Cerebral amyloid angiopathy (CAA) refers to the deposition of β-amyloid in the arteries of the cerebral cortex. It is commonly seen in Alzheimer's disease but can also occur in healthy elderly individuals. CAA can cause intracerebral hemorrhage, dementia, or transient neurological symptoms. The deposition damages blood vessels and increases the risk of hemorrhage. Imaging such as CT scans can detect hemorrhages characteristic of CAA, which are often lobar and cortical. Genetic factors like the ApoE genotype can influence the severity and presentation of CAA.
Tips, Pearls and Pitfalls of Spinal Cord MRIWafik Bahnasy
- Many neurological disorders simultaneously or consecutively affect the brain and spinal cord, however most neurologist find their comfort zone in attending the diagnosis via the brain access.
- This concept resulted in lagging of spinal cord imaging researches compared to brain ones and consecutive underestimation of the opportunity of an important tool sometimes essential to reach a definite diagnosis.
White matter hyperintensities, the invisible invaderWafik Bahnasy
WMHs is the most frequent type of CSVDs and a common incidental finding in MRI films of up to 70% of MRI images in individuals > 60 years, and 90% in those > 70 years.
Meticulous assessment of asymptomatic WMHs subjects reveals the presence of subtler cognitive, gait, balance and psychiatric disturbances.
On the occasion of National Epilepsy Day 2014, Dr. Rama Krishnan gave a talk titled "Integrated Diagnostics – A Unique Epilepsy Approach" at the Epilepsy Knowledge Forum in Chennai organised by Neurokrish & Trimed and Sponsored Medall.
Tips, Pearls and Pitfalls of Spinal Cord MRIWafik Bahnasy
- Many neurological disorders simultaneously or consecutively affect the brain and spinal cord, however most neurologist find their comfort zone in attending the diagnosis via the brain access.
- This concept resulted in lagging of spinal cord imaging researches compared to brain ones and consecutive underestimation of the opportunity of an important tool sometimes essential to reach a definite diagnosis.
White matter hyperintensities, the invisible invaderWafik Bahnasy
WMHs is the most frequent type of CSVDs and a common incidental finding in MRI films of up to 70% of MRI images in individuals > 60 years, and 90% in those > 70 years.
Meticulous assessment of asymptomatic WMHs subjects reveals the presence of subtler cognitive, gait, balance and psychiatric disturbances.
On the occasion of National Epilepsy Day 2014, Dr. Rama Krishnan gave a talk titled "Integrated Diagnostics – A Unique Epilepsy Approach" at the Epilepsy Knowledge Forum in Chennai organised by Neurokrish & Trimed and Sponsored Medall.
Stroke in people under 45 years of age is less frequent than in older populations but has a major impact on the individual and society. In this article we provide an overview of the epidemiology and etiology of young stroke.
Stroke is also known as Cerebrovascular Accident. This results in the sudden death of the brain cells due to the O2 deficiency when the blood flow to the brain is lost by obstruction/rupture of cerebral arteries which supplies to the brain. Stroke prevention requires the management of the many risk factors important to stroke development. It is important to diagnose stroke as early as possible to reduce the risk of more damage and functional loss. Stroke recovery is an inhomogeneous process, therefore, it is challenging to predict the actual post-stroke outcomes which assure a holistic approach. Rehabilitation can be provided in inpatient or outpatient departments to stroke survivors.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Radiological pathology of cerebral amyloid angiography
1. Professor Yasser Metwally
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INDEX |
INTRODUCTION
INTRODUCTION
Cerebral amyloid angiopathy (CAA) refers to the deposition of ß-amyloid in the media and
adventitia of small- and mid-sized arteries (and less frequently, veins) of the cerebral cortex
and the leptomeninges. It is a component of any disorder in which amyloid is deposited in
the brain, and it is not associated with systemic amyloidosis. CAA has been recognized as
one of the morphologic hallmarks of Alzheimer disease (AD), but it also is found often in
the brains of elderly patients who are neurologically healthy. While often asymptomatic,
CAA can present as intracranial hemorrhage (ICH), dementia, or transient neurologic
events. ICH is the most consistent effect of CAA. Although the vast majority of cases are
sporadic, 2 familial forms exist (ie, hereditary cerebral hemorrhage with amyloidosis
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[HCHWA]-Dutch type and HCHWA-Icelandic type). The severity of CAA is age related;
more than 50% of patients in the tenth decade of life have evidence of CAA. Increasing age
and the presence of AD are the only identified risk factors for CAA.
