Junctional scotoma (JS) is a visual field defect resulting from a lesion at the junction of the optic nerve and optic chiasm. The classic pattern is a central scotoma in the ipsilateral eye and a superotemporal visual field defect (respecting the vertical midline) in the contralateral eye. In ophthalmology, it is also called “combined scotoma” and is seen in compressive lesions at the optic nerve-chiasm junction.
Traquair junctional scotoma (JST) refers to a monocular temporal (or rarely nasal) hemianopic visual field defect in the ipsilateral eye from the same junctional lesion. It is named after the Scottish ophthalmologist Traquair, who described a monocular temporal scotoma in anterior chiasmal compression.
“Complete junctional scotoma” is a condition where both the superior and inferior temporal visual fields of the contralateral eye are defective, occurring when both the superior and inferior contralateral nasal fibers are affected. It may be seen in rapidly progressive cases such as metastatic tumors1).
In 1904, German ophthalmologist Herman Wilbrand reported a structure in which nasal crossing fibers detour in an arc within the contralateral optic nerve (Wilbrand’s knee). This anatomical structure was long used to explain the mechanism of junctional scotoma. However, in 1997, Horton showed in primate experiments that Wilbrand’s knee is an artifact of monocular enucleation, and in 2014, Shin et al. reported its existence in normal individuals using DTI, but Horton (2020) again argued it is an artifact. The existence of Wilbrand’s knee remains unresolved, but junctional scotoma is still observed clinically, and its anatomical basis is under debate3).
In a retrospective study of 53 cases of chiasmal compression, the patterns of visual field defects were reported as bitemporal hemianopia in 26%, junctional scotoma in 34%, and monocular visual field defect in 7%3).
JS is a binocular visual field abnormality consisting of a central scotoma on the side of the lesion plus a superotemporal quadrantanopia in the contralateral eye. JST is a monocular temporal (or nasal) hemianopic visual field defect in the eye on the side of the lesion, with the contralateral visual field preserved. Both arise from the same lesion at the optic nerve-chiasm junction, but the pattern differs depending on the type and extent of fibers affected.
Junctional Scotoma (JS)
Findings in the affected eye: Positive RAPD, optic atrophy, central scotoma.
Findings in the contralateral eye: Upper temporal visual field defect (respecting the vertical midline). In complete type, defect of the entire upper temporal quadrant.
Band atrophy: May appear in the contralateral eye due to damage to nasal fibers.
Junctional Scotoma of Traquair (JST)
Findings on the affected side: Positive RAPD, monocular temporal (or rarely nasal) hemianopic visual field defect.
Band atrophy: In the temporal hemianopia type, may appear in the affected eye.
Hourglass atrophy: In the nasal hemianopia type (rare) of JST, appears on the affected side due to atrophy of temporal fibers.
Other common clinical findings include the following.
Yes, it can. Cases have been reported where patients with paraganglioma metastasis (visual acuity 20/25) or meningioma (visual acuity 20/20) had junctional scotoma or Traquair junctional scotoma despite normal visual acuity 2,3). Normal visual acuity does not rule out visual field defects; formal automated perimetry is essential.
The most common cause of junctional scotoma is pituitary adenoma, followed by tumors of the skull base, vascular lesions, and inflammatory diseases.
Pituitary adenoma is the most common cause. Because it compresses the optic chiasm from directly below upward, the inferonasal retinal nerve fibers are easily damaged, leading to bitemporal hemianopia or junctional scotoma that is more pronounced superiorly. However, junctional scotoma is not necessarily caused only by pituitary adenoma; various causes such as meningioma, aneurysm, and optic neuritis exist.
The diagnosis of junctional scotoma requires a combination of automated perimetry, OCT, and imaging (MRI).
The roles of the main examination methods are shown below.
| Examination | Main role | Notes |
|---|---|---|
| Automated perimeter (HFA 24-2/30-2) | Accurate detection of visual field defects | Risk of missing defects with confrontation method |
| OCT (RNFL/GCC analysis) | Evaluation and early detection of nerve atrophy | Can detect abnormalities before visual field defects appear |
| Contrast-enhanced MRI | Visualization of compressive lesions | Coronal and sagittal views also essential |
Formal automated perimetry (Humphrey 24-2 or 30-2) is essential for accurate diagnosis of junctional visual field defects. Confrontation testing alone risks missing junctional scotomas. Visual field defect patterns that respect the vertical midline are important clues for differentiating from glaucomatous visual field defects.
Differentiation from NTG is particularly important. The following findings suggest a compressive lesion.
If contrast enhancement of the optic nerve or chiasm is observed after imaging, infectious (syphilis, tuberculosis), inflammatory (sarcoidosis, vasculitis), infiltrative (lymphoproliferative disorders), and demyelinating (MS, NMOSD, MOG antibody-related) conditions should also be considered in the differential diagnosis. In such cases, serological tests and cerebrospinal fluid examination should also be considered.
Yes. Reports indicate that up to 8% of NTG patients have compressive lesions of the anterior visual pathway 3). Cupping of the optic disc can also occur in compressive optic neuropathy, and 44% of non-glaucomatous optic atrophy cases are misdiagnosed as glaucoma. If RAPD, color vision abnormalities, disc/field mismatch, or temporal RNFL thinning are present, compressive lesions should be strongly suspected, and neuroimaging should be performed.
Treatment targets the underlying disease. Early intervention is crucial for recovery of visual function, as recovery becomes difficult once optic atrophy is evident.
The optic chiasm is a structure measuring 12–18 mm in transverse diameter, 8 mm in anteroposterior diameter, and 4 mm in height, located above the sella turcica and pituitary gland. Anteriorly, it contacts the cerebrospinal fluid of the subarachnoid space, and posteriorly it forms the floor of the third ventricle. The ophthalmic arteries, branching from the internal carotid arteries, run along both lateral sides.
The crossing ratio of optic nerve fibers is 53% from the nasal hemiretina (crossing fibers) and 47% from the temporal hemiretina (non-crossing fibers).
When a lesion occurs at the junction of the optic nerve and optic chiasm, it damages the ipsilateral optic nerve, causing a central scotoma, and simultaneously affects the contralateral inferior nasal retinal fibers (which pass through the anterior optic chiasm), resulting in a superior temporal visual field defect in the contralateral eye. If both superior and inferior nasal fibers on the contralateral side are affected, a complete junctional scotoma occurs1).
In junctional scotoma of Traquair, depending on the type of fibers affected, if the temporal fibers of the affected eye are damaged, it presents as temporal hemianopia (more common), and if the nasal fibers are damaged, it presents as nasal hemianopia (rare).
The pattern of visual field defects differs depending on the direction of compression.
Barton & Ozturan (2025) retrospectively analyzed 17 cases of junctional scotoma and reported that visual field defect patterns may help identify not only anatomical localization but also the type of underlying disease. Classic JS was associated with compressive lesions from the ventral side, while JS involving the inferior temporal quadrant suggested dorsal compression or non-compressive etiologies. The nasal visual field defect pattern in JST was also shown to be rarely associated with pituitary adenoma.
Advances in GCC (ganglion cell complex) analysis have shown the potential to detect chiasmal compression before visual field defects appear. Loss of nasal-temporal asymmetry in macular GCC analysis is noted as a very early sign, and its application as a predictive tool for postoperative visual recovery is also being studied3).
Although the cost-effectiveness of performing neuroimaging in all NTG patients is debated, the fact that up to 8% of NTG patients have compressive lesions of the anterior visual pathway suggests that neuroimaging should be actively performed at least in cases with atypical visual field defect patterns or prominent temporal RNFL thinning3).
