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In 1991 we proposed that while the syndrome of isolated intracranial hypertension might have many definite and probable causes, it has nonetheless a single unifying pathophysiological mechanism: namely, impairment of cerebrospinal fluid (CSF) reabsorption. For that reason, we also proposed then that it is best described by a single, unifying, inclusive term, namely, pseudotumor cerebri syndrome. Although it appears that there is, as far as nomenclature is concerned, now international agreement, there is as yet no agreement on pathophysiology and classification. Herein we outline our views on these matters and give our reasons. [ABSTRACT FROM AUTHOR]

Purpose: To review the extent and mechanism of the recovery of vestibular function after sudden, isolated, spontaneous, unilateral loss of most or all peripheral vestibular function – usually called acute vestibular neuritis. Methods: Critical review of published literature and personal experience. Results: The symptoms and signs of acute vestibular neuritis are vertigo, vomiting, nystagmus with ipsiversive slow-phases, ipsiversive lateropulsion and ocular tilt reaction (the static symptoms) and impairment of vestibulo-ocular reflexes from the ipsilesional semicircular canals on impulsive testing (the dynamic symptoms). Peripheral vestibular function might not improve and while static symptoms invariably resolve, albeit often not totally, dynamic symptoms only improve slightly if at all. Conclusions: The persistent loss of balance that some patients experience after acute vestibular neuritis can be due to inadequate central compensation or to incomplete peripheral recovery and vestibular rehabilitation has a role in the treatment of both. [ABSTRACT FROM AUTHOR]

Syringomyelia is an important cause of neurological deficit. Most cases of non-traumatic syringomyelia occur in association with a Chiari malformation. We present three unusual examples of syringomyelia with such an association. The first case is that of syringomyelia in a young woman with Marfan’s syndrome, a spontaneous CSF leak and intractable intracranial hypotension. The second is a woman with long-standing lumbo-peritoneal shunt for pseudotumour cerebri who developed an acquired Chiari malformation. A young woman with a Dandy-Walker cyst that herniated into the upper cervical canal is the third case. These cases provide a basis for discussion of the pathogenesis and management of syringomyelia and the Chiari malformation in such cases. [ABSTRACT FROM AUTHOR]

Objective: To examine the properties and potential clinical uses of myogenic potentials to bone conducted sound.Methods: Myogenic potentials were recorded from normal volunteers, using bone conducted tone bursts of 7 ms duration and 250-2000 Hz frequencies delivered over the mastoid processes by a B 71 clinical bone vibrator. Biphasic positive-negative (p1n1) responses were recorded from both sternocleidomastoid (SCM) muscles using averaged unrectified EMG. The best location for stimulus delivery, optimum stimulus frequency, stimulus thresholds, and the effect of aging on evoked response amplitudes and thresholds were systematically examined. Subjects with specific lesions were studied. Vestibular evoked myogenic potentials (VEMP) to air conducted 0.1 ms clicks, 7 ms/250-2000 Hz tones, and forehead taps were measured for comparison.Results: Bone conducted sound evoked short latency p1n1 responses in both SCM muscles. Ipsilateral responses occurred earlier and were usually larger. Mean (SD) p1 and n1 latencies were 13.6 (1.8) and 22.3 (1.2) ms ipsilaterally and 14.9 (2.1) and 23.7 (2.7) ms contralaterally. Stimuli of 250 Hz delivered over the mastoid process, posterosuperior to the external acoustic meatus, yielded the largest amplitude responses. Like VEMP in response to air conducted clicks and tones, p1n1 responses were absent ipsilaterally in subjects with selective vestibular neurectomy and preserved in those with severe sensorineural hearing loss. However, p1n1 responses were preserved in conductive hearing loss, whereas VEMP to air conducted sound were abolished or attenuated. Bone conducted response thresholds were 97.5 (3.9) dB SPL/30.5 dB HL, significantly lower than thresholds to air conducted clicks (131.7 (4.9) dB SPL/86.7 dB HL) and tones (114.0 (5.3) dB SPL/106 dB HL).Conclusions: Bone conducted sound evokes p1n1 responses (bone conducted VEMP) which are a useful measure of vestibular function, especially in the presence of conductive hearing loss. For a given perceptual intensity, bone conducted sound activates the vestibular apparatus more effectively than air conducted sound. [ABSTRACT FROM AUTHOR]

