Neuro-Ophthalmic Literature Review

Neuro-Ophthalmic Literature Review Carmen Chan, Evan Price, John H. Pula, Matthieu Robert, Michael Vaphiades, An-Guor Wang, and Sui Wong HIV NEURORETINAL DISORDER Jabs DA, Drye L, Van Natta ML, Thorne JE, Holland GN; Studies of the Ocular Complications of AIDS Research Group. Incidence and long-term outcomes of the human immunodefıciency virus neuroretinal disorder in patients with AIDS. Ophthalmology 2015;122:760–768. Patients with acquired immunodeficiency syndrome (AIDS) can have subtle abnormalities of vision (e.g. decreased contrast sensitivity, abnormal colour vision, visual field loss, abnormal results on other psychophysical tests) in the absence of ocular infection or media opacity. This is presumed to be caused by an ‘‘HIV neuroretinal disorder’’. A neuroretinal origin of the visual loss is supported by decreased retinal nerve fibre layer thickness on optical coherence tomography (OCT) and autopsy results of AIDS patients showing loss of optic nerve axons. In this paper, the authors used decreased contrast sensitivity as a marker for human immunodeficiency virus (HIV) neuroretinal disorder and analysed the contrast sensitivity data of the Longitudinal Study of the Ocular Complications of AIDS (LSOCA). LSOCA is a prospective, multi-centred observational cohort study of patients with AIDS, which recruited patients from 19 US centres. Out of the 1822 patients available for analysis, 294 (16%) had the HIV neuroretinal disorder at enrolment. HIV neuroretinal disorder was more common in women and African Americans, and it was associated with hepatitis C infection, low CD4 count, and detectable HIV RNA in the blood. Patients with HIV neuroretinal disorder tended to have a mildly but significantly reduced visual acuity and Humphrey visual field mean deviation at baseline; and the presence of HIV neuroretinal disorder was associated with a significantly higher risk of bilateral visual impairment and mortality during follow-up. The authors estimated that the cumulative incidence of HIV neuroretinal disorder was up to 50% 20 years after AIDS diagnosis. Therefore, HIV neuroretinal disorder is an important differential diagnosis of ‘‘visual loss of unknown cause’’ in AIDS patients. Carmen Chan LAMINA CRIBROSA QUALITIES ON EDI FOUND TO BE DETERMINANTS OF RNFL THICKNESS Lee EJ, Kim TW, Kim M, Kim H. Influence of lamina cribrosa thickness and depth on the rate of progressive retinal nerve fiber layer thinning. Ophthalmology 2015;122:721–729. In this prospective, observational study, the authors investigate the association of lamina cribrosa thickness (LCT) and lamina cribrosa depth (LCD) with rate of thinning of the retinal nerve fibre layer (RNFL) as measured by spectral-domain (SD) optical coherence tomography (OCT). One hundred ten eyes with primary open-angle glaucoma (POAG) were followed by SD OCT for at least 2.5 years. LCD and LCT were assessed by enhanced depth imaging (EDI) SD OCT. In prior experimental studies, posterior displacement (increased LCD) and thinning of the lamina cribrosa have been shown to precede RNFL loss. Increased LCD and decreased LCT have been demonstrated histologically in glaucomatous eyes. However, this is the first known report to demonstrate that increased LCD and decreased LCT precede thinning of the RNFL on SD OCT and contribute to an increased rate of RNFL thinning. Notably, the authors also identified an LCD breakpoint (489.7 mm) when Davies’ test was 152 employed, implying that LCD became a statistically significant determinant of RNFL thickness specifically when it was greater than this value. The authors note that it would be interesting to investigate whether increasing LCD has biomechanical implications in addition to its serving as a marker of lamina cribrosa displacement. They also posit that decreased LCT may impart a biomechanical disadvantage, possibly through pinching of axons and relative blockade of axoplasmic flow or through compression of laminar capillaries. They also note that pseudoexfoliation glaucoma patients with the same disease severity have a thinner LCT than their POAG counterparts, as well as a worse prognosis. Evan Price VISION IS PAINTED BY EMOTION Vuilleumier P. Affective and motivational control of vision. Curr Opin Neurol 2015;28:29–35. The ways that we perceive our surroundings are influenced directly by our emotions. In this review, the author shows exactly how directly affective inputs can modulate our experience of the visual world. Through thorough citing of recent research, it is shown that visual targets with emotional meaning (such as faces expressing fear and violent scenes) are found faster in visual search tasks and serve as better distractors. They are judged as sharper and more vivid when compared with images with equal luminance and contrast. Eye tracking studies reveal that they attract more total fixations and first fixations than details related to brightness or contrast. In addition, emotional face and body