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T. Lim and M. M. Thurnher

Fig. 6.9 Proven tuberculous meningitis with multiple ring enhancing tuberculomas in the basal cistern (a–c). With disease progression, there was perineural spread with thickened and enhancing cranial nerves (d–f, red arrows) (Reprinted with permission from Thurnher, M.M.,

small medial lenticulostriate and thalamo-perforating branches, resulting in basal ganglia and thalamus infarctions. These can be sensitively demonstrated using DWI, and MRA or black blood, high-resolution, thin-section 3D black blood, black CSF vessel wall imaging (VWI) (Fig.6.10) sequences can reveal narrowed enhancing vasculitic vessels (other infectious causes of vasculitis include aspergillosis and varicella zoster virus (VZV) infection).

Tuberculoma is the most common parenchymal form of CNS; imaging appearances depend on the different stages of infection; and tuberculomas heal by resolving or calcifying. Early, non-caseating tuberculomas show homogenous, nodular enhancement with low signal on T1-weighted images and high signal on T2-weighted images, and surrounding oedema. Solid caseating tuberculomas show variable signal intensity due to paramagnetic free radicals. Liquifying caseating tuberculomas resemble pyogenic abscess in signal and enhancing characteristics but are typically smaller with less surrounding oedema. Tuberculous abscesses are rarer, larger, multilocu-

Sundgren, P.C. (2020). Intracranial Infection and Inammation. In: Hodler, J., Kubik-Huch, R., von Schulthess, G. (eds) Diseases of the Brain, Head and Neck, Spine 2020–2023. IDKD Springer Series. Springer, Cham)

lated and are often indistinguishable from pyogenic abscess. Miliary TB with innumerable small enhancing lesions at the grey-white matter junction typically occurs in immunocompromised patients with widespread extracranial disease. Spinal cord/meningeal TB, including osteomyelitis/disc infection, and psoas abscess, should also be sought.

Key Points

• Characteristic complications of tuberculosis. – Thick leptomeningeal enhancement affecting

basal cisterns. – Hydrocephalus. – Tuberculomas. – Tuberculous abscesses. – Vasculitic stenosis/beading and infarction (espe-

cially basal ganglia/thalamus). – Cranial nerve enhancement and pachymeningitis.

6 Intracranial Infection andInammation

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Fig. 6.10 Tuberculous vasculitis: Time-of-ight MR angiography shows signal dropout in the right worse than left middle cerebral artery (MCA). Contrast-enhanced black blood, black CSF vessel wall imag-

6.7 Viral Infections

6.7.1 Herpes Simplex Virus

HSV-1 is the commonest cause of acute encephalitis syndrome, comprising 10–20% of identiable viruses. Typical ndings include unilateral or bilateral asymmetric swelling and hyperintensity on T2-weighted/FLAIR images, affecting hippocampus, anterior and medial temporal lobes and insular cortex (but often sparing the basal ganglia) (Fig.6.11). There is sometimes haemorrhage, DWI restriction, and contrast enhancement (compared to autoimmune encephalitis, see Sect. 6.8.1).

Key Points

• Many viral causes of encephalitis have yet to be identied.

• HSV-1 is the commonest virus and affects the hippocampus/temporal lobe.

• LGI1 antibody limbic encephalitis often mimics HSV-1 infection.

• Many arboviruses affect the thalamus bilaterally, sometimes with blood products.

• Varicella zoster virus is a major cause of vasculopathy and stroke in children.

ing shows linear enhancing vessel wall from vasculitis of the MCA branch artery, and enhancing subacute infarction of the right caudate nucleus

6.7.2 Arboviruses andOther Viruses

Arthropod-borne pathogens are spread by mosquitos, ticks, or other vectors. They include Japanese encephalitis virus (JEV), dengue virus (DENV), and Zika viruses and typically have geographic and seasonal variability. In patients with bilateral thalamic involvement (especially with haemorrhage), JEV and inuenza-associated encephalitis (IAE) should be considered (Fig. 6.12). IAE is most common in children under 5years of age, the elderly, and patients with co-morbidities. Enterovirus and rabies virus infections can involve the brainstem; VZV infection is a major cause of vasculopathy and ischemic stroke in children.

