The document provides an overview of central nervous system infections and tumors, detailing types of infections such as meningitis and encephalitis, and their clinical features and diagnosis. It also explains various brain tumor types, including gliomas, neuronal tumors, meningiomas, and peripheral nerve sheath tumors, with a focus on their characteristics, symptoms, and genetic aspects. Additionally, it discusses familial tumor syndromes like neurofibromatosis and tuberous sclerosis, summarizing their clinical implications.

1. Dr. P.Sravani., M.D.,
Assistant professor.
Govt. medical college
Anantapur

2. CENTRAL NERVOUS SYSTEM
 Normal cells:
1. neurons
2. glia:
a) derived from neuroectoderm
macroglia: astrocytes,
oligodendrocytes,
ependymocytes.
b) from bone marrow: microglia
3. cells of meninges, blood cells

9. INFECTIONS

10. TYPES OF INFECTIONS
1. Acute meningitis
2. Acute focal suppurative infections
3. Chronic bacterial meningoencephalitis
4. Viral meningoencephalitis
5. Fungal meningoencephalitis.

11. INFECTIONS
 Meningitis (generally* bacterial)
 E. coli, Strep B (neonates)
 H. influenzae (children)
 Neisseria meningitidis (adults)
 Strep. pneumoniae, Listeria (elderly)
 PMNs in CSF, INCREASED protein, REDUCED glucose
 Encephalitis (generally viral)
 Arboviruses, HSV, CMV, V/Z, polio, rabies, HIV
 Lymphs and macrophages in perivascular “Virchow-Robbins”
spaces
 Meningoencephalitis
*viral, chemical, tumoral

12. INFECTIONS
Routes:
 Hematogenous most common
 Direct implantation traumatic, iatrogenic.
 Local extension from sinusitis, caries,
osteomyelitis
 PNS viruses – rabies, herpes zoster.

13. ACUTE MENINGITIS
 Meningitis: Inflammation of leptomeninges &
CSF within subarachnoid space
 Meningoencephalitis: Inflammation of meninges
and brain parenchyma.
Types:
 Acute pyogenic ( bacterial),
 Acute aseptic (viral).

14. CLINICAL FEATURES
 Meningeal irritation & neurologic impairment
 Headache, photophobia, irritability, clouding of
consciousness, neck stiffness
 CSF: purulent, high pressure, high neutrophils,
high protein, markedly low glucose, bacteria +.
 Waterhouse Friderichsen syndrome: meningitis
 adrenal hemorrhagic infarcts.

16. ACUTE MENINGITIS

17. Acute aseptic (viral) meningitis
 ECHO, Coxsackie, non-paralytic poliomyelitis
 Less fulminant clinical course
 C/F: Meningeal irritation, fever, altered
consciousness
 CSF: lymphocytic pleocytosis, moderately high
protein, normal glucose.
Acute focal suppurative infections
 Brain abscess
 Subdural empyema (IN SINUSITIS)
 Extradural abscess (IN OSTEOMYELITIS)

18. Predisposing factors:
 Direct implantation during skull fractures
 Local extention of infection –Otitis media, Sinusitis,
mastoiditis
 Acute bacterial endocarditis
 Cyanotic congenital heart diseases
 Chronic pulmonary sepsis as in bronchiectasis
 C/F: Signs of raised ICP & progressive focal deficits.
 CSF: High pressure, high WBC, high protein, normal
sugar.
BRAIN ABSCESS

19. Gross: discrete, liquefactive necrosis,
fibrous capsule, edema.

21. MICROSCOPY
 Exuberant granulation tissue with
neovascularization around necrosis  edema,
 Fibroblasts of vessels  collagen of capsule.

22. CT BRAIN ABSCESS

23. SUBDURAL EMPYEMA

24.  Chronic bacterial meningoencephalitis
A) TB
B) neurosyphilis
C) neuroborreliosis (Lyme Disease)
A) TB:
 C/F: headache, vomitings, confusion
 CSF: moderate pleocytosis mononuclear cells or
mixture of polymorphonuclear and mononuclear
cells, high protein, low or normal glucose.

25.  Gross: gelatinous or fibrinous exudate in S.A. space
Diffuse meningoencephalitis:
 Discrete, white granules over leptomeninges
 Mixture of lymphocytes, plasma cells & macrophages.
 Granulomas, caseous necrosis, giant cells.
 Obliterative endarteritis.
 Acid fast stains – bacilli.
Tuberculoma:
 Well circumscribed intra parenchymal masses, may
cause mass effect
 Central core of caseous necrosis, surrounded by TB
granulomatous reaction

26. TUBERCULOMA

27. Viral meningoencephalitis:
 Viruses:HSV 1 &2, VZV, CMV, Polio, Rabies, HIV.
Fungal:
 Candida albicans, mucor, aspergillus
fumigatus, cryptococcus neoformans.

