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02 April 2024 : Case report  China (mainland)

[In Press] Oculomotor Nerve Palsy Induced by a Cerebral Developmental Venous Anomaly: A Case Report and Comprehensive Review

Unknown etiology, Challenging differential diagnosis, Unusual or unexpected effect of treatment

Jianying Zhang12ABEF, Sisi Wang1EF, Ying Jiang3BE, Yue Zhang2ABE

DOI: 10.12659/AJCR.943363

Am J Case Rep In Press; DOI: 10.12659/AJCR.943363  

Available online: 2024-04-02, In Press, Corrected Proof

Publication in the "In-Press" formula aims at speeding up the public availability of the pending manuscript while waiting for the final publication. The assigned DOI number is active and citable. The availability of the article in the Medline, PubMed and PMC databases as well as Web of Science will be obtained after the final publication according to the journal schedule

Abstract

BACKGROUND
Symptoms caused by developmental venous anomalies (DVAs) are usually mild and unspecific. Despite the benign nature of DVAs, they can occasionally be symptomatic.
CASE REPORT
A 67-year-old woman presented with sudden diplopia and left eyelid ptosis for 10 days. A neurologic examination revealed left complete oculomotor nerve palsy. Other neurologic deficits, including eye pain or pulsatile tinnitus, were not detected. Furthermore, the visual acuity was normal. Additionally, no retinal hemorrhage, venous dilatation, or fundus tortuosity were observed. No ischemia lesions or neoplasms were observed in MRI, and no widening or enhancement of the cavernous sinus was detected in post-contrast T1-weighted images, but magnetic resonance tomography cerebral angiography (MRTA) detected an offending vessel compressing the left oculomotor nerve in the fossa interpeduncular. We hypothesized that oculomotor nerve palsy (ONP) was caused by an abnormal arterial structure. However, digital subtraction angiography (DSA) revealed no aneurysm or abnormal arterial structure in the arterial phase, while a tortuous and dilated collecting vein was detected in the venous phase, connecting the left temporal lobe to the left cavernous sinus. This indicated a typical caput medusae appearance, suggesting the mechanism of oculomotor palsy caused by compressive impairment of the DVA. The patient refused microvascular decompression surgery, and ONP persisted after 30 days. Management was conservative, with spontaneous resolution at 60 days and no recurrence during the 2-year follow-up.
CONCLUSIONS
ONP is rarely caused by DVAs, which are easily ignored due to their benign nature. Cerebral vein examinations are advised for patients exhibiting clinical symptoms of unknown etiology.

Keywords: Case Reports; Conservative Treatment

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American Journal of Case Reports eISSN: 1941-5923
American Journal of Case Reports eISSN: 1941-5923