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Brain & Heart Thrombosis, essential thrombocythemia, and recurrent stroke
A B C D
Figure 2. Computed tomography (CT) and magnetic resonance angiogram including vessel wall imaging. (A and B) CT angiogram showing good
collaterals and robust bilateral posterior communicating arteries (blue arrows). (C and D) Magnetic resonance imaging showing thrombus in the proximal
basilar artery (blue arrows) but no significant finding in the vessel wall imaging.
A B C
Figure 3. Magnetic resonance imaging revealed evolving acute infarct at left paramedian pons and right lateral aspect of pons adjacent to cerebellar
hemisphere. (A) Magnetic resonance angiography; (B) computed tomography angiogram; (C) revealed the site of basilar thrombus (marked by blue
arrows).
The angiogram this time revealed the same findings as the treating physicians and his family decided against it as
during the previous admission. A repeat MRI of the his condition showed improvements. The following variables
brain revealed the new infarct at the pons (at the left were used to help distinguish ICAD in the current case:
paramedian pons and right lateral aspect of the pons location of thrombus in proximal basilar artery (classic for
next to the cerebellar hemisphere, where it was evolving ICAD-related occlusion), persistent distal basilar artery filling
during this presentation) with no evidence of bleeding. because of good posterior communicating artery (Figure 2),
Despite the mild fluctuations in clinical symptoms, with the 2 stroke in middle cerebellar peduncle (classic location
nd
an obvious speech impediment, his NIHSS score remained of watershed infarct in posterior circulation secondary to
at two, showing stable vitals. A 48-h Holter monitoring ICAD), and rapid improvement in both occasions (despite
and echocardiography did not yield remarkable findings. failed recanalization of occluded basilar artery), which pointed
Thus, considering the possibility of antiplatelet resistance, toward transient collateral failure because of hemodynamic
we then replaced clopidogrel with ticagrelor (90 mg twice compromise, which was possible in this situation.
daily) while maintaining the same medications, such as In both occasions, the patient showed improvements
aspirin and high-dose statin for the patient. On the 4 day, post-thrombolysis, concurrent with an NIHSS score
th
the patient was given enoxaparin 40 mg twice daily (at a drop from almost 18 to 2, without any hemorrhagic
lower dose to avoid bleeding episode) along with ticagrelor transformation. There were intact flows proximal and
and statin (aspirin was stopped), to dissolve the thrombus; distal to the thrombus, which indicate a possible chronicity
his condition was put on close monitoring. We did an MRA of the thrombus. In light of this, we did not proceed with
with vessel wall imaging but found no enhancement of the endovascular therapy in any occasion, and fortunately, the
vessel wall or any additional findings. During follow-up, patient successfully recovered afterward. After 8 months
his condition remained stable with apixaban 5 mg twice of follow-up, he experienced no further deterioration.
daily (replacement of enoxaparin) and ticagrelor and The findings of a repeat MRI of the brain with vessel wall
atorvastatin 80 mg. imaging remained unchanged (Figure 2).
st
nd
Sixteen days after the 1 stroke, the 2 stroke happened,
which was suspected through the ICAD detection and based 3. Discussion
on the failure of the conservative treatment administered. Essential thrombocythemia is a myelodysplastic syndrome
Basilar stenting was considered for treating the patient, but and represents a rare cause of stroke where both the
Volume 2 Issue 3 (2024) 3 doi: 10.36922/bh.3741

