Many patients with vertigo can see various types of nystagmus in the acute phase, and some patients with vertigo or dizziness do not have nystagmus on physical examination. Sometimes, patients have nystagmus, but do not have symptoms of vertigo or dizziness, but simply show a balance disorder. So, what is the relationship between vertigo and nystagmus? As one of the most frequent positive signs in patients with vertigo/dizziness, nystagmus has an important localizing diagnostic significance. A full understanding and analysis of nystagmus plays an important role in better understanding vertigo and neurological disorders. Nystagmus, or nystagmus for short, is an involuntary, biphasic, rhythmic, reciprocal oscillatory eye movement that can be physiologic or pathologic due to an inability to sustain gaze at the target and a slow movement of the eye to one side away from the gaze target, followed immediately by a rapid corrective eye jump back. In understanding nystagmus, we first need to classify it. There can be several ways to classify nystagmus according to different criteria: physiological or pathological nystagmus; acquired or congenital; monocular or binocular; according to the direction of nystagmus: horizontal or vertical (upward or downward jumping) or torsional nystagmus; or multidirectional nystagmus; according to the waveform: jumping (with slow and fast phases) or oscillatory (more or less the same speed or amplitude); gaze-induced or non-gaze induced nystagmus. By observing nystagmus, the most important aim is to clarify whether the nystagmus is pathological, central or peripheral, and identifying the waveform helps to localize the lesion. Physiologic or pathologic nystagmus Physiologic causes of nystagmus include optokinetic nystagmus (e.g., occurring when you are looking at trees in a moving car), vestibular stimulation (e.g., hot and cold water tests), and nystagmus occurring during extreme gaze. Physiological causes of nystagmus are difficult to avoid, but at this time nystagmus is usually transient and rarely becomes a chief complaint. Congenital or acquired nystagmus The distinction between congenital and acquired nystagmus is not difficult and is mainly made by age. Congenital nystagmus is usually a horizontal oscillatory nystagmus that can be exacerbated by gaze. Sometimes congenital nystagmus is associated with albinism and blindness. However, acquired nystagmus can also have a similar presentation, so age is a better differentiator. The nystagmus waveform is an important observation. Understanding some of the physiological and pathophysiological mechanisms involved in the formation of nystagmus will help to better understand the association between the waveform and the site of the lesion. Among them, vertical nystagmus has a strong localization diagnostic significance, including up-beating nystagmus and down-beating nystagmus. Upward-hopping nystagmus is a pontine lesion caused by damage to the ventral tegmental tract emanating from the superior vestibular nerve nucleus. the VTT transmits excitatory signals from the vestibular nerve upward to the nucleus accumbens through the full length of the ventral pontine. Therefore any lesion on this pathway can lead to upward jumping nystagmus. In addition, lesions in the caudal part of the medulla oblongata can also lead to similar nystagmus. Downbeat nystagmus is usually caused by a lesion in the cerebellar vermis, which subsequently leads to inhibition of the SVN-VTT pathway, followed by an increase in relative activity, facilitating the emergence of the slow phase of upbeat nystagmus. Downbeat nystagmus is seen in structural lesions at the cervicomedullary junction, such as Chiari malformation. Other possible etiologies include any type of cerebellar choroidal lesion.