1/53. Effects of blood glucose levels on performance in activities of daily living: a case example of a diabetic man with an acquired brain injury.Dysfunctional blood glucose regulation and sequelae of acquired brain injury (ABI) can affect behavioural training in brain injury rehabilitation. The relationship is examined between blood glucose levels and performance in three activities of daily living (ADL) skills (showering, toileting, and dressing) in a 21-year-old male with ABI and Type I diabetes mellitus. Multiple daily glucometer readings were obtained both pre- and post-treatment. Skills training involved graduated prompting and reinforcement to develop independence in ADLs. Assessment and teaching occurred initially in hospital, and then was presented at home. Results show a strong negative relationship between daily fluctuations in blood glucose levels and performance; no relationship was found between daily mean levels and performance. Implications for treatment approaches for diabetic individuals with ABI are discussed.- - - - - - - - - - ranking = 1keywords = brain (Clic here for more details about this article) |
2/53. Central brain herniation secondary to juvenile diabetic ketoacidosis.We present the CT, MR, and autopsy findings of central brain herniation in a 9-year-old boy undergoing treatment for diabetic ketoacidosis (DKA). Severe cerebral edema resulting in central brain herniation is an uncommon complication of the treatment of DKA but carries with it high morbidity and mortality. Radiologic imaging and autopsy findings in this case revealed striking infarctions of central brain structures.- - - - - - - - - - ranking = 1.1666666666667keywords = brain (Clic here for more details about this article) |
3/53. Normal pressure hydrocephalus in diabetic patients with recurrent episodes of hypoglycemic coma.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.- - - - - - - - - - ranking = 0.5keywords = brain (Clic here for more details about this article) |
4/53. Bilateral optic atrophy following diabetic ketoacidosis.diabetic ketoacidosis (DKA) can result in neuropathic abnormalities of the somatic and the autonomous nervous systems. We report the case of a 50-year-old man with Type 1 diabetes of 20-year duration who after severe DKA lost vision in his right eye and only retain partial vision in his left. This case demonstrates that optic neural tissue is vulnerable to haemodynamic and metabolic complications of DKA.- - - - - - - - - - ranking = 0.038845942812329keywords = nervous system (Clic here for more details about this article) |
5/53. Acute painful diabetic neuropathy: two patients with recent insulin-dependent diabetes mellitus.Two young men developed an acute painful peripheral neuropathy a few weeks after being diagnosed to suffer from an insulin-dependent diabetes mellitus. In both cases, peripheral nerve biopsy exhibited a few features of acute axonal degeneration. Additionally, in the first case there was a lymphocytic infiltrate around an endoneurial capillary, and in the second case there were several mast cells in the endoneurium of every fascicle examined. A few months later, the acute pain had disappeared in both cases. Only a few cases of acute painful diabetic neuropathy have been reported so far. A vascular origin seems unlikely and metabolic disorders are probably due to a contemporary severe weight loss. An auto-immune mechanism is an alternative explanation.- - - - - - - - - - ranking = 26.846986647653keywords = metabolic disorder (Clic here for more details about this article) |
6/53. Mutation analysis of the human adipocyte-specific apM-1 gene.BACKGROUND: The aim of this study was to analyse the human adipocyte-specific apM-1 gene for sequence variations. methods: sequence analysis was performed in 344 randomly chosen blood samples using a capillary sequencer. RESULTS: Whereas no mutations were detected in intronic regions and in 2.7 kb of the promoter, two sequence variations were found within the coding sequence of apM-1. For both mutations, a polymerase chain reaction-(PCR) based restriction fragment length polymorphism (RFLP) analysis was developed, which provided a rapid screening method. A conservative T --> G transition at nucleotide 45 within exon-2 [Gly15Gly] was detected with an allelic frequency of 0.9 for the wild-type allele and 0.1 for the mutated allele. In addition, a missense point mutation at nucleotide 331 within exon-3 [Tyr111His] was detected with an allelic frequency of 0.97 for the wild-type allele and 0.03 for the mutated allele. This mutation replaces a tyrosine by an histidine within the carboxyterminal globular domain of apM-1. Concerning the Gly15Gly polymorphism, the TT genotype was found in 275 subjects (79.9%), the TG genotype in 67 subjects (19.5%) and the GG genotype in 2 subjects (0.6%): one with maturity onset diabetes of young age (MODY-diabetes) and one with Lipoatrophic Diabetes Syndrome (LPDS). Concerning the Tyr111His polymorphism, the TT genotype was found in 328 subjects (95.4%), the TC genotype in 15 subjects (4.3%) and the CC genotype in 1 subject (0.3%). CONCLUSION: The existence of two yet unknown mutations within the apM-1 gene was demonstrated and RFLP analysis was established for rapid screening. Well defined cohorts of patients are necessary to determine the putative role of apM-1 gene mutations in the pathogenesis of metabolic disorders.- - - - - - - - - - ranking = 26.846986647653keywords = metabolic disorder (Clic here for more details about this article) |
