1/27. Oscillopsia and pseudonystagmus in kidney transplant patients.PURPOSE: Modern immunosuppressants have improved the success of kidney transplantation for renal failure patients. They also may induce neurotoxic effects including tremor. We report two cases of pseudonystagmus and oscillopsia in transplant patients caused by immunosuppressant-induced head tremor and gentamicin-induced vestibulotoxicity. methods: case reports. Head tremor, static visual acuity, and dynamic visual acuity were measured. Vestibular function was evaluated with ice water calorics. RESULTS: Both patients had significant head tremor and pseudonystagmus. Head stabilization improved static visual acuity. Dynamic visual acuity revealed a 4-line and 10-line loss of visual acuity, respectively. CONCLUSIONS: These findings of pseudonystagmus and oscillopsia are likely to become more prevalent as more renal failure patients receive transplants. Improvement may be seen with reduction of immunosuppressant, reduction of stimulant intake, use of medications to reduce head tremor, and vestibular rehabilitation.- - - - - - - - - - ranking = 1keywords = nystagmus (Clic here for more details about this article) |
2/27. Superior canal dehiscence syndrome.OBJECTIVE: To present the symptoms, signs, and findings on diagnostic tests of patients with the superior canal dehiscence syndrome and to describe the surgical procedures used to treat the dehiscence in five patients. DESIGN AND SETTING: Prospective study of a series of patients identified as having this syndrome at a tertiary care referral center. patients AND RESULTS: Seventeen patients with vertigo, oscillopsia, or both evoked by intense sounds or stimuli that caused changes in middle ear and/or intracranial pressure were identified over a 4-year period. The evoked eye movements had vertical and torsional components, with the direction corresponding to the effect of the stimuli in causing excitation (Valsalva against pinched nostrils, tragal compression, sounds) or inhibition (Valsalva against a closed glottis or jugular venous compression) of the affected superior semicircular canal. Thirteen (76%) of these patients also experienced chronic dysequilibrium that was often the most debilitating symptom. Dehiscence of bone overlying the superior semicircular canal on the affected side was confirmed with computed tomographic scans in each case. Surgical procedures through the middle fossa approach to plug or resurface the superior canal were performed in five patients (canal plugging in three cases and resurfacing of the dehiscence without plugging in two). The debilitating symptoms resolved or improved after the procedures. Signs of vestibular hypofunction, without loss of hearing, were noted in one patient after plugging of the superior canal and in one other patient after resurfacing of the canal. CONCLUSIONS: The superior canal dehiscence syndrome is identified based on characteristic symptoms, signs, and computed tomographic findings. The clinical presentation and findings can be understood in terms of the effect of the dehiscence on the physiology of the labyrinth. The syndrome is a treatable cause of vestibular disturbance.- - - - - - - - - - ranking = 5.5686847200639E-5keywords = vertical (Clic here for more details about this article) |
3/27. Inferior vestibular neuritis.Sudden, spontaneous, unilateral loss of vestibular function without simultaneous hearing loss or brain stem signs is generally attributed to a viral infection involving the vestibular nerve and is called acute vestibular neuritis. The clinical hallmarks of acute vestibular neuritis are vertigo, spontaneous nystagmus, and unilateral loss of lateral semicircular function as shown by impulsive and caloric testing. In some patients with vestibular neuritis the process appears to involve only anterior and lateral semicircular function, and these patients are considered to have selective superior vestibular neuritis. Here we report on two patients with acute vertigo, normal lateral semicircular canal function as shown by both impulsive and caloric testing, but selective loss of posterior semicircular canal function as shown by impulsive testing and of saccular function as shown by vestibular evoked myogenic potential testing. We suggest that these patients had selective inferior vestibular neuritis and that contrary to conventional teaching, in a patient with acute spontaneous vertigo, unilateral loss of lateral semicircular canal function is not essential for a diagnosis of acute vestibular neuritis.- - - - - - - - - - ranking = 0.14285714285714keywords = nystagmus (Clic here for more details about this article) |
4/27. Vergence-mediated modulation of the human horizontal angular VOR provides evidence of pathway-specific changes in VOR dynamics.The horizontal vestibulo-ocular reflex (VOR) evoked by passive, high-acceleration, head-on-body rotations (head thrusts) while viewing a far (124-cm) or near (15-cm) target was recorded (scleral search coil) in four subjects with normal vestibular function and in one subject with unilateral vestibular hypofunction. For responses in the subjects with normal vestibular function, the latency of responses relative to the onset of head movement was 7.5 /- 1.5 ms for the VOR and 21.6 /- 1.2 ms for the vergence-mediated increase in VOR gain. The gain of the VOR at the peak of the velocity response while viewing a far target was 1.01 /- 0.06; while viewing a near target, it was 1.25 /- 0.08 (p <0.003). The responses were modeled with two pathways based on the different latencies. The "far-viewing" pathway was represented by a constant gain term. The "near-viewing" pathway was represented by a first-order lead term, a gain that was dependent on viewing distance, and a delay. Analysis of the responses revealed that the lead term was greater for the adducting than the abducting eye. In the subject with unilateral vestibular hypofunction, ipsilesional responses showed no change in VOR gain with respect to viewing distance. Contralesional responses retained the vergence-dependent increase in gain. A bilateral model was developed based on the data from the subjects with normal vestibular function. Simulations of this model when inputs were eliminated from one side predict the changes observed in the subject with unilateral vestibular hypofunction. The response asymmetries arise because the near-viewing pathway is more susceptible to inhibitory cutoff than is the far-viewing pathway.- - - - - - - - - - ranking = 0.003672781538991keywords = horizontal (Clic here for more details about this article) |
