Evaluating the function of cranial nerves I and II

Understanding the anatomical relationships in the organization of cranial nerves I (olfactory) and II (optic) can help you to recognize the lesions that affect them. In this jam-packed video from our Clinical Neurology Essentials course, you'll learn how these cranial nerves mediate sight and smell, the types of lesions that affect them, and how Parkinson's disease can affect a patient's sense of smell. You'll also discover the four everyday items that you should keep in your office to assess olfaction—and the one item you should never use!

Confidently choose and perform the most appropriate neurologic examination for any patient! With our Clinical Neurology Essentials course, you'll learn and master basic and advanced examination skills, neuroanatomy, and the art of asking the right questions, so that you can interpret examination findings and localize pathologies with ease. Don't forget to register for a free trial account to access Chapter 1 now!

[00:00:00] Although not technically found in the brainstem, the optic and olfactory nerves are best studied with the other cranial nerves. They are important clinically so we are going to expand on their evaluation and clinical importance. Let's start by looking at the olfactory nerve, cranial nerve I, which is responsible for the sense of smell. The olfactory nerve is made up of the olfactory bulb and tract. The olfactory bulb connects with the

[00:00:30] nasal mucosa through the cribriform plate. This is a series of perforations in the bone which allows excellent fibers to pass through into the bulb to synapse with neurons there. The bulb is intimate with the cribriform plate. The nasal mucosal chemoreceptors which are sensitive to odors send out axons which then enter the olfactory bulb via the cribriform plate. In the bulbs, they interact with the dendrites of the cells present in the bulb.

[00:01:00] The axons of these cells make up the olfactory tracts. The tracts carry the axons of these second-order neurons to their targets in the entorhinal cortex, amygdala, and primary olfactory cortex located in the temporal lobe. Fibers pass through the anterior commissure, a structure providing a connection between hemispheres, so odors are perceived in cortex bilaterally. Once the signals reach these structures,

[00:01:30] one becomes aware of odors, but odors are actually identified in the frontal lobes which also receives input transmitted from the temporal lobes. So how can we test olfaction? There are elaborate kits available to test smell but for bedside testing, one only needs a commonly recognized or differ a substance and a way to blind the patient. Again, testing each nostril separately is important. Spices

[00:02:00] such as clove, anise, cinnamon make great substances to test and you can keep them in a sample blood test tube in a drawer or in a medical bag quite easily. Some other items readily available in a pinch might be mint-flavored toothpaste, a cigarette, or even a piece of mint or cinnamon chewing gum. Do not use volatile chemicals which can irritate the mucosa and lead to a false positive affirmation of smell being intact. There are several

[00:02:30] important clinical anatomical correlations related to cranial nerve I. The olfactory nerve is found at the base of the brain and can be affected by pathology arising in the bone or membrane surrounding the brain. Its unique location and intimacy with the skull base creates clinical circumstances that can affect its function. Movement of the brain within the cranial vault is common during blunt force head trauma. There is an acceleration-deceleration injury which can tear the fibers

[00:03:00] of the olfactory nerves penetrating olfactory bulb through the cribriform plate. Subfrontal meningioma is an occasional cause of dementia in patients. When present, the tumor may cause pressure on the olfactory bulb and tract causing anosmia on that side. Patients with Parkinson's disease often will exhibit early loss of smell. They sense smells less acutely with 70% to 100% of patients reporting such issues. The mechanism is not completely

[00:03:30] understood but probably has to do with the loss of neurotransmitter functions, in this case, between the frontal lobes and olfactory bulbs. Next, let's take a look at the anatomy of cranial nerve II. Cranial nerve II, the optic nerve, is primarily responsible for vision. Cranial nerve II consists of the optic nerve, the optic chiasm, and we'll see in a minute, this is the site of crossing over, the optic tract and the optic radiations.

