Case report

Geert Schurgers ‍ ‍,1 Baer M G Arts,1,2 Alida A Postma,2,3 Anna de Kort4,5
1

Department of Psychiatry and
Neuropsychology, Maastricht
University Medical Centre+,
Maastricht, The Netherlands
2
Maastricht University School
for Mental Health and
Neuroscience, Maastricht, The
Netherlands
3
Department of Radiology and
Nuclear Medicine, Maastricht
University Medical Centre+,
Maastricht, The Netherlands
4
Department of Neurology,
Radboud University Medical
Center, Nijmegen, The
Netherlands
5
Radboud University Donders
Institute for Brain Cognition
and Behaviour, Nijmegen, The
Netherlands
Correspondence to
Geert Schurgers;
​geert.​schurgers@​mumc.​nl
Accepted 13 January 2021

© BMJ Publishing Group
Limited 2021. Re-­use
permitted under CC BY-­NC. No
commercial re-­use. See rights
and permissions. Published
by BMJ.
To cite: Schurgers G,
Arts BMG, Postma AA,
et al. BMJ Case Rep
2021;14:e238922.
doi:10.1136/bcr-2020238922

SUMMARY
Cerebral amyloid angiopathy (CAA) is a condition
characterised by accumulation of amyloid beta protein
(Aβ) in the wall of cerebral blood vessels which increases
the risk of intracranial haemorrhage and contributes to
cognitive impairment. We describe the case of a man
around the age of 70 with ’probable’ CAA according to
the modified Boston criteria and severe depression whose
depression was treated successfully with electroconvulsive
therapy (ECT). To the best of our knowledge, there are no
earlier published reports of ECT in a patient with CAA. We
briefly discuss possible safety measures for these patients,
the impact of ECT on cognition in CAA and a possible
influence of ECT on Aβ clearance.

BACKGROUND

Cerebral amyloid angiopathy (CAA) is characterised by accumulation of amyloid beta protein
(Aβ) in the wall of cerebral blood vessels, mainly
cortical and leptomeningeal arterioles.1 It increases
the risk of spontaneous intracranial haemorrhage
and contributes to cognitive impairment.2 3 Possible
psychiatric manifestations include personality
changes, behavioural disturbances and/or depression.4 Diagnosis depends on the modified Boston
criteria using pathologic, radiographic and/or clinical information.5 CAA is common: clinicopathological studies show a prevalence of 55%–59% in
the demented and 28%–39% in the non-­demented
elderly population.6
Here, we describe the case of an elderly man with
a history of intracranial haemorrhage with underlying ‘probable’ CAA according to the modified
Boston criteria who underwent a successful course
of electroconvulsive therapy (ECT). To the best
of our knowledge, there are no earlier published
reports of ECT in a patient with CAA. ECT is one
of the most effective procedures for the treatment
of depression with no absolute contraindications.7
Extra caution seems warranted in patients with a
history of intracranial haemorrhage since ECT
causes transient haemodynamic changes such as
increased heart rate and blood pressure.8 However,
successful ECT has been reported in a patient with
recent subarachnoid haemorrhage9 or in the presence of subdural haemorrhage.10
This case is an example of a fundamental part
of modern ECT practice: weighing potential benefits against risks and side-­effects. After presenting
the case, we discuss possible safety measures for
patients with CAA, the impact of ECT on cognition in CAA and a possible influence of ECT on Aβ
clearance.

CASE PRESENTATION
Our patient was a man around the age of 70 who
was hospitalised due to spontaneous cerebral haemorrhage 12 months before admission to our psychiatric ward. MRI of the brain at the time of the
cerebral haemorrhage revealed subarachnoid haemorrhage in the right central and precentral sulcus
and a small focus of intraparenchymal bleeding in
the left parietal lobe. The MRI scan also showed
multiple microbleeds and superficial siderosis, both
compatible with ‘probable’ CAA.5 Clinical signs of
the stroke were minor disturbances of fine motor
skills of the left hand but the patient recovered fully
within weeks.
In the following months, the patient developed
pain and loss of strength in his left leg. After extensive investigation, these problems were deemed
functional. Six weeks prior to his hospitalisation
at our ward, the patient’s physiotherapist told him
no further improvement regarding his leg was to be
expected. Since then the patient started to develop
depressive symptoms for the first time in his life
such as low mood, loss of interest in his surroundings, disrupted sleep, excessive worries and restlessness. Delusional thoughts (such as the false idea
that he was going to lose his house) and catatonic
signs (such as mutism, staring and perseveration)
appeared in the following weeks. Ultimately, the
patient was hospitalised at the psychiatric ward of
our general university hospital after a primary care
physician referred him to the emergency department. Psychotic depression with catatonia was the
preliminary diagnosis. Together with the aforementioned symptoms, the patient showed remarkable cognitive dysfunction such as disorientation,
impaired memory and apraxia. The patient’s wife
stated that her husband showed no signs of cognitive dysfunction up until the moment he started
developing depressive symptoms.

