The Occipital Lobe

The occipital lobe can be roughly divided into two areas: the primary visual cortex, or V1 for short, and the visual association cortices V2 to V5. V1 corresponds to what is known as Brodmann area 17. Due to the special layering of the neurons in the cortex, this region has a stripe that is even visible to the naked eye, which is why the region is also called area striata. It is located largely on the medial, inward-facing side of the hemispheres at the occipital pole of the brain, thus forming the wall of the sulcus calcarinus.

V1 receives incoming nerve impulses, known as afferents, via optic radiation from the lateral geniculate nucleus (CGL for short, part of the thalamus), whereby its 1.5 million fibers now face an impressive 200 million cortex neurons. This may sound a little bureaucratic, but it is in fact a necessity for complex processing, as will become apparent.

The primary visual cortex is retinotopically organized. This means that each point on the retina corresponds to a specific small cortical area in V1, with neighborhoods remaining intact. Although the fovea, the point of sharpest vision on the retina, is only 1.5 millimeters in diameter, it occupies four-fifths of V1. This reflects the interconnection of cells in the retina, because in the fovea there is one ganglion cell per photoreceptor – or to put it more simply: the “resolution” is particularly high here. Both ensure that we can process what we see in focus in the best possible way.
 

Like the entire isocortex, the primary visual cortex is divided into six laminae, or layers, although it is significantly more complex than the rest of the cortex. The individual layers differ in structure and function, but are strongly interconnected.

Of particular interest for sensory areas in general is layer IV, which receives the afferents of the sensory neurons – although the first processing steps already take place in the previous stations of the visual pathway, e.g., in the retina and the CGL. Layer VI in the primary visual cortex now receives this information in a rather complex interconnection pattern. It is particularly thick, so that it is subdivided into sublayers A, B, and C (the latter subdivided again into α and β).

Two examples of the network may suffice here: The cells of layer 4Cα mainly receive input from the magnocellular fibers of the GLC. These fibers carry information that primarily deals with the movement of objects and are in turn forwarded to layer 4B. There are also parvocellular fibers, which are more object- and pattern-oriented. These mainly terminate in 4Cβ, and their cells in turn project into layers 2 and 3. This is already the beginning of the dorsal and the ventral streams of cortical visual processing.

In addition to this horizontal structure, there is also a vertical one, whose functional units were described as “columns” by Vernon Mountcastle (*1918) in the mid-1950s. Just as an aside: Nobel Prize winner David Hubel (*1926), who has done significant work in researching the visual system, would rather compare them to slices of toast. 

Mountcastle's columns build on each other: several orientation columns – in which so-called “simple cells” detect the alignment of a line between 0 and 180 degrees –together form an eye dominance column. Understanding their structure and distribution across the surface of the cortex proved to be quite difficult – comparable to trying to cut a lawn with nail scissors, as David Hubel later wrote. In fact, these “eye dominance columns” are not distributed alternately to the right and left, but overlap through horizontal and diagonal connections, becoming blurred at the boundaries. Today, a right and a left eye dominance column are combined to form a “hypercolumn,” each of which represents a small section of the outside world. This complex structure is one of the reasons for the enormous number of stimulus-processing cells in V1.

From above, the “blobs” descend into these orientation and eye dominance columns, which can only be detected using a special coloring technique. They are involved in the processing of color. David Hubel later explained the name “blobs” as follows: “We call them ‘blobs’ because the term is both vivid and unambiguous ... and because it seems to annoy our competitors.”

Blobs have a diameter of a quarter of a millimeter, in which five or six neurons can be derived. These neurons are often doubly complex in their behavior: for example, they react to red in the center with excitation and to central green with inhibition. The opposite is true in the surrounding area. Blobs have no orientation specificity, unlike the area in between – the interblobs. However, the size of their area of responsibility can be calculated: approximately 200 different color tones in about 500 steps of brightness and at least 26 levels of saturation result in over 2.5 million possibilities.
 

The primary visual cortex is surrounded by several visual association areas. The classic secondary visual cortex consists of V2 and V3 (according to Brodmann areas 18 and 19), whose inputs originate primarily from V1. The primary visual cortex projects point by point and in an orderly manner onto the secondary visual cortex. Secondary processing spreads to other areas, while these higher processing areas simultaneously send feedback.

Overall, the magnocellular and parvocellular pathways continue beyond the occipital lobe – toward the parietal lobe as the magnocellular dorsal stream, and toward the temporal lobe as the parvocellular ventral stream. On both pathways, color, shape, movement, and space are increasingly refined, partly in areas with a very high degree of specialization. For example, there are areas for the perception of faces or the distinction between familiar and unfamiliar objects.

Lesions in the primary visual cortex prevent the processing of corresponding impulses at the affected site. This results in deficits in the visual field – in the worst case, complete destruction of V1 results in what is known as cortical blindness: although the retina and visual pathway are intact, the patient is completely blind.
Deficits in the secondary visual cortex do not lead to visual field defects. Rather, patients are no longer able to classify or recognize what they see. This can affect colors, shapes, or even faces. In this case, the condition is referred to as visual agnosia. Synesthesia and visual hallucinations also appear to be caused by disorders of the secondary visual cortex.

First published on September 23, 2011
Last updated on August 28, 2025