Structure of the retina

In addition to the serially arranged photoreceptors, bipolar cells, and ganglion cells shown in Figure 28.1, the retina contains two sets of neurons arranged transversely: horizontal cells and amacrine cells (Figure 28.4). A total of eight layers are described for the retina as a whole.

Figure 28.4 The layers of the retina. (1) Pigment layer; (2) photoreceptor layer; (3) outer nuclear layer; (4) outer plexiform layer; (5) inner nuclear layer; (6) inner plexiform layer; (7) ganglion cell layer; (8) nerve fiber layer.

Action potentials are generated by the ganglion cells, providing the requisite speed for conduction to the thalamus and midbrain. For the other cell types, distances are very short and passive electrical charge (electrotonus) is sufficient for intercellular communication, whether by gap-junctional contact or transmitter release.

Cone and rod bipolar neurons

Cone bipolar neurons

Cone bipolar neurons are of two types. ON bipolars are switched on (depolarized) by light, being inhibited by transmitter released in the dark. They converge onto ON ganglion cells. OFF bipolars have the reverse response and converge onto OFF ganglion cells (Figure 28.5).

Figure 28.5 Retinal circuit diagram. (Adapted from Massey and Redburn, 1987.) A, amacrine cell; C, cone; CB, cone bipolar neuron; GC, ganglion cell; H, horizontal cell; N, nexus (gap junction); R, rod; RB, rod bipolar.

Rod bipolar neurons

Rod bipolar neurons are all hyperpolarized by light. They activate ON and OFF ganglion cells indirectly, by way of amacrine cells (Figure 28.5).

Foveal specialization

The relative density of cones increases progressively, and their size diminishes progressively, from the edge of the fovea inwards (Figure 28.6). The central one-third of the fovea, little more than 100 µm wide and known as the foveola, contains only midget cones. Two special anatomical features assist the foveal cones in general, and the midget cones in particular, in transducing the maximum amount of information concerning the form and color values of an object under direct scrutiny. First, the more superficial layers of the retina lean outward from the center, and their neurites are exceptionally long, with the result that the outer two-thirds of the foveola are little overlapped by bipolar cell bodies and the inner third is not overlapped at all; light reflected from the object strikes the cones of the foveola without any diffraction. Second, fidelity of central transmission is enhanced by one-to-one synaptic contact between the midget cones and midget bipolar neurons, and between these and midget ganglion cells. Outside the foveola, the amount of cone-to-bipolar-to-ganglion cell convergence increases progressively.

Figure 28.6 (A) Horizontal section of the right eyeball at the level of the optic disk and fovea centralis. (B) Enlargement from (A). Recurrent axons sweep around the fovea as shown in C. (C) Surface view of fovea centralis and neighboring retina. Cones have been omitted at intervals to show the ‘chain’ sequence of neurons. BCL, bipolar cell layer; GCL, ganglionic cell layer.

Optic nerve, optic tract

The optic nerve is formed by the axons of the retinal ganglion cells. The axons acquire myelin sheaths as they leave the optic disc.

The number of ganglion cells varies remarkably between individuals, from 800,000 to 1.5 million. Since every ganglion cell contributes to the optic nerve, the number of axons in the optic nerve is correspondingly variable.

The retinal ganglion cells are homologous with the sensory projection neurons of the spinal cord. The optic nerve is homologous with spinal cord white matter, and is not a peripheral nerve. As explained in Chapter 9, true peripheral nerves, whether cranial or spinal, contain Schwann cells and collagenous sheaths, and are capable of regeneration. The optic nerve contains neuroglial cells of central type (astrocytes and oligodendrocytes) and is not capable of regeneration in mammals. In addition, the nerve is invested with meninges containing an extension of the subarachnoid space – a feature largely responsible for the changed appearance of the fundus oculi when the intracranial pressure is raised (papilledema, Ch. 4).

