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title: "Normal Aging Brain"
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docid: "2a315550-b2ea-4afe-a2ef-f93a2209f276"
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breadcrumbs:
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- "Brain"
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- "Diagnosis"
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- "Pathology-Based Diagnoses"
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- "Acquired Toxic/Metabolic/Degenerative Disorders"
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- "Dementias and Degenerative Disorders"
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- "Normal Aging Brain"
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---
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# KEY FACTS
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- ## Terminology
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- ↓ overall brain volume with advancing age
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- Reflected in relative ↑ CSF spaces
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- ## Imaging
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- Broad spectrum of "normal" on imaging in elderly
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- "Successfully aging brain"
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- Smooth, thin, periventricular, high signal rim on FLAIR is normal
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- White matter hyperintensities (WMHs) absent/few
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- ↓ total brain volume
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- Selective atrophy of white matter (not gray matter) predominates
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- ± punctate hippocampal Ca⁺⁺
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- Enlarged perivascular (Virchow-Robin) spaces
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- WMHs ↑ in number/size after 50 years
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- Focal high signal intensity in splenium of corpus callosum
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- GRE/SWI
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- Increasing mineralization of basal ganglia with age
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- "Black line" in visual, motor/sensory cortex
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- Microbleeds are relatively common in aging patients
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- Lower prevalence than in cerebral amyloid disease & Alzheimer disease
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- ## Top Differential Diagnoses
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- Mild cognitive impairment
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- Alzheimer disease
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- Sporadic subcortical arteriosclerotic encephalopathy
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- Vascular dementia
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- Frontotemporal lobar degeneration
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- ## Clinical Issues
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- WMHs correlate with age, silent stroke, hypertension, female sex
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- ## Diagnostic Checklist
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- Cannot predict cognitive function from CT/MR
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- If brain volume loss appears disproportionate to age, look for potential neurodegenerative or systemic causes
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# TERMINOLOGY
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- ## Definitions
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- ↓ overall brain volume with advancing age
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- Reflected in relative ↑ CSF spaces
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# IMAGING
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- ## General Features
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- ### Best diagnostic clue
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- "Successfully aging brain"
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- Thin, periventricular, high-signal rim
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- Absent/few white matter hyperintensities (WMHs)
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- Mild shrinkage of selected cerebellar regions
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- ### Location
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- Selective atrophy of white matter (WM) predominates, not gray matter (GM)
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- Striatum (primarily caudate nucleus, putamen)
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- ### Size
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- ↓ total brain volume
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- Absolute striatal size
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- Caudate ↓ linearly with age
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- Putamen remains relatively stable
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- Relative striatal size (ratio of absolute size:total brain volume)
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- Caudate remains relatively stable
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- Putamen ↑ linearly with age
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- ### Morphology
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- Brain tissue ↓, CSF volume ↑
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- Reflects overall WM volume loss > focal WMHs
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- Rounded appearance of dilated ventricles, sulci ↑
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- Strong correlation between WM volume and CSF volume: Measure of overall brain atrophy
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- ## CT Findings
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- ### NECT
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- Enlarged ventricles, widened cortical sulci
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- Patchy periventricular low densities
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- ± symmetrical, punctate calcifications in globi pallidi (GP)
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- ± curvilinear vascular Ca⁺⁺
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- ± punctate hippocampal Ca⁺⁺
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- ### CECT
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- No parenchymal enhancement
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- ## MR Findings
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- ### T1WI
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- Mild but symmetric ventricular enlargement, proportionate prominence of subarachnoid spaces
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- Mild but significant age-related shrinkage of
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- Posterior vermis (lobules 6, 7, and 8-10)
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- Cerebellar hemispheres
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- Apparent age invariance of anterior vermis, ventral pons
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- Enlarged perivascular (Virchow-Robin) spaces
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- Common in aging, considered reflection of cerebral small vessel disease
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- Isointense to CSF on all sequences
