Unusual presentation of more common disease/injury

Case report

Cortical laminar necrosis in a case of migrainous
cerebral infarction
Vikram Khardenavis,1 Davala Krishna Karthik,2 Sharvari Kulkarni,3
Anirudda Deshpande4
1

Miraj Medical College, Miraj,
Maharashtra, India
2
Department of Radiology,
Surya Diagnostics, Warangal,
Telangana, India
3
Maharashtra Institute of
Medical Education and
Research, Pune, Maharashtra,
India
4
Department of Neurology,
Vinayaka Neuro Multispecialty
Clinic, Warangal, Telangana,
India
Correspondence to
Dr Anirudda Deshpande,
​dr.​anirudda.​deshpande@​gmail.​
com
Accepted 16 March 2018

Summary
We report a 27-year-old woman, a known case of
classical migraine headache, on oral contraceptive pills.
She had a severe episode of migraine with visual aura
attack, which continued late into the night. The next early
morning, her headache persisted and she developed
abrupt onset of dysarthria, right hemiparaesthesias. She
attributed symptoms to her long-standing headache
problem, and hence did not seek medical help for
the next two weeks. The symptoms persisted despite
her headache subsiding over the next 24 hours. She
worsened 2 weeks later during another such episode of
headache. This time, she developed right hemiparesis.
The patient was admitted with provisional diagnosis of
stroke. MRI of the brain showed left temporoparietal
lesion and was radiologically compatible with cortical
laminar necrosis.Extensive work-up was done to rule
out other causes of young stroke. The patient improved
with antiplatelets, antimigraine prophylaxis and stroke
rehabilitation therapy.

Background

Cortical laminar necrosis (CLN) is a less common
form of infarction where there is a selective pan-necrosis of cerebral cortex comprising glia, neuron
and blood vessels with relative or absolute sparing
of underlying white matter. It is frequently associated with hypoglycaemic or hypoxic encephalopathy, in some cases of status epilepticus. It is rarely
associated with migrainous infarction.

Case presentation

We report a 27-year-old female patient, with history
of hemicranial headaches since her adolescence.

Often, the episode of headache used to be preceded
by visual perceptions of bright star-shaped objects
‘floating’ in front of her eyes. These symptoms
usually lasted for a few minutes. Other associated
features during the episodes of headache were photophobia, phonophobia and severe nausea. The episode
of headache usually lasted more than 4–6 hours on an
average, sometimes 1–2 days. She was never on any
medication for migraine prophylaxis or triptans for
acute episodes of migraine. She recalled her mother
having episodes of such severe headaches on and off
for many years. There was no history of alcohol,
nicotine and narcotic substance abuse. On the
evening before the fateful day, she had a prolonged
episode of migraine (preceded by visual aura) which
continued into early next morning for 24–36 hours.
With ongoing headache, she developed dysarthria
along with paraesthesias of right half of the body, a
day after the onset of her headache. She did not seek
medical help for 2 weeks. On experiencing weakness
in right upper and lower limb after 2 weeks from the
primary event, she decided to visit the hospital. On
examination, vitals were normal and her National
Institutes of Health Stroke Scale was 4, suggestive of
minor stroke.
Her Rankin scale was +2 as she had slight
disability such that she was unable to carry out all
previous activities, but able to look after her own
affairs without assistance. The patient also had left
upper motor neuron facial paralysis, left pronator
sign. There was no evidence of neck stiffness.
Clinical diagnosis of cerebrovascular accident was
made. MRI of the brain showed gyral enhancement
in the left temporoparietal region (figures 1–3).
The patient was extensively evaluated for various
causes leading to stroke in young; however, these
tests were negative. The patient responded favourably to antiplatelet medication and antimigraine
medication.

Investigations

To cite: Khardenavis V,
Karthik DK, Kulkarni S, et al.
BMJ Case Rep Published
Online First: [please
include Day Month Year].
doi:10.1136/bcr-2017221483

Figure 1 MRI of the brain with contrast (axial view)
showing gyral enhancement in the left temporoparietal
area, suggestive of cortical laminar necrosis.

Chest roentgenography, 12-lead electrocardiography, two-dimensional echocardiography, bilateral
carotid Doppler, routine haematological screening,
routine biochemical profile, urinalysis, serology for
syphilis, HIV, ELISA, immunological blood tests
(extractable nuclear antigen, antinuclear antibodies,
lupus anticoagulant, IgG and IgM anticardiolipin
antibodies, rheumatoid factor) and procoagulant
panel (protein C&S, antithrombin 3, factor V
Leiden mutation and homocysteine).