28. VIRAL
ENCEPHALITIS
PERIVASCULAR
LYMPHOCYTIC
“CUFFING”

30. Meningitis Acute
bacterial
Viral Fungal Tuberculous
Csf pressure
90-180mm of
water
Increased Normal-
mild
increased
Increased Increased
Leucocytes
0-5cells
1000-
10,000
5-300 40-400 100-600
Proteins/mg/
dl
(15-45)
100-500 <100 50-300 50-300
Glucose
50-80 mg/dl
<40 normal decreased <45

31. CNS TUMORS
 Features:
1. Difficult to distinguish benign from malignant,
eg. Benign astrocytoma infiltrates large region of
brain.
2. Difficult to resect without neurological
impairment.
3. Lethality based on site. Eg, meningioma 
compresses medulla  cardiorespiratory arrest.
4. Different pattern of spread. Metastasis outside
brain is rare, spread through CSF common 
seedling along brain & spinal cord.

32. CLASSIFICATION:
 Gliomas : astrocytoma,
oligodendroglioma,
ependymoma.
 Neuronal tumors: ganglion cell tumors,
cerebral neuroblastoma,
central neurocytoma
 Poorly differentiated: medulloblastoma,
atypical teratoid/ rhabdoid
tumor

33.  Other parenchymal tumors:
primary CNS lymphoma,
germ cell tumors,
pineal parenchymal tumors
 Meningiomas
 Metastatic tumors
 Peripheral nerve sheath tumors:
schwannoma,
neurofibroma,
MPNST.

34. CNS TUMORS
SYMPTOMS?
 Headache
 Vomiting
 Mental Changes
 Motor Problems
 Seizures
 Increased Intracranial Pressure
ANY localizing CNS abnormality

35. ASTROCYTOMAS
 80% of adult primary brain tumors.
 Site: cerebral hemisphere, also in cerebellum,
brain stem, spinal cord.
 Age: 4th to 6th decade.
 C/F: seizures, headache, focal neurologic deficits.
 WHO Grading: grade expressed as “I - IV”.
grade I/IV : pilocytic astrocytoma
II/IV: diffuse fibrillary astrocytoma (well
differentiated)
III/IV: anaplastic astrocytoma
IV/IV: glioblastoma

36. Genetics:
 Low grade: inactivation of p53, over expression of
PDGF-A & its receptor.
 High grade: additional mutations of tumor
suppressor genes like RB gene.
Pilocytic astrocytoma (WHO I)
 Site: cerebellum, also in 3rd ventricle, optic nerves,
rarely cerebrum.
 Age: Children & young adults,
 p53 mutations rare.
 Benign.

37.  Slow growth
 Gross:
 Cystic, with a mural nodule in the wall of cyst.

38. MICROSCOPY
 Bipolar cells, long, thin
hair like cytoplasmic
processes.
 Rosenthal fibers-
granular, brightly
eosinophilic, elongated
cytoplasmic masses
 Microcysts +

39. DIFFUSE FIBRILLARY ASTROCYTOMA
 WHO grade II/IV
 Gross:
 Poorly defined, gray, infiltrative tumor that
expands and distorts the invaded brain.
 Size : few cms to huge replacing hemisphere.

40. firm or soft, gelatinous, cystic degeneration

41. Microscopy:
 Well differentiated
 Tumor cells infiltrate adjacent brain for some
distance
 Mild to moderate increase in number of glial cell
nuclei.
 Variable nuclear pleomorphism
 Intervening feltwork of fine, GFAP positive
astrocytic cell processes  fibrillary background.

42. ASTROCYTOMA

43. Anaplastic astrocytoma:
 WHO grade III/IV
 More densely cellular
 More nuclear pleomorphism
 Mitotic figures +
Glioblastoma:
 Was called as glioblastoma multiforme (GBM)
 2 types:
 Primary: de novo, elderly, poor prognosis
 2nd ary : from low grade astrocytoma, young,
better prognosis.

