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Interleukin‐1β and febrile seizures: From bench to bedside

changes. Using a monoclonal antibody (L 42) against the prion protein (PrP), we found typical synaptic staining in the neocortex, basal ganglia, thalamus, and cerebellum (molecular and granular layer). No prominent PrP staining was noted in the brainstem. So far UBN, especially as the initial clinical sign, has not been described in CJD. Other ocular motor disturbances (such as saccadic pursuit, horizontal nystagmus) were reported in only a few patients who had an early stage of the disease in association with cerebellar ataxia and dementia. Cerebellar symptoms and cognitive impairment manifested in our patient a few weeks after the initial UBN. UBN is thought to reflect an imbalance of vertical vestibuloocular reflex tone. Alternatively, a mismatch in the neural coordinate systems of saccade generation and neural velocity-to-position integration due to deficiency of the latter may cause UBN. UBN is associated with brainstem lesions in the tegmentum of the pontomesencephalic junction and in the medulla near the perihypoglossal nuclei. There is, however, also evidence that the cerebellum (in particular, the vermis) is involved. It has been hypothesized that up-down asymmetries in the brainstem–cerebellar network (which normally stabilizes vertical gaze) account for vertical nystagmus. The neuropathological findings of a major involvement of the cerebellum of our patient is in agreement with a cerebellar cause of UBN. In conclusion, CJD may initially manifest with dizziness and an ocular motor disorder such as UBN.