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Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
Imaging of infection of brain and its linings
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Imaging of infection of brain and its linings

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  • 1. MODERATOR: DR R.K. GOGOI Presenter Dr CHARUSMITA CHAUDHARY
  • 2. infection of brain and its linings 2  There has been a significant decrease in the morbidity and mortality of patients with intracranial infections with the advent of computed tomography (CT) scanning and magnetic resonance imaging (MRI Recent advances in technology  positron emission tomography (PET)  single photon emission computed tomography (SPECT)  diffusion imaging  proton magnetic resonance spectroscopy (MRS). additional imaging modalities to use in the evaluation of intracranial infection
  • 3. Source  Risk factoRs :  diabetes mellitus  alcoholism  malignancy  agammaglobulinemia  radiation therapy and chemotherapy  steroids  HIV 3  Hematogenous spRead  diRect extension infection of brain and its linings
  • 4. Forms of Intracranial infections Cerebritis  Abscess Empyema Granuloma  Encephalitis Meningitis Osteomyelitis 4infection of brain and its linings
  • 5. Forms of Intracranial infections CEREBRITIS: focal usually pyogenic without capsule or pus formation ABSCESS: pyogenic encapsulated pus containing cavity  EMPYMA: an abscess forms in an enclosed or potential space epidural or subdural GRANULOMA: : a focal, more or less encapsulated, inflammatory lesion usually chronic, without pus formation 5infection of brain and its linings
  • 6. Forms of Intracranial infections continue….. Encephalitis: direct infection of the brain, usually viral and often diffuse  Meningitis: infection of the meninges, may be suppurative or granulomatous 6infection of brain and its linings
  • 7. MENINGITIS 7infection of brain and its linings
  • 8. Leptomeningitis The pachymeninges make up the dura mater, which consists of the periosteum and a meningeal layer. The leptomeninges consist of the pia and arachnoid 8infection of brain and its linings
  • 9. Leptomeningitis  inflammation of the leptomeninges and the adjacent subarachnoid space  Characteristic pathogens  Bacterial meningitis or purulent meningitis  Non-bacterial meningitis often referred to as aseptic meningitis Can be divided into  acute pyogenic (bacterial),lymphocytic (viral), and chronic (TB) meningitisThe diagnosis is usually made clinically.  The role of neuroimaging is to exclude complications of meningitis (e.g., abscess, ventriculitis, empyema) 9infection of brain and its linings
  • 10. Causative organism 10infection of brain and its linings
  • 11. Aseptic Meningitis All non-bacterial causes of meningitis Typically less ill appearing than bacterial meningitis Most common cause is viral HSV  type II Enterovirus (coxsackie, echovirus)  Affects all ages  Generally self-limited illness
  • 12. Aseptic Meningitis  Other Viral  HIV  Lymphocytic choriomeningitis virus  Arbovirus  Mumps  CMV  EBV  VZV  Adenovirus  Measles  Rubella  Rotavirus  Influenza and parainfluenza  Other infectious  Borrelia burgdorferi  Mycobacterium tuberculosis  Treponema pallidum  Mycoplasma pneumoniae  Rickettsia, erlichia, brucella  Chlamydia  Fungal  Cryptococcus  Coccidiodes  Histoplasmosis  Parasitic  Angiostrongylus  Toxoplamosis  Medication  NSAID’s  Bactrim  Pyridium  Malignancy  Lymphoma and leukemia  Metastatic carcinoma  Autoimmune  Sarcoid  Behcet’s  SLE
  • 13. Pathogens- Special Situations VP shunts/penetrating head trauma- Staph epi Neural tube defects- Staph aureus, enteric organisms T-cell defects (HIV)- cryptococcus, listeria Sinus fracture- Strep pneumo Asplenia (HgB SS)- Neisseria, H. flu, S. pneumo Terminal compliment deficiency- Neisseria 13infection of brain and its linings
  • 14. Clinical Presentation  Clinical manifestations are due to local immune response to bacteria  Ensuing inflammatory response increases blood- brain permeability  Cerebral edema  Increased ICP  Local thrombosis and infarction 14infection of brain and its linings
  • 15. Clinical Presentation Con’t… 15infection of brain and its linings
  • 16. Pathological responses  INITIALLY: vascular congestion, edema, and minute hemorrhages CT and MRI findings may be normal early in the disease process  ONCE INFECTION PROGRESSES NECT :obliteration of the basal cisterns. results from a combination of hypervascularity in the acutely inflamed leptomeninges and exudate in the subarachnoid space. Diffuse cerebral swelling may be seen. Contrast-enhanced CT scan : show enhancement in the basal cisterns and sylvian fissure, regardless of the causative organism 16infection of brain and its linings
  • 17. Imaging continue… Routine MRI scans :obliteration of the basal cisterns on T1-weighted images.  Fluid-attenuated inversion recovery (FLAIR) sequence may show hyperintensity of the cerebrospinal fluid (CSF) within the subarachnoid space in contrast to the hypointense CSF in the ventricles. Abnormal cortical hyperintensity may be seen on T2-weighted images.  Contrast-enhanced MRI studies may show basal cisternal and sylvian enhancement as well as enhancement deep within the cortical sulci 17infection of brain and its linings
  • 18. Meningitis 18infection of brain and its linings
  • 19. complications Early complications abscess, subdural empyema, ventriculitis, and infarction.  Late complications subdural effusion, encephalomalacia, hydrocephalus, and atrophy 19infection of brain and its linings
