Search PubMed⌕ Search

Biomedical subjects

D J Ewing

Publications and source records attributed to D J Ewing.

At least 55 records · Page 3Linked to original sources
PubMed1988

Somatosensory and visual evoked potentials in insulin-dependent diabetics with mild peripheral neuropathy.

Using somatosensory and visual evoked potential techniques we have looked for evidence of central neuropathy in a group of insulin-dependent diabetics with mild peripheral neuropathy. The N9, N13, and N20 components of the somatosensory evoked potential were significantly (P less than 0.001) delayed in the diabetic group compared with the control subjects. There was a small but non-significant increase in the interpeak N13-9 and N20-13 latencies in the diabetic group. The visual evoked potential (P100) showed a small but insignificant delay. The delay in cerebral evoked potentials was mostly attributable to peripheral neuropathic damage and no firm evidence was obtained in favour of central diabetic neuropathy.

Adult↗
PubMed1988

Noradrenaline response to edrophonium in primary autonomic failure: distinction between central and peripheral damage.

The effects of intravenous edrophonium on plasma noradrenaline were studied in 12 subjects with primary autonomic failure. 5 had clinical features of central autonomic damage, 4 with parkinsonism (PD) and 1 with multiple system atrophy (MSA); the other 7 had clinical features of progressive autonomic failure without detectable central neurological damage (PAF). After edrophonium all but 1 subject showed falls in heart rate of about 6 beats/min; there were no consistent blood pressure changes. The 5 PD/MSA patients all had normal plasma noradrenaline responses to edrophonium, with rises of 35-66% within 2-8 min of injection. 6 of the 7 PAF patients had no response or very small responses (-6 to +11%), while the other subject had a normal response (70% rise). The noradrenaline response to edrophonium may provide a simple way to differentiate between central and peripheral autonomic damage.

Aged↗
PubMed1988

Ocular autonomic function in progressive autonomic failure.

Ocular autonomic function was assessed in 4 patients with progressive autonomic failure (PAF) and age-matched control subjects, by measurement of the pupil cycle time, and determination of autonomic denervation hypersensitivity of the iris. Pupil cycle time was abnormal in all patients with PAF; sustained pupil cycling was absent in 5 of the 8 eyes tested of the PAF patients, compared with only 16 eyes from 70 control subjects. Pupil constriction in response to 2.5% methacholine, indicative of parasympathetic denervation hypersensitivity, was significantly increased in patients with PAF (p less than 0.001), whilst pupil dilation in response to 0.5% phenylephrine, indicative of sympathetic denervation hypersensitivity, was also significantly higher in the PAF patients (p less than 0.001). The results suggest that ocular autonomic function may provide a sensitive early indicator of generalised autonomic dysfunction.

Aged↗
PubMed1988

Abnormalities of autonomic function in the Lambert Eaton myasthenic syndrome.

Two cases of Lambert Eaton syndrome unassociated with an underlying malignancy are described. Both had mild autonomic symptoms but markedly abnormal autonomic function tests. These results are suggestive of a widespread defect in cholinergic transmission in addition to that at the skeletal neuromuscular junction.

Aged↗
PubMed1988

Chronic and remitting painful diabetic polyneuropathy. Correlations with clinical features and subsequent changes in neurophysiology.

Twenty-nine diabetic patients (19 men, 10 women) aged 19-71 yr with newly developed painful polyneuropathy were studied prospectively for 12-18 mo. Pain remitted completely in 16 patients within 12 mo, but continued in the other 13 patients. At presentation, no differences were found in the type or prevalence of symptoms or neurophysiological measurements (electrophysiology and cardiovascular autonomic function tests) between the patients whose pain remitted and those whose pain continued. Most electrophysiological measurements improved slightly in remitting patients but deteriorated slightly in those whose pain continued to reveal a significant difference (P less than .05) between the groups on final review. Similarly, abnormal autonomic nerve function improved slightly when pain remitted but worsened or persisted in patients whose pain continued, again revealing a significant difference between the groups (P less than .05) on final review. We also observed that pain remission usually occurred if the onset of symptoms shortly followed some sudden metabolic change (e.g., rapid improvement in glycemic control, ketoacidosis, anorexia nervosa) when the duration of diabetes was relatively short or when considerable weight loss preceded the onset of pain. We suggest that remitting and chronic painful diabetic polyneuropathy have distinctive clinical features at presentation and detectable neurophysiological differences during their symptomatic evolution.

