Brain Imaging E-Book

Bodo Kress

• Herausgeber: Thieme
• Kategorie: Fachliteratur
• Sprache: Englisch

Seitenzahl: 257

Veröffentlichungsjahr: 2007

Beschreibung

Dx-Direct is a series of eleven Thieme books covering the main subspecialties in radiology. It includes all the cases you are most likely to see in your typical working day as a radiologist. For each condition or disease you will find the information you need -- with just the right level of detail. Dx-Direct gets to the point: - Definitions, Epidemiology, Etiology, and Imaging Signs - Typical Presentation, Treatment Options, Course and Prognosis - Differential Diagnosis, Tips and Pitfalls, and Key References ...all combined with high-quality diagnostic images. Whether you are a resident or a trainee, preparing for board examinations or just looking for a superbly organized reference: Dx-Direct is the high-yield choice for you! The series covers the full spectrum of radiology subspecialties including: Brain Gastrointestinal Cardiac Breast Urogenital Spinal Head and Neck Musculoskeletal Pediatric Thoracic Vascular

Leseprobe

Direct Diagnosis in Radiology

Brain Imaging

Klaus Sartor, MD

Professor of NeuroradiologyDirector, Division of NeuroradiologyDepartment of NeurologyUniversity of Heidelberg Medical CenterHeidelberg, Germany

Stefan Haehnel, MD

Associate Professor of NeuroradiologyAssistant Director, Division of NeuroradiologyDepartment of NeurologyUniversity of Heidelberg Medical CenterHeidelberg, Germany

Bodo Kress, MD

Clinical Associate Professor of NeuroradiologyDirector, Division of NeuroradiologyDepartment of Radiology and NeuroradiologyHospital NordwestFrankfurt am Main, Germany

336 Illustrations

ThiemeStuttgart · New York

Library of Congress Cataloging-in-Publication Data is available from the publisher.

This book is an authorized and revised translation of the German edition published and copyrighted 2006 by Georg Thieme Verlag, Stuttgart, Germany. Title of the German edition: Pareto-Reihe Radiologie: Gehirn.

Translator: John Grossman, Schrepkow, Germany

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Contents

1   Trauma

B. Kress

Cerebral Contusion

Diffuse Axonal Injury

Subdural Hematoma (SDH)

Epidural Hematoma

Traumatic Subarachnoid Hemorrhage

Cerebral Edema

Herniation Syndromes

Skull Fracture

2   Inflammation

S. Haehnel

Multiple Sclerosis (MS)

Postinfectious Encephalomyelitis (ADEM)

Herpes Simplex Encephalitis

Cerebral Abscess

Meningitis

Cerebral Vasculitis

Toxoplasmosis

Progressive Multifocal Leukoencephalopathy (PML)

Tuberculosis of the CNS

CNS Cysticercosis

3   Aneurysms

S. Haehnel

Subarachnoid Hemorrhage (SAH)

Saccular Aneurysm

Fusiform Aneurysm

4   Vascular Malformations

S. Haehnel

Cavernous Hemangioma

Venous Dysplasia

Capillary Telangiectasia

Pial Arteriovenous Malformation (AVM)

Cranial Dural Arteriovenous Fistula

Variants of Vascular Anatomy

Vascular Compression Syndromes

5   Stroke

S. Haehnel

Ischemic Brain Infarction

Cerebral Microangiopathy

Primary Intracerebral Hemorrhage

Amyloid Angiopathy

Vascular Dissection

Impaired Venous Drainage

Diffuse Hypoxic Brain Damage

6   Tumors

B. Kress

Meningioma

Higher Grade Gliomas

Brain Metastasis

Low-Grade Astrocytoma

Primary CNS Lymphoma

Sellar Masses

Nerve Sheath Tumors

Oligodendroglioma

Pilocytic Astrocytoma

Medulloblastoma

Pineal Tumors

Epidermoid

Embryonal Tumors

Ependymoma

Glioneuronal Tumors

Hemangioblastoma

Gliomatosis Cerebri

Choroid Plexus Papilloma

7   Cysts

B. Kress

Arachnoid Cyst

Virchow-Robin Spaces

Pineal Cyst

Colloid Cyst

Rathke Cleft Cyst

Choroid Plexus Cyst

8   Meninges

B. Kress

Meningeal Carcinomatosis

Reactive Meningeal Enhancement

CNS Sarcoidosis

9   Ventricles and Cisterns

S. Haehnel

Obstructive Hydrocephalus

Idiopathic Normal-Pressure Hydrocephalus

Pseudotumor Cerebri

10 Leukoencephalopathies

S. Haehnel

Wallerian Degeneration

Alzheimer Disease

Central Pontine Myelinolysis

Toxic Leukoencephalopathies

Reversible Posterior Leukoencephalopathy

Multiple System Atrophy

Wilson Disease

Hepatic Encephalopathy

Amyotrophic Lateral Sclerosis (ALS)

