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Clinical neurology

CASE REPORT

Posterior reversible encephalopathy syndrome with
thalamic involvement during vasopressor treatment
of vertebrobasilar vasospasm after subarachnoid
hemorrhage
Thomas Philip Madaelil,1 Rajat Dhar2
1

Department of
Neuroradiology, Mallinckrodt
Institute of Radiology,
Washington University School
of Medicine, St Louis, Missouri,
USA
2
Department of Neurology,
Washington University School
of Medicine, St Louis, Missouri,
USA
Correspondence to
Dr Thomas Philip Madaelil,
Department of Neuroradiology,
Mallinckrodt Institute of
Radiology, Washington
University School of Medicine,
St Louis, MO 63110, USA;
madaelilt@mir.wustl.edu
Republished with permission
from BMJ Case Reports
Published 11 December 2015;
doi:10.1136/bcr-2015-012103

ABSTRACT
Hemodynamic augmentation is the primary medical
intervention employed to reverse neurological deficits
associated with vasospasm and delayed cerebral
ischemia following aneurysmal subarachnoid
hemorrhage. Failure to improve despite induced
hypertension (IH) may raise concern for persistent
hypoperfusion and prompt even more aggressive blood
pressure augmentation. However, posterior reversible
encephalopathy syndrome (PRES) is a hyperperfusion
syndrome reported as a rare complication of IH that may
confound this picture. We report a case of PRES with
prominent thalamic involvement and impaired level of
consciousness secondary to blood pressure augmentation
for the treatment of symptomatic vertebrobasilar
vasospasm. Recognition of this syndrome in distinction
to worsening ischemia is particularly critical, as
normalization of blood pressure should lead to rapid
clinical improvement.

Accepted 2 November 2015

BACKGROUND
Hemodynamic augmentation, primarily consisting
of induced hypertension (IH), forms the cornerstone of medical therapies to improve cerebral perfusion and reverse delayed cerebral ischemia (DCI).
A number of complications of IH are well recognized, primarily cardiopulmonary decompensation
and hemorrhagic transformation of stroke.
Hypertensive encephalopathy attributable to breakthrough of cerebral hyperperfusion and development of cerebral edema (including the characteristic
posterior reversible encephalopathy syndrome
(PRES) pattern of white matter change) has also
been reported in a few cases. Recognition of PRES is
critical in this setting, as worsening mental status in
the setting of DCI may be misattributed to worsening vasospasm and ischemia. In response, blood
pressure may be further raised, placing the patient at
risk of irreversible complications like intracranial
hemorrhage. Instead, blood pressure needs to be
cautiously lowered to reverse edema while avoiding
recurrence of ischemia. Thalamic involvement is
rare in PRES and may lead to further diagnostic confusion, especially in the setting of vertebrobasilar
(VB) vasospasm and altered level of consciousness.
To cite: Madaelil TP,
Dhar R. J NeuroIntervent
Surg 2016;8:e45.

CASE PRESENTATION
A 55-year-old man presented with Hunt and Hess
grade 4 diffuse (modified Fisher 4) subarachnoid

hemorrhage and was found to have a distal superior cerebellar artery aneurysm which was subsequently coil occluded. His neurologic examination
improved after ventriculostomy placement for
hydrocephalus; he was extubated on post-bleed day
2 and was able to follow commands at that time.
His seizure prophylaxis was discontinued on postbleed day 3. On day 7 he was more lethargic and
underwent conventional cerebral angiography that
revealed moderate bilateral vasospasm of M1 and
A1 branches, and he was treated with intra-arterial
verapamil. Phenylephrine infusion was started concurrently for reversal of DCI, with the goal of
raising mean arterial pressure (MAP) from a baseline
level of 80–100 mm Hg to 110–120 mm Hg and
subsequently to 120–130 mm Hg, at which point
his examination improved; he was more alert and
able to respond and follow commands. He was subsequently weaned off pressors but a few days later
his mental status again worsened. Repeat angiography on day 12 revealed worsened vasospasm in
the VB system, which was treated with intra-arterial
verapamil. Vasopressors were restarted and MAPs
raised to 130–140 mm Hg. This time his neurologic
deficits did not improve and he underwent EEG
monitoring to exclude non-convulsive seizures. No
seizures were detected and pressors were continued.
The next day he underwent repeat angiography to
reassess vasospasm; this showed persistent posterior
circulation narrowing, again treated with verapamil.
On returning to the ICU after angiography, he had a
generalized tonic-clonic seizure with further worsening of mental status requiring intubation and
reinitiation of anticonvulsants.

INVESTIGATIONS
Head CT (figure 1) on the day prior to his seizure
showed hypodensity in the posterior white matter
with subtle left thalamic hypodensity. MRI (figure
2) performed after the seizure confirmed severe
bilateral posterior-predominant FLAIR-positive
diffusion-weighted imaging-negative signal abnormality
with
prominent
bilateral
thalamic
involvement.

DIFFERENTIAL DIAGNOSIS
At the time that his mental status continued to
worsen despite attempts to reverse deficits with IH,
the primary concern was for refractory DCI and
worsening vasospasm. Hypodensity on CT could

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Clinical neurology
lowered further and more aggressively. He was weaned off
phenylephrine and MAP returned to baseline levels (80–
90 mm Hg) over 6–12 h.

OUTCOME AND FOLLOW-UP
By the next day the patient was waking up easily, regarding, and
starting to respond to commands. He was extubated and able to
converse, swallow, and ambulate within 24 h. He had no further
seizures and follow-up imaging 1 week later showed resolution
of signal changes, confirming the presumptive diagnosis of
PRES. The patient was discharged to an acute rehabilitation
facility 2 weeks later.