[00:04:00] The optic nerves transmit images from the retina of the eye back through the lateral geniculate bodies of the thalamus and into the optic radiations which passed in part to the temporal lobe and parietal lobe before ending in the visual cortex of the occipital lobes. There are projections of the axons of the lateral geniculate body to the superior colliculus as well. Images from the retinas are sorted through the chiasm so that each visual field is represented

[00:04:30] in the contralateral hemisphere. To do this, the temporal fibers from each retina cross to the opposite side through the chiasm. So from the right visual field of each eye shown here in blue, the images from each retina are reformed in the left hemisphere. The optic nerve along with the oculomotor nerve, cranial nerve III, is important for the pupillary light reflex. Light on the retina triggers the efferent light reflex pathway carried by the optic nerve

[00:05:00] which synapses in the Edinger-Westphal nucleus or EWN. The EWN sends a signal to parasympathetic neurons carried in the oculomotor nerve which synapse in the ciliary ganglia and innervates sphincter pupillae in the iris causing miosis or constriction of the pupil. The optic nerves enter the skull via the optic canals. The optic chiasms sits above the region of the skull base named sella turcica. This region

[00:05:30] is a fossa that contains the pituitary gland which is attached to the thalamus by a stalk. So how can we test the function of the optic nerve? A primary examination tool for the optic nerve is your light source for documenting the pupillary responses. First, we look for pupil size and regularity and ambient light, preferably low light. Then we check responses both the direct light called the direct reflex and check the consensual response in the pupil not being directly illuminated,

[00:06:00] this should mimic the direct response. Then we shift the light between pupils to ensure the reactivity is appropriate. Occasionally, we see asymmetry in the pupil's size. This is called anisocoria. Pupil asymmetry can occur for a variety of reasons and we need to distinguish between a pathologic asymmetry and a benign change. To do so, one needs to carefully observe the response to light. In benign anisocoria, pupil responsive to light are usually equal in both eyes

[00:06:30] although one would see a residual difference between the pupils which remain stable. If the pupil is unreactive on one side, further testing is needed to determine a cause. We can also examine the optic nerve by assessing the optic cup using fundoscopic evaluation. The specifics of fundoscopic examination are beyond the scope of this course but simply put the optic cup is a concavity within the optic disc from which the blood vessels emerge. Normally, the border around

[00:07:00] the optic cup will appear distinct. The character of the blood vessels in their visibility through their course are important landmarks to note. Swelling of the optic disc will blur the border or margin and obscure the blood vessels. Visual acuity can be checked at the bedside by using a Snellen handheld card held at about four inches from the face. There are several important clinical anatomical correlations related to cranial nerve II as well. Optic neuritis refers to an inflammation of

[00:07:30] the optic nerve which damages myelin. It presents with blurred vision or loss of vision and often eye pain, either generalized aching or ache with eye movement. It can be seen as a part of multiple sclerosis or as a clinically isolated syndrome. When isolated, it might represent an inflammation of a post-infectious nature. Papillitis is optic neuritis that is very near the disc, thus, it is an inflammation of the disc. However, most often the inflammation of

[00:08:00] optic neuritis occurs behind the eye and in these cases is called retrobulbar neuritis. The afferent pupillary defect is a sign of optic neuritis. When the light is shown in one eye, that eye normally constricts. The other eye also have constricts in a consensual response. When you swing the flashlight to the opposite eye, the consensually constricted pupil should remain constricted due to the direct light reflex. If you have an efferent pupillary defect, the effective

[00:08:30] eye will appear to enlarge when the flashlight is swung into it. Just like the olfactory nerve, the optic nerve is in close proximity to bony structures and it can be affected by pathology arising in the bone or the membrane surrounding the brain. Remember that the optic chiasm sits above the sella turcica which is a fossa in the skull bone that contains the pituitary gland. Suprasellar extension of a pituitary tumor often compresses the optic chiasm, the region where the temporal retinal images cross.

[00:09:00] This results in a peculiar lesion known as bitemporal hemianopsia. Other masses that can affect this region include craniopharyngiomas, dermoid tumors, metastasis, and meningiomas.