Hyon-Ah Yi

Infarction in the Territory of Anterior Inferior Cerebellar Artery Spectrum of Audiovestibular Loss

Background and Purpose— To define the detailed spectrum of audiovestibular dysfunction in anterior inferior cerebellar artery territory infarction. Methods— Over 8.5 years, we prospectively identified 82 consecutive patients with anterior inferior cerebellar artery territory infarction diagnosed by MRI. Each patient completed a standardized audiovestibular questionnaire and underwent a neuro-otologic evaluation, including bithermal caloric tests and pure tone audiogram. Results— All but 2 (80 of 82 [98%]) patients had acute prolonged vertigo and vestibular dysfunction of peripheral, central, or combined origin. The most common pattern of audiovestibular dysfunction was the combined loss of auditory and vestibular function (n=49 [60%]). A selective loss of vestibular (n=4 [5%]) or cochlear (n=3 [4%]) function was rarely observed. We could classify anterior inferior cerebellar artery territory infarction into 7 subgroups according to the patterns of neuro-otological presentations: (1) acute prolonged vertigo with audiovestibular loss (n=35); (2) acute prolonged vertigo with audiovestibular loss preceded by an episode(s) of transient vertigo/auditory disturbance within 1 month before the infarction (n=13); (3) acute prolonged vertigo and isolated auditory loss without vestibular loss (n=3); (4) acute prolonged vertigo and isolated vestibular loss without auditory loss (n=4); (5) acute prolonged vertigo but without documented audiovestibular loss (n=24); (6) acute prolonged vertigo and isolated audiovestibular loss without any other neurological symptoms/signs (n=1); and (7) nonvestibular symptoms with normal audiovestibular function (n=2). Conclusions— Infarction in the anterior inferior cerebellar artery territory can present with a broad spectrum of audiovestibular dysfunctions. Unlike a viral cause, labyrinthine dysfunction of a vascular cause usually leads to combined loss of both auditory and vestibular functions.

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.

Apogeotropic central positional nystagmus as a sole sign of nodular infarction

Positional vertigo and nystagmus without associated neurological symptoms and signs are characteristic features of benign paroxysmal positional vertigo (BPPV). Although positional nystagmus may occur with caudal cerebellar infarction including the nodulus, positional nystagmus is usually associated with other neurological signs such as spontaneous or gaze-evoked nystagmus, perverted head-shaking nystagmus, cerebellar dysmetria, or severe gait ataxia with falling. We present a patient with nodular infarction who had positional vertigo with nystagmus as a sole manifestation. Video-oculography showed apogeotropic positional horizontal nystagmus during head turning while supine, which was consistent with apogeotropic BPPV involving the horizontal canal. MRI disclosed acute infarct in the nodulus. Nodulus infarction should be considered in a patient with positional nystagmus, especially when the presenting symptoms and signs are consistent with BPPV involving the horizontal canal.

Body lateropulsion as an isolated or predominant symptom of a pontine infarction

Background: Lateropulsion of the body—that is, falling to one side—is a well-known clinical feature of stroke in the posterior circulation. Body lateropulsion as an isolated or predominant manifestation of a pontine stroke has not been reported previously. Objective: To elucidate the possible mechanisms of patients presenting with body lateropulsion as an isolated or predominant symptom of an isolated pontine infarction. Methods: Between May 2004 and February 2006, out of 134 patients admitted with an isolated pontine stroke, we identified 8 (6%) consecutive patients in the Keimyung University Stroke Registry who had body lateropulsion as the main presenting symptom. Results: All lesions were localised to the paramedian tegmentum just ventral to the fourth ventricle. All except one showed a uniform pattern of body lateropulsion, in which the direction of falling was away from the side of an infarct. In two patients body lateropulsion was the sole clinical manifestation, whereas the other patients had other neurological signs. All but one patient had contraversive tilting of the subjective visual vertical (SVV). In all cases, the direction of SVV tilt corresponded to the direction of body lateropulsion. The mean net tilt angle was 6.1°. Conclusions: Based on the known anatomy of ascending vestibular pathways, SVV tilting and MRI findings, it is concluded that body lateropulsion probably results from damage to the graviceptive pathway ascending through the paramedian pontine tegmentum.

