A 29-year-old female presented with headache and gait imbalance. She had a history of pulmonary tuberculosis treated for one year. MRI of the brain showed multiple supra-tentorial lesions with ring enhancement, the largest in the right temporal lobe extending into the midbrain. Based on the history of tuberculosis and imaging findings, the lesions were determined to be multiple tuberculomas. Differential diagnoses for multiple ring-enhancing lesions include infections like tuberculomas and abscesses, as well as tumors and inflammatory conditions. Distinguishing between neoplastic and non-neoplastic causes is important to guide appropriate treatment.

1. MULTIPLE RING
ENHANCING BRAIN
LESIONS
PRESENTED BY
DR SUMIYA ARSHAD

2. CASE PRESENTATION
 Patient Perveen 29 years of age presented with complains of:
 Headache
 Imbalance gait
 She was a suspected case of tuberculous meningitis and tuberculomas
 Known case of pulmonary TB. On ATT for past 01 year
 MRI brain with contrast was performed

3. MRI BRAIN WITH CONTRAST
 Multiple variable size supra tentorial brain parenchymal lesions larger one in
right sided temporal lobe is seen extending inferiorly and involving right
aspect of mid brain causing minimal pressure effect. It is shows heterogeneous
hypointesnisty on T2WI within it.
 Another lesion in deep temporal lobe anteriorly
 Similar intensity variable lesions seen in left sided temporal lobe.
 These lesions show post contrast ring enhancement.
 Right sided leptomeningeal thickening is noted along side the sylvian fissure.

7. CONCLUSION
 Multiple supratentorial parenchymal lesions with the larger one in right
temporal lobe extending inferiorly to involve the mid brain with post
contrast ring enhancement --- suggestive of multiple tuberculomas
keeping in view the history of tuberculosis.

8. INTRODUCTION
 Multiple ring enhancing lesions are a commonly encountered
neuroimaging abnormality.
 Can be caused by a variety of infectious, neoplastic and inflammatory
diseases.
 Distinguishing between neoplastic and non neoplastic etiology is
extremely important because a misdiagnosis can lead to unwarranted
neurosurgery and exposure to toxic chemotherapy or potentially harmful
brain irradiation.

9. CLINICAL FINDINGS
 Clinically, they manifest as:
 recurrent seizures
 visual impairment
 focal neurological deficit
 Signs of raised intracranial pressure (severe headache, vomiting and papilledema).
 If cerebral edema is severe, patients may develop loss of sensorium and posturing
of limbs because of transtentorial brain herniation.

10. DIFFERENTIAL DIAGNOSIS
INFECTIVE
 Tuberculomas
 Pyogenic abscess
 Neurocysticercosis
 Echinococcus infection
 Amebic brain abscess
 NEOPLASTIC
 Metastases
 Glioblastoma
 Primary CNS lymphoma
 INFLAMMATORY & DEMYELINATING
 Tumefactive multiple sclerosis
 ADEM
 Radiation necrosis

11.  In developing and poor countries, the spectrum of etiologies of multiple
ring-enhancing lesions of the brain is likely to be different from developed
countries; as infective pathologies are more frequently encountered.

12. TUBERCULOMAS
 Central nervous system (CNS) tuberculosis (TB) is a serious form of TB, due to
haematogenous spread of Mycobacterium tuberculosis (MT).
 Represent a common neurological disorder in developing countries,
accounting for 10% to 30% of all intracranial masses
 Intracranial tuberculomas are the least common presentation of CNS TB and
can occur with or without tuberculous meningitis.
 Numerous small tuberculomas are common in patients with miliary pulmonary
tuberculosis.
 The diameter of these lesions usually ranges from 1 mm to 5 cm.

13. CLINICAL FEATURES
 Tuberculomas often present with symptoms and seizures, signs of raised
intracranial pressure and focal neurological deficit without evidence of
systemic disease.

14. RADIOGRAPHIC FEATURES
CT SCAN
 Hypo to iso dense lesions are seen with edema and necrosis appearing as
a low attenuating area on CT scan.
 Once the granuloma has begun to organize, there may be high
attenuation, contrast enhancement and calcification, as well as ring
enhancement and a variable degree of surrounding edema.
 The enhancement may be homogenous or there may be a central
radiolucent area corresponding to the central zone of necrosis.

16. A well defined hypo dense lesion with central hyper dense foci and surrounding edema is seen in the right
frontal lobe. On post contrast imaging the lesion shows peripheral ring enhancement.