Dear Sirs, Radiotherapy for patients with node-positive head and neck cancer (HNC) and certain subtypes of lymphoma improves overall survival but can result in longer term damage to the carotid arteries and carotid sinus, including blood pressure regulatory structures [[1]-[3]]. In our patients, baroreflex failure occurred independently of carotid stenosis; only one patient (Case 2) had significant carotid disease. The magnitude of early BP lability may reflect the degree of baroreflex dysfunction or variability in compensatory BP regulation from non-baroreflex pathways including central mechanisms, adaptation of the renin-angiotensin-aldosterone system, or cardio-pulmonary reflexes [[5], [9]]. Fluctuating blood pressure (BP) was defined as excessive diurnal fluctuation in BP according to the expert clinician (documented history of labile or fluctuating hypertension). [Extracted from the article]

Objectives: To compare acute nystagmus characteristics of posterior circulation stroke (PCS) and acute vestibular neuritis (AVN) in the emergency room (ER) within 24 h of presentation. Methods: ER-based video-nystagmography (VNG) was conducted, recording ictal nystagmus in 101 patients with PCS (on imaging) and 104 patients with AVN, diagnosed on accepted clinical and vestibular test criteria. Results: Patients with stroke in the brainstem (38/101, affecting midbrain (n = 7), pons (n = 19), and medulla (n = 12)), cerebellum (31/101), both (15/101) or other locations (17/101) were recruited. Common PCS territories included posterior-inferior-cerebellar-artery (41/101), pontine perforators (18/101), multiple-territories (17/101) and anterior-inferior-cerebellar-artery (7/101). In PCS, 44/101 patients had no spontaneous nystagmus. Remaining PCS patients had primary position horizontal (44/101), vertical (8/101) and torsional (5/101) nystagmus. Horizontal nystagmus was 50% ipsiversive and 50% contraversive in lateralised PCS. Most PCS patients with horizontal nystagmus (28/44) had unidirectional "peripheral-appearing" nystagmus. 32/101 of PCS patients had gaze-evoked nystagmus. AVN affected the superior, inferior or both divisions of the vestibular nerve in 55/104, 4/104 and 45/104. Most (102/104) had primary position horizontal nystagmus; none had gaze-evoked nystagmus. Two inferior VN patients had contraversive torsional-downbeat nystagmus. Horizontal nystagmus with SPV ≥ 5.8 °/s separated AVN from PCS with sensitivity and specificity of 91.2% and 83.0%. Absent nystagmus, gaze-evoked nystagmus, and vertical-torsional nystagmus were highly specific for PCS (100%, 100% and 98.1%). Conclusion: Nystagmus is often absent in PCS and always present in AVN. Unidirectional 'peripheral-appearing' horizontal nystagmus can be seen in PCS. ER-based VNG nystagmus assessment could provide useful diagnostic information when separating PCS from AVN. [ABSTRACT FROM AUTHOR]

