Moussavou Cedrick
Wernekink commissure syndrome was first described in 1941 by Lhermitte, but it wasn't until 1958 that it made its first appearance in a publication at the 22nd International Neurological Meeting. This syndrome takes its name from the first illustrations made in 1840 by Franz Joseph Julius Wilbrand, the successor of Friedrich Christian Wernekink (1798-1835). Wernekink's commissure syndrome is characterized by the combination of bilateral cerebellar ataxia with dysarthria or anarthria, associated with occasional internuclear ophthalmoplegia and delayed-onset palatal myoclonus (Holmes tremor), secondary to caudal paramedian midbrain infarction.
Maryam Sotoudeh Anvari
Rajesh Kumar, Brijesh Kumar*, Ashutosh Kumar, Ajay Kumar, Manish Singh
Shanmugam Rajendran
Shuai Liu
Objective: To investigate the changes of retinal thickness and P-ERG signals in adult patients with anisometropic and strabismic amblyopia. Methods: Sixty patients with monocular adult amblyopia, including 30 Anisotropic Amblyopes (AA group) and 30 Strabismic Amblyopes (SA group), were enrolled in our study at the outpatient clinic of The Hefei First Peoples Hospital of Anhui medical University from June 2019 to November 2020. Retinal Nerve Fiber Layer (RNFL) thickness was measured within 3.4 mm diameter range surrounding the optic nerve, and Ganglion Cell Complex (GCC) layer thickness within 6 mm diameter range surrounding the fovea by an Optovue RTVue Optical Coherence Tomography (OCT) in both amblyopic and fellow eyes. The amplitude and latency of P50 and N95 in Pattern-Electroretinogram (P-ERG) were recorded by a Roland electrophysiology instrument under two stimulation conditions with different temporal and spatial frequencies that were designed to bias the parvocellular and magnocellular pathways respectively. Data between amblyopic and fellow eyes was statistically analyzed by paired t test. The correlation between axial length and parameters of OCT and P-ERG was examined by Pearson correlation test. Results: Changes in RNFL thickness: In the AA group, RNFL thickness in temporal sector was significantly thinner (p=0.033), while that in the nasal, superior and inferior sectors increased (p<0.05) compared with fellow eyes. In SA group, no significant difference (each sector p>0.05) was found between amblyopic eyes and fellow eyes. Changes in GCC thickness compared with fellow eyes, in the AA group, GCC layer thickness of amblyopic eyes was significantly increased (p=0.039), whereas in the SA group, we did not find a significant difference between amblyopic eyes and fellow eyes (p>0.05). P-ERG stimulated mode biased the parvocellular pathway when compared with fellow eyes (n=15), in the AA group, the amplitudes of P50 (p=0.004) and N95 (p=0.038) were significantly decreased in amblyopic eyes, but no significant latent time difference (p>0.05) was found. In the same stimulus pattern, no statistically significant difference (n=15, p>0.05) between amblyopic eyes and fellow eyes was found in the amplitude and latency of P50 and N95 in the SA group. P-ERG stimulated mode biased the magnocellular pathway the amplitude and latency of P50 and N95 showed no statistically significant difference (p>0.05) in either the AA group or the SA group. We found no significant correlation between axial length and OCT, P-ERG parameters (p>0.05) in either group. Conclusion: Our results showed that the alterations in structure and function of retina that could be seen in adult anisometropic amblyopia were not found in adult strabismic amblyopia group. We thought the functional loss in anisometropic amblyopia was more bias to the parvocellular pathway. These findings indicated that the pathological mechanisms were different between anisometropic and strabismic amblyopia.
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