Convergence‐Retraction Nystagmus Associated with Dorsal Midbrain Lesions in Three Dogs

Convergence-retraction nystagmus is an irregular, jerky nystagmus in which both eyeballs rhythmically converge and retract into the orbit, particularly on attempting an upward gaze. In humans it is seen as part of Parinaud’s syndrome, also known as dorsal midbrain syndrome, in which a lesion of dorsally located midbrain structures (the ventral pretectum, the periaqueductal area, and the medial longitudinal fasciculus in the dorsal tegmentum) prevents upward or downward movement of the eyes. It has been hypothesized that convergence-retraction nystagmus is caused by damage (ischemia, neoplasia, compression, or demyelination) to supranuclear fibers that have an inhibitory effect on the convergence neurons or divergence neurons in the midbrain, resulting in a sustained discharge of medial rectus and other extraocular muscle neurons. The rostral interstitial nuclei of the medial longitudinal fasciculus (RINMLF) of the midbrain, located dorsal to the oculomotor nuclei, contain the final relays producing all vertical saccades, and hence it has been suggested that Parinaud’s syndrome may result from damage to their neuronal cell bodies, as well as their afferent and efferent pathways. Convergence-retraction nystagmus is a highly localizing clinical sign that to the best of our knowledge has not yet been described in the dog. Here, we report 3 large breed dogs that were presented with convergenceretraction nystagmus and in which magnetic resonance imaging (MRI) identified focal lesions within the dorsal midbrain. Case 1: An 11-year, 5-month-old male neutered Staffordshire Bull Terrier was presented with a 14-day history of acute onset, nonprogressive vestibular ataxia with lethargy and disorientation. General physical examination was normal. On neurological examination, the dog was found to be mildly obtunded with a mild right-sided head tilt and circling to the right. Convergence-retraction nystagmus was noted (Video S1), with decreased vestibulo-ocular reflex bilaterally. The remainder of the neurological examination was normal and the findings were considered consistent with a right brainstem neurolocalization. The CBC results were within reference intervals (RIs). Serum biochemistry results included a mildly increased alkaline phosphatase (ALKP) activity (313 U/ L; RI, 19–285 U/L), alanine transferase (ALT) activity (171 U/L; RI, 13–88 U/L), and calcium concentration (2.73 mmol/L; RI, 2.13–2.7 mmol/L). Serum thyroxine and thyroid-stimulating hormone (TSH) concentrations were within normal limits. Prothrombin time and activated partial thromboplastin time were within normal limits. Noninvasive blood pressure assessment identified a pressure of 170–175 mmHg. Urine-specific gravity was 1.043, and urine chemistry dipstrip analysis and sediment examination were normal. A Baermann test for Angiostrongylus was negative. The dog underwent general anesthesia. A combination of acepromazine maleate (0.01 mg/kg IV) and methadone (0.1–0.2 mg/kg IV) was used for premedication, followed by induction with propofol (4–6 mg/kg IV) and maintenance of anesthesia with isoflurane in oxygen. A MRI examination was performed and included T2weighted (T2W) (repetition time, [TR] [ms], echo time [TE], [ms] 3333/110) sagittal and transverse images, T2W fluid attenuated inversion recovery (FLAIR) (TR/TE, 3612/80, inversion time [TI] [ms] 2000) transverse images, and T2*W fast field echo (FFE) transverse images. Sagittal and transverse, T1-weighted (T1W) (TR/TE, 515/15) images were acquired before and after IV administration of gadolinium contrast (0.1 mmol/kg, gadobutrol). Slice From the Clinical Science and Services, Royal Veterinary College, University of London, Hatfield, Herts UK (Crawford, Beltran, Lam, Kenny). The work was conducted at the Royal Veterinary College. Corresponding author: A.H. Crawford, Clinical Science and Services, Royal Veterinary College, University of London, Hawkshead Lane, North Mymms, Hatfield, Herts AL9 7TA, UK; e-mail: ahcrawford@rvc.ac.uk. Submitted February 3, 2016; Revised April 10, 2016; Accepted April 21, 2016. Copyright © 2016 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals, Inc. on behalf of the American College of Veterinary Internal Medicine. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes. DOI: 10.1111/jvim.13966 Abbreviations: