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The records of 113 consecutive patients with a suspected gastrointestinal motility disorder referred between January 1988 and July 1991 were retrospectively reviewed. The aims were to identify the prevalence of autonomic dysfunction in those with or without associated neurological disease and to determine the diagnostic value of testing for autonomic dysfunction. All patients had gastrointestinal manometry (3 hours fasting, 2 hours fed), 94 of 113 underwent testing of sympathetic adrenergic and cholinergic function and cardiovagal cholinergic function. All tests were scored in a standard manner. There was a significant (p < 0.05) but modest (r = 0.28) rank correlation between autonomic and motility scores. This correlation was stronger (r = 0.67, p = 0.01) in diabetic patients. The number of patients in each group with autonomic dysfunction was as follows: irritable bowel syndrome nine of 33, idiopathic upper gastrointestinal dysmotility six of 21, diabetes mellitus nine of 13, identified non-diabetic neurological syndromes six of nine, postvagotomy or abdominal surgery three of 11, and myopathic pseudo-obstruction two of seven. Autonomic testing is useful in the assessment of autonomic involvement outside the gastrointestinal tract. Logistic discriminant analysis showed that autonomic function testing did not add to the diagnostic value of motility tests in distinguishing between patients with and without irritable bowel syndrome, although a slight improvement was indicated for identifying neuropathic dysmotilities. Thus, the aetiological role of general autonomic dysfunction in irritable bowel syndrome and idiopathic and postvagotomy dysmotilities deserves further study. The addition of autonomic function tests does not add substantially to the diagnostic accuracy of clinical, radiological, endoscopic, and manometric techniques in most patients referred for evaluation of a suspected motility disorder.
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PMID:Autonomic dysfunction in gastrointestinal motility disorders. 847 90

The serum concentration of lipoprotein(a) [Lp(a)], lipids, lipoproteins, apolipoprotein A-I, and apolipoprotein B were determined in 228 patients with cerebral infarction, composed of 87 cases of asymptomatic lacunar infarction, 99 cases of lacunar infarction, and 42 cases of atherothrombotic infarction, and in a control group of 138 healthy subjects with normal MRI. Observations were made on the distribution of Lp(a), Lp(a) and other risk factors for cerebral infarction and these were statistically analyzed, primarily by multiple logistic regression analysis. The diagnosis of these cases was based on the Classification of Cerebrovascular Diseases III of the National Institute of Neurological Disorders and Stroke. The following results were obtained. 1) Lipoprotein (a) (1) Lp(a) did not show a normal distribution with the curve showing a gradual declining slope to the right. It was therefore considered not appropriate in our analysis to use as a means or standard deviation. (2) The 25th percentile, 50th percentile, and 75th percentile of the control group were 5.0 mg/dl, 11.0 mg/dl, and 22.4 mg/dl, respectively. In studying the distribution in these percentile ranges by subtypes of infarction, an increase in cases showing values greater than the median of the control group was observed in asymptomatic lacunar infarction, lacunar infarction, and atherothrombotic infarction, when compared to the control group. In asymptomatic lacunar infarction and lacunar infarction in particular, Lp(a) showed a significantly higher value compared to the control group. (3) However, by multiple logistic regression analysis to adjust for age and sex, Lp(a) did not show a significant odds ratio for asymptomatic lacunar infarction, lacunar infarction and atherothrombotic infarction. 2) Various serum lipids and other parameters (1) The various serum lipids did not show any involvement in asymptomatic lacunar infarction. However, involvement of HDLC and Apo A-I in lacunar infarction and atherothrombotic infarction was observed with the odds ratios in lacunar infarction being 4.2 with a confidence interval of 2.9-9.4 and 4.7 with a confidence interval of 2.2-10.1, and the odds ratios in atherothrombotic infarction being 3.1 with a confidence interval of 1.1-9.0 and 9.6 with a confidence interval of 3.0-30.5, respectively. (2) Involvement of diabetes mellitus in asymptomatic lacunar infarction and lacunar infarction was small, but a strong involvement in atherothrombotic infarction was observed with the odds ratio being 4.3 with a confidence interval of 1.2-16.2. (3) Involvement of hypertension in asymptomatic lacunar infarction and lacunar infarction was observed with the odds ratios being 2.6 with a confidence interval of 1.4-5.2 and 5.6 with a confidence interval of 2.4-13.0, respectively, but the involvement in atherothrombotic infarction was low. The foregoing results indicated that there was no involvement of Lp(a) as a risk factor for any type of cerebral infarction, unlike its involvement in coronary heart diseases. Only blood pressure was involved as a risk factor for asymptomatic lacunar infarction, but for lacunar infarction not only blood pressure but also HDLC and Apo A-I were involved as risk factors. HDLC, Apo A-I, and diabetes mellitus were involved as risk factors for atherothrombotic infarction, but the involvement of hypertension was minimal.
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PMID:Lipoprotein(a) and other risk factors for cerebral infarction. 856 15

