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Background: It is unknown whether the development of cerebral microbleeds (MBs), small areas of signal loss on T2*-weighted gradient-echo imaging (GRE), follows a slow or a rapid process. We hypothesized that MBs may develop rapidly after certain critical events, such as strokes, and investigated the frequency, location, and factors associated with the formation of new MBs after acute ischemic stroke. Methods: We retrospectively examined 237 consecutive acute ischemic stroke patients who underwent MRI within 24 hours and follow-up MRI during the week after symptom onset. We defined new MBs as MBs that newly appeared on follow-up GRE outside the infarcted area. We examined the association of new MBs with demographics, risk factors, laboratory data, baseline MBs, and small vessel disease (SVD; leukoaraiosis and lacunar infarctions). Results: Seventy-five patients (31.6%) had baseline MBs, and 30 (12.7%) developed new MBs. Multiple logistic regression analysis indicated that the presence of baseline MBs (odds ratio [OR] 5.72, 95% confidence interval [CI] 2.12–15.42, p = 0.001) and severe SVD (OR 2.94, 95% CI 1.12–7.77, p = 0.03) independently predicted the development of new MBs. Of the 56 new MBs, 29 (51.8%) appeared in the lobar location, 17 (30.4%) appeared in the deep location, and 10 (17.9%) appeared in the infratentorial location. Conclusions: This study suggests that new microbleeds (MBs) can develop rapidly after acute ischemic stroke. Baseline MBs and severe small vessel disease are predictors for the development of new MBs. Further studies will be needed to investigate the clinical implications and mechanisms of these findings.

Background: Anti-GQ1b antibody has been found in Miller Fisher syndrome (MFS), Guillain-Barre syndrome (GBS) with ophthalmoplegia, Bickerstaff brainstem encephalitis (BBE), and acute ophthalmoplegia without ataxia (AO). The aim of this study was to determine the clinical features of AO associated with anti-GQ1b antibody. Methods: We retrospectively collected 34 patients with anti-GQ1b antibody syndrome. Of these patients, 31 patients had ophthalmoplegia. The patients with ophthalmoplegia were classified into MFS (n = 13), AO (n = 11), GBS with ophthalmoplegia (n = 6), and BBE (n = 1). We analyzed clinical features and patterns of external and internal ophthalmoplegia of AO, and neuro-ophthalmologic findings were compared with those of other anti-GQ1b syndromes with ophthalmoplegia. Results: AO was observed in 11 (32.4%) of the 34 patients with anti-GQ1b antibody. External ophthalmoparesis was present in all the patients and included mixed horizontal-vertical (n = 7), pure horizontal (n = 3), and pure vertical gaze palsy (n = 1). Binocular involvement was common, but unilateral ophthalmoparesis was also observed in 27.3%. Other findings included ptosis (n = 5, 45.5%) and internal ophthalmoplegia (n = 6, 54.5%). Other anti-GQ1b antibody syndromes had prominent neurologic signs including ataxia, weakness, and facial palsy in addition to ophthalmoplegia. The patterns of neuro-ophthalmologic findings did not differ between AO and other anti-GQ1b antibody syndromes with ophthalmoplegia. Conclusions: Acute ophthalmoplegia (AO) commonly occurs in anti-GQ1b antibody syndrome and manifests as various combinations of external and internal ophthalmoplegia. Internal ophthalmoplegia is fairly common and unilateral involvement may occur in AO.

Using the 10-item Spielberger Trait Anger Scale, the authors interviewed 145 patients with stroke regarding inability to control anger or aggression (ICAA). Poststroke depression and emotional incontinence were also assessed. ICAA was present in 47 patients (32%) and was closely related to motor dysfunction, dysarthria, emotional incontinence, and lesions affecting frontal-lenticulocapsular-pontine base areas. ICAA seems to be one of the major behavioral symptoms in patients with stroke.

Periodic alternating nystagmus (PAN) is characterized by periodic reversal of horizontal jerky nystagmus with a null period of several seconds. Damage to the uvulonodulus or to their connections with the brainstem vestibular nuclei has been suggested as a mechanism of PAN.1,2 However, PAN has rarely been reported in circumscribed cerebellar lesion.3 We report a patient with isolated nodular infarction who developed PAN without fixation in association with perverted head-shaking nystagmus (HSN) and loss of tilt suppression of the postrotatory nystagmus. This is the first report of PAN in circumscribed cerebellar infarction, and provides further evidence that PAN occurs due to dysfunction of cerebellar nodulus. A 69-year-old man with a history of hypertension developed acute vertigo with nausea/vomiting and postural imbalance. On examination, we observed spontaneous horizontal nystagmus in the primary position which reversed its direction with a cycle of approximately 2 minutes and a transition period of several seconds by using video Frenzel goggles (SLMED, Seoul, Korea) (see the video on the Neurology Web site at www.neurology.org). The …

A 54-year-old man developed sudden left-sided headache and diplopia. There was complete left ophthalmoplegia and decreased sensation in the ophthalmic and maxillary divisions of the trigeminal nerve. CT angiography showed an aneurysm in the supraclinoid portion of the left internal carotid artery (figure). An emergent …

A 20-year-old man with bilateral medial medullary infarction showed transition of bowtie and upbeat nystagmus into hemi-seesaw nystagmus. Follow-up MRI revealed near complete resolution of the right medullary lesion. This transition of nystagmus suggests that the upbeat nystagmus was generated by bilateral lesions in the ascending pathways from both anterior semicircular canals (SCC), and that the hemi-seesaw nystagmus was caused by damage to the pathway from the left anterior SCC.

Rotatory vertigo mostly develops in vestibular disorders while presyncopal dizziness usually reflects generalized cerebral ischemia due to a cardiovascular cause.1 Nevertheless, contrary to established wisdom, patients with cardiovascular disorders frequently report vertigo.1,–,3 However, the mechanism of so-called cardiogenic vertigo remains unknown. Furthermore, no study has explored vestibular dysfunction during a spontaneous episode in a patient with cardiogenic vertigo. The previous studies of induced syncope suggest that the vertigo may result from cerebellar ischemia and vestibular function was in fact assessed in one of these studies.4,5 We observed downbeat nystagmus during the presyncopal attack with vertigo in a patient with recurrent asystole due to sick sinus syndrome. ### Case report. A 67-year-old woman presented with recurrent rotatory vertigo, nausea, and palpitation for 3 months. The patient reported that the vertigo had lasted for 5–10 seconds, and occurred 2–3 times per week, which became more frequent for the previous several days. She had a history of mitral valve replacement 10 years before. Between the episodes, the …