Humans have main lacrimal glands and accessory lacrimal glands. The main lacrimal glands comprise the orbital and palpebral lobes, which are located in the superotemporal area of the orbit. The palpebral lobe lies below the aponeurosis of the levator palpebrae superioris and is in contact with the superior and lateral conjunctival fornices.1 Even in healthy subjects, the palpebral lobe is seen through the conjunctiva when the eyelid is elevated. Therefore, optical coherence tomography (OCT) scanning of the exposed palpebral lobe can be used to visualize the parenchyma of the palpebral lobe just beneath the conjunctiva.

Glaucoma is a leading cause of irreversible blindness worldwide.1 Increased intraocular pressure is a major risk factor for the development and progression of glaucoma; lowering intraocular pressure remains the current focus of glaucoma treatment.2,3 The efficacy of topical glaucoma therapy depends on patient adherence and poor adherence may lead to greater fluctuation in intraocular pressure.3,4 One prerequisite to achieving adherence to therapy is correct identification of medications. This is of particular importance for patients taking >1 medication with unique dosing schedules to avoid both under treatment and unnecessary side effects.

The standard of care for diagnosis of peripheral vitreoretinal pathology (such as retinal breaks, tears, or holes) is to perform indirect ophthalmoscopy with scleral depression; however, this is only supported by the “lowest strength of evidence.”1 For the patient, scleral depression causes discomfort owing to mechanical pressure on the globe. The few published reports in the literature on the topic of scleral depression describe the technique of scleral depression, but do not provide any comparison with examination without scleral depression.

Anterior ischemic optic neuropathy (AION), is classified as arteritic (giant cell arteritis [GCA]) or nonarteritic AION (NAION). Varicella zoster virus (VZV) vasculopathy causes symptoms and signs of AION.1–4 Because VZV is present in temporal arteries (TAs) of most patients with GCA1,5 and ischemic optic nerve and retinal pathologies,2,3 we examined GCA-negative TAs from seven AION patients for VZV.

Melanin, hemoglobin, and carotenoids are the dominant influences in the color of human skin.1 Yellowish discoloration of the eyelid skin is commonly a result of lipid-laden histiocytes in the dermis (xanthoma, xanthelasma), or cysts of the cutaneous adnexa. A distinct entity labeled “orange palpebral spots” has recently been described in the dermatologic literature.2 We have encountered 3 patients with a similar finding and suggest an expansion of the label to “yellow-orange palpebral spots” based on the coloration observed.

Normally, postnatal development of the human retina involves centrifugal displacement of the inner retinal layers (IRLs) from the fovea, centripetal migration of the cone photoreceptors into the fovea, and elongation of the photoreceptors with age.1,2 It is not clear whether retinal development in infants and young children with achromatopsia (ACHM) occurs in a similar way and whether any retinal changes that occur are progressive in early childhood.