Ischemia and diabetic neuropathy

Nukada, Hitoshi

doi:10.1016/b978-0-444-53480-4.00023-0

Cited by 66 publications

(62 citation statements)

References 150 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…After transient ischemia and reperfusion, acute inflammation of the diabetic nerve is seen. Resident macrophages are activated and recruited for macrophage infiltration [47]. The onset of acute facial palsy after the embolization of cerebral venous [48] or dural arteriovenous fistulas [49] provides some evidence of this.…”

Section: Primary Ischemiamentioning

confidence: 99%

The etiology of Bell’s palsy: a review

et al. 2019

View full text Add to dashboard Cite

Bell's palsy is the most common condition involving a rapid and unilateral onset of peripheral paresis/paralysis of the seventh cranial nerve. It affects 11.5-53.3 per 100,000 individuals a year across different populations. Bell's palsy is a health issue causing concern and has an extremely negative effect on both patients and their families. Therefore, diagnosis and prompt cause determination are key for early treatment. However, the etiology of Bell's palsy is unclear, and this affects its treatment. Thus, it is critical to determine the causes of Bell's palsy so that targeted treatment approaches can be developed and employed. This article reviews the literature on the diagnosis of Bell's palsy and examines possible etiologies of the disorder. It also suggests that the diagnosis of idiopathic facial palsy is based on exclusion and is most often made based on five factors including anatomical structure, viral infection, ischemia, inflammation, and cold stimulation responsivity.

show abstract

Section: Primary Ischemiamentioning

confidence: 99%

The etiology of Bell’s palsy: a review

et al. 2019

View full text Add to dashboard Cite

show abstract

“…In DN condition, cold allodynia precipitate due to loss of Aδ fibers which lead to sensitization of cold receptors (Ranjithkumar et al, 2013). Reports suggest that degeneration of the nerve fibers occurs due to hyperglycemia mediated ischemia (Nukada, 2014). In this study insulin treatment alone showed reduction in cold allodynia condition which might be linked to the reduction of hyperglycemia.…”

Section: Discussionmentioning

confidence: 99%

Bioactive Fraction of Annona reticulata Bark (or) Ziziphus jujuba Root Bark along with Insulin Attenuates Painful Diabetic Neuropathy through Inhibiting NF-κB Inflammatory Cascade

Kandimalla

Dash²,

Kalita

et al. 2017

Front. Cell. Neurosci.

View full text Add to dashboard Cite

The present study explains the neuroprotective ability of bioactive fractions of Annona reticulata bark (ARB) and Ziziphus jujuba root bark (ZJ) along with insulin against diabetic neuropathy. By using different solvents of increasing polarity ARB and ZJ were undergone for bioactive guided fractionation. The neuroprotective ability of the all the plant fractions were tested against H2O2 induced toxicity in SHSY5Y neuroblastoma cell lines and DRG neuronal cells. Among all the fractions tested, the methanol extract of ARB and ZJ (ARBME and ZJME) and its water fractions (ARBWF and ZJWF) exhibited significant neuroprotection against H2O2 induced toxicity in SHSY5Y cells and DRG neuronal cells. Further both the active fractions were tested against streptozotocin (55 mg/kg i.p.) induced diabetic neuropathy in male Wistar rats. Body weight changes, blood glucose levels and pain threshold through hot plate, tail immersion, cold plate and Randall-Sillitto methods were measured throughout the study at weekly interval. After completion of the drug treatment period, all the animals were sacrificed to measure the sciatic nerve lipid peroxidation, antioxidative enzyme levels (SOD, catalase, and GSH) and cytokine levels (IL-1β, IL-6, IL-10, TNF-α, iNOS, and NFκB) through ELISA and western blotting analysis. Results of this study explain that ARBME, ZJME, ARBWF, and ZJWF along with insulin potentially attenuate the thermal, mechanical hyperalgesia and cold allodynia in diabetic neuropathic rats, where insulin treatment alone failed to diminish the same. Reduction of sciatic nerve oxidative stress, NF-κB and iNOS mediated inflammatory cascade and normalization of abnormal cytokine release confirms the possible mechanism of action. The present study confirms the neuroprotective ability of ARB and ZJ against painful diabetic neuropathy through inhibiting oxidative stress and NF-κB inflammatory cascade.

show abstract

“…Human and animal models have shown endoneurial hypoxia caused by a reduction in nerve blood flow and increased endoneurial vascular resistance. There is strong evidence that ischemia is crucial in DSPN nerve fiber degeneration and loss [63]. Yet, Jaramillo et al [64] notes resistance of the action potential to inactivation by the neural ischemia observed in diabetic patients, allowing continued function at reduced levels.…”

Section: Discussionmentioning

confidence: 99%

Nerve decompression and neuropathy complications in diabetes: Are attitudes discordant with evidence?

Nickerson¹

2017

Diabetic Foot & Ankle

View full text Add to dashboard Cite

External neurolysis of the nerve at fibro-osseous tunnels has been proprosed to treat or prevent signs, symptoms, and complications in the lower extremity of diabetes patients with sensorimotor polyneuropathy. Nerve decompression is justified in the presence of symptomatic compressed nerves in the several fibro-osseous tunnels of the extremities, which are known to be frequent in diabetes. Quite a body of literature has accumulated reporting results after such nerve decompression in the leg, describing pain relief and sensibility improvement, as well as balance recovery, diabetic foot ulcer prevention, curtailed ulcer recurrence risk, and amputation avoidance.Historical academic hesitance to endorse surgical treatments for pain and numbness in diabetes was based primarily on the early retrospective reports’ potential for bias and placebo effects, and that the hypothetical basis for surgery lies outside the traditional etiology paradigm of length-dependent axonopathy. This reticence is here critiqued in view of recent studies using objective, measured outcome protocols which nullify such potential confounders. Pain relief is now confirmed with Level 1 studies, and Level 2 prospective information suggests protection from initial diabetic foot ulceration and most neuropathic ulcer recurrences. In view of the potential for nerve decompression to be useful in addressing some of the more difficult, expensive, and life altering complications of diabetic neuropathy, this secondary compression thesis and operative treatment methodology may deserve reassessment.

show abstract

Ischemia and diabetic neuropathy

Cited by 66 publications

References 150 publications

The etiology of Bell’s palsy: a review

The etiology of Bell’s palsy: a review

Bioactive Fraction of Annona reticulata Bark (or) Ziziphus jujuba Root Bark along with Insulin Attenuates Painful Diabetic Neuropathy through Inhibiting NF-κB Inflammatory Cascade

Nerve decompression and neuropathy complications in diabetes: Are attitudes discordant with evidence?

Contact Info

Product

Resources

About