  • 20. 20 Contrast-enhanced MRI more sensitive than contrast-enhanced CT in detection of meningitis and its complications The MRI differential diagnosis includes only meningeal carcinomatosis infection of brain and its linings
  • 21. Grp b streptococcal meningitis Leading cause of newborn meningitis in developed countries Best diagnostic clue: Meningoencephalitis in anewborn 21infection of brain and its linings
  • 22. 22infection of brain and its linings
  • 23. PACHYMENINGEAL ENHANCEMENT may be seen as a normal finding -- the dura mater does not produce a blood-brain barrier. dural reflections of the falx and tentorium. intracranial hypotension, meningiomas, metastatic disease, lymphoma, and granulomatous disease] Postoperative meningeal enhancement may be pachymeningeal or leptomeningeal in appearance. 23infection of brain and its linings
  • 24. Subdural Effusion irritation of the dura by the infectious agents or its by-products or by inflammation of subdural veins with loss of fluid and albumin into the subdural space. H. influenzae is a common pathogen On neuroimaging, effusions look similar to CSF and are frequently seen in the frontal region.  On contrast study , no evidence of abnormal enhancement The subdural effusion usually resolves spontaneously 24infection of brain and its linings
  • 25. infection of brain and its linings 26 INTRACRANIAL EMPYEMA
  • 26. Subdural empyema  collection of pus between dura and leptomeninges  as a complication of meningitis, paranasal sinusitis, otitis media, osteomyelitis, or a penetrating wound of the skull  Frontal sinusitis is the most common cause  Route: retrograde fashion through a dural sinus or through bridging veins  even when small, usually cause focal neurologic deficits  considered a neuro-surgical emergency because of its progressive clinical course.  Despite recent improvement in surgical technique and antibiotics, mortality remains high (25% to 40%).  Complications :venous thrombosis and infarction 27infection of brain and its linings
  • 27. CT scan -hypodense or isodense crescentic or lenticular area adjacent to the inner table of the skull CECT -enhancement of the medial rim may be seen Enhancement of the margin of the empyema is characteristic better visualized with MRI than with CT. 28infection of brain and its linings
  • 28. Epidural Empyema collection of pus between the dura and calvaria,  complication of otitis media, mastoiditis, sinusitis, or osteomyelitis of the skull.  not as toxic as that with subdural empyema. Displacement of the falx and dural sinuses away from the inner table of the skull, an important and useful sign indicating the epidural location of a collection 29infection of brain and its linings
  • 29. Epidural Empyema 30infection of brain and its linings
  • 30. Epidural Empyema  T2-weighted MR images , A hypointense rim, representing inflamed dura, in an epidural, but not a subdural, empyema  , epidural empyema may extend into the subgaleal space through emissary veins or adjacent 31 Epidural empyema, like epidural hematoma, can across the midline but is limited by the sutures . In contrast, a subdural collection of any kind cannot cross the midline but is not limited by the sutures infection of brain and its linings
  • 31. 32infection of brain and its linings
  • 32. Encephalitis  refers to diffuse inflammation of the brain with a parenchymal infiltration of inflammatory cells, usually caused by virus.  The brain damage is due to a combination of intracellular viral growth and the host's inflammatory response  Common herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2 33infection of brain and its linings
  • 33. INTRODUCTION unusual manifestation of human viral infection as most viruses do not attack the human CNS. Viruses vary in their potential to cause CNS infections. some cause relatively benign infections, others cause prominent neurologic symptoms  Overall, viruses are the most common cause of meningoencephalitis (3.5-7.4 per 100000 persons per year in USA). 34infection of brain and its linings
  • 34. INTRODUCTION Viral encephalitides can be divided into 4 types acute viral encephalitis postinfectious encephalomyelitis slow viral infections of the CNS chronic degenerative CNS disease of viral origin 35infection of brain and its linings
  • 35. VIRUSES THAT CAUSE MENINGOENCEPHALITIS  Herpes simplex virus (HSV-1, HSV-2)  Other herpes viruses: varicella zoster virus (VZV), cytomegalovirus (CMV), Epstein-Barr virus (EBV), human herpes virus 6 (HHV6)  Adenoviruses  Influenza A  Enteroviruses, poliovirus  Measles, mumps and rubella viruses  Rabies  Arboviruses—for example, Japanese B encephalitis, St Louis encephalitis virus, West Nile encephalitis virus, Eastern, Western, and Venezuelan equine encephalitis virus, tick borne encephalitis viruses, Chandipura virus, Dengue virus, chikungunya, KFD.  Bunyaviruses—for example, La Crosse strain of California virus  Reoviruses—for example, Colorado tick fever virus  Arenaviruses—for example, lymphocytic choriomeningitis virus  Paramyxovirus – Nipah virus, hendra virus Modified from Chaudhury and Kennedy Postgrad Med J. 2002;78:575 36infection of brain and its linings
  • 36. VIRUSES THAT CAUSE MENINGOENCEPHALITIS cont. Sporadic ; HSV1 and 2, Mumps, EB, adenovirus, rabies etc Epidemic; Arboviruses, influenza, enteroviruses, emerging viruses (Nipah). 37infection of brain and its linings
