Medial strabismus (esotropia) at rest associated with contralateral paramedian thalamic ischemic infarction in 2 dogs

Abstract

Pseudoabducens paralysis resulting in resting medial strabismus (esotropia) is a rare consequence of a contralateral paramedian thalamic ischemic infarction in people. To date, esotropia has been reported in dogs in association with ipsilateral abducens neuropathy or extraocular myopathy, but not secondary to thalamic lesions. A 7-year-old male neutered Border Collie and a 12-year-old female neutered cross-breed dog were presented with peracute nonprogressive vestibular ataxia. Neurological 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 identified a left paramedian thalamic lacunar ischemic infarct in both dogs. Interruption of descending inhibitory pathways that decussate in the subthalamic region and innervate 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.

FIGURE 1

Photograph of the dog (case 1) diagnosed with a left paramedian thalamic ischemic infarct and a right contralateral resting medial strabismus (esotropia).

FIGURE 2

MRI of the head of case 1 including T2W transverse (A), T2W sagittal (B), T2 FLAIR transverse (C), T1W precontrast transverse (D), and DWI transverse (E) sequences, revealed a sharply‐marginated homogeneous lesion (arrowhead), that was T2W and T2W FLAIR hyperintense, T1W hypointense compared to the gray matter and noncontrast enhancing with restricted diffusion in DWI and ADC map in the left thalamus extending paramedian from the ventral level of the mesencephalic aqueduct to the ventral thalamus. This lesion was consistent with a left ventral lacunar paramedian thalamic ischemic infarct.

FIGURE 3

MRI of the head of case 1 including T2W transverse (A), T2W sagittal (B), T2 FLAIR transverse (C), T1W postcontrast transverse (D), DWI dorsal (E) and ADC map dorsal (F) sequences, revealed a sharply‐marginated, homogeneous lesion (arrowhead) that was T2W and T2 FLAIR hyperintense, T1W isointense compared to the gray matter, and noncontrast enhancing with restricted diffusion in DWI and ADC map lesion in the rostral aspect of the left thalamus. This lesion was consistent with a left ventral lacunar paramedian thalamic ischemic infarct.

FIGURE 4

Schematic illustration of the disrupted pathways in dogs with pseudoabducens palsy.