17. MRI
T1WI
 Iso intense to grey-matter
 may have central region of hyper intensity representing caseation
T2WI
 Iso intense to grey-matter
 may have central region of hypo intensity representing gliosis and abundant
monocyte infiltration
 lesions are surrounded by vasogenic edema
T1 C+ (Gd)
 usually appears as ring-enhancement
 may appear as a conglomerate enhancing mass

19. ENHANCEMENT PATTERNS
 Tuberculomas on contrast administration appear as nodular or ring-like
enhancing lesions.
 Tuberculomas frequently show varied types of enhancement, including
irregular shapes, ring-like shapes, open rings and lobular patterns. Target-
like lesions are common.

22. PYOGENIC BRAIN ABSCESS
 Potentially life threatening condition requiring prompt diagnosis and
treatment.
 Results from pathogens growing within the brain initially as cerebritis, then
later demarcating into cerebral abscess. Haematogenous spread is
recognized as the most common source.
 Risk factors include: congenital heart diseases, endocarditis, IV drug
abusers, lung abscess, empyema thoracis, Sino nasal infections, dental
abscess and systemic sepsis.

23. RADIOGRAPHIC FEATURES
CT SCAN
 Pre and post contrast scans should be obtained.
 Typical appearance includes:
 Ring of iso or hyper dense tissue of uniform thickness representing capsule
of the abscess which show ring enhancement on post contrast scans.
 Some mass effect, usually not as marked in relation to the extent of
edema.
 Ventriculitis --- bad prognostic sign; enhancement of ependymal.
 Obstructive hydrocephalus due to ventricular spread may occur.

24. MRI
T1WI
 The central zone of liquefying necrosis in a mature abscess is slightly hyper
intense to CSF.
 Peripheral low intensity --- vasogenic edema.
 Capsule is commonly iso to slightly hyper intense to brain parenchyma.
 Significant post contrast ring enhancement.
T2WI
 Iso to hypo intense to CSF, does not attenuate on FLAIR.
 Peripheral high intensity --- vasogenic edema.
 Capsule --- intermediate to low signal thin rim.

27. NEUROCYSTICERCOSIS
 Caused by CNS infection with pork tape worm Taenia Solium.
 There is a variable time interval between the point of infection and the onset of symptoms ranging
from 1-30 years.
 Can be both intra or extra axial. Commonest locations are: subarachnoid space over the cerebral
hemispheres, parenchyma, basal cisterns, ventricles.
 Usually, the lesions are <20 mm in diameter. The lesions are often multiple and most often do not have
extensive oedema.

28. RADIOGRAPHIC FETURES
 Extra-intestinal infection undergoes specific imaging changes as it
progresses through four stages of infection. Imaging findings depend
upon location and stage of infection.
 VESICULAR STAGE:
 Cyst with dot sign
 CSF intensity
 Hyper intense scolex on T1 can be seen sometimes
 No enhancement is typical, however faint enhancement of the wall and the
scolex can be seen.

29. COLLOID VESICULAR STAGE :
 Cyst fluid becomes turbid
 CT = hyper attenuating to CSF
 MRI T1WI = hyper intense to CSF
 Surrounding edema
 Cyst and the wall become thickened and brightly enhances.
 Scolex can still be seen as a eccentric focus of enhancement.
 GRANULAR NODULAR:
• Edema decreases
• Cyst retracts
• Enhancement persists but is less marked.

30.  NODULAR CALCIFIED:
• End stage calcified cyst remnant
• No edema
• No enhancement
• Signal drop out on T2WI
• Some intrinsic high T1v signal may be present

33. METASTASES
 Brain metastases are estimated to account for approximately 25-50% of
intracranial tumors in hospitalized patients.
 Due to great variation in imaging appearances, these metastases present a
common diagnostic challenge.
 80% of brain metastases can be accounted for by five primary tumors :
• lung cancer
• renal cell carcinoma
• melanoma
• breast cancer
• GI tract adenocarcinoma majority being colorectal CA.

34.  80% of metastases localize to the cerebral hemispheres, 15% localize to
the cerebellum and 3% localize to the basal ganglia.
 Macroscopically metastases are relatively well demarcated from the
surrounding parenchyma and usually there is a zone of peritumoural
edema out of proportion with the tumor size.

35. RADIOGRAPHIC FEATURES
CT SCAN
 PRECONTRAST IMAGING:
the mass may be iso dense, hypo dense or hyper dense (classically melanoma)
compared to normal brain parenchyma with variable amounts of
surrounding vasogenic edema.
 POST CONTRAST:
enhancement is also variable and can be intense, punctate, nodular or ring-
enhancing if the tumor has out grown it's blood supply.

