Case presentation
A 47-year-old man was brought to a nearby hospital presenting with:
sudden vertigo; vomiting; and gradual right-sided hemiparesis that
eventually evolved to quadriparesis, without any previous medical
illness. Computed tomography of his brain revealed no abnormal densities
at the brainstem and a computed tomography angiogram (CTA) of his brain
revealed a proximal basilar artery occlusion. He was referred to our
institution 11 hours after initial onset under the basis of being
treated with mechanical thrombectomy. Upon arrival he was intubated but
was alert and keenly responsive. Neuroexamination showed left horizontal
opthalmoplegia, a motor power grade of 2/5 on the left side, and
hemiplegia on the right side that ultimately correlated to a National
Institute of Health Stroke Scale score of 21. A brain MRI shortly after
the examination demonstrated restricted diffusion at bilateral pons,
with greater restriction on the left side, including a restricted
diffusion at bilateral cerebellar hemispheres (figure1). Magnetic
resonance angiography (MRA) of his brain demonstrated the same findings
that were seen in the CTA. Following a discussion with his wife, we
agreed to continue with endovascular treatment. After two attempts of
stent retriever thrombectomy, complete recanalization was achieved
(figure2). Antiplatelet therapy was applied for 24 hours after the
procedure. The following day, an MRI and brain MRA follow up revealed
hypersignal intensity at bilateral pons and cerebellar hemispheres that
both appeared more distinctive than the initial MRI however remained
limited to the same region (figure3). Electrocardiography monitoring and
transthoracic echocardiogram were unremarkable. He was fed via
nasogastric tube, received daily physical therapy and was admitted in
the stroke unit for 12 days before being referred for further
rehabilitation at his previous hospital. He was discharged with an
evaluated NIHSS score of 18.
Neuroexamination one month
after his discharge revealed normal left horizontal opthalmoplegia, and
an improved left motor power grade of 4/5. However neither his right
side motor power nor his dysphagia had improved. At one-year, a
telephone and video call follow up had shown substantially improved
swallowing and his wife showed evidence of him being ambulant. One-year
MRI follow-up was not done since the patient lives far from our
institution and had trouble with transportation. However, the patient
was able to ambulate despite being previously being quadriplegic as a
result of the infarct, which had shown no evidence of improvement after
the MT was done – his ability to now live independently is diagnostic
in its own right.
Discussion At many stroke centers across the
world, acute BAO is commonly treated via endovascular therapy however it
is currently inconclusive as to what method of treatment is the best.
The current hypothesis of why this treatment works best on based upon
early recanalization. The recanalization rate of endovascular treatment
is far superior to that of intravenous thrombolytic drugs. This
implicates the more aggressive treatment to achieve the best outcome.
Despite the DWI and ADC that were positive in detecting restricted
diffusion, the treatment provided to our patient overcame that general
rule of the affected areas being irreversibly infarct. Only few reports
have shown restricted diffusion of DWI and ADC at the pons being
reversible – however these reports did highlight the uncertainty of
whether or not reversibility equates to a better clinical
outcome.3 Unlike these reports, our case uniquely
showed restricted diffusion of DWI and ADC at the pons before we
proceeded with the mechanical thrombectomy – with DWI, ADC and FLAIR at
24 hours showing an even more distinct infarct at the bilateral pons.
Despite the extensively established infarct at the pons, his condition
gradually improved until he was limitedly ambulant.
The amazing motor outcome of this bilateral pontine infarct could be
explained by the reorganization of the unaffected corticospinal and
corticobulbar tract (CST).4 Interestingly, the level
of the pontine infarct can determine several characteristics of the
motor outcome since different levels of the pons display different
characteristics of the CST. At the lower pons, the compactness of the
CST is higher than that of the upper pons – as it is measured in
fractional anisotropy (FA) – despite the upper pons having a larger CST
area.5 This suggests a linear neural structure of the
CST that increases in density from upper to lower which could also
clinically correlate to motor outcome.5 Upper pontine
infarcts have been reported to have better clinical outcomes than
patients with lower pontine infarcts.6 In our case,
the patient had a middle pontine infarction. In a report by Kim et al.,
it suggests that middle pons infarctions led to severe hemiparesis
whereas lesions of similar size in the paramedian rostral pons lead to
dysarthria and clumsy hand syndrome (DA-CH).7 This
demonstrates that different presentation of symptoms occur depending on
the level of pontine infarct.7 The limitation of this
report is that it is exclusively reporting single hemisphere pontine
infarcts however we can make a correlation to our patient if we approach
it as two single hemisphere pontine infarct cases rather than one
bilateral pontine infarct. Our patient had a greater defined lesion on
the left hand side which may be attributed to his severe right side
hemiparesis that still lingered a month after recanalization; similarly,
the lesser defined lesion on the right hand side may have led to his
quicker left side motor recovery of 4/5 with persistent dysarthria. This
supports both ideas of severe hemiparesis and DA-CH occurring depending
on the level of infarction. In a study by Zhang et al., findings
demonstrate that the CST was associated with motor function recovery
after 90 days of pontine infarction, but after 180 days the CST no
longer associated with such recovery, which suggests that recovery even
after severe pontine infarcts could result in motor
redevelopment.8 We can easily see this on our patient
where in the less severe right side lesion, recovery was achieved before
90 days and it may be attributed to CST reorganization, however on the
more severe left side lesion the patient only recovered full motor
function after a year which may suggest that the CST was not involved in
recovery anymore. Multiple instances of motor pathway salvaging were
found which has also been reported on many
occasions.8-11 Suggested mechanisms of this include
the peri-infarct CST taking over all motor function or even the lateral
CST dominating major movement. 9-11 We suggest that it
was the peri-infarct CST that assisted in motor recovery of the right
side lesion, since if the lateral CST were to assist in recovery then it
would also be involved as the peri-infarct CST of the left side lesion.
However since there was limited recovery a month after recanalization
with regards to the right side motor movements we refute this claim.
Additionally, since he didn’t have any previous medical illness and was
young those factors too might have contributed to his recovery. We
understand that conducting diffusion tensor imaging (DTI) would have
been highly diagnostic and would have provided substantial evidence
about the motor recovery of the patient however he had refused to come
in for a follow up MRI.
After the MT, his basilar artery had appeared normal without any
remaining stenosis. This leads us to suspect that the cause of the
stroke was likely from emboli of undetermined origins. Cumulatively,
with other reports that indicated restricted diffusion findings in a
bilateral pontine infarct, imaging solely may or may not predict a poor
clinical outcome hence, recanalization of an acutely occluded basilar
artery should be carefully considered. 12,13 More
studies are necessary to determine whether recanalization with
endovascular treatment or intravenous thrombolysis has a role in this
situation