Before a fluctuating unilateral ptosis can be attributed to ipsilateral midbrain stroke,alternative etiologies must be thoroughly excluded

Letter to the editor

We were interested to read the article by Cai et al. ¹ about a 60-year-old woman with unilateral, fluctuating ptosis and an ipsilateral diffusion-weighted imaging midbrain lesion that was claimed to be the cause of the ptosis. In the report, ptosis was attributed to the selective affliction of the levator palpebral muscle branch. Ptosis spontaneously resolved 1 month after onset under acetylsalicylic acid and atorvastatin treatment. ¹ We have the following comments.

The first issue refers to the diagnosis of midbrain infarction. ¹ The lesion shown in Figure 2 represents either a stroke or an artifact. An ischemic stroke would also be visible on a sagittal image. Cytotoxic edema is characterized by hypointensity in apparent diffusion coefficient imaging. An older lesion would show up as a hyperintensity or isointensity on T2/fluid-attenuated inversion recovery images.

The second point relates to the screening for cardiovascular risk factors. ¹ Although the patient had no arterial hypertension or diabetes and normal long-term electrocardiography recordings, it is conceivable that other risk factors such as smoking, hyperlipidemia, coagulation disorders, platelet disorders, carotid artery stenosis, or atrial fibrillation were present.

The third point relates to the clarification of myasthenia. Because the clinical presentation (worsening at night), the association with generalized fatigue, and the clinical tests (positive neostigmine test, positive fatigue test, and positive ice pack test) were suggestive of myasthenia, it would have been helpful to also test the patient for antibodies against low-density lipoprotein receptor-related protein 4, titin, thymoma, and presynaptic calcium channels to rule out a myasthenic syndrome. A myasthenic syndrome may be also caused by an occult malignancy and previously undetected immunological disease. Furthermore, the reported fluctuating nature of the ptosis suggests a neuromuscular transmission disease rather than a stroke.

The fourth point is that Figure 3 shows that the superior oblique fibers run through the third nerve fascicle, which is definitely not the case.

The fifth point refers to the statement that “a partial decussation of the subnucleus rectus superior within the oculomotor nucleus leads to a contralateral innervation of the levator palpebrae superioris, which is why the nuclear ptosis is bilateral.” ¹ The nucleus rectus superior does not supply the levator palpebrae superioris (LPS) muscle, nor is the supply to the LPS contralateral. The nuclei for the LPS muscles on both sides are supplied by a single caudal central nucleus. Unlike the superior rectus muscle, there is no decussation of these fibers, which is why the nuclear ptosis is bilateral. This is because the fibers of the superior rectus muscle in the fascicle of the third nerve are very close to those of the LPS and were probably affected. A slight weakness of the superior rectus muscle was observed in a video.

Lastly, we disagree with the statement in the discussion that Lambert–Eaton syndrome is caused by antibodies against presynaptic acetylcholine receptor antibodies; this syndrome is instead caused by antibodies against presynaptic calcium channels.

To summarize, this interesting study has limitations that put the results and their interpretation into perspective. To differentiate between a true stroke and an artifact, the criteria for an ischemic stroke in multimodal magnetic resonance imaging must be met. To state that a midbrain lesion is responsible for ptosis, the patho-anatomical constellation must match.