Anatomy clinical correlates: Olfactory (CN I) and optic (CN II) nerves

It's time to stop and smell the roses! Or... perhaps stop and see the clinical correlates of cranial nerve 1 and cranial nerve 2? Common sayings aside, this video will focus on the olfactory nerve, or cranial nerve 1, which allows us to experience smells, and your optic nerve, or cranial nerve 2, which allows us to see the world around us. Both of these nerves are prone to injury along their pathways, so knowing their anatomy can help us locate the different types of lesions that affect these nerves and understand why they are prone to injury.

Let’s start with the olfactory nerve. The olfactory nerve consists of chemoreceptors found in the nasal mucosa, and their axons make up rootlets that project through the cribriform plate of the ethmoid bone. These rootlets then synapse in the olfactory bulb, which rests on top of the cribriform plate, and this thin bony plate makes up the roof of the nasal cavity.

Fast acceleration and deceleration movements, such as a high impact car crash, can cause shearing and tearing of these rootlets as they travel through the cribriform plate. Head trauma, such as a direct blow to the nose, can also fracture the thin cribriform plate, putting the olfactory nerve at risk of injury. The fracture can injure both the rootlets passing through it, or the bulb resting on top of it.

Fracture of the cribriform plate can sometimes present with cerebrospinal fluid rhinorrhea, which is cerebrospinal fluid leaking from the nose - not to be confused with an ordinary runny nose from a cold! Damage to the olfactory nerve can cause anosmia, which means loss of smell. As smell is extremely important in the perception of taste, most individuals with anosmia actually complain of loss of taste. Clinical testing of anosmia is usually not performed, and diagnosis is made by asking the individual if they’ve lost their sense of taste or smell.

One clinical condition that is associated with dysfunction of the olfactory nerve is called Kallmann syndrome. This syndrome occurs when there is a failure of development and migration of neurons from the olfactory placode during fetal development. This structure normally gives rise to both the olfactory nerves responsible for smell, as well as the neurons that secrete gonadotropin releasing hormone, or GnRH. The GnRH neurons migrate from the olfactory placode and settle in the hypothalamus, from where they control secretion of sex hormones, sexual development and reproduction. Therefore, individuals with Kallmann syndrome present with issues related to low GnRH production such as failure to start or complete puberty, delayed growth, low sperm count and amenorrhea, as well as a decreased sense of smell, known as hyposmia, or complete anosmia.