Книги по МРТ КТ на английском языке / MR Imaging in White Matter Diseases of the Brain and Spinal Cord - K Sartor Massimo Filippi Nicola De Stefano Vincent Dou

27.5

Parasitic Infections

The most common parasitic infections that affect the CNS are (Chang et al. 1991; Gray et al. 2004):

Protozoal infections:

a)Amebiasis

b)Cerebral malaria

c)Toxoplasmosis that develops in the CNS of HIVinfected patients

d)Trypanosomiasis

Metazoal infections:

c)Echinococcus multilocularis (Taenia multilocularis) from foxes

d)Toxocariasis (Toxocara canis and Toxocara cati), which may produce visceral larva migrans and CNS manifestations in children

e)Paragonimiasis (Paragonimus westermani) from infected crabs or crayfish

Other parasitic infections including sparganosis, trichinosis (Trichinella spiralis), strongylosis, schistosomiasis may also develop in the CNS.

The three taenias, responsible for neurocysticer-

sule of an abscess has a host origin. The cystic wall is not detectable by the host immunologic system till the larva dies. The symptoms often arise after the death of the parasite, when the host response can occur. However, the location of the cyst may be also responsible for symptoms such as seizures, mass effect or CSF occlusion, before the death of the parasite.

27.5. 1

Cysticercosis (Taenia solium)

Cysticercosis is the most common parasitic infection of the CNS and is endemic in all countries, particu-

larly in Latin America (Gray et al. 2004). The larvae enter the intestinal wall and develop in the brain, the subarachnoid space, or the ventricles (del Brutto et al. 2001). Once the scolex is established, it makes itself immunologically invisible to the host and, consequently, incites no inflammatory reaction. Live cysts are isointense to CSF with all pulse sequences. No enhancement is seen within the cyst wall while the organism is alive (Fig. 27.10). The scolex may be seen as a 2-4 mm mural nodule in the cyst wall. There is no associated edema.

When the organism dies, an inflammatory granulomatous response occurs. The clinical manifestations are seizures or focal deficits. The wall enhances, and there is associated vasogenic edema (Fig. 27.10a,

a

Fig. 27.9a–c. Mycotic aneurysm. a Contrast-enhanced CT. Small enhancing lesion adjacent to the right parietal cortex. Note the incidental finding of a venous angioma on the left hemisphere. b T2* MR imaging. Presence of magnetic susceptibility, probably due to hemosiderin surrounding the mycotic aneurysm. c Selective right carotid-artery angiogram. The small mycotic aneurysm appears filled by the contrast agent on an anterior parietal branch of the middle cerebral artery

c, h). The dead cyst commonly calcifies (Fig. 27.10f). Patients treated with praziquantel may develop acute symptoms because of the simultaneous death of all live cysts (Fig. 27.10c). Subarachnoid cysts may often produce secondary obstructive hydrocephalus (Fig. 27.10d, e).

b

c

most common sites of development in humans are the liver, lung and bone. The brain is affected in less than 5% of patients. It is usually a single, unilocular and quite large cyst. When the cyst ruptures, it produces an inflammatory reaction.

27.5.2

Hydatid Cysts (Echinococcus granulosus)

Human Echinococcus granulosus contamination occurs by accidental ingestion of contaminated dog feces. The disease is endemic in the Mediterranean regions, the Middle East, and Latin America. The

27.5.3

Echinococcus multilocularis

This is a rare parasitic infection that usually has a fatal issue. The cysts are recognizable by their resemblance to wine grapes.

27.5.4 Toxoplasmosis

Toxoplasma gondii is distributed worldwide and infects more than 500 million humans (Ramsey and Dean 1997). It does not cause clinical intracranial infection in immunocompetent hosts, and, consequently, was rarely seen prior to the onset of the AIDS epidemia. However, toxoplasmosis may infect the embryo, producing diffuse necrotic lesions of the cortex, cerebral malformations and intracranial calcifications, especially in the periventricular regions (Gray et al. 2004).

Toxoplasmosis is the most common cerebral mass lesion encountered in the HIV-positive patient (Ramsey and Dean 1997). This is the first diagnosis to evoke when CNS manifestations occur with rapid progression in HIV-infected patients. The imaging appearance might be ubiquitous, but the antibiotic treatment is very efficient. Thus, AIDS patients with rapid CNS manifestations should be treated for toxoplasmosis regardless of the imaging features. The diagnosis might be reconsidered if the treatment is inefficient. With HAART (highly active antiretroviral therapy) treatment, the incidence of toxoplasmosis has dropped (Gray et al. 2003). Now, toxoplasmosis is encountered in patients who are unaware of their viral status for HIV. It is not rare that patients presenting inaugural seizures and several brain lesions are positive for HIV. This diagnosis must be evoked by the radiologist.

