The clinical syndrome and etiological mechanism of infarction involving the nucleus prepositus hypoglossi.

BACKGROUND

The human nucleus prepositus hypoglossi (NPH), which is known to be a neural integrator of horizontal eye movement, may also serve vestibular function. The present study investigated the clinical spectrum and etiological mechanism of isolated, small infarctions involving the NPH area demonstrated on MRI.

METHODS

The subjects of this study were 18 consecutive patients with a small infarction involving the NPH that was demonstrated by diffusion-weighted MRI. We assessed their clinical features according to the level involved (pons or medulla oblongata) and determined etiological mechanisms that may cause infarction in this region.

RESULTS

Vertigo and nausea/vomiting were the presenting symptoms in all patients. Sixteen patients showed truncal ataxia (contralateral falls in 11 patients and bilateral falls in 3). Gaze-evoked nystagmus was observed in 13 patients. In addition to those NPH-related symptoms, ipsi- lateral peripheral facial palsy and horizontal gaze palsies, including internuclear ophthalmoplegia and horizontal conjugate gaze palsy, were commonly associated with pontine lesions, and dysphagia was common in medullary lesions. Ten out of 18 patents showed significant stenosis (>or=50%) of the relevant vertebral artery. Two patients had aortic atheroma >4 mm, and 1 patient had atrial fibrillation.

CONCLUSIONS

Clinical features of vertigo, contralateral falls and gaze-evoked nystagmus are suggestive of an NPH lesion. Accompanying signs of ipsilateral facial palsy of the peripheral type and/or horizontal gaze palsies are highly specific for a pontine NPH lesion. Large-artery atherosclerosis was the most common causative mechanism of infarctions involving the NPH area.