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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetes mellitus is characterized by recurrent metabolic abnormalities which postmortem studies suggest might be associated with degenerative changes in the central nervous system. Acute hypoglycemia does indeed lead to cognitive impairment, whereas acute hyperglycemia in the absence of ketoacidosis or hyperosmolarity does not. Insulin-dependent diabetes mellitus is associated with cognitive deficits that tend to be relatively slight, inconsistent between different studies, and unrelated to clinical indicators; they can be ascribed as plausibly to psychogenic factors as to degenerative disease. In contrast, cognitive impairment in noninsulin-dependent diabetes mellitus is more conspicuous in tests of learning and memory, consistently associated with a patient's level of glycemic control, and more plausibly to be ascribed to structural neuropathology. Nevertheless, in both cases the deficits in question are unlikely to interfere significantly with patients' everyday functioning.
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PMID:Cognitive function in diabetes mellitus. 228 78

The case of a 57 year old man with cognitive impairment, hypertension and insulin dependent diabetes mellitus caused by phaeochromocytoma is reported. One year after removal of the tumour there was a significant improvement with the full scale IQ increasing by 15 points, normotension and minimal glucose intolerance. Possible mechanisms accounting for reversible cognitive impairment in such a situation are discussed. No previous reports of this association have been discovered.
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PMID:Phaeochromocytoma as a cause of reversible dementia. 380 23

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.
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PMID:Regional cerebral blood flow in IDDM patients: effects of diabetes and of recurrent severe hypoglycaemia. 817 39

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.
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PMID:Hypoglycemia-induced cognitive dysfunction in diabetes mellitus: effect of hypoglycemia unawareness. 858 58

Hypoglycemia elicits a characteristic sequence of responses in healthy humans. These responses (and their arterialized venous glycemic thresholds) include: 1) Decreased insulin secretion (approximately 4.5 mmol/L). 2) Increased glucose counterregulatory hormone (glucagon, epinephrine, growth hormone and cortisol) secretion (approximately 3.6-3.8 mmol/L). 3) Symptoms of hypoglycemia (approximately 3.0 mmol/L). 4) Cognitive dysfunction (approximately 2.6 mmol/L). Thus, insulin secretion decreases as plasma glucose levels fall within the physiological range, and counterregulatory hormone secretion increases as plasma glucose levels fall just below the physiological range at substantially higher glucose levels than those required to produce symptoms and impair cognitive function. These data are entirely consistent with the body of evidence that insulin, glucagon and epinephrine stand high in the hierarchy of redundant glucoregulatory factors that prevent, as well as correct, hypoglycemia. When the same methods are used, these thresholds are remarkably reproducible from laboratory to laboratory. Nonetheless, the glycemic thresholds are dynamic rather than static. They vary in relation to recent antecedent glycemia. For example, lower plasma glucose concentrations are required to elicit autonomic, including epinephrine, and symptomatic responses in patients with well controlled IDDM, a phenomenon best attributed to recent antecedent iatrogenic hypoglycemia. This is the basis of the clinical syndrome of hypoglycemia unawareness, which is now known to be reversible with scrupulous avoidance of iatrogenic hypoglycemia. The latter also at least partially reverses reduced epinephrine responses to hypoglycemia, a key component (in the setting of absent glucagon responses) of the syndrome of defective glucose counterregulation. While perhaps seemingly adaptive, these threshold shifts appear to be maladaptive since both defective glucose counterregulation and hypoglycemia unawareness are associated with substantially increased rates of severe iatrogenic hypoglycemia in people with IDDM.
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PMID:Hierarchy of physiological responses to hypoglycemia: relevance to clinical hypoglycemia in type I (insulin dependent) diabetes mellitus. 913 76

