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
20 - Herpes Simplex Encephalitis
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
As herpes simplex encephalitis (HSE) may clinically simulate stroke or tumor and early treatment is a must, identification by imaging is imperative and MRI is the method of choice. The process usually initially involves the mesial temporal lobes but may quickly extend to the insula (classically skipping the basal ganglia), the frontobasal regions, along the interhemispheric region, and then to the rest of the temporal, frontal and parietal lobes. Areas involved tend to be bilateral with generally asymmetrical degree of involvement. All lesions are of low T1 and high T2 signal, bright on DWI and with reduced diffusion on ADC maps. The advantage of FLAIR and especially DWI sequences is that the abnormalities are much more conspicuous early in the process. Contrast enhancement, particularly of the involved cortex, occurs in the later stages and meningeal enhancement may also be present. Hemorrhage may occur at any time of the infection. Perfusion study shows normal to low relative cerebral blood volume, as in other infectious and inflammatory processes. In addition to high choline and NAA, MR spectroscopy shows lipids and lactate. CT may show edema involving the temporal lobes but usually becomes positive only in advanced disease and should not be used to make the initial diagnosis. The abnormal signal in the mesial temporal lobes in patients with HHV-6 encephalopathy tends to be transient in contrast to persistent abnormality in patients with HSE.
- Type
- Chapter
- Information
- Brain Imaging with MRI and CTAn Image Pattern Approach, pp. 41 - 42Publisher: Cambridge University PressPrint publication year: 2012
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