Spectrum of diabetic neuropathies.

Autonomic Diabetes Neuropathy Radiculoplexus Treatment-induced neuropathy

Journal

Diabetology international
ISSN: 2190-1678
Titre abrégé: Diabetol Int
Pays: Japan
ID NLM: 101553224

Informations de publication

Date de publication:
Apr 2020
Historique:
received: 11 12 2019
accepted: 29 12 2019
entrez: 25 3 2020
pubmed: 25 3 2020
medline: 25 3 2020
Statut: epublish

Résumé

The diabetic state results in neuropathy. The main causative mechanism is hyperglycemia, although microvascular involvement, hypertriglyceridemia, as well as genetic and immune mechanisms may be contributory. There is a growing spectrum of types of diabetic neuropathies that differ based on the type of fibers involved (e.g. myelinated, unmyelinated, autonomic, somatic), distribution of nerves involved, and mechanisms of neuropathy. The most common type is distal sensory neuropathy (DSN), which affects the distal ends of large myelinated fibers, more often sensory than motor, and is often asymptomatic. The next-most common is distal small fiber neuropathy (DSFN), which largely affects the unmyelinated fibers and carries the phenotype of burning feet syndrome. Diabetic autonomic neuropathy (DAN) occurs when widespread involvement of autonomic unmyelinated fibers occurs, and patients can be incapacitated with orthostatic hypotension as well as neurogenic bladder and bowel involvement. Radiculoplexus diabetic neuropathy causes proximal weakness and pain, usually in the lower extremity, and has a combination of immune, inflammatory, and vascular mechanisms. The nerve roots and plexus are involved. These patients present with proximal weakness of a subacute onset, often with severe pain and some autonomic failure. Finally, rapid and sustained reduction of blood glucose can result in treatment-induced diabetic neuropathy (TIND), which largely affects the sensory and autonomic fibers. This occurs if HbA1c is rapidly reduced within 3 months, and the likelihood is proportional to the original A1c and the size of the reduction.

Identifiants

pubmed: 32206478
doi: 10.1007/s13340-019-00424-7
pii: 424
pmc: PMC7082443
doi:

Types de publication

Journal Article Review

Langues

eng

Pagination

87-96

Informations de copyright

© The Japan Diabetes Society 2020.

Déclaration de conflit d'intérêts

Conflict of interestThe authors declare that they have no conflicts of interest.

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Auteurs

Hideyuki Sasaki (H)

1Wakayama Medical University, Wakayama, Japan.

Nobutoshi Kawamura (N)

2Kawamura Hospital, Gifu, Japan.

Peter J Dyck (PJ)

3Department of Neurology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905 USA.

P James B Dyck (PJB)

3Department of Neurology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905 USA.

Mikihiro Kihara (M)

Hidaka Hospital, Takasaki, Japan.

Phillip A Low (PA)

3Department of Neurology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905 USA.

Classifications MeSH