Delayed visual deterioration after pituitary surgery--a review introducing the concept of vascular compression of the optic pathways.
BACKGROUND
Delayed visual deterioration after pituitary surgery has been attributed to secondary empty sella syndrome and downward herniation of the optic nerves and chiasm, but the pathophysiological basis of this condition is still a matter of debate.


METHODS
According to the literature, prior radiation therapy, previous visual impairment and transcranial surgery constitute risk factors for delayed visual deterioration. Radiation-induced vascular changes and/or strangulation of the optic nerves or chiasm are thought to compromise local blood flow. Downward herniation of the optic pathways was present in the majority of cases, but did not correlate with visual symptoms and signs, while dense scarring of the chiasm was a reproducable finding in all surgically explored cases. Indentations in the upper margin of the optic nerves or chiasm caused by the A1 segments of the anterior cerebral arteries have been reported repeatedly. As perichiasmal scarring constitutes the most consistent finding, the intimate relationship between artery and nerve with consecutive pulsatile pressure may constitute a causative factor in delayed visual dysfunction after pituitary surgery. The authors therefore introduce the concept of vascular compression, which is illustrated with a personal case of a successful decompression procedure with teflon interposition between the A1 segment and the non-herniated optic nerve to treat visual loss eight months following removal of a hemorrhagic pituitary adenoma.


CONCLUSIONS
Clinicians should be aware that surgical exploration via a transcranial approach is indicated in cases of progressive visual loss late after pituitary surgery, no matter whether downward displacement of the optic pathways is present on imaging studies or not. Special attention should be paid intra-operatively to the dissection of the intimate relationship between the anterior cerebral arteries and the optic nerves and chiasm.
Thomé
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C
Department of Neurosurgery, University Hospital Mannheim, University of Heidelberg, Mannheim, Germany. claudius.thome@nch.ma.uni-heidelberg.de
Zevgaridis
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D
D020771:Anterior Cerebral Artery / Q000473:pathology / Q000503:physiopathology; D002921:Cicatrix / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D019299:Decompression, Surgical / Q000592:standards; D018450:Disease Progression; D005260:Female; D006801:Humans; D008875:Middle Aged; D019635:Neurosurgical Procedures / Q000009:adverse effects*; D009897:Optic Chiasm / Q000098:blood supply / Q000293:injuries* / Q000473:pathology; D020221:Optic Nerve Injuries / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D010900:Pituitary Diseases / Q000473:pathology / Q000601:surgery*; D010902:Pituitary Gland / Q000473:pathology / Q000601:surgery; D011183:Postoperative Complications / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D019736:Prostheses and Implants / Q000592:standards; D011878:Radiotherapy / Q000009:adverse effects; D012658:Sella Turcica / Q000473:pathology / Q000601:surgery; D013997:Time Factors; D016896:Treatment Outcome; D015354:Vision, Low / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology