Indian Journal of Pathology and Microbiology
Home About us Instructions Submission Subscribe Advertise Contact e-Alerts Ahead Of Print Login 
Users Online: 1653
Print this page  Email this page Bookmark this page Small font sizeDefault font sizeIncrease font size

  Table of Contents    
Year : 2022  |  Volume : 65  |  Issue : 5  |  Page : 153-163
Role of imaging in CNS infections

Department of Radiology, Apollo Hospitals, Sheshadripuram, Bangaluru, Karnataka, India

Click here for correspondence address and email

Date of Submission27-Nov-2021
Date of Decision18-Jan-2022
Date of Acceptance19-Feb-2022
Date of Web Publication11-May-2022


Neuroinfections are seen in both adults and children. These can result in serious morbidity and if left untreated and/or associated with comorbidities can be life threatening. Cross-sectional imaging like computed tomography (CT) and magnetic resonance imaging (MRI) are advised by the clinicians for the diagnosing, confirmation of the diagnosis, assess any complications of the infection, and also for follow up. Though CT is the initial imaging investigation commonly asked by the clinician, due to its lesser soft tissue resolution, early brain changes may not be seen on CT. MRI has better soft tissue resolution with no ionizing radiation to the patient and helps in detecting the early signs of infection. Appropriate MRI, not only helps the radiologist to reduce the number of possibilities of the causative organism but also differentiates tumors from infection. However, CT is useful to assess the bony changes and also easily available and affordable cross-sectional imaging modality worldwide. The review summarizes the approach of the radiologist to central nervous system (CNS) infections and their typical imaging characteristic features.

Keywords: Cerebral abscess, cross-sectional imaging, encephalitis, meningitis, neuroinfections

How to cite this article:
Sharath Kumar G G, Adiga CP, Iyer PP, Goolahally LN. Role of imaging in CNS infections. Indian J Pathol Microbiol 2022;65, Suppl S1:153-63

How to cite this URL:
Sharath Kumar G G, Adiga CP, Iyer PP, Goolahally LN. Role of imaging in CNS infections. Indian J Pathol Microbiol [serial online] 2022 [cited 2022 May 24];65, Suppl S1:153-63. Available from: https://www.ijpmonline.org/text.asp?2022/65/5/153/345050

   Introduction Top

Imaging in CNS infections is a broad and important topic of discussion as imaging plays a crucial role in the diagnosis due to their specific features. CT and MRI are the choices of imaging modality in neuroinfections. Neurosonogram plays a small but significant role in detecting intracranial infections in the early infantile period when fontanelle are open.[1] Contrast MRI is the ultimate imaging modality of choice in neuroinfections. The limitation of CT being usage of ionizing radiation and suboptimal visualization of posterior fossa.[2] In this article, we have discussed the imaging approach to the CNS infections and reviewed their characteristic appearances.

   Radiological approach to neuroinfections Top

Neuroinfections can be caused by various organisms which include bacterial, viral, fungal, protozoan, or parasitic etiology or can also be due to prions, which are self-catalyzing endogenous proteins [Figure 1]. Every organism may not have specific imaging features but many have characteristic imaging pattern, knowledge of these imaging characteristics is discussed in the further sections. The initial evaluation of any neuroinfections is established by clinical history, physical examination and CSF evaluation. The approach of a radiologist for these infections is summarized in [Figure 2]. Preliminary imaging is mainly performed to rule out associated complications or and to exclude signs of raised intracranial pressure which is a contraindication for lumbar puncture. Imaging also helps in identifying the predisposing conditions like CSF leak/bony defects/congenital anomalies of CNS which is responsible for recurrent infection.
Figure 1: Classification of neuroinfections based on type of organisms

Click here to view
Figure 2: Approach to neuroinfections

Click here to view

CNS infections are categorized clinically and radiologically into meningitis, cerebritis, abscess, ventriculitis and extra-axial collections or combinations of these.[3]

Meningitis being a clinical diagnosis and confirmed by CSF evaluation, the role of imaging is to recognize the contraindications for doing lumbar puncture, monitor to look for complications associated with meningitis and identify any predisposing causes for recurrent meningitis.

Imaging may be completely normal in early uncomplicated meningitis. Early features in plain CT are obliteration of the cortical sulcal spaces and/or ventriculomegaly, especially third ventricular recess and rounded dilatation of the temporal horns of the lateral ventricle.[4] Contrast CT would depict meningeal thickening and enhancement only in approximately 50% of cases.[4] MRI is superior to CT due to the higher sensitivity especially in picking up meningeal enhancement. Fluid Attenuation Inversion Recovery (FLAIR) sequence has an inherent component of T1 weighting that enables visualization of contrast enhancement and along with its T2 prolongation as well as magnetization transfer effect, it has been shown to be particularly sensitive to detect leptomeningeal enhancement.[5] Post contrast FLAIR is superior to T1 post-contrast and pre-contrast FLAIR in picking up leptomeningeal enhancement [Figure 3](a) and [Figure 3](b) with sensitivity of ~96%, whereas the sensitivity of post contrast T1 was ~68%.[4],[5] Since T2 prolongation and T1 shortening are synergistic, contrast enhanced FLAIR is more sensitive for subtle abnormalities than either FLAIR alone or post-contrast T1 alone.[5] Inflammation along the dura defines pachymeningitis and inflammation in the subarachnoid space gives rise to leptomeningitis [Figure 3](c) and [Figure 3](d).
Figure 3: Meningitis and pyogenic cerebral abscess. (a) FLAIR MRI axial section through the brain shows no significant signal changes in the basal cisternal spaces (arrows). (b) Post-contrast FLAIR MRI axial section through the brain shows hyperintensity in the basal cisternal spaces (arrows). (c) Post-contrast T1 MRI axial section through the brain shows thickening of the dura along the right temporo-occipital convexity (arrows). (d) Post-contrast T1 MRI axial section through the brain reveals enhancement in the subarachnoid spaces (arrow). (e) DWI MRI axial section through the brain shows restricted diffusion in the right frontal lobe (f). (g) Axial section MRI T2 weighted image through the brain shows left frontal lobe pyogenic abscess with outer hypointense rim and inner relatively hyperintense rim. (f) Axial section MR susceptibility weighted image through the brain shows right occipital lobe abscess with similar outer hypointense and inner hyperintense rim

Click here to view

Infection spreading to the brain parenchyma leads to cerebritis which can further lead to abscess formation. Cerebritis may be focal, diffuse, or bilateral and imaging may show involvement of grey matter especially on DWI-MRI and FLAIR. Pattern of cortical involvement on imaging helps to narrow down the differential diagnosis in infective encephalitis and also help to look for complications, prognostication, follow-up, and differential diagnosis.

Brain abscess can be intra/extra axial and can also involve brainstem, cranial nerves, and spinal cord. Imaging including MR Spectroscopy in cerebral abscess helps to narrow the differential diagnosis as different organisms exhibit characteristic imaging features.[6] Few other sequences like 3D constructive interference in steady state (CISS)/fast imaging employing steady state acquisition (FIESTA) help to assess cranial nerve involvement or to detect any lesion in the subarachnoid space and in intraventricular location. Vascular involvement is assessed by doing CT or MR angiogram. MR perfusion also has a role in neuroinfections and helps in differentiating the infection from other etiologies by considering the cerebral blood volume. Spread of infection to involve adjacent bones/soft tissue where CT and MRI play a complimentary role to each other.[7]

Imaging patterns in CNS infections based on the organisms

Bacterial infections

Pyogenic infections are most common in adult and pediatric population. This may result in meningitis, cerebral abscess, subdural and epidural collections and thrombophlebitis.

The causative agents of pyogenic infection include streptococcal pneumoniae and Group B streptococci, H. influenzae, Nisseria meningitides, listeria monocytogenes, enterobacter, and bacterioides. Most common among these is streptococcal pneumoniae.

In neonates/early infants, sonogram also plays a role in meningitis. The sonographic findings in meningitis include echogenic thickened sulci of more than 2 mm, hydrocephalus, thickened, irregular and echogenic ependymal lining and echogenic debris within the ventricular cavity and localization of abscess.[1]

Acute bacterial meningitis is the commonest CNS infection in children as well as adults. In post-contrast MRI, meningeal enhancement pattern is linear against nodular enhancement in granulomatous conditions.[8]

Early cerebritis (one to four days) is seen as an ill-defined hypodense area in the cerebral parenchyma on CT. These show restrictions on diffusion, appears hyperintense on T2/FLAIR images and shows no or minimal enhancement in post-contrast images.

In late cerebritis (four to nine days), the central area appears hypodense on CT, hyperintense on T2 with iso to hypointense T2 peripheral rim, suggestive of necrosis. This part shows restricted diffusion with surrounding perilesional vasogenic edema [Figure 3](e) & [Figure 3](f). There is incomplete capsule in this stage. On post-contrast imaging, there is thick nodular or diffuse, irregular enhancing rim with central non-enhancing area. In second week, complete capsule is seen suggesting early abscess phase. Predisposing conditions and respective location of brain abscess is shown in [Table 1].
Table 1: Predisposing conditions and corresponding locations of the cerebral abscess

Click here to view

The capsule of the abscess appears iso or hyperdense on CT with T2 hypointense rim. On MRI, double rim sign may be seen in cerebral abscesses and is helpful in distinguishing an abscess from glial neoplasm. On both susceptibility weighted imaging (SWI) and T2 weighted images, it consists of two concentric rims surrounding the abscess cavity, outer one of which is hypointense, and the inner one relatively more hyperintense [Figure 3](g) and [Figure 3(h). Cerebral abscesses capsule appears typically smooth and complete against the irregular/nodular thickening and incomplete ones seen in glial neoplasms.[9] Enhancement of the capsule, visualization of daughter abscess are other features of this phase. MR Spectroscopy shows peaks of amino acids like valine, leucine, and isoleucine at 0.9 ppm which are sensitive indicators. The presence of acetate peaks at 1.9 ppm with or without succinate at 2.4 ppm favors anaerobic origin of bacterial infections.[10] Following successful treatment, the resonance peaks disappear. Tubercular brain abscess has smooth, lobulated, and crenated walls with core restricted diffusion. MR Spectroscopy shows predominant lipid-lactate peak without amino acid peaks.[11] Fungal brain abscess has intracavitary projections showing restricted diffusion. MR Spectroscopy shows predominant lipid-lactate peak with multiple peaks between 3.6 and 3.8 ppm assigned to trehalose.[11]

On MR perfusion imaging, the abscess capsule typically shows low relative cerebral blood volume (rCBV) values in the early phase. In the late abscess phase, which is more than second week to few months, the necrotic cavity reduces in size with progressive decrease in the intensity of capsular enhancement. T2 hypointensity of the rim may persist for years. There may be higher rCBV value of the capsule of the abscess in late-stage mimicking tumor.[3]

Spread of infection into the ventricles secondary to bacterial meningitis or rupture of abscess into the ventricular cavity results in pyogenic intraventricular empyema/ventriculitis which shows FLAIR hyperintensity and restriction on diffusion with periventricular edema. This is commonly seen in diabetics, post-traumatic, and post-neurosurgical patients.[8],[12]

Subdural or epidural collection or empyema due to purulent nature show restricted diffusion and rim enhancement. There may be adjacent dural enhancement in epidural empyema. Inflammation of the arteries and veins or secondary vasospasms, though not specific for bacterial meningitis result in cerebral infarction ormycotic aneurysms, where there is focal dilatation of arteries.