Although largely identical to an abscess, the lesion is not encapsulated, which accounts for the histologic classification of encephalitis rather than abscess (Zimmerman 2000; Gray et al. 2004). In the majority of cases, multiple mass lesions are present, and they may be located anywhere within the brain. The basal ganglia and the cortical-subcortical junction are more affected.

The imaging findings in the beginning include a mass effect with or without a slight, not well-demar- cated, contrast enhancement (Fig. 27.11a). Later, the enhancement is quite similar to an abscess, like a ring (Fig. 27.11c, d). The central necrosis is typically hyperintense on FLAIR and T2-weighted images. DWI reveals heterogeneous intensity (Fig. 27.11e), and the ADC is usually increased. Hemorrhage is not present at the time of initial diagnosis. Signs of hemorrhage are present when the patient is treated with antibiotics. High signal intensity from methemoglobin is seen on non-enhanced T1-weighted images, leading to confirmation of the diagnosis in patients under treatment (Fig. 27.11f).

In patients who are not improving with antibiotics, the diagnosis of toxoplasmosis must be reconsidered, with the primary goal of differentiating toxoplasmosis from lymphoma. Although it is rare, lymphoma is the second most common causes of mass lesions in patients with AIDS (Ramsey and Dean 1997). Lymphoma lesions are usually single and located in the deep gray and white matter (basal ganglia and corpus callosum).Lymphoma is often hypointense on T2-weighted images. There is mild, adjacent edema, with a mass effect lower than expected. Enhancement is usually diffuse but may be of a ring appearance, especially when the lesion is superior to 3.5 cm. Single photon emission CT (SPECT) with radioactive thallium can be used to confirm the diagnosis of lymphoma prior to therapy. Inflammatory lesions, including toxoplasmosis, are negative on SPECT, while lymphoma uptakes the radioactive thallium. When the diagnosis cannot be established non-invasively, biopsy is necessary. Non-Hodgkin lymphoma type B is the most common. Its outcome is, unfortunately, fatal.

27.5.5

Toxocara canis and Toxocara cati Infections

These are dog and cat nematodes. Human infection occurs by accidental ingestion of their eggs passed from pet animals. The liver, lung and peritoneum are most frequently involved. They produce focal lesions in the white matter, which spontaneously resolve. Vasculitis or granulomas around the larvae may form in the parenchyma (Fig. 27.12a, b) (Dousset et al. 2003). The death of the parasite in the brain is followed by a non-encapsulated granulomatous reaction (Gray et al. 2004).

27.6

Mycotic Infections

CNS fungal infections are possible in exposed populations such as immunocompromised patients with AIDS, leukemia, diabetes mellitus, renal diseases, those under aggressive chemotherapy and in intravenous drug abusers with unsterilized materials (Harris and Enterline 1997).

The most frequent fungal infections are: cryptococcosis due to Cryptococcus neoformans, aspergillosis, mucormycosis, candidiasis and histoplasmosis. They are responsible for meningitis in infections

might be involved, usually by the spread of the granuloma along the perivascular Virchow-Robin spaces. Inflammatory pseudotumors may also affect the cavernous sinuses, the orbits and, rarely, the hypophysis sellae.

CT or MRI features of granulomatous meningitis are cisternal enhancement, usually following the vessel routes. Thus, contrast-enhanced images are critical in establishing the diagnosis of granulomatous meningitis. Basal meningitis often leads to hydrocephalus. There is often compromise of the vascular system, with secondary infarction or hemorrhage. The combination of hydrocephalus and deep infarction in a young adult should, therefore, always raise the suspicion of granulomatous meningitis (Zimmerman 2000).

The differential diagnosis of granulomatous infectious meningitis is neoplastic carcinomatous meningitis (Aparicio and Chamberlain 2002). It has a predilection for the retro-cerebellar cisterns. Sarcoidosis has a predilection for the suprasellar cistern, often producing thickening of the pituitary stalk (Ulmer and Ester 1991). Enhancement along the course of the cranial nerves is characteristic of sarcoidosis but can also be seen in lymphoma.

