Bacillary Layer Detachment (BALAD) is an OCT finding showing a separation within the retina occurring between the external limiting membrane (ELM) and the ellipsoid zone (EZ)—that is, at the site of the photoreceptor inner segment myoid zone (MZ) 5).
The term “bacillary” originates from neuroanatomist Polyak’s 1941 definition of the photoreceptor inner and outer segments (IS-OS) as the “bacillary layer.” BALAD was formally named in 2018 when Mehta et al. reported this OCT finding in patients with toxoplasmosis and pachychoroid disease 1),3),5),9).
Although the incidence is rare, reports are increasing annually. In exudative AMD (nAMD) cohorts, the incidence is 4.5% (20 of 442 eyes), and in the HAWK trial it was reported as 7.2% 4). In Vogt-Koyanagi-Harada disease, a high incidence of 47% has been shown 9), and the frequency varies greatly by disease category. The disease-specific frequencies in reported cases are: VKH 47%, APMPPE 11%, sympathetic ophthalmia 7.3%, choroidal neovascularization 6.2%, toxoplasmosis 5.5%, and AIm 5.5% 9).
The first report of “intraretinal fluid accumulation in the outer retina” was by Maruyama & Kishi in 2009, in patients with Vogt-Koyanagi-Harada disease 9).
In nAMD, it is found in 4.5–7.2% of cases; in Vogt-Koyanagi-Harada disease, up to 47%. It is a rare but important finding, often appearing in the acute or exudative phase of the disease.
Subjective symptoms depend on the underlying disease. Representative examples are shown below.
Inflammatory diseases (e.g., toxoplasmosis, Vogt-Koyanagi-Harada disease) often have acute onset3),6). In contrast, degenerative diseases and those based on choroidal neovascularization (CNV) follow a gradual course.
BALAD is diagnosed by OCT. Characteristic findings are shown below.
Structure of BALAD
Location of the hyporeflective cavity: A separation cavity formed between the ELM and EZ (photoreceptor IS myoid)5)
Reflectivity within the cavity: Contains floating hyperreflective material of moderate reflectivity1),4)
Shape: Characteristic pear-shaped (piriform) with an acute angle at the base
SRF co-occurrence: Often accompanied by subretinal fluid (SRF)5)
Multimodal Imaging
FAF: Central hypoautofluorescence with a surrounding hyperautofluorescent ring1)
OCTA: In nAMD, subretinal neovascularization can be detected4)
Common locations: Fovea > Parafovea > Peripapillary
CRT examples: In 3 nAMD cases, 929 μm, 598 μm, and 543 μm were recorded4)
Choroidal thickening is observed in 93.8% of BALAD cases8).
There are two subtypes of BALAD associated with rhegmatogenous retinal detachment (RRD)2).
SRF is a hyporeflective fluid space between the RPE and neurosensory retina. In contrast, BALAD is a separation occurring between the ELM and EZ (myoid), and it also differs in that it contains hyperreflective material of moderate reflectivity within the cavity. Judgment is made based on both location and reflectivity characteristics.
BALAD is not a single disease but is observed in a heterogeneous group of diseases sharing common OCT findings.
Inflammatory Diseases
Infectious (non-granulomatous): Toxoplasma retinochoroiditis3), endogenous fungal endophthalmitis9)
Infectious (granulomatous): Tuberculous serpiginous-like choroiditis (SLC)6)
Non-infectious: Vogt-Koyanagi-Harada disease, sympathetic ophthalmia, acute posterior multifocal placoid pigment epitheliopathy, AIm. COVID-19-related (steroid use + systemic inflammatory state) 8)
Degenerative and vascular diseases
Neovascular age-related macular degeneration (nAMD): The most commonly reported degenerative disease 1),4),5)
Pachychoroid-related: CSCR (central serous chorioretinopathy) 7),8). In high hyperopia, short axial length → choroidal congestion → CSCR pathway can lead to BALAD 7)
Other vascular diseases: Hypertensive retinopathy, preeclampsia, diabetic retinopathy, retinal vein occlusion 5)
Tumors, trauma, and drug-induced
Tumors: Choroidal osteoma, choroidal lymphoma, choroidal metastasis
Trauma: Blunt trauma, choroidal rupture, rhegmatogenous retinal detachment 2)
Drug-induced: Dabrafenib, trametinib (MEK/BRAF inhibitors)
The following shows the differential diagnosis from diseases with OCT findings similar to BALAD.
| Disease | Location of cavity | Intracavitary reflectivity |
|---|---|---|
| BALAD | Between ELM and EZ | Moderate reflectivity |
| SRF/SRD | Between RPE and neurosensory retina | Low reflectivity (anechoic) |
| Retinoschisis | Within the neurosensory retina | Connecting strands present |
There is no specific treatment for BALAD itself. Treating the underlying disease leads to resolution of BALAD.
