Pinpointing lesions in the occipital lobe
In this video, from our Clinical Neurology Essentials course, you'll learn how to recognize and understand the structure and functions of the occipital lobe.
Visual defects are common with occipital lobe lesions, so recognizing and understanding the structure and functions of the occipital lobe is fundamental to helping your patients. In this video, from our Clinical Neurology Essentials course, you'll review the major anatomical characteristics of the occipital lobe and learn how to interpret useful clinical data that can help you to localize lesions and recognize key disorders of the region.
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[00:00:00] Anteriorly, the occipital lobe is separated from the parietal lobe by the parietooccipital sulcus. The occipital lobe is separated from the temporal lobe by the calcarine sulcus, which contains the calcarine cortex. As we'll see in a moment, this region is important for vision. The primary visual cortex, Brodmann area 17, occupies the upper and lower lips of the calcarine sulcus on the medial surface of the hemisphere. This is called
[00:00:30] the calcarine cortex. As its name suggests, it is the primary brain region involved in vision. The visual association cortex, Brodmann areas 18 and 19, also known as the secondary and tertiary visual cortices include the rest of the occipital lobe and the posterior part of the parietal lobe. It is involved in object recognition, perception of color, and other aspects of vision. There are many
[00:01:00] important clinical anatomical correlations involving the occipital lobe. When bilateral occipital lobe lesions such as infarcts occur, the patient will demonstrate cortical blindness. Often the patient does not recognize they are blind. In fact, they often confabulate or makeup descriptions of what they see. This collection of signs and symptoms is called Anton's syndrome. This can also occur with lesions affecting one occipital pole, which can provoke
[00:01:30] brief physiologic functional abnormality in the opposite occipital cortex for a short period of time. This produces temporary cortical blindness and results in Anton's syndrome. However, this process will reverse spontaneously with time. This induced physiologic dysfunction is called diaschisis. Visual field defects are common with occipital lobe lesions. Before looking at these in more detail, let's briefly review the visual pathways.
[00:02:00] First order neurons arise in the retina from rods and cones and then synapse with retinal ganglion cells, the second order neurons. The axons of these second order neurons make up the optic nerves and travel to the chiasm where the nasal fibers cross to the opposite lateral geniculate body and the temporal fibers remain ipsilateral and terminate in the lateral geniculate body. Third order neurons then leave the lateral geniculate body forming the optic radiations
[00:02:30] in Meyer's loop, which travel through the temporal and parietal lobes and terminate in the visual cortex. Since the visual pathways travel through the temporal and parietal lobes before entering the occipital lobe, we need to consider the entire path in order to localize a deficit. You should begin by observing the portion of the visual field where the image strikes the retina. Lesions involving the macula, the central area of the retina, lead to macular or central vision loss. Lesions of the
[00:03:00] optic nerve before the chiasm will result in complete visual loss from that eye. Lesions in the optic chiasm will lead to bitemporal hemianopsia where vision in the temporal fields of both eyes is lost. Lesions of the optic tract will lead to congruent hemianopsia, a loss of vision on the same side in both eyes. As we've discussed previously, lesions of the temporal lobe affecting Meyer's loop result in superior quadrantanopsia and lesions of the dorsal optic radiation
[00:03:30] in the parietal lobe, lead to inferior quadrantanopsia. Lesions of the optic radiation in the parietooccipital region, lead to macular sparing hemianopsia. As you’ll remember from our discussions of the temporal lobes, language processing occurs largely in the temporal lobes of the dominant hemisphere. In a right-handed person, that means when reading information from the left visual field it will be processed by the right visual cortex and would normally be conveyed
[00:04:00] to the language centers in the left hemisphere by passing through the corpus callosum. However, if a lesion occurs in the left visual cortex, the patient loses all input to the right visual field. Additional damage to the corpus callosum will prevent passage of visual information from the right visual cortex, and left visual field to the left parietal language processing regions. Thus, although the patient will be able to see the words, in this case,
[00:04:30] the patient will be unable to read written language. However, they will still be able to write sentences producing written language since this is not affected by the loss of visual information processing. This is called alexia without agraphia. Seizures involving the occipital lobe generally produce unformed visual hallucinations that may include sparkles of light and odd patterns of light and color. In contrast, remember that seizures in the temporal lobe produced
[00:05:00] formed visual hallucinations.