6.7.3 Progressive Multifocal Leukoencephalopathy

Progressive multifocal leukoencephalopathy (PML) is a demyelinating disease caused by reactivation of JC virus (a polyomavirus) infection in immunocompromised patients, especially people living with HIV.Typical features are bilateral asymmetric frontal or/and parietooccipital subcortical U bre white matter involvement (very rarely is periventricular white matter affected rst); the middle cerebellar peduncle, pons, peri-dentate white matter may also be affected, but isolated spinal cord lesions are rare. Classic PML is typically hyperintense on T2-weighted and FLAIR images, low or iso-

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Fig. 6.11 Herpes simplex virus type 1: bilateral asymmetric (worse on the right) swelling and increased signal on T2-weighted, DWI, and FLAIR images involving the medial temporal lobe (especially the hippocampus) and insula cortex (see Fig.6.15 for comparison)

T. Lim and M. M. Thurnher

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Fig. 6.12 Japanese encephalitis (a) FLAIR image shows bilateral symmetric high-signal lesions in the thalamus. (b, c). Most of the lesions show high signal on DWI and mixed ADC values. (Reprinted

signal on T1-weighted images, without enhancement, vasogenic oedema, or mass effect (Fig.6.13). DWI appearances vary according to stage of disease, with restricted diffusion in newer lesions or the advancing edge of active infection/

with permission from Ramli NM, Bae YJ.Structured Imaging Approach for Viral Encephalitis. Neuroimaging Clin N Am. 2023 Feb;33(1):43–56)

demyelination. Inammatory PML (with enhancement, vasogenic oedema, and mass effect) is a less common presenting phenotype or may be visualized in IRIS.

6 Intracranial Infection andInammation

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Fig. 6.13 Progressive multifocal leukoencephalopathy: T2-weighted images before (left) and after (right) antiretroviral therapy showing reduced extent of high signal in the subcortical white matter

6.8 Inammatory Diseases oftheCNS

Immune-mediated inammatory diseases of the CNS (Fig. 6.14) may be encountered by radiologists in patients with known cancer (paraneoplastic syndromes), in patients with known rheumatological diseases (e.g. systemic lupus erythematosus SLE, Sjogren’s disease), in patients after a viral infection (e.g. acute disseminated encephalomyelitis or ADEM), and nally as mimics of infection based on typical MRI patterns [5, 6]. Many of the imaging patterns of leptomeningitis, pachymeningitis, encephalitis, or vascular disease, described in the preceding sections of this chapter may also be caused by non-infectious inammation. Familiarity with these inammatory mimics may help diminish morbidity and future disability by facilitating appropriate treatments early, avoiding invasive brain biopsy, and triggering appropriate CT of the chest, abdomen, and pelvis to screen for underlying cancer or sarcoidosis.

6.8.1 Autoimmune andLimbic Encephalitis: LGI1 Antibody Encephalitis

The cause of acute encephalitis syndrome can be either infective or noninfective. Clinically, limbic encephalitis often presents with anterograde memory loss, seizures, behavioural or psychiatric symptoms, with MRI abnormalities affecting the hippocampus and medial temporal lobes bilaterally. Leucine-rich glioma inactivated 1 (LGI1) antibody is the commonest cause of limbic encephalitis mimicking HSV-1 infection (Fig. 6.15). Fever, a fulminant clinical course, unilateral involvement, absence of basal ganglia involvement, DWI restriction, and contrast enhancement, all favour HSV-1. Other autoimmune encephalitis is less consistent in their imaging

appearance; MRI in NMDA receptor encephalitis is more often normal, white matter abnormalities in MS, ADEM and MOG may mimic PML, and bilateral caudate and putamen abnormalities may be seen in anti- CV2/collapsin response mediator protein 5 (CRMP5) antibodies in occult small cell lung cancer. Brainstem, cerebellar, and spinal cord lesions are also associated with multiple autoimmune pathologies.

6.8.2 Leptomeningeal Enhancement: Neurosarcoidosis

This multisystem inammatory granulomatous disease has a predilection to affect the leptomeninges (50%, especially basal meninges, mimicking TB), pituitary gland, optic and facial cranial nerves, and spinal meninges (Fig. 6.16). Differentiation of neurosarcoidosis from TB can be difcult or impossible by imaging alone.

Key Points

• Neurosarcoidosis can affect different brain/spine compartments and mimics tuberculosis.

• Focal pachymeningeal disease can be caused by TB, syphilis, Lyme disease, sarcoidosis, IgG4related disease, antineutrophil cytoplasmic antibody associated (ANCA), and tumours such as meningioma or metastasis.

• Autoimmune CNS vasculitis has variable, often nonspecic imaging ndings.

• Many antibodies in paraneoplastic and immunemediated inammatory diseases have yet to be identied.