gestures incite increased activity in extrastriate cortex on functional magnetic resonance imaging (fMRI) and electroencephalography (EEG). Interestingly, they also bring about more activity in areas of earlier visual processing (V1), which the author argues accounts for the perceptual advantage of these types of stimuli. The amygdala, which is known to be central to emotional learning and assessment, has been found to project to V1. In patients with amygdalar damage, visual cortex sees less of an incremental boost in signal on fMRI and EEG from emotional stimuli than it does in controls. It is also noted that the amygdala exhibits spatial correspondence, with a greater response seen to emotional stimuli in the contralateral hemifield. It is possible that this has implications in attentional orientation. Although most of these findings can be replicated with reward stimuli, the functional anatomy of the reward system’s contribution to vision is less well known. It is suspected to involve the basal ganglia, dopaminergic projections from the midbrain, and possibly the amygdala as well. The author also notes that these findings have possible applications in rehabilitation of visual disorders. For example, in patients with hemispatial neglect, visual stimuli that are consistently presented with loud white noise in a Pavlovian manner are better detected in neglected space on later testing than are non-conditioned visual stimuli. In addition, when patients with neglect are rewarded for finding certain visual targets in their neglected field, they preferentially shift their search strategy to that field. Interestingly, the subset of these patients with basal ganglia damage showed less shift in their search bias. The author concludes that our understanding of affectional and motivational modulation of vision is in its nascent stages and that therapeutic application of our understanding should be further investigated. Evan Price HOW DO ER DOCTORS EVALUATE PAEDIATRIC HORNER? Cahill JA, Ross J. Eye on children: acute work-up for pediatric Horner’s syndrome. Case presentation and review of the literature. J Emerg Med 2015;48:58–62. This paper takes a specific scenario—a child with Horner syndrome—and presents it from the perspective of an emergency room (ER) physician. It behoves us to be aware of what non-neuro-ophthalmologists know about the diseases we treat and what their literature reports to them. In this case, the authors first give a brief review of the anatomy and differential diagnosis of ptosis and anisocoria in both adults and children, then focusing on the specific topic of how paediatric Horner is evaluated. They acknowledge that there is little consensus, and without stating it specifically, imply correctly that there are no high-level studies to guide us. Although there are several papers that recommend no evaluation beyond physical examination for paediatric Horner, this paper does not focus on if to evaluate, rather how and what to evaluate. The authors acknowledge that it may not be necessary to work up paediatric Horner in the emergency room, per se (carotid dissection is not expected in paediatrics as it is in adults), but if evaluation is initiated, a flow chart of recommendations is offered for guidance. The role of Neuro-Ophthalmic Literature Review 153 ! 2015 Informa Healthcare USA, Inc. diagnostic eye drops (hydroxyamphetamine, cocaine) is essentially disregarded, and there is no mention of the limitations of urine catacholamine testing. The authors admit to lack of guidance regarding modality of imaging (computed tomography [CT] versus magetic resonace imaging [MRI]) and ultimately, how and what to image is left to the specific resources of the ER physician. In general, though, this report should be essential reading for emergency room physicians. It’s too bad the authors didn’t recommend involvement of a neuro-ophthalmologist early to help guide the workup. John H. Pula GANGLION CELL AND INNER PLEXIFORM LAYER THICKNESS IN OPTIC PATHWAYS LESIONS Moon H, Yoon JY, Lim HT, Sung KR. Ganglion cell and inner plexiform layer thickness determined by spectral domain optical coherence tomography in patients with brain lesions. Br J Ophthalmol 2015;99:329–335. The authors retrospectively studied the visual fields (VF); the ganglion cell and inner plexiform layer (GCIPL) thickness; and the peripapillary retinal nerve fibre layer (pRNFL) thickness in 98 patients with brain lesions and 58 healthy controls. Their results showed good correlations between VF deficits, GCIPL thickness maps, and pRNFL thickness profiles, suggesting the interest of studying GCIPL thickness map modifications in patients with optic pathways lesions. Matthieu Robert KNOBLOCH SYNDROME AND THE ROLE OF COL18A1 IN HUMAN CORTICAL DEVELOPMENT Caglayan AO, Baranoski JF, Aktar F, Han W, Tuysuz B, Guzel A, Guclu B, Kaymakcalan H, Aktekin B, Akgumus GT, Murray PB, Erson-Omay EZ, Caglar C, Bakircioglu M, Sakalar YB, Guzel E, Demir N, Tuncer O, Senturk S, Ekici