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BASIC PATHOLOGICAL BASIC PATHOLOGICAL ASPECTS ASPECTS
OF OF NERVOUS SYSTEM NERVOUS SYSTEM
PATHOLOGYPATHOLOGYEsti D. S. Soetrisno B.
Rino PattiataDepartement Anatomic Pathology Faculty of Medicine
University of Indonesia
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BASIC PATHOLOGICAL MANIFESTATION
OF SOME DISTURBANCESDYS – 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 IUFDAPLASIA : There is only NS Streak Formation
abortionHYPOPLASIA : Failure to growth of all or partial part of NS
Hypotrophy (Micro Insize) Hypofunction / Fatal
e.g Microensephaly, Arnold – Chiary Syndrome
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Hyperplasia : Overgrowth parts of NS e.g Macroensephaly,
Hydrocephallus, Function?
Hypertrophy: True Hypertrophy / Pseudo Hypertrophy
Defect On Enclosing of the Neural TubeThere 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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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
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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
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CNS CELLSCNS CELLS
NEURONGLIAL CELL
– ASTROCYTE– OLIGODENDROGLIA– EPENDYMA– MICROGLIA
CHOROID PLEXUS CELL
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NEURONNEURON
ASTROCYTEASTROCYTE
OLIGO DENDROGLIAOLIGO DENDROGLIA
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NeuronNeuron 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)
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PIGMENTED NEURONPIGMENTED NEURON( SUBSTANTIA NIGRA )
neuromelanin
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ATROPHIC NEURONATROPHIC NEURON
hyperchromatic
Loss of neurons
* global/regional reduction (atrophic)
* single neuron
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ATROPHICATROPHICCEREBRAL CORTEXCEREBRAL CORTEX
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CYTOPLASM FLUID ACCUMULATIONCYTOPLASM FLUID ACCUMULATION
NUCLEUSNUCLEUS NISSL SUBSTANCE
MARGINATION
CHROMATOLYSIS
Injured neuron swell → cytoplasm swell → chromatolysis: response to injury
Reversible/death
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CENTRAL CHROMATOLYSIS
ANTERETROGADE DEGENERATION
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AstrocyteAstrocyte
Support neuronsPromote repair
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ASTROCYTEASTROCYTE
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GLIOSISGLIOSIS
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.
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GLIOSISGLIOSIS
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GEMISTOCYTEGEMISTOCYTE
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OLIGODENDROGLIAOLIGODENDROGLIA
Neuroectodermal originMyelin-producing cells during late
gestational period and early neonatal
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EPENDYMAEPENDYMA
Modulate fluid transfer between the cerebrospinal fluid and CNS
During gestation some viral target the ependymal cell → aqueductus stenosis → congenital hydrocephalus
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EPENDYMEPENDYM
CANALIS CENTRALISCANALIS CENTRALIS
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MICROGLIAMICROGLIA
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
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MICROGLIA MICROGLIA (PHAGOCYTE)(PHAGOCYTE)
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ACTIVATED MICROGLIAACTIVATED MICROGLIA
MYELINOLYMYELINOLYSISSIS
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INTRA NUCLEAR
INCLUSION( CYTOMEGALO VIRUS )( CYTOMEGALO VIRUS )
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NEGRI BODY NEGRI BODY INTRACYTOPLASM (RED)INTRACYTOPLASM (RED)(RABIES ENCEPHALITIS)(RABIES ENCEPHALITIS)
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NEURONOPHAGIANEURONOPHAGIA
PMN NEUTROPHIL
VASCULAR VASCULAR DILATATIONDILATATION(HYPEREMIA)(HYPEREMIA)
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HYDROCHEPALUSHYDROCHEPALUS
TYPE :1. COMMUNICANS :
obstruction occurs outside ventricle system
2. NON-COMMUNICANS3. EXVACUO
(COMPENSATED)
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HYDROCEPHALUSHYDROCEPHALUSPrimary 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
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SITES OF OBSTRUCTION OF CSF PATHWAY
1. Subarachnoid space
2. Arachnoid granulationes
3. Plexus choroid
4. Lateral ventricle
5. 3rd ventricle
6. Cerebral aqueduct
7. 4th ventricle
8. Exit foramina
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OBSTRUCTED AQUADUCT SYLVIOUSOBSTRUCTED AQUADUCT SYLVIOUS( BRAIN TUMOR)( BRAIN TUMOR)
