Diabetic neuropathy. Structural analysis of nerve hydration by magnetic resonance spectroscopy

Griffey, Richard H.

doi:10.1001/jama.260.19.2872

Cited by 25 publications

(23 citation statements)

References 34 publications

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“…Although the sequence of events is not well understood, investigators propose that microvascular vasoconstriction, edema, and ischemia play a role in development of DPN. Endoneurial edema increases pressure [128], thereby causing capillary closure and subsequent nerve ischemia with irreversible damage [129,130] Diminished endoneurial blood flow and ischemia, as measured with laser Doppler, may result from decreased nerve density and innervation of vessels [131,132]. Nerve ischemia stimulates activation of PKC β, increases vascular endothelial growth factor (VEGF) production and decreases NO-dependent vasodilation, exacerbating nerve damage [118,[133][134][135][136][137][138][139][140].…”

Section: Vascularmentioning

confidence: 99%

Pathophysiology and Treatment of Diabetic Peripheral Neuropathy: The Case for Diabetic Neurovascular Function as an Essential Component

Kles

Vinik²

2006

CDR

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Worldwide, diabetes and its complications are major causes of morbidity, decreased quality of life, mortality and increasing health care costs. Patients with diabetes attempt to control blood pressure, lipids and blood glucose levels to decrease their risk of macrovascular and microvascular complications, such as diabetic peripheral neuropathy (DPN). Even with control of these risk factors for vascular disease, many patients still develop complications. Targeted therapies to the underlying mechanisms of diabetic neuropathy are essential to slow the progression of the disease. This review describes the signs, symptoms and diagnosis of DPN. Additionally, new therapies and the complex etiology that contributes to the development of diabetic neuropathy are described (oxidative stress, hyperglycemia, advanced glycated end products, autoimmunity, neurotrophic factors and protein kinase C beta).

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Section: Vascularmentioning

confidence: 99%

Pathophysiology and Treatment of Diabetic Peripheral Neuropathy: The Case for Diabetic Neurovascular Function as an Essential Component

Kles

Vinik²

2006

CDR

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“…Type VI collagen is increased in the endoneurium surrounding groups of Schwann cells, with types IV, V, and VI increased around endoneurial microvessels. In several studies using noninvasive magnetic resonance spectroscopy (Griffey et al, 1988;Eaton et al, 1996), hydration was increased in nerves from both asymptomatic and symptomatic diabetic patients but not in those receiving treatment with aldose reductase inhibitors. Endoneurial fibrosis is evident in feline diabetic neuropathy, as are fibroblasts with glycogen accumulation (Mizisin et al, 2002).…”

Section: Endoneurial Connective Tissuementioning

confidence: 99%

Mechanisms of diabetic neuropathy

Mizisin

2014

Handbook of Clinical Neurology

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“…11 There are multiple possible explanations for this phenomenon, including the observation that the conversion of glucose to sorbitol osmotically increases intraneural water content, creating nerve edema. [12][13][14] Normally, the nerve courses through fixed anatomical structures with an already low tolerance for any nerve size variation. 15,16 Therefore, swelling will put the nerve at risk for compression within its anatomical "tunnel," causing entrapment that will lead to both distal nerve ischemia (by means of compression of the vaso nervorum 17 ), and a decrease in axoplasmic flow.…”

Section: Pathophysiologymentioning

confidence: 99%