Double depressor palsy after bilateral paramedian thalamus infarction

Abstract

PurposeWe report a rare case of double depressor palsy after bilateral paramedian thalamus infarction.MethodsCase Summary: A 47‐year‐old male presented with complaints of diplopia upon awakening. He had atrial fibrillation, mitral valve regurgitation, aortic valve regurgitation and a history of spleen infarction 1 year prior. His right eye was hypertrophic and right eye downgaze was limited unilaterally of equal degree in adduction and abduction. Right eye horizontal and upward movements were intact. Left eye movement was intact in all directions. Pupillary light reflex response and convergence test were normal. Nystagmus was not observed.ResultsThe patient was diagnosed with double depressor palsy of the right eye. Magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) of the brain showed an old infarction of the left thalamus and diffusion MRI showed acute infarction of the right thalamus. The patient's daily warfarin dose was 2 mg and was increased to 5 mg with cilostazol 75 mg two times a day. Seven weeks later, the patient's ocular movement revealed near normal muscle action and, subjectively, the patient was diplopia‐free.ConclusionsThe patient presented with bilateral thalamic lesions and was diagnosed double depressor palsy. The paramedian territory is supplied by the paramedian (or thalamoperforating) arteries which arise from the P1 segment of the PCA. The paramedian arteries often supply the rostral midbrain. Thus, bilateral thalamic infarctions can be presented with or without rostral midbrain lesions. The bilateral lesions of rostal midbrain including riMLF can cause double depressor palsy. However, the lesions of bilateral riMLF infarction were too small to be seen in imaging study. So there was no obvious lesion over the rostral midbrain. Otherwise, there may be another unknown vertical movement mechanism.