Unusual association of diseases/symptoms

CASE REPORT

Simultaneous transient global amnesia and right
MCA stroke after Valsalva manoeuvre
Ariel Fernando Mariaca,1 Jose Manuel Valdueza,1 Christian Gaebel,2
Manuel Gomez-Choco3
1

Neurology, Neurological
Center, Segeberger Kliniken, Bad
Segeberg, Germany
2
Radiology, Neurological Center,
Segeberger Kliniken, Bad
Segeberg, Germany
3
Department of Neurology,
Hospital Sant Joan Despi Moises
Broggi, Sant Joan Despi, Spain
Correspondence to
Dr. Manuel Gomez-Choco,
​mgomezch@​csi.​cat
Accepted 3 April 2017

This case highlights the importance of taking into
account the clinical information to be able to understand the results of ancillary investigations.

onset acute confusion. His wife described that
shortly after having ‘opened his bowels’ he repeatedly started to ask where they were and what they
were doing there, but he was not able to remember
the answers his wife gave to him and repeatedly
asked the same questions. She immediately called
the paramedics and as a stroke was suspected he
was urgently referred to the hospital.
The initial neurological examination did not
show any focal neurological deficit but an overt
amnestic syndrome was present at that moment. He
was constantly asking the same questions (‘where
am I?’, ‘what are we doing here?’) and was not
able to recall any information he was given after a
short time interval, but there were not any cognitive
deficits otherwise. The amnestic episode subsided
completely after 4 hours, and the patient and his
wife described that it was the first time that he had
suffered an episode like that. In view of the clinical
symptoms, the patient was diagnosed with transient
global amnesia (TGA).

CASE PRESENTATION

INVESTIGATIONS

SUMMARY
A 61-year-old man suffered an episode of transient
confusion and anterograde amnesia after a Valsalvarelated manoeuvre. The MRI diffusion weighted imaging
(DWI) sequences showed a left hippocampal and two
right parietal lesions that were deemed as acute. The MR
angiography disclosed a high-grade stenosis in the right
middle cerebral artery as was described by a transcranial
colour-coded ultrasound as well. Ultrasound investigation
of the jugular veins showed a right jugular venous reflux
after a Valsalva manoeuvre. The patient was diagnosed
with transient global amnesia based on clinical grounds
and the right parietal lesions were considered as silent
strokes. The Valsalva manoeuvre could have played as a
common trigger for both diseases.

BACKGROUND

A 61-year-old man with a medical history of high
blood pressure presented to hospital with sudden

To cite: Mariaca AF,
Valdueza JM, Gaebel C, et al.
BMJ Case Rep Published
Online First: [please
include Day Month Year].
doi:10.1136/bcr-2016218990

Figure 1 Brain MRI showed a left hippocampal
diffusion-weighted hyperintense lesion (arrow, A) not
evident on FLAIR sequence (B). The right parietal lesions
were clearly visible on both diffusion-weighted and fluid
attenuated inversion recovery (FLAIR) sequences (arrows,
C and D). The MR angiography disclosed a high-grade
stenosis in the right middle cerebral artery (arrow, E).
The prominent right posterior cerebral artery signal
(arrowheads, E) denotes leptomeningeal collateral flow
activation.

The laboratory investigations excluded toxic, infectious or metabolic causes and an electroencephalogram was normal. The initial cranial CT was unremarkable but the brain MRI revealed small cortical
lesions hyperintense on the DWI sequences. One of
them was located in the left hippocampus and two
in the right parietal region. The time-of-flight MR
angiography (MRA) disclosed a high-grade stenosis
in the right middle cerebral artery (MCA) (figure 1).
The duplex ultrasound investigation showed
non-significant carotid atherosclerosis. The transcranial colour-coded sonography (TCCS) revealed
an increased flow velocity that reached a peak
systolic velocity (PSV) of 313 cm/s at a depth of
53 mm in the right M1-MCA. A mild poststenotic
flow was detected in the right M2-MCA branches.
In comparison with the left side, the right P2-/
P3-PCA segments had an increased PSV without
turbulence (75 cm/s vs 54 cm/s). Both A1-anterior cerebral artery and the left M1-MCA segment
showed normal flow parameters (figure 2).
The investigation of the internal jugular
veins (IJVs) showed a right-dominant IJV defined
by a larger area and higher flow velocity. During
a Valsalva manoeuvre (VM), valve competence was
demonstrated on the left side. On the right side, a
marked reflux that lasted up to 1.28 s confirmed an
incompetent IJV valve (figure 3). The investigation

