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Biomedical subjects

J G Llewelyn

Publications and source records attributed to J G Llewelyn.

At least 19 recordsLinked to original sources
PubMed1998

Epineurial microvasculitis in proximal diabetic neuropathy.

Amongst the focal and multifocal neuropathies that are associated with diabetes mellitus one of the most common is a proximal predominantly motor lower limb neuropathy. Recent evidence has indicated that, at least in a proportion of cases, this may have an inflammatory basis. We have examined a consecutive series of 15 cases of proximal diabetic neuropathy (diabetic amyotrophy). These were characterized by proximal pain and asymmetric proximal or generalized lower limb muscle weakness, associated in some cases with radicular sensory involvement. Two-thirds of the patients had an accompanying distal symmetric sensory polyneuropathy. Biopsy of the intermediate cutaneous nerve of the thigh, a sensory branch of the femoral nerve, showed epineurial microvasculitis in 3 patients and nonvasculitic epineurial inflammatory infiltrates in another case. In a further case, microvasculitis was found in both in the sural nerve and a quadriceps muscle biopsy specimen. The detection of inflammatory changes appeared to be correlated with the occurrence of sensory radicular involvement. Whether similar changes are present in muscle nerves in this predominantly motor syndrome requires further study. Nevertheless, the present observations confirm the view that secondary vasculitic or other inflammatory reactions may contribute to some forms of diabetic neuropathy.

Aged↗
PubMed1997

Spontaneous bilateral carotid and vertebral artery dissection presenting as a Collet-Sicard syndrome.

Spontaneous dissection of the internal carotid arteries usually presents with unilateral headache, neck pain, focal ipsilateral cerebral ischaemic symptoms and a Horner's syndrome. Lower cranial nerve palsies are only rarely observed. We report a case of carotid and vertebral dissections presenting as a unilateral palsy of the ninth to twelfth cranial nerves (Collet-Sicard syndrome).

Abducens Nerve↗
PubMed1995

Diabetic neuropathy.

The possible role of growth factors in diabetic neuropathy is under investigation and offers new insights into the effect of diabetes on nerve function. The search continues to identify the pathogenic mechanisms involved, many of which will be interlinked.

Diabetic Neuropathies↗
PubMed1994

Glucose and leucine uptake by rat dorsal root ganglia is not insulin sensitive.

Dorsal root ganglia from rats were incubated with 3-O-methyl-[14C]glucose, and [3H]leucine in the presence or absence of insulin in order to determine whether insulin influences the uptake of glucose and amino acids by the cells of the ganglion. No effect was detected. A significant proportion (38%) of the uptake of [3H]leucine was shown to be inhibited by ouabain and therefore energy dependent, utilizing Na+K(+)-ATPase. The activity of this enzyme is known to be impaired in dorsal root ganglia in diabetic rats, as is the uptake of amino acids; these phenomena are therefore unlikely to be due to a direct effect of reduced circulating insulin levels. The relevance of these findings to theories as to the causation of diabetic neuropathy is discussed.

3-O-Methylglucose↗
PubMed1991

Rubidium (86Rb+) influx into dorsal root ganglia and sciatic nerve endoneurium of control and streptozotocin-diabetic rats: comparison with enzymatic Na,K-ATPase activity.

Streptozotocin (STZ)-induced diabetes in the rat causes a significant reduction in ouabain-sensitive Na,K-ATPase pumping activity measured by 86Rb+ influx, in sciatic endoneurium (by 54%) and dorsal root ganglia (by 22%). For endoneurium, the change is similar to that of ouabain-sensitive enzymatic Na,K-ATPase activity (42%), but in dorsal root ganglia, the decrease in enzymatic Na,K-ATPase activity was much greater. 86Rb+ efflux from dorsal root ganglia showed no difference between diabetic and control animals, confirming that the abnormal 86Rb+ influx reflects Na,K-ATPase function and not abnormal membrane permeability. The significance of these findings to pathogenetic mechanisms in diabetic neuropathy is discussed.

Animals↗
PubMed1991

Aldose reductase activity and myo-inositol levels in sciatic nerve and dorsal root ganglia of the diabetic mutant mouse [C57/BL/Ks (db/db)].

