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
5 - Methanol Intoxication
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
Initial CT and MRI studies in patients following methanol ingestion may be normal. CT and MRI performed at least 24 h after ingestion demonstrate characteristic bilateral necrosis of the putamina, which appear hypodense and edematous on CT and hyperintense on T2-weighted MR images. Hemorrhagic foci can also be seen within the putaminal lesions and other basal ganglia may be involved. Contrast-enhanced MR images may demonstrate peripheral enhancement of putaminal and subcortical lesions in the acute phase of injury. Optic nerve MR imaging reveals nonspecific T2 hyperintensity. Other findings seen in patients who survive for several days are non-enhancing areas of necrosis within the peripheral white matter, with sparing of the subcortical white matter U-fibers.
Pertinent Clinical Information
Symptoms of methanol intoxication usually begin after a 12- to 24-h latent period following ingestion. Patients typically experience visual disturbances, including decrease in visual acuity, visual field defects, color blindness, hyperemia of the optic discs, and peripapillary nerve fiber edema, and neurologic symptoms, including weakness, headache, and dizziness. Gastrointestinal complaints (pain, nausea, and vomiting) are also common. With larger consumed doses, seizures, stupor, and coma may occur. Laboratory evaluations will reveal a severe metabolic acidosis. Patients who survive methanol poisoning may have permanent blindness or irreversible neurologic impairments.
- Type
- Chapter
- Information
- Brain Imaging with MRI and CTAn Image Pattern Approach, pp. 11 - 12Publisher: Cambridge University PressPrint publication year: 2012