Wernicke Encephalopathy

Superficial Siderosis of the Brain

11 Congenital Malformations

S. Haehnel

Chiari Malformations

Defective Migration

Anomalies of the Corpus Callosum

Dandy-Walker Complex

Periventricular Leukomalacia (PVL)

Neurofibromatosis Type I (Von Recklinghausen Disease)

Neurofibromatosis Type II

Tuberous Sclerosis (Bourneville-Pringle Disease)

Sturge-Weber Syndrome

Von Hippel-Lindau-Syndrome

Holoprosencephaly

12 Artifacts in MRI

S. Haehnel, B. Kress

13 Postoperative Changes

B. Kress, S. Haehnel

    Index

Abbreviations

ACTH

Adrenocorticotropic hormone

ADC

Apparent diffusion coefficient

ADEM

Acute disseminated encephalomyelitis

AIDS

Acquired immunodeficiency syndrome

ALS

Amyotrophic lateral sclerosis

ANA

Antinuclear antibody

ANCA

Antineutrophil cytoplasmic antibodies

AVM

Arteriovenous malformation

C

Cervical vertebra

CADASIL

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy

CBF

Cerebral blood flow

CNS

Central nervous system

CSF

Cerebrospinal fluid

CT

Computed tomography, computed tomogram

CTA

CT angiography

DNT

Dysembryoplastic neuroepithelial tumor

DSA

Digital subtraction angiography

EGFR

Epidermal growth factor receptor

F

Female

FLAIR

Fluid-attenuated inversion recovery

HIV

Human immunodeficiency virus

HSV

Herpes simplex virus

HU

Hounsfield unit

IR

Inversion recovery

IV

Intravenous

M

Male

MALT

Mucosal associated lymphoid tissue

MELAS

Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes

MIP

Maximum intensity projection

MR

Magnetic resonance

MRA

Magnetic resonance angiography

MRI

Magnetic resonance imaging

MRS

Magnetic resonance spectroscopy

MS

Multiple sclerosis

MT

Magnetization transfer

PDGF

Platelet derived growth factor

PET

Positron emission tomography

PML

Progressive multifocal leukoencephalopathy

PVL

Periventricular leukomalacia

rCBF

Regional cerebral blood flow

rMTT

Relative mean transit time

ROI

Region of interest

rrCBV

Relative regional cerebral blood volume

SAH

Subarachnoid hemorrhage

SDH

Subdural hematoma

SPECT

Single-photon emission computed tomography

STH

Somatotropic hormone

TE

echo time

TOF

Time of flight

TRUE FISP

True fast imaging with steady state precession

V2

Maxillary nerve

V3

Mandibular nerve

1 Trauma

Cerebral Contusion

Definition

Epidemiology

The most common type of bleeding in craniocerebral trauma.

Etiology, pathophysiology, pathogenesis

Traumatic intra-axial bleeding • Injury to cerebral parenchyma • May occur in combination with other forms of hematoma (subdural, subarachnoid, intracerebral) in up to 20% of all cases • Localization: frontobasal, occipital, parietal.

Imaging Signs

Modality of choice

CT.

CT findings

Hypodense in the acute stage, later hyperdense with a hypodense halo (perifocal edema) • Size: a few millimeters to several centimeters • Bleeding at point of impact and contrecoup bleeding are present, whereby the size of the contrecoup hemorrhage can be larger than that at the point of impact • There may be a mass effect depending on the size of the hemorrhage and the extent of the edema:

– Cerebral swelling with reduced definition of the cortex.

– Midline displacement.

– Compression of ventricular system with obstructed flow of CSF.

– Compression of the cisterna ambiens.

MRI findings

Not indicated in diagnosing acute cases • High sensitivity for older hemorrhages (subacute to chronic) • Hypointense susceptibility artifact on T2*-weighted images • Signal intensity on T1- and T2-weighted images corresponds to that of the bleeding in the respective stage of the hemoglobin breakdown process (p. 101).

