Cerebral amyloid angiopathy

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Cerebral amyloid angiopathy (CAA) is a cerebrovascular disorder caused by the accumulation of cerebral amyloid-β (Aβ) in the tunica media and adventitia of leptomeningeal and cortical vessels of the brain. The resultant vascular fragility tends to manifest in normotensive elderly patients as lobar intracerebral haemorrhage. It is, along with Alzheimer disease, a common cerebral amyloid deposition disease.

Epidemiology

Cerebral amyloid angiopathy can be divided into sporadic (spontaneous) and familial forms.

Sporadic CAA

Cerebral amyloid angiopathy is a frequent incidental finding, found on screening gradient-recalled echo imaging in up to 16% of asymptomatic elderly patients ⁴. Autopsy studies have found a prevalence of approximately 5-9% in patients between 60 and 69 years, and 43-58% in patients over the age of 90 ⁴.

Autopsy of patients who have evidence of Alzheimer disease have found cerebral amyloid angiopathy in the vast majority of cases (90%). This rate is still high (20-40%) in non-demented elderly individuals ¹⁴.

Importantly it is usually notassociated with systemic amyloidoses.

Familial CAA

Familial cerebral amyloid angiopathies are a rare group of disorders usually encountered as an autosomal dominant condition ¹⁴. They mainly differ from spontaneous CAA in earlier age of onset, typically in middle to late middle age ¹⁴.

Clinical presentation

Cortical vessel involvement results in intracerebral haemorrhage, either as lobar haemorrhages or rarely cerebellar haemorrhages ¹⁹, which present as stroke, or smaller lobar cerebral microhaemorrhages, which are often only detected radiologically ¹⁵. Vessel damage in corticosubcortical regions can also result in ischaemic leukoencephalopathy ⁷. It is thought that lobar cerebral microhaemorrhages and ischaemic leukoencephalopathy play a role in the development of cognitive impairment that is independent to Alzheimer disease ¹⁵, although recurrent lobar haemorrhages can also cause step-wise decline in cognitive function.

Leptomeningeal vessel involvement results in convexal subarachnoid haemorrhage, which can present with transient focal neurologial symptoms (TFNS) or "amyloid spells", especially when localised to the central sulcus ¹⁶, which is in close proximity to the primary motor and sensory cortices. These TFNS are classically described as recurrent, stereotyped, spreading paraesthesias lasting several minutes but there is a wide spectrum of presentations encompassing both positive (spreading paraesthesia or visual symptoms) and negative (paresis, aphasia or dysphagia) phenomenology ¹⁷. It is important to differentiate TFNS from sensory transient ischaemic attacks and migraine with aura.

Uncommonly an inflammatory reaction may be incited and patients can present in a more subacute fashion with declining cognitive performance, seizures, headache and stroke like episodes (without haemorrhage) ^1,11. This known as cerebral amyloid angiopathy-related inflammation and is discussed separately.

Occasionally mass like lesions, known as cerebral amyloidoma, have been reported ^3,14. This is not to be confused with cerebral amyloidosis seen in patients with systemic amyloidosis.

The Boston criteria ⁷and newer Modified Boston criteria ⁹are a combination of clinical, radiographic and pathological criteria which are used to assess the probability of cerebral amyloid angiopathy.

Pathology

~~cerebral~~Cerebral amyloid angiopathy is characterised by the deposition of ß-amyloid (Aß-40) in the tunica media and tunica adventitia of small and medium sized arteries of the cerebral cortex and leptomeninges ⁴. This is associated with fibrinoid degeneration with ~~spearation~~separation of the tunica media and tunica intima, and microaneurysm formation ¹. Amyloid is an eosinophilic, insoluble protein, located in the extra-cellular space, and stains with Congo red yielding apple green birefringence when viewed with polarized light ³. It is important to note that amyloid deposition is also encountered in other clinical scenarios including spongiform encephalitis ¹.

