下眼瞼向き眼振など認められた橋傍正中動脈梗塞 (BAD) の1例

抄録

　A-76-year-old woman presented with abrupt onset of imbalance during standing and walking. Neurological examination revealed slight truncal ataxia and downbeat nystagmus on lateral gaze while wearing Frenzel goggles. MRI showed pons infarction (right paramedian perforating artery territory), which led to the diagnosis of branch atheromatous disease (BAD). ENG revealed downbeat nystagmus (DBN) occurring at the primary eye position and lateral gaze in the dark, but not during vertical gaze. Abnormal eye movements, such as square wave jerks and saccadic intrusions were also observed in the dark. While the horizontal pursuit was almost normal, saccadic pursuit was noted during vertical pursuit. Horizontal OKN and OKAN were well induced. The rightward saccade was relatively hypometric, while the upward saccade was slightly hypermetric (overshoot). In contrast to reports of DBN being generally caused by cerebellar flocculus/paraflocculus lesions, there are scarce reports of DBN resulting from discrete brainstem lesions. According to the aforementioned reports, DBN is conceivably induced by interruption of the neural pathways between the brainstem and the cerebellar flocculus/paraflocculus. There are three main neural pathways conveying important signals about eye movements from the brainstem to the flocculus/paraflocculus, namely, the pathways via the nucleus reticularis tegmenti pontis (NRTP), via the central tegmental tract to the inferior olive, and via the paramedian tract (PMT) neurons. In our case, we speculated that the DBN was most likely caused by damage to the PMT neurons induced by the pons infarction, as follows. PMT neurons, which represent several cell groups of neurons associated with both horizontal and vertical eye movements which project to the flocculus/paraflocculus and vermis, are present in the paramedian region of the lower brainstem; these neurons transmit vestibular information from the anterior semicircular canals to the cerebellum, forming a cerebellum-brainstem feedback loop. Therefore, damage to PMT neurons could cause disruption of this feedback loop, resulting in DBN.