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Corneal confocal microscopy for assessment of corneal nerve morphology in patients with acquired and hereditary demyelinating polyneuropathy

Poster Details

First Author: S.Akkaya Turhan TURKEY

Co Author(s):    E. Keskiner Ozturk   P. Kahraman Koytak   K. Uluc   H. Alibas   T. Tanrıdag   E. Toker     

Abstract Details

Purpose:

To evaluate corneal nerve and immune cell alterations in patients with acquired [chronic inflammatory demyelinating polyneuropathy (CIDP)] and hereditary demyelinating polyneuropathy (PNP) and compare with healthy volunteers.

Setting:

Marmara University School Of Medicine, Department Of Ophthalmology, and  Department Of Neurology

Methods:

A total of 31 patients with CIDP (n=15) and hereditary PNP (n=16) and 32 age-matched control subjects were enrolled in this study. Corneal nerve fiber density (CNFD), branch density (CNBD), and fiber length (CNFL) were quantified by the use of in vivo corneal confocal microscopy (IVCCM, Heidelberg Retinal Tomography III Rostock Cornea Module). For all sub-basal nerve plexus images, automatic CCMetrics software (University of Manchester, UK) was used for the quantitative analysis of the nerve fibers.  Cell infiltrates were analyzed manually in a blinded fashion.

Results:

CNFD, CNFL were significantly reduced in patients with CIDP compared with the control group  (p=0.03, p=0.006, respectively).  In hereditary PNP group; only CNFD was significantly reduced compared with the control group. Total infiltrative cell count and corneal nerve fiber tortuosity (CNFT) were significantly increased in CIDP group (p=0.005, p=0.001, respectively).There was no difference in cell counts between hereditary PNP group and the control group. CCM parameters were significantly lower in patients with neuropathic pain compared to those without pain in both patient groups. Moreover, a significant correlation was found between the CCM parameters and certain electrophysiological parameters in all patients.

Conclusions:

IVCCM may be a useful non-invasive tool to assess the small fiber involvement and axonal degeneration, mainly responsible for the long-term disability in these patients, and to elucidate the underlying pathophysiological mechanisms.

Financial Disclosure:

None

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