Biomed Imaging Interv J 2007; 3(1):e15
© 2007 Biomedical Imaging and
Stroke in elderly
S Kunanayagam1, MRCP,
BJJ Abdullah2,*, MBBS, FRCR,
G Kumar2, FRCR
1 Department of Medicine, Faculty of Medicine,
University of Malaya, Kuala Lumpur, Malaysia
2 Department of Biomedical Imaging, Faculty of Medicine, University
of Malaya, Kuala Lumpur, Malaysia
Madam X is a 70-year-old lady. She was admitted to the
accident and emergency department after 3 episodes of generalized tonic clonic
seizure lasting approximately 10 minutes each. Each episode aborted
spontaneously. She was drowsy on arrival. Her only past medical history was
that of occasional forgetfulness with no history of hypertension.
CT scans performed at the time of admission have been presented
What are the CT scan findings?
What is the most likely diagnosis?
What are the possible differential diagnoses based on the above
Briefly list the clinical manifestations of this condition.
Describe the pathological changes seen in this condition.
What investigation would you perform to obtain a definitive diagnosis?
1. What are the CT scan findings?
A large hyperdense focus is present within the brain
parenchyma of the right fronto-parietal lobe consistent with acute intracerebral
haematoma (long black arrow). A surrounding oedema (short black arrows) exists with
some midline shift towards the left side (arrowheads).
2. What is the most likely diagnosis?
The most likely diagnosis is cerebral amyloid angiopathy. Intracerebral
hemorrhages (ICH) account for approximately 12% of all strokes  and their
substantial morbidity and mortality exceed that of ischemic stroke [2, 3].
In Asian countries, ICH causes up to 30% of all strokes.
Cerebral amyloid angiopathy is caused by the deposition of
[beta]-amyloid in the media and adventitia of small arteries and capillaries of
the meninges and cerebral cortex. It is now recognized as a common cause of
primary lobar intracerebral hemorrhage in elderly persons, and is associated
with frequent hemorrhage recurrence and the presence of asymptomatic petechial
3. What are the possible differential diagnoses based on
the above findings?
The 4 differential diagnoses would include
Haemorrhagic transformation of an ischaemic stroke (Figure 3)
Arteriovenous malformation (AVM) (Figure 4)
Hypertensive haemorrhage (Figure 5)
4. Briefly list the clinical manifestations of this
The clinical manifestation varies according to the site and final
sphere of blood at cessation of bleeding. The size of the bleed determines the
clinical spectrum, from asymptomatic to fatal. The clinical spectrum varies
from being asymptomatic [4, 5] to headaches and seizures for smaller lobar haemorrhages
with hemiplegia and depressed levels of consciousness for large lobar haemorrhages
. Another important clinical manifestation, though less common, are spells
of weakness or parasthesia.
5. Describe the pathological changes seen in this
Cerebrovascular amyloidosis is a stagnant beta-fibrillosis
of arterioles, arising from failure of brain egress of beta-amyloid, after amyloid
precursor protein cleavage within brain parenchyma. The lobar distributions of
changes reflect an impairment of amyloid removal from brain interstitial fluid
and Virchow-Robin spaces. Hypertension, by contrast, , displays vascular
changes characterized by early proliferation of arteriolar smooth muscle,
followed later by apoptotic smooth muscle cell death and collagen deposition.
Eventually excess or deficient collagen deposition can lead respectively to
arteriolar occlusion, ectasia or both. Collagen has no contractile capability
and is brittle, unable to withstand breakage due to pulse pressure. Arterioles
physiologically bring down both blood pressure and pulse pressure, but
excessive dilatation results in Charcot-Bouchard aneurysms, which are fusiform,
not saccular structures. The distribution of hypertensive haemorrhage reflects
the high pulse pressure of arterioles immediately downstream from major end
arteries with minimal intervening branching.
Both diseases cause similar brittle arterioles with poor
contractile capability, therefore accounting for early growth of haematomas
when they rupture. Fibrin globes form in concentric spheres and attempt to seal
off the site of bleeding. The size of the final sphere of blood at cessation of
bleeding determines the clinical spectrum, from asymptomatic to fatal. Since
arteriolar bleeding is slower than arterial bleeding, several hours exist where
intervention may be useful with recombinant factor VIIa or other therapies. The
high pulse pressure and brisk interstitial fluid pumping in Virchow-Robin
spaces deep within the brain selectively protects against amyloidosis, while
leaving these basal arterioles vulnerable to hypertensive damage. Hypertensive haemorrhages
occur deep within the centrencephalon, while amyloid haemorrhages occur in a
lobar distribution, where pulse pressure and bulk flow are less, away from the
major feeding vessels of the brain. The brain distributions of hypertensive and
of amyloid haemorrhages are thus different and complementary .