The course until BALAD resolution for each disease is shown.
| Underlying disease | Treatment | Expected time to BALAD resolution |
|---|---|---|
| nAMD | Anti-VEGF injection | Rapid resolution |
| VKH disease | IV methylprednisolone | 2–5 days |
| Toxoplasma | TMP-SMX + steroid | Within 1 week |
| Tuberculous SLC | ATT + prednisone | Approximately 2 months |
| CSCR | Laser photocoagulation | Approximately 16 days |
The first-line treatment for nAMD is anti-VEGF intravitreal injection, and BALAD disappears rapidly after treatment1),4),5). The main drugs and doses are as follows5).
Jung JJ et al. (2021) reported two cases in which BALAD completely disappeared after a single bevacizumab injection5). In the first case, best-corrected visual acuity improved from 20/80 to 20/25, and in the second case, from 20/160 to 20/50. A case has also been reported in which CRT decreased from 929 μm to 310 μm and best-corrected visual acuity improved from CF to 20/50 after six aflibercept injections4).
Desai & Tyagi (2023) reported that in toxoplasmic retinochoroiditis, TMP-SMX (160/800 mg twice daily for 2 months) alone resulted in persistent inflammation and enlargement of BALAD, but the addition of prednisolone 50 mg/day led to resolution of BALAD within one week 3).
For tuberculous SLC, combination therapy with ATT (rifampicin + isoniazid + pyrazinamide + ethambutol) plus prednisone 60 mg/day has been reported to resolve BALAD within 2 months 6).
Laser photocoagulation (532 nm, 250 μm, 50 mW, 200 ms) for CSCR-related BALAD associated with high hyperopia has been reported to resolve BALAD within 16 days 7). In CSCR patients using steroids, discontinuation of steroids should be considered 8).
The choice of surgical procedure for rhegmatogenous retinal detachment-related BALAD depends on the subtype 2).
Intravitreal injection of voriconazole 100 μg/0.05 mL combined with systemic antifungal therapy has been reported to resolve BALAD within 3 weeks 9).
BALAD often resolves with treatment of the underlying disease. In nAMD, anti-VEGF injections; in inflammatory diseases, steroids and antibiotics can make BALAD disappear. However, even after BALAD resolves, long-term visual impairment may persist, for example, 77% of nAMD cases develop subretinal fibrosis within 4 years 4).
The inner segment (IS) of photoreceptors is functionally divided into two zones.
The structural vulnerability of the MZ provides the anatomical basis for BALAD formation.
Mehta et al. proposed two factors in BALAD formation 5).
Rapid influx of proteinaceous fluid through defects in the RPE/Bruch membrane complex elevates the ELM. Additionally, subretinal hemorrhage may form fibrin adhesions between the EZ and RPE, leading to cleavage in the MZ 5).
Choroidal thickening is observed in 93.8% of BALAD cases 8). In Vogt-Koyanagi-Harada disease and acute posterior multifocal placoid pigment epitheliopathy, choroidal ischemia is thought to induce BALAD.
Tangential forces at the macula are thought to disrupt the Müller cell cone, leading to ELM detachment and splitting in the MZ 2).
Govetto et al. (2023) proposed the possibility of a “foveation mechanism” in which healthy parafoveal cones migrate centripetally to reconstruct the fovea during BALAD repair after rhegmatogenous retinal detachment 2). Since post-mitotic cones cannot replicate, this hypothesis suggests foveal regeneration through migration rather than new formation.
The myoid zone (MZ) is structurally less robust than the ELM or EZ and represents an anatomical weak point. It is known that artificial separation easily occurs at this site in tissue specimens 5),9). When hydrostatic pressure from the choroid increases, splitting occurs at this weak point, leading to BALAD formation.
Flindris et al. (2025) reported that BALAD associated with nAMD is a biomarker indicating an aggressive disease phenotype 4). It was shown that 77% of nAMD eyes with BALAD developed subretinal fibrosis within 4 years. This suggests that BALAD may serve not only as an OCT finding but also as a prognostic indicator.
In more than half of BALAD cases, gradual recovery of EZ and IZ is observed 9). Since cone photoreceptors are post-mitotic and cannot replicate, the aforementioned foveation mechanism (centripetal migration for foveal reconstruction) may be key to recovery 2).
There has been a report of choroidal neovascularization occurring after the disappearance of BALAD associated with endogenous fungal endophthalmitis 9), suggesting that BALAD may form a substrate for choroidal neovascularization through damage to the outer retinal layers.
The precise histopathological correlation of BALAD remains unestablished 1),4),5). Currently, most reports are case reports or small case series, and large-scale prospective studies are needed to elucidate the natural course and prognostic factors of BALAD.