5/27. Acute peripheral vestibular deficits after whiplash injuries.We report 3 patients who had acute peripheral vestibular dysfunction minutes to hours after a car collision with whiplash injury without head trauma. The accident was a frontal collision in 1 case, a rear impact in the second, and lateral in the third. All patients complained immediately of cervicalgia, headache, acute vertigo with a sensation of erroneous body movements, and slipping of image with head movements. A sudden sensation of tilting of the environment when driving, tinnitus, and hyperacusis were also described. The otoneurologic findings showed bilateral canalolithiasis in 1 patient and an acute peripheral vestibular deficit in 2 patients. Tilt of the subjective visual vertical was measured in all patients. Cerebral magnetic resonance imaging yielded normal findings. As angular and linear accelerometers, the vestibular organs are directly exposed to high forces generated by whiplash mechanisms. vertigo generated by peripheral vestibular lesions is probably underestimated in whiplash injuries and may often be incorrectly attributed to cervical or cerebral lesions.- - - - - - - - - - ranking = 5.5686847200639E-5keywords = vertical (Clic here for more details about this article) |
6/27. Nodulus infarction mimicking acute peripheral vestibulopathy.The authors report two patients with cerebellar infarctions in the territory of the medial branch of the posterior inferior cerebellar artery who had vertigo, spontaneous ipsilesional nystagmus, and contralesional truncal lateropulsion. Although one of the two patients had slight dysmetria, overall signs closely mimicked those of acute peripheral vestibulopathy. The authors suggest that interruption of nodulouvular inhibitory projections to vestibular nuclei may account for the vestibular signs.- - - - - - - - - - ranking = 0.14285714285714keywords = nystagmus (Clic here for more details about this article) |
7/27. Anterior canal failure: ocular torsion without perceptual tilt due to preserved otolith function.A patient with anterior semicircular canal dehiscence syndrome underwent surgical patching that caused an isolated dysfunction of the left anterior semicircular canal postoperatively. He exhibited significant ocular torsion toward the side of the affected labyrinth (17 degrees excyclotropia of the ipsilateral eye), but no displacement of the subjective visual vertical. This dissociation suggests that an isolated ocular torsion may occur after an anterior semicircular canal lesion. A combined ocular torsion and subjective visual vertical tilt, which is usually seen with vestibular lesions, requires an associated otolith dysfunction.- - - - - - - - - - ranking = 0.00011137369440128keywords = vertical (Clic here for more details about this article) |
8/27. Caloric eye-tracking pattern test: visual suppression and the possibility of simplified differential diagnosis between peripheral and central vertigo.During the examination of patients who complain of vertigo or who have equilibrium disorders, often identifying the etiology of the disorders is difficult (i.e., determining whether it is dependent on a peripheral or a central vestibular disorder). To attempt to determine the etiology in these cases, we devised a new method: the caloric eye-tracking pattern test. In normal subjects and in patients with peripheral disorders, as is well-known, caloric nystagmus has little influence on the eye-tracking pattern. In contrast, in patients with central vestibular disorders, caloric nystagmus evoked abnormalities in the eye-tracking pattern, either superimposed or as saccades, despite the fact that the eye-tracking pattern before caloric stimulation was normal. These findings result from the visual suppression mechanism to vestibular nystagmus. We can conclude that the visual suppression to vestibular nystagmus is evoked more strongly by pursuing a moving visual stimulus than by gazing at a stationary target. These results are interesting, not only from the physiological viewpoint but from the clinical viewpoint. The differential diagnosis should include both peripheral and central vertigo.- - - - - - - - - - ranking = 0.57142857142857keywords = nystagmus (Clic here for more details about this article) |
9/27. noise exposure and its effect on the labyrinth, Part II.The neurootological data of 12 patients attending our ear, nose, and throat clinic were analyzed. The patients submitted to a neurootological routine evaluation consisting of patient history recording and audiometric and equilibriometric investigations (i.e., electronystagmography). The conclusion was that many tinnitus patients--even those who had no vestibular symptoms--showed some disturbance in the vestibular tests, such as spontaneous and positional nystagmus and nystagmus alternans. Laurikainen came to the same conclusion in 1995, after examining 10 patients with sudden deafness but no vestibular complaints. It is recommended that all patients with noise exposure, sudden deafness, and tinnitus of the severe disabling type undergo a complete cochleovestibular investigation.- - - - - - - - - - ranking = 0.28571428571429keywords = nystagmus (Clic here for more details about this article) |
10/27. A case of Cronkhite-canada syndrome with vestibular disturbances.A 66-year-old Japanese man with Cronkhite-canada syndrome (CCS) presented with complaints of long-lasting dysequilibrium. On neuro-otological examination, he showed gaze-evoked nystagmus at the rightward and leftward gaze, and saccadic pursuit. On the caloric test, he showed no response in either side, and on the head-impulse test he showed bilateral loss of vestibule-ocular reflexes around the yaw axis, while he had bilateral normal responses on the vestibular-evoked myogenic potential testing. Neuro-otological findings suggested that he had lesions in the peripheral vestibular system as well as the central nervous system. Neurological disorders such as sensory neuropathy have been reported in patients with CCS. This patient's balance problems could be due to CCS itself.- - - - - - - - - - ranking = 0.14285714285714keywords = nystagmus (Clic here for more details about this article) |
| | Next -> |