiological responses to hypoglycaemia are affected differentially by antecedent hypoglycaemia with sweating and adrenaline responses remaining impaired for at least adrenaline responses remaining impaired for at least 5 days.
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PMID:Prolonged but partial impairment of the hypoglycaemic physiological response following short-term hypoglycaemia in normal subjects. 869 Jan 70

There is little information concerning the physiological response to hypoglycaemia induced by sulphonylureas. We compared the physiological and symptomatic responses to insulin and tolbutamide induced hypoglycaemia in 8 normal subjects. While infusing either insulin or tolbutamide, we used a glucose clamp to maintain blood glucose at 4.5 mmol l-1 for 30 min and lowered it to 2.9 mmol l-1 for a further 30 min. Mean peripheral insulin levels during the insulin infusion arm in comparison with the tolbutamide infusion were not significantly different during the euglycaemic plateau: 106 +/- 4 vs 77 +/- 15 mU l-1 (mean +/- SEM) (mean difference 29 mU l-1, 95% CI -22 to 80; p = NS) but were greater during the hypoglycaemic plateau: 106 +/- 3.5 vs 21.0 +/- 4.0 mU l-1 (mean difference 85 mU l-1, 95% CI 72 to 98; p < 0.0001). Portal insulin concentrations, calculated from C-peptide data were not significantly different during the euglycaemic plateau with insulin as compared to tolbutamide. However, during hypoglycaemia portal insulin concentrations were significantly higher 15 min from the start of the plateau, during insulin infusion. During hypoglycaemia induced by either insulin or tolbutamide there were similar peak responses of glucagon: 124 +/- 14 vs 128 +/- 7 ng l-1 (mean difference -4, 95% CI -39 to 31; p = NS) and adrenaline: 2.9 +/- 0.4 vs 2.8 +/- 0.3 nmol l-1, (mean difference 0.1, 95% CI -0.9 to 1.0; p = NS). Increases in tremor and sweating and deterioration in reaction time were similar during both periods of hypoglycaemia as were increases in total: 18.5 +/- 1.4 vs 19.6 +/- 2.2 (mean difference -1.0, 95% CI -3.8 to 1.8; p = NS) and autonomic: 8.9 +/- 0.9 vs. 9.9 +/- 1.3 (mean difference -1.1, 95% CI -5.9 to 3.6; p = NS) symptom scores. We conclude that there is no difference in the glucagon, sympathoadrenal, cognitive or symptomatic response during hypoglycaemia induced by either insulin or tolbutamide. This suggests that the different insulin concentrations produced by these contrasting models of hypoglycaemia had no effect on the physiological response and patients taking sulphonylureas can be expected to develop similar warning symptoms to those on insulin.
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PMID:Similar physiological and symptomatic responses to sulphonylurea and insulin induced hypoglycaemia in normal subjects. 884 97


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