Tubercular etiology

As the name suggests, it is caused by mycobacterium tuberculosis and can cause meningitis (most common), tuberculomas, abscess, complications like hydrocephalus, vasculitis, infarcts, mycotic aneurysms, and cranial neuropathies. There is often co-existent pulmonary tuberculosis.

In tubercular meningitis (TBM), the subpial exudates are seen in basal cisterns, base of frontal and temporal lobes and the superior aspect of the cerebellum. In the late stages of the disease, it extends to the convexities and to the ependymal surfaces of the ventricles. Hydrocephalus, if present, suggests poor prognosis. Infarctions occur in any arterial territory but characteristically affect penetrating vessels supplying basal ganglia. Caudate infarction is more specific with underlying TBM.[13]

Tuberculomas can be noncaseating, caseating, and calcified. Noncaseating ones are hyperintense on T2 showing homogeneous contrast enhancement. Caseating ones with central liquefaction shows T2 hypointense rim with central hyperintensities with or without diffusion restriction and ring enhancement.[13] Caseating tuberculoma with solid center shows T2 shortening and ring-like enhancement. Multiple tuberculomas may come together and forma a coalescent mass. MR spectroscopy show prominent lipid peak at 1.3 ppm and also a lactate peak. Guanidinoacetate peak at 3.8 ppm is characteristic of tuberculomas.[14]


Tick borne disease caused by Borrellia species causes meningoradiculitis. Non-specific meningeal and parenchymal involvement may be present, resulting in meningitis and/or encephalitis. Cranial nerve root if involved, may show non-nodular thickening and enhancement. Facial nerve is commonly involved among all the nerves. The most important differential diagnosis in Lyme disease with white matter lesions is multiple sclerosis which also shows involvement of the calloso-septal interface, periventricular white matter.[8],[15] Orbital myositis is another complication of Lyme disease.


Treponema pallidum being the causative organism, manifests with neurotoxic and vasculotoxic effects. The imaging features are nonspecific which include meningitis and encephalitis, lesions similar to small vessel ischemic disease changes, predominantly involving middle cerebral artery territory. Acute lacunar infarcts may occur. Cranial nerve involvement is not uncommon. Post-contrast T1 sequences help in assessing the cranial nerves. Medial temporal signal changes, hydrocephalus, and gumma formation are other imaging characteristic findings in syphilis.[8] Tabes dorsalis is a late manifestation of untreated Neurosyphilis characterized by progressive degeneration of spinal cord nerve cells especially involving posterior columns mimicking subacute combined degeneration.[16]

Gummas are the granulation tissue which is dural based and show ring or nodular homogeneous enhancement. These Gummas appear hypodense on CT.[16] MR angiogram may demonstrate vascular occlusion involving large, medium-, and small-sized arteries secondary to inflammation of the vessel wall and fibrosis.


It is an anerobic bacteria with predilection for cerebellum and brainstem. Nonspecific findings include meningitis, meningoencephalitis, and rhombencephalitis. Cerebellum and brainstem involvement (Rhombencephalitis) may result in cranial nerve nuclei and subcortical abscess formation in brainstem and thalami.[17]


Rocky mountain spotted fever, epidemic typhus, and Q fever are the most common rickettsia infections. Imaging findings include diffuse meningeal enhancement, cerebral edema, and infarction.[18] There may be multiple petechial hemorrhages which are seen as areas of multiple tiny foci of blooming on SWI images. Multiple small periventricular and subcortical infarcts are also been reported and is known as Starry sky appearance.[19] This is seen as multiple bright hyperintense spots on FLAIR and DWI. In some cases, transient signal abnormalities in splenium of corpus callosum may be seen known as Boomerang sign, which represent cytotoxic lesions of corpus callosum (CLOCCs).

Viral infections

Viruses affecting the brain and spine are neurotrophic and are many in number. These viruses cause meningitis, meningoencephalitis, encephalomyelitis, and encephalomyeloradiculitis. Pathogenesis is by direct viral invasion, inflammation and immune response to viral antigen (Molecular mimicry). Acute viral encephalitis can mimic metabolic encephalopathy, autoimmune encephalopathy, infections post-infectious process other than viral etiology. Specific diagnosis requires polymerase chain reaction test on cerebrospinal fluid. Imaging plays an important role in the diagnosis and follow up. Though most of the viruses show non-specific imaging findings, few of them have characteristic imaging appearances which help in narrowing the differential diagnoses. Most important imaging sequences are diffusion weighted imaging (DWI), FLAIR, and contrast study.

Viral encephalitis can involve any age group and may be primary through direct spread or secondary through the spread of infection from other site.[20] Largely, the host response to viral infection of the CNS is responsible for the pathophysiology and imaging findings seen in affected patients.

