Central Vertigo

Abstract

Central vertigo can clinically manifest in three ways: Acute onset of vertigo and dizziness, recurrent attacks and chronic central vertigo. In patients with acute onset of symptoms it is essential to differentiate between central and peripheral vertigo because this has major diagnostic and therapeutic implications. A differentiation can most often be achieved by a careful neuroophthalmological and neuro-otological bedside examination. One should look in particular for the following five signs of central lesions: skew deviation/vertical divergence (as a component of the ocular tilt reaction), gaze-evoked nystagmus contralateral to a spontaneous nystagmus, saccadic smooth pursuit, acute nystagmus in combination with a nonpathological head-impulse test and central fixation nystagmus. The most frequent forms of central vertigo with recurrent attacks are vestibular migraine and episodic ataxia type 2. Clinically relevant types of chronic or chronic progressive central vertigo are neurodegenerative disorders affecting the cerebellum which are often associated with cerebellar ocular motor dysfunction, in particular downbeat nystagmus. Treatments of choice for a prophylactic therapy of vestibular migraine are betablocker, topiramate or valproic acid. A new treatment option for episodic ataxia type 2 and downbeat nystagmus are aminopyridines (potassium channel blockers).

Do central vestibular findings predict abnormal findings on magnetic resonance imaging?

“…Central vertigo can manifest in three ways: by acute onset of vertigo and dizziness, by recurrent attacks and through chronic vertigo. 4 In a clinical setting, a detailed history provides clues to differentiate between peripheral and central causes of vertigo. 5 Physical, neuro-ophthalmological and neuro-otological examination at the bedside can help to confirm the diagnosis.…”

“…The most common causes of central vertigo with recurrent attacks are vestibular migraine and episodic ataxia type 2. 4,9 A study by Swartz and Kern showed that those with migraine are four times more likely than those without migraine to have white matter hyperintensities in MRI scans. 10 This is in contrast to our findings where 31 individuals (45.5 per cent) with migraines had white matter hyperintensities in MRI scans versus 37 individuals with migraines (54.4 per cent) who did not have MRI abnormalities (Table 1).…”

Vestibular migraine: diagnostic difficulties and treatment optimization

“…Центральные вестибулярные синдромы в большинстве случаев представляют собой впервые остро возникающие головокружения, но далеко не всегда сопровождающиеся дополнительной очаговой симптоматикой, поэтому следует проверить дополнительные признаки центральных вестибулярных поражений [16]: нарушение нормального положения глазных яблок; взориндуцированный нистагм, контрлатеральный спонтанному; нарушение плавного слежения с появлением саккад; нормальный тест поворота головы при остро возникшем головокружении; центральный нистагм при фиксации взора.…”