Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 29-year-old man with Cockayne's syndrome (CS), presenting reversible ischemic neurological deficit is reported. In his past history, hearing disturbance developed at 6 years old and visual disturbance at 12 years old. His parents have consanguinious marriage. He came to our hospital complaining of right-sided hemiparesis and speech disturbance. He was 115.8 cm tall and his weight 20 kg. The characteristic manifestation of CS, i. e., dwarfism, mental retardadation, cachectic feature, retinal atrophy, neural deafness and calcification of bilateral basal ganglia were all noticed. A CT scan on admission revealed marked brain atrophy as well as the intracranial calcifications, while no lesions compatible with his neurological findings were detected. Cerebral ischemic state was mostly suspected. Following up with conservative therapy by the use of fibrinolytic agent, his neurological deteriorations disappeared on the 4th hospital day. Cerebral angiograms showed stenotic lesions of both C1-C2 portion of the left internal carotid artery and the right middle cerebral artery, and the aneurysm in the right internal carotid artery. Such atherosclerotic vascular change as observed in the cerebral angiograms in this case have progressed rapidly for his age. In this case, diabetes mellitus and hyperlipoproteinemia such as increased total cholesterol, increased triglyceride, decreased HDL and increased apoprotein B and C II were complicated for the risk factor of the atherosclerosis. It's controversial that early progress of atherosclerosis is due to ideopathic original feature of CS or to the secondary change from these complications.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cockayne's syndrome presenting cerebral ischemic attack: case report]. 379 Mar 68

30 patients aged between 45 and 78 years and who had suffered from transient global amnesia (TGA), were seen at the Department of Neurology, Pordenone Public Hospital, in the period 1978 to 1982. 25 patients had one or more risk factors for cerebrovascular disease, such as hypertension, cardiac abnormalities, diabetes and hyperlipidemia. EEG examination revealed abnormal activity only in 7 patients. Brain Computed Tomography showed cerebral atrophy in 10 and hypodense lesions in 3 patients. 16 patients had been followed up for a mean interval of 20 months. During the follow-up period, 4 patients had recurrent TGA and one had a transient ischemic attack in the vertebrobasilar arterial system. In the follow-up group, 15 patients showed permanent memory impairment. The high incidence of risk factors for cerebrovascular disease seems to confirm that TGA is probably due to transient cerebral ischemia. The high rate of permanent memory impairment, almost always connected with the coexistence of cerebrovascular risk factors, is not in agreement with the postulated good prognosis of TGA.
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PMID:Transient global amnesia. 651 86

A case of reversible catatonia in a well controlled insulin-dependent diabetic is described. The course of catatonia was characterized by very high CSF lactate values (serial semiautomatic determinations) during more than one month, beyond the clinical recovery. The CSF lactate elevations seem to reflect cerebral hypoxia. The uncommon coincidence of diabetes with cerebral atrophy, mental weakness, and perceptive deafness migh suggest the classification of this case of diabetes in the group 'associated with certain conditions and syndromes'.
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PMID:Catatonia with high CSF lactate in a case of diabetes with associated conditions. 722 10

CT examination in 100 patients affected by chronic cerebrovascular insufficiency showed a normal picture in 16 cases, while 84 subjects showed different degrees of atrophy, generalised and focal, controlateral or sometime omolateral to the infarct, with differing patterns. The mean age of subjects with normal CT was significantly lower in comparison with patients with definite atrophy. Besides the neurological picture and the time course, the patients' psychiatric status was also assessed: no definite relationship seems to exist between psychiatric disturbances and brain atrophy. Pseudobulbar syndrome was found in 46 cases and many of them showed cortical and mainly ventricular atrophy. This picture was very seldom found in patients with vertebro-basilar insufficiency. Localised cortical atrophy, on the contrary, was often associated with ischaemic stroke. The incidence of predisposing risk factors (hypertension, diabetes mellitus or high lipid levels) was greater in subjects with brain atrophy and older age than in patients with normal CT scan.
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PMID:[CT findings in chronic cerebrovascular insufficiency (author's transl)]. 729 86

