Objectives

Figure 14-1 The visual pathway from the retina to the visual cortex showing visual field defects. (1) Ipsilateral blindness. (2) Binasal hemianopia. (3) Bitemporal hemianopia. (4) Right hemianopia. (5) Right upper quadrantanopia. (6) Right lower quadrantanopia. (7) Right hemianopia with macular sparing. (8) Left constricted field as a result of end-stage glaucoma. Bilateral constricted fields may be seen in hysteria. (9) Left central scotoma as seen in optic (retrobulbar) neuritis in multiple sclerosis. (10) Upper altitudinal hemianopia as a result of bilateral destruction of the lingual gyri. (11) Lower altitudinal hemianopia as a result of bilateral destruction of the cunei.

E.The lateral geniculate body is a six-layered nucleus. Layers 1, 4, and 6 receive crossed fibers; layers 2, 3, and 5 receive uncrossed fibers. The lateral geniculate body receives input from layer VI of the striate cortex (Brodmann area 17). It also receives fibers from the ipsilateral temporal hemiretina and the contralateral nasal hemiretina. It projects through the geniculocalcarine tract to layer IV of the primary visual cortex (Brodmann area 17).

F.The geniculocalcarine tract (visual radiation) projects through two divisions to the visual cortex.

1.The upper division (Figure 14-3) projects to the upper bank of the calcarine sulcus, the cuneus. It contains input from the superior retinal quadrants, which represent the inferior visual field quadrants.

a.Transection causes a contralateral lower quadrantanopia.

b.Lesions that involve both cunei cause a lower altitudinal hemianopia (altitudinopia).

2.The lower division (see Figure 14-3) loops from the lateral geniculate body anteriorly (Meyer loop), then posteriorly, to terminate in the lower bank of the calcarine sulcus, the lingual gyrus. It contains input from the inferior retinal quadrants, which represent the superior visual field quadrants.

a.Transection causes a contralateral upper quadrantanopia (“pie in the sky”).

b.Transection of both lingual gyri causes an upper altitudinal hemianopia (altitudinopia).

G.The visual cortex (Brodmann area 17) is located on the banks of the calcarine fissure. The cuneus is the upper bank. The lingual gyrus is the lower bank. Lesions cause contralateral hemianopia with macular sparing. The visual cortex has a retinotopic organization:

1.The posterior area receives macular input (central vision).

2.The intermediate area receives paramacular input (peripheral input).

3.The anterior area receives monocular input.

110 Chapter 14

Light

Figure 14-2 Histology of the retina. The retina has ten layers: (1) pigment epithelium layer (PEL), (2) layer of rods and cones (LRC), (3) outer limiting membrane (OLM), (4) outer nuclear layer (ONL), (5) outer plexiform layer (OPL), (6) inner nuclear layer (INL), (7) inner plexiform layer (IPL), (8) ganglion cell layer (GCL), (9) nerve fiber layer (NFL), and (10) inner limiting layer (ILL). The tight junctions binding the pigment epithelial cells make up the blood–retina barrier. Retinal detachment usually occurs between the pigment layer and the layer of rods and cones. The central artery of the retina perfuses the retina to the outer plexiform layer, and the choriocapillaris supplies the outer five layers of the retina. The Müller cells are radial glial cells that have support function. Myelin of the central nervous system (CNS) is produced by oligodendrocytes, which are not normally found in the retina. (Adapted from Dudek RW. High-Yield Histology. Baltimore, MD: Williams & Wilkins; 1997:64, with permission.)

Lesion A of visual radiations to sup. bank of calcarine sulcus

Lat. geniculate body

Field defects

A

Lower r. homonymous quadrantanopia

Calcarine sulcus

B

Lesion B of visual radiations to inf. bank of calcarine sulcus

Figure 14-3 Relations of the left upper and left lower divisions of the geniculocalcarine tract to the lateral ventricle and calcarine sulcus. Transection of the upper division (A) results in right lower homonymous quadrantanopia. Transection of the lower division (B) results in right upper homonymous quadrantanopia. (Reprinted from Fix JD. BRS Neuroanatomy. Baltimore, MD: Williams & Wilkins; 1997:261, with permission.)

III The Pupillary Light Reflex Pathway (Figure 14-4) has an afferent

limb (CN II) and an efferent limb (CN III). It includes the following structures:

A.Ganglion Cells of the Retina, which project bilaterally to the pretectal nuclei.

B.The pretectal nucleus of the midbrain, which projects (through the posterior commissure) crossed and uncrossed fibers to the accessory oculomotor (Edinger–Westphal) nucleus.

C.The accessory oculomotor (Edinger–Westphal) nucleus of CN III, which gives rise to preganglionic parasympathetic fibers. These fibers exit the midbrain with CN III and synapse with postganglionic parasympathetic neurons of the ciliary ganglion.

D.The ciliary ganglion, which gives rise to postganglionic parasympathetic fibers. These fibers innervate the sphincter pupillae.

IV The Pupillary Dilation Pathway (Figure 14-5) is mediated by the

sympathetic division of the autonomic nervous system. Interruption of this pathway at any level causes ipsilateral Horner syndrome. It includes the following structures:

A.The hypothalamus. Hypothalamic neurons of the paraventricular nucleus project directly to the ciliospinal center (T1–T2) of the intermediolateral cell column of the spinal cord.

B.The ciliospinal center of Budge (T1–T2) projects preganglionic sympathetic fibers through the sympathetic trunk to the superior cervical ganglion.

C.The superior cervical ganglion projects postganglionic sympathetic fibers through the peri-

vascular plexus of the carotid system to the dilator muscle of the iris. Postganglionic sympathetic fibers pass through the tympanic cavity and cavernous sinus and enter the orbit through the superior orbital fissure.