At the optic chiasm, fibers from the nasal hemiretina (medial half-retina) enter the contralateral optic tract, whereas those from the temporal (lateral) hemiretina remain uncrossed and enter the ipsilateral tract.

As already noted in Chapter 26, some optic nerve fibers enter the suprachiasmatic nucleus of the hypothalamus. This connection has been invoked to account for the beneficial effect of bright artificial light, for several hours per day, in the treatment of wintertime depression.

Each optic tract winds around the midbrain and divides into a medial and a lateral root.

Geniculocalcarine tract and primary visual cortex

The geniculocalcarine tract, or optic radiation, is of major clinical importance because it is frequently compromised by vascular disorders or tumors in the posterior part of the cerebral hemisphere. It travels from the lateral geniculate body to the primary visual cortex.

The anatomy of the optic radiation is shown in Figures 28.7–28.10. Fibers destined for the lower half of the primary visual cortex sweep forward into the temporal lobe, as Meyer’s loop, before turning back to accompany those traveling to the upper half. The tract enters the retrolentiform part of the internal capsule and continues in the white matter underlying the lateral temporal cortex. It runs alongside the posterior horn of the lateral ventricle before turning medially to enter the occipital cortex.

Figure 28.7 Left optic radiation. LGB, Lateral geniculate body.

Figure 28.8 A dissection of the visual pathways, viewed from below.

(Photograph reproduced from Gluhbegovic, N. and Williams, T. W. (1980) The Human Brain, by kind permission of the authors and of J.B. Lippincott, Inc.)

Figure 28.9 Diagram of the visual pathways. The two visual fields are represented separately, without the normal overlap.

Figure 28.10 Pathway from the visual field of the left eye to the primary visual cortex. T denotes the temporal (outer) half of the left visual field; N denotes the nasal (inner) half of the left visual field.

In the left retina and optic nerve (ON), the neural representation of the image is reversed side to side. It is also inverted top to bottom. The right retina and optic nerve are inactive because this eye is shielded.

At the optic chiasm (OC) the axons forming the nasal half of the left optic nerve cross the midline and form the medial half of the right optic tract (OT). Those forming the lateral half of the nerve form the lateral half of the left optic tract. Each set synapses in the corresponding lateral geniculate body (LGB).

The optic radiations (OR) are fan-like (cf. Figure 28.7), with the axons carrying the foveal input initially in the middle of the fan.

As they approach the occipital pole, the foveal axons (red) in both hemispheres move to the back and enter the posterior part of the primary visual cortex (PVC). Note the striped pattern of delivery to the cortex on both sides. The blank intervals between are the same width and contain the axons and cortex responsible for the visual field of the right eye. SC, superior colliculus.

The primary visual cortex occupies the walls of the calcarine sulcus along its entire length (the sulcus is 10 mm deep). It emerges onto the medial surface of the hemisphere for 5 mm both above and below the sulcus, and onto the occipital pole of the brain for 10 mm. Its total area is about 28 cm². In the freshly cut brain, it is easily identified by a thin band of white matter (the visual stria of Gennari) within the gray matter – hence an alternative term, striate cortex. The left and right eyes are represented in the cortex in alternating stripes called ocular dominance columns (Figure 28.9).

Retinotopic map

The contralateral visual field is represented upside down. The plane of the calcarine sulcus represents the horizontal meridian. Retinal representation is posteroanterior, with a greatly magnified foveal representation in the posterior half of the calcarine cortex (Figure 28.10).

The clinical effects of various lesions of the visual pathway are described in Clinical Panel 28.1.

Clinical Panel 28.1 Lesions of the visual pathways

The following points arise in testing the visual pathways:

• The patient may be unaware of quite extensive blindness – sometimes even of a hemianopia.

• Large visual defects can often be detected by simple confrontation, as follows. The patient covers one eye at a time, and focuses on the examiner’s nose. The examiner, seated opposite, looks the patient in the eye while bringing one or other hand into view from various directions, with the index finger wiggling.

• In a blind area, the patient does not see blackness; the patient does not see anything.