Clinical Aspects

Typical presentation

Often unspecific, depending on the extent of bleeding • Headache • Vomiting • Nausea • Vertigo • Alertness is impaired, occasionally to point of loss of consciousness • Hemiparesis • Oculomotor impairment.

Treatment options

Surgical treatment is rarely indicated • Observation and control of edema are usually sufficient • Bleeding into the ventricular system may require drainage of cerebrospinal fluid.

Course and prognosis

This depends on the extent of the bleeding.

What does the clinician want to know?

Localization • Extent • Mass effect • Impingement • Rupture into the ventricular system • Obstructed flow of CSF.

Fig. 1.1 Hemorrhagic contusion in the superior frontal gyrus, 24 hours old. Axial CT.

Differential Diagnosis

The various forms of bleeding can occur in combination, rendering a differential diagnosis difficult.

Hemorrhagic infarction

– Significant perifocal edema usually present initially

– Significantly reduced ADC

Venous infarction

– Atypical location of hemorrhage (e.g. temporooccipital)

– No history of trauma

– Significant surrounding edema usually present initially

Congophilic hemorrhage

– Usually multifocal hemorrhages (T2*-weighted MR image)

– Additional signs suggestive of microangiopathy

Tips and Pitfalls

CT too early: Cerebral contusion may only be detectable after several hours. Therefore, a follow-up examination of intubated patients is indicated within six hours • Conscious patients should undergo a follow-up examination the following day.

Fig. 1.2a,b Bifrontal hemorrhagic contusion 3–4 days old. Axial T2*-weighted MR image (a) and axial T1-weighted MR image (b). Loss of signal due to susceptibility artifact on T2*-weighted images (a). Hyperintense signal (methemoglobin) on the T1-weighted image (b).

Selected References

Parizel P et al. Intracranial hemorrhage: Principles of CT and MRI interpretation. Europ Radiol 2001; 11 (9): 1770–1783

Struffert T et al. Schädel- und Hirntrauma. Radiologe 2003; 43: 861–877

Wiesmann M et al. Bildgebende Diagnostik akuter Schädel-Hirn-Verletzungen. Radiologe 1998; 38: 645–658

Diffuse Axonal Injury

Definition

Etiology, pathophysiology, pathogenesis

Stretched or torn nerve fibers • Loss of neurons • Petechial hemorrhage where perineural vessels are involved • Only about 20% of the lesions are hemorrhagic • Only half of the cases are posttraumatic; drug use is the next most common cause (recurrent hypoxia) • Disorder is most commonly supratentorial, in order of decreasing incidence: frontotemporal white matter—corpus callosum— brainstem.

Imaging Signs

Modality of choice

MRI.

CT findings

Findings are often unimpressive in the acute phase • Follow-up examinations demonstrate hemorrhages measuring a few millimeters at the corticomedullary junction • Edema is absent • Lesions in the corpus callosum and brainstem are difficult to detect • Nonhemorrhagic shear injuries cannot be diagnosed • Atrophy is a late sign of a shear injury.

MRI findings

T2*-weighted images will show a hemosiderin effect from hemorrhagic shear injuries • The apparent diffusion coefficient (ADC) is reduced • Usually at the corticomedullary junction • Linear or oval shaped • No surrounding edema • Often demonstrated only by histologic findings as many injuries are not detectable on MR images, especially nonhemorrhagic injuries.

Clinical Aspects

Typical presentation

The critical clinical condition is inconsistent with the “harmless” CT findings • Consciousness is severely impaired • Decerebrate rigidity • Convulsions • Intubation indicated.

Treatment options

No specific therapy is available • Control of edema • Management of acute complications.

Course and prognosis

Poor prognosis • Protracted convalescence • Atrophy indicative of loss of neurons.

What does the clinician want to know?

Differentiate from a “normal” cerebral contusion • Course.

Fig. 1.3 Diffuse axonal injury. Axial CT. Streaklike hemorrhages in the white matter (arrows). Hemorrhage in the corpus callosum and cingulate gyrus.

Differential Diagnosis

Contusion hemorrhage

– Perifocal edema

– Typically frontobasal and also occipital

Subarachnoid hemorrhage

– Blood in the sulci

Calcifications

– Do not show dynamic development on follow-up studies

Microangiopathy

– Periventricular location

– Located deep in white matter

– Does not show dynamic development on follow-up studies at short intervals

Tips and Pitfalls

Failing to consider diffuse axonal injury • An MRI study need not be obtained in the early phase, i.e., within the first seven days. Only in this phase is it possible to demonstrate the injury on the basis of the reduced apparent diffusion.