Glucose, polyol (sorbitol, fructose), and myo-inositol levels were estimated in peripheral nerve tissue of the diabetic mutant mouse [C57/BL/Ks (db/db)]. At 26 and 40 weeks of age, there was significant accumulation of glucose, sorbitol, and fructose. Tissue myo-inositol levels were lower than those in age-matched control animals at 40 weeks, but not at 26 weeks. Polyol changes in mouse nerve were less marked than those in rat nerve. In dorsal root ganglia, there was also an increase in glucose, sorbitol, and fructose, with a decrease in myo-inositol concentration. These findings show that there is increased aldose reductase activity in peripheral nerve tissue of the diabetic mutant mouse.

Aldehyde Reductase↗
PubMed1991

Sural nerve morphometry in diabetic autonomic and painful sensory neuropathy. A clinicopathological study.

Observations have been made on a selected series of insulin-dependent patients with neuropathy, subdivided into three groups: (1) severe autonomic neuropathy with an accompanying painless sensory neuropathy; (2) severe autonomic neuropathy with a chronic painful sensory neuropathy; and (3) chronic or acute painful sensory neuropathy with no autonomic neuropathy. All three groups showed a loss of large and small myelinated nerve fibres in sural nerve biopsy specimens which was greater in Groups 1 and 2. Regenerative activity was prominent in all three groups, but least in Group 3. Teased fibre studies showed evidence both of axonal regeneration and remyelination. Active fibre degeneration was rare. Measurements of g ratio (axon diameter:total fibre diameter) gave no indication of axonal atrophy. The density of unmyelinated axons was reduced in all three groups, as was their median diameter. Vibration sense threshold was positively correlated with the total number of myelinated fibres and thermal sensory threshold with median unmyelinated axon diameter but not with total unmyelinated axon numbers. No correlation between the occurrence of pain and active degeneration of myelinated fibres or with regenerative activity either in myelinated or unmyelinated axons was detectable. Assessment of differential loss of large or small myelinated nerve fibres was difficult because of the presence of large numbers of small regenerating myelinated axons. The results are discussed in relation to the concept of 'diabetic small fibre neuropathy' and the causation of pain in diabetic neuropathy.

Adult↗
PubMed1990

Morphometry of endoneurial capillaries in diabetic sensory and autonomic neuropathy.

Nerve biopsies were obtained from 27 patients with diabetic neuropathy. All had a symmetric distal sensory and autonomic neuropathy or a purely sensory neuropathy. Mean age was 39.8 years (range 23-57 years). Two patients had Type 2 (non-insulin-dependent) diabetes mellitus and the remainder Type 1 (insulin-dependent) diabetes. Morphometric observations on endoneurial capillaries were compared with results from organ donor control cases and from patients with type 1 hereditary motor and sensory neuropathy. The area of the lumen of the capillaries did not differ between the three groups. The area occupied by the capillary endothelial cells in transverse section and the number of endothelial cell nuclei were increased both in the patients with diabetic neuropathy and hereditary motor and sensory neuropathy, as was the thickness of the surrounding basal laminal zone. 'Closure' of endoneurial capillaries in diabetic neuropathy, reported in another study, was not confirmed. Capillary density and nearest-neighbour distances were similar in the diabetic and organ donor control cases. Capillary density was reduced in the patients with hereditary motor and sensory neuropathy, this being related to increased fascicular area consequent upon the presence of hypertrophic changes. The presence of thickening of the pericapillary basal laminal zone and endothelial cell hyperplasia both in diabetic and hereditary motor and sensory neuropathy, the latter being a neuropathy in which a vascular basis can be discounted, makes it difficult to use such changes as an argument favouring a vascular cause for diabetic neuropathy. There were differences in the basal laminal zone between the diabetic and hereditary motor and sensory neuropathy cases suggesting that the reduplicated basal lamina was more persistent in the diabetic patients.

Adult↗
PubMed1989

Polypeptide and glycoprotein abnormalities in dorsal root ganglia of streptozotocin-diabetic rats.

