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Biomed Imaging Interv J 2007; 3(1):e15
doi: 10.2349/biij.3.1.e15
© 2007 Biomedical Imaging and Intervention Journal


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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



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Clinical Scenario

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 (Figure 1)

1.        What are the CT scan findings?

2.        What is the most likely diagnosis?

3.        What are the possible differential diagnoses based on the above findings?

4.        Briefly list the clinical manifestations of this condition.

5.        Describe the pathological changes seen in this condition.

6.        What investigation would you perform to obtain a definitive diagnosis?



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Answers

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 [1] 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 hemorrhages.

3. What are the possible differential diagnoses based on the above findings?

The 4 differential diagnoses would include

1.        Haemorrhagic transformation of an ischaemic stroke (Figure 3)

2.        Haemorrhagic tumour

3.        Arteriovenous malformation (AVM) (Figure 4)

4.        Hypertensive haemorrhage (Figure 5)

4. Briefly list the clinical manifestations of this condition.

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 [6]. Another important clinical manifestation, though less common, are spells of weakness or parasthesia.

5. Describe the pathological changes seen in this condition?

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 [7].

6. What further investigation would be useful for a definitive diagnosis?

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 comparative analyses.

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 [8].

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 infarction.

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.



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PEARLS

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.

         Haemorrhages occur in a lobar distribution while hypertensive haemorrhages occur deep within the centrencephalon.

         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).




REFERENCES

  1. Qureshi AI, Tuhrim S, Broderick JP et al. Spontaneous intracerebral hemorrhage. N Engl J Med 2001; 344(19):1450-60.   [Medline]
  2. Counsell C, Boonyakarnkul S, Dennis M et al. Primary intracerebral hemorrhage in the Oxfordshire Community Stroke Project. Prog Cerebrovasc Dis 1995; 5:26-34.  
  3. Dennis MS, Burn JP, Sandercock PA et al. Long-term survival after first-ever stroke: the Oxfordshire Community Stroke Project. Stroke 1993; 24(6):796-800.   [Medline]
  4. Okazaki H, Reagan TJ, Campbell RJ. Clinicopathologic studies of primary cerebral amyloid angiopathy. Mayo Clin Proc 1979; 54(1):22-31.   [Medline]
  5. Greenberg SM, Finklestein SP, Schaefer PW. Petechial hemorrhages accompanying lobar hemorrhage: detection by gradient-echo MRI. Neurology 1996; 46(6):1751-4.   [Medline]
  6. Greenberg SM, Vonsattel JP, Stakes JW et al. The clinical spectrum of cerebral amyloid angiopathy: presentations without lobar hemorrhage. Neurology 1993; 43(10):2073-9.   [Medline]
  7. Auer RN, Sutherland GR. Primary intracerebral hemorrhage: pathophysiology. Can J Neurol Sci 2005; 32 Suppl 2:S3-12.   [Medline]
  8. Knudsen KA, Rosand J, Karluk D et al. Clinical diagnosis of cerebral amyloid angiopathy: validation of the Boston criteria. Neurology 2001; 56(4):537-9.   [Medline]

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: basrij@um.edu.my (B.J.J. Abdullah).


Please cite as: Kunanayagam S, Abdullah BJJ, Kumar G, Stroke in elderly, Biomed Imaging Interv J 2007; 3(1):e15
<URL: http://www.biij.org/2007/1/e15/>

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