  • 37. VIRUSES THAT CAUSE MENINGOENCEPHALITIS Indian scenario  In India, most common cause for epidemic encephalitis JE  Other viruses cause sporadic meningoencephalitis include herpes, mumps, measles and polio  In children enterovirus 71, mumps, measles, and JE are major causes. Others include herpes, varicella ,rubella and dengue  Emerging viruses with threat potential – Nipah, chandipura, chikungunya . 38infection of brain and its linings
  • 38. Pathogenesis CNS access of the virus can be through two routes  Hematogenous (eg. Arboviruses) –most common  Intraneuronal ( eg. HSV, rabies, varicella zoster) After hematogenous entry transient viremia→ → seeding of reticuloendothelial system, replication→ secondary viremia seeding of CNS→ → 39infection of brain and its linings
  • 39. Pathology: Gross: variable degree of meningitis, brain swelling, congestion and hemorrhage. Some viruses preferentially attack certain brain sites  Herpes virus – temporal neocortex, pons JE- thalamus, basal ganglia, substantia nigra, hippocampus This may reflect as fairly characteristic imaging findings 40infection of brain and its linings
  • 40. Imaging CT Hypoattenuated lesions affecting grey matter, deep gray matter and white matter. Focal or generalized brain swelling Focal hemorrhage +- enhancement MRI More sensitive T2 hyper and T1 hypo to isointense single or multifocal lesions +- enhancement +-hemorrhage infection of brain and its linings 41 DWMRI oIn acute stage- DW may show ↑ or equal lesions compared to conventional MR. In later stages may show less lesions[1,2]
  • 41. CONGENITAL CMV Transplacental transmission of human herpes virus Best diagnostic clue o Microcephaly o Cerebral calcification (40-70%) • Periventricular (sub ependymal) o Cortical gyral abnormalities • Agyria ~ pachygyria ~ diffuse polymicrogyria ~ focal cortical dysplasia o Cerebellar hypoplasia o Myelin delay or destruction Location: Dystrophic periventricular Ca++ has predilection for germinal matrix zones 42infection of brain and its linings
  • 42. IMAGING CT Findings o Cerebral parenchymal Ca++ (40-70%) • Periventricular (subependymal) o Ventricular dilatation and WM volume loss o Focal regions of WM low attenuation o Cortical gyral abnormalities o Cerebellar hypoplasia MR Findings • TIWI  o Periventricular subependymal foci of Tl shortening due to Ca ++  o Ventricular dilatation and periventricular WM volume loss 43infection of brain and its linings
  • 43. CONGENITAL HIV Vertical HlV 1 infection early in-utero/late pregnancy, at delivery or, by breast-feeding Imaging Findings • Best diagnostic clue: Basal ganglia Ca++, volume loss MRA: Fusiform vasculopathy Image Interpretation Pearls • Consider HIV if bilateral symmetrical calcifications in BG are found in a child> than 2 months 44infection of brain and its linings
  • 44. CONGENITAL HIV Scattered Ca++ • Hydrocephalus Periventricular Ca++ 45infection of brain and its linings
  • 45. Herpes encephalitis 46infection of brain and its linings
  • 46. Herpes simplex encephalitis most common endemic encephalitis in the USA (2 per million) and causes 10-20% of all viral encephalitis.  In India exact incidence is not known and it is under diagnosed due to lack of awareness and diagnostic facilities Early diagnosis is important because AV therapy can decrease mortality and morbidity. HSV1 causes 95% of HSE. Most commonly occurs due to virus reactivation. HSV2 causes 80-90% of neonatal encephalitis [1] Panagaria A. Neurol In. 49:360; 2001. 47infection of brain and its linings
  • 47. Herpes simplex encephalitis  Definitive diagnosis: PCR, intrathecal antibodies, brain biopsy – take time and may be false negative in early disease [1].  Imaging helps in establishing an early diagnosis. 1) Akyldz BN Paeditr Emerg Care 24;377 :2008. 48infection of brain and its linings
  • 48. Herpes simplex encephalitis 49infection of brain and its linings
  • 49. Usually bilateral Hemorrhage and enhancement seen Basal ganglia tend to be spared or involved in contiguity with the TL. Pons may be involved [Tien AJR:161,1993] MR is more sensitive and shows lesions earlier than CT or SPECT infection of brain and its linings 50 Herpes simplex encephalitis
  • 50. 51infection of brain and its linings
  • 51. Herpes simplex encephalitis Rare paraneoplastic syndrome limbic system, often bilateral Active seizures may disrupt BBB, cause signal abnormalities and enhancement 52infection of brain and its linings
  • 52. HSV 2 Both HSV1 and 2 are commonly prevalent in Indian population. (Mixed=83%, HSV1=10%, HSV2=1%) [1] HSV2 along with TORCH agents are major causes of neonatal encephalitis. Infections result from maternal birth canal or transplacental spread Unlike HSV1, HSV2 infection in neonates is diffuse. 1.Shivaswami 2005. IJDVL 71:26 53infection of brain and its linings
  • 53. HSV 2 Imaging findings are nonspecific. CT scans in early disease may be negative or show subtle areas of low density . Conventional MR and DWI show lesions better.  Lesions may be multifocal involving almost any area of brain or limited to temporal lobes brainstem and cerebellum. Watershed infarcts may be seen [1]  In-utero infections can result in microcephaly, encephalomalacia or calcification. 1)Vossough.2008. Neuroradiol 50:355 54infection of brain and its linings