Fig. 1.4a,b Coronal T2*-weighted (a) and axial T1-weighted MR images (b). Susceptibility artifact on the T2*-weighted image (a). After a few days the hemorrhages are also recognizable on the T1-weighted images by their hyperintense signal (b).

Selected References

Chan J et al. Diffuse axonal injury: detection of changes in anisotropy of water diffusion by diffusion-weighted imaging. Neuroradiology 2003; 45: 34–38

Niess C et al. Incidence of axonal injury in human brain tissue. Acta Neuropathol 2002; 104: 79–84

Struffert T et al. Schädel- und Hirntrauma. Radiologe 2003; 43: 861–877

Subdural Hematoma (SDH)

Definition

Epidemiology

Incidence: 10–20% of all patients with craniocerebral trauma.

Etiology, pathophysiology, pathogenesis

Acute or chronic accumulation of blood between the dura mater and arachnoid • Usually venous bleeding • Acute subdural hematomas are an absolute emergency indication • Combinations with other forms of hematoma (subdural, subarachnoid, intracerebral) may occur in up to 20% of all cases • In 95 % of all cases, the lesion is supratentorial (especially frontoparietal) • Bilateral hematoma is present in 15% of all cases.

Imaging Signs

Modality of choice

CT.

Findings on plain skull radiography

Obsolete study as it can only demonstrate a fracture, but not a cerebral hemorrhage.

CT findings

Acute subdural hematoma: Hyperdense crescent-shaped hemorrhage along the brain (early acute components can appear hypodense) • Not bounded by sutures • Significant mass effect: midline displacement (may be absent in bilateral hematomas) • Obstructed flow of CSF, blockage of the interventricular foramen of Monro • Reduced demarcation between gray and white matter • Cisterna ambiens obliterated • In infratentorial hematomas the cerebellar tonsils are displaced into the foramen magnum • The medial temporal lobe may become impinged in the tentorial notch • Usually there is no visible fracture • Frequently occurs in combination with intra-axial bleeding • Postoperative contralateral rebleeding may occur in response to removal of the tamponade.

Chronic subdural hematoma: Isodense or hypodense extra-axial collection of blood in a crescent along the brain • Lesion crosses suture lines • With isointense hematomas, the midline displacement is often the only detectable sign of a hematoma (selecting a wider CT window than normal is helpful) • The contrast enhancement of the cerebral vessels after IV administration of contrast agent aids in differentiating the hematoma from brain tissue • Significant mass effect • Usually there is no fracture.

MRI findings

MRI is not indicated in an acute subdural hematoma • In a chronic subdural hematoma, MRI can be used to estimate the age of the lesion (signal intensity of the hemoglobin breakdown products is helpful in a medical opinion, p. 101).

Fig. 1.5 Acute hemorrhage in a chronic subdural hematoma. Axial CT. Acute blood with mass effect is visualized next to chronic hypodense blood (*). In contrast to acute epidural hematoma, the subdural hematoma is concave and not limited by cranial sutures.

Clinical Aspects

Typical presentation

Acute subdural hematoma: Absolute emergency indication • Clinical findings are similar to epidural hematoma • Nausea, vomiting, headache, unconsciousness • The patient’s condition can dramatically worsen very rapidly • Anisocoria or suddenly fixed pupils are an alarm signal but a late sign • Patients are often intubated.

Chronic subdural hematoma: Clinical signs are relatively mild compared with CT findings • Headache, nausea, vomiting, vertigo • Slowed reactions, listlessness, signs of dementia • Hemiparesis symptoms occur rarely • Follow-up examination is indicated within 6–24 hours of initial examination, depending on clinical findings.

Treatment options

Craniotomy • Immediately indicated in subdural hematoma; treatment the next day may be acceptable in chronic hematoma.

Course and prognosis

Chronic subdural hematomas may recur • Prognosis is usually poor due to concomitant administration of drugs such as acetylsalicylic acid and clopidogrel.

What does the clinician want to know?

Extent • Midline displacement • Size of basal cisterns • Obstructed flow of CSF.