The cranial computerized axial tomography (CAT) findings in groups of patients with epilepsy, migraine, hypertension, and other general medical disorders have been reviewed to assess the frequency and patterns of focal and diffuse brain damage. In addition to demonstrating focal lesions in a proportion of patients with seizures and in patients presenting with a stroke, the CAT scan showed a premature degree of cerebral atrophy in an appreciable proportion of patients with long-standing epilepsy, hypertension and diabetes, and in some patients with migraine, valvular and ischaemic, heart disease, chronic obstructive airways disease, and chronic renal failure. The value of CAT as a means of screening for brain damage in groups of individuals at risk is discussed.
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PMID:Computerized axial tomography in the detection of brain damage. 2. Epilepsy, migraine, and general medical disorders. 746 20

MRI findings and risk factors for vascular dementia were evaluated with multi-variate analysis in 96 multi-infarct patients without dementia and 40 multi-infarct patients with dementia (MID). Only subjects with small infarcts in the territory of the perforator artery or deep white matter were studied. The diagnosis of MID was diagnosed according to DMS-III criteria and Hachinski's ischemia score. Location and area of patchy high-intensity areas including small infarcts, the degree of periventricular high intensity (PVH), and the degree of brain atrophy were examined with MR images. Independent variables were: history of hypertension, diabetes mellitus, other complications; systolic and diastolic blood pressure, atherosclerotic index, hematocrit, history of smoking, level of education, and activities of daily life (ADL). Hayashi's quantification method II was used to analyze the data. The most significant correlation was found between history of hypertension and dementia (partial correlation coefficient: 0.39). Significant correlations were also found between ADL and dementia (0.32), between thalamic infarction and dementia (0.31), and between PVH and dementia (0.27). Age, brain atrophy index, and history of diabetes mellitus contributed little to dementia. The contribution to dementia did not differ significantly between right and left patchy high-intensity areas on MR images. Location of infarcts, except for bilateral thalamic infarcts and large PVH, contributed little to dementia. Thus it would be difficult to base a prediction of the prevalence of vascular dementia on MRI findings. However, both hypertension and ADL contribute to vascular dementia and both are treatable, which may be significant for the prevention of dementia.
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PMID:[Difference in MRI findings and risk factors between multiple infarction without dementia and multi-infarct dementia]. 749 60

This longitudinal study was performed to clarify the relation between brain atrophy and common carotid hemodynamics. A total of 147 patients, including 70 males and 77 females, who had neither neurologic deficits nor organic lesions on computed tomography of the brain, were enrolled in this study. The ages of the patients ranged from 47 to 76 years (mean: 62 years) at the first diagnosis of brain atrophy. The patients were divided into three groups: 66 controls without hypertension or diabetes mellitus (Group I), 60 with hypertension (Group II) and 21 with both hypertension and diabetes mellitus (Group III). Brain atrophy was diagnosed by caudate head index (CHI). Mean blood flow volume (BF) at the right common carotid artery was measured by an ultrasonic quantitative flow measurement system. Both CHI and BF were measured twice at a mean interval 6.5 years. Increment in CHI per year (delta CHI) and decrement in mean blood flow volume per year (delta BF) were calculated. delta CHI of Group I and Group II had a significant relation with aging. delta CHI of Group III showed a larger increase than that of both Group I and Group II in subjects in the sixties. delta CHI had a significant relation with delta BF in each group. These results indicate that complication of both HT and DM, or decrement in mean blood flow volume may cause brain atrophy to progress.
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PMID:[A longitudinal study of brain atrophy and its relation with background factors and common carotid hemodynamics]. 769 44

