Clinical Correspondence

Occipital ischaemic stroke after visual
snow phenomenon – a case report

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! International Headache Society 2021
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DOI: 10.1177/0333102420985444
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Teresa Catarci

Abstract
Background: Persistent migraine with aura and neuroimaging examinations revealing ischaemia in the contralateral
cortex may be associated with migrainous infarction. Despite being a neurological symptom that is distinct from migraine
with aura, the visual snow phenomenon may also be associated with cerebral ischaemia. Here we describe a patient who
reported short-lasting daily symptoms of visual snow that affected his entire visual field before becoming continuous and
left-sided following acute occipital brain ischaemia.
Case report: In February 2017, a 74-year-old retired male was referred to our headache outpatient clinic with a
diagnosis of recent right occipital cerebral ischaemia and migraine with aura. The patient reported visual snow symptoms
that had changed from being bilateral and temporary to left-sided and permanent one day upon awakening; after being
admitted to hospital a few hours later, he discovered he had had a stroke. He said he had never had any symptoms of
migraine with aura. The visual snow phenomenon disappeared completely after about 1 year.
Conclusions: In our patient, a temporary daily visual snow phenomenon reversed to a persistent one. This phenomenon occurred in the part of his visual field that had been affected by the ischaemic occipital stroke, as typically happens
in migrainous infarction. We hypothesise that the occipital lesion disrupted the inhibitory circuits, leading to a quadrantopic persistent visual snow. Since the mechanism may be the same as that observed in migrainous infarction, though
with a different pathophysiology, it is possible to speculate that the aura in this case is the result, as opposed to the
cause, of stroke in most patients.
Keywords
Visual snow, migraine with aura, migrainous infarction, case report
Date received: 1 April 2020; revised: 11 November 2020; accepted: 3 December 2020

Introduction
Visual snow (VS) has recently been clinically characterised as a pan-field visual disturbance described as constant tiny dots resembling the noise of a detuned
analogue television. Although VS is reported to be a
distinct disorder from migraine with prolonged aura
(1), the latter is one of the most frequent misdiagnoses
in patients suffering from VS (2).
Migrainous infarction is a rare type of stroke. It is
considered a complication of migraine when one or
more than one aura symptom, during a typical
migraine with aura attack, is associated with an ischaemic brain lesion in the appropriate territory, as demonstrated by neuroimaging (3).
We describe a patient who reported short-lasting
daily symptoms of VS in his entire visual field for
about 40 years. One day he awoke with a continuous

left-sided VS phenomenon and was diagnosed as
having had a right occipital stroke. To the best of
our knowledge, this is the first report of an ischaemic
stroke after VS and one that raises important considerations about the pathophysiology of this
phenomenon.

Headache Outpatient Clinic, Azienda Sanitaria Locale Roma 1, Rome,
Italy
Corresponding author:
Teresa Catarci, Headache Outpatient Clinic, Azienda Sanitaria Locale
Roma 1, Poliambulatorio Luzzatti, Via Luzzatti 8, 00185 Rome, Italy.
Email: teresa.catarci@aslroma1.it

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Case report
In February 2017, a 74-year-old male was referred to
our headache outpatient clinic with a diagnosis of previous cerebral ischaemia due to migraine with aura. He
had a history of hypertension and hypercholesterolemia, both of which had successfully been treated by
means of telmisartan, ezetimibe and omega 3.
In 2011 he had undergone radiotherapy to treat
vocal cord cancer. Worthy of note is the fact that he
had stopped taking low-dose aspirin in 2014 because of
a peptic ulcer. In March 2016; that is, 1 year before
coming to our outpatient clinic, he had been admitted
to the emergency department owing to persistent visual
symptoms that had started 8 h before. The emergency
neurologist interpreted them as “flickering lights”. As
the neurological examination disclosed a left visual
field impairment, the patient was admitted to the neurological ward and was diagnosed with possible protracted migraine aura without headache. He underwent
an ECG, epiaortic vessel sonography and an EEG, all
of which were unremarkable. MRI with medium contrast and angio-MRI disclosed a right posterior occipital hyper-intense lesion in fluid-attenuated inversion