Associations

Alzheimer's disease
- pathological cerebral amyloid angiopathy changes are seen in ~80% of those with Alzheimer's disease (Aß-42) ^5-13
- ~40% of those with cerebral amyloid angiopathy have Alzheimer's dementia type symptoms

Radiographic features

Findings reflect the various manifestations of the disease:

cerebral haemorrhage
- usually superficial (lobar)
- appearance will vary according to age of bleed (see blood on MRI)
microhaemorrhages
- not seen on CT
- small focal regions of signal drop out best seen on T2* sequences (gradient echo, echo-planar, SWI) as regions of blooming ¹²
- may be difficult to see on conventional T1 and T2 sequences ⁴
- tend to be corticosubcortical (grey-white matter junction) in distribution, but can also be in the cerebellum
- tend to spare the basal ganglia and pons (c.f. hypertensive microhaemorrhages) ^{4, 14}
convexal subarachnoid haemorrhage
- appearance will vary according to age of bleed (see blood on MRI), but is best acutely seen on CT and T2 FLAIR ¹⁸
cortical superficial siderosis
- not seen on CT
- curvilinear regions of signal drop out localised to one of more sulci best seen on T2* sequences (gradient echo, echo-planar, SWI) ⁹
- thought to be a chronic sequela of covexal subarachnoid haemorrhage ⁹
- may be seen in up to 60% of patients ⁹
- not present infratenorially (c.f. superficial siderosis of the CNS)
ischaemic leukoencephalopathy
- CT: diffuse low density of the white matter
- MR: white matter hyperintensity on T2 weighted scans without involvement of subcortical U-fibres (c.f. cerebral amyloid angiopathy related inflammation) ⁷

Radiographic features of cerebral amyloid angiopathy related inflammation and cerebral amyloidoma are discussed separately.

Differential diagnosis

hypertensive microangiopathy
- haemorrhages, including microhaemorrhages, are typically located in basal ganglia, pons and cerebellum
- not associated with subarachnoid haemorrhage or superficial siderosis
multiple cavernoma syndrome
- lesions have a random distribution
- random size, although Zabramski classification Type IV cavernous malformations are indistinguishable from cerebral microhaemorrhages related to CAA
- often characteristic cavernous malformations can be identified
haemorrhagic metastases (e.g. melanoma)
- lesions have a variable size and can often be larger than microhaemorrhages
- enhancing
diffuse axonal injury
- lesions are typically located at the grey-white matter junction, in the corpus callosum and in more severe cases, in the brainstem
neurocysticercosis
- nodular calcified stage visible on CT or phase-filtered SWI
- random distribution
fat embolism syndrome
- 'starfield' pattern of distribution
- lesions also show restricted diffusion on DWI and are likely visible on other sequences
radiation induced vasculopathy
- microhaemorrhages have a very similar appearance (similar pathophysiology)
- distribution related to treatment field

