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)

Hypoglycaemia is the most common complication affecting people with Type 1 insulin dependent diabetes mellitus. Its onset is characterized by symptoms which include sweating, tremor, palpitations, loss of concentration and tiredness. As part of a research project to investigate the mechanisms of hypoglycaemia we have developed an ambulatory system to monitor and record pulsatile changes in blood flow, pulse interval, body temperature and skin impedance. The system uses a pocket computer (Atari Portfolio) to collect and store the data on a memory card. The analogue system consists of two thermocouples, an infrared photoplethysmograph and skin impedance monitoring circuit. To conserve power the system is programmed to make measurements for 2 min every 10 min: using this regimen over 16 h of data can be stored. Data collected during a spontaneous overnight hypoglycaemic episode are presented and also a comparison between continuous and intermittent data collection during a period of induced hypoglycaemia. The system is being used to investigate the physiological responses to hypoglycaemia but could easily be adapted for monitoring other physiological signals.
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PMID:A portable system for monitoring physiological responses to hypoglycaemia. 902 91

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.
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PMID:A comparative study of responses to acute hypoglycaemia induced by human and porcine insulins in patients with Type 1 diabetes. 916 11

Hypoglycemia is often associated with typical, but not specific symptoms. A differentiation is made between neuroglucopenic symptoms (e.g., confusion, somnolence) on the one hand, and those that arise as a result of the counterregulatory response of the sympathetic nervous system (e.g., tremor, sweating), on the other. The diagnosis of hypoglycemia can cause considerable problems, in particular when only isolated single symptoms present (e.g., confusion, psychosis, seizures, coma). For the elective clarification of recurrent hypoglycemia, further diagnostic examinations (e.g., fasting with determination of hormones, measurement of insulin) are employed in addition to the patient's history. For differential diagnostic considerations not only organic causes, but also adverse drug reactions and a factitious genesis must be excluded. In the event of an emergency (e.g., hypoglycemic coma) the usual form of treatment is the administration of glucoses or glucagon.
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PMID:[Hypoglycemia. Symptoms, differential diagnosis, therapy]. 917 11

Symptomatic episodes of documented hypoglycaemia were characterized with the aid of a 3-month diary in a single-centre, unselected group of 161 children and adolescents with Type 1 diabetes mellitus, treated mainly (81%) with multiple-dose insulin therapy. Patients and families were asked to write in the diary all the symptomatic episodes in which blood glucose concentration proved to be < or =3 mmol l(-1) before treatment. Of the patients, 83 (52%) had a total of 287 hypoglycaemic episodes (0.6 attack per month per patient). The majority of the attacks, 221 (77%), were mild (patients > or =6 years able to treat themselves). Only two attacks were severe, resulting in coma and/or convulsion. The most common dominant symptoms were weakness (29%), tremor (20%), hunger (14%), and drowsiness (12%). Of all the dominant symptoms, 39% were classified as autonomic, 20% neuroglycopenic, and 41% non-specific. In children under 6 years, autonomic symptoms were less common than in adolescents 15 years or over (34% vs 57%, p = 0.01). In conclusion, the incidence of documented symptomatic hypoglycaemia was low. The symptoms were more often neuroglycopenic or non-specific than autonomic, especially in young children.
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PMID:Documented symptomatic hypoglycaemia in children and adolescents using multiple daily insulin injection therapy. 963 24

Hypoglycemic episodes were studied in two large populations of prepubertal (332 subjects, aged 6-11 years) and adolescent (200 subjects, aged 12-18 years) diabetic children. We confirmed the majority of published data on incidence and causes of hypoglycemia and added some new information on the complex symptomatology and fear of hypoglycemia. Longer duration of IDDM induced a change in the symptomatology of hypoglycemia, consisting of a reduced occurrence of autonomic symptoms, namely tremor, and a parallel increased experience of neuroglycopenic symptoms, particularly drowsiness, difficulty in concentrating, and lack of coordination. The latter symptoms were found more frequently in patients with partial unawareness, more severe episodes and higher fear of hypoglycemia. These observations draw attention to the neuroglycopenic symptoms as important warning cues of hypoglycemia. We emphasized the necessity of observing the change in the frequency of symptoms experienced by patients, in particular autonomic and neuroglycopenic symptoms, in order to educate patients to preserve a normal awareness of hypoglycemia and prevent severe episodes.
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PMID:Problems of hypoglycemia arising in children and adolescents with insulin-dependent diabetes mellitus. The Diabetes Study Group of The Italian Society of Pediatric Endocrinology & Diabetes. 964 56

A 59-year-old woman was hospitalized in hypoglycemic coma. Although hypoglycemia was promptly reversed, she was in a somnolent, restless state with tachycardia, tremor, profuse sweating, and high body temperature. Thyrotoxic storm was highly suspected and vigorous antithyroid regimens gradually brought her up to normal mental and cardiovascular states in several days. However, profound generalized myopathy necessitated the maintenance with a respirator. One month later, an episode of angina pectoris was followed by generalized convulsion, coma, and death in a few days. Neuroimaging study disclosed posterior leukoencephalopathy syndrome. This case is instructive in that hypoglycemic coma may masquerade the major symptomatology of thyrotoxic storm, and that profound myopathy and angiopathic or angiospastic processes of the brain and the heart may interfere with the outcome.
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PMID:Hypoglycemic coma masquerading thyrotoxic storm. 1056 48

