Meningitis encephalitis hydrocephalus glioma

1. CNS PATHOLOGY
BY : MS. SAILI GAUDE
PRINCIPAL
SHIVAM COLLEGE OF NURSING, AMIRGADH

2. 1)HYDROCEPHALUS

3. Definition
• Increased volume of Cerebrospinal fluid within the skull along with dilatation of
the ventricles

5. INTERNAL HYDROCEPHALUS
• Hydrocephalus involving ventricular dilatation
EXTERNAL HYDROCEPHALUS
• Hydrocephalus without ventricular dilatation
• Localised collection of CSF in subarachnoid space

6. SOURCEAND CIRCULATIONOF CSF
• Choroid plexus epithelium and ependymal cells of the ventricles produces CSF- 120 to 150ml
• CSF is secreted by choroid plexus in each lateral ventricles
• CSF flows through interventricular foramina into 3rd ventricles
• Choroid plexus in third ventricles adds more CSF
• CSF flows down cerebral aqueduct to 4th ventricles
• Choroid plexus in 4th ventricles adds more CSF
• CSF flows out 2 lateral apertures and one median aperture
• CSF fills subarachnoid spaces and bathes external surfaces of brain and spinal cord
• At arachnoid villi, CSF is reabsorbed into venous blood of dural venous sinuses
PRODUCTION OF CSF
CIRCULATION OF CSF
REABSORBTIONOF CSF

7. FLOW DIAGRAM OF CSF CIRCULATION
LATERALVENTRICLES
FORAMENOF MONRO
THIRDVENTRICLES
AQUEDUCT OF SLYVIUS
FOURTHVENTRICLES
FORAMENOF MAGENDIEAND LUSHKA
SUBARACHNOID SPACEOF BRAINAND SPINAL CORD

9. TYPES AND ETIOPATHOGENESIS
PRIMARY HYDROCEPHALUS
• Most commonest
SECONDARY HYDROCEPHALUS
• Uncommon

10. PRIMARY HYDROCEPHALUS
• Actual increase in the volume of CSF within skull along with elevated intracranial
pressure
• Possible mechanisms of primary hydrocephalus
• 1) Obstruction of CSF flow
• 2) Overproduction of CSF
• 3) Deficient resorption of CSF

11. OBSTRUCTIVE HYDROCEPHALUS
• Most commonest type of primary hydrocephalus
• Depending on the site of obstruction, further classified as:
• 1) Non communicating hydrocephalus
• 2) Communicating hydrocephalus

12. 1) NON COMMUNICATING
HYDROCEPHALUS
• When the site of obstruction of CSF pathway is in the third ventricles or at fourth
ventricles
• Ventricular system enlarges
• CSF cannot pass into subarachnoid space
• Accumulation of CSF
• Causes :
• 1) Congenital – stenosis of aqueduct, Arnold chiari malformation, gliosis of
aqueduct, intrauterine meningitis
• 2) Acquired- Expanding lesions inside skull eg tumors, inflammatory lesions,
hemorrhage

13. 2) COMMUNICATING HYDROCEPHALUS
• When obstruction to the CSF flow is in the subarachnoid spaces at the base of the
brain, it results in enlargement of the ventricular system but CSF flows freely
between dilated ventricles and spinal cord.
• Causes are non obstructive in nature :
• 1) Overproduction of CSF- Choroid plexus pappiloma
• 2) Deficient reabsorbtion of CSF – after meningitis , subarachnoid hemorrhage

14. SECONDARY HYDROCEPHALUS
• Less common
• Compensatory increase of CSF due to loss of neural tissue without associated rise
in intracranial pressure
• Eg . Cerebral atrophy and infarction

15. MORPHOLOGY
• GROSS MORPHOLOGY
• Dilatation of ventricles
• Thinning and stretching of brain
• Engorgement of scalp vein
• Fontanelle remains open
• HISTOLOGICALLY
• Damage to ependymal lining of ventricles
• Periventricular interstitial edema

16. MENINGITIS

19. DEFINITION
• Inflammation of all layers of meninges and CSF within the subarachnoid space
• Pachymeningitis- inflammation of dura matter
• Leptomeningitis- inflammation of pia and arachnoid matter
• Chemical meningitis- when non bacterial irritants causes meningitis
• Meningeal carcinomatosis – cancer cells infiltrate the meninges

20. ETIOPATHOGENESIS
1. ACUTE PYOGENIC (Bacterial)
2. ACUTEVIRAL (Aseptic)
3. CHRONIC ( Bacterial or Fungal)

21. 1) ACUTE PYOGENIC MENINGITIS
• Acute infection of the pia and arachnoid mater
• Neonates – E.Coli, Proteus, Group B streptococci
• Infants and Children – H. Influenza
• Adolescents and young adults- Nesseiria meningitidis
• Blood stream
• Adjacent foci of infection
• Iatrogenic- during lumbar puncture or during surgery
ETIOLOGY
ROUTESOFTRANSMISSION

22. • CSF becomes purulent
• Accumulation of purulent CSF in subarachnoid space esp at the base of brain
• Meningeal artery becomes engorged and prominent
• In severe cases ventricles may get inflamed called as the ventriculitis
GROSSAPPEARANCE

23. • Subarachnoid space is filled with plenty of neutrophils
• Meninges also contains neutrophils
• Gram staining may show different causative bacteria
• Arachnoid fibrosis can be seen
• Adhesive arachnoiditis in which the arachnoid mater starts to stick to the adjacent
mater can be seen
MICROSCOPICALLY

24. • Fever
• Headache
• Vomitting
• Drowsiness
• Convulsion
• Coma
• Purpuric rash
• Neck rigidity
CLINICAL FEATURES