Herpes simplex virus (HSV) is the most common cause of sporadic fatal encephalitis. It can cause acute, subacute, chronic, and also chronic granulomatous encephalitis in children where there are nodular granulomas in brain parenchyma.[21]

Neonatal herpes simplex encephalitis (HSE) is most commonly caused by the Herpes simplex virus type 1 (HSV 2) which causes diffuse non-specific encephalitis. In adults and children more than six months, more than 90% of HSV encephalitis cases are due to Herpes simplex 1 virus (HSV1).

Imaging especially MRI in HSV1 encephalitis gives characteristic imaging pattern which is very specific and enables us to initiate the treatment at the earliest [Figure 4](a). Human Herpes Virus 6 (HHV6) Mimics HSV encephalitis and other limbic encephalitis on imaging. Extra temporal involvement is very rare in HHV6 as compared to HSV.
Figure 4: Various viral encephalitis. (a) T2 Wt MRI coronal section through the brain shows hyperintensities in the right insular cortex, left frontal and temporal lobes (arrows) consistent with Herpes simplex virus 1 encephalitis. (b) T2 Wt MRI axial section through the brain shows hyperintense and edematous bilateral thalami (arrows), findings consistent with flavivirus encephalitis (Japanese encephalitis). (c) SWI MRI axial section through the brain shows rim of blooming in bilateral cerebellar hemispheres (arrows) depicting Dengue hemorrhagic encephalitis. (d) DWI MRI axial section through the brain shows increased signal in bilateral periventricular white cerebral matter and splenium of corpus callosum (arrows) suggesting Rotavius encephalitis. (e) T2 Wt MRI axial section through the brain in Rabies encephalitis showing bilateral basal ganglialhyperintensities (asterisks). (f) DWI MRI axial section through the brain shows multifocal involvement of cortices and basal ganglia (arrows) in Ebstein-Barr virus infection. (g) T2 MRI axial section through the brain in Enterovirus encephalitis through the brain shows involvement of dorsal pons (arrows). (h) DWI MRI axial section through the brain in CMV encephalitis shows increased signal in periventricular regions (arrows). (i) FLAIR MRI axial section through the brain shows small hyperintense foci in the white matter (arrowheads) consistent with chikungunya infection. (j) T2 Wt axial section through the brain shows hyperintensities in bilateral subcortical and central white matter (arrows) in COVID-19 encephalitis

Click here to view

Flavivirus genus includes wide range of viruses and important ones are Japanese encephalitis (JE), Dengue and west Nile encephalitis (WNE) viruses have specific predilection for bilateral thalamic, subthalamic regions, and cerebellar white matter involvement [Figure 4](b). Hemorrhage is more common in Dengue than JE/WN [Figure 4](c). JE have predilection to substantia nigra and in many cases it mimics HSV encephalitis.

WNE is often associated with nerve root enhancement and signal changes in the anterior horn cells of the spinal cord. Co-existence of NCC and JE is well known.

Brainstem is the most common site of involvement in enterovirus infection (EV71). Signal intensity changes are seen in the dorsal aspect of the pons, medulla, midbrain, and dentate nuclei [Figure 4](g). Pontine tegmentum is the most common site of brainstem involvement. Ventral pontine lesions, substantia nigra, and dentate nuclei can also be affected. Spinal cord central grey matter involvement is also known whereas, supratentorial involvement is extremely rare.

Causes of specific encephalitis syndromes associated with viral infections

Limbic encephalitis- HSV1, HHV6

Cerebellar - Varicella zostervirus (VZV), Epstein-Barr virus (EBV), Mumps

Parkinsonian - JEV, WNV, St. Louis, Nipah

Rhombencephalitis - JEV, WNV, EV71, Rabies

Encephalomyelitis - JEV, WNV, EV71, Polio, Rabies, VZV, HSV, cytomegalovirus (CMV), EBV

Imaging features of some of the viruses with their frequent locations of involvement are shown in [Table 2] and [Figure 4](a), [Figure 4](b), [Figure 4](c), [Figure 4](d), [Figure 4](e), [Figure 4](f), [Figure 4](g), [Figure 4](h), [Figure 4](i), [Figure 4](j).[22],[23],[24],[25]
Table 2: Imaging characteristics of viral infection

Click here to view

Fungal infections


Mucoralesthough known to affect the central nervous system, it became a cause of serious morbidity and mortality during the coronavirus disease 2019 (COVID-19) pandemic. Known predisposing factors include diabetes, over use of steroids, immunocompromised state, and unhygienic environment. The most common route of spread of infection to the brain is through the paranasal sinuses with possible involvement of orbit. Hence, the name rhino-orbito-cerebral mucormycosis (ROCM). In ROCM, contrast MRI is the diagnostic modality of choice to confirm, assess extent of disease, and also follow-up post-treatment.

Imaging protocol for ROCM includes, CT/contrast enhanced MRI of the brain, orbit and paranasal sinuses. CT angiogram may be included to look for thrombus and aneurysm or pseudoaneurysm. There are three to four stages depending on the site of the infection as described below [Table 3]. CT is necessary to look for bone erosions or any osteomyelitis.[26]
Table 3: Stages of ROCM

Click here to view

Vision loss due to optic ischemic neuropathy in mucormycosis necessitates to look for diffusion restriction of the optic nerve. Mucor may involve other cranial nerves apart from optic nerve especially trigeminal and infraorbital nerves. Infection spreading into the brain parenchyma results in cerebritis and abscess formation. The fungal abscess shows diffusion restriction of the wall of the abscess with no central restriction as compared to central restriction in pyogenic abscess representing target sign. The wall of the abscess shows intracavitary projections.