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OBSTRUCTIVE OBSTRUCTIVE HYDROCEPHALUSHYDROCEPHALUS
( NEOPLASM )( NEOPLASM )
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OBSTRUCTIVE HYDROCEPHAL
US( INFECTION )( INFECTION )
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OBSTRUCTIVE HYDROCEPHALUS( GLIAL TISSUE POST VIRAL INFECTION)( GLIAL TISSUE POST VIRAL INFECTION)
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TRAUMATRAUMAPenetrating 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
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HIGH VELOCITY BULLET WOUND HIGH VELOCITY BULLET WOUND
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LOW VELOCITY BULLET WOUNDLOW VELOCITY BULLET WOUND
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HEMORRHAGIC TRACTHEMORRHAGIC TRACT (PENETRATING WOUND)
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Subdural hematomaSubdural 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
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Subdural hematomaSubdural 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
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CHRONIC SUBDURAL HEMATOMACHRONIC SUBDURAL HEMATOMA(INNER NEOMEMBRANE)
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EPIDURAL HEMATOMAEPIDURAL 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
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EPIDURAL HEMATOMAEPIDURAL 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
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EPIDURAL HEMATOMAEPIDURAL HEMATOMA(FRONTO PARIETAL)
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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
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TRANSTENTORIALTRANSTENTORIALHERNIATIONHERNIATION
(MIDBRAIN DISPLACED)(MIDBRAIN DISPLACED)
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GLIOBLASTOMAGLIOBLASTOMAMULTIFORMEMULTIFORME
HEMORRHAGEHEMORRHAGEHERNIATIONHERNIATION
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Head, generalized cerebral atrophy – Head, generalized cerebral atrophy – CTscanCTscan
DEGENERATIVE DISORDERSDEGENERATIVE DISORDERS
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DEGENERATIVE DISORDERSDEGENERATIVE DISORDERS
Brain, cerebral cortex, Alzheimer Brain, cerebral cortex, Alzheimer disease, silver staindisease, silver stain
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Brain, cerebral cortex, neuritic plaque Brain, cerebral cortex, neuritic plaque stained for tau protein and beta-amyloid stained for tau protein and beta-amyloid
DEGENERATIVE DEGENERATIVE DISORDERSDISORDERS
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Brain, substantia nigra, Lewy bodiesBrain, substantia nigra, Lewy bodies
DEGENERATIVE DISORDERSDEGENERATIVE DISORDERS
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ALZHEIMERALZHEIMER
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AlzheimerAlzheimer
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
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Spinal cord, amyotrophic lateral sclerosis Spinal cord, amyotrophic lateral sclerosis (A) and normal (B)(A) and normal (B)
DEGENERATIVE DISORDERSDEGENERATIVE DISORDERS
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Brain, Creutzfeldt-Jakob diseaseBrain, Creutzfeldt-Jakob disease
DEGENERATIVE DISORDERSDEGENERATIVE DISORDERS
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Prion diseasePrion disease(spongiform encephalopathies)(spongiform encephalopathies)
Transmissible neurodegenerative diseaseInfectious agents is prionHuman prion gene (PRNP) express cell-
surface glycoprotein bound to plasmalemma by glycolipid anchor
PrPc and PrPsc not differ in sequence except 3 dimensional conformation an patterns of glycosylation
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Prion diseasePrion 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
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Prion diseasePrion disease
SporadicInheritedIatrogenicNew variant CJD
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SporadicSporadic
75%1: 1.000.000Polymorphisme codon 129 Classical features
– Dementia– Myoclonus– Periodic spike-wave complexes
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GeneticGenetic
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
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IatrogenicIatrogenic
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)
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New variant CJDNew 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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