26. • Lumbar puncture may show :
• 1) Cloudy or purulent CSF
• 2) Increased CSF pressure
• 3) Increased protein levels in CSF
• 4) Decreased sugar in CSF
• 5) Increased Neutrophils in CSF
• Gram staining of culture of CSF
• 1) Shows the causative organisms
• Polymerase chain reaction may also be used
DIAGNOSTIC FINDINGS

27. 2) ACUTEVIRAL MENINGITIS
• Also called acute lymphocytic meningitis or Aseptic meningitis
• Most common cause-Viral
• Benign self limiting disorder
• Entero virus
• ECHO virus
• Coxsackie virus
• Epstein Barr virus
• Mumps
• Herpes simplex
CAUSATIVEORGANISMS

28. • Brain edema
• Inflammation of meninges
• Mild to moderate amount of lymphocytes are seen in CSF
• Inflammatory infiltrate in pia and arachnoid mater
GROSSAPPEARANCE
MICROSCOPICALLY

29. • Headache
• Meningeal irritability
• Hyperpyrexia
• Meningeal rigidity
• Weakness
• Complete recovery without specific therapy
CLINICAL FEATURES

30. • Clear or cloudy CSF
• Increased pressure more than 250mmHg
• Increased protein levels in CSF
• Normal CSF glucose levels
• Increased lymphocytes in CSF
• CSF bacteriologically sterile
DIAGNOSTICTEST

31. 3) CHRONIC MENINGITIS
• 2 disorders under this are :
1)TUBERCULOUS
MENINGITIS
2) CRYPTOCOCCAL
MENINGITIS

32. • Most common in children
• May occur as a part of miliary tuberculosis
• Immunosupression may cause it
• Commonly seen in multidrug resistanceTB
• Causative organism – M. tuberculosis
TUBERCULOUS MENINGITIS

33. • Occurs in immunocompromised patients as secondary infection
• Usually starts from a pulmonary lesion
• Important cause of meningitis in AIDS patient
CRYPTOCOCCAL MENINGITIS

34. • Thick greenish gelatinous pus
• Common at bases
• Many tubercles are present on the meninges- 1 to2 mm in diameter
• Brain edema
• In cryptococcal meningitis the exudate is less and gelatinous
GROSSAPPEARANCE

36. • Exudate comprises of mixture of cells of both acute and chronic inflammatory cells
• Granulation and giant cells
• Zeil – neilson staining – AFB +ve
• Cryptococci seen on Indian ink preparation
MICROSCOPICALLY

37. • Low grade fever
• Headache
• Vomiting
• Malaise
CLINICAL FEATURES

38. • CSF is clear
• When allowed to settle, CSF may show a small clot formation
• Increased pressure- above 300 mmHg
• Increased protein in CSF
• Decreased glucose content
• Increased leucocyte count in CSF
• Special stains demonstrates the micro-organisms responsible for meningitis
DIAGNOSTIC FINDINGS

39. ENCEPHALITIS

40. • Infection of brain parenchyma
• Causative organism- any organism
• Normally occurs as a secondary infection after meningitis
• Tuberculosis and neurosyphilis are only 2 causes of primary infection which causes
a brain lesion called as brain abscess
• The cerebral cortex is the place where this micro-organisms are found the most
and thus it may causes cerebritis
DEFINITION

41. • TRANSMISSION :
• A) Direct implantation- during fracture of skull or surgery of the skull
• B) Local extension of the infection- sinusitis, otitis media, mastoiditis etc
• C) Blood spread- Especially infection from heart such as endocarditis, may spread
through blood to brain
• PATHOLOGICAL CHANGES
• Cerebral abscesses are destructive lesions
• Walled off by pyogenic membrane
1. BACTERIAL ENCEPHALITIS

42. • GROSS APPEARANCE:
• Abscess with central necrosis surrounded by fibrous capsule and edema
• Multiple abscesses
• Can occur in any lobe – frontal, parietal and cerebellum
• MICROSCOPICALLY
• Central liquefactive necrosis
• Acute and chronic inflammatory cells
• Neovascular blood vessels
• Edema
• Fibrous capsule
• Gliosis

43. • Range of viruses can cause this disorder
• Preceding infection in other tissues
• Virus replication occurs outside brain
• Than affects nervous system
• ENTRY OF MICRO-ORGANISM
• Via gastrointestinal tract
• Skin and mucus membrane
• Transplacental
• Body fluids
• Animal bite
2)VIRAL ENCEPHALITIS

44. • Inflammation of cortex, basal ganglia and brain stem
• Herpes simplex- temporal lobe
• Diffuse parenchymal infiltrate of lymphocytes, plasma cells and macrophages
• Clusters of glial cells
• Presence of specific inclusion bodies
PATHOLOGICAL CHANGES

45. • Necrotizing area
• Hemorrhage
• Eosinophillic
• Inflammatory infiltrate
• Edema
• Vascular congestion
• Pyramidal cells are seen in case of rabies
MORPHOLOGY

46. • Infection of ependymal cells and glial cells
• Owl eye like big inclusions seen inside nucleus or cytoplasm in cytomegalovirus
infection
• Negri bodies- a small bullet shaped intra cytoplasmic inclusion seen in rabies
• Microglial nodules
MICROSCOPICALLY

47. • Usually develop by blood stream
• Systemic deep mycoses somewhere else in the body causes it
• Common in immunosuppressed individuals
• Common causative organisms- candida, mucormycosis, histoplasma, aspergillus,
cryptococci
• Protozoal causes- malaria, toxoplasmosis, amoebiasis etc
3) FUNGAL ENCEPHALITIS

48. THE END