Adult↗
PubMed1987

Abnormal diurnal urinary sodium and water excretion in diabetic autonomic neuropathy.

1. Diurnal patterns of urine output and sodium and potassium excretion were studied in 10 diabetic patients with and 10 without autonomic neuropathy, and in 10 normal subjects. 2. The diurnal patterns of excretion in the diabetic patients with autonomic neuropathy differed significantly from the two other groups, as a smaller proportion of the 24 h output of urine, sodium and potassium was excreted during the day and a larger proportion was excreted at night. 3. Similar changes were noted in the diurnal patterns of urinary kallikrein excretion in diabetic patients with autonomic neuropathy, and urinary kallikrein output correlated significantly with urine volume but not with urinary sodium excretion. 4. The diurnal patterns of excretion of urinary prostaglandin E2 and 6-keto-PGF1 alpha were not significantly different in diabetic patients with autonomic neuropathy. 5. Nocturia was a common complaint in this group, and the number of nocturnal voidings correlated with night urine volume. There was no evidence of premature bladder emptying. 6. The changes observed in the day/night urine output and sodium excretion could not be explained by glycosuria, insulin regimens, impaired renal function or abnormal diurnal prostaglandin excretion; their possible relevance to the diurnal changes of urinary kallikrein excretion is discussed.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Increased bronchial reactivity to histamine in diabetic autonomic neuropathy.

1. Twelve male diabetic patients inhaled nebulized histamine in doubling concentrations from 0.03 mg/ml to 32 mg/ml until they reached the maximum concentration or until their forced expiratory volume in 1 s (FEV1.0) fell by at least 20%. Six had evidence of severe autonomic neuropathy (DAN), while the other six did not. 2. More of the DAN group decreased their FEV1.0 on histamine inhalation by at least 20% (P less than 0.02) and more of them decreased their maximal flow at 50% vital capacity by at least 20% than those in the group without DAN (P less than 0.05). 3. The fall in FEV1.0 and in maximal flow at 50% of vital capacity was greater (P less than 0.05) in the DAN group than in the group without DAN. 4. This suggests that diabetic patients with autonomic neuropathy have increased bronchial reactivity to histamine. This could either be due to differential damage of the respiratory autonomic nerves or, alternatively, to denervation hypersensitivity.

Autonomic Nervous System Diseases↗
PubMed1987

Effects of beta-adrenoceptor blockade on heart rate and physiological tremor in diabetics with autonomic neuropathy. A comparative study of epanolol, atenolol and pindolol.

Eight diabetics with autonomic neuropathy were given single oral doses of epanolol (200 mg), atenolol (50 mg), pindolol (5 mg) and placebo in a double-blind randomised order at weekly intervals. Supine resting heart rate, physiological tremor and blood glucose were measured before, 2 and 4 h after dosing, and ambulatory heart rate monitored for 24 h. Supine resting heart rate was significantly lowered by atenolol both at 2 and 4 h, and increased on pindolol at 4 h. Heart rate was unaffected by epanolol compared with placebo. Heart rate during the 'waking' period (14.00-23.00 h) was lower than placebo after epanolol and atenolol but unaffected by pindolol. During the 'sleeping' period (23.00 h-08.00 h) heart rate was significantly increased by pindolol, lowered with atenolol and unaffected on epanolol. Pindolol significantly increased physiological tremor at 4 h. No differences were seen between epanolol, atenolol and placebo. Plasma glucose was significantly increased by pindolol 2 h after dosing. These results suggest that pindolol probably produces its partial agonist activity at both beta 1- and beta 2-adrenoceptors, while the partial agonist activity of epanolol is beta 1-selective. Despite abnormal cardiovascular reflex tests in these diabetics, the heart rate responses obtained in this study after beta-adrenoceptor blockade were surprisingly normal, and suggest that the concept of 'cardiac denervation' in diabetes requires modification.

Adrenergic beta-Antagonists↗
PubMed1987

Cardiovascular reflexes in multiple sclerosis.

Cardiovascular autonomic function was studied in 50 patients with multiple sclerosis using 5 simple non-invasive tests: the heart rate responses to the Valsalva manoeuvre, deep breathing and standing, and the blood pressure responses to standing and sustained handgrip. Abnormalities of one or more tests were found in 37 subjects. There was a variable distribution of abnormalities with most occurring in the heart rate response to deep breathing and the blood pressure response to sustained handgrip. This pattern contrasts with that in diabetics and probably reflects the scattered central pathological lesions of multiple sclerosis.

