There are different types of brain diseases associated with cranial nerve dysfunction (including cerebral venous thrombosis, infection, subarachnoid hemorrhage, vasculitis, cerebral infarction, emergent hypertension, etc.), but the clinical presentation and radiographic findings in our case did not support their diagnosis. It has been documented that microemboli complications are the adverse effect of invasive procedures such as CA [
2]. Since the incidence rate of acute stroke after PCI is 0.56%, it can be suggested that our patient experienced an ischemic event of unilateral abducens. This can happen due to microembolism during PCI resulting in left lateral rectus palsy [
11]. Moreover, the proposed mechanisms of it include the formation of blood clots within the catheter and arterial wall along with their displacement. Moving the catheter may also dislodge atheromatous material, direct damage to the vessel wall by using the wire resulting in dislodging of atheromatous plaque. In PCI, the catheter itself may be responsible for dislodging plaques while entering the vessels before balloon dilation. The risk of embolic complications may be associated with prolonged and challenging procedures [
12].
Contrast-induced neurotoxicity (CIN) is another plausible differential diagnosis. This rare complication has been reported in patients undergoing PCI [
13]. CIN results within minutes after contrast injection and can present in different ways, including seizure, focal neurological deficit, visual loss, encephalopathy, ophthalmoplegia, and cerebellar dysfunction [
14]. The proposed risk factors are renal dysfunction and injection of large volumes of contrast agents [
15]. Since our patient had medical history of diabetes mellitus, he received only 150 cc of contrast agent. The impairment of cranial nerves in CIN cases is rare. In 2010, Guimaraens
et al. reported two cases of a 71-year-old man and a 49-year-old woman who underwent vertebral and clavicle arteriography followed by aortic angiography with the involvement of cranial nerve [
16]. In 1989, Lantos presented a case in which eye movement paralysis also developed in a 51-year-old man after carotid angiography [
17]. Following coronary angiography, additional cases have been documented. In 2013, Vasavada
et al. reported a case where a patient underwent angioplasty and experienced temporary unilateral partial oculomotor nerve palsy [
18]. Similarly, Drummond and Wuebbolt reported a case of bilateral ophthalmoplegia in a 61-year-old woman following PCI [
7]. Other instances of ophthalmoplegia after CA were reported by Yu and Dangas [
19] and Caillé
et al. [
20]. Eggenberger
et al. conducted an analysis on 110 patients with internuclear ophthalmoplegia (INO) and found that 5 of them experienced isolated INO during intravascular surgery [
6]. Patients with CIN may present different radiographic findings. As initial CT scans could be normal, cerebral edema, cortical enhancement, subcortical enhancement, and hyperdensity in the subarachnoid space or parenchyma may also appear but be mistaken with intracerebral or subarachnoid hemorrhage [
19,
21‐
23]. If a significant amount of contrast is administered, regardless of its osmolality, it can potentially disrupt the blood–brain barrier and cause neurotoxicity in the absence of preexisting brain pathology [
24,
25]. Additionally, our patient experienced temporary lateral rectus palsy after undergoing PCI, which could potentially be linked to contrast-induced neurotoxicity. Extra-axial lesions including vasculopathy are also another plausible differential diagnosis for isolated abducens nerve palsy. In the majority of cases, abducens nerve palsy resulting from a lesion in the intrapontine fascicle is manifested with other neurological symptoms [
10]. Thus, in such cases, it is better to perform precise examinations including MRI [
26]. However, our patient had a history of diabetes mellitus and MRI revealed no signs of pontine infarction.