Essential tremor (ET) is generally regarded as a benign monosymptomatic condition with tremor being the sole neurological manifestation. Structural brain abnormalities are not considered part of the syndrome. Over recent years, however, it has become increasingly clear that a cerebellar pathology might be involved in the disease process [1, 2]. Neuropathological studies associated Purkinje cell loss with ET [3], whereas brain imaging demonstrated in many cases atrophic changes in different lobules of the cerebellum [4]. It should be mentioned, however, that there are also studies which failed to show an association of ET and cerebellar pathology [5]. Reports on clinical cerebellar signs in ET are sparse [1, 6]. Here, we present an ET case exhibiting saccadic intrusions with features of ocular flutter (OF). A 74-year-old woman presented with gradual onset of hand tremor over the last three decades. The tremor worsened with stress or intense physical exercise and improved after ingestion of small amounts of alcohol. Her father had similar symptoms but never sought medical advice. She also complained of dizziness and oscillopsia lasting ‘‘a few seconds’’ many times a day for at least 10 years. On examination, a postural tremor of both hands, more pronounced on the left, was noted. Finger-to-nose test was slightly impaired, but heel–knee–shin was unremarkable. The eyes showed infrequent (1–2/min), rapid, conjugate, horizontal oscillations occurring in bursts, leading to the clinical diagnosis of OF. No other ocular motor abnormalities were noted. Recording of eye movements confirmed the clinical impression, showing bursts of fast phases without intersaccadic intervals (Fig. 1a). Intraburst frequency was 10 Hz, and interburst frequency was 0.5 Hz in a 4-min record. Surface electromyography (EMG) recordings of the wrist extensors revealed a postural tremor frequency of 6–6.5 Hz (Fig. 1c). We put the patient on primidone, slowly titrated up to a daily dose of 375 mg. Upon reexamination 2 months later, hand tremor had virtually disappeared (Fig. 1d), although the patient reported a mild tremor of the left hand during emotional excitement. Interestingly, ocular flutter was also absent both clinically and in a 7-min-long record (Fig. 1b). Importantly, she could not recall any oscillopsias in the last couple of weeks. OF is a pathological form of saccadic intrusions consisting of back-to-back horizontal saccades [7]. It is considered a subtype of opsoclonus, the former being characterized by multidirectional fast phases of varying amplitudes. The pathophysiology of OF and opsoclonus is still controversial. It is assumed that abnormal Purkinje cell activity in the cerebellum leads to reduced inhibition on the fastigial nucleus. This results in enhanced inhibition of brainstem omnipause neurons, which, in turn, renders saccadic burst neurons free to oscillate [8, 9]. Recent modeling, however, is based on a dysfunction of the brainstem saccadic generator while cerebellar abnormalities are believed to be secondary to brainstem oscillations [10]. Nonetheless, available functional neuroimaging data conform to the cerebellar hypothesis of OF genesis [11, 12]. The present case exhibited ocular flutter linked with mild oscillopsia for presumably more than 10 years. Thus, this long period largely rules out causes such as encephalitis or paraneoplastic disease. The fact that both tremor E. Anagnostou (&) E. Kararizou I. Evdokimidis Department of Neurology, Eginition Hospital, University of Athens, Vas. Sophias Avenue 74, 11528 Athens, Greece e-mail: granavan@yahoo.com