Deposition of amyloid damages the media and adventitia of cortical and leptomeningeal
vessels, leading to thickening of the basal membrane, stenosis of the vessel lumen, and
fragmentation of the internal elastic lamina. This can result in fibrinoid necrosis and
microaneurysm formation, predisposing to hemorrhage. Some evidence suggests that the
amyloid is produced in the smooth muscle cells of the tunica media as a response to damage
of the vessel wall (perhaps by arteriosclerosis or hypertension). Although CAA may be
found more commonly in women than men at autopsy, the incidence of ICH is the same in
women and men. Hemorrhage occurs at the same age in men and women.
The true incidence and prevalence are hard to specify, as definite CAA can be diagnosed
only at postmortem. However, estimates can be made based on autopsy series and the
incidence of lobar ICH. A series of 400 autopsies found evidence of CAA in the brains of
18.3% of men and 28% of women aged 40-90 years. In a series of 117 brains of patients
with confirmed AD, 83% had evidence of CAA. The prevalence of CAA increases with
advancing age; in some autopsy series it has been found in 5% of individuals in the seventh
decade but in 50% of those older than 90 years. CAA is estimated to account for up to 15%
of all ICH in patients older than 60 years and up to one half of nontraumatic lobar ICH in
patients older than 70 years (approximately 15-20 cases per 100,000 people per y). CAA
and CAA-related hemorrhage are particularly common in elderly individuals with AD and
Down syndrome.
Conditions associated with cerebral amyloid angiopathy
o Intracerebral hemorrhage
The most consistent clinical effect of CAA is lobar ICH. Lobar ICH is associated with a
lower mortality rate (11-32%) and a better functional outcome than hypertensive deep
ganglionic bleeds. Of individuals with CAA-related hemorrhage, 25-40% have a
recurrence, with the highest risk in the first year. Recurrent hemorrhages can occur
simultaneously or several years later. They are associated with a high mortality rate (up to
40%). Patients with a previous hemorrhage are at greater risk for subsequent hemorrhages
than those with no history. Hypertension may exacerbate the tendency to CAA-related
hemorrhage and vice versa. Cortical petechial hemorrhage can be epileptogenic. Familial
forms of CAA are associated with hemorrhage at younger ages, by the third or fourth
decade in the Icelandic form and by the sixth decade among the Dutch kindreds.
o
Dementia
Cognitive impairment of Alzheimer type is a common feature of CAA. More than 40% of
patients with ICH-related hemorrhage have some degree of dementia. In some cases, the
cognitive changes can precede the ICH. The relationship between CAA and AD is close.
CAA, which is present in 80-85% of patients with AD, is severe in one third to two thirds of
these patients. CAA is the most significant microscopic abnormality in 10-15% of patients
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diagnosed with AD by clinical criteria. CAA and AD coexist pathologically at rates greater
than predicted by chance. Arterial ß-amyloid in CAA is nearly identical to senile plaque ßamyloid. Vascular lesions can play a significant physiopathologic role and can contribute to
the development of dementia in AD. The severity of CAA is correlated with the presence of
ischemic or hemorrhagic lesions in the brains of patients with AD, and CAA is associated
with gross strokes but not with subcortical lacunae. However, a direct causal link between
the 2 disorders has not been established, and the association could be due to shared risk
factors such as the presence of apolipoprotein (ApoE) e4. Some patients with CAA present
with a progressive dementia that entails rapid cognitive decline over days or weeks. This
rapid progression could be due to the additive effects of severe vascular amyloid, cortical
hemorrhages and infarctions, white matter destruction, and accumulation of neuritic
plaques.
o
Vasculitis
Few cases of vasculitis of various types (giant cell arteritis, rheumatoid vasculitis, primary
angiitis of the CNS) associated with CAA have been reported. No consensus exists as to
whether the pathologic abnormalities are related causally or whether the appearance of
vasculitis is a reaction to CAA-induced angiopathic changes.