Fig. 1.6a,b Chronological development of a chronic subdural hematoma in CT images. Two to three weeks after the hemorrhage, the hematoma exhibits densities approximately equal to that of brain tissue (a). This makes it difficult to delineate hematoma from brain tissue (arrowheads). During the further clinical course, the density of the hematoma decreases to values similar to CSF (b).

Differential Diagnosis

Epidural hematoma

– Convex, crescentic

– Does not cross suture line

Subarachnoid hematoma

– Blood is visible in the sulci

– No midline displacement

Intracerebral hematoma

– Bleeding into cerebral parenchyma

Subdural abscess

– Septic clinical syndrome

– Comorbidities usually present

– Hypodense or isodense to brain tissue, significant contrast enhancement

– No history of recent trauma

Tips and Pitfalls

Failing to detect bilateral isodense chronic subdural hematomas.

Fig. 1.7 Acute subdural hematoma in the posterior longitudinal fissure and in a frontal location. Axial CT.

Selected References

Maxeiner H. Entstehungsbedingungen, Quellen und Typologie von tödlichen Subdural-blutungen. Rechtsmedizin 1998; 9 (1): 14–20

Struffert T et al. Schädel- und Hirntrauma. Radiologe 2003; 43: 861–877

Wiesmann M et al. Bildgebende Diagnostik akuter Schädel-Hirn-Verletzungen. Radiologe 1998; 38: 645–658

Epidural Hematoma

Definition

Epidemiology

Frequency: 1–5% of all patients with craniocerebral trauma • In 5% of these cases bilaterally (occasionally only after surgical decompression of one side).

Etiology, pathophysiology, pathogenesis

Acute, usually traumatic bleeding between the inner table and dura mater • Usually the result of arterial injury (middle meningeal artery in 85% of all cases) • Venous bleeding occurs in 15% of all cases (diploic veins, dural venous sinus, especially in infratentorial hematomas) • May occur in combination with other forms of hematoma (subdural, subarachnoid, intracerebral) in up to 20% of all cases • Localization: usually temporoparietal.

Imaging Signs

Modality of choice

CT.

Findings on plain skull radiography

Obsolete study as the film can only demonstrate a fracture, but not the extent of bleeding • Obtaining a plain skull film merely delays relevant diagnostic studies.

CT findings

Semiconvex shape • Hyperdense • Acute, uncoagulated blood components can also be hypodense • The hematoma cannot cross suture lines as the dura mater is firmly attached to the bone along the boundaries of the calvaria • Significant mass effect: midline displacement • Reduced demarcation between gray and white matter • Obstructed flow of CSF (blockage of the interventricular foramen of Monro) • Cisterna ambiens narrowed (the medial temporal lobe may become impinged in the tentorial notch) • The hematoma can rapidly expand • Usually there is a displaced calvarial fracture • Postoperative contralateral rebleeding (epidural or intracerebral) may occur in response to removal of the tamponade.

MRI findings

Not indicated because of the long time required to organize and perform the examination.

Clinical Aspects

Typical presentation

Absolute emergency that can rapidly become life threatening • Nausea, vomiting, headache, unconsciousness • The patient’s condition can dramatically worsen very rapidly • Anisocoria or suddenly fixed pupils are an alarm signal but a late sign • Patients are often intubated.

Treatment options

Surgery is usually indicated • Unconscious patients with an epidural hematoma not requiring surgery should have a follow-up CT within six hours • Conscious patients who can undergo neurologic evaluation may have a follow-up CT the next day • Patients with an epidural hematoma not requiring surgery must remain under observation (ideally in the intensive care unit).

Course and prognosis

With early craniotomy, the prognosis is good; otherwise mortality is high.

What does the clinician want to know?

Extent • Midline displacement • Obstructed flow of CSF.

Fig. 1.8a,b Epidural hematoma. Axial CT. Convex, hyperdense mass close to the calvaria. The sutures are a natural barrier for epidural hematomas because here the dura mater is firmly attached to the calvaria (a). Epidural hematomas typically occur in the setting of a fracture (b).

Differential Diagnosis

Subdural hematoma

– Crosses suture line

– Significant mass effect even with minimal thickness

– Symptoms milder, especially in chronic hematomas

– Often no visible fracture

Subarachnoid hematoma

– Blood visible deep in the sulci

– No midline displacement

Intracerebral hematoma

– Bleeding into cerebral parenchyma

Epidural abscess

– Septic clinical syndrome

– Comorbidities usually present

– Hypodense or isodense to brain tissue

– No history of recent trauma

Fig. 1.9 Postoperative epidural bleeding. Axial CT. Acute epidural hematomas can also contain hypodense components (arrow). This is acute blood that has not yet coagulated. The air inclusions are residues of the operation.

