1. CNS
Dr. Amitabha Basu. MD

3. Topic
Edema of brain
Herniation
Hydrocephalous
Vascular diseases

4. Edema Vasogenic edema : Seen in case of abscess and Neoplasm.
Fluid accumulate in the interstitial space.
Cytotoxic Edema:
intracellular fluid accumulation due to Hypoxic Cell Injury.

5. Herniation of brain matter in severe case.
Edema: complication
Herniation of brain matter in severe case.

6. Herniation

7. Herniation Etiology: Due to mass effect. Tumor, Trauma( blood clot),
Infection induced edema.

8. Types Transtentorial Herniation (uncal gyral )
Subfalcine herniation (cingulate gyrus )
Tonsillar Herniation

9. Transtentorial Herniation [Uncus]
Involved Brain : Uncus: medial portion of the temporal lobe
Cause : A Mass in the temporal area.
Clinical effects:
Posterior cerebral artery compression : Occipital infarct.
Ipsilateral dilated pupil [ stretching of CN III

10. Subfalcine Herniation (involve Cingulate gyrus )

11. Subfalcine herniation
Involved Brain : cingulate gyrus
Cause : A Mass in temporal/fontal(?) lobe
Clinical effect:
Anterior Cerebral Artery compression : Weakness and Sensory abnormality of the leg typically occur with a Meningioma. R

12. Tonsillar Herniation
Herniation of the cerebellar tonsil through foramen Magnum.
It is life threatening : causes compression of the vital respiratory center.
Complication: Secondary Brain stem or Duret hemorrhage.

13. Duret hemorrhage
Kinking of the penetrating median and paramedian pontine arteries – a branch off the basilar artery.
Pons
Spinal cord

14. Secondary Brain stem or Duret hemorrhage
Causes:
Tonsillar Herniation
Gliomas

15. Hydrocephalus
The Thinker

16. Hydrocephalus:
Def: Accumulation of excessive CSF within the Ventricular System.
Etiology:
Decreased resorption of the CSF.
Overproduction of CSF (in a choroid plexus tumor-a papillary tumor in ventricle).

17. 2 Types
1. Non communicating Hydrocephalous. Obstruction within the ventricular system.
2. Communicating Hydrocephalous. the obstruction is in the subarachnoid space or venous sinuses.

18. Non communicating Hydrocephalous (0bstructive) ; Cause
Medulloblastoma,
Ependymoma
No communication between ventricles and subarachonoid space.

19. Communicating Hydrocephalous.
Meningitis- adult.
Subarachnoid hemorrhage- obstruction in subarachnoid space (SAP)- adult

20. Hydrocephalous by meningitis
Early acute phage: obstruction of the SAP by exudates.
Late chronic phage: obstruction of the SAP by fibrosis.

21. Morphology of hydrocephalous
Infant : Dilated ventricles, enlarged cranium (increase Head circumference), atrophy of cortex of brain.
Adult:
Dilated ventricle, Atrophy of cortex, enlargement of cranium does not take place- dementia.

22. Child and adult
Sunset sign

23. Clinical features Infants & young children:
Signs symptoms of increased ICP- irritability, impaired conscious level, and vomiting.
Adult:
Early: Signs symptoms of increased ICP- headache, vomiting, papilledema and deteriorating conscious level.
Late: Dementia.

24. Persistence of the memory : Salvador Dali
Vascular Diseases
Persistence of the memory : Salvador Dali

25. Vascular Diseases GENERAL FEATURES TYPES ETIOPATHOLOGY MORPHOLGY
CLINICAL FEARYRES WITH INVESTIGATIONS.

26. RISK FACTORS OF ISCHEMIC BRAIN INJURY::
AGE
DURATION OF THE HYPOXIA
TEMPERATURE [HYPOTHERMIA PROTECT HYPOXIC BRAIN DAMAGE]

27. Three categories' Global Hypoxic Ischemic Encephalopathy.
Local infarct [ 80 % of the total]
Hemorrhage.

28. A. Global Hypoxic Ischemic Encephalopathy.
It occur when the systolic blood pressure goes
below 50mmHg.
Cause:
Cardiac arrest (due to myocardial infarct, cardiac arrhythmias),
Aspiration of foreign objects, drowning.
Early feature: border zone infract
Late features: Laminar cortical necrosis

29. Border zone infarct: Watershed infarct : May follows a Hypotensive episode.
Lesion lies at the boundary between the anterior and middle cerebral artery territories.

30. Morphology: Global Hypoxic Ischemic Encephalopathy.
Laminar cortical necrosis : A LINEAR ZONE OF SOFTENING DISCOLORATION IN THE CORTICAL MANTLE.

31. B. Infarct Caused by Local obstruction in blood vessels.
Thromboembolism and other embolisms
HAEMORRHAGE, Atheroma
Hypertension
Risk: hypertension, smoking, diabetes mellitus.
Most common form called “Strokes”.
Age : 7th Decades
Sex : Male > Female.

32. Thrombo-embolism Most common in Middle cerebral Artery.
Source of emboli:
Mural thrombus in the left ventricle of the heart,
Atherosclerotic plaques involving more proximal arteries (especially the carotid arteries).

33. Description of Morphological Changes of brain infarct.
Microscopical changes
After 12 hours : Red neuron and neutrophils infiltration.
36 to 48 hours : Non-hemorrhagic or hemorrhagic infarct (due to reperfusion).
By 10 days : liquefaction occur : presence of macrophages and surrounding reactive gliosis.
1– 6 months: a cystic cavity will form (remote infarct).

34. Red neuron
Normal
Hemorrhagic infarct

35. Liquefactive necrosis
Tissue shows macrophage and microglial proliferation in this time. CT shows enhancing lesion.

36. Remote infarct ( cavity )

37. Remote infarct ( cavity )
In the wall of the cavity= shows reactive astrocytes with reactive gliosis.
An CT would show enhancing shadow.

38. Shower embolization Multiple small hemorrhage: fat embolism, amniotic fluid embolism

39. Hypertension induced infarct
Lacunar infarcts
Site: The pons.

40. What are the signs infarction?
Clinical features
What are the signs infarction?
TIA: transient ischemic attack: persists < 24 hours.
Stroke: >24 hours
Sudden numbness or weakness on one side of the face, arm or leg .
Sudden trouble speaking or understanding.
Sudden trouble seeing.

41. Clinical Features: If middle cerebral Artery is effected.
Contralateral hemiparesis and spasticity.
Visual Field abnormality
In some case speech aphasia.

42. End of Stroke
Guernica