Mariaca AF, et al. BMJ Case Rep 2017. doi:10.1136/bcr-2016-218990

1

Unusual association of diseases/symptoms
stenosis were considered incidental findings. Aspirin and statins
were added to his antihypertensive medication. After 3 years of
follow-up, the patient remained clinically stable without any
changes on the TCCS and MRA. The left-sided hippocampal
lesion was not detectable in the FLAIR sequences at that time.

DISCUSSION

Figure 2 The transcranial colour-coded sonography disclosed
high-flow velocities at a depth of 53 mm in the right MCA (A) with a
poststenotic flow in M2 segments (B), corresponding to a high-grade
stenosis. The right PCA (C) showed increased velocities compared with
the contralateral PCA (D) which suggested collateral flow carried by
leptomeningeal collateral. M1-MCA-R: M1 segment of the right MCA.
M2-MCA-R: M2 segment of the MCA. P2/3-PCA-R: P2-P3 segments of
the right PCA. P2/3-PCA-L: P2-P3 segments of the left PCA. MCA, middle
cerebral artery; PCA, posterior cerebral artery.
of the intracranial veins showed normal flow signals in all
examined vessels including the basal vein of Rosenthal (BVR),
the deep middle cerebral vein, the vein of Galen (VG), and the
straight sinus (StS). A mild flow velocity reduction was observed
during a forced VM in the examined BVR.
Cardiological work-up including transoesophageal echocardiography and 24-hour telemetry showed neither cardiac nor
aortal sources of emboli.
Considering the left-sided hippocampal lesion and the clinical presentation and evolution, a TGA was diagnosed whereas
the right-sided ischaemic lesions and high-grade M1-MCA

Figure 3 (A) Left IJV with undulating flow and low flow velocities
at rest and physiological flow arrest during a Valsalva strain. Note
the sharp and short retrograde flow resembling physiological valve
closure (arrow). (B) Right IJV with undulating but mostly anterograde
flow direction with higher flow velocities compared with the left IJV
at rest. An abnormal flow reflux is seen during a Valsalva strain of
1.28 s. IJV, internal jugular vein.
2

Herein we describe a 61-year-old patient who suffered a first
episode of TGA after a Valsalva-related manoeuvre. The DWI-MRI
revealed a hyperintense lesion in the Sommer sector of the left
hippocampus and two small parietal acute ischaemic lesions likely
to be embolic in the context of a high-grade MCA stenosis.
Hippocampal DWI-positive lesions have been previously
described in TGA. These lesions are reversible and can be found
in up to 84% of the cases between 24 and 74 hours after symptoms onset.1 2 Compared with lesions observed in patients with
transient ischaemic attack (TIA), TGA DWI-positive lesions
appear later, tend to be smaller and do not lead to permanent
FLAIR hyperintensities.3
The pathogenesis of TGA is controversial and several mechanisms have been proposed, including epilepsy, arterial ischaemia and venous congestion. Although an amnestic syndrome
can be caused by an ischaemic stroke, it usually appears as part
of other neurological symptoms.4 5 Furthermore, patients with
TGA usually have lower rates of vascular risk factors and future
vascular events than patients with TIA, arguing against an ischaemic aetiology for TGA.6
Venous congestion has also been considered a potential pathological mechanism given the close temporal relationship observed
in many cases between VM and episodes of TGA. VM leads to a
transient increase of the intrathoracic pressure that can limit the
venous reflux coming from the head and limbs.7 The resulting
venous congestion might block the draining veins of the medial
temporal lobe and especially the inferior ventricular vein (IVV),
where the anterior hippocampus drains.8 The IVVs merge on
both sides into the BVR. Both BVR drain into the singular VG
and/or StS and then preferentially into the left transverse sinus
(TS) and left IJV. Subsequently, venous reflux into the dominant
IJV might affect both hippocampal areas.
A cessation or decrease of anterograde venous flow during
repetitive VM can be assessed with ultrasonography and indicates competent jugular valves, whereas retrograde flow indicates
internal jugular valve insufficiency (IJVVI). A cut-off value of 0.88 s
has been defined to securely differentiate between transient physiological reflux (<0.88 s) caused by valve closure and real IJVVI
(>0.88 s).9 IJVVI is present in approximately 30% of healthy
subjects.10
A series of ultrasound studies found a significantly higher,
mostly unilateral IJVVI prevalence in patients with TGA
compared with controls.11–16 The largest study, analysing 142
patients and 40 controls found an IJVVI in 80% of patients
with TGA and in 25% of controls.12 In selected patients with an
antecedent VM, IJVVI was even seen in up to 100%.10
However, the side of affected IJV valve does not always seem
to match the observed StS drainage pattern, as demonstrated
in a combined ultrasound–MRI study. However, the number of
analysed patients was too small to draw definite conclusions.16
Using MRA at rest, a higher proportion of retrograde venous
flow—distal of the IJV valves—was reported in patients with
TGA.17 However, this observation has not been confirmed by
others.18 Other authors suggest that patients with TGA can
have an increased prevalence of stenosis of the jugular veins
and hypoplasia of the TS.19 Furthermore, ultrasound studies
Mariaca AF, et al. BMJ Case Rep 2017. doi:10.1136/bcr-2016-218990

