Reminder of important clinical lesson

CASE REPORT

Apathetic syndrome from carotid dissection:
a dangerous condition
Carmela Gerace,1 Fabio Massimo Corsi,2 Giovanna Comanducci2
1

Department of Neurology,
Azienda Ospedaliera S.CamilloForlanini, Roma, Italy
2
Department of Neurosciences,
Azienda Ospedaliera S.CamilloForlanini, Roma, Italy
Correspondence to
Dr Carmela Gerace,
c.gerace@tiscali.it

SUMMARY
Isolated behavioural disturbances can mimic psychiatric
diseases and delay diagnosis of acute brain disease. We
reported the case of a patient with carotid dissection
manifesting only with apathetic syndrome that was
initially considered as a possible postpartum depression,
causing a threatening diagnostic delay.

TREATMENT
Anticoagulant treatment and blood pressure monitoring were immediately started.

OUTCOME AND FOLLOW-UP
BACKGROUND
Sometimes acute ischaemic lesions of the brain
manifest themselves only with behavioural disturbances. In these cases, a diagnosis can be delayed
with dangerous effects for the patient. Apathy is a
well known symptom of stroke, but it has been
described in patients after the acute phase of the
disease. We did not find other case in which it has
been the first and sole manifestation in patients
with acute ischaemic brain damage.

CASE PRESENTATION
A 27-year-old woman was referred to emergency
room for behavioural disturbances. She had delivered a healthy child 12 days before, the delivery
went well and it did not last too long. Then she
had become indifferent for 3 days, since she had
headache for 1 day. Her husband described that she
was often quiet, distant, she did not even talk with
him naturally, sometimes she answered with strange
words to his questions and it appeared she could
not explain her behaviour.
Her medical history was unremarkable and she
did not take any medicine.
She had no fever and the brain CT and laboratory blood examinations were normal.
A postpartum depressive disorder was supposed
based only on behavioural symptoms of the patient
and her recent delivery because there were no
other social, familiar or psychiatric risk factors for
depression. She was referred to a psychiatrist who
did not fully agree with diagnosis of depressive disorder. The patient was then visited by a neurologist
who noticed a very mild aphasic expressive disorder together with apathetic behaviour and sent
the patient to the emergency room for immediate
investigations about possible left hemispheric
lesion.
To cite: Gerace C,
Corsi FM, Comanducci G.
BMJ Case Rep Published
online: [ please include Day
Month Year] doi:10.1136/
bcr-2013-009686

(ICA) dissection with apparent loss of flow of
middle cerebral artery (MCA; figure 1).

INVESTIGATIONS
Brain MRI and MRI angiography, performed after
12 h from patient’s arrival in the emergency room,
showed acute ischaemic stroke in the head of the
left caudate nucleus and left internal carotid artery

Gerace C, et al. BMJ Case Rep 2013. doi:10.1136/bcr-2013-009686

On the second day after admission to neurology
department the patient was alert, responsive, motor
and verbal inertia with decreased spontaneous
activity were evident, the speech was non-fluent
(rare anomias and prolonged latency in responding
to questions), with preserved comprehension, repetition while writing and reading. Mini-Mental State
Examination was 29/30; no other neurological
signs were present. After 1 month the patient was
well and there were no symptoms in her daily life
activities; only mild inertia was present.

DISCUSSION
ICA dissection is a frequent cause of stroke in
young patients.1 Risk factors that can lead to dissection include a neck injury and diseases of the inner
wall of the artery. The reason why dissection
occurred in our otherwise healthy young patient is
unknown, but we could consider significant, as risk
factor, possible neck movements and strains related
to her recent delivery. Common symptoms in a
carotid dissection are cervical pain and headache,
Horner’s syndrome, paralysis of the cranial nerves
and subsequently cerebral and retinal ischaemia.
Carotid artery dissection may be associated with
permanent deficits or even fatal outcomes due to
central nervous system ischaemia. Multiple lesions
are often evident with diffusion-weighted MRI in
many patients with carotid dissection. This observation would favour anticoagulation in prevention
and treatment of stroke from carotid dissection
because it suggests that artery-to-artery embolism
rather than haemodynamic compromise is the main
underlying mechanism in carotid dissection stroke.2
Our patient’s MRI angiography showed signs of
ICA dissection and apparent loss of flow of MCA
while an ischaemic lesion only developed in the
caudate head. Possible explanations of this finding
are the following:
1. Embolic occlusion, distal to the dissection flap,
of the penetrating artery nourishing the caudate
head while the MCA is not occluded but the
blood flow is markedly lowered and slow, being
insufficient to give the ‘signal void’ in MRI
imaging, but enough to avoid ischaemic lesion of
MCA territory.
1

