From the olfactory mucosa to the olfactory bulb, the olfactory nerve is the first cranial nerve to conduct olfactory information via markless nerve fibers. Specific disorders of the olfactory nerve include anosmia and hyposmia. They may also occur as a result of skull base fracture.
What is the olfactory nerve?
Odors travel from the olfactory mucosa to the brain via the olfactory nerve. The olfactory nerve thereby forms both the first cranial nerve of a total of twelve and the first link in the olfactory pathway, which maps the course of olfactory information transmission. Accordingly, disturbances in this area lead to pathological deterioration of the sense of smell (hyposmia) or to complete failure (anosmia). Since the olfactory nerve does not consist of brainstem neurons, but is composed of the axons of the olfactory cells, some sources in the literature do not consider it to be a cranial nerve in the strict sense. However, for traditional reasons, medicine still considers the olfactory nerve to be a cranial nerve; the same is true for the optic nerve or optic nerve, which has similar properties.
Anatomy and structure
The olfactory nerve consists of fibers, which are also known to anatomy as olfactory filaments or fila olfactoria. They are the nerve fibers of cells located in the olfactory mucosa, where they respond to olfactory stimuli. They are found exclusively in the regio olfactoria. From there, the olfactory nerve runs across the lamina cribrosa to the bulbus olfactoriusi’in the brain. In total, the olfactorius nerve consists of 20-25 bundles, which in turn are composed of the individual nerve fibers (axons). Unlike other neurons, the nerve fibers that unite to form the olfactory nerve are marbless, as they do not have a myelin sheath. The myelin sheath arises from Schwann’s cells and electrically insulates the axons. This increases the speed of information transmission. Conversely, for the olfactory nerve (which lacks this insulating layer), this means that its signals travel more slowly than the impulses of other nerves. Among the cranial nerves, the olfactory nerve represents the shortest.
Function and tasks
The function of the olfactory nerve is to transmit olfactory information. Although humans are not among the most odor-sensitive creatures in the animal kingdom, their olfactory mucosa has 30 million olfactory cells distributed over 10 cm2. The olfactory cell has sensitive receptors on its surface. Stimulation changes the properties of the cell membrane and the biochemical balance of the sensory cells shifts. As a result, depolarization occurs: the electrical voltage changes and can now continue through the nerve fibers. The long extensions of the cells reach into the olfactory bulb (bulbus olfactorius), which is already located in the brain. No synapse or interconnection is necessary; the transmission of the electrical signal is therefore particularly efficient. The bulbus olfactorius contains the pyramidal mitral cells, which as a group form the tractus olfactorius. Via this second neuron, the signal finally reached the olfactory center of the brain, which neuroscientists refer to as the primary olfactory cortex or trigonum olfactorium. This is where the initial processing takes place in the central nervous system before the brain processes the olfactory information in higher areas.
Diseases
Two clinical pictures specifically affect the olfactory nerve: anosmia as well as hyposmia. The latter describes a reduction in the ability to smell, whereas people suffering from anosmia lose the sense of smell completely. In functional anosmia, affected individuals theoretically still have a residual ability to smell, but its practical significance is no longer present. A special form of olfactory loss is partial anosmia, which leads to the loss of the ability to smell certain odors without other olfactory perceptions having to be impaired. Medical science classifies these clinical pictures among the quantitative olfactory disorders; their causes are manifold. Neurodegenerative diseases such as Parkinson’s disease, Alzheimer’s disease or multiple sclerosis are possible causes of hyposmia and anosmia, as are traumatic effects. Skull base fracture is one of the frequent traumatic causes of quantitative olfactory disorders, especially in the case of a frontal fracture.Biochemical causes include zinc deficiency as well as medications such as ACE inhibitors, antihistamines and certain antidepressants. In addition, chlorine and benzene gases can damage the olfactory system, as can infections with viruses, inflammation, tumors, and swelling. Congenital anosmia does not necessarily have to be due to a maldevelopment or lesion of the olfactory nerve, but can also affect other members of the information transmission system; however, the cause is usually in the olfactory pathway, which includes the olfactory nerve. A special form of congenital anosmia manifests itself in the context of Kallmann syndrome; in this case, the olfactory disorder is accompanied by an underfunction of the ovaries or testes and can thus prevent or delay pubertal development. In addition, a movement disorder of the hands (synkinesia) and missing attachments for teeth and/or brain bars are possible; other disorders are also possible. Kallmann syndrome results from a mutation in the genetic material and is hereditary. Regardless of their cause, anosmia and hyposmia can cause psychological distress; in the case of causes such as neurodegenerative diseases, the psychological symptoms of the respective underlying disease are added, with depressive symptoms being particularly common. Despite intact taste buds and nerves, olfactory dysfunction also limits the perception of taste, as the two sensory modalities are closely related and smell significantly influences the taste of food.
