Neurology

Left homonymous hemianopia:

Follow Up Questions/Answers

Could you present me with your findings, please?

• This patient has a left-sided homonymous hemianopia.
• Reduced left-sided sensation on her face.
• Reduced hearing on her left side as well.
• I would like to complete this examination by
o Taking a full history from the patient
o performing an upper and lower limb neurological examination
• The symptoms are most likely due to a right-sided middle cerebral artery infarct or
a lesion affecting the right hemisphere.
Thinking about your examination of the limbs, what other signs might you be interested
in?
• Increased tone
• Reduced power
• Hyperreflexia
• Any evidence of clonus.
Returning for a moment to the cranial nerve examination, you mentioned that she has a
visual field defect. Could you talk me through how the nature of that visual field defect
helped you localise the lesion?
• This visual field defect was a left-sided homonymous hemianopia which respected
the midline.
• Showed no evidence of macular sparing.
• If this were a posterior cerebral artery stroke, you would expect macular sparing.
This was not present on examination.
• More consistent with a middle cerebral artery stroke.
• Would also fit with the left-sided sensory changes.
Let us move away from the neurological examination and think of what other physical
signs we might want to look for in a case such as this.
• I would like to
o Palpate the patient's pulse.
o See if there is any irregularity to the pulse such as atrial fibrillation (can
increase your risk of stroke).
o Auscultate the carotids, listening for any evidence of a bruit (could indicate
stenosis in that vessel).
o Listen to the heart, auscultating for any evidence of a cardiac murmur
(could suggest valvular heart disease, increasing the risk of stroke further).
Are there any other measurements that could be done at the bedside which would be
important in assessing stroke risk?
• Blood pressure (hypertension is associated with stroke).
Let us move on and think a little about initial investigations. If this lady came into A&E with
these signs, how would you proceed?
• I would arrange an urgent CT brain (if this patient has no other contraindications on
history or examination)
• If the CT scan showed no evidence of haemorrhage, she could be a candidate for
thrombolysis therapy.
Neurology

What if it were a different situation, and she comes to your clinic in outpatients and this
was a more chronic scenario. How would you proceed under those circumstances?
• It would be important to arrange:
o A MR brain (characterise those changes in the right hemisphere)
o An ECG (see if the patient is in sinus rhythm)
o A blood pressure measurement
o A Carotid Doppler scan.
And what are the findings you might be interested in looking at on the carotid Doppler
scan?
• Looking for evidence of stenosis to see if that could be a cause of the stroke.
If you found stenosis, what action would that lead to?
• Look at the degree of stenosis within the carotid vessels.
• If suitable for endarterectomy therapy, then we could arrange that.
Now let us say we’ve done the ECG; this didn’t show an abnormality. We have done the
carotid dopplers and there was no significant stenosis. What further tests could you do to
investigate the cause of the stroke?
• Look more closely for evidence of paradoxical atrial fibrillation using a 24-hour or 5-
day heart monitor.
Let’s say we do that; we measure for 5 days and there is no evidence of paradoxical atrial
fibrillation. Are there any other tests we could do?
• Arrange an echocardiogram (looking for any structural cause for these symptoms).
Neurology
Left homonymous hemianopia:

