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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 34-year-old man presented with classic glucagonoma syndrome manifested by weight loss, dermatitis, stomatitis, anemia, and mild diabetes mellitus. The diagnosis of glucagonoma was made by light and electron microscopic demonstration of a metastatic alpha cell carcinoma in a liver biopsy specimen. Plasma glucagon concentration was abnormally high. The patient also had symptoms and signs of involvement of the central nervous system. Radionuclide and CAT scans of the brain, negative CSF cytology and myelography excluded the possibility of metastases or other space-occupying lesions. Glucagon was demonstrated in the CSF. We postulate that the neurologic symptoms were due to direct or indirect effect of this hormone on the brain. Following therapy with streptozotocin and 5-fluorouracil, the patient had a subjective and objective clinical and hormonal remission of his disease including amelioration of his neurological impairment.
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PMID:Neurologic involvement in glucagonoma syndrome: response to combination chemotherapy with 5-fluorouracil and streptozotocin. 22 32

In a series of examinations of more than 1000 psychiatricneurological patients we tried to state the effects of diabetes mellitus on the nervous system. We attempted to diagnose the diabetic metabolic error by means of using the oral glucose tolerance test (100 g glucose), the plasma insulin levels and many other laboratory-technical examinations (altogether about 23 000 individual tests). It was found that 21,6% of the patients had a pathological glucose tolerance, 29.6% of them had a pathological insulin response and 5,5% of them showed a known and manifest diabetes mellitus. The comparison between the number of patients with a metabolic disturbance and the frequency of sick persons to be expected epidemiologically shows that an influence exercised by the diabetic metabolism may be stated in neurological and psychic disturbances of cerebral sclerosis and polyneuropathy. The central syndromes are more frequent than the peripheric ones. Mainly low plasma insulin is present. As a rule, pathological results may be seen more often during pathological glucose tolerance in electroencephalography, pneumencephalography, CSF-examinations, personality and intelligence states. This suggests that a diffuse disturbance upon the nervous system comes from the diabetic metabolism, without any acute metabolic disturbance which we did not find among our patients. This disturbance is evident clinically as so-called diabetic polyneuropathy and also encephalopathy. In opposition to that very often pathological changes can be seen by technical research methods in other neurological and psychiatric diagnoses without influencing essentially the autonomous progress of the psychiatricneurological illness.
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PMID:[Diseases of the central nervous system in diabetes mellitus]. 61 60

Blood and CSF gases, as well as the level of lactate and pyruvate in blood and CSF were determined in 43 cases. of severe stroke with softening of the brain. It transpired that the CSF lactate level is the best prognostic indicator of survival. CSF values above 2,5 mMol/1 in apoplexy imply a very unfavourable prognosis. The CSF lactate level is also a very useful prognostic indicator in patients suffering from diabetes and/or uraemic metabolic disorders. As the determination of CSF lactate presents no tecnical difficulties and furnishes valuable prognostic information it would merit inclusion as a routine procedure in relevant cases.
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PMID:[Lactacidosis of the cerebrospinal fluid in apoplexy as indicator of prognosis (author's transl)]. 66 6