o
Microbleeds in cerebral amyloid angiography
Cerebral microbleeds are defined radiologically as small, rounded, homogeneous,
hypointense lesions on T2*-weighed gradient-recalled echo (T2*-GRE) and related MRI
sequences that are sensitive to magnetic susceptibility.[11] Scharf et al. were the first to
report on small, intracerebral black dots of signal loss on T2-weighted spin-echo MRI in
patients with hypertensive cerebrovascular disease and intracerebral hemorrhage (ICH)
associated with ischemic white matter disease and lacunar infarcts.[12] They called these
lesions ‘hemorrhagic lacunes’, and their further characterization using T2*-GRE MRI
sequences led to the current radiologic definition of ‘microbleeds’, a term coined by
Offenbacher and colleagues in 1996.[13] A key feature of Cerebral microbleeds is that they
are not seen well on conventional computed tomography or MRI scans. Available
histopathological studies suggest that Cerebral microbleeds radiological lesions are due to
tiny bleeds adjacent to abnormal small vessels, being mainly affected by hypertensive
angiopathy (arteriolosclerosis – usually lipohyaline degeneration related to hypertension)
or cerebral amyloid angiopathy (CAA).[14]
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Figure 1. A postmortem section of the brain
showing a cortical microbleed (arrow) in a
patient with Alzheimer’s disease and CAA
CLINICAL PICTURE OF CEREBRAL AMYLOID ANGIOGRAPHY
History
CAA is frequently asymptomatic. However, it can present as one of several
clinicopathologic entities. The most frequent are ICH and dementia.
CAA most often comes to clinical attention because of ICH. Symptoms may range
from transient weakness to coma, depending on the size and location of the
hemorrhage. Patients may have recurrent episodes.
o The most common symptom at onset is headache (60-70% of patients).
Frontal hematomas produce bifrontal headache pain; parietal bleeds, usually
unilateral temple pain; temporal hematomas, ipsilateral eye and ear pain;
and occipital bleeds, ipsilateral eye pain.
o Vomiting (in 30-40%) tends to occur early.
o Seizures occur at onset in 16-36%. Seizures are most commonly partial, with
symptoms determined by the location of the ICH. As many as half of the
patients present in status epilepticus.
o Coma at presentation has been reported in a small proportion of patients
(0.4-19%). Decreased level of consciousness, which is related to the size and
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location of the hematoma, results from compression of the contralateral
hemisphere or brain stem or increased intracranial pressure.
Dementia may be manifested by any of several patterns of cognitive dysfunction.
Some patients present with rapid progression from a normal baseline to profound
dementia in a couple of years. Other patients can have a more protracted course,
which is more typical of that seen in AD.
Stereotyped transient neurologic events commonly consist of focal weakness,
paresthesias, or numbness. In some cases, these events may be prodromes to larger
hemorrhages.
o The symptoms spread to contiguous body parts over 2-10 minutes, and they
may involve areas in several vascular territories. These events are probably
due to small cortical petechial hemorrhages that lead to focal seizures. The
rate of spread is akin to that seen in migraine; some have proposed that they
may represent spreading depression of neuronal activity.
o Some patients present with transient confusion or episodes of visual
misperceptions.
Uncommon presentations of CAA
o CAA can be associated with ischemic strokes; in some of these patients, a
coexistent vasculitis can be found. The causal relationship with CAA is
unclear.
o CAA is found in patients with autosomal dominant dementia, spasticity, and
ataxia without ICH.
o CAA is reported in patients with vascular malformations, postirradiation
necrosis, spongiform encephalopathies, and dementia pugilistica.
o CAA can present as a mass lesion; this has been related to the existence of an
"amyloidoma" with accumulation of amyloid in the brain parenchyma or to
edema and gliosis that result from the vascular lesion.
Physical
Physical findings depend on the clinicopathological entity associated with CAA in a
particular patient.
The features of ICH depend on the location of the bleed. Strict isolation of features
from each lobe frequently is not possible because of extension of hematoma to other
lobes, mass effect, and increased intracranial pressure.
o Frontal: Depending on the size and location, frontal ICH may present with
any symptoms from weakness of one limb to impaired consciousness with
contralateral hemiparesis, hemisensory loss, and horizontal gaze palsy. Left
hemispheric lesions can present with aphasia, and more anterior lesions lead
to an abulic state with frontal release signs.
o Parietal: Hemisensory loss, homonymous hemianopsia, hemi-inattention, and
apraxia are all signs of parietal ICH.
o Temporal: Dominant hemisphere hematomas lead to aphasia and
hemianopia; nondominant hemisphere hematomas produce a confusional
state.
