BASIC PATHOLOGICAL ASPECTS OF NERVOUS SYSTEM PATHOLOGY

1. BASIC PATHOLOGICAL ASPECTS OF NERVOUS SYSTEM PATHOLOGY Esti D. S. Soetrisno B. Rino Pattiata Departement Anatomic Pathology Faculty of Medicine University of Indonesia

2. BASIC PATHOLOGICAL MANIFESTATION OF SOME DISTURBANCES DYS – NEURO EMBRYOGENESIS • ABORTION / INTRA-UTERINE FETAL DEATH (IUFD) • ABNORMALITIES : TERATOGENIC, MONSTER, CONGENITAL ANOMALY AGENESIS : There is no processus (anlage) of all or partial part of NS  No formation of NS  IUFD APLASIA : There is only NS Streak Formation  abortion HYPOPLASIA : Failure to growth of all or partial part of NS  Hypotrophy (Micro Insize)  Hypofunction / Fatal e.g Microensephaly, Arnold – Chiary Syndrome

3. Hyperplasia : Overgrowth parts of NS e.g Macroensephaly, Hydrocephallus, Function? Hypertrophy: True Hypertrophy / Pseudo Hypertrophy • Defect On Enclosing of the Neural Tube There is “Cele” Formation, or Spina Bifida Formation (Occulta/Aperta) e.g Meningocele, Encephalo -/ Myelo – Meningcocele, Syringo -Encephalo –/ Myelo – Meningcocele (Syringo Myelia)

6. DYS – HISTOGENESIS : incorrect migration and/or naturation – differentation ECTOPIC : mature tissue found in abnormal places HETEROPIC : intermingled of some mature tissuesin abnormal places HAMARTOMA : abnormal composition of mature tissues at its normal places NEOPLASMA (GEN MUTATION) : benign and malignant

7. DYS – NEUROANATOMY Abnormalities of anatomy / location of NS - Dyslocation - Reverse of Several Centre DYS - NEUROCHEMISTRY - NEUROPHYSIOLOGY INHIBIT : Slow Conduction – Slow Movement / Analysis / etc EXCITE : Rapid / Hyperactivity (ies) DYS – REGULATION / CONTROL : UNCONTROL MOVEMENT – PATHOLOGICAL REFLEXES DYSFUNCTIONAL IMPULS CONDUCT

8. CNS CELLS • NEURON • GLIAL CELL • ASTROCYTE • OLIGODENDROGLIA • EPENDYMA • MICROGLIA • CHOROID PLEXUS CELL

9. OLIGO DENDROGLIA NEURON ASTROCYTE

10. Neuron • Effector cells of Nervous System • Neuron loss with progressive aginh • Neuron of CNS cannot effectively regenerate axons over long distance → limit ability of CNS to respond to different type of injury • Infarct transects internal capsule creates permanent motor deficiti • Neuron in CNS don’t remyelinate → demyelinating disease causes permanent functional deficit (multipel sclerosis)

11. PIGMENTED NEURON ( SUBSTANTIA NIGRA ) neuromelanin

12. ATROPHIC NEURON hyperchromatic Loss of neurons * global/regional reduction (atrophic) * single neuron

13. ATROPHIC CEREBRAL CORTEX

14. CHROMATOLYSIS Injured neuron swell → cytoplasm swell → chromatolysis: response to injury Reversible/death CYTOPLASM FLUID ACCUMULATION MARGINATION NUCLEUS NISSL SUBSTANCE

15. CENTRAL CHROMATOLYSIS ANTERETROGADE DEGENERATION

16. Astrocyte • Support neurons • Promote repair

17. ASTROCYTE

18. GLIOSIS • Reaction to injury • Proliferation of astrocyte • Evolves in hours to day and persists to an extent that is usually commensurate with the severity of injury • Reactive astrocyte : gemistocytic astrocyte: exentric plump nuclei, eosinophilic cytoplam • Glial scar: composed of reactive astrocytes and their processes.

