Author’s reply:

Considering the brief case description of Shiihara and Takahashi [6], we agree on the diagnosis of opsoclonus–myoclonus syndrome (OMS) following an infection with Mycoplasma pneumoniae although “jerky movements” are difficult to distinguish from a cerebellar ataxia.

The presence of autoantibodies against glutamate receptors (GluR) rises the question whether the consciousness of the patient was affected or not [2], which is important for the diagnosis of a possible encephalitis. Besides, it may be crucial to rule out other tumors than neuroblastoma, e.g., teratomas and carcinomas [1].

The normal findings of the cerebrospinal fluid (CSF) examination without either pleocytosis or positive antibodies on day 30 are surprising. This contrasts with other published cases of autoimmune encephalitis with positive anti-GluR-delta2 antibodies [4, 5].

One of the main messages of our communication in this journal was the need for a prompt treatment with corticosteroids starting in the first week of disease manifestation [3]. This was also described in cases of anti-GluR-delta2 antibody-positive encephalitis [7]. Intravenous immunoglobulins may have a place as a second line therapy. One can speculate that the extended course described by Shiihara and Takahashi may be the result of a delay in therapy.

Given the lack of remaining CSF or serum in our three patients, we cannot contribute to the question whether anti-GluR-delta2 antibodies are pathognomonic for OMS following an infection with M. pneumoniae. However, we would encourage the detection of anti-GluR-delta2 antibodies in serum and CSF in future cases of OMS following an infection with M. pneumoniae to further elucidate the role of these antibodies.