The vertiginous syndromes are classified into two large groups-peripheral vertigo and central vertigo-depending on the information system that is altered:


Possible causes of peripheral vertigo include labyrinthine lesions such as Ménière's disease, cranial trauma, labyrinthitis or labyrinth inflammations secondary to viral infections, complicated meningitis or otitis, or drugs (aminoglycosides, furosemide) or alcohol. Other causes are paroxysmal positional vertigo, vestibular neuritis after upper respiratory infections and tumors such as acoustic neurinoma. The onset is usually abrupt and intense, in the form of self-limiting episodes, with intense vegetative symptoms and exacerbation of symptoms with head movement. Hearing symptoms may occur more frequently, while other neurological symptoms are rare. The nystagmus is usually horizontal-rotating with the rapid phase on the opposite side of the lesion and improves with the fixation of the gaze. The first three causes of peripheral vestibular vertigo are:


Benign paroxysmal positional vertigo is defined as the appearance of brief episodes of vertigo caused by changes in position, usually when turning in bed, when lying down or getting up, when bending, straightening or extending the neck, and that they reproduce when adopting the trigger position. It is the most common cause of peripheral vertigo. This disorder may be due to cephalic injury, viral labyrinthitis or vascular occlusion or, more commonly, presenting as an idiopathic phenomenon. There seems to be a detachment of otoliths from the saccule or the utricle, which move towards the posterior semicircular canal, and when moving freely, obstruct the flow of the endolymph and its absorption. Benign paroxysmal positional vertigo usually improves with canalicular relocation maneuvers. The disease is spontaneously resolved, and the patient recovers completely within approximately three months.


It is the second most frequent cause of peripheral vestibular vertigo. It is characterized by recurrent spontaneous attacks of vertigo, fluctuating hearing loss, tinnitus and aural fullness. The attack of vertigo reaches a maximum intensity within a few minutes of the beginning and then slowly subsides in the following hours. The patient perceives a sensation of instability and dizziness after an acute episode. In most cases the symptom can be located in the affected ear due to auditory discomfort. In the early stages, the sensorineural hearing loss is low frequency and completely reversible, but in late stages residual hearing loss is observed and can affect the middle and high frequencies. The syndrome reaches an extinction phase that results in severe permanent hearing loss but cessation of vertigo. The pathological correlation is established by an excessive accumulation of endolymph that produces dropsy. As the volume of endolymph increases, the membranous labyrinth expands until it breaks, producing hearing loss and vertigo.

The treatment is mainly aimed at preventing osmotic changes in the endolymph. Medications, such as vasodilators and diuretics, are useful in many patients. It is recommended to follow a diet low in sodium and restricting the consumption of caffeine and tobacco. Specific treatment of any underlying allergy by immunotherapy or suppression of food allergens is also recommended. This treatment is usually insufficient for the control of vertigo episodes, which is why a surgical procedure is necessary.


It is the third most frequent cause of peripheral vestibular vertigo. It presents with severe and sudden rotational vertigo that can last several days. Nausea and vomiting are common, however, there is no hearing loss or other focal neurological signs. Residual instability may persist for several weeks once the vertigo subsides, while in the elderly it may persist for months. About 50% of patients report having an upper respiratory infection a few weeks before the onset of vertigo. Histopathological studies reveal atrophy of one or more vestibular nerve trunks and of the sense organs. The treatment consists of the administration of vestibular suppressants, antiemetics and adequate hydration for prolonged vomiting.


Among the possible causes of central vertigo include multiple sclerosis, cerebrovascular accident, neuropathies affecting the cranial nerves, temporal epilepsy, tumors of the posterior fossa and cerebellopontine angle and transient ischemia of the brainstem due to involvement of the vertebrobasilar territory. Sometimes vertigo can appear as a preamble to a migrainous crisis or in basilar migraine, as well as due to some drugs such as phenytoin, quinidine, amino-glucosides, etc. Central vertigo is usually more insidious and constant, less intense and is not related to the movements of the head; the vegetative symptoms are milder and may be accompanied by other neurological deficiencies. There are usually no auditory symptoms. Nystagmus is not as characteristic as in peripheral involvement.