We present a case of opsoclonus- myoclonus ataxia following Lyme and Anaplasma infection with positive CSF- detected NIF-IgG antibodies.

A 62-year-old man presented with headaches, fever, and malaise after discovering multiple ticks on his lower extremities.  He was diagnosed with Anaplasma Phagocytophilum by serum PCR. After five days of oral antibiotics, he started experiencing imbalance with frequent falls, myoclonus, and confusion.  Examination revealed disorientation, opsoclonus-myoclonus, hypometric saccades, and appendicular and truncal ataxia.  MRI of the brain was normal.  CSF analysis demonstrated a lymphocytic pleocytosis (160 WBC/cubic mL) and elevated protein (243 mg/dL). CSF Lyme titer was markedly positive (16.2); but, because of a high CSF albumin level, the titer was considered equivocal. The patient was treated with intravenous doxycycline and then discharged home on oral doxycycline. His symptoms worsened at home and was admitted for IV ceftriaxone. CSF demonstrated improved lymphocytic pleocytosis (139 WBC/cubic mL) and protein (98 mg/dL). CSF autoimmune encephalitis panel demonstrated a markedly elevated neuronal intermediate filament (NIF) titer of 1:16 with positive light and heavy chain antibodies. This was suspected to have been triggered by the Lyme and Anaplasma infections. Symptoms resolved on ceftriaxone. Repeat CSF examination eight days later still showed a positive immunofluorescence assay for anti-NIF antibodies, but the CSF titer was now less than 1:2.

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The detection of CSF-detected NIF-IgG antibodies in this patient suggests an overlap between the two most common causes of opsoclonus: parainfectious and autoimmune encephalitis. The anti NIF antibodies support cerebellar (vermal) dysfunction as a mechanism for opsoclonus-myoclonus ataxia and also provide a hypothesis for co-existent saccadic hypometria and opsoclonus, as the vermis plays a role in both initiation and termination of saccades.