INVESTIGATIONS
Routine blood testing and urinalysis showed no
abnormalities. On admission to the psychiatric
ward, brain MRI was repeated which showed
similar results compared with the MRI scan 12
months earlier with no new cerebrovascular lesions
(see figure 1). Cerebrospinal fluid (CSF) analysis
revealed decreased levels of Aβ40 and Aβ42 (2632
(ref. >3200) and 385 (ref. >500) ng/L, respectively) with normal tau and phospho-­tau levels (340
(ref. <350) and 48 (ref. <85) ng/L, respectively).
The CSF sample showed no signs of inflammation of the central nervous system such as elevated
leucocyte count or protein levels. When assessing

Schurgers G, et al. BMJ Case Rep 2021;14:e238922. doi:10.1136/bcr-2020-238922

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Successful electroconvulsive therapy for depression in
a man with cerebral amyloid angiopathy

Case report

Figure 1 MRI (A, B, C) and CT (D) images of the brain made prior
to electroconvulsive therapy. White matter hyperintensities (straight
white arrows) classified as Fazekas grade 2 are seen at T2-­weighted
(A) and fluid-­attenuated inversion recovery images (B). Subarachnoid
haemorrhage (black arrowheads) in the right parietal region is seen at
susceptibility weighted imaging (SWI) (C) and CT (D) with superficial
siderosis in this region at SWI (C). Intraparenchymal haemorrhage
(white arrowhead) in the left parietal gyrus is seen at SWI (C) and CT
(D). Microbleeds (bended arrows) are seen at SWI (C).

Prior to hospitalisation, our patient was treated with sertraline
up to 100 mg daily on an outpatient basis for several weeks with
no success. Once he was hospitalised, lorazepam (1 mg three
times a day) was initiated which led to the disappearance of the
catatonic symptoms. Nortriptyline was started (50 mg once daily
resulting in a therapeutic blood level of 134 µg/L) together with
haloperidol (0.5 mg once daily) to treat the depressive symptoms
and nihilistic delusions.
Despite psychopharmacological treatment for several weeks,
the patient’s condition worsened. Eventually, a course of ECT
was initiated. Evidence-­based guidelines or case reports of ECT
in patients with CAA were lacking. A neurologist specialised
in neurovascular disease advised to avoid severe elevations in
blood pressure during the procedure. To achieve this, the beta
blocker esmolol (50 mg before the seizure, 50 mg once again
after the seizure if needed) and the opioid agonist alfentanil
(0.25–0.5 mg before the seizure) were administered intravenously to this 89 kg weighing man together with the usual
anaesthetic (etomidate 20 mg) and muscle relaxant (succinylcholine 100 mg). Using this medication combination, the ictal
and postictal systolic blood pressure did not exceed 160 mm
Hg and the diastolic blood pressure stayed well below 100 mm
Hg; these values were comparable to blood pressure measurements on non-­ECT days. The patient underwent bitemporal
ECT treatments twice weekly for a total of six ECT sessions
(seizure duration 35–67 s on electroencephalogram) with the
use of a Thymatron System IV device (Somatics, LLC, Lake
Bluff, Illinois, USA). The following device parameters were
used: pulse width=0.5 ms, frequency=50–70 Hz, stimulus
duration=6.8–7.8 s and total charge=352–555 mC.

OUTCOME AND FOLLOW-UP

Systemic causes of mood dysregulation such as anaemia and
hypothyroidism were ruled out through blood testing. The (sub)
acute time course of the cognitive deterioration and normal tau
levels in the CSF made an advanced neurodegenerative condition such as Alzheimer’s disease (AD) unlikely. Although AD
and CAA are overlapping conditions,11 the fact that not only
Aβ42 but also Aβ40 levels in the CSF were decreased pointed to
CAA rather than AD.12 13 Delirium was considered unlikely since
apart from disorientation typical symptoms of delirium such as
altered or fluctuating consciousness were absent. Also, typical
causes of delirium such as infection or electrolyte disturbances
were ruled out. Brain MRI excluded an acute cerebrovascular
cause of the rapid cognitive decline. Psychotic depression was
thus considered the main diagnosis and the patient was treated
accordingly.