  • 54. Axial T2WI MR shows areas of high signal in frontal lobes WM due to acute H5V-2 Axial T1WI MR shows diffuse cystic encephalomalacia and prominent CSF-containing spaces Scattered Ca++, hydrocephalusPeriventricular Ca++, 55infection of brain and its linings
  • 55. HIV Encephalitis Syndrome of cognitive, behavioral, and motor abnormalities attributed to direct HIV effect on brain, in the absence of opportunistic brain infections Location: Bilateral periventricular and centrum semiovale WM, basal ganglia, cerebellum, brainstem 56 Best diagnostic clue: Combination of atrophy and symmetric, periventricular or diffuse white matter (WM) disease suggests HIVE infection of brain and its linings
  • 56. 57infection of brain and its linings
  • 57. Introduction mosquito borne Flaviviral encephalitis.  Pigs and heron like birds are main amplifiers. leading cause of acute meningoencephalitis affecting children and adults in the world. JE is endemic to Indian subcontinent, particularly in the NE state of Assam Epidemics occur in the summer rainy season which favor breeding of mosquitoes. First recognized in India in 1955, Epidemics occur every year in several Indian states since the first in WB(1973). 59infection of brain and its linings
  • 58. Pathology 1)Tiroumourougane. Postgrad. Med. J. 2002; 78: 205 60infection of brain and its linings Some neurons have specific receptors with strong affinity for JEV [1
  • 59. Lesions of JE are most commonly seen in the thalami and substantia nigra, Basal ganglia, cerebral cortex, hippocampi, midbrain, pons, medulla and cerebellum lesions are also seen. Lesions hyperintense on T2 and FL and iso to hypo on T1 with local or generalized brain swelling. No enhancement. Hemorrhagic change has been reported from India [1]. MRI is the investigation of choice with reported sensitivity of 89-100% compared to CT (38-55%) [1,2]. DWI has been reported to help in early diagnosis and in assessing temporal evolution of lesions[1]  Was helpful in making an early diagnosis in JE showing additional lesions 1)Kalita. J Neurol Sci 2000; 174: 3 61infection of brain and its linings Imaging
  • 60. Evolution of lesions in JE 62infection of brain and its linings
  • 61. Temporal lobe involvement in JE Fairly characteristic pattern of TL involvement with posterior hippocampal involvement and sparing of anterior temporal lobe and neocortex. Insula occasionally involved Associated lesions characteristic of JE usually seen in thalamus, SN, BG etc. Can help differentiate from HSE [1] 1)Handique AJNR 2006 27:1027 63infection of brain and its linings
  • 62. infection of brain and its linings 64 T2 DWI PATTERN 1 DWI>T2 [1]
  • 63. Neurocysticercosis and JE More than a casual relationship between NCC and JE has been suggested by many studies in China and India [1,2,3] Co-infections have been advocated as prognosticator of poor outcome[1] 1.Desai Epidemiol Infect 1997;118:165 2. Shankar. Ind J Med Res 1983; 78:431 3. Liu. Chinese Med J 1957;75:1010 65infection of brain and its linings
  • 64. Neurocysticercosis and JE asymmetric with lateralization to the side of the brain having maximum NCC or a cyst with edema. were more florid with significantly higher amount of abnormal CT scans and more abnormal MR imaging more common in children. Altered immune status in co-infections were suggested by significantly lowered levels of JE IgM. 66infection of brain and its linings
  • 65. infection of brain and its linings 67 co-infection
  • 66. Mumps, measles and varicella Mumps, measles and varicella viruses may occasionally cause acute encephalitis besides its primary infectious manifestations.  Acute measles encephalitis is much more common than the more well known (amongst radiologists) SSPE In a study of VE in children from India, 10% was caused by mumps, 7% by measles and 1.8% by varicella [1] (1) Karmarkar. Ind JPaediatr.2008;75:801 68infection of brain and its linings
  • 67. Mumps, measles and varicella Very few large scale imaging studies exist for these encephalitis as the findings are non specific. Mumps encephalitis shows white matter and brainstem lesions[1]. Measles shows lesions in the basal ganglia with multifocal lesions in the gray and white matter, thalamus (rare) with gyriform enhancement of gray matter lesions [2]. Varicella shows multifocal cortical lesions[3] (1)Koyama Int Med 2000 ;39:499 (2) Lee. Neuroradiol 2003; 45:100 (3) Tien AJR 19937; 161:16 69infection of brain and its linings
  • 68. Enterovirus 71 MRI revealed lesions in the brainstem and cerebellum in 71% patients with rhombencephalitis. Anterior horn cells showed lesions in patients with flaccid paralysis [1] In study from India lesions were also described in the thalamus, basal ganglia, parieto occipital, frontal, temporal lobes, substantia nigra besides brainstem and cerebellar involvement [2] 1) Huang. New Eng J Med. 1999;341:936 (2) Karmarkar. Ind JPaediatr.2008;75:801 70infection of brain and its linings
  • 69. Dengue Dengue is caused by a mosquito borne flavivirus like JE. Neurologic manifestations in dengue fever, hemorrhagic fever and Shock syndrome have been thought to be due to encephalopathy Recent reports have shown that dengue virus can cause neuroinvasion and encephalitis [1,2] (1) Lum. Am J Trop Med Hyg. 1996;54:256 (2) Muzaffar. Sing Med J 2006;47:975 71infection of brain and its linings
  • 70. Dengue infection of brain and its linings 72 From. Muzaffar. Sing Med J 2006;47:975 Imaging studies have shown cerebral edema, lesions in the hippocampus and temporal lobes
