Tommaso Davini, Carlotta Remelli, Chiara Mattei, Swan Specchi, Roberta Biserni, Marco Bernardini

Background

Horner syndrome (HS) is a neurological disorder caused by disruption of the sympathetic innervation to the eye, producing miosis, ptosis, enophthalmos, and third eyelid protrusion. In dogs, many cases are idiopathic, particularly in male golden retrievers. However, in human medicine, internal carotid artery dissection (ICAD) is a well-recognized cause of isolated HS. Prior to this report, ICAD had not been documented as a cause of HS in dogs. This case describes clinical and imaging findings consistent with ICAD as the underlying cause of HS in a golden retriever.

Methods

A 5-year-old male golden retriever presented with subacute onset of left-sided ptosis, miosis, and third eyelid protrusion, consistent with isolated left HS. Neurological and systemic examinations were otherwise normal. Magnetic resonance imaging (MRI) of the head, including T1-weighted fat-saturated (FATSAT), T2-weighted, and 3D time-of-flight magnetic resonance angiography (TOF-MRA) sequences, and total-body computed tomography (CT) with angiography were performed to investigate potential causes.

Results

MRI revealed progressive luminal narrowing of the left internal carotid artery (ICA), loss of normal flow void, and marked T1 hyperintensity within the ICA lumen—findings characteristic of a thrombosed false lumen or intramural hematoma. CT angiography confirmed vessel narrowing and irregularity, particularly above the carotid bifurcation. No other lesions were detected along the oculosympathetic pathway, and the remainder of the imaging studies were normal. Based on these findings, a presumptive diagnosis of left ICAD was made as the underlying cause of postganglionic HS.

Limitations

Pharmacologic localization testing (e.g., phenylephrine response) was not performed, which could have confirmed postganglionic involvement. As a single case report, generalizability is limited. Histopathologic confirmation was not available, and MRI and CT findings served as the diagnostic basis.

Conclusions

This case represents the first reported instance of Horner syndrome secondary to presumed internal carotid artery dissection in a dog. MRI and CT findings mirrored those described in humans with ICAD, indicating a similar pathophysiological mechanism. The study highlights the diagnostic value of magnetic resonance angiography (MRA) in canine patients with isolated HS and suggests that ICAD should be included in the differential diagnosis. Incorporating MRA sequences into MRI protocols for HS may improve detection of vascular causes previously labeled as idiopathic.

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