The ECT course was successful. Already after the first treatment, a clear improvement was seen as psychomotor retardation
decreased significantly and the patient appeared remarkably more
communicative. By the fourth treatment, the patient reported a
dramatic improvement in his mood. ECT was stopped after the
sixth treatment because remission was achieved. The total score
on the clinician-­rated Inventory of Depressive Symptomatology
decreased from 25 pre-­ECT (indicating moderate depression,
probably an underestimation due to difficulties performing a
complete assessment of symptoms due to the severe mood and
cognitive disturbance) to seven post-­ECT (indicating remission
of depressive symptomatology). The subscore for anxiety on the
Hospital Anxiety and Depression Scale decreased from 13/21 to
1/21, for depression from 13/21 to 4/21.
To assess whether the ECT was inflicting additional cerebral
lesions, brain MRI was repeated after the fourth ECT treatment.
No changes in the extent of superficial hemosiderosis or white
matter hyperintensities and the number of microbleeds were
observed nor new lesions or oedema. We did not observe any
complications during the ECT course although cognitive problems persisted. The MMSE scores dropped from 25/30 pre-­ECT
to 24/30 during the ECT course. Three weeks post-­ECT, a neuropsychological re-­
evaluation took place. The patient’s MMSE
score now was 29/30 and improvements in working speed,
attention and executive functions were seen, most likely due to
resolution of depressive symptomatology. In contrast, impairments in memory and visuoconstructional abilities persisted (see
table 1). The remaining cognitive impairment was attributed to
the cognitive side-­effects of ECT and pre-­existing cerebrovascular damage. Cognition improved in the months after ECT and

2

Schurgers G, et al. BMJ Case Rep 2021;14:e238922. doi:10.1136/bcr-2020-238922

the patient’s cognitive functions, he attained a score of 25/30 on
the Mini Mental State Examination (MMSE). More extensive
neuropsychological examination objectified deficits in mental
processing speed, attention, executive functions, memory and
visuoconstruction (see table 1).

DIFFERENTIAL DIAGNOSIS

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TREATMENT

Case report
Overview of specific neuropsychological tests performed prior to ECT and 3 weeks after completion of the ECT course

Name of test

Cognitive functions assessed

CST

►► CST A: attention, processing speed
►► CST A: extremely low
►► CST B: attention, processing speed
(Z=−4.32)
►► CST C: mental flexibility
►► CST B: low average
►► CST interference score: mental flexibility
(Z=−1.45)

Performance pre-­ECT

►► CST interference score: extremely low

(Z=−4.81)
(Z=−6.84)

►► SCWT 1: extremely low

►► SCWT 1: average

►► SCWT 2: low average

►► SCWT 2: low average

►► SCWT 3: average

►► SCWT 3: average

►► SCWT interference score: average

►► SCWT interference score: average

►► Writing: extremely low (Z=−3.9)
►► Reading: extremely low (Z=−2.56)

►► Writing: borderline/low (Z=−1.77)
►► Reading: low average (Z=−1.19)

(Z=−2.08)
(Z=−1.30)

(Z=0.1)

Processing speed, writing, reading

(Z=1.31)

►► CST interference score: extremely
low

(Z=−0.51)

LDST

(Z=−0.94)

►► CST B: superior

►► CST C: extremely low

(Z=−2.81)
►► SCWT 1: attention, processing speed
►► SCWT 2: attention, processing speed
►► SCWT 3: selective attention, ability to
inhibit cognitive interference
►► SCWT interference score: inhibition

►► CST A: low average

►► CST C: extremely low

(Z=−3.32)

SCWT

Performance post-­ECT

(Z=−0.05)
(Z=−1.09)
(Z=−0.42)
(Z=−0.31)

BADS

Executive functions

Total score 3 (impaired)

Total score 11 (borderline)

15-­Words Test

Memory: immediate recall, delayed recall,
recognition

►► Immediate: borderline (Z=−1.61)
►► Delayed: extremely low (Z=−2.94)
►► Recognition: borderline (Z=−1.61)

►► Immediate: extremely low (Z=−2.38)
►► Delayed: extremely low (Z=−2.14)
►► Recognition: borderline (Z=−1.95)

VAT

Memory: learning visual associations

Percentile 1 (extremely low)