Prevention of stroke caused by carotid bifurcation stenosis can be achieved by accurate identification and evaluation of patients at risk. A consensus report from the National Institute of Neurologic Disorders and Stroke has standardized diagnostic criteria and symptoms related to this disease. Recent prospective, randomized trials have identified effective treatment for both asymptomatic and symptomatic carotid stenosis. The risk factors for carotid stenosis are similar to those for atherosclerosis--hypertension, diabetes, cigarette smoking and hyperlipidemia. A carotid bruit is the most common clinical finding, although its positive predictive value is only about 60 to 70 percent. Recent clinical trials have identified patient groups that benefit from surgical and medical therapy, depending on the degree of carotid stenosis and the presence or absence of symptoms. Symptomatic patients with carotid stenosis greater than 70 percent benefit from surgical therapy. Asymptomatic patients who have carotid stenosis greater than 60 percent and are good surgical candidates should be referred for surgical consultation.
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PMID:Prevention of stroke caused by carotid bifurcation stenosis. 862 32

A new autosomal dominant syndrome in a Swedish pedigree is described. Five patients were affected with cerebellar ataxia and sensorineural deafness. Four of these patients had symptoms of narcolepsy. Optic atrophy, other neurological abnormalities and psychiatric symptoms developed with increasing disease duration. Three patients had non-neurological disease in addition, including diabetes mellitus in two and hypertrophic cardiomyopathy in one. Autopsy with neuropathological examination was performed in one case. Molecular studies focused on the short arm of chromosome 6, including the HLA DR2 locus associated with narcolepsy and the (CAG)n repeat at the spinocerebellar ataxia type 1 (SCA1) locus. Biochemical investigation of muscle biopsy of one case indicated mitochondrial dysfunction with selective decrease in ATP production for substrates that normally give the highest rates. The activity of glutamate dehydrogenase was reduced, indicating a low mitochondrial density. We postulate an autosomal dominant genetic factor responsible for this syndrome. Linkage was excluded to HLA DR2, and a normal sized SCA1 repeat was observed. We conclude that a locus predisposing to ataxia, deafness and narcolepsy exists outside this region of chromosome 6.
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PMID:Autosomal dominant cerebellar ataxia deafness and narcolepsy. 874 54

Free radicals are defined as atoms or molecules that contain one or more unpaired electrons. The toxicity of many xenobiotics is associated with the metabolic activation of foreign compounds to form free radicals or with the production of reactive oxygen species as superoxide anion, hydroxyl radicals or hydrogen peroxide which are responsible for the tissue damaging effects as lipid peroxidation, and DNA and protein damage. Oxidative stress associated with production of reactive oxygen species is believed to be involved not only in the toxicity of xenobiotics but also in the pathophysiology of aging, and various age-related diseases, including cataracts, atherosclerosis, neoplastic diseases, diabetes, diabetic retinopathy, chronic inflammatory diseases of the gastrointestinal tract, aging of skin, diseases associated with cartilage, Alzheimer's disease, and other neurologic disorders. The cellular sources of free radicals and reactive oxygen species, the biological targets of free radicals, and clinical conditions which are associated with free radical production and tissue damage are reviewed. In addition, potential therapeutic approaches to the prevention of free radical damage are considered. Free radical-induced injury can explain many clinical conditions.
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PMID:The role of free radicals in toxicity and disease. 885 68

The purpose of this investigation was to compare self-reported health-related quality of life (HRQOL) in epilepsy compared to another neurological condition or a non-neurological chronic illness. Patients with epilepsy (N = 271), multiple sclerosis (N = 85) and diabetes (N = 555) completed a generic measure of HRQOL (RAND 36-Item Health Survey 1.0 (SF-36)), and the eight SF-36 scale scores were compared across groups, adjusting for differences in sociodemographic characteristics and co-morbid medical conditions. Patients with multiple sclerosis reported significantly worse HRQOL compared to both the epilepsy and diabetes groups (who did not differ from one another) on the Physical Functioning, Role Limitations-Physical, Energy, and Social Function scales. Patients with epilepsy and multiple sclerosis did not differ from one another but reported significantly lower HRQOL scores than the diabetes group on the Emotional Well-Being and Role Limitations-Emotional scales. However, the epilepsy group reported better health perceptions compared to the diabetes and multiple sclerosis patients. Generic measures of HRQOL appear useful in identifying some effects of neurological disease, but disease-targeted supplements may be required to more clearly identify the impact of epilepsy on quality of life.
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PMID:A comparison of health-related quality of life in patients with epilepsy, diabetes and multiple sclerosis. 888 69

