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Los daños en la sustancia blanca (DSB), detectados como hiperintensidades en las imágenes de RM ponderadas en T2, representan la enfermedad de pequeños vasos cerebrales, y están considerados como un factor de riesgo potencial de trastornos de la memoria y disfunción cognitiva. No se ha evidenciado suficientemente que la disfunción cognitiva en pacientes con enfermedad de Alzheimer esté causada por DSB y la patología β-amiloide (Aβ). El objetivo de estudio fue evaluar la relación entre los DSB y el metabolismo de la glucosa cerebral en pacientes con disfunción cognitiva, tras el ajuste de la carga cerebral de Aβ. Incluimos en este estudio transversal a ochenta y tres sujetos con desempeño cognitivo que oscilaba entre normal y demencia, a quienes se realizó RM cerebral y PET con Florbetaben (18F) y PET con 18F-FDG. Utilizamos la escala Fazekas para cuantificar los DSB en la RM cerebral ponderada en T2. Estimamos cuantitativamente la carga cerebral de Aβ y el metabolismo de la glucosa cerebral utilizando el análisis del volumen de interés. Evaluamos las diferencias del metabolismo de la glucosa cerebral regional entre los grupos de bajo DSB (escala Fazekas < 2) y alto DSB (escala Fazekas ≥ 2). Realizamos un análisis de regresión lineal múltiple ajustado por edad, sexo y carga cerebral de Aβ, para evaluar la relación entre la puntuación de la escala Fazekas y el metabolismo de la glucosa cerebral. El metabolismo de la glucosa cerebral regional para los lóbulos bilateral frontal, temporal, córtices parietales, y lóbulos límbicos en el grupo de alto DSB fueron significativamente menores que los del grupo de bajo DSB. Existieron correlaciones negativas significativas entre la puntuación de la escala Fazekas y el metabolismo de la glucosa cerebral regional en los córtices bilateral frontal, bilateral temporal y córtices parietales izquierdos, y lóbulos límbicos bilaterales. Los análisis de regresión lineal múltiple revelaron que la puntuación de la escala Fazekas era un determinante independiente del metabolismo de la glucosa en los córtices bilateral frontal y temporal y los lóbulos límbicos. Los DSB están asociados a un descenso del metabolismo de la glucosa cerebral. Nuestros hallazgos sugieren que la enfermedad de los pequeños vasos, así como lo patología de Aβ, pueden contribuir a la disfunción cognitiva en pacientes con enfermedad de Alzheimer. White matter lesions (WMLs), detected as hyperintensities on T2-weighted MRI, represent small vessel disease in the brain and are considered a potential risk factor for memory and cognitive impairment. It has not been sufficiently evident that cognitive impairment in patients with Alzheimer's disease is caused by WMLs as well as β-amyloid (Aβ) pathology. The aim of this study was to evaluate relationship between WMLs and cerebral glucose metabolism in patients with cognitive impairment after adjustment of cerebral Aβ burden. Eighty-three subjects with cognitive performance ranging from normal to dementia, who underwent brain MRI and 18F-florbetaben positron emission tomography (PET) and 18F-fluorodeoxyglucose PET, were included in this cross-sectional study. The Fazekas scale was used to quantify WMLs on brain T2-weighted MRI. The cerebral Aβ burden and cerebral glucose metabolism were quantitatively estimated using volume-of-interest analysis. Differences in the regional cerebral glucose metabolism were evaluated between low-WML (Fazekas scale < 2) and high-WML (Fazekas scale ≥ 2) groups. Multiple linear regression analysis adjusted for age, sex and cerebral Aβ burden was performed to evaluate the relationship between the Fazekas scale score and cerebral glucose metabolism. The regional cerebral glucose metabolism for the bilateral frontal, temporal, and parietal cortices, and limbic lobes in the high-WML group were significantly lower than those in the low-WML group. There were significant negative correlations between the Fazekas scale score and regional cerebral glucose metabolism in the bilateral frontal, bilateral temporal and left parietal cortices, and bilateral limbic lobes. Multiple linear regression analysis revealed that the Fazekas scale score was an independent determinant of the glucose metabolism in the bilateral frontal and temporal cortices and limbic lobes. WMLs are associated with decreased cerebral glucose metabolism. Our findings suggest that small vessel disease, as well as Aβ pathology, may contribute to cognitive impairment in patients with Alzheimer's disease. [ABSTRACT FROM AUTHOR]