To estimate the relationship between aging, dementia and changes observed on magnetic resonance imaging (MRI) seen in elderly patients with cerebral thrombosis, MRI findings in 103 patients with an initial stroke event (thrombosis group) were compared with those of 37 patients with hypertension/diabetes (high risk group) and 78 patients without those disorders (low risk group). In addition to the causative lesions in the thrombosis group, periventricular hyperintensities (PVH), spotty lesions (SL), silent infarctions (SI), ventricular dilatation (VD), and cortical atrophy (CA) were analyzed in these groups. Infarctions located in the internal capsule/corona radiata were the most frequent causative lesion. Compared to the low risk group, a high incidence of patchy/diffuse PVH, SI, and severe CA was seen in both the thrombosis group and the high risk group. Widespread PVH and multiple SL increased with age in the thrombosis group, while severe CA was seen in each group. SI and VD tended to increase after age 60, though they were not significant. Dementia, diagnosed in 40 out of 78 patients, increased with age. Multivariate analysis revealed the degree of the effects of MRI findings on dementia to be marked in PVH, brain atrophy, causative lesions, and SL, in that order. These results indicated that diffuse PVH and brain atrophy, developing with age, promoted dementia in the elderly with vascular lesions. Moreover, they suggested that a variety of silent brain lesions recognized on MRI other than infarction can affect symptoms in the elderly.
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PMID:[Brain MRI findings in patients with initial cerebral thrombosis and the relationship between incidental findings, aging and dementia]. 772 91

Aim of this study was to investigate a) if through Magnetic Resonance Imaging (MRI) it was possible to reveal cerebral alterations in patients with insulin-dependent diabetes mellitus (IDDM); b) if there was any correlation with hypoglycemic episodes, glycometabolic control, microvascular alterations and diabetic peripheral neuropathy. For this purpose ten ID-DM patients under treatment with human insulin, aged 19-30 yr with the disease, the duration being from 1 to 19 yr, were investigated by MRI using a Philips Gyroscan. Spin Echo sequences were used with images in T1 T2 in sagittal and axial planes. To measure the ventricular dilatation the cerebroventricular index (CVI) was evaluated. The MRI has put in evidence in 7/10 patients a dilatation in the lateral ventricles and subarachnoidal spaces of the cerebral vault and the cerebellum clearly due to cerebral atrophy. The CVI mean values (34.78 +/- 2.92) were statistically (p < 0.001) higher in diabetic patients respect to control subjects (CVI mean values 27.5 +/- 1.58). These alterations did not present clear correlations with the degree of glycometabolic control, duration of disease, number of symptomatic hypoglycemic episodes and threshold for hypoglycemic symptoms, retinal microvascular alterations, microalbuminuria, diabetic peripheral neuropathy. The clinical or functional relevance of CVI changes and the exact pathogenic mechanism remains to be clarified.
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PMID:Evidence by magnetic resonance imaging of cerebral alterations of atrophy type in young insulin-dependent diabetic patients. 793 Mar 74

We report a patient with mitochondrial encephalomyopathy presenting parkinsonism, as well as her brother who had ataxia but not parkinsonism. Both patients had myopathy, deafness, and insulin-dependent diabetes mellitus. The proband was a 55-year-old woman, who has developed progressive difficulty in walking and slowness of movement since 53 years of age, becoming bed-ridden at 55. Neurological examination revealed mental impairment, a masked face, Myerson's sign, vertical supranuclear ophthalmoplegia, and severe sensorineural deafness, hypokinesia, rigidospasticity, and weakness of the extremities. But tremor and cerebellar ataxia were absent. Her 48-year-old brother gradually developed weakness of the lower extremities and drunken gait over a few years. On neurologic examination, vertical supranuclear ophthalmoplegia, moderate sensorineural deafness, and cerebellar ataxia were present, but parkinsonism was absent. Three other siblings were reported to have died in early childhood. Cranial MR imaging showed cerebral atrophy and mild atrophy of the cerebellar vermis as well as mild periventricular hyperintensities in T2-weighted images in both patients. However, no infarcts were seen. Laboratory investigations revealed slightly elevated lactate and pyruvate levels in the proband and elevation of pyruvate in her brother. A biopsy specimen obtained from the quadriceps muscle showed ragged-red fibers with modified Gomori trichrome staining, and a decrease of complex I+III and complex II+III activity in the proband. Mitochondrial DNA (mtDNA) analysis using the polymerase chain reaction and restriction enzyme Apa I showed a point mutation in the tRNA(Leu)(UUR)) gene (an A to G transition at nucleotide 3243) in both patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Mitochondrial encephalomyopathy associated with parkinsonism and a point mutation in the mitochondrial tRNA(Leu)(UUR)) gene]. 802 31


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