Correction: Magnetic resonance imaging pattern recognition of metabolic and neurodegenerative encephalopathies in dogs and cats

Maria Miguel-Garces^1*Rita Gonçalves²Rodrigo Gutierrez-Quintana³Patricia Álvarez⁴Katrin Melanie Beckmann⁵Emili Alcoverro⁶Melania Moioli⁷Edward Ives⁸Megan Madden⁹Sergio A. Gomes¹⁰Evelyn Marie Galban¹¹Tim Bentley²Koen Santifort^12,13An Vanhaesebrouck¹⁴Chiara Briola^15,16Patricia Montoliu^17,18Unai Ibaseta¹⁹Inés Carrera²⁰

• ¹Southern Counties Veterinary Specialists, Ringwood, United Kingdom
• ²University of Liverpool Small Animal Teaching Hospital, Neston, United Kingdom
• ³Small Animal Hospital, School of Biodiversity, One Health and Veterinary Medicine, University of Glasgow, Glasgow, United Kingdom
• ⁴Neurology and Neurosurgery Department, Pride Veterinary Referrals, Independent Vetcare (IVC) Ltd, Derby, United Kingdom
• ⁵Section of Neurology, Department of Small Animals, Vetsuisse Faculty Zurich, University of Zurich, Zurich, Switzerland
• ⁶ChesterGates Veterinary Specialists, Chester, United Kingdom
• ⁷Division of Clinical Radiology, Department of Clinical Veterinary Medicine, Vetsuisse Faculty University of Bern, Bern, Switzerland
• ⁸Anderson Moores Veterinary Specialists, Winchester, United Kingdom
• ⁹Royal (Dick) School of Veterinary Studies, University of Edinburgh, Edinburgh, United Kingdom
• ¹⁰Dovecote Veterinary Hospital, Castle Donington, United Kingdom, Castle Donington, United Kingdom
• ¹¹Neurology and neurosurgery Department, University of Pennsylvania School of Veterinary Medicine, Philadelphia, Pennsylvania, USA, Philadelphia, United States
• ¹²IVC Evidensia Small Animal Referral Hospital Arnhem, Neurolohy, Arnhem, The Netherlands., Arnhem, Netherlands
• ¹³IVC Evidensia Small Animal Referral Hospital Hart van Brabant, Neurology, Waalwijk, The Netherlands, Waalwijk, Netherlands
• ¹⁴University of Cambridge Queen's Veterinary School Hospital, Cambridge, United Kingdom
• ¹⁵The Ralph Veterinary Referral Centre, Marlow, United Kingdom
• ¹⁶VetCT, Cambridge, United Kingdom, Cambridge, United Kingdom
• ¹⁷Ars Veterinaria SLP, Barcelona, Spain
• ¹⁸Hospital Veterinari Costa Brava, Girona, Spain, Girona, Spain
• ¹⁹Neurology and Neurosurgery Department, Hospital Veterinario Menes, Gijón, Asturias, Spain, Gijon, Spain
• ²⁰VetOracle, Norfolk, United Kingdom, Norfolk, United Kingdom

