Pusher syndrome in patients with cerebellar infarctions?

Abstract

Acute supratentorial unilateral stroke can lead to an impairment of head and body posture and balance that manifests as an active pushing away from the non-paralyzed side in order to maintain an upright posture, i.e., socalled pusher syndrome (PS). Besides supratentorial lesions [1–3], there have also been claims of PS occurring in patients with cerebellar lesions [4]. Thus, we aimed to answer the question whether the PS can be found regularly in patients with cerebellar lesions. A total of 19 patients with acute cerebellar stroke, documented by magnetic resonance imaging (MRI) (time since lesion, mean ± standard deviation (SD): 4.0 ± 2.2 days) were classified based on the criteria of the Scale for Contraversive Pushing [1]. All patients underwent neurootological examinations including otolith testing by means of the subjective visual vertical (SVV) [5, 6]. None of the patients showed PS (mean score 0). However, if the criterion of a ‘‘pathological tilt’’ of SVV of [2.5 on our data is applied [5], 9 patients (48%) presented with contralesional tilt (9.1 ± 7.1 ) and 5 (26%) with ipsilesional tilt of SVV (5.1 ± 2.9 ). Five patients (26%) had no pathological tilt. Thus, our data indicate that PS is not a common sign in patients with acute cerebellar lesions, whereas an otolith deficit with tilts of SVV regularly occurred [6]. Therefore, contrary to a cortical level where an association between PS and SVV tilt was reported [3, 7] and points toward otolith dysfunction in PS patients, at a cerebellar level such an association could not be verified by our data. Indeed, one might even speculate that PS does not exist in cerebellar stroke patients. The case report describing a patient with gait ataxia that presented 1 week later with a ‘‘strong pusher behavior when standing’’ whereas ‘‘independent sitting was possible, but not standing without help’’ [4] has to be discussed with caution. The authors attributed these signs to a PS toward the affected side caused by a large cerebellar infarction [4]. The lesion site of the infarction could only be documented by CT scan. However, CT scan’s resolution is not adequate to detect small brainstem lesions at the medullary level which often accompany cerebellar infarctions. Indeed, an additional small affection of the medulla might be an important aspect since lateral medullary lesions can cause severe body lateropulsion, i.e., a strong irresistible tendency to fall to one side even with the eyes open [8–10]. This ipsilateral axial lateropulsion might appear similar to PS and, thus, can be mixed up, especially when it occurs in the standing and not in the sitting body position as was the case in patient described by Paci and Nannetti [4]. Body lateropulsion in medullary infarcts may occur without signs of vestibular dysfunction (e.g., tilts of SVV) and without limb ataxia: it reflects an impairment of vestibulospinal postural control caused by a lesion of the descending lateral vestibulospinal tract as described with three-dimensional brainstem mapping based on MRI [10]. Body lateropulsion with limb ataxia is probably the consequence of impaired or absent proprioceptive information caused by a lesion of the ascending dorsal spino-cerebellar tract [10]. The observation of the present data that patients with cerebellar lesions show contraor ipsilesional tilt of SVV B. Baier (&) M. Dieterich Department of Neurology, University of Mainz, Langenbeckstr. 1, 55131 Mainz, Germany e-mail: baierb@uni-mainz.de