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- 1. CNS PATHOLOGY BY :MS. SAILI GAUDE PRINCIPAL SHIVAM COLLEGE OF NURSING, AMIRGADH
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- 3. Definition • Increased volumeof Cerebrospinal fluid within the skull along with dilatation of the ventricles
- 5. INTERNAL HYDROCEPHALUS • Hydrocephalusinvolving 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 OFCSF CIRCULATION LATERALVENTRICLES FORAMENOF MONRO THIRDVENTRICLES AQUEDUCT OF SLYVIUS FOURTHVENTRICLES FORAMENOF MAGENDIEAND LUSHKA SUBARACHNOID SPACEOF BRAINAND SPINAL CORD
- 9. TYPES AND ETIOPATHOGENESIS PRIMARYHYDROCEPHALUS • Most commonest SECONDARY HYDROCEPHALUS • Uncommon
- 10. PRIMARY HYDROCEPHALUS • Actualincrease 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 • Mostcommonest 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 • Lesscommon • 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
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- 19. DEFINITION • Inflammation ofall 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 PYOGENICMENINGITIS • 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 becomespurulent • 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 spaceis 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 puncturemay 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 • Meningealirritability • Hyperpyrexia • Meningeal rigidity • Weakness • Complete recovery without specific therapy CLINICAL FEATURES
- 30. • Clear orcloudy 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 commonin 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 inimmunocompromised patients as secondary infection • Usually starts from a pulmonary lesion • Important cause of meningitis in AIDS patient CRYPTOCOCCAL MENINGITIS
- 34. • Thick greenishgelatinous 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 comprisesof 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 gradefever • Headache • Vomiting • Malaise CLINICAL FEATURES
- 38. • CSF isclear • 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
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- 40. • Infection ofbrain 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 ofviruses 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 ofcortex, 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 ofependymal 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 developby 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
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