There was a mistake in the caption of figure [3] as published. The superior longitudinal fasciculus was incorrectly cited as the affected structure: "Dorsal (A) and transverse plane T2-weighted images at the level of the thalamus (B,C) The corrected caption of figure [3] appears below."Dorsal (A) and transverse plane T2-weighted images at the level of the thalamus (B,C) of a dog with presumptive diagnosis of osmotic demyelination syndrome. There are bilateral and symmetric hyperintensities affecting the thalamus (long white arrows) (A-C) and extending into the subthalamus (dashed long white arrows) (C). A specific region of the grey matter is also affected, corresponding with the claustrum (short black arrows) (B)."The original version of this article has been updated. Adding/removing text In the abstract, the superior longitudinal fasciculus was incorrectly cited as the affected structure and was described as a novel finding: "Metabolic/neurodegenerative encephalopathies encompass a wide list of conditions that share similar clinical and magnetic resonance imaging (MRI) characteristics, challenging the diagnostic process and resulting in numerous tests performed in order to reach a definitive diagnosis. The aims of this multicentric, retrospective and descriptive study are: (I) to describe the MRI features of dogs and cats with metabolic/neurodegenerative encephalopathies; (II) to attempt an MRI recognition pattern classifying these conditions according to the involvement of grey matter, white matter or both; and (III) to correlate the MRI findings with previous literature. A total of 100 cases were recruited, comprising 81 dogs and 19 cats. These included hepatic encephalopathy (20 dogs and three cats), myelinolysis (five dogs), intoxications (seven dogs and one cat), thiamine deficiency (two dogs and seven cats), hypertensive encephalopathy (three dogs and two cats), neuronal ceroid lipofuscinosis (11 dogs and one cat), gangliosidosis (three dogs and two cats), fucosidosis (one dog), L-2hydroxyglutaric aciduria (13 dogs and one cat), Lafora disease (11 dogs), spongiform leukoencephalomyelopathy (one dog) and cerebellar cortical degeneration (four dogs and two cats). None of the hepatic encephalopathies showed the previously described T1-weighted hyperintensity of the lentiform nuclei. Instead, there was involvement of the cerebellar nuclei (8/23), which is a feature not previously described. Dogs with myelinolysis showed novel involvement of a specific white matter structure, the superior longitudinal fasciculus (5/5). Thiamine deficiency affected numerous deep grey nuclei with novel involvement of the oculomotor nuclei (3/9), thalamic nuclei, subthalamus and cerebellar nuclei (1/9). Cats with hypertensive encephalopathy had a more extensive distribution of the white matter changes when compared to dogs, extending from the parietal and occipital lobes into the frontal lobes with associated mass effect and increased brain volume. Lysosomal storage disease showed white matter involvement only, with neuronal ceroid lipofuscinosis characterised by severe brain atrophy when compared to gangliosidosis and fucosidosis. All patients with L-2-hydroxyglutaric aciduria had a characteristic T2-weighted hyperintense swelling of the cerebral and cerebellar cortical grey matter, resulting in increased brain volume. Lafora disease cases showed either normal brain morphology (5/11) or mild brain atrophy (6/11). Dogs with cerebellar cortical degeneration had more marked cerebellar atrophy when compared to cats. This study shows the important role of MRI in distinguishing different metabolic/neurodegenerative encephalopathies according to specific imaging characteristics."This has been corrected to read:"Metabolic/neurodegenerative encephalopathies encompass a wide list of conditions that share similar clinical and magnetic resonance imaging (MRI) characteristics, challenging the diagnostic process and resulting in numerous tests performed in order to reach a definitive diagnosis. The aims of this multicentric, retrospective and descriptive study are: (I) to describe the MRI features of dogs and cats with metabolic/neurodegenerative encephalopathies; (II) to attempt an MRI recognition pattern classifying these conditions according to the involvement of grey matter, white matter or both; and (III) to correlate the MRI findings with previous literature. A total of 100 cases were recruited, comprising 81 dogs and 19 cats. These included hepatic encephalopathy (20 dogs and three cats), myelinolysis (five dogs), intoxications (seven dogs and one cat), thiamine deficiency (two dogs and seven cats), hypertensive encephalopathy (three dogs and two cats), neuronal ceroid lipofuscinosis (11 dogs and one cat), gangliosidosis (three dogs and two cats), fucosidosis (one dog), L-2-hydroxyglutaric aciduria (13 dogs and one cat), Lafora disease (11 dogs), spongiform leukoencephalomyelopathy (one dog) and cerebellar cortical degeneration (four dogs and two cats). None of the hepatic encephalopathies showed the previously described T1-weighted hyperintensity of the lentiform nuclei. Instead, there was involvement of the cerebellar nuclei (8/23), which is a feature not previously described. Dogs with myelinolysis showed novel involvement of a specific grey matter structure, the claustrum (5/5). Thiamine deficiency affected numerous deep grey nuclei with novel involvement of the oculomotor nuclei (3/9), thalamic nuclei, subthalamus and cerebellar nuclei (1/9). Cats with hypertensive encephalopathy had a more extensive distribution of the white matter changes when compared to dogs, extending from the parietal and occipital lobes into the frontal lobes with associated mass effect and increased brain volume. Lysosomal storage disease showed white matter involvement only, with neuronal ceroid lipofuscinosis characterised by severe brain atrophy when compared to gangliosidosis and fucosidosis. All patients with L-2-hydroxyglutaric aciduria had a characteristic T2-weighted hyperintense swelling of the cerebral and cerebellar cortical grey matter, resulting in increased brain volume. Lafora disease cases showed either normal brain morphology (5/11) or mild brain atrophy (6/11). Dogs with cerebellar cortical degeneration had more marked cerebellar atrophy when compared to cats. This study shows the important role of MRI in distinguishing different metabolic/neurodegenerative encephalopathies according to specific imaging characteristics."The original version of this article has been updated. The superior longitudinal fasciculus was incorrectly cited as the affected structure and was described as a novel finding. This error appears in the Results section and the Discussion. The correct structure involved in dogs with myelinolysis is the claustrum.A correction has been made to the section Results, subsection endogenous malfunction and toxins -Myelinolysis/osmotic demyelination syndrome, Paragraph Number 9: "The brain volume was normal in all cases (5/5). Patients showed both grey and white matter structures affected with the presence of bilateral, symmetric intra-axial lesions. The grey matter structures affected included thalamus (5/5) and subthalamus (1/5). Regarding the white matter, a specific anatomical region located immediately lateral to the internal capsule was affected in all cases (5/5), corresponding with the superior longitudinal fasciculus (Figure 3). All lesions were homogenous, hyperintense in T2W and FLAIR, isointense in T1W and without contrast enhancement."The correct statement is: "The brain volume was normal in all cases (5/5). Patients showed grey matter structures affected with the presence of bilateral, symmetric intra-axial lesions. The grey matter structures affected included thalamus (5/5), subthalamus (1/5) and a specific anatomical region located immediately lateral to the internal capsule (5/5), corresponding with the claustrum (Figure 3)."The original version of this article has been updated.A correction has been made to the section Discussion, subsection Osmotic demyelination syndrome, Paragraph Number 5: "A novel finding not previously described was the involvement of a specific white matter structure seen in all patients, the superior longitudinal fasciculus. The superior longitudinal fasciculus is a type of long association fibre contained within the white matter that connects the frontal cortex with the parietal and the occipital cortex (27). The reason for the susceptibility of this specific region in these patients is unknown and histopathological correlation is required to confirm the nature of the changes."The correct statement is: "A novel finding not previously described was the involvement of a specific grey matter structure seen in all patients, the claustrum. The claustrum is a component of the basal nuclei (27). The reason for the susceptibility of this specific region in these patients is unknown and histopathological correlation is required to confirm the nature of the changes."The original version of this article has been updated.