Acute unilateral peripheral and central vestibular lesions can cause similar signs and symptoms, but they require different diagnostics and management. We therefore correlated clinical signs to differentiate vestibular neuritis (40 patients) from central ''vestibular pseudoneuritis'' (43 patients) in the acute situation with the final diagnosis assessed by neuroimaging. Skew deviation was the only specific but non-sensitive (40%) sign for pseudoneuritis. None of the other isolated signs (head thrust test, saccadic pursuit, gaze evoked nystagmus, subjective visual vertical) were reliable; however, multivariate logistic regression increased their sensitivity and specificity to 92%.The 1-year prevalence of vestibular vertigo in the general population is 5%, 1 and it accounts for approximately 1% of all emergency department visits.2
The recurrence rate in patients with a mean follow-up of 10 years was 50%. Most recurrences (80%) were within the first year after treatment, irrespective of the liberatory maneuver applied. None of the patients observed a recurrence after a symptom-free period of 8 years. Recurrences were seen significantly more often in women (58% versus 39%). The recurrence rate of patients in the seventh decade was half that of those in the sixth decade (p=0.0009). A history of three or more BPPV attacks prior to treatment indicated a higher risk of impending multiple recurrences in about two-thirds of the patients.
Structural brain abnormalities associated with congenital nystagmus (CN) are still unknown. In some patients with CN additional sensory, metabolic, or gross structural alterations can be detected. In the present study voxel-based morphometry was used to compare the gray matter (GM) brain volumes of 14 individuals with CN without associated sensory, metabolic, or obvious structural alterations (i.e., idiopathic CN) to those of a group of controls. Further, GM brain volumes were correlated with nystagmus severity as measured by sway path. Intergroup comparison exhibited significant volume increases in the human motion sensitive complex V5/MT+, the fusiform gyrus, and the middle occipital gyrus bilaterally in CN. These volume increases may be associated with excess visual motion stimulation due to involuntary retinal slip of the visual scene. A positive correlation (linear model) of nystagmus sway path with cerebellar GM volume was seen in the following areas: vermal parts VIII-X as well as hemisphere lobule II, hemisphere VI, crus I, crus II, and lobule VII-IX bilaterally. There is evidence that the reported GM volume changes in the vestibulo-cerebellum, which correlated with nystagmus sway path, might be related to the subjects‘ attempt to maintain fixation, rather than be due to the generation of nystagmus.
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