27.7.2 Vasculitis

Vasculitis may be the result of direct spread from the leptomeninges along the perivascular spaces or direct invasion and growth within the lumen of the vessel. It also can be the result of an immune reaction at the endothelial level, without infectious agents. Infarcts occur in the deep gray matter or in the cortex.

27.7.3

Acute Disseminated Encephalomyelitis

Acute disseminated encephalomyelitis is an autoimmune disorder that is similar to multiple sclerosis, except that it is monophasic (Talbot et al. 2001). Acute disseminated encephalomyelitis occurs with a latency of 1 week to several weeks after viral exposure or vaccination. In most of the cases, multiple lesions are present at the same time in the white matter, affecting the gray matter in at least one-third of cases. The disease may produce multifocal demyelination similar to viral encephalitis or multiple sclerosis. Enhancement is inconstant, although frequent. In most cases, improvement is

good under steroids. Death is possible in the most severe cases.

References

Anderson DJ, Goldstein LB, Wilkinson WE et al (2003) Stroke location, characterization, severity, and outcome in mitral vs aortic valve endocarditis. Neurology 61:1341–1346

Aparicio A, Chamberlain MC (2002) Neoplastic meningitis. Curr Neurol Neurosci Rep 2:225–235

Bonthius DJ, Karacay B (2002) Meningitis and encephalitis in children. An update. Neurol Clin 20:1013–1038

Burtscher IM, Holtas M (1999) In vivo proton MR spectroscopy of untreated and treated brain abscesses. AJNR Am J Neuroradiol 20:1049–1053

Cecil KM, Lenkinski RE (1998) Proton MR spectroscopy in inflammatory and infectious brain disorders. Neuroimaging Clin N Am 8:863–880

Chang KH, Cho YS, Hesselink JR et al (1991) Parasitic diseases of the central nervous system. Neuroimaging Clin N Am 1:159–178

Collie DA, Sellar RJ, Zeidler M et al (2001) MRI of CreutzfeldtJakob disease: imaging features and recommended MRI protocol. Clin Radiol 56:726–739

Collie DA, Summers DM, Sellar RJ et al (2003) Diagnosing variant Creutzfeldt-Jakob disease with the pulvinar sign: MR imaging findings in 86 neuropathologically confirmed cases. AJNR Am J Neuroradiol 24:1560–1569

Dal Canto MC (1997) Mechanisms of HIV infection of the central nervous system and pathogenesis of AIDS-dementia complex. Neuroimaging Clin N Am 7:231–242

Del Brutto OH, Rajshekhar V, White AC Jr et al (2001) Proposed diagnostic criteria for neurocysticercosis. Neurology 57:177–183

Desprechins B,Stadnik T,Koerts G et al (1999) Use of diffusionweighted MR imaging in differential diagnosis between intracerebral necrotic tumors and cerebral abscesses.AJNR Am J Neuroradiol 20:1252–1257

Dousset V, Armand JP, Lacoste D et al (1997) Magnetization transfer study of HIV encephalitis and progressive multifocal leukoencephalopathy. AJNR Am J Neuroradiol 18:895–901

Dousset V, Sibon I, Menegon P (2003) Cerebral vasculitis due to Toxocara canis (or catis) origin. J Radiol 84:89–91

Gray F, Chretien F, Vallat-Decouvelaere AV et al (2003) The changing pattern of HIV neuropathology in the HAART. J Neuropathol Exp Neurol 62:429–440

Gray F, de Girolami U, Poirier J (2004) Basic neuropathology, 4th edn. Elsevier, Philadelphia

Harris DE, Enterline DS (1997) Fungal infections of the central nervous system. Neuroimaging Clin N Am 7:187–198

Lai PH, Ho JT, Chen WL et al (2002) Brain abscess and necrotic brain tumor: discrimination with proton MR spectroscopy and diffusion-weighted imaging. AJNR Am J Neuroradiol 23:1369–1377

Maezawa Y, Hirasawa A, Abe T et al (2002) Successful treatment of listerial brain abscess: a case report and literature review. Intern Med 41:1073–1078

Martindale JL, Geschwind MD, Miller BL (2003) Psychiatric and neuroimaging findings in Creutzfeldt-Jakob disease. Curr Psychiatry Rep 5:43–46

Osborn RE, Byrd SE (1991) Congenital infections of the brain. Neuroimaging Clin N Am 1:105–118

Phuong LK, Link M, Widjdicks E (2002) Management of intracranial infectious aneurysms: a series of 16 cases. Neurosurgery 51:1145–1151