  • 71. Rabies encephalitis Transmitted by bites of infected animals or by transplants. 100% fatal. In India rabies occurs in all parts of the country except in Lakshadweep, Andaman and Nicobar islands. 73infection of brain and its linings
  • 72. infection of brain and its linings 74
  • 73. Nipah virus encephalitis paramyxovirus spread to man from fruit-bats or pigs infected by fruit-bats.  Subsequent spread from man to man occurs. First identified in Malaysia and Singapore in 1988-89, outbreaks have occurred in Bangladesh (2001-4,5)and Siliguri (2001). Case fatality in India and Bangladesh was 75%[1] (1) Halder. Ann Ind Acad Neurol 2006;9:137 75infection of brain and its linings
  • 74. Nipah virus encephalitis MR shows fairly characteristic findings with small T2 hyperintense white or gray matter lesions with transient T1 hyperintense punctate cortical lesions in subacute phase [1] (1) Lim. Radiol 2002;222:219 infection of brain and its linings 76
  • 75. Other emerging viruses Chandipura virus is transmitted to humans possibly by sandflies and primarily causes encephalitis in children. Major outbreaks have occurred in Gujarat, Andhra Pradesh, Madhya Pradesh and Maharashtra with fatality rates of 50-80%. Brainstem encephalitis has been reported.  CT and MRI scans have showed no abnormality in few (CT=5,MR=1)reported patients from India [1,2]. No large scale imaging studies available. Other emerging viruses that ocassionally cause encephalitis include Chikungunya and KFD. 77infection of brain and its linings
  • 76. ADEM acute Disseminated Encephalomyelitis an immune response to a preceding viral infection or vaccination neurologic signs and symptoms 5 days to 2 weeks later. Both humoral and cell-mediated immunity  A hypersensitivity reaction to a myelin . Perivenous demyelination is the hallmark of the disease The disease primarily involves white matter, but change may also be apparent in gray matter and brain stem The differential diagnosis includes multiple sclerosis, vasculitis, and embolic infarction.  In later stages of the disease, encephalomalacia, ventriculomegaly, and atrophy may be seen. 78infection of brain and its linings
  • 77. Other Encephalitides Creutzfeldt-Jakob Disease human spongiform encephalopathy that results from an infection by a prion transmission has been traced to inoculations by injections of human growth hormone, transplantation of corneas, and implantation of cerebral electrodes butchers and meat handlers are at greater risk of contracting the disease variant ;bovine spongiform encephalopathy (so-called mad cow disease). The infective prion is a proteinaceous particle that contains little or no nucleic acid. The disease occurs in adults in their late 50s 79infection of brain and its linings
  • 78. infection of brain and its linings 80  Cortical gray matter involvement without cerebral atrophy may represent an early phase of the disease.  [ In contrast to Creutzfeldt-Jakob disease, wherein bilateral involvement of the corpus striata and thalami is seen on the imaging studies, the bovine spongiform encephalopathy is characteristically demonstrated by bilateral thalamic pulvinar hyperintensity on T2-weighted and FLAIR images . A, FLAIR image demonstrates hyperintensity in both thalami, in the periatrial white matter, and in the anterior cingulated gyri. B, Diffusion-weighted image shows restricted diffusion in both thalami and cingulated gyri
  • 79. Subacute Sclerosing Panencephalitis measles virus seen in children and young adults with previous measles infection 3 to 9 years earlier CT scans low-density changes in subcortical white matter as well as in basal ganglia.  MRI studies show hyperintensity in the periventricular white matter, subcortical white matter, basal ganglia, cerebellum, and pons on T2- weighted and FLAIR images.[ Abnormal signal intensity on T2-weighted and FLAIR images involving the splenium of corpus callosum can occur.  Atrophy is a late-stage finding. 81infection of brain and its linings
  • 80. Reye's Syndrome disease of unknown etiology in children.  It usually follows a viral infection such as type A or B influenza and varicella . Exogenous toxins, such as salicylates, and intrinsic metabolic defects have been implicated as other factors CT scans show diffuse low density of the supratentorial structures, a finding consistent with diffuse cerebral edema.[124] 82infection of brain and its linings
  • 81. Encephalitis in Immunocompromised Patients Human ImmunodefIcIency VIrus encepHalItIs neurotropic virus causes a subacute form of encephalitis CT scans low density in the periventricular white matter.  MRI hyperintensity in the periventricular white matter on T2-weighted and FLAIR images Normal neuroimaging studies do not exclude HIV encephalitis. 83infection of brain and its linings
  • 82. Encephalitis in Immunocompromised Patients Progressive Multifocal Leukoencephalopathy a JC virus infecting the oligodendrocyte seen in immunocompromised patients.  affects all parts of the brain, including the cerebellum, and does not have the propensity to involve the parieto- occipital region, as previously describe 84infection of brain and its linings