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T. Lim and M. M. Thurnher

Leptomeninges Pachymeninges

Neurosarcoidosis

Beh et syndrome IgG4 related disease

Sjogren syndrome and rheumatoid arthritis

Primary and secondary CNS vasculitis

Differential: infectious meningitis, subarachnoid hemorrhage, meningioma

Cortical and subcortical area

NMDAR, GABA A/B, DPPX

ADEM, MOG, AQP4, MS

Differential: PML, lymphoma, anoxic injury, inherited leukodystrophies

Striatum

CRMP5/CV2, DR2, NMDAR, LGI1

SLE

Differential: CJD, anoxic injruy, toxic metabolic causes, toxoplasmosis, cryptococcus, Wilson disease

The meninges

Neurosarcoidosis

Granulomatosis with polyangiitis, ANCAassociated vasculitis

Rheumatoid arthritisGFAP

Idiopathic hypertrophic pachymeningitis

Differential: infectious meningitis, meningioma, intracranial hypotension

Pituitary and sellar

Neurosarcoidosis

IgG4 related disease

Granulomatosis with polyangiitis, (ANCA)

CNS histiocytosis

Brainstem

See Table 10-1

Limbic system

Immune-mediated

Targeting membrane proteins: NMDAR, LGI1,

CASPR2, AMPAR, DPPX, GABA B, IgLON5

Targeting nuclear or cytoplasmic proteins:

ANNA1/Hu, GAD65, Ma2/Ta, CRMP5/CV2

Differential diagnosis

Viral etiologies: HSV1, CMV, adenovirus, HHV6, VZV, WNV

Bacterial etiologies: syphilis

Infiltrative glioma

Peri-ictal and postictal changes

Diencephalon (thalamus and hypothalamus)

Ma1-2, NMDAR, IgLON5, DPPX, AQP4

Neurosarcoidosis, Beh et syndrome, CNS histiocytosis

Differential: Wernicke encephalopathy, Whipple disease, deep venous thrombosis, arboviruses

Cerebellum

Paraneoplastic and autoimmune: ANNA1/Hu, ANNA2/Ri, PCA1/Yo, mGLuR1, GAD65, KLH11, Septin-5 and-7 IgGs

Differential: Viral or postinfectious cerebellitis, celiac disease, neurodegeneration such as SCA

Fig. 6.14 Autoimmune and inammatory central nervous system (CNS) disorders and radiographic differential diagnoses based on typical location. (Reprinted with permission from Wahed LA, Cho

TA.Imaging of Central Nervous System Autoimmune, Paraneoplastic, and Neuro-rheumatologic Disorders. Continuum (Minneap Minn). 2023 Feb 1;29(1):255–291)

Fig. 6.15 LGI1 antibody encephalitis. Axial and coronal T2-weighted and FLAIR images showing bilateral symmetrical swelling and increased signal in the hippocampus (see Fig.6.11 for comparison)

6.8.3 Pachymeningeal Enhancement: IgG4Related Diseases

with IgG4 related spectrum of disease, including orbital pseudotumor. Commonly, IgG4 disease affects the pancreas,

biliary tract, kidneys, retroperitoneum/aorta, and thorax. In IgG4-related disease is a multisystem chronic progressive broinammatory autoimmune disease; as the disease denition is updated, some conditions are now felt to overlap

the head and neck (second commonest site of presentation

after the pancreas), the salivary (especially submandibular),

lacrimal, and pituitary glands may be affected, and localized

6 Intracranial Infection andInammation

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Fig. 6.16 Axial FLAIR (a) and T1-weighted post-contrast administra- tion (b) demonstrate diffuse, focal, increased FLAIR signal in the underlying brain parenchyma and focal left-sided leptomeningeal enhancement in a patient with neurosarcoidosis. (Reprinted with per-

mission from Thurnher, M.M., Sundgren, P.C. (2020). Intracranial

Infection and Inammation. In: Hodler, J., Kubik-Huch, R., von

Schulthess, G. (eds) Diseases of the Brain, Head and Neck, Spine

2020–2023. IDKD Springer Series. Springer, Cham)

def

Fig. 6.17 Thick, dural enhancement is observed bilaterally frontally and along the falx (b–f). T2-high-signal intensity is also seen in the parenchyma of both frontal lobes, reecting compression of the brain parenchyma (a) (Reprinted with permission from Thurnher, M.M.,

or diffuse pachymeningeal thickening and enhancement can be seen (Fig. 6.17). Tissue biopsy is the gold standard for diagnosis but MRI typically shows low signal on both T1-

Sundgren, P.C. (2020). Intracranial Infection and Inammation. In:

Hodler, J., Kubik-Huch, R., von Schulthess, G. (eds) Diseases of the

Brain, Head and Neck, Spine 2020–2023. IDKD Springer Series.