Reminder of important clinical lesson

Figure 1 MRI axial diffusion-weighted imaging sequences (A) and apparent diffusion coefficient (B) with acute ischaemic infarct of the head of
left caudate nucleus (arrow); MRI angiography (C) with left internal carotid dissection (large arrow) and normal right carotid (small arrow).

2. Global hypoperfusion of the left hemispheric ICA territory
with haemodynamic lesion only in caudate head due to local
critic unbalance between oxygen and substrate need and
blood flow.
The most prominent clinical features of caudate vascular
lesions are behavioural and cognitive abnormalities, more often
apathy and abulia, characterised by decreased spontaneous activity and prolonged latency in responding to questions and other
stimuli. These clinical findings are caused by dysfunction of cortical zones due to loss of striatal efferent projections from the
caudate nucleus.3 It has been reported that about half of apathetic patients could remain in this condition for a long time.
Apathy can be more evident when associated with older age and
cognitive impairment.4

Learning points

Contributors CG gave substantial contribution to the conception and design,
acquisition of the data, interpretation of the data and drafting the article. FMC gave
substantial contribution in revising manuscript and to the final approval of the
version published. GC gave contribution in revising manuscript.
Competing interests None.
Patient consent Obtained.
Provenance and peer review Not commissioned; externally peer reviewed.

REFERENCES
1
2

3
4
5

Rubinstein M, Peerdeman Saskia M, van Tulder Maurits W, et al. A systematic review
of the risk factors for cervical artery dissection Sidney. Stroke 2005;36:1575–80.
Engelter Stefan T, Brandt T, Debette S, et al. For the Cervical Artery Dissection in
Ischemic Stroke Patients (CADISP) Study Group. Antiplatelets versus anticoagulation
in cervical artery dissection. Stroke 2007;38:2605–11.
Emre K, Dilek E, Kaan B. Acute caudate vascular lesions. Stroke 1999;30:100–8.
Caeiro JL, Ferro JM, Costa J. Apathy secondary to stroke: a systematic review and
meta-analysis. Cerebrovasc Dis 2013;35:23–39.
Starkstein SE, Leentjens AFG. The nosological position of apathy in clinical practice.
J Neurol Neurosurg Psychiatry 2008;79:1088–92.

▸ Apathy secondary to stroke is a more frequent
neuropsychiatric disturbance than depression.
▸ Patient history is always very important, especially when a
patient manifests behavioural or cognitive disturbances.
▸ Although apathic-abulic syndrome can be a symptom of
psychiatric disease, it is also very often found in a great
variety of neurological and medical conditions.5
▸ Correct identification of isolated neurological apathy and its
causes can be challenging in the emergency department.
▸ In this patient diagnostic delay due to misinterpretation of
apathetic symptoms could be very dangerous because
diagnostic delay of carotid dissection can provoke increased
morbidity and mortality.

2

Gerace C, et al. BMJ Case Rep 2013. doi:10.1136/bcr-2013-009686

Reminder of important clinical lesson

Copyright 2013 BMJ Publishing Group. All rights reserved. For permission to reuse any of this content visit
http://group.bmj.com/group/rights-licensing/permissions.
BMJ Case Report Fellows may re-use this article for personal use and teaching without any further permission.
Become a Fellow of BMJ Case Reports today and you can:
▸ Submit as many cases as you like
▸ Enjoy fast sympathetic peer review and rapid publication of accepted articles
▸ Access all the published articles
▸ Re-use any of the published material for personal use and teaching without further permission
For information on Institutional Fellowships contact consortiasales@bmjgroup.com
Visit casereports.bmj.com for more articles like this and to become a Fellow

Gerace C, et al. BMJ Case Rep 2013. doi:10.1136/bcr-2013-009686

3