Visual field and OCT are two most commonly used clinical examine methods for nerve injury disorder, such as glaucoma and intracranial tumor. And the Cluster analysis program in Octopus perimeter, which is designed according to the distribution of RNFL, can sensitively detect regional dysfunction when there are minimal visual field abnormalities. Perdicchi’s study showed within normal VF and abnormal ganglion cell complex (GCC) eyes of hypertension or early stage glaucoma, all of the 23 eyes showed abnormal results with cluster analysis[8]. Some studies had shown the correlation between the structure and function in glaucoma patients with Humphrey or Octopus perimeter and OCT[9–11]. Generally these studies all found a topographic correlation in VF and OCT. But few studies have explored the topographic correlation in intracranial tumor patients with Octopus perimeter and OCT, fewer are about cluster analysis.
Our study shows a relative weak correlation between the MD of OP clusters with the thickness of RNFL in seven of ten OP clusters in those intracranial tumor patients (cluser1, 5, 6–10), most correlation coefficient absolute value is less than 0.45. While in the glaucoma patients, with each OP cluster, we find moderate correlations in more than one RNFL sector, which is similar with other studies[12–14]. Also the map (Fig. 2) shows the topographic structure-function relationship in glaucoma. Previous studies also showed a moderate association between RNFL thickness in each sector with VF region either in Octopus or Humphrey perimetry in glaucoma patients[9–11], a structure-function map which is similar with ours was created.
We assume the result may correlate with the different retinal ganglion cells (RGCs) damage mechanisms in glaucoma and intracranial tumor. It is well-known that glaucoma is characterized by the damage to RGCs axons initialing at the optic nerve head with different mechanisms, such as intraocular pressure mechanical compression, vascular disorders, immunologic influence, and oxidative stress. That may lead to the direct retrograde damage to the RGCs, following with the RNFL thinning and VF defect. Also some studies show glaucoma optic disk change correlated with the intraorbital optic nerve measurement and chiasmal size[15–17], which suggest glaucoma may also lead to anterograde degeneration post optic disk. Therefore, glaucoma may produce a bidirectional nerve injury from the optic nerve head.
While intracranial tumors cause the retrograde degeneration on the visual pathway, the pathologic changes starts from the distal axonal and progresses centripetally, which is also found in other central nervous system pathologies such as cerebral infarction, head trauma, multiple sclerosis[18–20]. That includes two conditions. Tumor arising near the sella turcica causing the axonal or terminal lesions between the eye and the lateral geniculate body, leads to the direct retrograde degeneration[6]. Whereas, tumors arising post lateral geniculate body cause damage to the optic radiation after the tertiary neurons in the visual pathway and lead to the trans-synaptic retrograde retinal degeneration (TRD). It also causes the RNFL thinning and the optic nerve head vessel density decrease[18, 21, 22]. This is mechanically different from the damage of RGCs and axons in glaucoma.
Previous research showed the chiasmal lesion caused more prominent optic nerve head vessel density decrease than postgeniculate lesion, which indicated the direct retrograde degeneration might be more prominent than TRD[22]. And our study shows the RNFL thinning is less prominent than glaucoma’ RGCs’ degeneration, both of the direct and trans-synaptic retrograde induced by the intracranial tumor. Whether the RNFL damage extent is negative correlated with the distance from the initial site of injury to the RGCs remains unknown and need more research to prove.
Another hypothesis is that the weak structure-function correlation in intracranial tumor patients is mightly due to the less injury of RNFL caused by direct or trans-synaptic retrograde. Our study yields two age and VF matched groups, of glaucoma and intracranial tumor, and shows more severe RNFL damage, smaller rim area, larger cup volume and larger C/D (P < 0.05) in the glaucoma patients. Also some study showed the optic chiasmal Compression might cause the cell-inner plexiform layer thinning without RNFL changing in the early phase of some intracranial tumors[23, 24]. However, Orman’s study showed, pituitary tumors might have RNFL thinning and RGCs degeneration without VF defect[25]. These inconsistencies in structure and function may also lead to the weak structure-function correlation in those intracranial tumor patients.
In the contrast to the intracranial tumor, in our study, at the same age range and VF MD levels, glaucoma patients have more severe RNFL and optic nerve head damage. The logistic regression analysis shows the RNFL loss tending to the diagnosis of glaucoma; the VF damage is inclined to the diagnosis of intracranial tumor. Few studies had ever explored the RNFL difference between those two VF-affected diseases. This may provide some information for the antidiastole.
There are some limitations in our study. First, the smaller number of participants may introduce some selection bias. Second, there are not enough post-geniculate participants to analysis the direct and transsynaptic retrograde degeneration respectively. The same problem exists in the angle-closed and open glaucoma cases. Further study should be conducted to explore more detailed information.
In conclusion, due to few correlation coefficients, intracranial tumor has a weak correlation between the RNFL thickness and Octopus visual field MD, compared with the glaucoma. RNFL and optic nerve head damage was more prominent in glaucoma patients when compared to intracranial tumor patients. OCT and Octopus visual field may provide more information for the antidiastole of intracranial tumor and glaucoma.