Cranial multineuropathy with hypoglossal nerve involvement in a patient with anti-Ku autoantibodies
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LETTER TO THE EDITOR
Cranial multineuropathy with hypoglossal nerve involvement in a patient with anti-Ku autoantibodies Chiara Sist 1
&
Mara Turri 2 & Igor Florio 2 & Francesco Teatini 2
Received: 17 July 2020 / Accepted: 15 November 2020 # Fondazione Società Italiana di Neurologia 2020
Cranial multineuropathy involving facial and trigeminal nerves is a well-described possible manifestation of an autoimmune disease associated with anti-Ku antibodies. We present the case of a patient with anti-Ku antibodies and monolateral hypoglossal palsy. A 61-year-old man was admitted to our department for numbness sensation involving both cheeks. Symptoms appeared some months before on the right cheek, with subsequential spreading to the nose, the contralateral cheek, and the oral cavity. The patient could not feel food textures and this fact prevented him from chewing properly, so he lost weight within few months. Afterwards he complained burning sensation over the left part of the tongue. Raynaud’s syndrome had occurred some months before. His past medical history revealed a recent diagnosis of chronic gastritis; no other medical relevant conditions were reported. The patient had no familiarity for neurologic or rheumatologic diseases. Clinical examination showed hypoesthesia involving the region of the second and third trigeminal branches bilaterally and the oral cavity. Mild central facial palsy and a deviation of the tongue to the left on protrusion were present. Needle examination confirmed left axonal hypoglossal nerve damage. No clinical or neurophysiological signs of neurogenic nor myogenic damage were detected on either upper or lower limbs. The patient did not complain myalgia, muscle weakness, or arthralgia. No skin changes were detected. The patient underwent brain magnetic resonance imaging (MRI), which did not detect signs of gadolinium enhancement * Chiara Sist [email protected] 1
Department of Neurosciences, Biomedicine and Movement Sciences, Section of Clinical Neurology, University of Verona, Verona, Italy
2
Department of Neurology/Stroke Unit, San Maurizio Hospital, Bolzano, Italy
nor nerve thickening. Conversely, whole body positron emission tomography-computed tomography (PET-CT) showed interstitial lung disease (ILD). A pathological 18fluorodeoxyglucose (18-FDG) uptake in the gastric region and at the gastro-duodenal junction consistent with anamnestic chronic gastritis was also noted. Screening for antineuronal antibodies by indirect immunofluorescence assay on HEp-2 cells revealed strong positivity of ANA (titer 1:1280), with speckled pattern. According to the International Consensus on ANA Patterns (ICAP), ENA, SSc, and inflammatory myopathy profile were performed, and immunoblot identified the presence of anti-Ku antibodies. Serum anti-ganglioside antibodies were not found and creatine kinase levels were normal. Lumbar puncture was also performed, but cerebrospinal fluid examination did not show pleocytosis, abnormal cell count, hypoglycorrhachia, oligoclonal bands or onconeural antibodies.
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