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recovery (FLAIR) images due to occlusion of a posterior cerebral artery (medial occipital branch) and an
acute ischaemic stroke in diffusion-weighted images
(Figure 1).
He was discharged 6 days later with a diagnosis of
cerebral ischaemia and was prescribed antiplatelet
treatment with clopidogrel.
A few weeks after discharge, paroxysmal atrial
fibrillation was detected by 24-h ECG and the patient
was prescribed novel anticoagulants instead of clopidogrel. One month later, a computerised visual field
detected superior left homonymous quadrantopia.
When we first examined the patient, he said that
ever since he had been in his 30s, he had had sudden
attacks of impaired vision. These attacks lasted
approximately 5 min and were similar to a badly
tuned TV channel with little spots moving in the
entire visual field, with the occasional vision of floaters
and afterimages, which caused little or no disability.
Prior ophthalmological tests had, according to the
patient, been normal. He also stated that he had never
had any significant headaches or migraine with aura.
Following the stroke, the VS symptoms became persistent and localized in his left upper visual field.

Figure 1. MRI images without medium contrast showing restricted diffusion-weighted scans of the right posterior occipital region as
per acute ischaemia.

Catarci
Although he no longer saw floaters, he told us that he
had suffered from tinnitus for the last couple of years.
In contrast to the emergency neurologist’s report, he
told us that he had never seen any flickering lights. In
addition to confirming the presence of the visual field
impairment, the neurological examination disclosed
bilateral hypoacusia with left tinnitus. We therefore
made a diagnosis of persistent VS phenomenon secondary to an occipital stroke. A control MRI and visual
field were performed, though the result remained
unchanged. When the patient returned to the clinic
nine months later; that is, 2 years after the stroke, referring temporary diplopia lasting about 1 min, he was readmitted to the hospital for a further evaluation. The
neuroimaging examination was again unchanged
though his folate levels were found to be lower than
when he had previously been admitted. It was noteworthy that the patient no longer perceived the VS, whether permanent or temporary, whereas the visual loss
remained unchanged. The patient was oblivious to
exactly when the phenomenon had subsided but
retained a vague memory of the VS owing to the disabling effect of the lack of vision.

Discussion
We describe, for the first time, a patient in whom a
temporary daily VS phenomenon reversed to a persistent phenomenon and was temporally associated with a
contralateral ischaemic occipital stroke. This has also
been reported to occur in migrainous infarction.
Although typical VS is described as continuous, we
believe that the visual symptoms in our patient before
the stroke fulfil most of the diagnostic criteria. When
he had a thromboembolic stroke, which is likely to
have been due to paroxysmal atrial fibrillation, he
was not taking any antiplatelet treatment. He developed a symptomatic VS phenomenon, similar to the
one he had previously experienced, localised this time
in his upper left visual field. We believe that the VS he
had previously experienced may be interpreted as a
temporary and global imbalance in inhibitory visual
circuits; that is, with the stroke resulting in a localised
permanent disruption. This hypothesis is supported by
recent data showing that the metabolism of the lingual
gyrus, which is one of the cerebral areas supplied by the
medial branch of the posterior cerebral artery, is
altered in VS patients (4).
About 1.5 years after the stroke, the patient still complained of visual impairment in his upper left visual field
whereas the VS phenomenon persisted for approximately 1 year before disappearing. Interestingly, even the VS

