Olfactory hypersensitivity is an increased sensitivity to olfactory odor stimuli is a clinical manifestation of olfactory disorders. Olfactory impairment is a partial or total decrease, loss or abnormality of olfactory function. The olfactory nerve is the nerve fiber of the olfactory epithelium across the sieve plate to the olfactory bulb. The ability to smell is a characteristic of the olfactory cells in the nasal mucosa. Injury to the nasal mucosa, olfactory bulb, olfactory filament or central nervous system connection may affect the sense of smell. Clinical manifestations are hyposmia, olfactory loss, olfactory deficit, olfactory inversion, phantom smell and increased sensitivity to olfactory stimuli. The pathogenesis of olfactory hypersensitivity and the molecular biology of olfaction are unknown. Among them, meningiomas, metastases or infiltrative tumors of the anterior cranial sulcus artery or frontal lobe. They can compress the olfactory bulb and olfactory tract leading to olfactory impairment. Many tumors in the anterior cranial sulcus, as well as tumors in the saddle area and paracranial area invade the olfactory nerve and cause olfactory hyposmia and loss of smell; lesions in the frontal lobe such as glioma and brain abscess can develop to a certain extent; in a few cases, increased intracranial pressure, hydrocephalus and cranial surgery can also produce olfactory impairment. In cranial trauma, the olfactory filaments of the olfactory nerve via the sieve plate can be torn or the olfactory bulb can be shredded (contusion). Due to the fracture of the skull base in the anterior cranial sulcus involving the sieve plate, unilateral loss of smell is often seen and cerebrospinal fluid nasal leakage may occur; in the case of hedonic brain injury with occipital force, the contusion is mainly concentrated in the orbital gyrus of the frontal lobe, which happens to be the site of the bilateral olfactory nerves, showing a bilateral loss of smell, sometimes persistent.