A central issue in interpreting the Romberg’s test is whether itsapplication is that of a binary clinical sign (i.e. it is either presentor absent), or whether it finds utility as a form of posturography,whereby the result is interpreted in the context of a continuum(wherein normal values are set according to age).

In 2009 we surveyed 49 neurologists at the Australian and NewZealand Association of Neurologists Annual Scientific Meeting andthe members of a division of General Practice in Melbourne, Austra-lia, regarding their understanding, method and interpretation of theRomberg’s test. There was very little consistency in the responses tothe eight item written survey within and between the two groupssurveyed.

We proffer some tentative recommendations on nomenclature.

doi:10.1016/j.jocn.2010.07.091

91. Audiovestibular sarcoidosisDavid J. Szmulewicz, John A. Waterston

The Alfred Hospital, VIC

We report on two patients with biopsy proven audiovestibularsarcoidosis. Their presentations included that of hearing impair-ment, vertigo and gait unsteadiness. On examination there was evi-dence of sensorineural hearing loss, a positive head impulse test andgait ataxia. The clinical findings were confirmed by formal oto-neu-rology testing, the results of which included sensorineural hearingloss with poor speech discrimination, semi-circular canal hypofunc-tion and abnormal auditory brainstem responses. MRI of the brainrevealed enhancement of the vestibular nerves.

Both patients responded to high dose oral corticosteroid treat-ment, which reinforces the importance of thorough investigationshould the possibility of a reversible cause of audiovestibular dys-function exist. A review of the pertinent literature was undertaken.

doi:10.1016/j.jocn.2010.07.092

92. Hydroxychloroquine induced vacuolar myopathy mimickingacid maltaseJia Haur Tho a, Peter Blumbergs b

a Dept of Neurology, Gold Coast Hospital, QLDb Institute of Medical and Veterinary Science, SA

The antimalarials induce dysfunction of the autophagic-lysosomesystem resulting in pathologic autophagic vacuole formation. Wepresent a patient where the glycogen accumulation secondary todrug induced lysosomal dysfunction was so severe that a glycogenstorage disorder was initially suspected. A 74 year old woman witha past history of cutaneous lupus presented with dysphagia, reducedmobility and recurrent falls. She had been treated with hydroxychlo-roquine 400 mg daily together with prednisolone 5mg on alternatedays and rosuvastatin 5mg daily. There was no family history of neu-romuscular disease. General examination showed a cachectic elderlywoman without any skin rash. Neurological examination demon-strated proximal muscle weakness, quadriceps wasting, lowerextremity areflexia and reduced vibration sense. Routine blood testswere normal including creatinine kinase 105 U/L. Electrophysiologi-cal examination revealed proximal myopathic and distal neuropathicpatterns suggestive of a neuromyopathy. A muscle biopsy revealedsevere vacuolar myopathy with florid glycogen excess leading to ini-tial interpretation of glycogen storage disease. Electron microscopy

showed pathognomonic curvilinear bodies and disruption of musclefibres by vacuoles containing autophagic debris including myeloidbodies. A diagnosis of toxic myopathy with secondary glycogenaccumulation due to acquired lysosomal damage from hydroxychlo-roquine was made. Statins and prednisolone are potential myotoxicagents and may have contributed to her myopathy although the type2B fibre atrophy was not present.

Conclusion: An unusual case of hydroxychloroquine induced vac-uolar myopathy mimicking a glycogen storage disorder is presented.Muscle biopsy is the definitive diagnostic test in suspected hydrox-ychloroquine myopathy. Electron microscopy is essential to demon-strate the diagnostic curvilinear bodies.

doi:10.1016/j.jocn.2010.07.093

93. Worse stroke outcome in patients with atrial fibrillation maybe due to greater volumes of more severe hypoperfusionHans T.H. Tu a, Bruce C.V. Campbell a, Soren Christensen b, MarnieCollins c, Mark W. Parsons d, P Alan Barber e, Geoffrey A. Donnan f,Stephen M. Davis a

a Department of Neurology, Royal Melbourne Hospital, University ofMelbourne, VICb Department of Radiology, Royal Melbourne Hospital, University ofMelbourne, VICc Department of Mathematics and Statistics, University of Melbourne,VICd Department of Neurology and Hunter Medical Research Institute, JohnHunter Hospital, University of Newcastle, NSWe Department of Medicine, University of Auckland, New Zealandf Florey Neurosciences Institute, VIC

Background: Atrial fibrillation (AF) is associated with worse out-come following ischemic stroke, but the reasons for this remainunclear. We aimed to elucidate the pathophysiological determinantsof worse stroke outcome in patients with AF using serial MRI datafrom the EPITHET study.

Methods: Comparisons of infarct size, hypoperfusion volume,infarct growth, recanalisation, reperfusion, hemorrhage, strokeseverity, and response to thrombolysis were made between patientswith and without AF in the EPITHET study.

Results: AF was present in 42 of 101 patients. At baseline, AFpatients were older (79 vs 73 years, p = 0.02), had more severe neu-rological impairment (NIHSS 16 vs 11, p = 0.006), larger infarcts (29vs 15mL p = 0.04) and greater volumes of more severe hypoperfusion(Tmax P 8 Perfusion Weighted Image volume 70 vs 43mL, p = 0.01)compared to patients without AF. There were no differences in arte-rial occlusion site, infarct growth, recanalisation or reperfusion. Atoutcome, AF patients had larger infarcts (52 vs 16mL, p = 0.05),worse hemorrhagic transformation (29% vs 5%, p = 0.002 for paren-chymal hematomas) and higher mortality rates (31% vs 12%,p = 0.04). AF was an independent predictor of parenchymal hema-toma (OR 6.41, CI 1.53–26.81), but not mortality (OR 2.38, CI 0.79–7.10), after adjusting for baseline imbalances in age, tPA treatment,blood glucose, stroke size and severity.

Conclusions: Patients with AF have worse clinical and imagingoutcomes following ischemic stroke. This study suggests that theadverse effect of AF is due to greater volumes of more severely hyp-operfused tissue, leading to larger infarct size and greater risk ofsevere hemorrhagic transformation.

doi:10.1016/j.jocn.2010.07.094

Abstracts / Journal of Clinical Neuroscience 17 (2010) 1610–1638 1637