  • 83. Progressive Multifocal Leukoencephalopathy CT scans low-density lesions in white matter.  Early involvement -asymmetrical pattern, later disease -symmetrical and diffusely confluent. Contrast enhancement is usually absent but may occur.[155 . MRI shows a focal region of hypointensity in the white matter on T1-weighted images and hyperintensity on T2-weighted images . Involvement of the subcortical U- fiber is characteristic for PML, as opposed to other HIV- related encephalopathy. . MRI is more sensitive than CT in detecting abnormalities T2-weighted image shows high signal intensity in the parieto- occipital white matter bilaterally. 85infection of brain and its linings
  • 84. Cytomegalovirus Encephalitis affect the immunocompetent as well as immunocompromised patients cause meningoencephalitis or subacute encephalitis. CMV can produce demyelination and necrosis within the white matter. CMV is the most frequent cause of fetal and neonatal viral infection.  calcifications are usually in the subependymal region, whereas in infants with toxoplasmosis, calcifications are seen everywhere, including the periventricular region. 86infection of brain and its linings
  • 85.  CT scans show low density in the white matter, which may or may not enhance with contrast agents . MRI shows high signal intensity in the white matter on T2-weighted and FLAIR images and is more sensitive than CT in detecting leukoencephalitis Nonenhanced CT scans in a newborn show periventricular calcification and ventricular dilatation 87infection of brain and its linings Cytomegalovirus Encephalitis
  • 86. Cerebritis and Abscess 88infection of brain and its linings
  • 87. most brain abscesses are bacterial  streptococci accounting for the majority haematogenous dissemination, penetrating trauma or direct spread  Blood-borne infection can occur anywhere in the brain, but has a predilection for the territory of the middle cerebral arteries fever ,headache and focal neurological deficits. Brain abscesses are multiple in 10–50 per infection of brain and its linings 89
  • 88. stages in the evolution of cerebral abscess there are four stages 1. Acute cerebritis (the first 4 to 5 days). In early cerebritis, mild central nodular enhancement may be seen on contrast-enhanced CT or MRI scans infection of brain and its linings 90
  • 89. infection of brain and its linings 91 2. Late cerebritis (at 7 to 10 days). In the late cerebritis stage brain enhancement on CT scans Late cerebritis. A, Gadolinium-enhanced MRI study shows thick, smooth, ringlike enhancement with surrounding edema. B, Gadolinium-enhanced MRI study (coronal view) shows a second small, adjacent ringlike enhancement
  • 90. stages in the evolution of cerebral abscess 3. Early abscess (at 10 to 14 days). Formation of a collagenous capsule by fibroblasts is seen. The central necrotic area is liquefied. Surrounding edema persists. 4. Mature abscess (after 14 days). A decrease in surrounding edema gliotic reaction at outer margin of the abscess capsule. infection of brain and its linings 92 Usually, more than 2 weeks is required to form a firm capsule The wall of the mature abscess consists of three layers: (1) an inner inflammatory layer of granulation tissue containing macrophages, (2) a middle collagenous layer, and (3) an outer gliotic layer
  • 91. infection of brain and its linings 93 Abscess treated conservatively with antibiotics.
  • 92. infection of brain and its linings 94 Abscess caused by gas-forming organism. The most distinctive feature of abscess on imaging is the presence of a smooth, thin capsule with a moderate amount of cerebral edema. [57]  It is located at the corticomedullary junction and usually extends into the white matter. Nonenhanced CT scans show a low-density area with mass effect and compression of the ventricular system.  rupture of the abscess into an adjacent ventricle {medially into the ventricular system because the medial wall is thinner than the lateral wall
  • 93. Differential diagnosis  necrotic primary brain tumor, cystic metastatic tumor, infarction, resolving hematoma, cysticercosis, and thrombosed aneurysm Thick, nodular enhancing wall typical History of trauma or vascular lesion • Blood products present Enhancement often incomplete ring • Thick, nodular enhancing wall typical 95infection of brain and its linings Infarcts often show gyral enhancement, occasionally mimicking ring enhancementThe MRI differential diagnosis of abscess is similar to the CT diagnosis except for hematomas, which can be recognized by their characteristic MRI signal intensity patterns, depending on the age of the hematomas
  • 94. Ependymitis  Ventriculitis, or ependymitis, is an inflammation of the ependymal lining of the ventricular system  rupture of periventricular abscess or from retrograde spread of infection from the basal cisterns by way of the fourth ventricle  Hydrocephalus may result from intraventricular adhesions and septation caused by organization of intraventricular exudate and debris, resulting in blockage of the interventricular foramina.  A trapped fourth ventricle may result from obstruction of its outlets and the aqueduct because of ependymitis infection of brain and its linings 96
  • 95. infection of brain and its linings 97  NECT scan -normal or may show only slightly increased density in region of affected ependyma  MRI -marginal ventricular abnormality or only slightly increased signal intensity in the region of affected ependyma  proton-density-weighted images. The fluid within the ventricles may show slightly increased intensity,.  Contrast-enhanced CT or MRI studies show uniform, thin ependymal enhancement Gadolinium-enhanced MRI studies show thin, smooth ependymal enhancement in an AIDS patient with cytomegalovirus ependymitis.