Percentile 1 (extremely low)

Visuoconstruction tests (drawing of meander Visuoconstruction
pattern, cubes, honeycomb, clock)

Clock drawing ‘poor’, rest ‘wrong’
(rating: good—poor—wrong)

Cube drawing ‘poor’, rest ‘wrong’
(rating: good—poor—wrong)

BNT

Score 13/15
(above cut-­off, which is 12.5)

Score 14/15
(above cut-­off, which is 12.5)

Naming

Z-­scores <2.00 indicate impairment.
BADS, Behavioural Assessment of the Dysexecutive Syndrome; BNT, Boston Naming Test; CST, concept shifting task; ECT, electroconvulsive therapy; LDST, Letter Digit Substitution Test; SCWT,
Stroop Colour and Word Test; VAT, Visual Association Test.

To the best of our knowledge, this is the first case report of
successful ECT in a patient with ‘probable’ CAA. Given the
high prevalence of CAA in the elderly and the fact that ECT is
a preferred treatment method in severe late-­life depression,14 it
is likely that many patients with unrecognised CAA are treated
with ECT, without specific safety measures. Considering the low
rates of serious ECT-­related adverse events in large patient populations,15–17 one could argue that the risk of provoking intracerebral haemorrhage is probably low. However, Weisberg et al
reported a case of intracerebral haemorrhage following ECT in
which CAA was considered a possible underlying cause.18 It is
unclear whether or not specific safety measures (such as neuroimaging prior to/during ECT or interventions to reduce periprocedural blood pressure) provide safety benefits in patients with
probable CAA. Evidence-­
based guidelines on this matter are
lacking. Esmolol seems to be a good candidate to reduce blood
pressure and heart rate after electrical stimulation but shortening
of the seizure duration could possibly impede ECT efficacy.19
Adjuvant remifentanil has proven to reduce systolic blood pressure during ECT and may lengthen seizure duration if it allows
for a dose reduction of the main anaesthetic.20
In line with the available literature, our case suggests that
pre-­existing cognitive impairment or the presence of age-­related
brain changes should not withhold psychiatrists to treat elderly
patients with severe mood disorders with ECT. Since CAA is

frequently associated with cognitive impairment and cognitive
side-­effects after ECT are common, one could be worried about
a negative impact of ECT on cognition in patients with CAA.
However, when assessing our patient 3 weeks after the last ECT
treatment, his MMSE score and performance in a broader neuropsychological examination improved. In line with this, Obbels et
al recently reported an increase in MMSE scores during ECT
life depression,
treatment in a sample of patients with late-­
specifically in a subset of patients with a low (<24) baseline
MMSE score.21 In addition, in a recent study, Bouckaert et al did
not find any association between age-­related brain changes (such
as hippocampal atrophy, white matter hyperintensities and total
amyloid load) and ECT outcome.22 According to the authors,
‘ECT should be considered in subjects with late life depression
irrespective of accumulating age-­related brain pathology’.
Arguably, ECT could have therapeutic effects in CAA beyond
the treatment of depression. It is hypothesised that the cerebral Aβ
accumulation in CAA, as in AD, is not the result of excessive Aβ
production but rather of diminished clearance from the brain.11
Zimmerman et al demonstrated a small, but significant, transient
increase in four Aβ isoforms (1–42, 1–40, x−42, x−40) in the
plasma of depressed individuals 30 min after ECT.23 Kranaster
et al found an increase in Aβ1-42 in the CSF of ECT-­responders
which was positively correlated to the number of ECT sessions.24
It is tempting to speculate that such an Aβ increase in plasma or
CSF reflects increased Aβ clearance from the brain, perhaps due
to ECT-­induced transient opening of the blood–brain barrier.25
In another paper on the impact of ECT on Aβ, Vandenbulcke
et al reported the asymmetrical Aβ distribution in a patient

Schurgers G, et al. BMJ Case Rep 2021;14:e238922. doi:10.1136/bcr-2020-238922

3

remained stable thereafter, according to the patient’s wife. In the
year after ECT, there were no signs of depression relapse.