Post MJD, Sheldon JJ, Hensley GT et al (1986) Central nervous system disease in acquired immunodeficiency syndrome: prospective correlation using CT, MR imaging, and pathologic studies. Radiology 158:141–148

Prusiner SB (1987) Prions and neurodegenerative disease. N Engl J Med 317:1571–1581

Ramsey RG, Dean AD (1997) Central nervous system toxoplasmosis. Neuroimaging Clin N Am 7:171–186

Rich PM, Deasy NP, Jarosz JM (2000) Intracranial dural empyema. Br J Radiol 73:1329–1336

Talbot PJ, Arnold D, Antel JP (2001) Virus-induced autoim-

mune reactions in the CNS. Curr Top Microbiol Immunol 253:247–271

Tien RD, Felsberg GJ, Osumi AK (1993) Herpes virus infections of the CNS: MR findings. AJR Am J Roentgenol 161:167–176

Trotot PM, Gray F (1997) Diagnostic imaging contribution in the early stages of HIV infection of the brain. Neuroimaging Clin N Am 7:243–260

Tunkel AR, Pradhan SK (2002) Central nervous system infections in injection drug users. Infect Dis Clin North Am 16:589–605

Ulmer JL, Elster AD (1991) Sarcoidosis of the central nervous system. Neuroimaging Clin N Am 1:141–150

Zimmerman RD (2000) Infection. Proceedings of the Radiologic Society of North America Annual meeting RSNA categorial course in diagnostic radiology: neuroradiology. pp 45–63

Zimmerman RD, Weingarten KW (1991) Neuroimaging of cerebral abscess. Neuroimaging Clin N Am 1:1–16

CONTENTS

28.1Introduction 411

28.2Neuropathology 411

28.7Image-Guided Neurosurgery 432

28.8Integrating Multiple Biologic Parameters and Conclusions 436

References 436

28.1 Introduction

The American Cancer Society estimates that in the United States 16,800 new diagnosed intracranial neoplasms were diagnosed in 1999, more than double the number of diagnosed cases of Hodgkin’s disease and over half the number of cases of melanoma (DeAngelis 2001). A large number of intracranial tumours arise from brain tissue while others arise from meninges (meningiomas) and hematopoietic tissue (lymphomas). Metastases to the brain are even more common: more than 100,000 patients per year die with symptomatic intracranial metastases. Incidence rates have a first peak before 10 years of age, then they decline to increase again after 25 years of age, and decline again only after 85 years of age. Data from the last three decades are showing that brain-tu- mour incidence increases with age through life. In the last three decades, the incidence of primary brain tumours has increased in Europe, Japan and the United

A.Bizzi, MD

B.Pollo, MD

C.Marras, MD

Department of Neuroradiology,Istituto Nazionale Neurologico “Carlo Besta”, Via Caloria 11, 20133 Milan, Italy

States among people older than 65 years. However, this increase in rates is not real but it is attributed to improvements in management of common illnesses and better diagnostic workup of elderly patients.

This chapter will focus on the histopathology, biology, and imaging of the morphologic, metabolic and physiopathologic features of brain tumours, with particular attention to the most common type of primary intra-axial tumours: the glioma.

28.2 Neuropathology

The 2000 World Health Organization (WHO) classification of tumours of the nervous system is the most comprehensive to date, and it has received a large consensus among neuropathologists. It divides brain tumours into seven large categories: tumours arising from neuroepithelial tissue; from peripheral nerves; from the meninges; lymphomas and hematopoietic neoplasms; germ cell tumours; tumours of the sellar region and metastatic tumours.A simplified version of the WHO classification (Kleihues 2000) is presented on Table 28.1.

Among tumours of neuroepithelial tissue,the gliomas are by far the most common and best known. Gliomas include tumours arising from neoplastic transformation of astrocytes, oligodendrocytes, mixed gliomas and glial tumours of uncertain origin. The group of neuroepithelial tumours comprise also ependymomas, neuronal and mixed neuronal– glial tumours (as ganglioglioma), and embryonal tumours (as medulloblastoma). Much evidence has been recently reported in support of the hypothesis that brain tumours arise by transformation of proliferating neural stem cells. Neural stem cells are able to self-renew and differentiate into neurons and glia. Other masses may arise from normal constituents of the brain, such as hamartomas, or from embryologically misplaced tissues such as teratomas, dermoids and germinomas.