Endgames Picture Quiz

Visual impairment

BMJ 2013; 346 doi: https://doi.org/10.1136/bmj.f2163 (Published 10 April 2013) Cite this as: BMJ 2013;346:f2163

This article has a correction. Please see:

  1. Ramachandiran Nandhagopal, consultant neurologist
  1. 1Department of Medicine, College of Medicine and Health Sciences, Al-Khod, Zip 123, Muscat, Oman
  1. Correspondence to: R Nandhagopal rnandagopal{at}yahoo.com

A 66 year old man with diabetes presented to the emergency service six hours after the acute onset of visual loss in his left eye. Figure 1 shows the only neurological deficit that was elicited during bedside clinical examination. Serial electrocardiography showed an intermittent fast rhythm (which lasted for several hours), characterised by varying R-R intervals and absence of P waves, followed by a return to sinus rhythm. Cranial magnetic resonance imaging showed an area of infarction with haemorrhagic transformation. His medical history included episodes of palpitation and dizziness, for which he received a diagnosis of non-valvular atrial fibrillation.


Fig 1 Schematic representation of the clinical findings seen during bedside finger perimetry. OD=right visual field; OS=left visual field


  • 1 What clinical finding is depicted in fig 1?

  • 2 On the basis of the clinical sign seen in fig 1, can you localise the lesion (infarct)?

  • 3 How would you prevent recurrence of this patient’s new neurological symptoms?


1 What clinical finding is depicted in fig 1?

Short answer

Left homonymous superior quadrantanopia.

Long answer

Figure 1 shows a visual field defect (visual loss) in the right superior nasal quadrant and left superior temporal quadrant. Hence, the patient had left homonymous superior quadrantanopia. Although the quadrantanopic visual deficit was present on either side, the patient reported visual loss in the left eye only (the eye with the temporal visual field cut). This is the usual pattern of symptoms reported by patients with homonymous quadrantanopia or hemianopia.1 In other words, patients usually project the visual loss unilaterally to the eye with the temporal field cut. Hence, while examining the visual field, careful attention should be paid to the unrecognised visual defect (not verbalised by the patient) in the ipsilesional nasal field.

2 On the basis of the clinical sign seen in fig 1, can you localise the lesion (infarct)?

Short answer

Right inferior occipital (or occipitotemporal) region.

Long answer

The presence of homonymous quadrantanopia suggested a retrochiasmatic (posterior to the optic chiasm) lesion. The highly congruous visual field deficit suggests that the lesion was in a more posterior location rather than in the loop of optic radiation (Meyer’s loop) in the anterior temporal region. Because this patient’s visual field defect pointed to a right sided (non-dominant) brain lesion, associated findings should also be sought. These include visual inattention, visuospatial deficits and spatial disorientation in the preserved inferior visual quadrants, optokinetic nystagmus, prosopagnosia (problems with face recognition), altered prosody of speech, and tactile extinction by double simultaneous sensory testing at the bedside. The absence of these associated findings, the presence of vascular risk factors, and the acute onset of symptoms suggested a circumscribed vascular or stroke lesion that had damaged the visual pathway along the geniculo-calcarine tract, especially in the right inferior occipital region. In contrast, a vascular lesion that had damaged the optic radiation in the parietal region would result in inferior quadrantanopia.

In this patient, diffusion weighted magnetic resonance imaging (diffusion sensitivity factor b=1000 sec/mm2; fig 2A) showed a bright (hyperintense) signal in the inferior calcarine (occipital) cortex). This lesion was dark (hypointense) on apparent diffusion coefficient mapping (fig 2B) and showed areas of hypointensity (petechial haemorrhage) on susceptibility weighted magnetic resonance imaging (fig 2C), which is sensitive to blood products. These features confirmed an acute infarction in the inferior occipital cortex (in the distribution of a branch of the right posterior cerebral artery), with mild haemorrhagic conversion.


Fig 2 Brain magnetic resonance imaging. (A) Diffusion weighted axial image (b=1000 sec/mm2) showing a bright signal (arrow) in the right inferior occipital region; inset: magnetic resonance cerebral angiogram showing no flow abnormalities in the posterior cerebral arteries or basilar artery. (B) Corresponding apparent diffusion coefficient map showing a dark signal (arrow) in the right inferior occipital region. (C) Susceptibility weighted image, which is sensitive to blood products, areas of haemorrhage (arrowheads) as dark signal. These findings suggest the presence of an acute ischaemic infarction with mild haemorrhagic transformation

3 How would you prevent recurrence of this patient’s new neurological symptoms?

Short answer

Long term oral anticoagulation is needed to prevent further cardioembolic stroke episodes.

