ObjectiveStudies using conventional full‐field visual evoked potentials (ffVEP) have reported subtle abnormalities in patients with chronic inflammatory demyelinating polyneuropathy (CIDP). We hypothesize that these abnormalities can be detected in the majority of CIDP patients using enhanced methods.MethodsWe performed a cross‐sectional noninterventional study comparing 18 CIDP patients and 18 matched healthy controls using multifocal VEP (mfVEP) as a technique with enhanced sensitivity to detect conduction abnormalities across the spectrum of optic nerve fibers. Patients with confounding diseases (ophthalmologic, diabetes mellitus) were excluded.ResultsThe mean amplitude and latency, as well as the low‐contrast visual acuity, did not differ between CIDP patients and controls. Subanalyses revealed latency differences concerning the superior sector of the visual field. Severity markers of CIDP (ODSS, motor nerve conduction velocity) were associated with mfVEP latency delay.InterpretationWe could not adduce evidence for clinically or diagnostically relevant visual pathway involvement in CIDP. The latency differences identified were very subtle and restricted to the superior visual field which cannot be readily explained biologically, anatomically, or pathologically. In summary, we conclude that our study revealed no relevant differences in mfVEP parameters between CIDP patients and controls.

Background: Symptomatic carotid artery disease (CAD) may cause modified blood supply to the retina possibly leading to retinal structure changes. Results of previous studies in asymptomatic CAD were heterogeneous in retinal layer changes measured by OCT. The objectives of this prospective, non-interventional study were to investigate if structural retinal changes occur in symptomatic CAD patients with macroangiopathic ischemic stroke or transient ischemic attack (TIA). Methods: We used spectral-domain optical coherence tomography (SD-OCT) to cross-sectionally and longitudinally analyze the retinal morphology of CAD patients with macroangiopathic ischemic stroke or TIA not permanently affecting the visual pathway. We employed semi-automated segmentation of macular volume scans to assess the macular retinal layers' thickness and peripapillary ring scans to determine the peripapillary retinal nerve fiber layer thickness using the contralateral eye and eyes of microangiopathic ischemic stroke patients with matched age, gender, and vascular risk factors as control. Visual function and visual field deficits were assessed by multifocal visual evoked potentials (mfVEP). Results: Neither the thickness of retinal layers measured by SD-OCT in 17 patients nor the mfVEP latency or amplitude in 10 patients differed between the symptomatic stenotic, the contralateral internal carotid artery (ICA) side and the control group of 17 microangiopathic stroke patients at baseline. Furthermore, longitudinal investigations of 10 patients revealed no significant changes of any retinal layer 4 months after ischemic stroke or TIA. Conclusion: In conclusion, our study revealed no evidence for an impact of symptomatic carotid artery disease on retinal structure or functional impairment of the visual pathway.

Background: Visual field defects are a common and disabling consequence of stroke and a negative prognostic factor of patient's quality of life. They result from lesions in different parts of the visual system, most commonly the visual cortex and optic radiation. An important pathophysiological mechanism is transsynaptic retrograde degeneration (TRD). Methods: In a case series 21 patients with posterior cerebral artery (PCA) territory infarctions were analyzed by spectral-domain optical coherence tomography (SD-OCT) and multifocal visual evoked potentials (mfVEPs) cross-sectionally and longitudinally for up to 6 months. In OCT, symptomatic affected nasal and temporal sectors and corresponding visual fields in mfVEPs were compared to the contralateral side. Results: SD-OCT revealed a significant reduction (−2.92 ±2.53 µm, mean ± SD) of the symptomatic nasal macular retinal nerve fiber layer (RNFL) thickness and of the symptomatic temporal peripapillary RNFL after 6 months compared to baseline whereas the symptomatic temporal macular quadrant already showed a significantly thinner RNFL at baseline. The mfVEP first peak latency at baseline was significantly different (nasal visual field +11.69 ±11.17 ms, mean ± SD; temporal visual field +16.63 ±7.97 ms, mean ± SD) on the symptomatic compared to the asymptomatic field. The nasal visual fields partly recovered in amplitude and first peak latency of mfVEPs over the following 6 months compared to baseline. Conclusion: The dynamics of OCT and mfVEP outcomes for degeneration and recovery after PCA infarction differ between the nasal and temporal retinal sector. We postulate that retinal sectors may differ in their temporal pattern of TRD over time after retrogeniculate cerebral infarction.

Background: It is unknown whether microangiopathic ischemic strokes outside the visual pathway go along with subclinical changes of the retinal structure or the visual system. The objectives of this prospective noninterventional case series were to investigate if spectral-domain optical coherence tomography (SD-OCT) or multifocal visual evoked potentials (mfVEPs) can detect structural retinal changes or functional impairment of the visual system in patients with microangiopathic ischemic stroke. Methods: We used SD-OCT to cross-sectionally analyze the retinal morphology of 15 patients with microangiopathic ischemic stroke according to the Trial of Org 10172 in Acute Stroke Treatment (TOAST) classification not affecting the visual pathway. We employed semi-automated segmentation of macular volume scans to analyze the thickness of the macular retinal layers and peripapillary ring scans to investigate the retinal morphology in comparison to a control group without stroke. Visual function was assessed by the mfVEP technique in 13 microangiopathic ischemic stroke patients. Results: First peak latency of mfVEPs was significantly delayed in the microangiopathic ischemic stroke group compared to the control patients. Neither the retinal layers nor the mfVEPs' amplitude differed between the microangiopathic ischemic stroke patients and the control group. Conclusions: In conclusion, microangiopathic ischemic stroke patients presented a delayed first peak latency in mfVEPs as a sign of subclinical functional impairment of the visual pathway. However, our case series suggests no influence on retinal structure resulting from microangiopathic ischemic stroke outside the visual system. Larger and longitudinal studies are needed to confirm these mfVEP findings.