Antibodies to Neuronal Structures

Vinik, Aaron I.; Anandacoomaraswamy, Dharshan; Ullal, Jagdeesh

doi:10.2337/diacare.28.8.2067

Cited by 30 publications

(10 citation statements)

References 61 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…According to the traditional approach to the mechanism of neuropathy development, hyperglycemia causes nerve injuries [1]. However, some authors think that the chain of pathological processes in diabetes is initiated by disorders in the work of nerve endings in the pancreas [6,[13][14][15]. We previously described a possible mechanism of this disorders [4].…”

Section: Resultsmentioning

confidence: 99%

Immunoreactivity of Neuron-Specific Enolase (NSE) in Human Pancreas in Health and Type 1

et al. 2010

View full text Add to dashboard Cite

The role of neuron-specific enolase (glycolytic enzyme; marker of nerve fibers and Langerhans islet in human pancreas) in the development of type 1 diabetes mellitus was studied in autopsy specimens from 6 adult patients. Autopsied specimens of the pancreas from 7 subjects without carbohydrate metabolism disorders served as the control. Autopsied specimens of the pancreas from a child with the clinical diagnosis of type 1 diabetes mellitus, a child without carbohydrate metabolism disorders, and from 7 human fetuses of 15-40 weeks gestation were also studied. In control specimens, the neuron-specific enolase was detected in the pancreatic nerve fibers and Langerhans islets. Studies of pancreatic tissue specimens from adult patients with type 1 diabetes mellitus showed no immunopositive reaction to neuron-specific enolase in insulin-negative specimens. A possible mechanism of type 1 diabetes mellitus development is suggested.

show abstract

Section: Resultsmentioning

confidence: 99%

Immunoreactivity of Neuron-Specific Enolase (NSE) in Human Pancreas in Health and Type 1

et al. 2010

View full text Add to dashboard Cite

show abstract

“…[21,22] Oxidative stress depletes nitric oxide within the peripheral nerves and endothelium of the microvasculature by reducing endothelial nitric oxide synthase, altering nerve perfusion. [23] Dyslipidemia is also found to be associated with nerve damage in diabetes. Many theories had been postulated to explain the possible relationship between lipid disorders and peripheral neuropathy.…”

Section: Discussionmentioning

confidence: 99%

Electrophysiological study of the palmar cutaneous nerves in diabetics

Prasad¹,

Diwanji²

2018

Natl J Physiol Pharm Pharmacol

View full text Add to dashboard Cite

Background: Polyneuropathy in diabetics which may be asymptomatic, targets particularly sensory neurons and their axons, starting in their distal terminals. Aims and Objectives: Aim of the present study was to identify the presence of subclinical neuropathy in Type 2 diabetic patients with the help of sensory nerve conduction studies (NCS). Material and Methods: Diabetic and control groups underwent standard antidromic technique of sensory NCS and recording of sensory nerve action potentials (SNAPs) of the palmar digital branches of the median and ulnar nerves using Neuro perfect software on windows based computerized electromyographic/nerve conduction velocity/evoked response Mark II system and surface electrodes. Results: On comparing the parameters of NCS it was found that distal latency of both the nerves was higher in diabetics than controls with a statistically significant difference. Results also showed a statistically significant decrease in conduction velocities of both nerves in diabetics. The mean SNAP amplitudes for all tested nerves were found to be decreased significantly in diabetics. Conclusions: Sensory nerves are found affected in diabetics with no clinical sign and symptoms of neuropathy. NCS is a sensitive test which can be used to identify subclinical cases.

show abstract

“…The exact pathophysiological mechanisms are unknown, but might depend of antibodies to neuronal structures as seen in neuropathy associated with diabetes [6]. Furthermore, cytokines and growth factors have been suggested to play a role in initiating or maintaining neuropathic pain [7].…”

Section: Discussionmentioning

confidence: 99%

Intravenous immunoglobulin treatment in a patient with adrenomyeloneuropathy

et al. 2012

View full text Add to dashboard Cite

BackgroundAdrenomyeloneuropathy (AMN) is one of several phenotypes of the adrenoleukodystrophy spectrum caused by mutations in the ABCD1 gene on the X chromosome. An inflammatory component is part of the disease complex ranging from severe childhood CNS demyelination to spinal cord and peripheral nerve degeneration.Case presentationWe present a patient with clinical progressive AMN and severe lower limb pain. Longitudinal brain magnetic resonance spectroscopy showed a constant slightly elevated myoinositol/total creatine ratio during the five year treatment period, probably reflecting demyelination, microglial activation and gliosis, indicating an inflammatory response. The pain was refractory to conventional therapy but intravenous immunoglobulin (IVIG) treatment was highly efficient.ConclusionIVIG may be considered as a last resort for treatment of refractory pain in AMN patients with indications of an inflammatory component.

show abstract

Antibodies to Neuronal Structures

Cited by 30 publications

References 61 publications

Immunoreactivity of Neuron-Specific Enolase (NSE) in Human Pancreas in Health and Type 1

Immunoreactivity of Neuron-Specific Enolase (NSE) in Human Pancreas in Health and Type 1

Electrophysiological study of the palmar cutaneous nerves in diabetics

Intravenous immunoglobulin treatment in a patient with adrenomyeloneuropathy

Contact Info

Product

Resources

About