There may be retroclival collection as part of infection. Mycotic aneurysms or pseduoaneurysms with rupture and subarachnoid hemorrhage are also seen in ROCM. Plain CT soft tissue window helps in detecting intracranial hemorrhage. A spectrum of imaging features in mucormycosis has been summarized in [Figure 5](a), [Figure 5](b), [Figure 5](c), [Figure 5](d), [Figure 5](e), [Figure 5](f), [Figure 5](g), [Figure 5](h), [Figure 5](i), [Figure 5](j).
Figure 5: Spectrum of imaging findings in ROCM. (a) Fat saturated post contrast T1 WtMRI coronal section through the paranasal sinuses shows non enhancement of right inferior turbinate (short arrow) and right maxillary mucosa (long arrow) and soft tissue involvement (asterisk). (b) Fat saturated post-contrast T1 Wt MRI coronal section through the paranasal sinuses showing right medial rectus thickening and enhancement (long arrow) and non enhancement of hard palate (short arrow). (c) Fat saturated post-contrast T1 Wt MRI coronal section through the brain shows pachymeningeal thickening and enhancement (arrow), thickened, and enhancing right trigeminal nerve (arrowhead). (d) DWI MRI axial section through the brain shows acute infarcts in left frontal and occpital lobes (arrows). (e) DWI MRI axial section through the brain showing thick walled peripherally restricting fungal abscess in right frontal lobe (arrow). (f) Fat saturated post-contrast T1 Wt MRI axial section through the brain shows peripherally enhancing right frontal fungal abscess (arrow). (g) CT axial section through the brain shows subarachnoid hemorrhage in the basal cisternal spaces (arrowhead) and pseudoaneurysm in the P3 segment of left posterior cerebral artery (arrow). (h) MR TOF angiogram showing psuedoaneurysms in the basilar artery

Click here to view


Cerebral aspergillosis is seen in both immunocompromised and immunocompetent individuals with direct spread from the paranasal sinuses and hematogenous dissemination. May manifest in the form of abscess, cerebral infarcts due to angioinvasion, meningitis, ventriculitis, and acute or chronic rhinosinusitis.[26] Lesions may be nodular showing enhancement on post-contrast mimicking nerve sheath tumor, abscess, and mycotic aneurysms.[27] Lesions are characterized by intermediate to low signal intensity on T2WI, reflecting presence of ferromagnetic elements in the hyphae calcium and hemorrhage.[26],[27]


Cryptococcosis, an opportunistic infection is caused by cryptococcus neoformans. The imaging features include nonspecific leptomeningeal thickening or basal meningitis, dilated Virchow robin spaces in basal ganglia, thalamus, midbrain and cerebellum. Punctate T2 hyperintense foci as pseudocysts and cryptococcomas which show better enhancement on delayed post-contrast images may be seen [Figure 7](a) &[Figure 7](b). The dilatation of subarachnoid spaces and cisterns due to mucoid gelatinous exudates may occur.[28]
Figure 7: (a) T2 Wt MRI axial section through the brain shows dilated virchow robin spaces at bilateral basal ganglia in cryptococcosis (arrows). (b) Post-contrast T1 MRI axial section through the brain shows no enhancement of the dilated Virchow-Robin spaces. (c) T2 Wt MRI sagittal image through the brain shows ill definedhyperintensityin the right frontal lobe with adjacent tiny hyperintense foci depicting milky way sign in PML (arrow). (d) SWI MRI axial section through the brain shows juxtacortical susceptibility hypointense rim in PML (arrow). (e) FLAIR MRI axial section through the brain shows hyperintense cerebellar lesion abutting but sparing the dentate nucleus known as shrimp sign in PML (arrow). (f) T2 Wt MRI axial section through the brain in a case of toxoplasmosis shows concentric target sign in left frontal lobe. (g) T2 Wt MRI axial section through the brain in a case of toxoplasmosis shows eccentric target sign in right frontal lobe. (h) T2 Wt MRI axial section through the brain shows a well defined hyperintense cyst with a thin hypointense wall suggesting hydatid cyst. (i) DWI MRI axial section through the brain shows increased signal in the right frontal cortex (long white arrow), caudate nucleus and anterior putamen (short black arrow) in sporadic CJD. (j) FLAIR MRI axial section through the brain shows hyperintense bilateral posterior thalami (arrows) in variant CJD

Click here to view


Coccididomycosis, caused by dimorphic fungus, shows MCA cistern, leptomeningeal enhancement, granulomas, acute infarcts, and hydrocephalus.

Parasitic etiology

Neurocysticercosis (NCC)

NCC, the most common parasitic infection, is caused by Tenia solium are of four types based on the topographical distribution- meningeal (racemose), parenchymal, ventricular, and combination of the above. NCC may manifest in the form of meningitis/meningoencephalitis, focal granulomas, granulomatous meningitis, focal or multiple cysts and intraventricular cysts. Complications include hydrocephalus, ependymitis, and arteritis.[29]

Four stages of parenchymal NCC are vesicular stage – T2 hyperintense cyst with an eccentric hypointense focus without enhancement, Colloidal stage – ring enhancement of the cyst with perilesional edema, granulonodular degenerative stage – calcification begins and enhancement/edema reduces and the nodular calcified stage – neither enhancement nor edema.[30] Enhancement of the cyst remains for a longer duration. Degenerative cyst also enhances after contrast administration. Recurrent attacks or symptoms recurring after few or many years and perilesional edema in a patient with calcified granuloma indicate cysticercus infection than tuberculoma and is probably due to intermittent antigen sequestration by compacting degenerating cysticercosis. Heavily T2 WT sequences like 3D CISS/FIESTA is sensitive for detecting scolex or any lesion in the cisternal space or within the ventricles. MRS shows pyruvate peak at 2.4 ppm only in viable cysts and is also seen in other parasitic viable cysts of hydatid and coenurosis.[31]