We tested the hypothesis that as few as two weekly brief episodes of superimposed hypoglycemia (i.e., doubling the average frequency of symptomatic hypoglycemia) would reduce physiological and behavioral defenses against developing hypoglycemia and reduce detection of clinical hypoglycemia in patients with type 1 diabetes mellitus (T1DM). Compared with nondiabetic controls, six patients with well-controlled T1DM (HbA1c, 7.5 +/- 0.7% [mean +/- SD]) exhibited absent glucagon responses and reduced epinephrine (P = 0.0027), norepinephrine (P = 0.0007), pancreatic polypeptide (P = 0.0030), and neurogenic symptom (P = 0.0451) responses to hypoglycemia as expected. In these patients, 2 h of induced hypoglycemia (50 mg/dl, 2.8 mmol/l) twice weekly for 1 month, compared in a random-sequence crossover design with an otherwise identical 2 h of induced hyperglycemia (150 mg/dl, 8.3 mmol/l) twice weekly for 1 month, further reduced the epinephrine (P = 0.0001) and pancreatic polypeptide (P = 0.0030) responses, tended to further reduce the norepinephrine and neurogenic symptom responses to hypoglycemia, and reduced cognitive dysfunction during hypoglycemia (P = 0.0271), all assessed in the investigational setting. In the clinical setting, induced hypoglycemia did not alter overall glycemic control, but did reduce the total number of symptomatic hypoglycemic episodes detected by the patients from 49 to 30 per month and lowered the mean +/- SE self-monitored blood glucose level during symptomatic hypoglycemia from 51 +/- 2 mg/dl (2.8 +/- 0.1 mmol/l) to 46 +/- 3 mg/dl (2.6 +/- 0.2 mmol/l) (P < 0.01). It also reduced the proportion of low regularly scheduled self-monitored values that were symptomatic by approximately 33%. Thus as little as doubling the frequency of symptomatic hypoglycemia further reduced both the key epinephrine response and clinical awareness of developing hypoglycemia, changes reasonably expected to increase the risk of severe iatrogenic hypoglycemia in T1DM.
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PMID:Brief twice-weekly episodes of hypoglycemia reduce detection of clinical hypoglycemia in type 1 diabetes mellitus. 972 37

To test the hypothesis that glycemic thresholds for cognitive dysfunction during hypoglycemia, like those for autonomic and symptomatic responses, shift to lower plasma glucose concentrations after recent antecedent hypoglycemia in patients with type 1 diabetes mellitus (T1DM), 15 patients were studied on two occasions. Cognitive functions were assessed during morning hyperinsulinemic stepped hypoglycemic clamps (85, 75, 65, 55, and 45 mg/dl steps) after, in random sequence, nocturnal (2330-0300) hypoglycemia (48 +/- 2 mg/dl) on one occasion and nocturnal euglycemia (109 +/- 1 mg/dl) on the other. Compared with nondiabetic control subjects (n = 12), patients with T1DM had absent glucagon (P = 0.0009) and reduced epinephrine (P = 0.0010), norepinephrine (P = 0.0001), and neurogenic symptom (P = 0.0480) responses to hypoglycemia; the epinephrine (P = 0.0460) and neurogenic symptom (P = 0.0480) responses were reduced further after nocturnal hypoglycemia. After nocturnal hypoglycemia, in contrast to nocturnal euglycemia, there was less deterioration of cognitive function overall (P = 0.0065) during hypoglycemia based on analysis of the sum of standardized scores (z-scores). There was relative preservation of measures of pattern recognition and memory (the delayed non-match to sample task, P = 0.0371) and of attention (the Stroop arrow-word task, P = 0.0395), but not of measures of information processing (the paced serial addition task) or declarative memory (the delayed paragraph recall task), after nocturnal hypoglycemia. Thus, glycemic thresholds for hypoglycemic cognitive dysfunction, like those for autonomic and symptomatic responses to hypoglycemia, shift to lower plasma glucose concentrations after recent antecedent hypoglycemia in patients with T1DM.
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PMID:Impact of nocturnal hypoglycemia on hypoglycemic cognitive dysfunction in type 1 diabetes. 983 25