  • 96.   The differential diagnosis on CT and MRI studies includes ependymal seeding of intracranial neoplasm. The ependymal enhancement may be irregular or nodular if it is secondary to seeding of neoplasm, the clinical history may be helpful in arriving at the correct diagnosis typically nodular • Parenchymal disease usually present Ventricles typically not enlarged 98infection of brain and its linings
  • 97. Granulomatous Infection 99 Tuberculosis infection of brain and its linings
  • 98. Tuberculosis Mycobacterium tuberculosis  very young and very old persons are affected, with the highest incidence in the first 3 years of life Increased in incidence in immunocompromised patients, drug abusers, and patients with AIDS Tuberculous meningitis is the most frequent manifestation and tends to involve the basal leptomeninges.  Best diagnostic clue o Basilar meningitis + extracerebral TB (pulmonary) o Meningitis + parenchymal lesions highly suggestive 100infection of brain and its linings
  • 99. TBM pathology Penetration of meningeal vessel walls by haematogenous spread • Rupture of subependymal or subpial granulomata into the CSF 101infection of brain and its linings
  • 100. Tuberculous meningitis  involve the basal leptomeninges.  CT shows -  obliteration of the basal cisterns by isodense or slightly hyperdense exudate, which shows diffuse enhancement with IV contrast medium  The most useful CT criteria of abnormal basal meningeal enhancement are:  (A) linear enhancement of the middle cerebral artery cisterns;  (B) obliteration by contrast of the CSF spaces around normal vascular enhancement;  (C) Y-shaped enhancement at the junction of the suprasellar and middle cerebral artery cisterns and  (D) asymmetry of enhancement 102infection of brain and its linings
  • 101. infection of brain and its linings 103  MRI depicts the basal meningeal enhancement, hydrocephalus and basal ganglia infarcts with greater sensitivity than CT  Late sequelae of tuberculous meningitis include hydrocephalus, infarction, syringobulbia, and syringomyelia.
  • 102. Tuberculous meningitis differential diagnosis includes fungal meningitis, sarcoid and carcinomatous meningitis 104infection of brain and its linings
  • 103. tuberculoma found in any portion of the intracranial compartment When tuberculoma and tuberculous meningitis are seen together, the diagnosis of tuberculosis is easily made. 105 Tuberculoma pathophysiology • Hematogenous spread (GM-WM junction lesions) • Extension of meningitis into parenchyma via cortical veins or small penetrating arteries infection of brain and its linings
  • 104. 106  NECT scans isodense, hyperdense, or of mixed density  CECT- ringlike enhancement[152] or, less likely, areas of nodular enhancement  A central nidus of calcification with surrounding ringlike enhancement, known as the target sign, suggests tuberculoma.  Gadolinium-enhanced MRI studies show enhancing patterns similar to those on contrast-enhanced CT scans infection of brain and its linings
  • 105. 107 T1-weighted image shows isointense to hyperintense capsules with central pus and debris and surrounding edema. B, T2-weighted image shows the abscess capsules with an inner ring of hypointensity and an outer ring of hyperintensity; pus shows hyperintensity, and debris shows hypointensity. C, Gadolinium-enhanced MRI study shows smooth, ringlike enhancement of the abscess capsule infection of brain and its linings
  • 106. Neurosyphilis meningovascular syphilis syphilitic gumma  widespread thickening of the meninges, with lymphocytic infiltration involving the meninges and around the small vessels  CT shows multiple low- density areas involving both gray and white matter.  Contrast-enhanced CT scans show linear, nonhomogeneous enhancement.  Contrast-enhanced MRI studies may demonstrate meningeal enhancement in addition to a gyriform pattern of enhancement  consist of masses of granulation tissue and are rare  originate in the meninges and blood vessels and spread into the brain parenchyma.  On CT scans, gummas are well- delineated masses with ringlike or nodular enhancement.  On contrast-enhanced MRI, gumma shows nodular or ringlike enhancement. Cerebral atrophy may develop in patients with neurosyphilis 108infection of brain and its linings
  • 107. Fungal infection involve intracranial blood vessels, leptomeninges, and brain parenchyma. Intracranial infection is frequently secondary to pulmonary disease HIV, diabetes, pregnancy, and malignancy. CNS fungal infection displays neuroimaging features similar to those seen with tuberculosis 109infection of brain and its linings The fungi of yeast forms tend to spread hematogenously to the meningeal microcirculation, with resultant leptomeningitis attributable to their smaller size; the larger hyphal form more commonly involves the brain parenchyma, with resultant cerebritis or encephalitis
  • 108. Aspergillosis Aspergillus fumigatus infection is seen predominantly in immunocompromised patients hematogenous spread of pulmonary disease and less commonly caused by direct extension of disease in the nasal cavity and paranasal sinuses produces meningitis and meningo-encephalitis. 110infection of brain and its linings
  • 109. Patho physiology 111infection of brain and its linings
  • 110. Imaging CT scans low-density areas with little or no contrast enhancement and mass effect, representing areas of infarction  Incomplete ringlike contrast enhancement may be seen MRI studies demonstrate a peripheral ring of low signal intensity The ring of low signal intensity corresponds to a dense population of Aspergillus hyphal elements and small areas of hemorrhage histologically. 112infection of brain and its linings
  • 111. Cryptococcosis Cryptococcosis is the most common fungal infection in patients with AIDS . a yeast with a polysaccharide capsule CNS infection is usually secondary to pulmonary infectio nmeningitis, meningoencephalitis, or cryptococcal mass . Meningitis is the most common presentation. Ocular symptoms are common in patients with cryptococcal meningitis. infection of brain and its linings 113
  • 112. Mucormycosis infection of brain and its linings 114
