$336 Wednesday, November 9, 2005 Poster Abstracts

was ~-'9ms. VOR thresholds from SCDs were 10-40dB below normal ( l l0dB NHL). Eye rotation taxis of click VOR was aligned with superior canal axis; axis orthogonal to superior canal platte. Conclusions: As CT scan abnormality Call be observed in asylitpto- matte ear, tiffs reproducible and quantifiable click evoked VOR maybe a useful screening test for SCD.

0927 Patterns of Head-Shaking Nystagmus in Lateral Medullary Infarction

Choi, K, Oh, S, Park, S, Hail, M, Koo, J, Kim, J. Department of Neurology, Otolaryngology, Head and Neck Surgery College of Medicine, Seoul National University, Seoul National University Bundang Hospital

Background: Head-shaking nystagmus (HSN) may occur in patients with central as well as peripheral vestibular lesions. However, systematic study of HSN in central vestibulopathy has been sparse. We analyzed HSN in 12 patients with lateral medullary infarction to elucidate the patterns of HSN in central vestibulopathy, and discuss possible mechanisms involved. Methods: In 12 consecutive patients with lateral medullary infarction, HSN was recorded with 3-dimensional video-oculography or by using magnetic search coil technique. To induce HSN, horizontal head oscillation was delivered at 2 3 Hz for 15 seconds after pitching tile head forward by approximately 30 '>. The effect of visual fixation on HSN was also assessed. Results: Eleven of 12 patients exhibited HSN, which was ipsilesional horizontal with sntall vertical and torsional components. In five patients with contralesional spontaneous nystagnms, horizontal head oscillation immediately reversed direction of the spontaneous nystag- mus. Three patients showed unusually strong HSN with a maximum SPV more than 80%. Visual fixation markedly suppressed HSN in most patients. Conclusions: The ipsilesional HSN in lateral medullary infarction may be due to unilateral loss of nodulo-uvular inlffbition on tile velocity-storage. The suppression of HSN by fixation suggests sparing the projections from the floccuhis. The reversal of spontaneous nystagmus by head oscillation may be a sign suggesting central vesribulopathy.

0928 Nervous system hnpairntents of the patients with radiation4ndueed, vascular and noise-induced sensorineural hearing loss

Gaioviy, V ~. 1 Research Institute of 0 tolaryngology, Ukraine "s Academy of iVledieal Sciences,/@iv, Ukraine

The growing nmnber of patients with chronic and progressive heating deterioration, in particular in tile group of young people, makes this problem acute in both medical and social temts. The goal of this research was to determine typical characteristics of changes in the nervous system for the patients with the hearing loss of different etiology.

Diagnostics of 156 patients (187 males and 69 females) has been conducted clinically (neurologist, therapist, ophthalmologist) as well as with tile modern methods of diagnostics (MRI, EEG, hearing evoked potentials, ultrasound investigation).

Nervous system impairments were evidenced by changes in the other cranial nerves (most often nVII and nV) as well as cerebrovascalar pathology, in particular evident in case of hypertonic illness and brain atherosclerosis as encephalopathy. Therefore tile hearing nerve impairment is not selective. Apart from hearing loss these patients were often affected with headaches, dizziness, tinnitus. The cerebro- vascular changes of different severity (up to encephalopathy) were evident in all patients with the hearing loss disorder irrespective of etiology. The patients affected by Chernobyl nuclear accident had different levels of CNS affected with the pathological process and had manifested vestibular disorders. These patients often suffered from

persistent headaches, memory and sleep disorders. When affected by noise these patients initially developed disorders of functional character rather than organic nervous system disorder.

Therefore affection of hearing nerve is only one component in the large-scale picture of nervous system impairment and is registered sinmltaneously with cerebrovascalar disorders in all cases.

0929 White Matter Alteration in a Patient with Graves' Disease with Ophth~hnopathy: Association or Extrathyroidal Maniti~statioff. ~

Krone, A, Aydin, O, Karabudak, R. Hacettepe University, Medical Faculty, Neurology Department, Ankara, Turkey On dokuz iVlayis University, Medical Faculty, Department of Pediatric Neurology, Samsun, Turkey Aeettepe University, iVledieal Faculty, Neurology Department, Ankara, Turkey

Hashimoto thyroiditis and Graves' disease are the most common forms and the two extremes of a wide spectrum of mixed thyroid autoimmune conditions associated with several neurologic disorders. Several autoimmune disorders have been associated with the diagnosis of Graves disease.

Nineteen years old female patient has been adnfftted to our center for parasthesia of her legs and tile lower part of the body. She was diagnosed as Graves' diseases when she was 5 years old and subtotal tiroidectomy was applied when she was 10. On neurologic examination paresthesia below the level of T6 was detected. Besides position and vibration senses were impaired and cutaneous abdominal reflexes were all absent. Deep tendon reflexes of upper extrenffties were normal while hyperactive for lower extrenffties. Bilateral Babinski sign was detected. While her cranial MRI was normal, her thoracal MRI revealed plaques on the level o f T5-T6. Four months later she had another relapse of the same symptoms. For the follow up depending on her clinical and radiological signs she was diagnosed as multiple sclerosis. We introduce a case diagnosed as Graves' disease, having a high titer of attti-TPO antibody and normal thyroid functions as well as white matter abnormalities on her cranial and spinal MRI. The differential diagnosis of white matter lesions was discussed in the point of view for multiple sclerosis and neuronal involvement of Graves" disease.

0930 Central Paroxysmal positioning vertigo

Lee, JH 1. 2Department Of Neurology, Hallym University, Seoul, Korea

Background: Vertigo induced by head positioning is mostly caused by a peripheral vestibular syndromes, such as benign paroxysntal position- ing vertigo (BPPV). However, central lesion can lead to paroxysnml positioning vertigo (central PPV). We report two patients having acute infarct who presented with central PPV. Results: (Case 1) A 58-year-old man with diabetes mellitus suddenly developed episodic vertigo. Vertigo with nausea appeared right after head hanging maneuver, and lasted a few seconds up to about a minute. However, nystagntus was not definitely provoked by head positioning. There were no definite cerebellar dysfmtctions or oculomotor abnormalities. Brain MRI showed a small acute infarct located right dorsolateral to the fourth ventricle. One month later, similar episodic vertigo reappeared. Repeated MRI showed a newly developed infarct located left dorsolateral to tile 4th ventricle.

(Case 2) A 47-year-old man with nonvalvular atrial fibrillation suddenly developed positional vertigo. Apogeotrophic nystagmus with severe vertigo and nausea appeared just after head turning to the right side on supine position, and persisted for about one minute. He had no definite neurologic deficits except bilateral unsteady gait. Brain MRI showed acute infarcts involving cerebellar noduhis/uvula region. Conclusions; We reports two patients with central PPV with their imaging findings and clinical features. Dorsolateral to tile fourth ventricle and cerebellar nodulus/uvula region in our patients are