Springer, Cham)

and T2-weighted images, with homogeneous enhancement;

remission after steroid therapy (in almost 90%) can be a

helpful feature.

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T. Lim and M. M. Thurnher

6.8.4 Autoimmune CNS Vasculitis

tions, but ndings often not specic for the cause. Concentric

wall thickening favours vasculitis over atherosclerosis Cerebral vessel walls are inamed in CNS vasculitis, which

can be caused by primary angiitis of the CNS, or can be secondary to underlying systemic vasculitis (such as SLE, rheu-

(which tends to show eccentric thickening) on VWI but is

also not specic for the type of vasculitis. Diagnosis often

depends on biopsy. matoid arthritis, and Sjogren’s disease), or secondary to

infections (such as TB, VZV, or syphilis). MRI is nearly always abnormal, and a normal study can exclude vasculitis. Typical ndings include infarcts of different ages in different arterial territories (Fig. 6.18), sometimes accompanied by parenchymal or subarachnoid blood. DSA is more sensitive than MRA and CTA in detecting “beading”; alternating stenosis and dilatation in at least two separate vascular distribu-

6.8.4.1 Autoimmune CNS Vasculitis

Granulomatosis with polyangiitis (GPA)(previously called

Wegener’s granulomatosis) is a systemic vasculitis of small

and medium vessels and can rarely affect the CNS, character-

ized by high mortality. MRI typically shows focal granulo-

mas spreading from the frontal sinus, leptomeningeal contrast

enhancement, and white matter hyperintensities (Fig.6.19).

Fig. 6.18 Different imaging ndings in patients with known vasculitis; (a) hyperintense FLAIR lesions, (b) conuent white matter signal abnormalities, (c) leptomeningeal contrast enhancement, (d) cortical infracts, (e) multiple acute lacunar infarcts (Reprinted with permission

from Thurnher, M.M., Sundgren, P.C. (2020). Intracranial Infection and

Inammation. In: Hodler, J., Kubik-Huch, R., von Schulthess, G. (eds)

Diseases of the Brain, Head and Neck, Spine 2020–2023. IDKD

Springer Series. Springer, Cham)

6 Intracranial Infection andInammation

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ab c

Fig. 6.19 (a) Sagittal CT (bone window) demonstrates opacication of the frontal sinus. (b, c) Granuloma extension into the frontal lobes bilaterally with surrounding oedema and gliosis (Reprinted with permission from Thurnher, M.M., Sundgren, P.C. (2020). Intracranial

6.9 Concluding Remarks

Radiologists should be aware of the three characteristic imaging patterns in meningitis, abscess, and encephalitis. Clinical problem-solving based on MRI pattern recognition remains a fundamental skillset: our knowledge of typical features and their anatomical distribution enables us to process new data in novel infectious/inammatory agents considering past differential diagnosis. Conventional and advanced MRI techniques and new point-of-care scanners have the potential to improve diagnostic performance in CNS infections, especially in future outbreaks and pandemics (Fig. 6.20) [7]. Future advances in PCR technology, machine learning, and new MRI biomarkers hold great promise for elucidating the pathogen and immune-mediated mechanisms of neuronal damage and complications. The role and value of radiologists are enhanced by multidisciplinary team discussions, because “No man is an island”; we do not work in isolation, all of us are an essential part of the healthcare teams.

Infection and Inammation. In: Hodler, J., Kubik-Huch, R., von

Schulthess, G. (eds) Diseases of the Brain, Head and Neck, Spine

2020–2023. IDKD Springer Series. Springer, Cham)

Take-Home Messages

• Multimodal MRI, including post-contrast 3D T2-FLAIR, DWI, SWI, and vessel wall imaging is useful for problem-solving.

• Although CNS infection typically presents with characteristic patterns of meningitis, abscess, HSV-1 encephalitis, it is important to remember their mimics and differentiating features.

• Restricted diffusion on DWI has high sensitivity and specicity for meningitis and pyogenic abscess, respectively.

• HSV-1 infection and LGI1-antibody encephalitis can both cause medial temporal and hippocampal abnormalities.

• Specic infectious agents including HIV and TB may have characteristic MRI appearances and complications.

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T. Lim and M. M. Thurnher

Fig. 6.20 Summary of major emerging zoonotic outbreaks related to bats, 1994–2019. Conrmed bat-borne viruses include Hendra, Nipah, and SARS-CoV-1 viruses; bats are also suspected to be viral reservoirs for MERS, Ebola, and SARS-CoV-2 (cause of the current COVID-19 pandemic) viruses. Years when outbreaks occurred and conrmed or

References

1. Thurnher MM, Sundgren PC. Intracranial infection and inammation. In: Hodler J, Kubik-Huch R, von Schulthess G, editors. Diseases of the brain, head and neck, spine 2020–2023, IDKD Springer Series. Cham: Springer; 2020.

