Vascular Compression of the Anterior Optic Pathway: A Rare Occurrence?

Tsutsumi, Satoshi; Onο, Hideo; Yasumoto, Yukimasa

doi:10.1016/j.carj.2017.02.001

Cited by 7 publications

(7 citation statements)

References 20 publications

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“…It usually results in a slow progressive and painless structural and functional deterioration of optic nerve. The etiologic compressive masses can be varied in terms of different pathologic tissues, sizes, growth rates, biological behaviors, and systemic disturbances 1,2. Also, the retinotopic rearrangement of axonal fibers themselves at the site of compression can be region-specific along the pathway from intraocular, intraorbital, intracanalicular, intracranial parts of the optic nerve, chiasm, optic tract before synapse at the lateral geniculate body.…”

Section: Introductionmentioning

confidence: 99%

<p>Variable structure and function relationship of compressive optic neuropathy at the time of diagnosis</p>

Laowanapiban

Chirapapaisan

Kemahayung

et al. 2019

OPTH

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PurposeTo illustrate the structure–function relationship of compressive optic neuropathy (CON) at the time of diagnosis.Patients and methodsThirty-two eyes of newly diagnosed suprasellar CON and 60 healthy eyes were included in the study. The peripapillary retinal nerve fiber layer (RNFL) thickness and macular ganglion cell-inner plexiform layer (GCIPL) thickness were obtained using Cirrus spectral domain optical coherence tomography (SD-OCT). CON eyes were stratified based on the similar degree and pattern of both RNFL and GCIPL.ResultsFrom 32 eyes of newly diagnosed suprasellar CON eyes, 27 eyes had a predominantly nasal hemiretina thinning of macular GCIPL, 4 eyes showed a generalized macular thinning, and 1 eye showed a predominantly superior macular thinning. The corresponding temporal peripapillary RNFL thinning with nasal hemiretina GCIPL thinning were inconsistently manifested. Structure–function analysis of stratified CON eyes with similar thinning profiles showed that a range rather than a fixed value of visual field loss based on mean deviation (MD) index was associated to each thinning profile. The maximal limit of visual field loss range was ubiquitously nonrestricted to any structural thinning profile. While the minimal limit of the associated MD range was gradually reduced from 0 to about −16.0 dB, the nasal hemiretina macular GCIPL thinning was the only manifestation and decreased from 75 to 45 µm. However, the different degrees of temporal hemiretina macular GCIPL and superior–inferior peripapillary RNFL thinning were only seen in 10 of 32 eyes of which their nasal hemiretina GCIPL and temporal RNFL thinning had reached significant thinning. Interestingly when present, the minimal limit of associated MD range continued to decrease from −16.0 to −32.0 dB.ConclusionCON eyes can present with variable structure and function relationship at the time of diagnosis. Using structural parameters at the time of diagnosis to predict the prognosis should be used with caution.

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Section: Introductionmentioning

confidence: 99%

<p>Variable structure and function relationship of compressive optic neuropathy at the time of diagnosis</p>

Laowanapiban

Chirapapaisan

Kemahayung

et al. 2019

OPTH

View full text Add to dashboard Cite

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“…A recent study by Tsutumi et al of 183 patients suggested an 11% incidence while the previous study by Jacobson et al of 100 patients suggested a 17% incidence. 37,38 This would suggest other aetiologies of visual dysfunction must be excluded before interventions to alleviate vascular compression are considered. However, patients in the Tsutumi et al radiological study did not undergo full visual testing, so it is possible that patients had unidentified visual dysfunction.…”

Section: Discussionmentioning

confidence: 99%

“…However, patients in the Tsutumi et al radiological study did not undergo full visual testing, so it is possible that patients had unidentified visual dysfunction. 37 This feature also highlights that there is an incomplete understanding of the exact mechanism of loss of function in artery-nerve compression and interaction. As yet unidentified factors may be involved in leading AVP compression to manifest with symptomatic visual dysfunction.…”

Section: Discussionmentioning

confidence: 99%

“…Colour vision was also not routinely tested in the patients. As previously mentioned, such vascular compression of AVP structures may occur with a relatively high frequency in asymptomatic individuals, 37,38 rendering its role in causing unexplained visual field defects still difficult to define. Our group plans to undertake a study with 250 prospective consecutive MRIs from otherwise normal patients in order to establish the frequency of contact or compression of the AVP by any of the four arteries cited and assess for any ophthalmological findings.…”

Section: Discussionmentioning

confidence: 99%

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Intracranial Arterial Compression of the Anterior Visual Pathway

Jain

Kam

Chong

et al. 2019

Neuro-Ophthalmology

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Compression of anterior visual pathway (AVP) structures by intracranial arteries is observed not infrequently on neuroimaging. Whether or not such compression results in damage to these structures, however, remains unclear. This information is important to define as AVP compression by intracranial arteries may be a causative factor in patients with otherwise unexplained visual dysfunction. In a single centre, 37 patients with evidence of intracranial artery AVP compression demonstrated on magnetic resonance imaging were identified by retrospective review of case records over the period 2011-2017. Variables were collected, including patient demographics, visual acuity, visual fields, pupillary reactions and optic disc appearance for patients in the case series. Visual field deficits correlated with compression sites in the 37 patients examined. Internal carotid artery-optic nerve compression was the most frequent (unilateral compression n = 9, bilateral compression n = 14), followed by chiasmal compression by the anterior cerebral artery (n = 8) and a combination of optic nerve and chiasmal compression (n = 5). Visual acuity and visual fields were stable on follow-up (mean 4 years) in 24 of 26 cases (93%). We conclude that AVP compression by intracranial arteries may be a causative factor in unexplained visual dysfunction. The visual defects are largely non-progressive.

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“…These aneurysms are difficult to diagnose since they are manifested only by a gradual decrease in visual acuity and the development of CS. Aneurysm rupture resulting in subarachnoid hemorrhage may be clinically manifested by sudden headache, neurological deficit and decrease in visual acuity [20,29,30].…”

Section: Intrachiasmal Lesionsmentioning

confidence: 99%

Neuro-opthalmological aspect of chiasmal-and-sellar disorders

Vasyuta¹,

Pedachenko²

2018

Oftalmol Zh

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This article reviews the causes, pathogenesis, and major manifestations of chiasmal syndrome. In addition, it reviews the methods for diagnosing the condition, and the course of the syndrome in patients with various chiasmal-and-sellar disorders such as pituitary adenoma, craniopharyngioma, tuberculum sellae meningioma, and skull base aneurysm. The principle neuro-ophthalmological symptoms include decreased visual acuity, bitemporal visual field defects, and development of descending optic nerve atrophy. Early detection of ophthalmological symptoms is of critical importance for timely neurosurgical treatment.

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Vascular Compression of the Anterior Optic Pathway: A Rare Occurrence?

Abstract: Vascular compression of the ON and OC may not be an infrequent occurrence in the cranial cavity. Progressive and unexplainable visual impairment might possibly be caused by vascular-compressive neuropathy.

Cited by 7 publications

References 20 publications

<p>Variable structure and function relationship of compressive optic neuropathy at the time of diagnosis</p>

<p>Variable structure and function relationship of compressive optic neuropathy at the time of diagnosis</p>

Intracranial Arterial Compression of the Anterior Visual Pathway

Neuro-opthalmological aspect of chiasmal-and-sellar disorders

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