The contribution of the vertical semicircular canals to high-velocity horizontal vestibulo-ocular reflex (VOR) in normal subjects and patients with unilateral vestibular nerve section.

We have examined to what extent the vertical semicircular canals contribute to the nonlinearity of the horizontal VOR imposed by the driving of primary vestibular afferents into inhibitory cutoff at high velocities of head rotation (Ewald's second law). The gain (eye velocity/head velocity) of the horizontal component of the VOR with the head pitched down 30 degrees and pitched up 30 degrees was examined during constant-velocity rotations in normal subjects and patients following unilateral vestibular nerve section. In normal subjects, VOR gain decreases as chair velocity increases from 60-300 degrees/s when the head is pitched up, but VOR gain remains constant when the head is pitched down. This finding implies that the mechanism by which the gain of the horizontal VOR gain remains constant at all velocities of rotation depends upon the pattern of labyrinthine stimulation. Following unilateral nerve section, we found that the directional preponderance (DP) in horizontal VOR depends upon whether the head is pitched up 30 (mean asymmetry = 5%) or pitched down 30 degrees (mean asymmetry = 20%). This is what is expected based on the degree to which the lateral and vertical semicircular canals sense horizontal head acceleration with the head in different degrees of pitch. Hence, following unilateral vestibular lesions, the DP of horizontal VOR gain is most easily elicited at high velocities of head rotation and with the head pitched down 30 degrees. Evidence for DP at the bedside using the "head-shaking nystagmus" technique may be optimally elicited with the head pitched down 30 degrees.

Systemic vasculitis positive for circulating anti-neutrophil cytoplasmic antibodies and with predominantly neurological presentation.

A 57-year-old male patient suffering from dramatically deteriorating diffuse and focal central nervous system symptoms was admitted to hospital after a short prodromal period in a somnolent state. He was diagnosed as having systemic vasculitis positive for circulating anti-neutrophil cytoplasmic antibodies, primarily involving the brain, but also most other organ systems. Circulating anti-neutrophil cytoplasmic antibodies are highly specific for Wegener granulomatosis, though they have been detected in rare cases of other vasculitic syndromes. Central nervous system lesions as presenting signs in Wegener granulomatosis have to be regarded as rare. This case nonetheless suggests that Wegener granulomatosis has to be considered in patients with a predominantly cerebral manifestation of a vasculitic syndrome.

Diagnostic significance of tibial nerve somatosensory evoked potentials (spinal and cortical components) with spinal cord lesions.

Forty normal subjects were investigated with the somatosensory evoked potential technique following stimulation of the posterior tibial nerve in order to yield information upon normal values, and especially the origin of the cervical potential. Subsequently an electrophysiologic localization of tumours along the spinal cord was attempted in 18 patients with spinal tumours. In C2 recordings with Fz reference 3 components, N28, N30, and N34, are visible. Simultaneous cortical and cervical recordings with mastoid, knee, and neck references suggest a cranio-cervical origin of N28, a subcortical origin of N30 and a thalamic or thalamo-cortical origin of N34. In patients, the lumbar spinal cord potentials regularly yielded a useful additional information with respect to the tumour site. The cervical potentials added in 5 out of 18 patients additional information localizing the tumour within the spinal cord or brain-stem.

False-negative brainstem auditory evoked potential recordings in a case of multiple acoustic neuroma.

A case history is reported to demonstrate that electrophysiological testing (brainstem auditory evoked potentials, BAEP and stapedius reflex) may fail in the search for cerebello-pontine angle tumours. The clinical history began with repeated episodes indicating a disorder of the vestibular system. Repeated testing of BAEP exhibited normal curves before and after surgery on the right side. This case serves as a reminder that normal BAEP do not necessarily exclude the presence of an acoustic neuroma developing in the immediate vicinity of the vestibular nerve.

Brainstem auditory evoked potential abnormalities in vascular malformations of the posterior fossa.

Recent reports indicate that malformations of arteries and veins in the posterior fossa are a common cause of facial spasm and trigeminal neuralgia. More rarely they may also cause facial nerve paresis and hearing loss. When vascular malformations are present, brainstem auditory evoked potentials (BAEPs) sometimes show abnormalities similar to those usually recorded in patients with tumours in the cerebellopontine angle. In three patients with facial spasm, one with trigeminal neuralgia and one with facial paresis pathologically delayed absolute latencies and/or interpeak latencies of BAEPs associated with vascular malformations were found. It is concluded that those BAEP abnormalities associated with tumours in the posterior fossa may also be caused by vascular malformations. BAEPs are valuable aids to the diagnosis of such malformations.