The most common differential diagnosis of neurocysticercosis is tuberculoma and differentiating between the two is a common conundrum faced among the radiologists. However, there are few imaging features which are highly specific for differentiating these two conditions and are briefed in [Table 4] and [Figure 6](a), [Figure 6](b), [Figure 6](c), [Figure 6](d), [Figure 6](e), [Figure 6](f), [Figure 6(g), [Figure 6](h), [Figure 6](i), [Figure 6](j).
Table 4: Imaging differences between tuberculosis and neurocysticercosis

Click here to view
Figure 6: Characteristic findings in Tuberculomas. (a), (b), (c), and (d) T2 Wt MRI axial section through the brain showing target appearance which is seen as hypointensecentre and surrounding hyperintensity and an outer hypointense rim with adjacent hyperintense edema. (e) Post-contrast T1 MRI shows coalescent ring enhancing lesions in right occipital lobe (arrow). Imaging features of Neurocysticercosis. (f) CISS MRI axial section through the brain shows hyperintense lesions in left frontal lobe with hypointense rim and eccentric scolex (arrow). (g and h) T2 Wt and FLAIR MRI axial section through the brain shows content inversion (arrows). (i) Post-contrast T1 Wt MRI coronal section through the brain shows ring enhancing lesion with surrounding hyperintensity (arrow). (j) Post-contrast T1 Wt MRI axial section through the brain shows multiple tiny rings enhancing lesions, few of which showing conglomeration in left frontal lobe (arrow)

Click here to view


Toxoplasma gondii causes toxoplasmosis, commonly seen in immunocompromised individuals. The most common imaging finding is multifocal abscess, predominantly in the basal ganglia, thalamus, and grey-white matter junction. The sign described on T2 images is the concentric target sign which is seen as concentric alternating hypointense and hyperintense rims [Figure 7]f.[32],[33],[34] The eccentric target sign is another sign where there is a ring-shaped zone of peripheral enhancement with a small eccentric nodule along the wall on post-contrast CT and TI MR images [Figure 7](g). This sign is produced by the concentrically thickened vessels traversing the sulcus.[35]

Echinococcosis/Hydatid cyst

Echinococcosis, caused by echinococcusgranulosus – results in formation of a cyst and reaches a considerable size before the patient becomes symptomatic. The cysts are well-defined, thin walled, smooth, round lesions showing CSF intensity [Figure 7](H). The wall appears hypointense with a faint hyperintense perilesional halo on T2 images. If the cyst ruptures, it appears hyperintense on T1 and hypointense on T2 images and shows rim enhancement.[8] Pyruvate on MRS is seen in cestode family including echinococcus.

Melioidosis and sparganosis

Neuromelioidosis, caused by Burkholderiapseudomallei on imaging, shows features of cerebritis/micro abscesses along the white matter tract/cranial nerve involvement, especially trigeminal nerve, and dural venous sinus thrombosis.[36]

Cerebral sparganosis, caused by spirometra larva cestode, shows irregular or nodular enhancing lesions with punctate calcifications on CT. In MRI “tunnel sign” is characteristic, and depicts the moving track of migrating worm leading to inflammatory granulomas. Different stages of the disease may be seen in the same image due to longer duration of the disease.[37]


Progressive multifocal leukoencephalopathy (PML) is a secondary demyelinating disease caused by the reactivation of John Cunningham virus (JC virus) infecting pro-oligodendrocytes in patients with compromised immune systems. Subcortical frontal and parieto-occipital regions are commonly involved with special affinity to subcortical U-fibers [Figure 7](c) and [Figure 7](d). Isolated posterior fossa/corpus callosal involvement has also been reported [Figure 7](e). Long-standing lesions show juxtacortical SWI blooming. Rarely lesions may show peripheral enhancement and cause minimal or no mass effect.

Prion disease

Self-replicating dysmorphic protein accumulation in the neuronal cells results in neurodegenerative conditions which are popularly known as prion diseases or transmissible spongiform encephalopathies. There are five such diseases which include Creutzfeldt-Jakob disease (CJD), fatal familial insomnia, Gerstmann-Straussler-Scheinkerdisease, kuru, and lastly, variably protease-sensitive prionopathy. Among the above diseases, CJD is the commonest. Four types of CJDs to be aware of are variant type, sporadic type, inherited type, and iatrogenic type as described below. Cortical and basal ganglia hyperintensities (commonly caudate nucleus and anterior putamen) on T2 FLAIR and DWI are seen in sporadic type of CJD [Figure 7](i). The popular “pulvinar” and “Hockey stick” signs are seen in variant type of CJD, and appear as high signal in pulvinar regions of bilateral thalami and dorsomedial thalamic nuclei on T2 FLAIR and DWI, respectively [Figure 7](j). Rest of the prion diseases show non-specific changes on imaging like cerebral and/or cerebellar atrophy.[38],[39],[40]

   Conclusion Top

Imaging in CNS infections is a vast and emerging topic of discussion. Cross-sectional imaging, especially MRI plays a crucial role though there is considerable overlap in the findings. The approach to these infections is important to narrow down the list of differentials with knowledge of the type of microorganisms/their pathophysiology giving specific imaging pattern, which helps in establishing proper etiology and hence proper treatment.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