Objective: Patients with superior canal dehiscence (SCD) have large sound-evoked vestibular reflexes with pathologically low threshold. We wished to determine whether a recently discovered measure of the vestibulo-ocular reflex--the ocular vestibular evoked myogenic potential (OVEMP)--produced similar high-amplitude, low-threshold responses in SCD, and could differentiate patients with SCD from normal control patients. Methods: Nine patients with CT-confirmed SCD and 10 normal controls were stimulated with 500 Hz, 2 ms tone bursts and 0.1 ms clicks at intensities up to 142 dB peak SPL. Conventional VEMPs were recorded from the ipsilateral sternocleidomastoid muscle to determine threshold, and OVEMPs were recorded from electrode pairs placed superior and inferior to the eyes. Three-dimensional eye movements were measured with scleral dual-search coils. Results: In patients with SCD, OVEMP amplitudes were significantly larger than normal (p<0.001) and thresholds were pathologically low. The n10 OVEMP in the contralateral inferior electrode became particularly large with increasing stimulus intensity (up to 25 μV) and with up-gaze (up to 40 μV). Sound-evoked (slow-phase) eye movements were present in all patients with SCD (vertical: upward; torsional: upper pole away from the affected side; and horizontal: towards or away from the affected side), but began only as the OVEMP response became maximal, which is consistent with the surface potentials being produced by activation of the extraocular muscles that generated the eye movements. Conclusions: OVEMP amplitude and threshold (particularly the contralateral inferior n10 response) differentiated patients with SCD from normal controls. Our findings suggest that both the OVEMPs and induced eye movements in SCD are a result of intense saccular activation in addition to superior canal stimulation. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented in response to the article "Giant Cell Arteritis Presenting With Bilateral Vertebral and Axillary Artery Occlusions" in the previous issue.

Objective:To report the outcome of posterior semicircular canal occlusion surgery for intractable benign positional vertigo, regarding vertigo cure rate and hearing and balance outcomes.Methods:Retrospective review of 53 patients presenting with benign positional vertigo, unresponsive to repositioning manoeuvres, who eventually underwent posterior canal occlusion, over a 20 year period.Results:From 1991 to 2011, 5364 benign positional vertigo patients were treated in our balance disorders clinic; 53 of those who failed to respond to repositioning underwent posterior canal occlusion. All 53 were cured of their benign positional vertigo. Nine suffered some symptomatic permanent hearing loss (>20 dB at low and >25 dB at high frequencies). Ten patients suffered caloric vestibular function deterioration, with mild but permanent subjective imbalance in five; a further 10 patients with no post-operative caloric test changes also had some permanent imbalance. Benign positional vertigo later developed in the operated ear lateral canal in two patients and in the opposite ear posterior canal in eight patients. Two patients needed bilateral sequential posterior canal occlusion.Conclusion:Posterior canal occlusion is a highly effective treatment for intractable benign positional vertigo, with what is probably an acceptable risk to hearing and balance: five of six patients will have no hearing problem and nine of 10 no balance problem after surgery. [ABSTRACT FROM PUBLISHER]

If a patient, who is lying supine and looking upward, is given bone-conducted vibration (BCV) of the forehead at the hairline in the midline (Fz) with a clinical reflex hammer or a powerful bone conduction vibrator, short-latency surface potentials called ocular vestibular evoked myogenic potentials (oVEMP) can be recorded from just beneath the eyes. The early negative (excitatory) component (n10) is approximately equal in amplitude for both eyes in healthy subjects, but in patients with unilateral vestibular loss, the n10 component is significantly asymmetrical under the 2 eyes – the n10 component is small or absent under the eye on the side contralateral to the prior unilateral vestibular nerve removal, but of normal amplitude under the eye on the side contralateral to the healthy ear. The n10 component of the oVEMP response to BCV at Fz stimuli reflects vestibular and probably mainly otolithic function via crossed otolithic-ocular pathways, and so n10 asymmetry is a new way of identifying the affected side in patients with unilateral otolithic loss. Copyright © 2008 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Eye movement disorders are rarely reported in vitamin B12 deficiency. We describe two cases with eye movement disorder and vitamin B12 deficiency; one with bilateral internuclear ophthalmoplegia and the other with downbeat nystagmus. Both of the patients received replacement therapy but their eye movement disorders did not respond to treatment. We also review the nine previously reported cases. [ABSTRACT FROM AUTHOR]