Veins of the eyelids anastomose medially between the angular vein and branches of the SOV in the superior medial orbit in the region of the trochlea. Facial veins drain in­ feriorly and laterally to form the external jugular vein, which eventually joins the internal jugular in the neck.

Lasjaunias P, Berenstein A, ter Brugge KG. Clinical Vascular Anatomy and Variations. 2nd ed. Springer; 2001. Surgical Neuroangiography; vol 1.

A disturbance in visual function may be the result of pathology affecting any part of the afferent visual system, including the ret­ina, optic nerve, and visual pathways (Fig 1-21).

The afferent visual pathway begins within the ret­ina. Details of ret­i­nal anatomy can be found in BCSC Section 2, Fundamentals and Princi­ples of Ophthalmology, and Sec­ tion 12, Ret­ina and Vitreous. The following discussion focuses on key points relevant to neuro-­ophthalmology.

The absence of ret­i­nal receptors over the ONH creates a physiologic scotoma (blind spot), located approximately 15° from the fovea and mea­sur­ing approximately 5° by 7°. The fovea, which is approximately 1.5 mm in dia­meter (1 disc dia­meter), is located about 4 mm (approximately 2.5 disc dia­meters) from and 0.8 mm lower than the ONH.

By contrast, the ret­i­nal pigment epithelium is in direct contact with the ret­i­nal pho­ toreceptor cells. Between the outer and inner ret­i­nal layers, the ret­i­nal signal generated in rods and cones is pro­cessed primarily through the bipolar cells that synapse on ret­i­nal ganglion cells (RGCs). A subset of melanopsin-­containing RGCs, known as intrinsically photosensitive ret­i­nal ganglion cells (ipRGCs), serve primarily nonvisual light-­dependent functions such as the pupillary light reflex. Horizontal, amacrine, and interplexiform cells (which communicate horizontally between neighboring cells) permit signal pro­cessing within the ret­i­nal layers. The glial support cells—­Müller cells and astrocytes—­play an impor­ tant metabolic role.

The ratio of photoreceptor cells to RGCs varies depending on the region of the ret­ina. The ratio is highest in the periphery (at more than 1000:1) and lowest at the fovea (where an RGC may receive a signal from a single cone). The foveal bipolar cells and RGCs are displaced radially from the fovea, with the bipolar cells receiving input via long cone axons that make up the Henle layer. The radial nature of the Henle layer is responsible for the accumulation of fluid in the macula in a star-­shaped pattern.

The optic nerve begins anatomically at the ONH but physiologically and functionally within the RGC layer that covers the entire ret­ina. Although ganglion cell fibers coming from the nasal ret­ina can travel uninterrupted directly to the ONH, ­those coming from the temporal ret­ina must anatomically separate to enter the ONH at ­either the superior or the inferior pole in order to avoid the macula (Fig 1-22). This unique anatomy means that some of the nasal fibers (nasal within the macula) enter the ONH on its temporal side (within the papillomacular bundle). Defects in the nerve fiber layer include focal loss, which may appear as ­either grooves or slits or as reflections that parallel the ret­i­nal arte­ rioles where the internal limiting membrane drapes over the vessels. Diffuse loss of the nerve fiber layer is often more difficult to detect and brings the ret­i­nal vessels into sharp relief.

The first portion of the optic nerve, representing the confluence of approximately 1.0–1.2 million RGC axons, traverses the sclera through the lamina cribrosa, which con­ tains approximately 200–300 channels. The combination of small channels and a unique blood supply (largely from branches of the posterior ciliary arteries) likely plays a role in several optic neuropathies. Anterograde and retrograde axonal transport of molecules, subcellular organelles, and metabolic products occurs along the length of the optic nerve. The anterograde axonal transport system is further subdivided into slow, intermediate, and fast speeds. This energy-­dependent system, which requires high concentrations of oxygen, is sensitive to ischemic, inflammatory, and compressive pro­cesses.

Just posterior to the sclera, the optic nerve acquires a dural sheath that is contigu­ ous with the periorbita of the optic canal and an arachnoid membrane that supports and protects the axons and is contiguous with the arachnoid of the subdural intracranial space through the optic canal. This arrangement permits circulation of CSF around the optic nerve up to the ONH. Just posterior to the lamina cribrosa, the optic nerve also acquires a myelin coating, which increases its dia­meter from 1.5 mm (ie, in the ONH) to approxi­ mately 3 mm (6 mm including the optic nerve sheath). The myelin investment is part of the membrane of oligodendrocytes that join the nerve posterior to the sclera.

The intraorbital optic nerve extends approximately 25–30 mm to the optic canal, a length that allows unimpeded globe rotation as well as axial shifts within the orbit. The CRA and CRV travel within the anterior 10–12 mm of the optic nerve. The CRA supplies only a minor portion of the optic nerve circulation; most of the blood supply comes from pial branches of the surrounding meninges, which are in turn supplied by small branches of the OphA (see Fig 1-12). An approximate topographic repre­sen­ta­tion is maintained in the optic nerve. Peripheral ret­i­nal repre­sen­ta­tion is found more peripherally, and the pap­ illomacular bundle travels temporally and increasingly centrally within the nerve.