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experienced by our patient prior to the stroke did not
reoccur, a finding that may be due to the rearrangement
in visual circuitry described in some patients with
Charles Bonnet Syndrome (5). A recent paper on the
long-term follow-up in patients with migrainous infarction also reported a good functional outcome (6). A
recent retrospective analysis of a cohort of 58 patients
with VS did not report any vascular complications,
whereas anxiety and depression were frequently found
to coexist (7).
Migraine with aura and the VS phenomenon are two
distinct neurological symptoms that may be due to two
different pathophysiological mechanisms: a) Cortical
spreading depression and cerebral hypoperfusion in
the former (8); b) visual cortex hyperexcitability and
hyperperfusion in the latter (9).
In spite of this, the case we describe here suggests
that VS, like migraine aura, may be symptomatic of
stroke. Although migrainous infarction is believed to
be caused above all either by a spontaneous artery dissection or microembolism producing protracted oligoemia (10), our patient had clearly had a thromboembolic
stroke. It is therefore possible that the imbalance that
was observed in our patient – between visual cortical
inhibition and excitation due to the ischaemia of the
lingual gyrus – resulted in the VS, while the infarct in
the primary visual cortex caused the quadrantopic
visual loss. Patients with VS have been reported to display an imbalance of this nature (11), which suggests
that such patients may be more susceptible to a permanent VS phenomenon when an ischaemic insult occurs.
Migrainous infarction is, like VS infarction, a rare
condition. It accounts for only 0.32–1% of all strokes
in a recent series (12), while migraine with aura and the
VS phenomenon are considerably more common conditions. We hypothesise that the actual prevalence of
migrainous infarction may be even lower. It is possible
that patients with migraine with aura, like those with
VS, are more likely to develop visual symptoms during
occipital ischaemia and that the majority of migraines
with aura are the effect rather than the actual cause of
the stroke.
An increased awareness of VS phenomena among
neurologists may lead to more cases like ours being
disclosed, as well as to a more precise diagnosis and
characterisation of the clinical picture.
Our case raises two important clinical considerations: first, although VS is a neurological entity that
is distinct from migraine with aura, it may on occasion
be associated with a stroke in the occipital territory;
second, migrainous infarction might be a far rarer condition than is currently believed.

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Clinical implications
• Although VS is reported to be a neurological entity distinct from migraine with aura, occasionally it can
also be associated with a stroke in the occipital territory.
• Migrainous infarction might be a far much rarer condition than is currently believed.

Acknowledgements
The author wishes to thank Prof. Maurizio Corbetta for the
illuminating discussion about visual cortex physiopathology,
Ms Rosalinda Spallone for collaborating on the first English
version of the paper and Mr Lewis Baker for the final corrections. MRI scans courtesy of Dr Antonio Salerno of S.
Giovanni Hospital, Rome.

Consent
Written informed consent was obtained.

Declaration of conflicting interests
The author declared no potential conflicts of interest with
respect to the research, authorship, and/or publication of
this article.

Funding
The author received no financial support for the research,
authorship, and/or publication of this article.

References
1. Schankin CJ, Maniyar FH, Digre KB, et al. ‘Visual snow’
– a disorder distinct from persistent migraine aura. Brain
2014: 37; 1419–1428.
2. Robbins MS. Comment: Time for neurologists to see
visual snow. Neurology 2019: 93; 153.
3. Olesen J. Headache Classification Committee of the
International Headache Society. The International
Classification of Headache Disorders, 3rd edition.
Cephalalgia 2018: 38; 1–211.

4. Puledda F, Ffytche D, Lythgoe DJ, et al. Insular and
occipital changes in visual snow syndrome: A BOLD
fMRI and MRS study. Ann Clin Trans Neurol 2020; 7:
296–306.
5. Pang L. Hallucinations experienced by visually impaired:
Charles Bonnet Syndrome. Optom Vision Sci 2016; 93:
1466–1478.
6. Serrano F, Arauz A, Uribe R, et al. Long-term follow-up
of patients with migrainous infarction. Clin Neurol
Neurosurg 2018: 165; 7–9.
7. Van Dongen RM, Waaijer L, Onderwater GLJ, et al.
Treatment effects and comorbid diseases in 58 patients
with visual snow. Neurology 2019; 93: 1–6.
8. Lauritzen M. Pathophysiology of the migraine aura. The
spreading depression theory. Brain 1994; 117: 199–210.
9. Fatma Gokcem Yildiz FG, Turkyilmaz U and UnalCevik I. The clinical characteristics and neurophysiological assessments of the occipital cortex in Visual Snow
Syndrome with or without migraine. Headache 2019;
59: 484–494.
10. Olesen J, Friberg L, Olsen TS, et al. Ischaemia-induced
(symptomatic) migraine attacks may be more frequent
than migraine-induced ischaemic insults. Brain 1993;
116: 187–202.
11. McKendrick AM, Chan YM, Tien M, et al. Behavioral
measures of cortical hyperexcitability assessed in people
who experience visual snow. Neurology 2017; 88:
1243–1249.
12. Wolf ME, Szabo K, Griebe M, et al. Clinical and MRI
characteristics of acute migrainous infarction. Neurology
2011; 76: 1911–1917.