In spite of a history of more than 100 years, the pathoaetiology of multiple sclerosis is still unknown today. Research is based on three working hypotheses, i.e. on an immunopathological disease origin, on the conception that MS, as an infectious disease, is caused by a specific pathogen (slow virus infection) and on the assumption of a disturbance of basal metabolism or utilisation. The present position of the scientific foundation of the working hypotheses is presented in detail and supplemented by the results of our own investigations. Of particular interest are the geomedical studies which show that MS occurs more frequently in temperate climatic regions. In Europe, a latitude of 46 degrees forms a conspicuous boundary; in the USA this boundary is found at 38 degrees. North of this line there is a morbidity rate of 30 to 60 patients per 100 000 inhabitants, while south of it 15 cases at most per 100 000 inhibitants are found. Asia, especially in China and Japan, and tropical countries, where Multiple Sclerosis is practically unknown in the native populations, are exceptions. The observation that immigrants from areas with a low MS incidence into regions with a high risk of MS fall ill with the disease after years remains also unexplained. These peculiarities have given rise to the consideration whether there is a still unknown factor in the soil of high-risk areas or a specific pathogenic spectrum. In this connection, the question is also discussed whether the risk of MS in northern countries is associated with the excessive consumption of animal fat. The possible therapeutic and prophylactic significance of unsaturated fatty acids is emphasized. Our own results with the Schilling-test, determination of gastric acids, rubella titres in serum and cerebrospinal fluid, the immunofluorescence test of the serum and CSF, determination of tissue antigens (HLA) in families with multiple incidence of Multiple Sclerosis are discussed. On evaluation of a large series of patients, it is striking that Multiple Sclerosis and juvenile diabetes seem to be mutually exclusive (Schrader). Likewise, in MS statistics no other immunopathologic disease such as rheumatic diseases or bronchial asthma was found. Interestingly, also in 400 MS patients examined, hyperuricaemia or gout, which are widespread among the populace, were not found in a single case.
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PMID:[Pathogenesis of multiple sclerosis. Work-hypotheses and experimental data]. 84 79

Experience in the management of 100 cases of acromegaly is described. Three quarters of these had been referred directly to the endocrine clinic at the Middlesex Hospital. The remainder were referred from the Royal Post-graduate Hospital because they were thought unsuitable for yttrium implantation. The patients were studied by clinical assessment of severity, by measurement of basal growth hormone levels on three separate mornings, and by a review of possible complications. Particular attention was paid to diabetes, hypertension, cardiomegaly, respiratory, vascular and skeletal changes as well as visual field defect. Aggressive treatment was recommended in 77 patients. It was not recommended in the remainder on account of age, intercurrent illness or the apparent mildness of the condition. Fifty-nine patients were treated by trans-sphenoidal hypophysectomy. In 46 of the 59 patients the mean basal growth hormone level has been reduced to 5 ng/ml or less. In 39 this followed operation, in five operation and subsequent X-ray therapy and in two operation and the continuing effect of previously implanted yttrium. Of these 46 patients in whom the growth hormone level has been reduced to normal, 26 do not show any deficiency of anterior pituitary trophic hormones, 13 have gonadotrophin defect (in eight of these it was present before the operation) and seven require full replacement therapy. One patient died at home six weeks after the operation from a pulmonary embolus. There was one case of CSF rhinorrhoea which stopped spontaneously and three of acute frontal sinusitis. Trans-sphenoidal hypophysectomy is shown to be an effective means of treating acromegaly. If the basal level of growth hormone is not reduced to normal by six weeks after operation, it is recommended that a course of X-ray therapy should be given. This does not apply if irradiation has been used before operation.
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PMID:The treatment of acromegaly with special reference to trans-sphenoidal hypophysectomy. 115 91