7/53. Ketoacidosis accompanied by epileptic seizures in a patient with diabetes mellitus and mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS).We herein report a rare case of MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes) and diabetes mellitus with ketoacidosis. An 18-year-old female patient was diagnosed to have diabetes mellitus and insulin therapy was thereafter initiated. At 26 years of age, she was hospitalized for diabetic ketoacidosis, soon followed by a loss of consciousness, left-sided dysmetria, and ataxic speech. MELAS was diagnosed because of the presence of ragged red fibers in a muscle biopsy. At 33 years of age, she was admitted to our hospital because of ketoacidosis and partial status epilepticus. A blood gas examination revealed as follows; arterial pH, 6.88; bicarbonate, 2.1 mmol/l; base excess - 29.8 mmol/l. The serum level of glucose had also increased to 30 mmol/l. The serum levels of lactate and B-hydroxybutyrate were elevated to 11.4 mmol/l and 1,990 micromol/l, respectively. Ketoacidosis improved by fluid replacement and continuous intravenous insulin infusion. A brain MRI demonstrated hyperintensity areas on FLAIR images in the bilateral temporal lobes and the cerebellum. A proton MRS demonstrated the abnormal lactate accumulation in the bilateral temporal and occipital lobes. Since epileptic seizures are rare in patients with diabetic ketoacidosis, such seizures may indicate the existence of melas syndrome.- - - - - - - - - - ranking = 0.16666666666667keywords = brain (Clic here for more details about this article) |
8/53. anorexia nervosa, diabetes mellitus, brain atrophy, and fatty liver.An increased number of diabetes mellitus cases followed by the development of anorexia nervosa have been reported. In this report, the opposite has been observed in the case of a patient with anorexia nervosa who later developed insulin-dependent diabetes mellitus, associated with brain atrophy and fatty liver. The patient was treated with insulin, amitriptylene, and behavior modification. Significant improvement was noted on this regimen.- - - - - - - - - - ranking = 0.83333333333333keywords = brain (Clic here for more details about this article) |
9/53. Potential risk of serious oral infections in the diabetic patient: a clinical report.Diabetes has many manifestations, including increased vulnerability to bacterial and fungal infections, that may be of concern to the dental profession. Oral candidosis and other opportunistic fungal infections may be early, nonspecific signs of uncontrolled diabetes. Rhinocerebral involvement often extends to the paranasal sinuses, pharynx, palate, orbit, and brain, causing severe tissue destruction and necrosis. This clinical report describes a young woman with diabetes who developed mucormycosis of the maxilla. Tissue destruction resulted in loss of the entire premaxilla, the anterior half of the hard palate, and all maxillary teeth except for the right and left second molars. An interim clear acrylic resin prosthesis was fabricated to restore facial contours and speech and to allow mastication. This prosthesis subsequently was duplicated, and teeth were added for improved lip support, esthetics, and mastication.- - - - - - - - - - ranking = 0.16666666666667keywords = brain (Clic here for more details about this article) |
10/53. Prehospital cardiac arrest in diabetic ketoacidemia: why brain swelling may lead to death before treatment.An adolescent is reported with type 1 diabetes mellitus and diabetic ketoacidemia (DKA) who died from brain herniation prior to treatment with intravenous fluids and intravenous insulin. The pathophysiology of raised intracranial pressure (ICP) and water intoxication is discussed. As DKA evolves, water and electrolyte losses are replaced by very hypotonic fluids taken orally, leading to a physiologic excess of free water that would cause brain swelling prior to treatment. central nervous system acidosis may interfere with normal compensatory mechanisms that help prevent small increases in ICP. The pathophysiology of pre-treatment brain swelling has important implications for rehydration with intravenous fluids and treatment with insulin. Prevention of DKA is paramount as well as complete postmortem evaluation of patients who die from this disease.- - - - - - - - - - ranking = 1.205512609479keywords = brain, nervous system (Clic here for more details about this article) |
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