Etude ultrastructurale du nerf périphérique chez 16 diabétiques sans neuropathie clinique. Comparaisons avec 16 neuropathies diabétiques et 16 neuropathies non diabétiques

Vital, C; M, Le Blanc; Jm, Vallat; Cocquet, M; Vallat, M; Jc, Roques

doi:10.1007/bf00685323

Cited by 30 publications

(10 citation statements)

References 10 publications

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“…Atherosclerosis develops at an accelerated rate in arteries, arteriosclerosis in arterioles, and microangiopathy in capillaries, including those of nerves [35,367. The size of the focal lesions, their wedge shape, and the involvement of perineurium indicates that the responsible vessel is epineurial.…”

Section: Resultsmentioning

confidence: 99%

Pathogenesis of diabetic neuropathy

Johnson

Doll

Cromey

1986

Annals of Neurology

248

100

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Samples of lumbosacral trunk, posterior tibial nerve, and sural nerve obtained at autopsy from diabetic and nondiabetic patients without mononeuropathy multiplex were evaluated using 1-mu-thick epoxy sections and teased nerve fiber preparations. Focal fascicular lesions characterized by reduced density of myelinated axons within fascicles were found predominantly in the specimens from diabetics, mainly in the posterior tibial nerve and lumbosacral trunk. In severe examples, the perineurium and even surrounding epineurium were damaged, stamping the lesions as ischemic. In addition, identical lesions were found in biopsies of nerves of nondiabetics with vasculitis. Density of myelinated fibers at the three sites demonstrated a proximal-distal graded loss that was significantly greater in the diabetic samples. The loss from the lumbosacral trunk to the posterior tibial nerve was correlated with the density of focal lesions in the lumbosacral trunk in the diabetic (p = 0.025), indicating that distal fiber loss was partly due to the focal lesions. Teased nerve fiber abnormalities were common only in sural nerves of diabetics, suggesting that they are secondary. We conclude that beyond the possible metabolic abnormalities involved in the genesis of diabetic polyneuropathy, focal fascicular lesions, likely due to diabetic microangiopathy, are also important in the development of diabetic neuropathy.

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Section: Resultsmentioning

confidence: 99%

Pathogenesis of diabetic neuropathy

Johnson

Doll

Cromey

1986

Annals of Neurology

248

100

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“…Ballin and Thomas identified onion bulbs and teased nerve fiber findings suggesting recurrent demyelination and Vital reported both segmental demyelination and axonal degeneration. 69–71 Dyck demonstrated that the changes of axonal degeneration and regeneration were more frequent than those of segmental demyelination and remyelination, and in the setting of multifocal fiber loss, they concluded that axonal degeneration was the primary process. 50 Studies by Said of the sural nerves of patients with prominent small fiber sensory loss found pathologic evidence for both axonal degeneration, as well as both primary and secondary segmental demyelination.…”

Section: Epidemiologymentioning

confidence: 99%

Diabetic Neuropathy Part 1

et al. 2013

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Diabetes is the most common cause of neuropathy in US and neuropathies are the most common complication of diabetes mellitus affecting up to 50% of patients with type 1 and type 2 diabetes mellitus. Various types of neuropathies can be associated with diabetes mellitus.1 Symptoms usually include numbness, tingling, pain and weakness. Dizziness with postural changes can be seen with autonomic neuropathy. Metabolic, vascular and immune theories have been proposed for the pathogenesis of diabetic neuropathy. Pathologically axonal damage and segmental demyelination can be seen with diabetic neuropathies. Management of diabetic neuropathy should begin at the initial diagnosis of diabetes and mainly requires tight and stable glycemic control. Many medications are available for the treatment of neuropathic pain.

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“…27 The finding of reduced basal laminal thickness in our patients with CMS is unexpected but not surprising. One possibility is that it is not part of a neuropathic process but represents an adaptive phenomenon to life at high altitude.…”

Section: Discussionmentioning

confidence: 49%

Neurological manifestations in chronic mountain sickness: the burning feet-burning hands syndrome

Thomas¹,

King²,

Feng³

et al. 2000

Journal of Neurology, Neurosurgery &Amp; Psychiatry

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Objective-To characterise the clinical features and nerve biopsy findings in patients with chronic mountain sickness (CMS) living in the Peruvian Andes, with particular attention to the occurrence of the "burning feet-burning hands" syndrome. Methods-Symptoms and signs were documented clinically in 10 patients with CMS and compared with those in five healthy subjects all living at 4338 metres altitude. Sural nerve biopsies were obtained from three patients with CMS.The nerve fibre population and endoneurial microvessels were analyzed morphometrically. Results-All patients with CMS experienced burning and tingling paraesthesiae in the distal parts of their limbs. Similar but milder symptoms confined to the feet occurred in four of five controls. Three patients with CMS had a mild sensory neuropathy on examination, controls were clinically normal. Nerve biopsies showed a mild demyelinating neuropathy in all three with a reduction in the unmyelinated axon population in one. The endoneurial blood vessels showed a reduced thickness in the basal laminal zone compared with control values but were otherwise normal. Conclusions-Apart from well recognised symptoms and signs of CMS, the study has shown that such patients may also exhibit a mild sensory neuropathy. Its relation to the burning feet-burning hands syndrome, which was not confined to the patients but was also found in controls at altitude, is uncertain. The time course and pattern of the centrifugal resolution of the burning paraesthesiae complex on low altitude sojourn of high altitude natives raises the possibility that a mechanism involving altered axonal transport may be involved. The reduced thickness of the basal laminal zone of microvessels implies that adaptive structural changes to hypobaric hypoxia may also occur in peripheral nerve and are similar to those reported in other tissues of high altitude natives. (J Neurol Neurosurg Psychiatry 2000;69:447-452)

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Etude ultrastructurale du nerf périphérique chez 16 diabétiques sans neuropathie clinique. Comparaisons avec 16 neuropathies diabétiques et 16 neuropathies non diabétiques

Cited by 30 publications

References 10 publications

Pathogenesis of diabetic neuropathy

Pathogenesis of diabetic neuropathy

Diabetic Neuropathy Part 1

Neurological manifestations in chronic mountain sickness: the burning feet-burning hands syndrome

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