44. GLIOBLASTOMA
Gross:
 Variegated  firm &
white; soft & yellow
(necrosis); cystic
degeneration,
hemorrhages
 Apparently well
demarcated
 always infiltrates
adjacent brain

45. Microscopy:
 Anaplastic
astrocytoma + necrosis
& endothelial cell
proliferation.
 Necrosis:
serpentine/
geographic necrosis.

46. Geographic Necrosis
 Highly malignant
tumor cells crowd
along edge of necrosis
 ‘pseudopalisading’.

47. Glomeruloid body
 Endothelial hyperplasia:
Tufts of piled up
vascular cells  bulge
into lumen  form a ball
like structure
‘glomeruloid body’.

48. OLIGODENDROGLIOMA
 Age: 4th & 5th decades
 Site: cerebral hemisphere – white matter
 C/F: neurologic complaints lasting for years.
 Genetics: LOH for chromosomes 1p & 19q.
 Prognosis better than astrocytomas
 WHO Grade II/IV
Gross:
 Well circumscribed, gelatinous, grey masses
 Cysts, hemorrhages & gritty

49. OLIGODENDROGLIOMA-10X
 Delicate plexiform
network of
anastomosing
capillaries  ‘chicken
wire’ or ‘crow feet’
pattern.

50. Oligodendroglioma-40x
 Sheets of regular cells
with uniform spherical
nuclei with fine
granular chromatin,
clear halo around
nucleus  ‘fried egg
appearance’.

52. EPENDYMOMA
 1st two decades  4th
ventricle
 Adults  spinal cord,
common in
neurofibromatosis 2.
 C/F: obstructive
hydrocephalus
 Genetics: spinal type – NF2
gene alterations on chr 22.
 WHO grade II/IV
 Gross: Solid, papillary
masses extending from floor
of IV ventricle or spinal cord.

53. EPENDYMOMA
 Tumor cells form gland
like round structures 
rosettes or elongated
structures  canals
 As perivascular
pseudorosettes  cells
around vessels with
intervening zone of
GFAP +ve thin
ependymal processes
directed toward wall of
vessel.

55. MEDULLOBLASTOMA
 Neuroectodermal origin
 Poorly differentiated or embryonal.
 Composed of primitive, undifferentiated cells.
 Children Exclusively in cerebellum
 Adults  cerebral hemisphere
 C/F: obstructive hydrocephaluslethargy,
headache, morning emesis.
 Genetics: isochromosome 17q i(17q).

56. MEDULLOBLASTOMA
 Gross:
 Well circumscribed,
gray, friable

57. MICROSCOPY
 Extremely cellular
 Sheets of small
cells, little
cytoplasm,
hyperchromatic
nuclei which are
round or angulated
 Arranged as closely
packed sheets
 Abundant mitoses,

58.  Highly malignant tumor
 SRBCT.
 Infiltrate as linear cells into cerebellar cortex
penetrate pia  seed into SAS  CSF metastasis
as nodular masses upto cauda equina  “drop
metastasis”.

59. MENINGIOMA
 Benign tumors, arise from meningothelial cells of
arachnoid.
 Age: adults, sex- F:M::3:2
 Has progesterone receptors – rapid growth in
pregnancy
 Site: external surface of brain, also in ventricles.
Common in parasagittal convexity, wing of
sphenoid, olfactory groove, sella turcica
 Attached to dura.
 Solitary, multiple in NF2.
 Genetics: deletion of chr 22q12 which has NF2
gene.

60. Gross-meningioma
 round, encapsulated,
bosselated or polypoid
mass- meningioma

61. Histologic patterns:
 Syncytial or meningotheliomatous:
whorled clusters of cells without visible cell
membranes, tight groups & nests
 Fibroblastic:
elongated cells, dense collagen between cells
 Transitional:
syncytial and fibroblastic

62. MENINGIOMA
transitional type

63. PSAMMOMATOUS
MENINGIOMA
Numerous
psammoma
bodies, due to
calcification of
syncytial nests of
meningothelial
cells.

64.  Microcystic: loose spongy
 Secretory: intracytoplasmic droplets, PAS +ve.
 Atypical meningioma (WHO grade II/IV):
 lower grade meningiomas by the presence of
either a mitotic index of four or more mitoses per
10 high power fields or at least three atypical
features (increased cellularity, small cells with a
high nuclear-to-cytoplasmic ratio, prominent
nucleoli, patternless growth, or necrosis).
 Clear cell & chordoid variants

65.  Anaplastic (malignant) meningioma (WHO grade
III/IV):
 Papillary: pleomorphic cells around fibrovascular
core
 Rhabdoid: sheets of tumor cells with hyaline
eosinophilic cytoplasm

66. METASTATIC TUMORS
 Primaries from lung, breast, skin, kidney & GIT.
 Choriocarcinoma, a rare tumor, commonly
metastasizes
Gross
 Sharply demarcated masses at junction of grey &
white matters
 Well defined boundary between tumor & adjacent
brain
 Meningeal carcinomatosis:
tumor nodules stud over brain, spinal cord –
primaries from lung and breast.