Magnesium is an essential cofactor for many enzymatic reactions, especially those involved in energy metabolism. Deficits of magnesium are prevalent due to inadequate intake or malabsorption and due to the renal loss of magnesium that occurs in certain disease states (alcoholism, diabetes) and with drug therapy (diuretics, aminoglycosides, cisplatin, digoxin, cyclosporin, amphotericin B). Protracted deficits of magnesium in humans and animals result in neurological disturbances, including hyperexcitability, convulsions and various psychiatric symptoms ranging from apathy to psychosis, some of which can be reversed with magnesium supplementation, others requiring correction of the dysregulation mechanism. Although the role of magnesium in neuronal function is not completely understood, a lowering of CSF or brain magnesium can induce epileptiform activity and there is an association between decreased CSF magnesium and the development of seizures. CSF concentrations of magnesium are normally higher than magnesium plasma ultrafiltrate (diffusible) concentrations due to the active transport of magnesium across the blood-brain barrier. Under conditions of magnesium deficiency, CSF concentrations decline, although this decline lags behind and is less pronounced than the changes observed in plasma magnesium concentrations. Decreases in CSF magnesium concentrations correlate with the alterations observed in extracellular brain magnesium concentrations in animals following the dietary deprivation of magnesium. CSF magnesium concentrations can readily be repleted following magnesium supplementation, although high dose magnesium therapy, such as that used in the treatment of convulsions in eclampsia, will only increase CSF magnesium concentrations to a very limited degree (approximately 11-18 per cent) above physiological concentrations. Greater increases in CSF magnesium may occur in neonates since neonatal swine, following treatment with magnesium, have CSF magnesium concentrations that are similar to their plasma concentrations. There has been a recent resurgence of interest in magnesium deficiency and its neurological consequences due to the finding that magnesium, at physiological concentrations, blocks N-methyl-D-aspartate (NMDA) receptors in neurones. NMDA receptors are normally activated by glutamate and/or aspartate which represent the principal neurotransmitters for excitatory synaptic transmission in vertebrate CNS. Magnesium deficiency produces epileptiform activity in the CNS which can be blocked by NMDA receptor antagonists. Other mechanisms, including alterations in Na+/K(+)-ATPase activity, cAMP/cGMP concentrations and calcium currents in pre- and postsynaptic membranes, may also be at least partially responsible for the neuronal effects associated with low brain magnesium. Further studies are necessary to increase our understanding of the neurological implications of magnesium deficit in the central nervous system.
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PMID:Brain and CSF magnesium concentrations during magnesium deficit in animals and humans: neurological symptoms. 129 67

Pancreatic beta cell destruction in the non-obese diabetic (NOD) mouse is mediated by T lymphocytes and macrophages and accelerated by cyclophosphamide. We purified pancreatic T lymphocytes from the NOD mouse for comparative phenotypic and functional analysis with T lymphocytes from spleen, peripheral blood and regional lymph nodes. Pancreatic T lymphocytes from NOD-Wehi mice, which have an incidence of spontaneous diabetes of less than 5%, had a CD4:CD8 ratio of 1.25 +/- 0.23 compared with 2.44 +/- 0.31 for peripheral blood lymphocytes. After cyclophosphamide, the CD4:CD8 ratio of pancreatic lymphocytes increased to 2.30 +/- 0.24 at day 7. T lymphocytes bearing IL-2 receptors increased two- to three-fold in number and their secretion of GM-CSF/IL-3 and IFN-gamma increased to a maximum on day 7. Pancreatic insulin content and mRNA levels declined sharply between days 10 and 12, at which time the majority of pancreatic T lymphocytes in hyperglycaemic mice were CD8+ (CD4:CD8 ratio 0.63 +/- 0.04 compared to 4.14 +/- 1.05 in peripheral blood). The pancreatic T lymphocyte CD4:CD8 ratio in prediabetic NOD-Lt mice, which have an incidence of spontaneous diabetes of about 60% at 150 days, was similar to that in untreated NOD-Wehi mice, but 25% of their pancreatic CD8 T lymphocytes were IL-2-receptor positive. Thus, significant changes in the phenotype of NOD pancreatic T lymphocytes following cyclophosphamide were not reflected in peripheral blood or spleen T lymphocytes. The earliest change after cyclophosphamide was an increase in activated, predominantly CD4+ T lymphocytes; with the development of beta cell destruction and hyperglycaemia, pancreatic T lymphocytes were, as in human IDDM, predominantly CD8+.
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PMID:Characterization of pancreatic T lymphocytes associated with beta cell destruction in the non-obese diabetic (NOD) mouse. 167 32

