Glaucomatous Optic Neuropathy: Associated With Cognitive Impairment?

To the Editor: With great interest, we read the article by Kolomeyer et al1 reporting that the visual evoked potential (VEP) response to an isolated-check pattern decreases in cases with varying degrees of glaucoma. The isolated-check VEP measured the central visual function within a 10 by 10 degree visual field. It has been postulated that the low contrast, high temporal frequency isolated-check stimuli preferentially activate the magnocellular pathway of visual processing, and the magnocellular stream may be influenced early in glaucoma.2 However, the cause of the magnocellular stream dysfunction and consequently the decrease in the isolated-check VEP response in the patients with glaucoma remain to be elucidated. Cognitive impairment is common in old cases with glaucoma.3 On the other hand, a significantly enlarged optic cup to disc ratio has been reported in cases with cognitive dysfunction.4 Cognitive impairment is associated with central nervous system (CNS) neurodegeneration. The optic nerve as a part of CNS might also be influenced in brain neurodegeneration. Structural and functional assessments of the optic nerve provide evidences for CNS degeneration. Peripapillary retinal nerve fiber layer thickness decreases in patients with cognitive impairment.5 The function of the optic nerve has been evaluated using VEP. The VEP amplitude response decreases in cases with cognitive dysfunction6 even with mild cognitive impairment.7 Specifically, the response arises from the magnocellular stream of visual processing reduces.8 Both retinal and corticosubcortical evidences have been provided for the magnocellular pathway involvement in cases with cognitive dysfunction; however, the association between the current evidences and their cause and effect relationships remain unclear. The retinal ganglion cell loss in the magnocellular stream may be secondary to retrograde axonal degeneration. However, it remains obscure whether the axonal loss is a primary optic neuropathy with secondary CNS neurodegeneration or secondary to intracranial neurodegeneration or a combination of them. Consequently, the ocular biomechanical risk factors of glaucoma9 may initiate or speed up the optic neurodegeneration in glaucomatous optic neuropathy development. Taken together, the optic neuropathy in patients with glaucoma may be associated with brain neurodegeneration, and the reduced isolated-check VEP response in cases with primary glaucoma may be associated with cognitive impairment. In the future research, the VEP response needs to be correlated with cognitive function of patients with glaucomatous optic neuropathy. Since there are common neuropathologic changes and pathophysiological mechanisms in glaucoma and brain neurodegenerative diseases,10 there may be an association between glaucomatous optic neuropathy and cognitive dysfunction. Moreover, the investigation of their causal relationship is of particular interest. The glaucomatous optic neuropathy may result in or from brain neurodegeneration. Cognitive function plays an important role in patient adherence to the treatment for glaucoma. If it turns out that the VEP response correlates with cognitive function of cases with primary glaucoma, the VEP technique will help us to monitor their risk of poor adherence to the therapy. It will enable us to identify cases at risk of glaucoma progression even at the early stages of the disease. Poor cognitive function and poor adherence to the therapy put the patients at a high risk of the disease progression. The VEP technique as a feasible, available, inexpensive, and noninvasive tool will be more commonly used in glaucoma clinics to monitor the patients’ cognitive function and adherence to the treatment.


