Daniel R. Gold, DO, Departments of Neurology, Ophthalmology, Neurosurgery, Otolaryngology - Head & Neck Surgery, Emergency Medicine, and Medicine, The Johns Hopkins School of Medicine
This is a 50-yo-woman with imbalance, and with fixation removed on her examination (with Frenzel goggles), there was no spontaneous nystagmus. Using a handheld vibrator to vibrate the mastoids and vertex, there was a rightward slow phase and corrective leftward fast phase (left-beating nystagmus). Vibration is an excitatory vestibular stimulus, and when vestibular asymmetry is present, vibration can transiently exacerbate this asymmetry and generate a slow phase that is ipsilateral to the pathology/vestibular hypofunction (towards the right in this case). After hyperventilating the patient for 40 seconds, there was robust right-beating and torsional (towards right ear) nystagmus. Hyperventilation transiently alters neuronal conductivity across a demyelinated segment of the 8th cranial nerve (e.g., acoustic neuroma or neurovascular compression), and can generate excitatory>inhibitory pattern of nystagmus (excitatory in this case with contralesional, leftward slow phase, and ipsilesional, rightward fast phases). MRI demonstrated a right sided vestibular schwannoma which explained both the right hypofunction (LBN with vibration), and the excitatory pattern (RBN) of her hyperventilation-induced nystagmus.
1, patient with right sided vestibular schwannoma with nystagmus provoked by vibration and hyperventilation
Daniel R. Gold, D.O.
Spencer S. Eccles Health Sciences Library, University of Utah