   References Top

Gupta N, Grover H, Bansal I, Hooda K, Sapire JM, Anand R, et al. Neonatal cranial sonography: Ultrasound findings in neonatal meningitis-A pictorial review. Quant Imaging Med Surg 2017;7:123-31.  Back to cited text no. 1
Cuvinciuc V, Vargas MI, Lovblad KO, Haller S. Diagnosing infection of the CNS with MRI. Imaging Med 2011;3:689-710.  Back to cited text no. 2
Ferreira NPDF, Otta GM, do Amaral LLF, da Rocha AJ. Imaging aspects of pyogenic infections of the central nervous system. Top Magn Reson Imaging 2005;16:145-54.  Back to cited text no. 3
Mitchell BC, Dehkharghani S. Imaging of intracranial infectious diseases in adults. Appl Radiol 2014;43:6-15.  Back to cited text no. 4
Lee EK, Lee EJ, Kim S, Lee YS. Importance of contrast-enhanced fluid-attenuated inversion recovery magnetic resonance imaging in various intracranial pathologic conditions. Korean J Radiol 2016;17:127-41.  Back to cited text no. 5
Rangarajan K, Das CJ, Kumar A, Gupta AK. MRI in central nervous system infections: A simplified patterned approach. World J Radiol 2014;6:716-25.  Back to cited text no. 6
Honavar SG. Code Mucor: Guidelines for the diagnosis, staging and management of rhino-orbito-cerebral mucormycosis in the setting of COVID-19. Indian J Ophthalmol 2021;69:1361-5.  Back to cited text no. 7
  [Full text]  
Shih RY, Koeller KK. Bacterial, fungal, and parasitic infections of the central nervous system: Radiologic-pathologic correlation and historical perspectives. Radiographics 2015;35:1141-69.  Back to cited text no. 8
Toh CH, Wei KC, Chang CN, Hsu PW, Wong HF, Ng SH, et al. Differentiation of pyogenic brain abscesses from necrotic glioblastomas with use of susceptibility-weighted imaging. AJNR Am J Neuroradiol 2012;33:1534-8.  Back to cited text no. 9
Pal D, Bhattacharyya A, Husain M, Prasad KN, Pandey CM, Gupta RK. In vivo proton MR spectroscopy evaluation of pyogenic brain abscesses: A report of 194 cases. AJNR Am J Neuroradiol 2010;31:360-6.  Back to cited text no. 10
Hughes DC, Raghavan A, Mordekar SR, Griffiths PD, Connolly DJA. Role of imaging in the diagnosis of acute bacterial meningitis and its complications. Postgrad Med J 2010;86:478-85.  Back to cited text no. 11
Han KT, Choi DS, Ryoo JW, Cho JM, Jeon KN, Bae KS, et al. Diffusion-weighted MR imaging of pyogenic intraventricular empyema. Neuroradiology 2007;49:813-8.  Back to cited text no. 12
Sanei Taheri M, Karimi MA, Haghighatkhah H, Pourghorban R, Samadian M, DelavarKasmaei H. Central nervous system tuberculosis: An imaging-focused review of a reemerging disease. Radiol Res Pract 2015;2015:202806.  Back to cited text no. 13
Khatri GD, Krishnan V, Antil N, Saigal G. Magnetic resonance imaging spectrum of intracranial tubercular lesions: One disease, many faces. Pol J Radiol 2018;83:e524-35.  Back to cited text no. 14
Lindland ES, Solheim AM, Andreassen S, Quist-Paulsen E, Eikeland R, Ljøstad U, et al. Imaging in Lyme neuroborreliosis. Insights Imaging 2018;9:833-44.  Back to cited text no. 15
Nagappa M, Sinha S, Taly AB, Rao SL, Nagarathna S, Bindu PS, et al. Neurosyphilis: MRI features and their phenotypic correlation in a cohort of 35 patients from a tertiary care university hospital. Neuroradiology 2013;55:379-88.  Back to cited text no. 16
Xu R, Bai Y, Duan C, Zhao S, Chen X, Yang Q. Central nervous system Listeria monocytogenes infection mimicking central nervous system idiopathic inflammatory demyelinating disease. Infect Drug Resist 2019;12:255-9.  Back to cited text no. 17
Akgoz A, Mukundan S, Lee TC. Imaging of rickettsial, spirochetal, and parasitic infections. Neuroimaging Clin N Am 2012;22:633-57.  Back to cited text no. 18
Kontzialis M, Zamora CA. Teaching NeuroImages: Starry-sky appearance in Rocky Mountain spotted fever. Neurology 2015;85:e93.  Back to cited text no. 19
Jayaraman K, Rangasami R, Chandrasekharan A. Magnetic resonance imaging findings in viral encephalitis: A pictorial essay. J Neurosci Rural Pract 2018;9:556-60.  Back to cited text no. 20
[PUBMED]  [Full text]  
Love S, Koch P, Urbach H, Dawson TP. Chronic granulomatous herpes simplex encephalitis in children. J Neuropathol Exp Neurol 2004;63:1173-81.  Back to cited text no. 21
Granerod J, Davies NWS, Mukonoweshuro W, Mehta A, Das K, Lim M, et al. Neuroimaging in encephalitis: Analysis of imaging findings and interobserver agreement. Clin Radiol 2016;71:1050-8.  Back to cited text no. 22
Lee KY, Cho WH, Kim SH, Kim HD, Kim IO. Acute encephalitis associated with measles: MRI features. Neuroradiology 2003;45:100-6.  Back to cited text no. 23