DISCUSSION

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Table 1

Case report
REFERENCES

ORCID iD
Geert Schurgers http://​orcid.​org/​0000-​0003-​4343-​5242

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recent subarachnoid hemorrhage. J Ect 2018;34:e2–4.
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15 Blumberger DM, Seitz DP, Herrmann N, et al. Low medical morbidity and mortality
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Psychiatr Scand 2017;136:583–93.
16 Nuttall GA, Bowersox MR, Douglass SB, et al. Morbidity and mortality in the use of
electroconvulsive therapy. J Ect 2004;20:237–41.
17 Watts BV, Groft A, Bagian JP, et al. An examination of mortality and other adverse
events related to electroconvulsive therapy using a national adverse event report
system. J Ect 2011;27:105–8.
18 Weisberg LA, Elliott D, Mielke D. Intracerebral hemorrhage following electroconvulsive
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19 Boere E, Birkenhäger TK, Groenland THN, et al. Beta-­blocking agents during
electroconvulsive therapy: a review. Br J Anaesth 2014;113:43–51.
20 Takekita Y, Suwa T, Sunada N, et al. Remifentanil in electroconvulsive therapy: a
systematic review and meta-­analysis of randomized controlled trials. Eur Arch
Psychiatry Clin Neurosci 2016;266:703–17.
21 Obbels J, Vansteelandt K, Verwijk E, et al. MMSE changes during and after ECT in
late-­life Depression: a prospective study. Am J Geriatr Psychiatry 2019;27:934–44.
22 Bouckaert F, Emsell L, Vansteelandt K, et al. Electroconvulsive therapy response
in late-­life depression unaffected by age-­related brain changes. J Affect Disord
2019;251:114–20.
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of amyloid β peptides after electroconvulsive therapy. Brain Stimul 2012;5:25–9.
24 Kranaster L, Aksay SS, Bumb JM, et al. Electroconvulsive therapy selectively enhances
amyloid β 1-42 in the cerebrospinal fluid of patients with major depression: a
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Schurgers G, et al. BMJ Case Rep 2021;14:e238922. doi:10.1136/bcr-2020-238922

Learning points
►► This is the first case report of electroconvulsive therapy (ECT)

in a patient with depression and cerebral amyloid angiopathy
(CAA), a common condition among elderly characterised
by accumulation of amyloid beta protein (Aβ) in the wall of
cerebral blood vessels leading to intracranial haemorrhage
and cognitive impairment.
►► Following a vascular neurologist’s advice, we used a beta
blocker and opioid antagonist to limit blood pressure during
ECT and reduce the risk of cerebral haemorrhage. We
performed brain MRI after four ECT treatments to assess
whether ECT was inflicting additional cerebral lesions, which
was not the case. Evidence-­based guidelines on such safety
measures for patients with CAA are non-­existent.
►► Our case suggests ECT should be considered in elderly
patients with severe mood disorders even in the presence of
CAA.
►► Preliminary evidence suggests that ECT stimulates Aβ
elimination from the brain but further research is needed
before firm conclusions can be drawn.
Acknowledgements Dr Marcel M. Verbeek and Professor Pascal Sienaert,
renowned experts in the fields of CAA and ECT, respectively, provided additional
advice and assisted in selecting an appropriate journal for publication of the
manuscript. Dr Claire Wolfs assisted in interpreting and summarising the
neuropsychological findings.
Contributors GS was directly involved in the treatment of the patient described in
the article, took the initiative to write this case report and was the main author of
the manuscript. BMGA was the supervising psychiatrist involved in the treatment of
the patient and critically revised multiple versions of the manuscript. AAP critically
revised multiple versions of the manuscript, especially the parts on neuroradiological
aspects, and provided the images. AdK critically revised multiple versions of the
manuscript, especially the parts on clinical and pathophysiological aspects of
cerebral amyloid angiopathy.
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 AAP reports an institutional grant from Siemens Healthcare,
outside the submitted work.
Patient consent for publication Obtained.
Provenance and peer review Not commissioned; externally peer reviewed.
Open access This is an open access article distributed in accordance with the
Creative Commons Attribution Non Commercial (CC BY-­NC 4.0) license, which
permits others to distribute, remix, adapt, build upon this work non-­commercially,
and license their derivative works on different terms, provided the original work
is properly cited and the use is non-­commercial. See: http://​creativecommons.​org/​
licenses/​by-​nc/4​ .​0/.

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with AD 20 months after unilateral ECT, possibly due to ECT-­
induced alterations in Aβ deposition.26 Altered Aβ deposition
might be a consequence of glial cell activation by ECT.27 Clearly,
further research in this area is needed before firm conclusions
can be drawn. Unfortunately, we did not have the possibility to
re-­examine the CSF of our patient so we cannot make statements
on the impact of ECT on Aβ in this specific case.

Case report
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