Book contents
- Frontmatter
- Contents
- List of contributors
- List of abbreviations
- Preface
- Section 1 Bilateral Predominantly Symmetric Abnormalities
- 1 Hepatic Encephalopathy
- 2 Neurofibromatosis Type 1 – UBOs
- 3 Carbon Monoxide Intoxication
- 4 Pantothenate Kinase-Associated Neurodegeneration (Hallervorden–Spatz Syndrome)
- 5 Methanol Intoxication
- 6 Wilson Disease 12
- 7 Hypoxic Ischemic Encephalopathy in Term Neonates
- 8 Cryptococcosis
- 9 Gangliosidosis GM2
- 10 Leigh Disease
- 11 Deep Cerebral Vein Thrombosis (DCVT)
- 12 Creutzfeldt-Jakob Disease (CJD)
- 13 Global Cerebral Anoxia in Mature Brain
- 14 Wernicke Encephalopathy
- 15 Amyotrophic Lateral Sclerosis
- 16 Glutaric Aciduria Type 1
- 17 Subcortical Band Heterotopia
- 18 Bilateral Perisylvian Polymicrogyria (BPP)
- 19 Lissencephaly
- 20 Herpes Simplex Encephalitis
- 21 Limbic Encephalitis
- 22 CADASIL (Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy)
- 23 Megalencephalic Leukoencephalopathy with Subcortical Cysts
- 24 Canavan Disease
- 25 HIV Encephalopathy
- 26 Radiation- and Chemotherapy-Induced Leukoencephalopathy
- 27 Leukoaraiosis (Microangiopathy)
- 28 Periventricular Edema in Acute Hydrocephalus
- 29 Hypoglycemia
- 30 X-Linked Adrenoleukodystrophy (X-ALD)
- 31 Periventricular Leukomalacia (PVL)
- 32 Posterior Reversible Encephalopathy Syndrome (PRES, Hypertensive Encephalopathy)
- 33 Alexander Disease
- 34 Metachromatic Leukodystrophy
- 35 Neurodegenerative Langerhans Cell Histiocytosis (ND-LCH)
- 36 Remote Cerebellar Hemorrhage
- 37 Spontaneous Intracranial Hypotension
- Section 2 Sellar, Perisellar and Midline Lesions
- Section 3 Parenchymal Defects or Abnormal Volume
- Section 4 Abnormalities Without Significant Mass Effect
- Section 5 Primarily Extra-Axial Focal Space-Occupying Lesions
- Section 6 Primarily Intra-Axial Masses
- Section 7 Intracranial Calcifications
- Index
- References
27 - Leukoaraiosis (Microangiopathy)
from Section 1 - Bilateral Predominantly Symmetric Abnormalities
Published online by Cambridge University Press: 05 August 2013
- Frontmatter
- Contents
- List of contributors
- List of abbreviations
- Preface
- Section 1 Bilateral Predominantly Symmetric Abnormalities
- 1 Hepatic Encephalopathy
- 2 Neurofibromatosis Type 1 – UBOs
- 3 Carbon Monoxide Intoxication
- 4 Pantothenate Kinase-Associated Neurodegeneration (Hallervorden–Spatz Syndrome)
- 5 Methanol Intoxication
- 6 Wilson Disease 12
- 7 Hypoxic Ischemic Encephalopathy in Term Neonates
- 8 Cryptococcosis
- 9 Gangliosidosis GM2
- 10 Leigh Disease
- 11 Deep Cerebral Vein Thrombosis (DCVT)
- 12 Creutzfeldt-Jakob Disease (CJD)
- 13 Global Cerebral Anoxia in Mature Brain
- 14 Wernicke Encephalopathy
- 15 Amyotrophic Lateral Sclerosis
- 16 Glutaric Aciduria Type 1
- 17 Subcortical Band Heterotopia
- 18 Bilateral Perisylvian Polymicrogyria (BPP)
- 19 Lissencephaly
- 20 Herpes Simplex Encephalitis
- 21 Limbic Encephalitis
- 22 CADASIL (Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy)
- 23 Megalencephalic Leukoencephalopathy with Subcortical Cysts
- 24 Canavan Disease
- 25 HIV Encephalopathy
- 26 Radiation- and Chemotherapy-Induced Leukoencephalopathy
- 27 Leukoaraiosis (Microangiopathy)
- 28 Periventricular Edema in Acute Hydrocephalus
- 29 Hypoglycemia
- 30 X-Linked Adrenoleukodystrophy (X-ALD)
- 31 Periventricular Leukomalacia (PVL)
- 32 Posterior Reversible Encephalopathy Syndrome (PRES, Hypertensive Encephalopathy)
- 33 Alexander Disease
- 34 Metachromatic Leukodystrophy
- 35 Neurodegenerative Langerhans Cell Histiocytosis (ND-LCH)
- 36 Remote Cerebellar Hemorrhage
- 37 Spontaneous Intracranial Hypotension
- Section 2 Sellar, Perisellar and Midline Lesions
- Section 3 Parenchymal Defects or Abnormal Volume
- Section 4 Abnormalities Without Significant Mass Effect
- Section 5 Primarily Extra-Axial Focal Space-Occupying Lesions
- Section 6 Primarily Intra-Axial Masses
- Section 7 Intracranial Calcifications
- Index
- References
Summary
Specific Imaging Findings
Leukoaraiosis (LA) and white matter hyperintensities (WMH) are the interchangeable terms used for bilateral non-enhancing white matter abnormalities without mass effect that are hypodense on CT, of high T2 signal, and with increased diffusion (bright on ADC maps). The abnormalities can be punctate or patchy with irregular borders; they are often confluent and involving large areas of white matter, especially in the periventricular subependymal regions, where they may form “caps” and “rims”. The lesions tend to spare the temporal lobes and corpus callosum. T2 hyperintensities frequently also involve the deep gray matter structures. Microangiopathy is considered responsible for these imaging findings. There is a frequent coexistence of dilated perivascular spaces (PVS, Virchow–Robin spaces), lacunar infarcts, chronic microbleeds, and diffuse brain volume loss. Differentiation between PVS and lacunar infarcts is best accomplished with FLAIR images: hypodense areas with gliotic hyperintense borders are present in lacunar infarcts. A number of imaging grading systems have been formulated, but are rarely used in clinical practice.
Pertinent Clinical Information
WMH are almost universal in patients over 65 years of age and are also found in younger individuals. There is therefore a large overlap between asymptomatic aging individuals with LA and patients with vascular risk factors, such as arterial hypertension, hypercholesterolemia, diabetes mellitus, and amyloid angiopathy. LA is associated with lacunar infarcts and cerebral hemorrhages. Periventricular lesions are related to cognitive decline, whereas subcortical ones may be related to late-onset depression. Lesion extension is a predictor for the subsequent rate of progression.
- Type
- Chapter
- Information
- Brain Imaging with MRI and CTAn Image Pattern Approach, pp. 55 - 56Publisher: Cambridge University PressPrint publication year: 2012