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o
Occipital: Unilateral hemianopia or quadrantanopia
hallucinations often accompany occipital ICH.
and
visual
AETIOLOGY OF CEREBRAL AMYLOID ANGIOGRAPHY
Most cases are sporadic, although genetic predispositions exist. (eg, ApoE subtypes
confer different risk profiles.)
Most cases of CAA-related ICH are spontaneous, but they may be related to vessel
wall injury by atherosclerosis and hypertension. The risk of intracranial bleeding
following head trauma and neurosurgical procedures is increased in patients with
CAA. Some evidence suggests that CAA has a role in a substantial proportion of
anticoagulant- and thrombolytic-related hemorrhages.
Hereditary forms of CAA are due to specific gene mutations.
Hereditary cerebral hemorrhage with amyloidosis-Dutch type is an autosomaldominant disorder with complete penetrance.
o The age of onset of ICH is in the sixth decade (mean, 55 y). Eighty-seven
percent of those affected have ICH, and 13% have infarcts (deep).
o Some patients develop dementia without ICH.
o Amyloid deposits are found in cortical and leptomeningeal vessels;
parenchymal neurofibrillary tangles are not seen. Deposited amyloid protein
in these patients is identical to the amyloid protein seen in sporadic cases,
and the likely genetic defect is in the amyloid protein precursor protein
(APP) gene on chromosome 21.
Hereditary cerebral hemorrhage with amyloidosis-Icelandic type is also autosomal
dominant.
o Patients present with their first episode of ICH in the third or fourth decade,
with some patients dying from ICH aged as young as 15 years. A recent case
report has identified a family with late-onset dementia with and without
ICH.
o The amyloid angiopathy is more widely distributed in this type than in other
types, involving arteries in the cerebrum, cerebellum, and brain stem.
o The amyloid protein is a mutant of the cysteine protease inhibitor cystatin C.
Severity of angiopathy and fibrinoid necrosis closely correlate with the occurrence
of ICH.
The Boston Cerebral Amyloid Angiopathy Group has elaborated guidelines for the
diagnosis of CAA associated with ICH. Four levels of certainty in the diagnosis of
CAA are considered: definite, probable with supporting pathological evidence,
probable, and possible. The first 3 require that no other cause of hemorrhage has
been identified; they are yet to be validated but are clinically useful.
o Definite CAA: Full postmortem examination reveals lobar, cortical, or
corticosubcortical hemorrhage and evidence of severe CAA.
o Probable CAA with supporting pathological evidence: The clinical data and
pathological tissue (evacuated hematoma or cortical biopsy specimen)
demonstrate a hemorrhage with the aforementioned characteristics and some
degree of vascular amyloid deposition.
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o
o
Probable CAA: Clinical data and MRI findings (in the absence of a
pathological specimen) demonstrate multiple hematomas (as described
above) in a patient older than 60 years.
Possible CAA: This is considered if the patient is older than 60 years, and
clinical and MRI data reveal a single lobar, cortical, or corticosubcortical
hemorrhage without another cause, multiple hemorrhages with a possible
but not a definite cause, or some hemorrhage in an atypical location.
GENETIC OF CEREBRAL AMYLOID ANGIOGRAPHY
The severity of the angiopathy is associated with ApoE polymorphism. The ApoE e4
and e2 alleles are risk factors for CAA.
o The ApoE e2 allele also confers an increased risk of ICH in patients with
CAA. The ApoE e4 allele is associated with earlier onset of first hemorrhage
and carries a significant risk of concomitant AD.
o Patients with lobar ICH and the e2 or e4 allele have a greater risk of early
recurrence.
o These tests lack sensitivity and specificity and are not indicated as screening
or diagnostic procedures. However, they may be helpful prognostic tools in
identifying patients with a greater risk of early recurrence.
In cases of CAA-related ICH, laboratory studies should rule out other possible
etiologies.