Tips and Pitfalls

No follow-up examination • No observation on the ward • Failing to detect temporal polar epidural hematoma.

Selected References

Struffert T et al. Schädel- und Hirntrauma. Radiologe 2003; 43: 861–877

Wiesmann M et al. Bildgebende Diagnostik akuter Schädel-Hirn-Verletzungen. Radiologe 1998; 38: 645–658

Traumatic Subarachnoid Hemorrhage

Definition

Etiology, pathophysiology, pathogenesis

Bleeding into the subarachnoid space secondary to trauma • Rupture of veins or arteries • May occur in combination with hematomas at other sites (subdural, subarachnoid, intracerebral) in up to 20% of all cases • Typical localization: parietal.

Imaging Signs

Modality of choice

CT.

Findings on plain skull radiography

Obsolete study as the film can only demonstrate a fracture, but not the extent of bleeding.

CT findings

Streaks in the sulci isodense to blood • Typical localization: parietal • No midline displacement • No evidence of aneurysm on arterial CT angiography • Flow of CSF may be obstructed.

MRI findings

Prepontine hemorrhages are best visualized on proton density-weighted images (hyperintense signal in hypointense CSF) • Subarachnoid hemorrhages in the cerebral hemispheres are best visualized on FLAIR images (hyperintense signal of the sulci) • Chronic subarachnoid hemorrhages appear on T2*-weighted images as a hypointense coating over the surface of the brain (siderosis, p. 244).

Clinical Aspects

Typical presentation

Craniocerebral trauma dominates the clinical picture • An isolated traumatic subarachnoid hemorrhage is a rare finding • Headache, nausea, vomiting • Vertigo • Consciousness is impaired, occasionally to point of loss of consciousness • Obstructed flow of CSF.

Treatment options

Management of complications.

Course and prognosis

This depends on the severity of the craniocerebral trauma.

What does the clinician want to know?

Differentiate from a subarachnoid hemorrhage due to a ruptured aneurysm • Obstructed flow of CSF.

Fig. 1.10 Traumatic subarachnoid hemorrhage. Axial CT. Hyperdense frontoparietal subarachnoid space. Adjacent to this is a subdural hematoma on the left side.

Differential Diagnosis

The sensitivity of CT for demonstrating a subarachnoid hemorrhage is at most 90%; this means a normal CT does not exclude a subarachnoid hemorrhage • MRI has the same sensitivity as lumbar puncture.

Aneurysmal hemorrhage

– In the basal cisterns or prepontine region

– Proven aneurysm is diagnostic

– Differential diagnosis can be difficult, especially with uncertain trauma; such cases require identical diagnostic procedures as aneurysmal hemorrhage (CTA, DSA)

Fig. 1.11a,b Aneurysmal subarachnoid hemorrhage. Axial CT (a) and CTA (b). In contrast to traumatic subarachnoid hemorrhage, the greater portion of the blood in an aneurysmal hemorrhage is in the basal cisterns (a). Aneurysm demonstrated on arterial CTA (b, arrow).

Tips and Pitfalls

Misinterpreting a ruptured aneurysm as a traumatic subarachnoid hemorrhage • When in doubt, at least perform CT angiography.

Selected References

Grunwald I et al. Klinik, Diagnostik und Therapie der Subarachnoidalblutung. Radiologe 2002; 42: 860–870

Struffert T et al. Schädel- und Hirntrauma. Radiologe 2003; 43: 861–877

Wiesmann M et al. Nachweis der akuten Subarachnoidalblutung. FLAIR und Protonendichte-gewichtete MRT-Sequenzen bei 1,5 Tesla. Radiologe 1999; 39: 860–865

Cerebral Edema

Definition

Epidemiology

Frequency: Occurs in 20% of all severe craniocerebral trauma cases • Frequently accompanies tumors and infarctions as well.

Etiology, pathophysiology, pathogenesis

Inclusion of fluid in the brain parenchyma (vasogenic, cytotoxic) • Impaired cerebral vascular autoregulation • Hypoxia • The swelling can briefly occur secondary to trauma, but usually only a day or two later.