Sudden deafness as a sign of stroke with normal diffusion-weighted brain MRI.

Sudden deafness without associated neurological signs and symptoms is typically attributed to a viral inflammation of the labyrinth. Sudden deafness as a heralding manifestation of basilar occlusion has rarely been described. A 60-year-old male with hypertension presented with an acute onset of isolated sudden deafness with vertigo. On admission, initial brain MRI, including diffusion-weighted images, was normal. Two days after the onset of symptoms, the patient presented with an exacerbation of vertigo. A follow-up MRI scan revealed new infarcts involving the right middle cerebellar peduncle, right dorsolateral pons and right anterior cerebellum. In this patient, the acute onset of isolated sudden deafness with vertigo may have been a heralding manifestation of the pontocerebellar infarction.

Sudden bilateral simultaneous deafness with vertigo as a sole manifestation of vertebrobasilar insufficiency

A 68 year old woman presented with bilateral sudden simultaneous hearing loss and transient spontaneous vertigo as a sole manifestation of vertebrobasilar insufficiency. Extensive investigation to exclude other causes was unremarkable. Magnetic resonance imaging of the brain, including diffusion images, showed no abnormalities. A magnetic resonance angiogram showed severe stenosis of the middle third of the basilar artery. A pure tone audiogram showed moderate sensorineural-type hearing loss bilaterally. The localisation and mechanism of an isolated cochleovestibular dysfunction are discussed.

Relation between subcortical grey matter atrophy and conversion from mild cognitive impairment to Alzheimer's disease

Objective To investigate whether subcortical grey matter atrophy predicts progression from mild cognitive impairment (MCI) to Alzheimers disease (AD), and to compare subcortical volumes between AD, MCI and controls. To assess the correlation between subcortical grey matter volumes and severity of cognitive impairment. Methods We included 773 participants with three-dimensional T1-weighted MRI at 3 T, made up of 181 controls, who had subjective memory symptoms with normal cognition, 201 MCIs and 391 AD. During follow-up (2.0±0.9 years), 35 MCIs converted to AD (progressive MCI) and 160 MCIs remained stable (stable MCI). We segmented volumes of six subcortical structures of the amygdala, thalamus, caudate nucleus, putamen, globus pallidus and nucleus accumbens, and of the hippocampus, using FMRIBs integrated registration and segmentation tool. Results Analysis of variances, adjusted for sex and age, showed that all structures, except the globus pallidus, were smaller in AD than in controls. In addition, the amygdala, thalamus, putamen, nucleus accumbens and hippocampus were smaller in MCIs than in controls. Across groups, all subcortical greymatter volumes, except the globus pallidus, showed a positive correlation with cognitive function, as measured by Mini Mental State Examination (MMSE) (0.16<r<0.28, all p<0.05). Cox proportional hazards analyses adjusted for age, sex, education, Cambridge Cognitive Examination-Revised (CAMCOG-R) and MMSE showed that smaller volumes of the hippocampus and nucleus accumbens were associated with increased risk of progression from MCI to AD (HR (95% CI) 1.60 (1.15 to 2.21); 1.60 (1.09 to 2.35), p<0.05). Conclusions In addition to the hippocampus, the nucleus accumbens volume loss was also associated with increased risk of progression from MCI to AD. Furthermore, volume loss of subcortical grey matter structures was associated with severity of cognitive impairment.