The anabolic effects of clenbuterol have been recognized for a long time. Clenbuterol augments the expression of specific muscle proteins with a differential effect on type I and type II fibres. Furthermore, clenbuterol induces the synthesis of endogenous nerve growth factor (NGF) and may itself be a myotrophic factor released by neuron endings. Side effects include tremor and headache and dose dependent abnormalities of laboratory values (hypokalemia, hypoglycemia). After long-term medication increasing fatigue of muscles has been observed. Decreased expression of beta 2-adrenergic receptors may limit the expected functional improvement. The efficacy of clenbuterol as symptomatic treatment of amyotrophic lateral sclerosis has not been proved. Controlled treatment trials are warranted to assess this question.
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PMID:[Clenbuterol in amyotrophic lateral sclerosis. No indication for a positive effect]. 1063 19

Beta-adrenergic-blocking drugs (BABs) have a firm place in the therapy of cardiovascular conditions including angina and hypertension. Although all BABs are competitive inhibitors of beta-receptors, they may differ in their additional pharmacodynamics, i.e., beta1-(cardio)selectivity, partial agonistic activity (PAA), and pharmacokinetic properties. Understanding these additional properties would allow the physician to choose the more appropriate agent for some patients or for specific situations. beta1-Selective BABs may be of potential importance in patients with obstructive airway disease, peripheral vascular disease, and hyperlipidemia and in diabetic patients receiving antidiabetic drugs. These BABs may better control the increased blood pressure in response to hypoglycemia, exercise, or cigarette smoking. Nonselective BABs may be preferably used to decrease epinephrine-induced hypokalemia or to prevent myocardial infarction, and in certain circumstances (i.e., migraine, anxiety, thyrotoxicosis or essential tremor). BABs with PAA may theoretically cause a lesser degree of cardiodepression (reduction of heart rate at rest, cardiac output, and AV conduction), bronchospasm, and peripheral vasoconstriction and minor effects on plasma lipids. Withdrawal syndrome may be absent after BABs with PAA. The pharmacokinetic properties of the BABs such as absorption, bioavailability, elimination half-life, liver metabolization, interindividual variability, as well as pharmacological interactions depend on their hydrophilic/lipophilic ratio. The development of new BABs continues. It has been possible to incorporate into a drug molecule combinations of PAA, preferred beta1-blockade, and beta2-agonist activity. Even if these new agents cause less adverse effects (e.g., vasoconstriction, bronchospasm), their clinical significance remains to be established.
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PMID:Optimization of beta-blockers' pharmacology. 1152 10

In humans, the role of hypothalamic centers for activation of counterregulatory release of catecholamines and glucagon during hypoglycemia is unclear. To address this question, we investigated the counterregulatory response to acute insulin-induced hypoglycemia of glucagon, epinephrine, and norepinephrine in eight patients who had undergone transcranial surgery for a craniopharyngioma extending to the hypothalamic region. We compared the patients' responses with those of four patients suffering from hypopituitarism and of six healthy subjects. After the i.v. injection of 0.1 U of human insulin per kg of body weight in the patients or 0.15 U in healthy subjects, the plasma glucose concentrations decreased to similar minimum levels within 30 min in all three groups. All subjects recovered spontaneously from hypoglycemia within 2 h. In five of eight craniopharyngioma patients, only a small counterregulatory rise in plasma epinephrine (< or =2-fold) and norepinephrine could be observed (P < 0.05 for epinephrine and P = 0.22 for norepinephrine vs. healthy controls). During hypoglycemia, virtually no adrenergic symptoms (tremor, heart pounding, and anxiety) were reported by these five patients, and changes in the heart rate were diminished. In three craniopharyngioma patients, the counterregulatory increase in catecholamines was unimpaired, adrenergic symptoms were reported and a rise in heart rate was observed during hypoglycemia. In all craniopharyngioma patients, the counterregulatory glucagon response to hypoglycemia was preserved and orthostasis increased both catecholamines and the heart rate similar to in the patients with hypopituitarism as well as in the healthy controls. Our results demonstrate selective impairment of counterregulatory sympathoadrenal activation in patients who had undergone surgery for a craniopharyngioma extending to the hypothalamic region. This strongly suggests the involvement of hypothalamic centers in hypoglycemia-induced activation of the sympathoadrenal axis in humans. It remains unclear as to whether hypoglycemia-induced glucagon secretion is also controlled by the hypothalamus. However, a common hypothalamic center controlling both counterregulatory catecholamine and glucagon release is unlikely, and sympathoadrenal activation is not required for hypoglycemia-induced glucagon secretion in humans.
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PMID:Sympathoadrenal counterregulation in patients with hypothalamic craniopharyngioma. 1183 95

Following beta-phenylpyruvate injection, mice developed hypoglycemia clinically manifested as tachypnea, tremor, convulsions and death. To further investigate, neonatal mice were injected with beta-phenylpyruvate and their blood glucose determined and brain histology assessed. beta-Phenylpyruvate-injected mice exhibited higher mortality and neurophysiological changes as compared with controls, although without evidence of neural cell death. Accordingly, we hypothesize that the central neural damage in phenylketonuria might be caused by these recurrent beta-phenylpyruvate-induced hypoglycemic events.
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PMID:Glucose-lowering effect of beta-phenylpyruvate in neonatal mice: a possible mechanism for phenylketonuria-related neurodegenerative changes. 1264 57


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