MMK Muqit1*, CR Weir1, J Ballantyne2, FG Dunn3, NER Goodfield3
1. Tennent Institute of Ophthalmology, Gartnavel General Hospital, 1053 Great Western Road, Glasgow, G12 OYN
2. Department of Ophthalmology and Orthoptics, Stobhill Hospital, 133 Balornock Road, Glasgow, G21 3UW
3. Department of Cardiology, Stobhill Hospital, 133 Balornock Road, Glasgow, G21 3UW
*
Current address: Department of Ophthalmology, Leeds Teaching Hospitals NHS
Trust, Beckett Street, Leeds, LS9 7TF
Corresponding author: Mr Mahiul MK Muqit, Email. mmmk3@aol.com.
SMJ 2007 52(4): 54
Diplopia and gaze palsies are extremely disabling and distressing problems, especially in patients with significant cardiac co-morbidity. A case of Parinaud syndrome and oculomotor nerve palsy following coronary angiography (CA) is reported. These neuro-ophthalmic complications are not previously documented in the literature in association with CA. The case raises awareness of potential ocular motility deficits that may occur following CA. Potential risk factors during CA are analysed and the mechanisms of the embolic pathway are discussed.
Key
words: Coronary angiography, percutaneous, Parinaud, oculomotor
Patients with coronary artery disease (CAD) often undergo diagnostic coronary angiography (CA) and percutaneous intervention (PCI). Clinical indications include angina unresponsive to medical therapy and acute myocardial infarction (MI). PCI is a well-established non-operative method of myocardial revascularisation for atheromatous CAD. Neurological complications following these procedures occur in less than 1% of cases.1 Neuro-ophthalmic complications are rare, although branch retinal artery occlusion,2 bilateral ophthalmoplegia,3 internuclear ophthalmoplegia,4 and microembolic retinopathy5 have been described. We report the findings of a patient who developed disabling ocular motility deficits following CA.
Case
Report
A 68-year-old male underwent urgent CA for
post-infarct angina. The procedure was technically difficult, and three
catheters were used before a selective insertion of the left main coronary was
obtained. There was severe left-sided coronary artery disease. After the third
injection, the patient acutely developed a right hemiparesis, right upper motor
neurone facial palsy, dysphagia and expressive dysphasia. He was noted to have a
left partial third nerve palsy with pupillary involvement. An urgent CT scan was
normal and excluded brain haemorrhage. Following discussion with the stroke
specialist, he was thrombolysed using recombinant tissue-plasminogen activator.
His neurological status improved considerably over the following 24 hours. He
was referred for an ophthalmology opinion the following day, which confirmed the
oculomotor nerve palsy. He had no previous ocular or neurological history of
note. His visual acuities were 6/6 in each eye and the remainder of his ocular
examination was normal. He was managed conservatively with occlusion of the left
spectacle lens. A second CT scan was done on the third day to assess the extent
of the stroke post-thrombolysis. This demonstrated an infarct within the
thalamus on the left side (figure
1), and explained the Weber’s syndrome in our patient. He was reviewed in
the ophthalmology clinic one week later by which time he had developed signs
consistent with Parinaud syndrome namely bilateral weakness of both upgaze and
downgaze, and convergence retraction nystagmus. Over the following year his
orthoptic findings remained unchanged. The nystagmus caused significant problems
on close-up viewing of objects, however there was no oscillopsia. The diplopia
was controlled by a 15-dioptre base down Fresnel prism over his left spectacle
lens. The patient was reluctant to undergo future CA or PCI due to the
significant navigational problems associated with the diplopia.
Discussion
The occurrence of microembolic complications following invasive procedures such as CA is well documented.1 Whilst neurological complications are well reported, the neuro-ophthalmic complications are rare.1-4 To our knowledge this is the first report of both Weber’s syndrome and Parinaud syndrome in a patient following CA.
Whilst the precise aetiology of such complications is not fully understood various mechanisms6 have been postulated. Thrombus formation within and displacement from, both the catheter and the arterial wall may occur. Atheromatous material may be dislodged during catheter manipulation, whilst the wire may directly traumatise the vessel wall, and dislodge atheromatous plaque en route. During CA, the intracoronary contrast injection may introduce gaseous bubbles and cause coronary spasm. Before balloon dilatation in PCI, the catheter itself may dislodge plaques during the entry and withdrawal stages. Prolonged and technically difficult procedures may increase the risk of embolic complications developing. Multiple catheter manipulations at the coronary artery ostium were required in our case, and transcranial doppler studies6 have confirmed high microembolic signals during such manipulations.
The neuro-ophthalmic complications described above, which are secondary to ischaemia, may be explained on an anatomical basis. The vertical gaze centre is located within the dorsal midbrain, whilst the oculomotor nerve nucleus lies in the floor of the aqueduct of Sylvius at the level of the superior colliculus in the midbrain. The blood supply to the third nerve nuclear complex is the basilar artery, and the superior cerebellar artery supplies the superior tectal plate. The infarct seen in figure1 corresponds to a midbrain stroke syndrome, and we speculate that the following sequence of events may contribute to the aetiology. The catheter follows a retrograde route from descending aorta along the aortic arch, passing behind the ostia of the left subclavian artery (LSA) and then the left common carotid artery (LCCA). Any emboli dislodged from this point or closer to the coronary ostium, may flow anterogradely through the aortic arch and ascend the LCCA and the LSA. Emboli may similarly ascend the LSA to reach the left vertebral artery, with emboli passing to the left basilar artery circulation. Smaller particles could potentially reach the posterior communicating artery ganglionic branches and the superior cerebellar arteries, then lodge in the medial and lateral branches that supply the midbrain, resulting in the neuro-ophthalmic complications described above.
Conclusion
Whilst Parinaud syndrome and oculomotor nerve palsies are rare following coronary angiography and percutaneous intervention, diplopia and gaze palsies are extremely disabling and distressing problems, especially in patients with significant cardiac co-morbidity. It is important for cardiologists, ophthalmologists and orthoptists to be aware that such complications can develop. The risks of diplopia and nystagmus should be reflected in the information provided to the patient prior to consent being obtained.
References
2. Bucci FA Jnr, Dimitsopulos TM, Krohel GB. Branch retinal artery occlusion secondary to percutaneous transluminal coronary angioplasty. Br J Ophthalmol 1989; 73(4): 309-310.
3. Drummond GT, Wuebbolt G. Bilateral ophthalmoplegia during percutaneous transluminal angioplasty. Can J Ophthalmol 1990; 25(3): 152-155.
4. Eggenberger ER, Desai NP, Kaufman DI, et al. Internuclear ophthalmoplegia after coronary artery catheterisation and percutaneous transluminal coronary balloon angioplasty. J Neuroophthalmol 2000; 20(2): 123-126.
5. Teitelbaum BA. Asymptomatic unilateral microembolic retinopathy secondary to percutaneous transluminal coronary angioplasty. J Am Optom Assoc 1999; 70(9): 587-592.
6. Blackin CF, Bingham L, Grigg L, et al. Transcranial doppler detection of microemboli during percutaneous transluminal coronary angioplasty. Stroke 1998; 29(11): 2367-2370.