Structural-functional dissociation in glaucoma: an attempt to end controversy.

Dear Editor,

We read with interest the article titled “Evidence-based approach to glaucoma management” by Garudadri et al.[1] Standard automated perimetry (SAP) is the current standard in glaucoma diagnosis, but 20-40% retinal ganglion cells could be lost before a visual field defect could be picked up by SAP. The reported sensitivity and specificity of image technologies and their agreement with each other are far from ideal. Brain and eye have adaptive strategies to compensate scotoma. Safran and Landis[2] in a review article described the effects of plasticity in the adult visual cortex. Plasticity plays a crucial role in recovery from damage to the visual system. Cortical remapping generates a filling-in of visual field defects. Cortical rearrangement following lesions in the visual pathways helps to compensate for gaps in perception. Filling-in is a major cause of failure of patients with simple chronic glaucoma to recognize their visual defects at an early stage. Qing et al.,[3] have documented that more affected the visual field (SAP), the less affected the functional magnetic resonance image response. This phenomenon may imply a replasticity or a compensatory mechanism of the visual pathway. Peripheral scotoma may have a potentiating effect on the central reserved visual field. Decreased retina input may result in replasticity of the cortical neurons and enhance the information processing and integrity ability of the visual cortex. Measurement of blue chromatic thresholds in the macular region might make it possible to detect functional damage due to glaucoma prior to morphological changes of the optic nerve head of glaucoma patients. Probably a combination of decreased peripheral sensitivity with increased central retinal sensitivity may be suggestive of early glaucoma. Alzheimer's disease and Parkinson's disease cause retinal nerve fiber loss (RNFL). Evidence shows that microtubules in nerve fiber bundles are the major contributors for retinal nerve fiber layer birefringence, and microtubules are expected to disappear after the ganglion cells die. It remains to be clarified whether the time lag between cell death and microtubules disappearance or other subcellular changes differ between primary open angle glaucoma (POAG) and primary angle closure glaucoma. Preferred retinal locus (PRL) and oculomotor re-referencing are adaptive strategies of eye to compensate scotoma.[4] A PRL can be defined as a discrete retinal area that contains the center of target image for greater than 20% of a fixation interval. Oculomotor re-referencing is a phenomenon seen in patients who describe themselves as looking straight ahead when they are fixating with PRL (i.e., when the eye is not in the primary position). Fixation instability is a feature documented in early and moderate POAG.[5] This may be considered as an evidence for ocular adaptive strategy to compensate scotoma because eccentric fixation induces instability. Probably a combination of RNFL and recent onset fixation instability may improve sensitivity and specificity of image technologies. In conclusion, we agree with the authors advice that good history taking, proper clinical examination, documentation of details, supplemented with appropriate investigations, counseling, and proper follow-up enhance the care of the patient and family.