Observations were made on the polypeptide and glycoprotein composition of dorsal root ganglia from streptozotocin-induced diabetic rats by sodium dodecyl sulphate (SDS)-polyacrylamide gel electrophoresis (PAGE). Silver staining of one-dimensional gels failed to demonstrate any differences between diabetic and control animals. In two-dimensional studies, good resolution of polypeptides with a mass greater than 70 kDa was not obtained, but a number of important abnormalities in the polypeptide composition of diabetic ganglia were detected. Some polypeptides recognized in the gels from control ganglia were present in high concentrations in diabetic ganglia; other polypeptides, particularly a number of basic polypeptides of low molecular mass, were only identified in the diabetic rats. Three major polypeptides showed a small shift in their isoelectric point in the diabetic animals. The glycoprotein content of the ganglia was examined by lectin binding to both one- and two-dimensional gel separations. An increase in total glycoprotein content was evident in the diabetic ganglia. A number of polypeptides with a molecular mass between 70 and 110 kDa showed heavy glycosylation. Altered glycosylation of some specific polypeptides of lower molecular mass was also seen, 7 of these showing increased and 3 reduced glycosylation. The significance of these findings is discussed.

Animals↗
PubMed1988

Pattern of myelinated fibre loss in the sural nerve in neuropathy related to type 1 (insulin-dependent) diabetes.

Sural nerve biopsies were obtained from 17 diabetic patients with neuropathy. All patients except three had both a symmetric distal sensory and autonomic polyneuropathy related to Type 1 (insulin-dependent) diabetes mellitus; 3 patients had a purely sensory polyneuropathy. Mean age was 34.5 years (range 18-53 years). The biopsies were compared with specimens from an age-matched control series. Myelinated fibre loss in the diabetic nerves was found to be nonuniform. Although patchy fibre loss has been considered to favour a vascular basis, an identical pattern of nonuniform loss was observed in a series of sural nerve biopsies from patients with Type I hereditary motor and sensory neuropathy, a subgroup within the spectrum of peroneal muscular atrophy, mainly of autosomal dominant inheritance, and a condition in which a vascular causation can be discounted. Possible reasons for nonuniform fibre loss other than vascular disease are discussed.

Adult↗
PubMed1988

Water content, vasoactive intestinal polypeptide and substance P in intact and crushed sciatic nerves of normal and streptozotocin-diabetic rats.

Observations on streptozotocin-diabetic rats have confirmed overhydration of peripheral nerve. As in previous studies, the sorbitol and fructose content, when expressed in terms of wet weight of nerve was found to be increased and myo-inositol decreased. The reduction in myo-inositol content was less, although still significant, when expressed in terms of protein content. Nerve water content increased during Wallerian degeneration following a crush injury in both normal and diabetic animals, but was relatively less in the latter. Vasoactive intestinal polypeptide (VIP) concentrations were significantly increased in diabetic nerve, those for substance P being normal. Both became severely reduced during Wallerian degeneration following nerve crush and ligature. The significance of these findings is discussed. The accumulation of water in the endoneurial compartment may be related to impaired extraction by the perineurium, to which the increased VIP content may contribute. These changes are unlikely to be responsible for nerve fibre damage.

Animals↗
PubMed1987

Perineurial sodium-potassium-ATPase activity in streptozotocin-diabetic rats.

Perineurial sodium-potassium-ATPase activity was estimated in streptozotocin-diabetic rats and compared with that in control animals. Total ATPase activity was found to be reduced by 34% and ouabain-sensitive ATPase activity by 53%. This finding is significant in relation to the putative role of the perineurium as a metabolically active perifascicular diffusion barrier that regulates the composition of the endoneurial fluid, as is its possible relevance to the occurrence of endoneurial edema in diabetes.

Animals↗
PubMed1986

Acute painful diabetic neuropathy precipitated by strict glycaemic control.

A case of acute painful diabetic neuropathy that followed the establishment of strict glycaemic control using continuous subcutaneous insulin infusion is described. Sural nerve biopsy shortly after the onset of the acute painful syndrome showed no evidence of active nerve fibre degeneration; instead, the appearances were those of a chronic neuropathy with prominent regenerative activity. The suggestion is made that adequate diabetic control promoted regeneration and that the pain may have been related to the ectopic generation of impulses in regenerating axon sprouts.

Acute Disease↗