Large Ventricles
Bronwyn E. Hamilton, MD
DIFFERENTIAL DIAGNOSIS
Common
Aging Brain, Normal
Encephalomalacia, General
Obstructive Hydrocephalus
Meningitis
Subarachnoid Hemorrhage, NOS
Intraventricular Hemorrhage
Cerebral Atrophy, NOS
Chronic Hypertensive Encephalopathy
Multiple Sclerosis
Alcoholic Encephalopathy
Radiation and Chemotherapy
Diffuse Axonal Injury (DAI)
Post-Meningitis
Drug Abuse
Less Common
Alzheimer Dementia
Normal Pressure Hydrocephalus
Multi-Infarct Dementia
Frontotemporal Dementia
Rare but Important
Choroid Plexus Papilloma
Megalencephaly Syndromes
Huntington Disease
Creutzfeldt-Jakob Disease (CJD)
Inborn Errors of Metabolism (End-Stage)
ESSENTIAL INFORMATION
Key Differential Diagnosis Issues
Imaging most important to distinguish acutely obstructive causes from non-obstructive causes
Dementias best diagnosed clinically
Helpful Clues for Common Diagnoses
Aging Brain, Normal
Ventriculomegaly in proportion to sulci
Reflects atrophy from parenchymal loss
Encephalomalacia, General
Volume loss from many causes (prior stroke, trauma, surgery)
Focal, in areas of parenchymal tissue loss (with focal ventricular enlargement), or diffuse when global
Obstructive Hydrocephalus
Surgically emergent condition
Types of obstructive hydrocephalus
Intraventricular obstructive hydrocephalus (IVOH) = “non-communicating hydrocephalus”: Due to obstructed CSF at level of ventricles from focal mass effect
Extraventricular obstructive hydrocephalus (EVOH) = “communicating hydrocephalus”: Due to obstructed CSF resorption at level of sulci, meninges/arachnoid granulations
CSF overproduction (choroid plexus tumors)
Meningitis
Mild hydrocephalus typical, may be earliest imaging finding (EVOH)
Leptomeningeal enhancement
Complications: Cerebritis/abscess, effusions, ischemia
Subarachnoid Hemorrhage, NOS
Impaired CSF resorption (EVOH)
Subarachnoid blood, often aneurysmal
Intraventricular Hemorrhage
Impaired CSF resorption (EVOH)
Ventricular blood, often related to trauma or AVM
Cerebral Atrophy, NOS
Chronic Hypertensive Encephalopathy
Brain parenchymal changes due to long-standing effects of untreated or poorly treated systemic hypertension
May result in vascular dementia
Diffuse white matter (WM) atrophy with low density or high T2 signal
May have hemorrhagic foci on GRE (basal ganglia, thalamus, cerebellum)
Multiple Sclerosis
Periventricular WM pattern of T2 hyperintensities ± enhancement
Often dramatic callosal volume loss & ventriculomegaly
Lesions generally lack mass effect
Alcoholic Encephalopathy
Chronic alcohol abuse results in symmetric lateral ventricle enlargement & superior vermian atrophy
Wernicke involvement: Mamillary bodies, medial thalami, hypothalamus, periaqueductal gray matter
Radiation and Chemotherapy
Diffuse Axonal Injury (DAI)
DAI best seen on GRE, FLAIR, & DWI
Classic locations: Gray-white matter junctions, callosum, deep nuclei
Accompanied by late WM volume loss
Post-Meningitis
Late WM volume loss diffusely
May have encephalomalacia related to abscess, ischemia
Drug Abuse
Consider in young patients with ischemic or hemorrhagic strokes
Chronic: Volume loss
Helpful Clues for Less Common Diagnoses
Alzheimer Dementia
Parietal & temporal cortical atrophy with/disproportionate hippocampal volume loss is suggestive
Normal Pressure Hydrocephalus
Clinical triad of dementia, gait apraxia, & incontinence
Ventriculomegaly disproportionate to sulcal prominence, normal hippocampus
CSF flow studies can detect increased velocity
Multi-Infarct Dementia
Multifocal infarcts involving cortical gray matter, subcortical WM, & basal ganglia
Strokes of multiple ages & lacunes common
Often associated with arteriolosclerosis, WM hyperintensity
Frontotemporal Dementia
Anterior frontotemporal atrophy with WM hyperintensity; “knife-like gyri”
Helpful Clues for Rare Diagnoses
Choroid Plexus Papilloma
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