-Cerebral amyloid angiopathy (CAA) is a cerebrovascular disorder caused by the accumulation of cerebral amyloid-β (Aβ) in the tunica media and adventitia of leptomeningeal and cortical vessels of the brain. The resultant vascular fragility tends to manifest in normotensive elderly patients as <a href="/articles/lobar-haemorrhage">lobar intracerebral haemorrhage</a>. It is, along with <a href="/articles/alzheimer-disease-1">Alzheimer disease</a>, a common <a href="/articles/cerebral-amyloid-deposition-diseases">cerebral amyloid deposition disease</a>.<h4>Epidemiology </h4>Cerebral amyloid angiopathy can be divided into sporadic (spontaneous) and familial forms. <h5>Sporadic CAA</h5>Cerebral amyloid angiopathy is a frequent incidental finding, found on screening gradient-recalled echo imaging in up to 16% of asymptomatic elderly patients 4. Autopsy studies have found a prevalence of approximately 5-9% in patients between 60 and 69 years, and 43-58% in patients over the age of 90 4.Autopsy of patients who have evidence of Alzheimer disease have found cerebral amyloid angiopathy in the vast majority of cases (90%). This rate is still high (20-40%) in non-demented elderly individuals 14. Importantly it is usually not associated with systemic <a href="/articles/amyloidosis">amyloidoses</a>.<h5>Familial CAA</h5>Familial cerebral amyloid angiopathies are a rare group of disorders usually encountered as an autosomal dominant condition 14. They mainly differ from spontaneous CAA in earlier age of onset, typically in middle to late middle age 14.<h4>Clinical presentation</h4>Cortical vessel involvement results in <a title="Intracerebral haemorrhage" href="/articles/intracerebral-haemorrhage">intracerebral haemorrhage</a>, either as <a href="/articles/lobar-haemorrhage">lobar haemorrhages</a> or rarely <a title="Cerebellar haemorrhages" href="/articles/cerebellar-haemorrhage">cerebellar haemorrhages</a> 19, which present as stroke, or smaller lobar cerebral <a href="/articles/cerebral-microhaemorrhage">microhaemorrhages</a>, which are often only detected radiologically 15. Vessel damage in corticosubcortical regions can also result in ischaemic leukoencephalopathy 7. It is thought that lobar cerebral <a href="/articles/cerebral-microhaemorrhage">microhaemorrhages</a> and ischaemic leukoencephalopathy play a role in the development of cognitive impairment that is independent to <a href="/articles/alzheimer-disease-1">Alzheimer disease</a> 15, although recurrent <a href="/articles/lobar-haemorrhage">lobar haemorrhages</a> can also cause step-wise decline in cognitive function.Leptomeningeal vessel involvement results in convexal <a title="Subarachnoid haemorrhage (SAH)" href="/articles/subarachnoid-haemorrhage">subarachnoid haemorrhage</a>, which can present with transient focal neurologial symptoms (TFNS) or "amyloid spells", especially when localised to the central sulcus 16, which is in close proximity to the primary motor and sensory cortices. These TFNS are classically described as recurrent, stereotyped, spreading paraesthesias lasting several minutes but there is a wide spectrum of presentations encompassing both positive (spreading paraesthesia or visual symptoms) and negative (paresis, aphasia or dysphagia) phenomenology 17. It is important to differentiate TFNS from sensory <a href="/articles/transient-ischaemic-attack">transient ischaemic attacks</a> and <a href="/articles/migraine">migraine</a> with aura.Uncommonly an inflammatory reaction may be incited and patients can present in a more subacute fashion with declining cognitive performance, seizures, headache and stroke like episodes (without haemorrhage) 1,11. This known as <a href="/articles/cerebral-amyloid-angiopathy-related-inflammation">cerebral amyloid angiopathy-related inflammation</a> and is discussed separately. Occasionally mass like lesions, known as <a href="/articles/cerebral-amyloidoma">cerebral amyloidoma</a>, have been reported 3,14. This is not to be confused with <a href="/articles/cerebral-amyloidosis">cerebral amyloidosis</a> seen in patients with systemic amyloidosis. The <a href="/articles/boston-criteria">Boston criteria</a> 7 and newer <a href="/articles/modified-boston-criteria-for-cerebral-amyloid-angiopathy-1">Modified Boston criteria</a> 9 are a combination of clinical, radiographic and pathological criteria which are used to assess the probability of cerebral amyloid angiopathy.<h4>Pathology</h4>cerebral amyloid angiopathy is characterised by the deposition of ß-amyloid (Aß-40) in the tunica media and tunica adventitia of small and medium sized arteries of the cerebral cortex and leptomeninges 4. This is associated with fibrinoid degeneration with spearation of the tunica media and tunica intima, and microaneurysm formation 1. Amyloid is an eosinophilic, insoluble protein, located in the extra-cellular space, and stains with Congo red yielding apple green birefringence when viewed with polarized light 3. It is important to note that amyloid deposition is also encountered in other clinical scenarios including <a href="/articles/spongiform-encephalitis">spongiform encephalitis</a> 1.<h5>Associations</h5><ul><li>