Long answer

In the context of paroxysmal atrial fibrillation (fig 3), and the fact that the most common mechanism underlying ischaemic infarction in the distribution of the right posterior cerebral artery is embolism,2 the patient’s recent stroke with haemorrhagic conversion was thought to be caused by cardioembolism. This conclusion is backed up by the absence of a stenotic lesion or occlusion of the posterior cerebral arteries on angiography (fig 2A, inset).


Fig 3 Serial electrocardiography. The top recording (lead II) obtained on the afternoon of day 1 shows the presence of P waves (arrows) and a regular RR interval. In the middle recording (obtained about five hours after the first electrocardiogram), P waves are replaced by undulations of baseline or fibrillation waves, and RR intervals are irregular with a faster heart rate. In the bottom row (recorded on day 6), RR intervals are regular and P waves are again present. These features are suggestive of paroxysmal atrial fibrillation

The stroke risk stratification scheme for atrial fibrillation, CHA2DS2-VASc,3 4 5 returns a score of 4 points in this patient—diabetes: 1 point; previous or recent stroke or transient ischaemic attack: 2 points; age: 1 point. With a score greater than 2 points, this patient requires anticoagulation. The choice of drugs includes warfarin (an oral vitamin K antagonist) or newer drugs such as dabigatran6(direct thrombin inhibitor), rivaroxaban,7 and apixaban8 (both oral factor Xa inhibitors) to prevent future stroke in the long term (class I recommendation: evidence or agreement that the intervention or treatment is beneficial and effective; evidence level A: evidence from randomised clinical trials).5 Treatment with warfarin should aim for a target international normalised ratio of 2-3. Specific treatment of paroxysmal atrial fibrillation should be considered in close liaison with a cardiologist. The management of hyperglycaemia and hyperlipidaemia, if present, should also be optimised.

Patient outcome

Two years before this stroke, the patient had been diagnosed as having paroxysmal atrial fibrillation by his cardiologist on the basis of his symptoms of intermittent palpitation and dizziness and findings on Holter electrocardiography. He underwent chemical cardioversion with amiodarone (for the non-valvular paroxysmal atrial fibrillation), and this resulted in reversion to sinus rhythm. He was subsequently placed on a small dose of β adrenoceptor antagonist. Coronary angiography showed only mild atherosclerotic changes. His CHADS2 (previous stroke risk scoring scheme in the setting of atrial fibrillation) score at that time was 1 and he was prescribed aspirin along with a statin.

At the onset of the current episode he noticed transient loss of vision in both eyes (possibly cortical blindness due to embolic occlusion of the top of the basilar artery branching into bilateral posterior cerebral arteries). His vision subsequently improved to leave a trace of left homonymous quadrantanopia (probable fragmentation of emboli and embolic occlusion of a branch of right posterior cerebral artery leading to infarction in the right inferior occipital region; fig 2).

The day after stroke onset, he developed probable right occipital seizure with secondary generalisation (visual hallucination in his left hemifield followed by generalised tonic clonic limb movements), which was treated with a short course of anticonvulsant (levetiracetam). Echocardiography found no intramural cardiac thrombus, wall motion abnormalities, atrial septal defects, chamber enlargement, or valvular abnormalities. There was no evidence of deep venous thrombosis in his legs. After initial stabilisation, he was started on dabigatran. Statin and insulin were continued. Since then, he has been followed up regularly in the cardiology and neurology outpatient clinics.

In a patient with paroxysmal or persistent non-valvular atrial fibrillation, the CHADS2-VASc score is recommended for the assessment of stroke risk (class I recommendation; evidence level A). In patients who present with focal neurological deficits, an acute ischaemic stroke as a result of thromboembolism should be considered first (unless the patient has haemodynamically significant arterial stenosis or acute lacunar stroke). Long term oral anticoagulants are recommended to prevent future stroke (class I recommendation; evidence level A).5


Cite this as: BMJ 2013;346:f2163


  • Competing interests: The author has completed the ICMJE uniform disclosure form at www.icmje.org/coi_disclosure.pdf (available on request from the corresponding author) and declares: no support from any organisation for the submitted work; no financial relationships with any organisations that might have an interest in the submitted work in the previous three years; no other relationships or activities that could appear to have influenced the submitted work.

  • Provenance and peer review: Not commissioned; externally peer reviewed.

  • Patient consent obtained.


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