Multi-infarct dementia (MID) indicates a dementia disorder primarily caused by multiple cerebral infarcts. Since other pathogenetic mechanisms cause vascular dementia we evaluated clinical, CT scan and CSF neurochemical parameters of 134 MID and 67 PVD (probable vascular dementia) patients. We found no differences with regard to the presence of major risk factors. Only TIA/stroke episodes and focal neurological signs were significantly more frequent in MID than in PVD cases, an anticipable result on the basis of MID definition. CT scan findings showed a prevalence of subcortical with respect to cortical lesions in both groups, with a higher frequency in MID patients. Subjects with deep infarcts more frequently showed TIA/stroke episodes and diabetes mellitus. No differences were detectable in CSF monoamine metabolite levels. We conclude that in the majority of vascular dementias subcortical damage seems to have a major pathogenetic role.
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PMID:Is multi-infarct dementia representative of vascular dementias? A retrospective study. 169 87

The relative percentage of patients over 60 years who underwent operations in our clinic has greatly increased from 18% in 1874 to 27% in 1989. Postoperatively, difficulties may also result from additional medical problems, which may be cardiovascular, pulmonary, metabolic (especially diabetes mellitus), increased thromboembolism in origin as well as from the reduced tendency to neurological recovery in elderly patients. On the other hand, advances in diagnostics and surgical treatment often make it possible to help even these patients effectively today. The clinical pictures which are especially frequent in our hospital are specified below. Disc herniations: Soft nucleus-pulposus herniations occur in every age group. In elderly patients, the osseous constriction of the lumbar canal (especially by spondylarthrosis) often leads to spinal claudication. Functional myelography with myelograms taken in the sitting and the standing position is important for preoperative appraisal. On the basis of the clinical/neuroradiological findings, it may be decided whether a selective or an extended decompression is necessary. Larger-scale decompressions are mostly possible in this age group without postoperative instability, with good results in more than 80% of the cases. In our clinic, anterior microsurgical decompression without graft is the most frequently used procedure in cervical disc herniations/spondylosis, a method which is well tolerated by spinal cord and nerve roots: 75% simple anterior discectomies/spondylectomies compared to only 25% classical Cloward operations with bone grafts. We use intervertebral bone grafts only in severe spondylosis and/or instabilities, if necessary in combination with metal plates (e.g. in the context of cervical myelopathy). Craniocerebral injuries: Epidural hematomas and CSF fistulae, but also circumscribed space-occupying contusions have a relatively favorable prognosis in every age group. The older the patient, the more serious is the acute subdural hematoma, which is often associated with extensive contusions, although surprisingly good recoveries are occasionally possible postoperatively even here. Detailed scrutiny of all prognostically relevant factors is important. In borderline situations we give the patient a chance in order to take later action, depending on the course. Chronic subdural hematomas are especially frequent and readily dealt with surgically in patients over 60 years. The simple borehole drainage to the outside is often sufficient. In extensive excreting membranes, which are especially frequent in elderly patients, we prefer today a subdural-peritoneal drainage for six to eight weeks to the very much more burdensome craniotomy: The relatively simple operation allows an early mobilization and almost always a prompt healing. Hydrocephalus male resorptivus is also very much more frequent in this age group.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Neurosurgery in old age. I: Significance of the problem--herniated disk, spinal canal stenosis--craniocerebral injuries--chronic subdural hematoma--resorptive hydrocephalus]. 174 88

The cases of three patients with focal seizure associated to non-cetotic hyperglycemia are reported. Two patients presented motor epilepsy partialis continua (EPC). One case showed EPC as the first clinical manifestation of diabetes mellitus. Neurological exam was normal in all patients. CT and CSF were normal in the cases they were evaluated. Scalp EEG registered during a focal seizure revealed a bilateral temporal spiky activity. Glycemia levels were 455, 660 and 439 mg/dl. Two patients presented hyponatremia simultaneously. No patients had benefit with phenytoin or diazepam, and one patient got worse after them. Seizure control occurred after insulin and electrolytic treatment. It is important to diagnose this type of condition to avoid changes of non-cetotic hyperglycemia syndrome in a hyperosmolarity and coma state, disturbance which brings a higher mortality.
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PMID:[Focal seizures in nonketotic hyperglycemia]. 184 95


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