6. What further investigation would be useful for a definitive
Gradient � echo MRI (GE-MRI) accentuates the loss of MR signal
caused by iron containing deposits as a result of old haemorrhages. GE-MRI
identification criteria in almost all studies comprise a rounded area of marked
and homogeneous signal loss (Figure 4), not located in sulcal areas to avoid
confusion with flow void from cerebral vessels. Furthermore, symmetric subcortical
and hypointense lesions likely to represent focal calcification have to be
excluded. The size definition of cerebral micro-bleeds (maximum diameter) is
not quite consistent among the studies reviewed. Nonetheless, an upper diameter
limit of 10 mm was applied in almost 80% of subjects, and other major
identification criteria are very similar in all studies, thereby allowing for
Gradient-echo magnetic resonance imaging can been used to
detect the multiple asymptomatic lobar petechial haemorrhages typical of the
disease, and it can allow a presumptive diagnosis of cerebral amyloid angiopathy
to be made in vivo .
Focal areas of signal loss on GE MRI imaging pathologically
represent focal haemosiderin deposition associated with previous hemorrhagic
events. Cerebral microhaemorrhages have been noted in healthy elderly, ischemic
cerebrovascular disease, intracerebral haemorrhage (ICH), cerebral amyloid angiopathy
(CAA), and in cerebral autosomal dominant arteriopathy with subcortical
infarcts and leukoencephalopathy. Microhaemorrhages have been associated with
older age, hypertension, smoking, white matter disease, lacunar infarcts,
previous ischemic stroke, or ICH.
In CAA, microhaemorrhages predict both the risk of recurrent
lobar ICH and future clinical decline. In patients with ischemic cerebrovascular
disease, the number and location of microhaemorrhages may be associated with
executive dysfunction and may predict the occurrence of ICH and lacunar
When cerebral microhaemorrhages are diagnosed on MRI,
conclusions regarding their significance and associated risks should be made
based on the population examined. Further studies to characterise the
associated risks of cerebral microhaemorrhages in different stroke populations
are needed to use this imaging marker in therapeutic decisions.
Cerebral amyloid angiopathy
Recognized as a common cause of primary lobar intracerebral haemorrhage
in elderly persons.
Associated with frequent haemorrhage recurrence and the presence of
asymptomatic petechial haemorrhages.
occur in a lobar distribution while hypertensive haemorrhages occur deep within
Gradient-echo magnetic resonance imaging can been used to detect the multiple
asymptomatic lobar petechial haemorrhages.
Microhaemorrhages predict both the risk of recurrent lobar ICH and
future clinical decline.
Figure 1 Plain axial CT scan through the superior aspect of the brain.
Figure 3 Axial CT scan of the brain (plain). Hyperdense foci (haemorrhage) (long arrows) within the infarct (short arrows) in the territory of the left middle cerebral artery. There is intraventricular extension of haemorrhage (arrowhead).
Figure 4 Coronal MRI of the brain using a gradient echo sequence demonstrating a hypointense focus (arrows) in the left temporal lobe. This would be compatible with previous haemorrhage which was due to an AVM in this patient.
Figure 5 Hypertensive haemorrhage. There is a large haematoma (*) in the region of the right basal ganglia with associated cerebral edema. There is midline shift towards the left (short arrow). Normal left basal ganglia (long arrow).
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|Received 26 August 2006; received in revised form 31 October 2007; accepted 8 November 2006
Correspondence: Department of Biomedical Imaging, Faculty of Medicine, University of Malaya, 50603 Kuala Lumpur, Malaysia. Tel: +603-79492069; Fax: +603-79581973;
E-mail: firstname.lastname@example.org (B.J.J. Abdullah).
Please cite as: Kunanayagam S, Abdullah BJJ, Kumar G,
Stroke in elderly, Biomed Imaging Interv J 2007; 3(1):e15
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