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

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Presentation on theme: "BASIC PATHOLOGICAL ASPECTS OF NERVOUS SYSTEM PATHOLOGY Esti D. S. Soetrisno B. Rino Pattiata Departement Anatomic Pathology Faculty of Medicine University."— Presentation transcript:

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)

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6 DYS – HISTOGENESIS : incorrect migration and/or naturation – differentation ECTOPIC : mature tissue found in abnormal places HETEROPIC : intermingled of some mature tissues in 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 NEURON ASTROCYTE OLIGO DENDROGLIA

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

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 EPENDYM CANALIS CENTRALIS

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 NEURONOPHAGIA PMN NEUTROPHIL VASCULARDILATATION(HYPEREMIA)

30 HYDROCHEPALUS TYPE : 1.COMMUNICANS : obstruction occurs outside ventricle system 2.NON-COMMUNICANS 3.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 1.Subarachnoid space 2.Arachnoid granulationes 3.Plexus choroid 4.Lateral ventricle 5.3 rd ventricle 6.Cerebral aqueduct 7.4 th ventricle 8.Exit foramina

33 OBSTRUCTED AQUADUCT SYLVIOUS ( BRAIN TUMOR)

34 OBSTRUCTIVEHYDROCEPHALUS ( 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 mL

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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 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 : 3 rd cranial nerve Pupil fixed and dilated

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48 EPIDURAL HEMATOMA (FRONTO PARIETAL)

49 SITES OF HERNIATION 1.Cingulate gyrus under falx cerebri 2.Hippocampal uncus and parahippocampal gyrus over tentorium cerebeli 3.Cerebelar tonsilar through foramen magnum 4.Any defect in the dura and skull HERNIATION

50 TRANSTENTORIALHERNIATION (MIDBRAIN DISPLACED)

51 GLIOBLASTOMAMULTIFORMEHEMORRHAGE HERNIATION

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54 Head, generalized cerebral atrophy – CTscan DEGENERATIVE DISORDERS

55 Brain, cerebral cortex, Alzheimer disease, silver stain

56 Brain, cerebral cortex, neuritic plaque stained for tau protein and beta-amyloid DEGENERATIVE DISORDERS

57 Brain, substantia nigra, Lewy bodies Brain, substantia nigra, Lewy bodies DEGENERATIVE DISORDERS

58 ALZHEIMER

59 Alzheimer Amyloid β protein – Derived from APP – Normal degradation of APP: proteolytic middle domain – Alzheimer : proteolytic in either end Neurofibrillary tangles – Paired of helical filaments consisted of abnormal form of MAP: tau – Phosphorylation of tau results in a protein not associated with microtubules deprives cells of its microtubules effect – Impairing axonal transport & compromising neuronal function Genetic factors Apolipoprotein E

60 Spinal cord, amyotrophic lateral sclerosis (A) and normal (B) DEGENERATIVE DISORDERS

61 Brain, Creutzfeldt-Jakob disease DEGENERATIVE DISORDERS

62 Prion disease (spongiform encephalopathies) Transmissible neurodegenerative disease Infectious agents is prion Human prion gene (PRNP) express cell- surface glycoprotein bound to plasmalemma by glycolipid anchor PrP c and PrP sc not differ in sequence except 3 dimensional conformation an patterns of glycosylation

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64 Prion disease Kuru – Fore people – Trembling – Canibalism – Spongiform cerebral and cerebelum Creutzfeldt-Jacob disease (CJD) – Symptoms begin insidiously – 6 months exhibits severe dementia – 1 year : death

65 Prion disease Sporadic Inherited Iatrogenic New variant CJD

66 Sporadic 75% 1: Polymorphisme codon 129 Classical features – Dementia – Myoclonus – Periodic spike-wave complexes

67 Genetic 15% Gertsmann-Straussler-Scheiner syndrome(GSS) – Spinocerebelar ataxia with demntia Fatal familial insomnia – Profound disturbance of sleep-wake cycles – Sings of pyramidal and cerebellar dysfunctions – Mutation codon 178 PRNP gene

68 Iatrogenic Hormone injection – Human growth hormone (55 cases) – Human pituitary gondotropin (5 cases) Tissue grafts – Duramater (11 cases) – Cornea (1 case) – Pericardium (1 case) Medical devices – Depth electrode (2 cases) – Surgical instruments (not definitely proven)

69 New variant CJD Identified following surveillance following BSE epidemic in UK Mean age 26 years (compared to sporadic 65) Dysesthesia, none EEG of sporadic CJD Spngioform in basal ganglia and thalamus Extensive PrP plaques in cerebrum and cerebelum More PrP than sporadic CJD BSE is likely the source of vCJD

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72 Thank You


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