The pathophysiology of brain damage induced by severe hypoglycemia is still unknown. We experienced a case with type 1 diabetes and recurrent severe hypoglycemic coma who showed a central brain atrophy and an abnormal cerebrospinal fluid flow, suggesting normal pressure hydrocephalus. Following this case, the CSF flow was studied using 111In-DTPA cisternography in six consecutive diabetic patients admitted for repeated episodes of hypoglycemic coma. All the patients showed the central brain atrophy on computed tomography and four of them (67%) had the ventricular reflux, with delayed clearance of 111In-DTPA. Two patients with abnormal CSF flow showed cognitive dysfunction by WAIS or WAIS-R. In contrast, none of five randomly selected diabetic patients, without hypoglycemic coma showed abnormal CSF flow. Our results suggest the presence of normal pressure hydrocephalus in diabetic patients with recurrent hypoglycemic coma. It may associate with the cognitive dysfunction.
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PMID:Normal pressure hydrocephalus in diabetic patients with recurrent episodes of hypoglycemic coma. 1067 Sep 9

Hypoglycaemia is a common side effect of insulin therapy in type 1 diabetes. In patients with type 2 diabetes treated with blood-glucose lowering agents of the sulphonylurea group, hypoglycaemia is less frequent than in insulin-treated patients. In most patients strict metabolic control increases the risk of hypoglycaemia, but this risk may be reduced if patients are offered individualised insulin treatment in combination with active support and education. Previously experienced hypoglycaemic episodes and lack of endogenous insulin production are risk factors for repeated episodes. Patients with longstanding diabetes and loss of warning symptoms have increased risk of severe hypoglycaemic episodes, which may lead to loss of consciousness or convulsions. Driving performance is significantly disrupted at relatively mild hypoglycaemia, and persons with diabetes should not start driving when their blood glucose is in the 4-5 mmol/l range without prophylactic treatment. They ought to have carbohydrate-rich snacks easily available in the car and should stop driving if they feel hypoglycaemic. Repeated episodes of severe hypoglycaemia seem to be associated with cognitive dysfunction. When deciding the targets of blood-glucose lowering therapy, the risk of severe hypoglycaemia must be weighed against the beneficial effects of good metabolic control.
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PMID:[Hypoglycemia--a dreaded complication of diabetes]. 1147 34

Driving is a complex, multi-task activity that can be affected by cognitive impairment resulting from episodes of severe hypoglycaemia. Intensive insulin therapy increases the likelihood of severe hypoglycaemia but there have been few studies examining effects on driving skills. A survey carried out recently indicated that patients with type 1 diabetes had twice the incidence of driving accidents than their non-diabetic spouses or patients with type 2 diabetes. The motor accidents were associated with more frequent low blood glucose while driving and less frequent self-monitoring. In driving simulation tests it was found that driving has an intrinsic metabolic demand that can contribute to hypoglycaemia. Driving performance began to deteriorate at around 3.6 mmol/l but drivers frequently did not recognise and failed to treat the hypoglycaemia. Those who did self-treat had more driving relevant symptoms and less neuroglycopenia quantified by EEG alpha-theta differences. Patients should be recommended not to begin driving if blood glucose is below 4.5 mmol/l and should not continue to drive if they suspect that blood glucose has fallen below 4 mmol/l while driving. If hypoglycaemia is suspected patients should immediately pull off the road, measure blood glucose if possible, treat themselves as necessary and not resume driving until glucose and cognitive-motor function return to normal. The problems of driving and hypoglycaemia should be discussed with patients with diabetes and behavioural interventions instigated. To this end, Blood Glucose Awareness Training (BGAT) and Hypoglycaemia Anticipation, Awareness and Treatment Training (HAATT) have been developed and shown to markedly reduce incidence of driving mishaps.
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PMID:Driving mishaps and hypoglycaemia: risk and prevention. 1159 97


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