Medial cerebellar stroke presenting as a pure labyrinthine syndrome

Objective: Cerebellar stroke may mimick vestibular neuritis, a benign and usually self-limited neurologic disorder. On the basis of the clinical findings it is not always possible to differentiate between those two entities. However, the differential diagnosis is important because treatment and surveillance of patients are different, and misjudging cerebellar infarction may be fatal as it may lead to swelling and brainstem compression. Recent studies and case reports on cerebellar ischaemia have shown that cerebellar infarction presenting as a pure labyrinthine syndrome, so-called pseudo-vestibular neuritis, is more common than previously thought.

Methods: We here report two patients who developed a sudden onset of vertigo, nausea, vomiting, and truncal imbalance. Both had spontaneous rotatory nystagmus on examination and a tendency to fall to the side opposite to the fast phase of the nystagmus. They did not show any other cerebellar signs, such as dysmetria, dysarthria, abnormal smooth pursuit or saccadic lateropulsion.

Results: The initial brain CT scans were normal. We performed MRI because caloric vestibular stimulation produced regular responses in one case and because of severe cardiovascular risk factors in the other. In both patients it revealed medial cerebellar infarction involving the nodulus. Repeated electrooculography confirmed the absence of cerebellar oculomotor disturbances.

Conclusions: These cases again stress the importance of careful diagnostic workup in patients with acute vestibular syndrome. Caloric vestibular stimulation helps to differentiate between cerebellar infarction and peripheral vestibulopathy. Suspect findings require further diagnostic effort and early magnetic resonance imaging of the brain.

As previously assumed, interruption of inhibitory nodulovestibular Purkinje fibers seems to be the explanation for the ipsilesional spontaneous nystagmus in medial cerebellar stroke and nodulus infarction, because this causes an increased activity in the ipsilateral vestibular nucleus neurons in the brainstem.