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- Conform to course of penetrating arteries
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- Round/oval/curvilinear
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- Smooth, well-defined margins
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- Bilateral, often symmetrical; usually no mass effect
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- ↑ in number, size (> 2 mm) with age
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- Can be found in most areas
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- Midbrain, hippocampi, basal ganglia (BG), & centrum semiovale
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- Tend to cluster around anterior commissure
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- Inferior 1/3 of putamen, external capsule
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- ### T2WI
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- Focal/confluent periventricular WMHs
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- Number/size ↑ after 50 years; ~ universal after 65 years
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- Only rough correlation with cognitive function
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- Significant overlap with dementias
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- Infarct-like T2-hyperintense lesions
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- Seen in 1/3 of asymptomatic patients > 65 years
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- 70% < 10 mm
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- Mostly in BG, thalami
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- Probably represent clinically silent lacunar infarcts
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- ### FLAIR
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- Smooth, thin, periventricular hyperintense rim is normal
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- Focal high signal intensity in splenium of corpus callosum
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- BG and thalamic foci
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- Perivascular spaces suppress
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- Lacunar infarcts hyperintense
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- ### T2* GRE
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- SWI: Increasing mineralization of BG with age
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- Normal in GP, abnormal in thalamus
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- Can see linear "waves" or conglomerate mineralization in GP
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- Putaminal hypointensity less prominent until 8th decade
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- Microbleeds are common in aging brain
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- SWI demonstrates microbleeds in 20% of patients > 60 years and in 60-70% of patients > 80 years
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- Microbleeds are relatively common in aging patients
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- Lower prevalence than in cerebral amyloid disease & Alzheimer disease
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- BG, brainstem, and cerebellar microbleeds indicative of chronic hypertensive encephalopathy
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- Lobar and cortical microbleeds typical of amyloid angiopathy
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- SWI: "Black line" in visual, motor/sensory cortex
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- Common, normal in older patients
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- ### DWI
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- Small but significant ↑ water diffusibility
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- ADC ↑
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- DTI: Loss of fractional anisotropy in normal-appearing WM
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- ### T1WI C+
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- Age-related WMHs do not enhance
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- If enhancing, consider acute/subacute lacunar infarct or metastases
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- ### MRS
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- Metabolite distribution varies among different brain regions
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- Choline (Cho) content ↑ with aging
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- Creatine (Cr) ↑ with aging
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- N-acetyl aspartate (NAA) ↓ in cortex, centrum semiovale, temporal lobes
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- ## Nuclear Medicine Findings
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- ### PET
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- Metabolic alterations common
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- Global, regional changes in cerebral blood flow (CBF)
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- Gradual ↓ in regional CBF of GM, WM
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- Particularly in frontal lobes
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- Age-related shift from anterior to posterior cortical metabolism
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- Putamen receives primarily posterior cortical input
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- Caudate receives relatively more anterior cortical input
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- Relative glucose metabolic rate (rGMR) measured by FDG PET
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- With age, rGMR ↑ in putamen and ↓ in caudate
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- ↓ pre-/postsynaptic dopamine markers in BG
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- Tc-99m HMPAO SPECT, Xe-133 inhalation show regional, global reduction in CBF
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- ## Imaging Recommendations
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- ### Best imaging tool
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- MR with FLAIR, DWI, T2* GRE/SWI
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# DIFFERENTIAL DIAGNOSIS
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- ## Mild Cognitive Impairment
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- Overlap with normal on standard imaging studies
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- Associated with ↓ size and number of regions of brain activation in response to memory tasks despite normal-appearing brain on conventional MR
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- Higher calculated hippocampal ADCs (not visible)
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- Subtle hypoperfusion, hypometabolism in parahippocampal regions, cingulum, thalamus
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- ↓ NAA
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- [Alzheimer Disease](/document/alzheimer-disease/f71f5cf5-b1af-4c6d-b145-b4c10eec7b58)
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- Parietal and temporal cortical atrophy
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- Striking volume loss in hippocampi, entorhinal cortex
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- Often coexisting microvascular disease, WMHs
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- Striking temporoparietal hypometabolism, hypoperfusion
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- ↓ NAA, ↑ myoinositol (mI)
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- [Sporadic Subcortical Arteriosclerotic Encephalopathy](/document/chronic-hypertensive-encephalopathy/1afc1f3f-203d-4cdf-8d49-2283cb13d6db)