  • 113. Candidiasis -most common cause of human fungal infection and represents 75% of the fungal infections in patients with neoplasm present as meningitis, granuloma, or microabscess infection of brain and its linings 115 T1-weighted image reveals a hyperintense area in the left thalamus, consistent with focal hemorrhage. B, FLAIR image demonstrates abnormal hyperintense areas in the corpus striati bilaterally and in the left thalamus. C, Postcontrast image demonstrates patchy abnormal enhancement in the corpus striati bilaterally as well as in the left thalamus
  • 114. Cysticercosis one of the most common parasitic diseases involving the brain ingesting the ova of the pork tapeworm (Taenia solium), usually on unwashed, fecally contaminated vegetables or water By ingesting poorly cooked pork infected with cysticercosis, the human becomes the definitive host for T. solium through the anus-finger-mouth route. 117 Best diagnostic clue: Cyst with "dot" inside infection of brain and its linings intracranial compartment is involved in 60% to 90% of patients with cysticercosis meningobasal, parenchymal, intraventricular, or a combination of these sites Convexity subarachnoid spaces most common ( cisterns> parenchyma> ventricles)
  • 115. STAGES: Escobar, has identified four stages that the parasite undergoes within the brain parenchyma Vesicular stage (viable larva) Colloidal vesicular stage (degenerating larva) :Granular nodular (healing) stage Nodular calcified (healed) stage infection of brain and its linings 118
  • 116. 119 STAGES . . VESICULAR STAGE  the tiny (4- to 5-mm) live spherical larva  Smooth, thin-walled CYST , isodense to CSF, no edema  • Hyperdense "dot" within cyst = proto scolex  No (or mild) wall enhancement  COLLOIDAL VESICULAR STAGE.  Hyperdense cyst fluid with surrounding edema The cyst wall may show enhancement  The cyst fluid may show increased density with CT and intensity with MRI. The scolex begins to degenerate and shrink infection of brain and its linings
  • 117.  GRANULAR NODULAR STAGE Mild edema calcification may be identified within the scolex and along the cyst wall on CT scan  NODULAR CALCIFIED STAGE,  granular material appears completely mineralized, with the lesion having shrunk to one half or one fourth of the size of the original  Calcification is much better demonstrated on CT than on MRI 120infection of brain and its linings
  • 118. 121infection of brain and its linings
  • 119. Intraventricular cysticercosis potentially lethal The cysts can be identified by CSF density or signal intensity A thick, ring like enhancement associated with intraventricular cysticercosis 122infection of brain and its linings
  • 120. Echinococcosis CNS involvement is rare Hydatid disease, or echinococcosis, is the larval stage of Echinococcus granulosus definitive host of E. granulosus is the dog, intermediate hosts are sheep, cattle, and camels. Seizure, focal neurologic signs, and increased intracranial pressure are the usual clinical presentations . Extradural cysts have been reported 123infection of brain and its linings
  • 121. infection of brain and its linings 124  NECT or MRI appear as large intraparenchymal cystic lesions with sharp margins  Cyst fluid is of CSF density or signal intensity.  The lack of surrounding edema is an important feature differentiate this lesion from cerebral abscess.  Contrast enhancement may be seen partially or completely involving the wall. Calcification MAY SEEN
  • 122. Toxoplasmosis  Toxoplasma gondii, a protozoan  immunocompromised patients or in patients with AIDS  meningoencephalitis or as granulomas  Granuloma site corticomedullary junction, in the deep gray matter, or in the periventricular areas  NECT- show multiple low-density areas.  MRI studies are more sensitive in detecting the Toxoplasma lesions than contrast-enhanced CT scans infection of brain and its linings 125
  • 123. Rasmussen's Encephalitis childhood disease.  severe epilepsy and progressive neurologic deficits Characterized by hemispheric volume loss and difficult to control focal seizure activity partial motor seizure type and tend to be intractable Early in the disease process, CT and MRI findings may be normal. MRI may reveal hyperintensity in the white matter and putamen on T2-weighted images.[143]  PET imaging using 18 FDG may show decreased hemispheric activity. 127infection of brain and its linings
  • 124. (parieto-occipital most commonHemispheric infarction 128infection of brain and its linings
  • 125. Acute Necrotizing Encephalitis infants and children between 6 and 18 months of age history of mild antecedent illness elevated liver enzymes no focal neurologic or meningeal signs.  Etiology is unknown;  it may be postinfectious (HSV-6 or influenza A and B), immune mediated, or metabolic.  Prognosis is usually poor; less than 10% of patients recover completely.  Focal neurologic deficits are common sequelae 129infection of brain and its linings
  • 126. Acute Necrotizing Encephalitis  Thalamic lesions almost always become hemorrhagic  Enhancement in the margin of the thalami may be seen.  MRS may show elevated lipids, glutamate/glutamine complex, and lactate A, T1-weighted image reveals bilateral thalamic hemorrhage. B, FLAIR image demonstrates hyperintensity in both thalami with adjacent edema. 130infection of brain and its linings
  • 127. Intracranial infections take the following forms Cerebritis Abscess Empyema Granuloma Encephalitis Meningitis Osteomyelitis infection of brain and its linings 131
  • 128. 132 Even with appropriate antibiotics, mortality rate for bacterial meningitis is significant imaging can help in establishing a working diagnosis of viral encephalitis, and differentiate from other conditions such as ADEM and TBM. Keeping in mind the age, geographical location, climate and host immune status, imaging findings can help arrive at an etiological diagnosis of viral encephalitis. HSV encephalitis can be identified early for early AV therapy In epidemic situations the alert radiologist can point to the possible etiological agent eg. in JE, NVE and EV71E Can help in prognostication and identification of associated disease such as NCC with JE infection of brain and its linings
  • 129. 133infection of brain and its linings

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