Highlights: [•] This study investigated the frequency and detailed spectrum of autonomic dysfunction in patients with orthostatic dizziness. [•] Approximately 83% (180/217) of patients showed at least one abnormal autonomic testing result. We classified orthostatic dizziness into 11 groups according to the patterns of autonomic dysfunctions. [•] This study helps clinicians to understand the pattern and mechanism of autonomic dysfunction associated with orthostatic dizziness. [ABSTRACT FROM AUTHOR]

Abstract: Impairment of gaze holding mechanism and gaze-evoked nystagmus (GEN) in the vertical plane due to a focal brain lesion is usually caused by a failure of the vertical neural integrator, which is known to be localized in the interstitial nucleus of the Cajal in the upper midbrain. We report a patient with hemorrhagic stroke involving the paramedian pontine tegmentum who presented with vertical GEN due to a failure of vertical gaze holding mechanism and unilateral internuclear ophthalmoplegia. The possible structure taking a role as a vertical neural integrator in this patient might be the paramedian tract (PMT) neuron. [Copyright &y& Elsevier]

Abstract: A 70-year-old man presented with left-sided weakness and dysarthria. His brain MRI and magnetic resonance angiography demonstrated acute infarctions in the bilateral middle cerebral artery territories in a setting of agenesis of the right internal carotid artery (ICA) with transcavernous anastomosis, a rare developmental anomaly. In this setting, atherosclerotic disease in the unilateral common carotid artery or ICA can induce acute infarctions in the bilateral anterior circulation. [Copyright &y& Elsevier]

Abstract: Upbeat nystagmus (UBN) is typically increased with upward gaze and decreased with downward gaze. We describe a patient with acute multiple sclerosis who developed primary position UBN with a linear slow phase waveform, in which the velocity of nystagmus was intensified in downward gaze and decreased during upward gaze. Brain MRI showed high signal lesions in the paramedian dorsal area of the caudal medulla encompassing the most caudal part of the perihypoglossal nuclei. Clinicians should be aware of possibility of a caudal medullary lesion in a patient with UBN, especially when the velocity of the UBN is increased in downward gaze. [Copyright &y& Elsevier]

Abstract: Background and purpose: Vertebrobasilar ischemic stroke (VBIS) can cause acute hearing loss (AHL) because the vertebrobasilar system supplies most of the auditory system including the inner ear. The aim of this study was to assess the long-term prognosis of AHL associated with VBIS. Methods: Over 12.5years, 62 patients with AHL of a vascular cause who were followed for at least 1year (mean, 49.2months; SD, 24.4months) were enrolled in this study. Quantitative audiovestibular function testing was performed during the acute (mostly within 10days after symptom onset) and last follow-up periods in all patients. Results: On the last follow-up, approximately 65% (39/62) of the patients showed a partial (n=24) or complete (n=15) hearing recovery. All but 2 (97%) patients had acute vertigo and 56 (56/62, 90%) had a unilateral canal paresis to caloric stimulation on the side of the AHL. The most commonly infarcted territory on brain MRI was in the distribution of the anterior inferior cerebellar artery (55/62, 89%). Multivariable analysis showed that multiple risk factors for stroke [odds ratio (OR) 10.46, 95% confidence interval (CI) 1.72 to 13.7, p=0.011] and profound hearing loss [OR 3.92, 95% CI 1.03 to 14.97, p<0.046] predicted a poor outcome for recovery of hearing loss. Conclusions: Acute hearing loss associated with posterior circulation ischemic stroke exhibits a relatively good long-term outcome. Two or more risk factors for stroke and profound hearing loss are adverse prognostic factors for recovery of hearing loss of a vascular cause. [Copyright &y& Elsevier]