Adult↗
PubMed1987

Six-month treatment with sorbinil in asymptomatic diabetic neuropathy. Failure to improve abnormal nerve function.

The effect of long-term treatment with the aldose reductase inhibitor sorbinil (125 mg daily for 6 mo) was examined in 22 diabetic patients with subclinical abnormalities of nerve function. This was a placebo-controlled, double-blind crossover trial in which each of the two treatment periods lasted 6 mo. Peripheral nerve function was assessed electrophysiologically and by quantitative sensory testing; autonomic function was assessed by measurement of five cardiovascular reflexes and of mean heart rate from a 24-h ECG recording. Measurement of erythrocyte sorbitol concentrations demonstrated very significant inhibition of aldose reductase activity with sorbinil treatment, but no concomitant improvement in either peripheral or autonomic nerve function was observed.

Adult↗
PubMed1987

Noradrenaline response to edrophonium (Tensilon) and its relation to other autonomic tests in diabetic subjects.

Noradrenaline responses following 10 mg intravenous edrophonium were assessed in 32 insulin-treated diabetic men, allocated to 4 groups according to their responses to 5 cardiovascular autonomic tests. The group with the most severe autonomic involvement had no rise in plasma noradrenaline, in contrast to the other 3 groups, whereas the heart rate fell in all 4 groups. There were significant correlations between individual noradrenaline responses, cardiovascular reflex tests, 24 hour heart rate variation and pupil cycle time, depending on whether predominantly parasympathetic or sympathetic pathways or both were involved. These results indicate that the noradrenaline response to edrophonium cannot be used as a test of early sympathetic dysfunction in diabetics; and that autonomic nervous system involvement occurs simultaneously in different body systems.

Autonomic Nervous System Diseases↗
PubMed1986

Progression of subclinical polyneuropathy in young patients with type 1 (insulin-dependent) diabetes: associations with glycaemic control and microangiopathy (microvascular complications).

The progression of subclinical polyneuropathy over 2.5 years has been studied in a representative group of 75 young patients with Type 1 (insulin-dependent) diabetes (initial age 16-19 years). The relationships between changes in nerve function, glycaemic control and concurrently developing microvascular complications (retinopathy, microproteinuria) were investigated. Deterioration of motor, sensory and autonomic nerve function, retinopathy and microproteinuria was related to poor glycaemic control. In addition, there was an association between developing neural and microvascular complications which was not diminished when their common relationship to hyperglycaemia was taken into account. These findings suggest that, although poor glycaemic control is an essential permissive factor in the early development of diabetic polyneuropathy, other influences, shared with microvascular complications, must also be important.

Adolescent↗
PubMed1986

Correlation of cardiovascular and neuroendocrine tests of autonomic function in diabetes.

Six normal subjects and 16 insulin-dependent diabetics with varying degrees of autonomic damage each had blood sampled for norepinephrine and pancreatic polypeptide for fifteen minutes after a mixed meal and intravenous (IV) edrophonium (Tensilon). The normal subjects showed a brisk but short-lived rise in norepinephrine after edrophonium (average maximum increase 70% between 2 and 6 minutes), as did most diabetics. However, diabetics with cardiovascular reflex evidence of sympathetic damage showed no rise in norepinephrine. Pancreatic polypeptide concentrations increased up to 400% above baseline after a mixed meal in both the normal and the diabetic group with normal cardiovascular reflexes. There was no significant rise in pancreatic polypeptide either in the diabetics with parasympathetic damage alone or in those with additional sympathetic damage. These results provide further evidence for the diffuse nature of the damage in diabetic autonomic neuropathy.

Adult↗
PubMed1986

Autonomic neuropathy: its diagnosis and prognosis.

