Veterinary Internal Medicine PDF - 2024 - Medial Strabismus in Dogs

Summary

This article from the Journal of Veterinary Internal Medicine reports on two cases of medial strabismus (esotropia) in dogs, potentially linked to contralateral thalamic ischemic infarction. The study highlights the unusual neurological sign of esotropia as a possible diagnostic tool for such lesions in canines. Detailed clinical examinations and imaging are used to support findings.

Full Transcript

Received: 17 November 2023 Accepted: 15 December 2023 DOI: 10.1111/jvim.16986 CASE REPORT Medial strabismus (esotropia) at rest associated with contralateral paramedian thalamic ischemic infarction in 2 dogs Theofanis Liatis 1 | Ioannis N. Plessas 2...

Received: 17 November 2023 Accepted: 15 December 2023 DOI: 10.1111/jvim.16986 CASE REPORT Medial strabismus (esotropia) at rest associated with contralateral paramedian thalamic ischemic infarction in 2 dogs Theofanis Liatis 1 | Ioannis N. Plessas 2 | Holger Volk 3 | Danielle Whittaker 1 1 Queen Mother Hospital for Animals, Royal Veterinary College, University of London, Abstract Hatfield, UK Pseudoabducens paralysis resulting in resting medial strabismus (esotropia) is a rare 2 Davies Veterinary Specialists, Hitchin, UK 3 consequence of a contralateral paramedian thalamic ischemic infarction in people. To Department of Small Animal Medicine and Surgery, University of Veterinary Medicine date, esotropia has been reported in dogs in association with ipsilateral abducens Hannover, Hannover, Germany neuropathy or extraocular myopathy, but not secondary to thalamic lesions. A Correspondence 7-year-old male neutered Border Collie and a 12-year-old female neutered cross- Theofanis Liatis, Royal Veterinary College, breed dog were presented with peracute nonprogressive vestibular ataxia. Neurologi- Hatfield, UK. Email: [email protected] cal examination identified right esotropia, nonambulatory tetraparesis, right head tilt, vestibular ataxia and nystagmus. Lesions in both dogs were localized to the vestibular system with thalamic involvement. Magnetic resonance imaging of the brain identi- fied a left paramedian thalamic lacunar ischemic infarct in both dogs. Interruption of descending inhibitory pathways that decussate in the subthalamic region and inner- vate the contralateral motor nucleus of the oculomotor nerve leads to hypertonicity of the medial rectus. These cases indicate that esotropia is a rare but highly localizing sign in dogs with contralateral thalamic infarcts. KEYWORDS cerebrovascular accident, motor nucleus of oculomotor nerve, paramedian thalamus, pseudoabducens palsy, thalamic esotropia 1 | I N T RO DU CT I O N innervate the contralateral motor nucleus of the oculomotor nerve. Such a lesion results in tonic activation of the medial rectus muscle of Pseudoabducens paralysis or palsy refers to failure of ocular abduc- the contralateral eye and therefore contralateral resting medial stra- tion that is not caused by dysfunction of the abducens nerve, but bismus (esotropia).2,3 1 likely is a result of increased convergence activity to the eye. In In dogs, neuro-ophthalmological signs secondary to thalamic and humans, pseudoabducens paralysis is a rare neurological sign, and it midbrain ischemic infarcts have been reported rarely, and these signs has been described as ipsilateral or contralateral to an ischemic infarct include positional nystagmus, ipsilateral or contralateral positional at the midbrain-thalamic junction or thalamic-subthalamic region, ventral or ventrolateral strabismus, anisocoria with ipsilateral mydriasis, respectively.2 A paramedian thalamic lesion can cause interruption of Horner syndrome and pupillary light reflex deficits,4,5 whereas the descending inhibitory convergence pathways that traverse the convergence-retraction nystagmus and Collier's sign can be manifested paramedian thalamus and decussate in the subthalamic region to when the dorsal midbrain is affected.6,7 To date, esotropia has been reported in dogs in association with ipsilateral abducens neuropathy,8,9 extraocular myopathy10 and congenital abnormalities,11 but not second- Abbreviations: ADC, apparent diffusion coefficient; DWI, diffusion-weighted imaging; FLAIR, fluid attenuated inversion recovery. ary to thalamic lesions. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. © 2024 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals LLC on behalf of American College of Veterinary Internal Medicine. 1146 wileyonlinelibrary.com/journal/jvim J Vet Intern Med. 2024;38:1146–1151. 19391676, 2024, 2, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/jvim.16986 by Cochrane Colombia, Wiley Online Library on [17/11/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License LIATIS ET AL. 1147 Herein we describe esotropia as a localizing neurological sign of matter, had no mass effect or contrast enhancement and showed contralateral paramedian thalamic ischemic infarction in 2 dogs. restricted diffusion in diffuse weighting imaging (DWI) and apparent dif- fusion coefficient (ADC) mapping (Figure 2). This lesion was consistent with a left ventral lacunar paramedian thalamic ischemic infarct in the 2 | CASES vascular territory of the caudal perforating artery.5 Computed tomogra- phy of thorax and abdomen disclosed no lesions. Thrombotic profile 2.1 | Case 1 including viscoelastic coagulation monitoring was normal, whereas multi- ple electrode aggregometry analysis using arachidonic acid and adeno- A 7-year-old male neutered Border Collie was presented to the hospi- sine diphosphate reagents suggested increased platelet activation and tal for evaluation of peracute nonprogressive vestibular ataxia. therefore a possible thrombotic event. Physical examination was normal. Neurological examination identified The dog was hospitalized for 7 days and given supportive care, marked right head tilt, nonambulatory tetraparesis and marked including, IV fluid therapy, antinausea medications (maropitant, vestibular ataxia. The dog constantly rolled to the right side. Pos- 1 mg/kg IV q24h; ondansetron, 1 mg/kg IV q12h) and physiotherapy. tural reactions could not be assessed. Cranial nerve assessment The dog subsequently improved to ambulatory status and was dis- identified right esotropia (Figure 1), suspected upward gaze palsy charged from the hospital. The episodic head tremor completely with intact vestibulo-ocular reflex. Episodic nonintentional head resolved 9 days after the onset of the cerebrovascular accident. tremor with vertical direction from which the dog could be occa- sionally distracted also was present (Video 1). Neuroanatomical localization was consistent with a right-sided central vestibular 2.2 | Case 2 system lesion with suspected thalamic involvement based on the episodic head tremor. A 12-year-old female neutered cross-breed dog was presented to the Venous blood gas analysis, hematology, thyroid profile (ie, total hospital for evaluation of peracute nonprogressive vestibular ataxia. thyroxine and thyroid stimulating hormone concentrations), urinalysis Physical examination was normal. Neurological examination dis- and urine protein: creatinine ratio were within normal limits, whereas closed marked right head tilt, nonambulatory tetraparesis and serum biochemistry disclosed mild hypercholesterolemia (8.7 mmol/L; marked vestibular ataxia. The dog rolled to the right side. Postural reference interval [RI], 3.2-6.2 mmol/L) and increased C-reactive protein reaction assessment identified decreased hopping and paw place- (37.7 mg/dL; RI,

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