Hypoglossal nerve palsy after SARS-CoV-2 vaccination - report of two cases.

BACKGROUND: SARS-CoV-2 vaccination is associated with an increased risk for Bell's palsy and some other neurological disorders assumed to be of autoimmune origin. While facial nerve palsy is frequent and usually idiopathic, hypoglossal nerve palsy is rare, and a specific cause is almost always found. We firstly report two patients who developed isolated hypoglossal nerve palsy shortly after SARS-CoV-2 vaccination. CASE PRESENTATION: Two otherwise healthy patients, a 49-year-old man and a 39-year-old woman, developed unilateral hypoglossal nerve palsy 10 and 7 days after the second SARS-CoV-2-vaccination (AstraZeneca and BioNTech/Pfizer), respectively. In both subjects, needle electromyography showed denervation and rarefication of motor units. CT, MRI, examination of blood and CSF as well as ENT exam were unremarkable. In both subjects symptoms gradually improved. CONCLUSION: Due to close temporal relationship, the absence of other etiologies, and spontaneous improvement we suspect the vaccination as the cause for hypoglossal nerve palsy in both patients. This is further supported by the rarity of isolated hypoglossal nerve palsies, especially in idiopathic cases. We suggest the addition of hypoglossal nerve palsy to the list of neurological injuries potentially caused by SARS-CoV-2 vaccination.

Patients with breakthrough tick-borne encephalitis suffer a more severe clinical course and display extensive magnetic resonance imaging changes.

BACKGROUND AND PURPOSE: Tick-borne encephalitis (TBE) is a common viral disease in central Europe and Asia. Severe or even lethal neurological symptoms may ensue. With limited therapeutic options, active vaccination against the TBE virus (TBEV) is strongly recommended in endemic areas. A systematic analysis of the clinical picture and cerebral imaging findings associated with TBE was conducted with particular focus on patients who acquired TBE despite previous vaccination. METHODS: A cohort of 52 patients with serologically proven TBE treated at our centre in a 10-year period who received at least one cerebral magnetic resonance imaging (MRI) was retrospectively described. Extension of MRI changes was systematically assessed by an experienced neuroradiologist. Standard statistical procedures were performed. RESULTS: Fifty-two patients with a definite serological diagnosis of TBE were included. The most common presentation was encephalitis (67%). MRI showed TBE-associated parenchymal lesions in 33% of all patients. Sites of predilection included the periaqueductal grey, the thalamus and the brainstem. Ten patients had received at least one prior active or passive TBEV immunization. All of these had a maximal Rankin Scale score of at least 4. The median number of affected anatomical regions on MRI was significantly higher than in the non-vaccinated cohort. CONCLUSIONS: To our knowledge, this is the first study systematically describing the peculiarities of MRI in patients vaccinated against TBE. In addition to a severe clinical course, they exhibit more extensive MRI lesions than a non-vaccinated cohort. Possible reasons for these findings include incomplete seroconversion, more virulent TBEV strains or antibody-dependent enhancement.

CXCL13 as a diagnostic marker of neuroborreliosis and other neuroinflammatory disorders in an unselected group of patients.

BACKGROUND: The C-X-C motif chemokine ligand 13 (CXCL13) and its receptor CXCR5 play an important role in the homing of B-lymphocytes. As a biomarker in the cerebrospinal fluid (CSF), CXCL13 has increasingly been used for the diagnosis of neuroborreliosis (NB). We evaluated the diagnostic and prognostic potential of CXCL13 for NB and other neuroinflammatory diseases in an unselected cohort, paying attention to those patients particularly who might benefit from newly emerging CXCL13-directed therapies. METHODS: We report the CSF CXCL13 concentrations and other relevant baseline characteristics for an unselected cohort of 459 patients. We compare different diagnostic groups and analyse the sensitivity and specificity of CSF CXCL13 as a marker of NB. The course of the CXCL13 concentrations is reported in a subgroup of 19 patients. RESULTS: We confirm the high diagnostic yield of CXCL13 for NB in this unselected cohort. The optimal cut-off for the reliable diagnosis of NB was 93.83 pg/ml, resulting in a sensitivity and specificity of 95 and 97%, respectively (positive predictive value 55.9%, negative predictive value 99.8%), surpassing the sensitivity of both serological testing and PCR. CSF CXCL13 concentration showed a swift response to therapy. Non-NB patients with high CSF CXCL13 concentrations suffered from meningeosis neoplastica or infectious encephalitis. CONCLUSIONS: CXCL13 is a valuable tool for the diagnosis and assessment of therapeutic response in NB. Furthermore, our data point towards an emerging role of CXCL13 in the diagnosis and prognosis of viral encephalitis and meningeosis neoplastica. These results are of particular interest in the light of recently developed approaches to CXCL13-directed therapeutic interventions.