2. Thurnher MM. Bacterial infections. In: Barkhof F, Jäger R, Thurnher M, Rovira A, editors. Clinical neuroradiology. Berlin: Springer; 2019.

3. Duong MT, Rudie JD, Mohan S.Neuroimaging patterns of intracranial infections: meningitis, cerebritis, and their complications. Neuroimaging Clin N Am. 2023;33(1):11–41.

suspected intermediate hosts involved in virus spillover are also shown. *Indicates that although the 2014 Ebola outbreak was believed to have started with direct bat-to-human transmission, nonhuman primates have been implicated in previous Ebola outbreaks. ^Data accurate as of May 11, 2020. (Reprinted with permission of Duke-NUS Medical School)

4. Thurnher MM. Infections in immunocompromised patients. In: Barkhof F, Jäger R, Thurnher M, Rovira A, editors. Clinical neuroradiology. Berlin: Springer; 2019.

5. Graus F, Titulaer MJ, Balu R, etal. A clinical approach to diagnosis of autoimmune encephalitis. Lancet Neurol. 2016;15:391–404.

6. Wahed LA, Cho TA. Imaging of central nervous system autoimmune, paraneoplastic, and neuro-rheumatologic disorders. Continuum (Minneap Minn). 2023;29(1):255–91.

7. Goh GX, Tan K, Ang BSP, Wang L-F, Tchoyoson Lim CC. Neuroimaging in zoonotic outbreaks affecting the central nervous system: are we ghting the last war? Am J Neuroradiol. 2020;41:1760–7.

Open Access This chapter is licensed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.

org/licenses/by/4.0/), which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropri-

ate credit to the original author(s) and the source, provide a link to the Creative Commons license and indicate if changes were made.

The images or other third party material in this chapter are included in the chapter's Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the chapter's Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder.

Neuroimaging Update onTraumatic

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Brain Injury

ApostolosJ.Tsiouris andYvonneW.Lui

Abstract

Traumatic brain injury is a common injury worldwide that

affects individuals of all ages. Injuries can range in sever-

ity. Timely assessment of injury is important to triage

cases that may be severe and imminently life-threatening,

and neuroimaging is a critical component to the clinical

care of such patients. Injuries may occur in multiple

spaces from the extracranial soft tissues to the potential

spaces between meningeal layers to the brain parenchyma

itself. The neck and intracranial arterial and venous ves-

sels can also be injured with devastating sequelae. CT,

CTA, MRI, and MRA can all be useful in the assessment

of head injury. In particular, CT is often used as a rst-line

imaging modality to screen for acute intracranial injury.

MRI can be useful in patients who have discordance

between symptoms and CT ndings as well as in those

with more prolonged symptoms or who suffer chronic

sequelae of injury. Neuroimaging research is ongoing

using MRI to study the underlying pathophysiology of

head injury.

Keywords

Head trauma · Brain injury · CT · MRI

Learning Objectives

• Review imaging techniques used to help diagnose and evaluate patients with CNS trauma.

• Compare the utility of CT vs MRI in evaluating TBI patients with a spectrum of brain injuries.

• Show various forms of surgical vs non-surgical intracranial abnormalities resulting from head trauma.

Key Points

• CT is the primary imaging modality utilized to assess patients following CNS trauma in the urgent setting due to availability, speed, and few contraindications.

• Initial CT ndings can assist in the appropriate triage of patients that require urgent surgical management and those that would benet from non-surgical monitoring.

• MRI is useful in patients who suffer from neurologic symptoms out of proportion to initial CT imaging ndings and to assist in the detection of brain injuries below the sensitivity of CT.

A. J. Tsiouris Department of Radiology, New York-Presbyterian Hospital—Weill Cornell Medicine, New York, NY, USA e-mail: apt9001@med.cornell.edu

Y. W. Lui (*) Department of Radiology, New York University Langone Health/ Grossman School of Medicine, New York, NY, USA e-mail: Yvonne.lui@nyulangone.org

https://doi.org/10.1007/978-3-031-50675-8_7

7.1 Introduction

Traumatic brain injury (TBI) is a leading health concern with approximately 2.8 million reported emergency department visits in 2014in the United States. Of these, there is an estimated 288,000 TBI-related hospitalizations and 56,800 TBIrelated deaths [1]. The majority of these cases involve elderly adults over age 75years followed by young children [2] with a global incidence estimate of 100–749 cases per 100,000 [3]. These staggering numbers are themselves likely to be

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