Did poor eyesight influence Goya's late works? Medicine and art history in search for an interpretation of Goya's late paintings.

PURPOSE: The aim of this article is to 'determine' the scope of Goya's eyesight difficulties and assess the extent to which those difficulties might explain his style of painting in the last years of his life. METHODS: We analyse the correspondence and late works of the Aragonese painter Francisco de Goya y Lucientes (1746-1828), who has been admired for his use of colour, his energetic loose brushstrokes, his disregard for details and his bold compositions, as well as for his different artistic styles throughout his life. RESULTS: The evolution of Goya's style of painting in his later works seems to have been the consequence of an eyesight condition, probably age-related cataracts at an advanced stage. The faded dark backgrounds, which become blurred with the silhouette of the person portrayed, could indicate a certain degree of eye strain. This can be traced in all these works, but is especially evident in the unfinished portrait of Pío de Molina (1827-1828), as well as in the portraits of Mariano Goya, the artist's grandson (1827), and Jacques Galos (1826). CONCLUSION: It has been considered that the late and isolated Goya's sight problems were a belated consequence of his severe illness of 1792. Nevertheless, in our opinion, this is a simplistic explanation and, given the painter's age, it is logical to presume that their cause could be age-related lens opacities. This article argues that medicine may become a subsidiary science to art history, as it can provide empirical evidence of the way painters' illnesses may have a strong impact on their artworks.

Rhombencephalitis due to Listeria monocytogenes: A Clinicopathologic Study of a Case.

INTRODUCTION: Central nervous system infections caused by Listeria monocytogenes usually manifest in the form of meningitis or meningoencephalitis, and are more common among immunosuppressed patients. Brainstem encephalitis (rhombencephalitis) is less common and fatal if not recognized and treated early. CASE REPORT: We describe the case of a 40-year-old, immunocompetent male patient, who presented with initial symptoms of high fever and productive cough. Signs of brainstem involvement appeared later. A magnetic resonance imaging of the brain revealed a lesion of inflammatory appearance in the right medulla oblongata, and the cerebrospinal fluid test showed mononuclear pleocytosis. Blood and cerebrospinal fluid cultures were negative. He presented with a significant improvement with the start of ceftriaxone and subsequent association of corticosteroids, until he developed respiratory failure and died. The third blood cultures grew after his death and they were positive for L. monocytogenes. An autopsy was carried out, which showed necrotizing inflammation, with gram-positive bacilli in the brainstem and the cerebellum. CONCLUSIONS: A fatal delay in the diagnosis occurred, mainly because of the favorable clinical response to ceftriaxone and corticosteroids. This case reminds us that a febrile clinical presentation with brainstem involvement must generate the suspicion of a Listeria infection, and therefore ampicillin must be a part of the empirical treatment.

Carotid intima-media thickness as a predictor of response to cholinesterase inhibitors in Alzheimer's disease: an open-label trial.

BACKGROUND: Cholinesterase inhibitors are modestly effective in treating patients with Alzheimer's disease. However, there may be important inter-individual variations ranging from no improvement at all to significant improvement and long periods of stabilization. Carotid atherosclerosis is associated with cognitive decline in elderly people. OBJECTIVE: The objective of this study was to investigate whether carotid intima-media thickness (IMT) predicts response to cholinesterase inhibitors in Alzheimer's disease. PATIENTS AND METHODS: A series of 54 patients with mild to moderate Alzheimer's disease were enrolled consecutively in an open-label trial. At baseline, all patients were assessed on the following clinical scales: Mini-Mental State Examination, Clinical Dementia Rating, the Hachinski Ischemic Scale, Blessed Dementia Rating Scale, Alzheimer's Disease Assessment Scale-cognitive subscale (ADAS-cog), Neuropsychiatric Inventory (NPI) and a daily-living activities scale (Disability Assessment for Dementia [DAD]). Investigations included magnetic resonance imaging of the brain and a colour echo-Doppler scan of the carotid arteries to measure the maximum IMT. Patients were then commenced on galantamine treatment for 6 months, after which scores on the ADAS-cog, NPI and DAD scales were reassessed. RESULTS: A total of 50 patients completed the study. Their mean age was 77.78 years (SD 6.51 years); 34 patients were female. Galantamine treatment decreased the mean NPI score from 17.68 to 13.86 points, but this difference was not statistically significant (p=0.07). On the ADAS-cog scale, a modest and nonsignificant mean difference of -0.4 points (p=0.7) was observed. A weak (correlation coefficient r=0.4) but significant correlation between IMT and changes in clinical scale score was found, with low carotid IMT being shown to be a predictor of response on both the ADAS-cog (p=0.003) and NPI (p=0.006) scales; these findings were corroborated in multivariate analysis. For men, the correlation was stronger (r=0.7 and 0.8 for the ADAS-cog and NPI scales, respectively). CONCLUSION: Although the magnitude of effect was moderate, carotid IMT could be a significant predictor of clinical response to cholinesterase inhibitors in patients with Alzheimer's disease.

The cerebrovascular pathology in Alzheimer's disease and its influence on clinical variables.

Vascular pathology is frequently found in the brains of patients with Alzheimer's disease (AD). The aim of this study is to assess the frequency of vascular pathology in the brain in AD patients in a systematic manner and its clinical significance at presentation. A series of 51 patients with mild to moderate AD were consecutively enrolled. At baseline, every patient underwent the following clinical scales: Mini-Mental, Clinical Dementia Rating Scale, Ischemic Scale, Blessed Dementia Rating Scale, Alzheimer's Disease Assessment Scale Cognitive Subscale, Neuropsychiatric Inventory, and an Activities of Daily Living Scale (Disability Assessment for Dementia). We also carried out magnetic resonance imaging of the brain and color echo Doppler of carotids to measure the intima-media thickness. White matter hyperintensities were quantitatively evaluated with the Wahlund scale. We did not find correlation between intima-media thicknesses of carotids and clinical scales and between the Wahlund scale and clinical scales. The presence or absence of both microinfarctions and hypertension had no influence in the scores of the clinical scales. We conclude that the vascular component is common in AD but only as coincident pathology.