Pattern of otolith dysfunction in posterior inferior cerebellar artery territory cerebellar infarction

OBJECTIVES To document otolith dysfunction in patients with posterior inferior cerebellar artery (PICA) territory cerebellar infarction. METHODS From March to October 2006, 14 consecutive patients with PICA territory cerebellar infarctions (brainstem spared) diagnosed by brain MRI from the acute stroke registry at the Keimyung University Dongsan Medical Center were enrolled within 12 days of onset (mean 4.0 days). Otolith function tests included ocular torsion (OT), skew deviation, and subjective visual vertical (SVV) were performed. The extent of the cerebellar infarction was determined by previously validated MR anatomical templates. RESULTS All patients had an abnormal posture as a result of otolithic dysfunction. Eleven patients (79%) had at least one otolith-related test abnormality: abnormal tilt of SVV (79%), abnormal OT (29%), or skew deviation (21%). Two common patterns of otolith dysfunction were identified based on whether or not the nodulus was infarcted: 1) ipsilesional SVV tilt (mean 5.0 degrees at binocular viewing) without accompanying abnormal OT or skew deviation (nodulus spared); 2) contralesional SVV tilt (mean 11.3 degrees at binocular viewing) with concomitant abnormal OT and skew deviation (nodulus infarcted). Patients with type 1 infarcts (i.e., nodulus spared) fell toward the side of lesion while patients with type 2 infarcts (i.e., nodulus infracted) fell toward the opposite side. CONCLUSION Isolated PICA territory cerebellar infarction usually produces two distinct patterns of otolith dysfunction - Ipsilesional SVV tilt and falling without accompanying OT or skew deviation if the nodulus is spared and contralesional SVV tilt and falling with OT and skew deviation if nodulus is infarcted.

Drop attacks in elderly patients secondary to otologic causes with Meniere's syndrome or non-Meniere peripheral vestibulopathy

Many neurologists are unaware of the drop attack that may occur from an inner ear dysfunction especially in elderly. We studied the clinical features and results of quantitative audiovestibular tests in six elderly patients (> or =65 years of age) who presented with drop attacks attributable to an inner ear pathology. Group was divided into Menieres syndrome (4) or non-Meniere peripheral vestibulopathy (2). Standard dizziness questionnaire and quantitative audiovestibular function testing were performed. Episodes were described as a sudden push to the ground in four or a violent illusionary movement of environment leading to a fall in two. All cases gave a history of prior vertiginous episodes and vestibular testing revealed unilateral caloric paresis. Ipsilateral hearing loss was documented in four cases. Our results suggest that otologic causes should be considered in the differential diagnosis of the drop attack in elderly, even if the symptoms and signs were not consistent with Menieres syndrome.

Abnormal cervical vestibular-evoked myogenic potential in anterior inferior cerebellar artery territory infarction: Frequency, pattern, and a determinant

BACKGROUND There has been no systematic study that carefully investigates the characteristic features of abnormal cervical vestibular-evoked myogenic potential (cVEMP) response associated with the AICA territory infarction. OBJECTIVES To investigate the frequency, the characteristic patterns of abnormal cVEMP associated with AICA territory infarction, and the crucial site for producing abnormal cVEMP response in the AICA territory infarction. METHODS We studied 16 consecutive cases of unilateral AICA territory infarction diagnosed by brain MRI. VEMP was induced by a short click sound and was recorded in contracting sternocleidomastoid muscle. Each patient underwent a quantitative audiovestibular evaluation, including bithermal caloric test and pure tone audiogram. RESULTS Eight patients (50%) exhibited abnormal cVEMP response on the side of the AICA territory infarction. All patients with abnormal cVEMP showed an absent or decreased response in amplitude but no difference in latency. Patients with abnormal VEMP were significantly more likely to have canal paresis (CP), sensorineural hearing loss, or both compared with patients who had normal cVEMP. Conversely, abnormal cVEMP was more frequently observed among patients with CP than among those without CP. There was no difference in lesion sites according to brain MRI among patients with or without abnormal cVEMP response. CONCLUSIONS Our findings suggest that the peripheral vestibular structure with the inner ear probably plays a crucial role in producing abnormal cVEMP response associated with AICA territory infarction.