Key Words and Phrases

In this neurology station the candidate was asked to examine the cranial nerves and the
principal finding was a visual field defect. There was also evidence of sensory loss on the
left side of the face. One of the potential pitfalls of this case is that despite being asked to
examine the cranial nerves, the lesion is in the right cerebral hemisphere. This is an
important lesson to learn: cranial nerve examination may reveal pathology that does not
affect the cranial nerves themselves.
The candidate rapidly established that there was a visual problem, so he performed a
detailed examination of that component and used a red hat pin to carefully map out the
visual field defect. Remember the sensitivity of field testing with a moving finger is only
about 50% - using a pin increases this sensitivity to nearer 80%. In this case a left
homonymous hemianopia was found and there was no evidence of macular sparing.
This is a helpful observation – in posterior cerebral artery strokes we see macular sparing
due to the occipital pole receiving blood supply from the middle cerebral artery, so this
complete field defect would be consistent with right middle cerebral artery ischaemia,
assuming a vascular aetiology.
Having identified this field defect, the good candidate will be on the lookout for other right
hemisphere signs. In this case the candidate found reduced sensation in the left side of the
face. It would be all too easy to attribute this to trigeminal nerve damage, especially as you
have been told to examine the cranial nerves. This is an example of ‘framing’ bias.
However, if you interpret the field defect correctly, it will be apparent to you that this loss
of sensation likely reflects right hemisphere cortical damage, consistent with the notion of
a right middle cerebral artery stroke.
There are two ways of establishing the sensory loss is not due to trigeminal neuropathy.
First, you could test sensation on the neck or some other site without the trigeminal nerve
distribution. Alternatively, you could check the corneal reflex; this will be lost in cases of
trigeminal neuropathy but remains intact when the sensory loss is due to hemispheric
damage.
The remainder of the examination was unremarkable, and as is usually the case the lower
cranial nerves take much less time to examine than the visual components. There was mild
reduction in left-sided hearing, although this is unlikely to be related. However, new
unilateral hearing loss should always be taken note of and investigated.
The candidate performed a fluent and comprehensive cranial nerve examination on this
patient. He did not take the opportunity to check saccadic eye movements, but, due to the
dense field defect this would have been a difficult test to perform. It is worth remembering
that horizontal saccadic eye movements are a sensitive way to check for internuclear
ophthalmoplegia and vertical saccades can reveal early signs of a vertical supranuclear
gaze palsy.
The findings in this examination are not particularly subtle, so as an examiner I would be
expecting the signs to be picked up correctly and for an accurate diagnostic formulation to
be made. The presence of a left-sided visual field defect and left-sided sensory loss clearly
localise the lesion to the right hemisphere. The nature of the field defect, sharply
respecting the midline with macular sparing, is strongly suggestive of an ischaemic
aetiology.
It is, therefore, quite possible to conclude that the patient has had a partial middle
cerebral artery ischaemic stroke. We can say it is partial based on the absence of a clear
left-sided weakness. There is a differential diagnosis, and in principle other right
hemisphere lesions could produce these signs.
Neurology

Having found these signs, there are some other features that I would expect a good
candidate to look for. I would expect them to suggest proceeding to limb examination to
look for other signs of stroke – increased tone, weakness, sensory loss, hyperreflexia.
In addition to this, it would be appropriate to look for any evidence of the likely aetiology.
Simple bedside measures would include checking the pulse for atrial fibrillation, listening
to the heart for murmurs and auscultating for a right carotid for bruit. We would also
measure blood pressure and check the urine for glucose.
In a station such as this it would be reasonable to ask the candidate for a plan or
investigation. It makes sense to initially confirm the primary diagnostic hypothesis. This will
require cranial imaging; in the acute setting a CT brain scan is the investigation of choice,
but if this was a subacute or chronic situation a MRI brain scan would be the better option.
If the initial tests confirm ischaemic stroke, the next stage would be to investigate its
aetiology. This would mean getting carotid dopplers, as this is an anterior circulation
stroke. An echocardiogram can be performed to look for any evidence of cardiac
thrombus, and prolonged ECG monitoring is used to look for arrhythmias, specifically
paroxysmal atrial fibrillation.
Alternatively, the examiner may accept the diagnosis of ischaemic stroke and ask for a
treatment plan. This will depend on how acute the situation is. In the hyperacute scenario
attention needs to be given to the possibility of thrombolysis. In the longer-term one’s
thoughts need to turn to secondary prevention and addressing vascular risk factors. This
would mean consideration of anti-platelet therapy, a statin and an ACE inhibitor.