• Visual defects are described from the patient’s viewpoint, in terms of the visual fields.

• Possible sites of injury to the visual pathways are shown in Figure CP 28.1.1. The effects produced correspond to the numbers in the following list:

Lesions	Field defects
1 Partial optic nerve	Ipsilateral scotomaa
2 Complete optic nerve	Blindness in that eye
3 Optic chiasm	Bitemporal hemianopia
4 Optic tract	Homonymousb hemianopia
5 Meyer’s loop	Homonymous upper quadrantanopia
6 Optic radiation	Homonymous hemianopia
7 Visual cortex	Homonymous hemianopia
8 Bilateral macular cortex	Bilateral central scotomas

^a Patch of blindness.

^b Matching.

Notes on the numbered lesions

1 Eccentric lesions of the optic nerve produce scotomas in the nasal or temporal field of the affected eye. When a young adult presents with a scotoma, multiple sclerosis must always be suspected.

2 Total conduction blockage may follow head injury.

3 Compression of the middle of the chiasm is most often caused by an adenoma (benign tumor) of the pituitary gland.

4 Lesions of the optic tract are rare. Although homonymous (matching) visual fields are affected, the outer, exposed half of the tract tends to be more affected than the inner half, and the hemianopia is then described as incongruous.

5 Meyer’s loop may be selectively caught by a tumor in the temporal lobe.

6 Lesions involving the optic radiation include tumors arising in the temporal, parietal, or occipital lobe. The visual fields of both eyes tend to be affected to an equal extent (congruously). Tumors impinging on the radiation from below produce an upper quadrantic defect at first, whereas tumors impinging from above produce a lower quadrantic defect. The stem of the radiation occupies the retrolentiform part of the internal capsule and is often compromised for some days by edema, following hemorrhage from a branch of the middle cerebral artery (classic stroke, Ch. 35).

7 Thrombosis of the posterior cerebral artery produces a homonymous hemianopia. The notches in field chart no. 7 represent macular sparing. Sparing of the macular hemifields is inconstant.

8 Bilateral central scotomas are most often caused by a backward fall with occipital contusion.

Reference

Remington LA. Clinical anatomy of the visual system, ed 2. Butterworth-Heinemann; 2005.

Figure CP 28.1.1 Visual field defects following various lesions of the visual pathways.

Core Information

The embryonic retina is an outgrowth of the diencephalon. The embryonal optic cup is composed of an outer, pigment layer, an inner, nervous layer, with an intraretinal space between. The nervous layer contains three sets of radially disposed neurons, viz. photoreceptors, bipolar cells, and ganglion cells, and two tangential sets, viz. horizontal cells and amacrine cells. Except at the fovea centralis, light must pass through the other layers to reach the photoreceptors. The visual image is inverted and reversed by the lens. Two-thirds of the visual field are binocular, the outer one-sixth on each side being monocular. Visual defects are described in terms of visual fields.

Rod photoreceptors function in dim light and are absent from the fovea. Cones are most numerous in the fovea; they are responsive to shape and have three kinds of sensitivity to color. Ganglion cell responses are concentric, showing center-surround color opponency. M ganglion cells are relatively large, are movement detectors, and project their axons to the two magnocellular layers of the lateral geniculate body (LGB). P ganglion cells signal particular features of the image as well as color and project to the four parvocellular layers of LGB. LGB is binocular, receiving signals from the contralateral nasal hemiretina (via the optic chiasm) and from the ipsilateral temporal hemiretina. Both sets of axons arrive by the optic tract, which also gives offsets to the midbrain for lower-level visual reflexes.

The geniculocalcarine tract (optic radiation) arises from M and P cells of the LGB and swings around the side of the lateral ventricle to reach the primary visual cortex, in the walls of the calcarine sulcus.

Distinctive visual field defects occur following damage at any of the five major components of the visual pathway (optic nerve, optic chiasm, optic tract, optic radiation, visual cortex).