Book contents
- Frontmatter
- Contents
- List of contributors
- List of abbreviations
- Preface
- Section 1 Bilateral Predominantly Symmetric Abnormalities
- Section 2 Sellar, Perisellar and Midline Lesions
- 38 Rathke's Cleft Cyst
- 39 Pituitary Microadenoma
- 40 Lymphocytic Hypophysitis
- 41 Pituitary Macroadenoma
- 42 Ectopic Posterior Pituitary Lobe
- 43 Langerhans Cell Histiocytosis
- 44 Craniopharyngioma
- 45 Hypothalamic Hamartoma
- 46 Optic Glioma
- 47 Perisellar Meningioma
- 48 Hemangioma of the Cavernous Sinus
- 49 Tolosa–Hunt Syndrome
- 50 Carotid-Cavernous Sinus Fistula
- 51 Perisellar Aneurysm
- 52 Chordoma
- 53 Chondrosarcoma
- 54 Colloid Cyst
- 55 Aqueductal Stenosis
- 56 Progressive Supranuclear Palsy (PSP)
- 57 Joubert Syndrome
- 58 Rhombencephalosynapsis
- 59 Multiple System Atrophy (MSA)
- 60 Maple Syrup Urine Disease (MSUD)
- 61 Chiari 2 Malformation
- 62 Tectal Glioma
- 63 Brainstem Glioma
- 64 Duret Hemorrhage
- 65 Hypertrophic Olivary Degeneration
- 66 Osmotic Myelinolysis
- 67 Germinoma
- 68 Pineoblastoma
- 69 Pineal Cyst
- 70 Vein of Galen Aneurysmal Malformation (VGAM)
- 71 Corpus Callosum Dysgenesis
- 72 Septo-Optic Dysplasia
- 73 Holoprosencephaly
- 74 Atretic Parietal Encephalocele
- 75 Dermoid Cyst
- 76 Lipoma
- 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
66 - Osmotic Myelinolysis
from Section 2 - Sellar, Perisellar and Midline Lesions
Published online by Cambridge University Press: 05 August 2013
- Frontmatter
- Contents
- List of contributors
- List of abbreviations
- Preface
- Section 1 Bilateral Predominantly Symmetric Abnormalities
- Section 2 Sellar, Perisellar and Midline Lesions
- 38 Rathke's Cleft Cyst
- 39 Pituitary Microadenoma
- 40 Lymphocytic Hypophysitis
- 41 Pituitary Macroadenoma
- 42 Ectopic Posterior Pituitary Lobe
- 43 Langerhans Cell Histiocytosis
- 44 Craniopharyngioma
- 45 Hypothalamic Hamartoma
- 46 Optic Glioma
- 47 Perisellar Meningioma
- 48 Hemangioma of the Cavernous Sinus
- 49 Tolosa–Hunt Syndrome
- 50 Carotid-Cavernous Sinus Fistula
- 51 Perisellar Aneurysm
- 52 Chordoma
- 53 Chondrosarcoma
- 54 Colloid Cyst
- 55 Aqueductal Stenosis
- 56 Progressive Supranuclear Palsy (PSP)
- 57 Joubert Syndrome
- 58 Rhombencephalosynapsis
- 59 Multiple System Atrophy (MSA)
- 60 Maple Syrup Urine Disease (MSUD)
- 61 Chiari 2 Malformation
- 62 Tectal Glioma
- 63 Brainstem Glioma
- 64 Duret Hemorrhage
- 65 Hypertrophic Olivary Degeneration
- 66 Osmotic Myelinolysis
- 67 Germinoma
- 68 Pineoblastoma
- 69 Pineal Cyst
- 70 Vein of Galen Aneurysmal Malformation (VGAM)
- 71 Corpus Callosum Dysgenesis
- 72 Septo-Optic Dysplasia
- 73 Holoprosencephaly
- 74 Atretic Parietal Encephalocele
- 75 Dermoid Cyst
- 76 Lipoma
- 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
In central pontine myelinolysis (CPM) CT shows hypodensity in the central mid to lower pons, typically of a somewhat triangular shape with its base located posteriorly and resembling a trident, due to sparing of the corticospinal tracts. The brainstem is not expanded and the abnormality tends to regress and even disappear with time. The lesions are T2 hyperintense with usually less prominent T1 hypointensity. Hemorrhage is not present and contrast enhancement is absent or minimal. DWI shows the lesion to be bright and ADC maps reveal reduced diffusion. Diffusion changes may precede T2 findings by up to 24 hours. MRS may in the acute period show elevated choline, probably due to breakdown of myelin. NAA is decreased and lactate may occasionally be present. DTI may show swelling and displacement of white matter tracts but no frank destruction.
Extrapontine myelinolysis presents as areas of high T2 signal and reduced diffusion involving the supratentorial deep gray matter and/or the corpus callosum. Involvement of the deep gray matter occurs in 10% of patients with CPM. Involvement of the corpus callosum, primarily the body, is generally known as the Marchiafava–Bignami syndrome (MBS). The entire thickness of the callosum is affected, the anterior and posterior commissures as well as the subcortical U-fibers may be involved. The lesions are T1 hypointense and bright on T2 sequences. Peripheral contrast enhancement may occur during the acute to subacute periods. Reduced diffusion correlates with a worse prognosis.
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- Information
- Brain Imaging with MRI and CTAn Image Pattern Approach, pp. 135 - 136Publisher: Cambridge University PressPrint publication year: 2012