Moonis G, Filippi CG, Kirsch CFE, Mohan S, Stein EG, Hirsch JA, et al. The spectrum of neuroimaging findings on CT and MRI in adults with COVID-19. AJR Am J Roentgenol 2021;217:959-74.  Back to cited text no. 24
Ganesan K, Diwan A, Shankar SK, Desai SB, Sainani GS, Katrak SM. Chikungunya encephalomyeloradiculitis: Report of 2 cases with neuroimaging and 1 case with autopsy findings. AJNR Am J Neuroradiol 2008;29:1636-7.  Back to cited text no. 25
Sreshta K, Dave TV, Varma DR, Nair AG, Bothra N, Naik MN, et al. Magnetic resonance imaging in rhino-orbital-cerebral mucormycosis. Indian J Ophthalmol 2021;69:1915-27.  Back to cited text no. 26
[PUBMED]  [Full text]  
Marzolf G, Sabou M, Lannes B, Cotton F, Meyronet D, Galanaud D, et al. Magnetic resonance imaging of cerebral aspergillosis: Imaging and pathological correlations. PLoS One 2016;11:e0152475.  Back to cited text no. 27
Xia S, Li X, Li H. Imaging characterization of cryptococcal meningoencephalitis. Radiol Infect Dis 2016;3:187-191.  Back to cited text no. 28
White AC, Coyle CM Jr, Rajshekhar V, Singh G, Hauser WA, Mohanty A, et al. Diagnosis and treatment of neurocysticercosis: 2017 clinical practice guidelines by the infectious diseases society of America (IDSA) and the American society of tropical medicine and hygiene (ASTMH). Am J Trop Med Hyg 2018;98:945-66.  Back to cited text no. 29
Amaral L, Maschietto M, Maschietto R, Cury R, Ferreira NF, Mendonça R, et al. Ununsual manifestations of neurocysticercosis in MR imaging: Analysis of 172 cases. Arq Neuropsiquiatr 2003;61:533-41.  Back to cited text no. 30
Jayakumar PN, Srikanth SG, Chandrashekar HS, Kovoor JME, Shankar SK, Anandh B. Pyruvate: An in vivo marker of cestodal infestation of the human brain on proton MR spectroscopy. J Magn Reson Imaging 2003;18:675-80.  Back to cited text no. 31
Roche AD, Rowley D, Brett FM, Looby S. Concentric and eccentric target MRI signs in a case of HIV-associated cerebral toxoplasmosis. Case Rep Neurol Med 2018;2018:9876514.  Back to cited text no. 32
Mahadevan A, Ramalingaiah AH, Parthasarathy S, Nath A, Ranga U, Krishna SS. Neuropathological correlate of the “concentric target sign” in MRI of HIV-associated cerebral toxoplasmosis: Concentric Target Sign in Toxoplasmosis. J Magn Reson Imaging 2013;38:488-95.  Back to cited text no. 33
Benson JC, Cervantes G, Baron TR, Tyan AE, Flanagan S, Lucato LT, et al. Imaging features of neurotoxoplasmosis: A multiparametric approach, with emphasis on susceptibility-weighted imaging. Eur J Radiol Open 2018;5:45-51.  Back to cited text no. 34
Kumar GGS, Mahadevan A, Guruprasad AS, Kovoor JM, Satishchandra P, Nath A, et al. Eccentric target sign in cerebral toxoplasmosis: Neuropathological correlate to the imaging feature. J Magn Reson Imaging 2010;31:1469-72.  Back to cited text no. 35
Hsu CC, Singh D, Kwan G, Deuble M, Aquilina C, Korah I, et al. Neuromelioidosis: Craniospinal MRI findings in Burkholderiapseudomallei infection: Craniospinal MRI Findings in B. Pseuodomallei. J Neuroimaging 2016;26:75-82.  Back to cited text no. 36
Song T, Wang WS, Zhou BR, Mai WW, Li ZZ, Guo HC, et al. CT and MR characteristics of cerebral sparganosis. AJNR Am J Neuroradiol 2007;28:1700-5.  Back to cited text no. 37
Macfarlane RG, Wroe SJ, Collinge J, Yousry TA, Jäger HR. Neuroimaging findings in human prion disease. J Neurol Neurosurg Psychiatry 2007;78:664-70.  Back to cited text no. 38
Letourneau-Guillon L, Wada R, Kucharczyk W. Imaging of prion diseases. J Magn Reson Imaging 2012;35:998-1012.  Back to cited text no. 39
Haïk S, Galanaud D, Linguraru MG, Peoc'h K, Privat N, Faucheux BA, et al. In vivo detection of thalamic gliosis: A pathoradiologic demonstration in familial fatal insomnia: A pathoradiologic demonstration in familial fatal insomnia. Arch Neurol 2008;65:545-9.  Back to cited text no. 40

Correspondence Address:
Chaitra Parameshwara Adiga
Apollo Hospitals, Sheshadripuram, Near Mantri Square Mall, Bangaluru – 560020, Karnataka
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijpm.ijpm_1162_21

Rights and Permissions


  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7]

  [Table 1], [Table 2], [Table 3], [Table 4]


    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Email Alert *
    Add to My List *
* Registration required (free)  

    Radiological app...
    Article Figures
    Article Tables

 Article Access Statistics
    PDF Downloaded12    
    Comments [Add]    

Recommend this journal