+Cerebral amyloid angiopathy (CAA) is a cerebrovascular disorder caused by the accumulation of cerebral amyloid-β (Aβ) in the tunica media and adventitia of leptomeningeal and cortical vessels of the brain. The resultant vascular fragility tends to manifest in normotensive elderly patients as <a href="/articles/lobar-haemorrhage">lobar intracerebral haemorrhage</a>. It is, along with <a href="/articles/alzheimer-disease-1">Alzheimer disease</a>, a common <a href="/articles/cerebral-amyloid-deposition-diseases">cerebral amyloid deposition disease</a>.<h4>Epidemiology </h4>Cerebral amyloid angiopathy can be divided into sporadic (spontaneous) and familial forms. <h5>Sporadic CAA</h5>Cerebral amyloid angiopathy is a frequent incidental finding, found on screening gradient-recalled echo imaging in up to 16% of asymptomatic elderly patients 4. Autopsy studies have found a prevalence of approximately 5-9% in patients between 60 and 69 years, and 43-58% in patients over the age of 90 4.Autopsy of patients who have evidence of Alzheimer disease have found cerebral amyloid angiopathy in the vast majority of cases (90%). This rate is still high (20-40%) in non-demented elderly individuals 14. Importantly it is usually not associated with systemic <a href="/articles/amyloidosis">amyloidoses</a>.<h5>Familial CAA</h5>Familial cerebral amyloid angiopathies are a rare group of disorders usually encountered as an autosomal dominant condition 14. They mainly differ from spontaneous CAA in earlier age of onset, typically in middle to late middle age 14.<h4>Clinical presentation</h4>Cortical vessel involvement results in <a href="/articles/intracerebral-haemorrhage">intracerebral haemorrhage</a>, either as <a href="/articles/lobar-haemorrhage">lobar haemorrhages</a> or rarely <a href="/articles/cerebellar-haemorrhage">cerebellar haemorrhages</a> 19, which present as stroke, or smaller lobar cerebral <a href="/articles/cerebral-microhaemorrhage">microhaemorrhages</a>, which are often only detected radiologically 15. Vessel damage in corticosubcortical regions can also result in ischaemic leukoencephalopathy 7. It is thought that lobar cerebral <a href="/articles/cerebral-microhaemorrhage">microhaemorrhages</a> and ischaemic leukoencephalopathy play a role in the development of cognitive impairment that is independent to <a href="/articles/alzheimer-disease-1">Alzheimer disease</a> 15, although recurrent <a href="/articles/lobar-haemorrhage">lobar haemorrhages</a> can also cause step-wise decline in cognitive function.Leptomeningeal vessel involvement results in convexal <a href="/articles/subarachnoid-haemorrhage">subarachnoid haemorrhage</a>, which can present with transient focal neurologial symptoms (TFNS) or "amyloid spells", especially when localised to the central sulcus 16, which is in close proximity to the primary motor and sensory cortices. These TFNS are classically described as recurrent, stereotyped, spreading paraesthesias lasting several minutes but there is a wide spectrum of presentations encompassing both positive (spreading paraesthesia or visual symptoms) and negative (paresis, aphasia or dysphagia) phenomenology 17. It is important to differentiate TFNS from sensory <a href="/articles/transient-ischaemic-attack">transient ischaemic attacks</a> and <a href="/articles/migraine">migraine</a> with aura.Uncommonly an inflammatory reaction may be incited and patients can present in a more subacute fashion with declining cognitive performance, seizures, headache and stroke like episodes (without haemorrhage) 1,11. This known as <a href="/articles/cerebral-amyloid-angiopathy-related-inflammation">cerebral amyloid angiopathy-related inflammation</a> and is discussed separately. Occasionally mass like lesions, known as <a href="/articles/cerebral-amyloidoma">cerebral amyloidoma</a>, have been reported 3,14. This is not to be confused with <a href="/articles/cerebral-amyloidosis">cerebral amyloidosis</a> seen in patients with systemic amyloidosis. The <a href="/articles/boston-criteria">Boston criteria</a> 7 and newer <a href="/articles/modified-boston-criteria-for-cerebral-amyloid-angiopathy-1">Modified Boston criteria</a> 9 are a combination of clinical, radiographic and pathological criteria which are used to assess the probability of cerebral amyloid angiopathy.<h4>Pathology</h4>Cerebral amyloid angiopathy is characterised by the deposition of ß-amyloid (Aß-40) in the tunica media and tunica adventitia of small and medium sized arteries of the cerebral cortex and leptomeninges 4. This is associated with fibrinoid degeneration with separation of the tunica media and tunica intima, and microaneurysm formation 1. Amyloid is an eosinophilic, insoluble protein, located in the extra-cellular space, and stains with Congo red yielding apple green birefringence when viewed with polarized light 3. It is important to note that amyloid deposition is also encountered in other clinical scenarios including <a href="/articles/spongiform-encephalitis">spongiform encephalitis</a> 1.<h5>Associations</h5><ul><li>

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