Imaging Signs

Modality of choice

CT or MRI.

CT findings

Loss of demarcation between gray and white matter • Increase in the volume of brain parenchyma, decrease in the volume of the subarachnoid space and cisterns • White matter is hypodense • Mass effect is present, which may include herniation • Intact portions of the brain are visualized adjacent to edematous portions (for example, “white cerebellum sign”).

MRI findings

Loss of demarcation between gray and white matter • On T1-weighted inversion recovery images, the otherwise typical contrast between the hypointense gray matter and hyperintense white matter is no longer discernible • The apparent diffusion coefficient (ADC) is reduced in cytotoxic cerebral edema and increased in vasogenic and interstitial cerebral edema • Obstructed flow of CSF.

Clinical Aspects

Typical presentation

Life-threatening clinical syndrome • Patients usually require intubation and assisted respiration.

Treatment options

Control of edema: mannitol, appropriate physical steps • Hemicraniotomy where indicated.

Course and prognosis

Up to 50% mortality.

What does the clinician want to know?

Mass effect (extent of midline displacement in millimeters, impingement signs, obstructed flow of CSF, infarctions) • Signs of brain death.

Fig.1.12 Edema in the left cerebral hemisphere. Axial CT. Compared with the right side, the left sulci are less clearly delineated and the demarcation between gray and white matter is reduced.

Fig. 1.13 Hypoxia. Axial CT. Absence of demarcation between gray and white matter. The sulci are no longer delineated, indicating irreversible damage to the cerebral parenchyma.

Differential Diagnosis

Brain not yet fully myelinized

– Normal demarcation between gray and white matter, although no sulci can be delineated

– No asymmetry between the hemispheres

Tips and Pitfalls

Failing to identify herniation (p. 19).

Selected References

Karantanas A et al. Contribution of MRI and MR angiography in early diagnosis of brain death. Europ Radiol 2002; 12(11): 2710–2716

Struffert T et al. Schädel- und Hirntrauma. Teil 2: Intraaxiale Verletzungen, sekundäre Verletzungen. Radiologe 2003; 43: 1001–1016

Herniation Syndromes

Definition

Etiology, pathophysiology, pathogenesis

The falx and tentorium divide the intracranial space into two supratentorial spaces and an infratentorial space • A hemorrhage or cerebral edema forces brain tissue into an adjacent compartment: subfalcial herniation (midline displacement), transtentorial or tonsilar herniation • Herniation syndromes lead to ischemic lesions and obstructed flow of CSF, which may eventually cause death if they persist.

Imaging Signs

Modality of choice

CT.

CT findings

CT systems with multiple detectors allow multiplanar reconstructions that visualize the displacement of brain tissue.

Subfalcial herniation: Most common herniation syndrome • The septum pellucidum is displaced to the contralateral side (semiconvex course) • There is a risk of obstructed flow of CSF due to blockage of the interventricular foramen of Monro (the width of the temporal horns is a sensitive sign of this).

Transtentorial herniation: Displacement of portions of the midbrain inferiorly through the tentorium • Narrowing or complete occlusion (obliteration) of the cisterna ambiens • Usually with midline displacement • Obstructed flow of CSF due to compression of the sylvian aqueduct.

Tonsilar herniation: Infratentorial mass effect • Displacement of the cerebellar tonsils inferiorly through the foramen magnum • Obliteration of the prepontine cistern • The perimedullar halo of CSF is no longer present in the foramen magnum • Obstructed flow of CSF due to compression of the sylvian aqueduct and the fourth ventricle.

MRI findings

This modality is the second choice due to the time it requires • Multiplanar imaging can visualize the herniation syndrome in all planes • Secondary sequelae that can be visualized include: microhemorrhages (T2*-weighted images), cranial nerve lesions (T1-weighted gradient echo sequences after injection of contrast agent), hypoxic brain damage (diffusion-weighted images).

Clinical Aspects

Typical presentation

Severely ill patient, usually intubated and requiring assisted respiration • Life-threatening situation, especially where there is impingement in the tentorial notch and foramen magnum • Pupillomotor dysfunction • Brainstem syndrome with loss of corneal reflex, altered respiration, and cardiovascular dysfunction • Obstructed flow of CSF.

Fig. 1.14a,b Development of cerebral edema in craniocerebral trauma. Axial CT. At admission to the hospital (a) the prepontine cistern is still completely intact. Two days after trauma (b) there is significant infratentorial swelling. The intracranial portion of the cisterna magna at the foramen magnum is no longer visible. The cerebellar tonsils are displaced into the foramen magnum (inferior impingement).