Khardenavis V, et al. BMJ Case Rep 2018. doi:10.1136/bcr-2017-221483

1

Unusual presentation of more common disease/injury

Figure 2 MRI of the brain with contrast (coronal view) showing gyral
enhancement in the left temporoparietal area, suggestive of cortical
laminar necrosis.

Differential diagnosis

Demyelinating lesion, space-occupying lesion and venous infarct
secondary to cerebral venous thrombosis.

Treatment

Antiplatelet medication (aspirin) 150 mg once daily in the afternoon (after lunch), antimigraine medication (topiramate 25 mg
twice daily, flunarizine 10 mg once daily, naproxen 500 mg if
needed).

Outcome and follow-up

The patient responded favourably to antiplatelet medication,
antimigraine medications and physiotherapy.

Discussion

Migraine headache is a known yet less common cause of stroke
in young. Little is known about the exact demographics, and
statistical association between CLN and migrainous stroke is
not known; however, such previous study, with data extrapolated over 19 years, shows that only 10 of the 3808 consecutive

patients with stroke fulfilled the necessary criteria for migrainous
stroke and amounts to roughly 0.26% of total cases.1
Ischaemic strokes are more common than intracranial bleeds.
Around 40% of the cases had an active migraine attack while
they had the stroke.2 Classical migraine (with aura) is more
predisposed to vascular insufficiency than those who have simple
migraine headache.3 The exact pathophysiology of migrainous
infarction is not known. However, some of the possible mechanisms include vascular changes related to cortical spreading
depression vasospasm and hypercoagulability.4 5 Oxidative
stress-induced endothelial dysfunction may be a cause and effect
of migraine, leading to stroke.6 Migrainous stroke presenting
radiologically as CLN has been infrequently reported.7 8 CLN
has been noted in cases with metabolic disturbances, cerebral
hypoxia, drugs and infections. Potential mimickers for such
clinical presentation are mitochondrial encephalopathy, lactic
acidosis and stroke-like episodes, Fabry’s disease and ‘arterial
dissection’. The radiological findings in CLN show cortical
hyperintensity on T1-weighted images, usually from 2 weeks to
approximately 2 years after ischaemia. Fluid-attenuated inversion recovery hyperintensities appear later in the course of
illness. The curvilinear ‘gyriform’ enhancement on gadolinium
contrast is attributed to breakdown of the blood–brain barrier
necrosis of the blood vessels.9 Migrainous infarcts causing CLN
could be explained theoretically that the endothelial dysfunction
can in turn lead to breakdown of the blood–brain barrier.10

Learning points
►► Migrainous infarction is a less common, but important cause

of ‘stroke in young’.

►► Migrainous infarcts present as cortical laminar necrosis, an

infrequent radiological finding.

►► Vascular changes related to cortical spreading depression

vasospasm and hypercoagulability are some of the possible
mechanisms postulated to cause migrainous infarct.

Contributors VK and DKK made substantial contributions to the conception and
design of the work, acquisition, analysis and interpretation of the data. AD and SK
was involved in drafting the work and revising it critically for important intellectual
content. All authors approved the final version to be published.
Funding The authors have not declared a specific grant for this research from any
funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Patient consent Obtained.
Provenance and peer review Not commissioned; externally peer reviewed.
© BMJ Publishing Group Ltd (unless otherwise stated in the text of the article)
2018. All rights reserved. No commercial use is permitted unless otherwise expressly
granted.

References

Figure 3 MRI of the brain with contrast (sagittal view) showing gyral
enhancement in the left temporoparietal area, suggestive of cortical
laminar necrosis.
2

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3	Tzourio C, Tehindrazanarivelo A, Iglésias S, et al. Case-control study of migraine and
risk of ischaemic stroke in young women. BMJ 1995;310:830–3.
4 Kurth T. Migraine and ischaemic vascular events. Cephalalgia 2007;27:965–75.
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7 Kinoshita T, Ogawa T, Yoshida Y, et al. Curvilinear T1 hyperintense lesions representing
cortical necrosis after cerebral infarction. Neuroradiology 2005;47:647–51.
8	Arboix A, Massons J, García-Eroles L, et al. Migrainous cerebral infarction in the
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Khardenavis V, et al. BMJ Case Rep 2018. doi:10.1136/bcr-2017-221483

Unusual presentation of more common disease/injury
9	Arboix A, González-Peris S, Grivé E, et al. Cortical laminar necrosis related to
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10	Abbott NJ, Rönnbäck L, Hansson E. "Astrocyte– endothelial interactions at the blood–
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Khardenavis V, et al. BMJ Case Rep 2018. doi:10.1136/bcr-2017-221483

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