To the Editor:
With great interest, we read the article by Kolomeyer et al 1 reporting that the visual evoked potential (VEP) response to an isolated-check pattern decreases in cases with varying degrees of glaucoma. The isolated-check VEP measured the central visual function within a 10 by 10 degree visual field. It has been postulated that the low contrast, high temporal frequency isolated-check stimuli preferentially activate the magnocellular pathway of visual processing, and the magnocellular stream may be influenced early in glaucoma. 2 However, the cause of the magnocellular stream dysfunction and consequently the decrease in the isolated-check VEP response in the patients with glaucoma remain to be elucidated.
Cognitive impairment is common in old cases with glaucoma. 3 On the other hand, a significantly enlarged optic cup to disc ratio has been reported in cases with cognitive dysfunction. 4 Cognitive impairment is associated with central nervous system (CNS) neurodegeneration. The optic nerve as a part of CNS might also be influenced in brain neurodegeneration. Structural and functional assessments of the optic nerve provide evidences for CNS degeneration. Peripapillary retinal nerve fiber layer thickness decreases in patients with cognitive impairment. 5 The function of the optic nerve has been evaluated using VEP. The VEP amplitude response decreases in cases with cognitive dysfunction 6 even with mild cognitive impairment. 7 Specifically, the response arises from the magnocellular stream of visual processing reduces. 8 Both retinal and corticosubcortical evidences have been provided for the magnocellular pathway involvement in cases with cognitive dysfunction; however, the association between the current evidences and their cause and effect relationships remain unclear. The retinal ganglion cell loss in the magnocellular stream may be secondary to retrograde axonal degeneration. However, it remains obscure whether the axonal loss is a primary optic neuropathy with secondary CNS neurodegeneration or secondary to intracranial neurodegeneration or a combination of them. Consequently, the ocular biomechanical risk factors of glaucoma 9 may initiate or speed up the optic neurodegeneration in glaucomatous optic neuropathy development. Taken together, the optic neuropathy in patients with glaucoma may be associated with brain neurodegeneration, and the reduced isolated-check VEP response in cases with primary glaucoma may be associated with cognitive impairment. In the future research, the VEP response needs to be correlated with cognitive function of patients with glaucomatous optic neuropathy. Since there are common neuropathologic changes and pathophysiological mechanisms in glaucoma and brain neurodegenerative diseases, 10 there may be an association between glaucomatous optic neuropathy and cognitive dysfunction. Moreover, the investigation of their causal relationship is of particular interest. The glaucomatous optic neuropathy may result in or from brain neurodegeneration.
Cognitive function plays an important role in patient adherence to the treatment for glaucoma. If it turns out that the VEP response correlates with cognitive function of cases with primary glaucoma, the VEP technique will help us to monitor their risk of poor adherence to the therapy. It will enable us to identify cases at risk of glaucoma progression even at the early stages of the disease. Poor cognitive function and poor adherence to the therapy put the patients at a high risk of the disease progression. The VEP technique as a feasible, available, inexpensive, and noninvasive tool will be more commonly used in glaucoma clinics to monitor the patients' cognitive function and adherence to the treatment. The association between glaucoma and cognitive function remains controversial. [3][4][5] Regardless, the issue of cognitive impairment is pervasive in glaucoma. Patients with cognitive impairment are more likely to have unreliable or variable visual field tests, especially false negatives. 6,7 Studies have also suggested that optical coherence tomography may be affected by cognitive decline, as decreased retinal nerve fiber layer thickness has been reported in Alzheimer's disease. 8 Dr Norozpour makes some interesting points regarding the use of icVEP for the assessment of cognitive function. In fact, icVEP has been recommended as part of a battery of tests to assess perceptual/cognitive functions in individuals with schizophrenia during clinical trials. 9 There is evidence in the literature for anterograde transneuronal degeneration associated with glaucoma and possibly retrograde degeneration from brain to retina. 10 To the Editor:

Amir Norouzpour, MD
We read with great interest the article "Phacoemulsification versus Phacotrabeculectomy in primary angleclosure glaucoma with cataract: long term clinical outcomes" 1 by Hansapinyo and colleagues and would like to appreciate the work of the authors for the same.
Choosing phacoemulsification or phacotrabeculectomy in primary angleclosure glaucoma (PACG) patients with cataract has been a topic of great debate and there is no clear consensus on it.
We would like to highlight few points in the study which require some clarification.
In the present study, PACG has not been classified into early and advanced disease. The intraocular pressure (IOP) lowering requirement and subsequent need for antiglaucoma medications would vary according to the severity of the disease. Such randomization can give false results. Authors have mentioned that 10 patients in Phaco group required further trabeculectomy. Whether they were from medically controlIed IOP group or uncontrolled group is not clear.
Yag capsulotomy has been considered as additional surgery in both groups. Authors have found 6 and 4 patients in Phaco group and Phacotrab group, respectively, to have developed posterior capsular opacification. Out of which 2 and 3 patients in Phaco and