DISCUSSION

Figure 1 Non-contrast head CT performed to investigate the cause of
decreased mentation showing ill-defined posterior occipital hypodensity
(originally interpreted as ischemic change secondary to vasospasm)
(black arrows) and subtle left thalamic hypodensity secondary to
vasospasm. However, clinical suspicion for posterior reversible
encephalopathy syndrome (PRES) existed.

represent early changes of cerebral ischemia, although the
pattern was atypical. Involvement of the thalamus could represent ischemia relating to his known VB vasospasm. However,
given the symmetric posterior white matter abnormalities, PRES
was raised as an alternative diagnosis. This was confirmed by
MRI which ruled out primary cytotoxic ischemia causing bilateral thalamic signal abnormalities. Instead, the combination of
radiographic findings and lack of improvement at higher MAP
was highly suggestive of PRES.

TREATMENT
The patient was cautiously weaned off vasopressors, initially to
lower MAP to 110–120 mm Hg. Once MRI was performed to
exclude ischemia and confirm PRES, MAP targets were then

Blood pressure augmentation is commonly used to treat DCI.
However, awareness of treatment-related side effects should
guide titration of vasopressors. PRES is especially critical since it
is not often considered at first, but is a readily reversible cause
of altered mental status during IH treatment that may mimic
worsening DCI. Nine cases of PRES caused by hemodynamic
augmentation for treatment of vasospasm have been reported.1–
6
To our knowledge, this is the first case to prominently involve
the thalami in this setting. Although many theories have been
suggested in the pathogenesis of PRES, autoregulatory failure
with hyperperfusion is felt to be the most likely cause with
hypertension.7 PRES most commonly involves the posterior
white matter of the cerebral hemispheres, most apparent as
FLAIR hyperintensity in the parietal and occipital lobes.8
Thalamic involvement, although not common, may be seen in
up to 30% of cases.9 Additionally, a central PRES variant that
lacks typical parietal-occipital changes but almost always
involves the thalamus with basal ganglia and/or the brainstem
FLAIR hyperintensity has been described.10 Interestingly, lack of
sympathetic innervation of the posterior circulation may explain
the failure of autoregulation and increased risk of the syndrome
in VB territories.11 This pathophysiologic mechanism may have
tipped the scales in favor of hyperperfusion and PRES, with the
vasodilatory effect of intra-arterial verapamil superimposed upon
hemodynamic augmentation in an effort to maintain vessel
patency and perfusion in our patient with DCI. His presentation
with a seizure may be another clinical clue, as seizures are rare in

Figure 2 FLAIR and
diffusion-weighted images (A–D) from
brain MRI obtained immediately after
seizure post-angiography for treatment
of vertebrobasilar vasospasm showing
severe bilateral parieto-occipital (white
arrowheads) and left greater than right
thalamic (black arrows) FLAIR positive
signal abnormality. A small left
thalamic stroke (C) is present on the
diffusion-weighted image (white
arrow). Follow-up MRI performed
8 days later after cessation of
hemodynamic augmentation and
improved clinical mentation (E–H)
shows resolving FLAIR posterior white
matter changes and small residual left
thalamic infarct consistent with
posterior reversible encephalopathy
syndrome (PRES) with central thalamic
involvement.
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Clinical neurology
DCI but common with PRES. Including our case, seizures may
account for 20% of the initial presenting clinical signs for hemodynamic augmentation-induced PRES.1–7 Another contributing
factor could be the possible seizure-provoking effects of
intra-arterial verapamil. Only two cases of intra-arterial
verapamil-induced seizures for the treatment of symptomatic
vasospasm have been reported.12 13 Immediate reperfusion to
ischemic brain (with VB vasospasm) and/or acute hyperperfusion
are possible culprit mechanisms for seizure in this setting. This
phenomenon has also been reported in thrombolysis for acute
ischemic stroke where successful vessel recanalization and clinical
recovery is heralded by a seizure.14 15 The third clue was based
on imaging, as posterior cerebral hypodensity on head CT in the
setting of acute decompensation and hypertension fit the clinical
picture of PRES rather than ischemia/infarction.

Key messages
▸ Posterior reversible encephalopathy syndrome (PRES) should
be considered with hypertensive treatment of vasospasm,
especially if seizure or worsened mentation occurs with
greater hemodynamic augmentation and hypodensity is not
in the typical vascular territory or in a bilateral posterior
distribution.
▸ Thalamic and basal ganglia involvement in PRES may lead
to prominent disturbances in consciousness.
▸ Rapid reversal of deficits (and normalization of MRI) with
removal of the offending agent confirms a diagnosis of PRES.
▸ Although rare, intra-arterial verapamil can induce seizures
probably through an ischemic-reperfusion mechanism.

Patient consent Obtained.
Provenance and peer review Not commissioned; externally peer reviewed.

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Contributors Both authors contributed equally to the preparation of this article.
Competing interests None declared.

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Posterior reversible encephalopathy
syndrome with thalamic involvement during
vasopressor treatment of vertebrobasilar
vasospasm after subarachnoid hemorrhage
Thomas Philip Madaelil and Rajat Dhar
J NeuroIntervent Surg 2016 8: e45 originally published online December
18, 2015

doi: 10.1136/neurintsurg-2015-012103.rep
Updated information and services can be found at:
http://jnis.bmj.com/content/8/11/e45

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