36. MRI
 T1
• typically iso to hypo intense
• if hemorrhagic may have intrinsic high signal
• non-hemorrhagic melanoma metastases can also have intrinsic high signal due
to the paramagnetic properties of melanin
 T2
• typically hyper intense
• hemorrhage may alter this
 FLAIR
• typically hyper intense
• Hyper intense peritumoural edema of variable amounts

37.  T1C+
• enhancement pattern can be uniform, punctate, or ring-enhancing, but it is
usually intense
• delayed sequences may show additional lesions, therefore contrast-enhanced
MR is the current standard for small metastases detection

40. GLIOBLASTOMA
 Glioblastoma (GBM) is the most common adult primary intracranial
neoplasm.
 Carries the worst prognosis (WHO grade IV).
 These tumors are multifocal in 20% of patients and are rarely multi centric.
 Usually occur after the age of 40 years with a peak incidence between 65
and 75 years of age.
 There is a slight male preponderance with a 3:2 M:F ratio.
 Caucasians are affected somewhat more frequently than other ethnicities.

41.  Glioblastomas are typically poorly marginated, diffusely infiltrating necrotic
masses localized to the cerebral hemispheres. The supratentorial white
matter is the most common location.
 Infiltration beyond the visible tumor margin is always present.

42. RADIOGRAPHIC FEATURES
CT SCAN
 Irregular thick margins: iso to slightly hyper attenuating (high cellularity).
 Irregular hypo dense center representing necrosis
 Marked mass effect
 Surrounding vasogenic edema
 Hemorrhage occasionally seen
 Calcification is uncommon
 Intense irregular, heterogeneous enhancement of the margins is almost
always present

43. MRI
 T1
• hypo to iso intense mass within white matter
• central heterogeneous signal (necrosis, intra tumoral hemorrhage)
 T2/FLAIR
• Hyper intense
• surrounded by vasogenic edema
• flow voids occasionally seen
 T1 C+ (Gd)
• enhancement is variable but is almost always present
• typically peripheral and irregular with nodular components
• usually surrounds necrosis

45. TUMEFACTIVE MULTIPLE SCLEROSIS
 Tumefactive multiple sclerosis is a term used to describe patients with
established multiple sclerosis who develop large aggressive demyelinating
lesions.
 Most frequently encountered in women, usually young middle age.
 It is a separate entity then Tumefactive demyelinating lesions also
sometimes called mono focal acute inflammatory demyelination
(MAID), is a locally aggressive form of demyelination, usually manifesting
as a solitary lesion; greater than 2 cm that may mimic a neoplasm on
imaging.
 TMS and TDL have similar radiological appearance with different clinical
picture.

46. RADIOGRAPHIC FEATURES
CT SCAN
 Tumefactive multiple sclerosis plaques appears as hypo attenuating lesion
with ill-defined ring enhancement, central necrosis, perilesional edema and
minimal mass effect.

47. MRI
 Tumefactive demyelinating lesions tend to be large but with relatively little
mass effect or surrounding edema.
 T1 C+ (Gd)
• about half of tumefactive demyelinating lesions demonstrate contrast
enhancement.
• the enhancement pattern is usually in the form on an open ring and the
incomplete portion of the ring is on the gray matter side of the lesion

49. CONCLUSION
 Multiple ring enhancing lesions are a commonly encountered
neuroimaging abnormality. Distinguishing between neoplastic and non
neoplastic etiology is extremely important.
 Many features of the lesion as well as clinical presentation and patient
demographics need to be taken together to help narrow the differential.

50.  Helpful rules of thumb include:
 Enhancing wall characteristics
• thick and nodular favors neoplasm
• thin and regular favors abscess
• incomplete ring often opened toward the cortex favors demyelination
• intermediate to low T2 signal capsule favors abscess
• restricted diffusion of enhancing wall favors GBM or demyelination
 Surrounding edema
• extensive edema relative to lesion size favors abscess
• increased perfusion favors neoplasm (metastases or primary cerebral malignancy)

51.  Central fluid content
• restricted diffusion favors abscess
• absence of diffusion restriction favor a tumor with a central necrotic component
(classically a metastases)
 Number of lesions
• similar sized rounded lesions at grey white matter junction favors metastases or
abscesses
• irregular mass with adjacent secondary lesions embedded in the same region of 'edema'
favors GBM.
• small (<1-2cm) lesions with thin walls especially if other calcific foci are present
suggest Neurocysticercosis.

53. THANK YOU