Xenomelia is the oppressive feeling that one or more limbs of one's body do not belong to one's self. We present the results of a thorough examination of the characteristics of the disorder in 15 males with a strong desire for amputation of one or both legs. The feeling of estrangement had been present since early childhood and was limited to a precisely demarcated part of the leg in all individuals. Neurological status examination and neuropsychological testing were normal in all participants, and psychiatric evaluation ruled out the presence of a psychotic disorder. In 13 individuals and in 13 pair-matched control participants, magnetic resonance imaging was performed, and surface-based morphometry revealed significant group differences in cortical architecture. In the right hemisphere, participants with xenomelia showed reduced cortical thickness in the superior parietal lobule and reduced cortical surface area in the primary and secondary somatosensory cortices, in the inferior parietal lobule, as well as in the anterior insular cortex. A cluster of increased thickness was located in the central sulcus. In the left hemisphere, affected individuals evinced a larger cortical surface area in the inferior parietal lobule and secondary somatosensory cortex. Although of modest size, these structural correlates of xenomelia appear meaningful when discussed against the background of some key clinical features of the disorder. Thus, the predominantly right-sided cortical abnormalities are in line with a strong bias for left-sided limbs as the target of the amputation desire, evident both in our sample and in previously described populations with xenomelia. We also propose that the higher incidence of lower compared with upper limbs (∼80% according to previous investigations) may explain the erotic connotations typically associated with xenomelia, also in the present sample. These may have their roots in the proximity of primary somatosensory cortex for leg representation, whose surface area was reduced in the participants with xenomelia, with that of the genitals. Alternatively, the spatial adjacency of secondary somatosensory cortex for leg representation and the anterior insula, the latter known to mediate sexual arousal beyond that induced by direct tactile stimulation of the genital area, might play a role. Although the right hemisphere regions of significant neuroarchitectural correlates of xenomelia are part of a network reportedly subserving body ownership, it remains unclear whether the structural alterations are the cause or rather the consequence of the long-standing and pervasive mismatch between body and self.

Symptomatic recovery after acute vestibular neuritis (VN) is variable, with around 50% of patients reporting long term vestibular symptoms; hence, it is essential to identify factors related to poor clinical outcome. Here we investigated whether excessive reliance on visual input for spatial orientation (visual dependence) was associated with long term vestibular symptoms following acute VN. Twenty-eight patients with VN and 25 normal control subjects were included. Patients were enrolled at least 6 months after acute illness. Recovery status was not a criterion for study entry, allowing recruitment of patients with a full range of persistent symptoms. We measured visual dependence with a laptop-based Rod-and-Disk Test and severity of symptoms with the Dizziness Handicap Inventory (DHI). The third of patients showing the worst clinical outcomes (mean DHI score 36–80) had significantly greater visual dependence than normal subjects (6.35° error vs. 3.39° respectively, p = 0.03). Asymptomatic patients and those with minor residual symptoms did not differ from controls. Visual dependence was associated with high levels of persistent vestibular symptoms after acute VN. Over-reliance on visual information for spatial orientation is one characteristic of poorly recovered vestibular neuritis patients. The finding may be clinically useful given that visual dependence may be modified through rehabilitation desensitization techniques.

Alteplase resulted in a greater and faster improvement of the angiographic and hemodynamic variables compared with heparin. However, the high frequency of bleeding observed with alteplase in this trial suggests that patients should be carefully selected before thrombolytic therapy is given.

When qHIT is used as a reference, bHIT sensitivity is adequate and therefore clinically useful in the hands of both neuro-otological experts and non-experts. We advise performing quantitative head impulse testing with search coils or high speed video methods when bHIT is not conclusive.

Downbeat nystagmus is a frequent ocular motor sign in patients with lesions of the vestibulocerebellum. The upward drift in downbeat nystagmus is a combination of a gaze-evoked drift, due to an impaired vertical neural integrator, and a velocity bias. Using a three-dimensional turntable, we analyzed the influence of gravity on these two mechanisms. Patients with cerebellar downbeat nystagmus (n = 6) and healthy subjects (n = 12) were placed in various whole-body positions along the roll, pitch, and oblique vertical planes of the head. Ocular drift was monitored with scleral search coils. Although there was no gravity dependence of the vertical gaze-evoked drift, the vertical velocity bias consisted of two components: a gravity-dependent component that sinusoidally modulated as a function of body position along the pitch plane, and a gravity-independent component that was directed upward. The combination of the two components led to an overall drift that was minimal in supine and maximal in prone position. In healthy subjects, only the gravity-dependent component was present, but in a scaled-down manner. Our results suggest that the intact vestibulocerebellum minimizes an overacting otolith-ocular reflex elicited by pitch tilt and cancels an inherent upward ocular drift that is independent of gravity-modulated otolith signals.