Autonomic neuropathy is now well established as a relatively common and significant complication of diabetes mellitus. Its importance has been clarified in recent years during which the extent of autonomic control over all areas of body function has been defined. Using simple cardiovascular reflex tests, autonomic abnormalities can be demonstrated without any corresponding symptoms. The often stated concept of 'patchy' involvement in diabetic autonomic neuropathy should now be rejected as too should the view that autonomic neuropathy is either 'present' or 'absent' based on a single test result. When generalized and predominantly metabolic disturbances, as in diabetes, give rise to impaired nerve function, autonomic as well as somatic components of the nerve are affected. Where damage is severe this leads to the characteristic florid picture of symptomatic autonomic neuropathy with its particularly poor prognosis. For the physician in a busy clinic, much of the theoretical and experimental basis for autonomic neuropathy may not appear of direct relevance. However, he has now to be aware of the clinical implications of autonomic damage in the diabetic. This may have particular relevance in the care of the diabetic foot (see Chapter 10), the recognition of many of the vague symptoms associated with autonomic damage, the treatment of disabling features such as postural dizziness and nocturnal diarrhoea, and an awareness of the poor prognosis associated with symptomatic autonomic neuropathy. He will also need to be alert to the dangers of general anaesthesia in such patients, and the possibility of sudden unexpected deaths. Diabetic autonomic neuropathy causes widespread abnormalities, some of which are clinically apparent, some of which can be detected by sensitive tests, and others which have yet to be discovered. Inclusion of the neuropeptides and other hormones within the compass of autonomic control has opened up a whole new area of investigative interest, with many complex interrelationships which still need to be unravelled. This should lead to better understanding of the pathophysiological processes that cause damage to diabetic nerves. With so much research effort directed towards better glycaemic control and aldose reductase inhibitors (see Chapter 8), it may eventually be possible to reverse or prevent this potentially disabling and lethal complication of diabetes.

Autonomic Nervous System Diseases↗
PubMed1986

Pupil cycle time: a simple way of measuring an autonomic reflex.

Persistent regular oscillations of the pupil of the eye can be induced using a slit-lamp. The period of these oscillations, pupil cycle time (PCT), is simple to measure with a hand-held stop-watch. Evidence from pharmacological testing suggests that PCT is a sensitive measure of dysfunction of the parasympathetic efferent limb of the pupillary light reflex arc. This is confirmed by the finding that PCT is prolonged in a high proportion of patients with evidence of autonomic neuropathy judged by abnormalities of their cardiovascular reflexes. The method provides a simple, non-invasive way of quantifying an autonomic reflex and it may be of value in investigating patients with diseases affecting the autonomic nervous system.

Adult↗
PubMed1986

Chronic renal failure and cardiovascular autonomic function.

Autonomic function was assessed in 67 patients with chronic renal failure using a standardized battery of five cardiovascular reflex tests. The results showed that 38 (65%) had early or definite parasympathetic abnormalities, while 14 (24%) had additional sympathetic damage. There were no significant differences between those treated conservatively (n = 19), those on continuous ambulatory peritoneal dialysis (n = 8) and those on intermittent haemodialysis (n = 40). Cardiovascular autonomic damage is widespread among patients with chronic renal failure, however treated, and may have a number of clinical sequelae.

Adolescent↗
PubMed1986

Variable relationship between peripheral somatic and autonomic neuropathy in patients with different syndromes of diabetic polyneuropathy.

The relationship between abnormal peripheral nerve electrophysiology and abnormal cardiovascular autonomic function has been studied in four groups of diabetic subjects, comparable with regard to age, duration, and type of diabetes. Thirty-three had no symptoms of neuropathy, 28 had newly developed painful neuropathy, 24 had chronic painful neuropathy, and 21 had painless neuropathy with associated recurrent foot ulcers. In all three symptomatic groups, electrophysiology and autonomic function were more abnormal than in asymptomatic diabetic subjects. There was a significant overall relationship between peripheral nerve (electrophysiologic) and autonomic (cardiovascular reflex) dysfunction. However, when considered by groups, the degree of cardiovascular reflex abnormality was similar in the three symptomatic groups, whereas electrophysiology was appreciably worse in the foot ulcer group than in patients with painful neuropathy. Thus, patients with painful neuropathy had a higher ratio of autonomic (small fiber) abnormality to electrophysiologic (large fiber) abnormality. By contrast, foot ulceration was associated with the worst electrophysiologic (large fiber) abnormality. Heavier alcohol consumption and more severe retinopathy were also related to foot ulceration. In diabetic subjects with symmetrical sensory neuropathy, the relationship between large fiber and small fiber damage is not uniform. We conclude that there may be different etiologic influences on large and small fiber neuropathy in diabetic subjects and that the predominant type of fiber damage may determine the form of the presenting clinical syndrome.

Adult↗