In the last few years, several mitochondrial DNA mutations and deletions have been described in association with various human diseases. Mitochondrial disorders, though long regarded strictly as neuromuscular diseases, may in fact involve non-neuromuscular symptoms. Diabetes mellitus has been reported in patients presenting with large mtDNA rearrangements (deletion, deletion-duplication) or in association with mtDNA point mutations, generally in tRNA genes (tRNA(Leu(UUR)). Genetic studies have shown that these disorders occur in sporadic cases or can be maternally inherited. The main clinical feature of mitochondrial diabetes is its nearly-consistent association with other symptoms (deafness, neurologic disorders, cardiac failure, renal failure, etc.). This paper provides a review of different types of mtDNA abnormalities associated with diabetes and a study of the prevalence of mitochondrial diabetes mellitus.
Diabetes Metab 1996 Oct
PMID:Mitochondrial diabetes mellitus. 889 89

The quality of the epidemiological data on diabetic neuropathies remains poor for a variety of reasons. They include variability in 1) ascertainment of diabetes, 2) the clinical varieties of diabetic patients studied, 3) characterization of neurological dysfunction, 4) abnormal limits for neurological examinations and tests, 5) minimal criteria for neuropathy, 6) correct attribution of nondiabetic neurological disease, 7) correct attribution of type of neuropathy, 8) estimating neuropathy from use of multiple tests, and 9) estimating severity of polyneuropathy. We have tried to remedy these short-comings in the Rochester Diabetic Neuropathy Study (RDNS). It was not possible to adequately characterize and quantitate diabetic polyneuropathies using only one or two clinical or test abnormalities. To estimate severity of diabetic polyneuropathy, the results of the neurological examination and abnormalities of nerve conduction, quantitative sensory tests, and quantitative autonomic tests were combined into a composite score. One begins by scoring a standard test of neurological deficits (impairments) of the lower limbs (NIS[LL]) and adds to this transformed numbers for percentile abnormality of seven good functional tests. This NIS(LL)+7 tests score appears to provide a much more comprehensive and stable numeric score by which to diagnose and grade severity of diabetic polyneuropathy than does the use of individual clinical or test results. This test score should be useful as a measure of change in diabetic polyneuropathy for purposes of medical practice, epidemiology studies, and controlled clinical trials. The staging approach that we introduced previously continues to provide an important measure of overall severity of diabetic polyneuropathy, taking into account both symptoms and impairments.
Diabetes 1997 Sep
PMID:Approaches to improve epidemiological studies of diabetic neuropathy: insights from the Rochester Diabetic Neuropathy Study. 928 91

We report a rare case of achalasia coexistent with megacolon. The patient, a 25-year-old woman, presented at our hospital with a history of abdominal pain with distension, and was finally operated on for a megacolon. Five months later she presented symptoms of progressive dysphagia and heartburn. Oesophageal manometry of the upper and lower oesophageal sphincter and X-ray studies showed images compatible with achalasia. Oesophagomyotomy of the oesophagogastric junction (Heller procedure with Dor haemifundoplication technique) was performed. In the specimens taken for biopsy, neither pathology of the myenteric plexuses, nor atrophy of the muscle fibres was evident. Chagas' disease serological diagnosis for Trypanosoma cruzii, neurological disease, diabetes and all the pathological events related with neuromuscular disorders of the gastrointestinal tract proved negative. We believe that the pathological findings are related to a dysfunction of the physiological mediators of the upper and lower digestive tract motility. The present case is extraordinary and, to our knowledge, extremely rare. The association of the two pathological diseases is questionable, and the literature is reviewed.
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PMID:Idiopathic megacolon associated with oesophageal achalasia. 958 91

Both achalasia and Hirchsprung's disease arise from defects of innervation of the oesophagus and distal large bowel respectively. Their consequences are confined to disorders of motility in the relevant part of the gastrointestinal tract. Many neurogenic and primary muscle disorders are associated with abnormalities of gut motility. Stroke, even when unilateral, is commonly associated with dysphagia. Transcranial magnetoelectric stimulation has established that the pharyngeal phase of swallowing tends to receive its innervation principally from one hemisphere. In many neurological disorders, dysphagia is only one part of the clinical picture but in some--for example, the Chiari malformation--dysphagia may be the sole or major feature. Disturbances of small and large bowel motility, when seen in neurogenic disorders, are associated with autonomic neuropathy and are particularly common in diabetes mellitus. Primary muscle disorders can lead to dysphagia (for example, with polymyositis or oculopharyngeal dystrophy) or defects of large bowel motility (for example, with Duchenne's muscular dystrophy). Primary gut disorders particularly associated with neurological disease include pernicious anaemia, nicotinamide and thiamine deficiencies, selective vitamin E deficiency, and coeliac disease. Inflammatory bowel disease is associated with thromboembolic complications which may include the CNS, inflammatory muscle disease, and abnormalities on MRI of the brain of uncertain relevance. Whipple's disease is a rare condition which sometimes is largely or entirely confined to the CNS. In such cases, a particular neurological presentation can indicate the diagnosis.
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PMID:Neurology and the gastrointestinal system. 1040 May 14


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