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- Associated with hypertension
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- Numerous WMHs (overlap with normal)
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- Multiple lacunar infarcts
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- Lenticular nuclei, pons, thalamus, internal capsule, and caudate nuclei
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- Diffuse, confluent regions of periventricular WM involvement (leukoaraiosis)
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- [Vascular Dementia](/document/vascular-dementia/f59dab57-c511-4369-8fcc-592421a4b8d1)
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- Hyperintense lesions on T2WI and focal atrophy suggestive of chronic infarcts
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- [Frontotemporal Lobar Degeneration](/document/frontotemporal-lobar-degeneration/49510d0e-acf7-45cb-9eb1-53f8193b0b6d)
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- Asymmetric frontal, anterior temporal atrophy
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- T2 hyperintensity in frontotemporal WM
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- Dilated subarachnoid space over frontal lobes signifying atrophy
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- ↓ metabolic activity in frontotemporal cortices
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# PATHOLOGY
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- ## General Features
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- ### Etiology
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- Previous conception of aging: Substantial cortical neuronal loss with age
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- New: Predominant neuroanatomic changes
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- WM alterations, subcortical neuronal loss
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- Reduction in cell size > cell number
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- Neuronal dysfunction rather than loss of neurons/synapses
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- ↓ neuronal viability or function associated with accelerated membrane degradation &/or ↑ glial cell numbers
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- Loss of synapses and dendritic pruning in selected areas rather than globally
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- Some investigators consider accumulation of neurofibrillary tangles (NFTs) may be responsible for memory loss associated with aging
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- ### Genetics
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- Clearly affect aging of brain
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- Apolipoprotein E (*APOE*) and 6 novel risk-associated single nucleotide polymorphisms (SNPs) on chromosome 17q25 associated with brain pathology in aging
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- ## Gross Pathologic & Surgical Features
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- Widened sulci, proportionate large ventricles
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- Minor thinning of cortical mantle, predominant changes in subcortical WM
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- ## Microscopic Features
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- Degeneration of neurons and oligodendrocytes
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- ↓ myelinated fibers in subcortical WM
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- ↑ extracellular space, gliosis
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- Iron deposition in GP, putamen
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- WM capillaries lose pericytes, have thinner endothelium
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- Dilated perivascular spaces of Virchow-Robin
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- Extension of subarachnoid space that accompanies penetrating vessels into brain to level of capillaries
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- Senile plaques
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- Extracellular amyloid deposits in cerebral GM
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- Lewy bodies
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- Intraneuronal clumps of α-synuclein and ubiquitin proteins
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- Found in 5-10% of cognitively intact individuals
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- NFTs
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- Tau phosphorylation, mitochondrial dysfunction may precede full NFT formation
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- NFTs appear in small numbers in entorhinal and transentorhinal cortices early in aging (patients ~ 60 years)
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- NFTs may induce neural dysfunction, destruction of synapses, and, eventually, neuronal death
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# CLINICAL ISSUES
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- ## Presentation
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- ### Most common signs/symptoms
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- Normal cognitive function
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- Mild cognitive impairment correlates with ↑ risk of Alzheimer disease
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- ## Demographics
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- ### Age
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- > 60 years
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- ### Sex
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- Differences in striatal size
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- Relatively constant across lifespan in men
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- Variable across lifespan in women: Smaller in women aged 50-70 years than in men
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- Differences in rGMR
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- Caudate: Higher rGMR in women than men
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- Putamen: Equal rGMR in women and men
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- Greater dopamine transporters in caudate in women
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- ### Epidemiology
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- WMHs correlate with age, silent stroke, hypertension, female sex
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- ## Natural History & Prognosis
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- Parenchymal volume ↓, CSF spaces ↑ progressively
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- WMHs progressively ↑ with age
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# DIAGNOSTIC CHECKLIST
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- ## Consider
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- Striatum may mediate age-associated cognitive decline
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- ↓ volume, functional activity with age
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- ## Image Interpretation Pearls
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- Broad spectrum of "normal" on imaging in elderly
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- Cannot predict cognitive function from CT/MR
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- If brain volume loss appears disproportionate to age, look for potential neurodegenerative or systemic causes
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a71a0c8f-d105-4815-9edf-3fc113d5acc4
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