67. METASTASIS BRAIN

68. PERIPHERAL NERVE SHEATH TUMORS
 Schwannoma
 Neurofibroma
 MPNST
 Myelination by oligodendrocytes is shifted to
that by schwann cells within several millimeters
of substance of brain, as nerves exit brain & spinal
cord.
 Hence, they can arise within cranial vault.

69. SCHWANNOMA/NEURILEMMOMA
o Benign, arise from schwann cells
o Sites: cerebellopontine angle  vestibular branch
of VIII nerve  vestibular schwannoma / acoustic
neuroma
o C/F: tinnitus, deafness.
o Sensory nerves: branches of V nerve, dorsal roots.
o Gross: well circumscribed, encapsulated masses,
attached to nerve, but can be separated from it .
o Firm, grey
o Cystic change may be +.
o Soft, tan colored, “fish fleshy”

70. SCHWANNOMA

71. Microscopy:
 Mixture of 2 growth patterns of elongated cells
with regular, oval nuclei & cytoplasmic processes.
 Antoni A pattern:
 moderate to high cellularity ,
 cells arranged as fascicles,
 little stromal matrix.
 nuclear free zones of cytoplasmic processes that
lie between nuclear palisading  ‘verocay bodies’
 Antoni B pattern: hypocellular, loose meshwork
of cells with microcysts, myxoid areas

72. ANTONI A WITH
VEROCAY BODIES ANTONI B

73. NEUROFIBROMA
 Skin: cutaneous NF
 Peripheral nerve: solitary NF
 Arise sporadically or with NF1 plexiform NF
 Cutaneous – nodules , in dermis & fat,
as well demarcated, but unencapsulated masses
of spindle cells, highly collagenised stroma
 Plexiform: large nerve trunk, multiple, nerve
irregularly expanded.
 lesions cannot be separated from nerve,

74.  Microscopy: loose myxoid background, low
cellularity.
 Schwann cells - Elongated nuclei, extension of pink
cytoplasm
 Large, multipolar fibroblasts
 Inflammatory cells.
 Collagen bundles in the background of myxoid
areas look as shredded carrot
 Malignant transformation high for plexiform NF as
MPNST

75. MPNST (MALIGNANT SCHWANNOMA)
 High grade sarcomas, NF1 gene, p53 & p16
mutations.
 Gross: poorly defined, invades parent nerve,
necrosis
 Microscopy : schwann cells – elongated nucleus,
prominent bipolar cytoplasmic processes.
 As fascicles, bundles, storiform, herring bone,
geographic necrosis.

76. FAMILIAL TUMOR SYNDROMES
 Neurofibromatosis Type 1
 This autosomal dominant disorder, one of the
more common genetic disorders, having a
frequency of 1 in 3000, is characterized by
neurofibromas (plexiform and solitary), gliomas
of the optic nerve, pigmented nodules of the iris
(Lisch nodules), and cutaneous hyperpigmented
macules (café au lait spots).

77.  Neurofibromatosis Type 2 (NF2)
 This is an autosomal dominant disorder resulting
in a range of tumors, most commonly bilateral
eighth-nerve schwannomas and multiple
meningiomas. Gliomas, typically ependymomas
of the spinal cord

78.  Tuberous Sclerosis Complex
 Tuberous sclerosis is an autosomal dominant syndrome,
hamartomas and benign neoplasms involving the brain and
other tissues.
 Hamartomas within the CNS take the form of cortical tubers
and subependymal nodules;
 subependymal giant-cell astrocytomas are low grade
neoplasms that appear to develop from the hamartomatous
nodules in the same location.
 renal angiomyolipomas, retinal glial hamartomas,
pulmonary lymphangioleiomyomatosis and cardiac
rhabdomyomas.
 Cysts may be found at various sites, including the liver,
kidneys, and pancreas.
 Cutaneous lesions include angiofibromas, localized
leathery thickenings (shagreen patches), hypopigmented
areas (ash-leaf patches), and subungual fibromas.

79. THANK
YOU
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