Unusual association of diseases/symptoms
did not show a venous reflux during VM at least in the BVR
and StS.11 13
Apart from IJVVI findings in TGA, significantly higher rates
have also been observed in primary exertional headache,20 in
idiopathic intracranial hypertension,21 in patients with transient
monocular blindness, especially if recurrent and of undetermined origin,22 and also in leukoaraiosis.23
The case we are discussing herein is complex as it combines TGA
with concomitant silent brain infarctions. Silent DWI-positive
lesions can be observed in up to 5% of the cases in some groups
of patients.24 25 In our case ,the DWI-positive parietal lesions were
interpreted as incidental and presumably caused by an artery-toartery embolism coming from the high-grade right MCA stenosis.
However, apart from ‘lesions just found by chance’, it is
possible that those parietal lesions could share a common
origin with the episode of TGA and the left hippocampal
lesion. In that sense, phase IV of VM is characterised by a
sharp increase of the arterial blood pressure caused by both
increased sympathetic tone and systemic vascular resistance.
During this latest phase of the VM, an increase of the cerebral blood flow velocity is observed in the MCA when it is
monitored with transcranial Doppler.26 Accordingly, we could
hypothesise that the increase of the arterial blood pressure and
consequent stress over the surface of an intracranial stenosis
could favour plaque rupture and subsequently thrombosis and
embolism.27
This clinical case points out the importance of clinical history
and examination to make an accurate interpretation of the results
we get from ancillary investigations. Furthermore, although
merely hypothetical, our case also shows how two unrelated
diseases can happen at the same time given a common element
that is able to trigger different pathogenic mechanism.

Learning points
►► The clinical information that we get from our patients is

the cornerstone to understand the results of the ancillary
investigations.
►► A Valsalva manoeuvre can be the trigger for transient global
amnesia (TGA) and acute stroke.
►► Jugular vein insufficiency is more frequent in patients with
TGA.
►► In contrast to ischaemic lesions, TGA DWI-positive lesions do
not lead to permanent lesions on FLAIR sequences.
Contributors JMV and AFM: acquisition, analysis and interpretation of data and
critical review of the manuscript. CG: acquisition, analysis and interpretation of data.
MGC: interpretation of data, writing and critical review of the manuscript.
Competing interests None declared.
Patient consent Obtained.
Provenance and peer review Not commissioned; externally peer reviewed.

Mariaca AF, et al. BMJ Case Rep 2017. doi:10.1136/bcr-2016-218990

© BMJ Publishing Group Ltd (unless otherwise stated in the text of the article)
2017. All rights reserved. No commercial use is permitted unless otherwise expressly
granted.

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Mariaca AF, et al. BMJ Case Rep 2017. doi:10.1136/bcr-2016-218990