19. GLIOSIS

20. GEMISTOCYTE

21. OLIGODENDROGLIA • Neuroectodermal origin • Myelin-producing cells during late gestational period and early neonatal

22. EPENDYMA • Modulate fluid transfer between the cerebrospinal fluid and CNS • During gestation some viral target the ependymal cell → aqueductus stenosis → congenital hydrocephalus

23. CANALIS CENTRALIS EPENDYM

24. MICROGLIA • Phagocytic macrophage-derived cells • Reactions: changes in areas of injury • 2 pattern : focal and diffuse microgliosis • Microglial nodule: responses to viral or other infection. • Rod cells: prominent elongated nucleus • Gitter cells: response to necrosis: it will become phagocytic, accumulate lipid and other material

25. MICROGLIA (PHAGOCYTE)

26. ACTIVATED MICROGLIA MYELINOLYSIS

27. INTRA NUCLEAR INCLUSION ( CYTOMEGALO VIRUS )

28. NEGRI BODY INTRACYTOPLASM (RED) (RABIES ENCEPHALITIS)

29. VASCULAR DILATATION (HYPEREMIA) PMN NEUTROPHIL NEURONOPHAGIA

30. HYDROCHEPALUS • TYPE : • COMMUNICANS : obstruction occurs outside ventricle system • NON-COMMUNICANS • EXVACUO (COMPENSATED)

31. HYDROCEPHALUS • Primary hydrocephalus • Accompanied by increased intracranial pressure • Due to: • Obstruction • Congenital • acquired • Impaired CSF absorption • Excess CSF production • Secondary hydrocephalus • Compensatory to loss of cerebral tissue

32. SITES OF OBSTRUCTION OF CSF PATHWAY • Subarachnoid space • Arachnoid granulationes • Plexus choroid • Lateral ventricle • 3rd ventricle • Cerebral aqueduct • 4th ventricle • Exit foramina

33. OBSTRUCTED AQUADUCT SYLVIOUS ( BRAIN TUMOR)

34. OBSTRUCTIVE HYDROCEPHALUS ( NEOPLASM )

35. OBSTRUCTIVE HYDROCEPHALUS ( INFECTION )

36. OBSTRUCTIVE HYDROCEPHALUS ( GLIAL TISSUE POST VIRAL INFECTION)

37. TRAUMA • Penetrating wounds produce hemorrhage and blast effects. Velocity contributes a blast effect to a projectile • High-velocity : it disrupts tissues by its own mass and also centrifugal blast that enlarges the diameter → immediate death • Low-velocity • Seizures are threat in healed penetrating wounds, 6-12 mo after : collagenous tissue is displaced in the brain

38. HIGH VELOCITY BULLET WOUND

39. LOW VELOCITY BULLET WOUND

40. HEMORRHAGIC TRACT (PENETRATING WOUND)

41. Subdural hematoma • Significant cause of death from falls, assaults, vehicular acidents, sporting mishaps • Frontal/occipital area is struck by blunt object → cerebral hemispher displaced in an anteroposterior direction → hit against inner aspect • Soft cerebral tissue becomes compact then recoil → shearing effect • Usually stop after 25-30 mL

43. Subdural hematoma • Tissue response • Formation of granulation tissue → outer membrane • Fibroblast from outer membrane moved into the hematoma → inner membrane : 2 weeks • Evolution: • Reabsorbe leave a small amount of telltale hemosiderophage • Remain static, with potential for calcification • Enlarge : 6 months

44. CHRONIC SUBDURAL HEMATOMA (INNER NEOMEMBRANE)

45. EPIDURAL HEMATOMA • Middle meningeal artery branches splay across temporal-parietal area • Hemorrhage into epidural space, separating dura from calvaria • 4-8 hours: asymptomatic • 30-50 mL: intracranial pressure increased → exceed venous pressure → circulatory stagnation and cerebral ischemia → global cerebral hypoxia

46. EPIDURAL HEMATOMA • Cushing reflex : protective response • HR slow to increase ventricular filling • Myocardial contraction is forceful • Systolic pressure increased • Compensatory mechanism exhausted : temporal lobe displaced downward → transtentorial herniation • Herniation compress uncus/hyppocampus against midbrain and other structures : 3rd cranial nerve • Pupil fixed and dilated

48. EPIDURAL HEMATOMA (FRONTO PARIETAL)

49. HERNIATION • Cingulate gyrus under falx cerebri • Hippocampal uncus and parahippocampal gyrus over tentorium cerebeli • Cerebelar tonsilar through foramen magnum • Any defect in the dura and skull SITES OF HERNIATION

50. TRANSTENTORIAL HERNIATION (MIDBRAIN DISPLACED)