IMAGING OF CEREBRAL AMYLOID ANGIOGRAPHY
CT scan of the brain
o This procedure is the first choice for patients with suspected acute ICH.
o A single lobar hemorrhage with superficial location and cortical involvement
with or without local extension to the subarachnoid and intraventricular
spaces is suggestive of CAA-related hemorrhage. Evidence of multiple
hemorrhages restricted to lobar regions may be present.
o Hemorrhages are most common in the frontal and parietal lobes, involving
the cortex and subcortical white matter. Over time, several lobes may be
involved. Deep central gray nuclei, the corpus callosum, and the cerebellum
are sometimes affected. CAA is rarely the cause of putaminal, thalamic, or
brain stem hemorrhage.
o Pure subarachnoid, intraventricular, and subdural hemorrhages can be seen
but are rare. CAA should never be assumed to be the cause of an isolated
subarachnoid hemorrhage unless all other causes, particularly aneurysmal,
have been excluded.
o Patients with CAA-associated dementia have a leukoencephalopathy similar
to that seen in Binswanger disease. Atrophy also can be detected, particularly
in patients with cognitive impairment and a history of prior hemorrhage.
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MRI
o
o
o
o
MRI shows evidence of multiple cortical and subcortical large and small
petechial hemorrhages, even in patients without a history that suggests
previous hemorrhage.
MRI gradient-echo sequences show evidence of iron deposits, which
correspond to old hemorrhages. In patients who present with lobar
hemorrhages, the evidence of old petechial bleeds and microbleeds can help
in the diagnosis of CAA. Gradient-echo MRI also can be used as a marker of
disease progression and potentially can evaluate the effect of therapeutic
interventions.
Leptomeningeal enhancement is seen in patients with associated vasculitis.
Cerebral microbleeds are commonly associated with cerebral amyloid
angiopathy, Microbleeds are lobar in location in patients with cerebral
amyloid angiopathy
Figure 2. Lobar microbleeds on 3dimensional
T2*-weighted
gradientrecalled echo MRI in an 80 years old man
with dementia and cerebral amyloid
angiopathy.
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Figure 3. Example of
microbleeds
on
3dimensional
T2*-weighted
gradient-recalled echo MRI
in an 80 years old man with
Alzheimer dementia and
cerebral
amyloid
angiopathy. The microbleeds
are lobar in location.
HISTOPATHOLOGICAL FINDING IN CEREBRAL AMYLOID ANGIOGRAPHY
Histologic examination is required for definitive diagnosis. Pathologic samples are obtained
from hematoma evacuation, cortical biopsy, or postmortem specimens. The disease process
may be diffuse, so pathologic data may be lacking even in biopsy cases. The presence of
vascular amyloid is a sensitive marker for CAA-related hemorrhage. ß-amyloid consists of
twisted ß-sheet fibrils in vessel wall. It is a homogenous, intensely eosinophilic material that
gives a smudged appearance by light microscopy. When stained with Congo red and
visualized under polarized light, it gives a characteristic yellow-green (ie, apple green)
birefringence. When thioflavin T and S are used and visualized with ultraviolet light,
amyloid appears fluorescent. The presence of fibrinoid necrosis in amyloid-laden vessels is
relatively specific for CAA-related ICH. CAA, which involves cortical and leptomeningeal
vessels, is most common in the parietal and occipital lobes. The microangiopathy spares
white matter and deep gray structures. Parenchymal features found in the brains of
patients with CAA include patchy demyelination and loss of white matter, cortical
hemorrhages and infarcts, and neuritic plaques with or without neurofibrillary tangles.
Most patients with CAA-related ICH do not have AD.
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Figure 4. Lobar hemorrhage due to amyloid angiopathy, B Microscopic section of the brain
cortex, section has been stained with Congo Red for amyloid viewed with polarized light.
The section shows relatively preserved cortical neurons and the blood vessels shows
birefringence with polarized light. In some areas the walls of the blood vessels are yellowgreen (arrow). Diagnosis: Amyloid angiopathy, also known as congophilic angiopathy.
References
1. Case records of the Massachusetts General Hospital. Weekly clinicopathological
exercises. Case 22-1996. Cerebral hemorrhage in a 69-year-old woman receiving
warfarin [clinical conference] [published erratum appears in N Engl J Med 1996
Oct 10;335(15):. N Engl J Med 1996 Jul 18; 335(3): 189-96.
2. Ellis RJ, Olichney JM, Thal LJ, et al.: Cerebral amyloid angiopathy in the brains of
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