Treatment options

Control of edema, for example with mannitol • Appropriate physical steps • Decompression craniotomy.

Course and prognosis

Life-threatening situation with poor prognosis.

What does the clinician want to know?

Are the basal cisterns still demarcated? • Obstructed flow of CSF? • Signs of brain death?

Differential Diagnosis

Chiari malformation

– Cerebellar tonsils extend into the foramen magnum but secondary signs are absent (prepontine space not narrowed)

Asymmetrically positioned patient

– Septum pellucidum in the center

– No sequelae of trauma

Fig. 1.15 Axial CT. Significant midline shift with blockage of the foramen of Monro due to the right temporal hemorrhage (widening of the left lateral ventricle). Narrowing of the perimesencephalic cisterns (transtentorial herniation).

Tips and Pitfalls

Misinterpreting a Chiari malformation as impingement • Failing to note the width of the basal cisterns.

Selected References

Struffert T et al. Schädel- und Hirntrauma. Teil 2: Intraxiale Verletzungen, sekundäre Verletzungen. Radiologe 2003; 43: 861–877

Skull Fracture

Definition

Epidemiology

Frequency: Occurs in approximately 3% of all patients with craniocerebral trauma • Intracranial injury is present in 90% of all patients with skull fracture.

Etiology, pathophysiology, pathogenesis

Traumatic discontinuity of the calvaria or facial portion of the skull • Discontinuity of the inner and outer tables.

Imaging Signs

Modality of choice

CT.

Plain skull radiography

Such studies are obsolete as they cannot exclude intracranial injury • Guidelines of the German Society of Neuropediatrics specify CT as the modality of choice for primary diagnosis of craniocerebral trauma where available • Conventional radiographs are only helpful in isolated facial trauma (submentobregmatic “jug handle” view in a fracture of the zygomatic arch, occipitomental/occipitofrontal nasal sinus views in a midfacial fracture) • Look for indirect fracture signs (fluid levels, air).

CT findings

Should be recalculated in the bone algorithm and documented in the bone window, for example, w 400 c 1500 • Discontinuity of the calvaria traceable through several slices • Midfacial fractures require multiplanar reconstructions, for example, coronal in an orbital floor fracture and sagittal in a temporomandibular joint fracture • Fluid in the petrous bone or nasal sinuses is an indirect fracture sign in patients with craniocerebral trauma • Intracranial air is a sign of an open fracture of the frontal or temporal base • CSF leaks are difficult to diagnose; sometimes this is possible only with intrathecal contrast (CT with the patient prone).

MRI findings

In injuries to the atlantoaxial junction • Fat-saturated T2-weighted images show a hyperintense bone marrow edema.

Clinical Aspects

Typical presentation

Retrograde amnesia • Headache • Vomiting, nausea • Vertigo • Cranial CT is absolutely indicated in a unconscious patient with multiple trauma or in patients taking anticoagulants • Clinically asymptomatic patients do not require imaging studies (and especially not a plain skull radiograph).

Treatment options

Isolated nondisplaced skull fractures without associated intracranial bleeding are not treated • Displaced fractures can be an indication for surgery.

Fig. 1.16a,b Multiple skull base fractures (arrows; a) in the petrous bone, temporal bone, wall of the sphenoidal sinus, and muscular process of the mandible (arrow; b). High-resolution axial CT (a) and oblique sagittal reconstruction (b).

Course and prognosis

The prognosis for nondisplaced fractures without associated intracranial bleeding is good.

What does the clinician want to know?

Associated intracranial injury • Displacement of bone fragments.

Differential Diagnosis

Chronic fracture

– Rounded edges in contrast to acute fracture

– No corresponding soft-tissue swelling

Suture

– Not easy to differentiate from a fracture, especially in children

– Margin sclerosed

– Usually symmetrical

– At typical locations: lambdoid suture, temporozygomatic suture, sagittal suture, coronal suture

Ruptured suture

– Asymmetrically widened suture

– Usually with associated intracranial injury

Anomalies

– Various anomalies, especially at the skull base, for example bone defect in the floor of the orbit, lamina papyracea, occipital squama

– No accompanying symptoms, no hematoma, no soft-tissue swelling

– Clinical findings do not suggest injury

Fig. 1.17