tartu 2009 i - al-mustansiriya university11_08_… · axonal transport anterograde / orthograde...
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Tartu 2009 I Introduction to Neuropathology
& General Aspects
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Special Features of the CNS
Complex and diverse topography
Complex and diverse cytology
Axoplasmic transport
Myelin
3 classes of intermediate filaments –
neurofilaments, glial fibrillary acidic protein, vimentin
Neurotransmitters
Separate population of interstitial cells-glia
Blood brain barrier
Cerebrospinal fluid
Absent lymphatic vessels and lymph nodes
Special aspects of cranial cavity (intracranial pressure)
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Neuropathology – in a broader sense
Neurology of the
Central Nervous System
(Brain and spinal cord, incl. their coverings)
Peripheral Nervous System
(and its coverings)
Skeletal Muscle
Neuropathology in a limited sense
Neuropathomorphology
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General Neuropathology =
Neuropathology-related Special Features
Cell Pathology
General „Organ Pathology“
General Principles of neuropathologic disease groups
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Neuropathology of
Nerve cells blood brain barrier
Glial cells peripheral nerves
Oligodendroglia skeletal muscle
Astroglia and Ependyma
Microglia
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Keyhole Neuropathology
Brain biopsy
Nerve biopsy
extracerebral biopsy in
neurodegenerative diseases
in adults
in children
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General Principles of Neuropathologic Groups of
Diseases
Neurodegenerative Diseases
Neurometabolic Diseases
Inflammatory Diseases
Infections
Autoimmune processes
Toxic Diseases
Malformations
Tumors
Circulation Diseases
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I. Pathologic Reactions in the CNS
II. Brain Edema
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Neuronal Reactions
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Pathology of Neuronal Processes
Dendrites
Axons
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Axonal Transport
Anterograde / Orthograde
Fast:
I 100 - 400 mm/day - Polypeptides
II 20 - 70 mm/day - Polypeptides
III 3 - 20 mm/day - Polypeptides
Slow:
IV / V 0,1 - 4 mm/day - Components of cytoskeleton
and membrane skeleton and
associated proteins incl.
cytoplasmic enzymes
Retrograde
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Pathology of Neuronal Processes
Wallerian degeneration
Retrograde reaction
Anterograde transneuronal degeneration
Retrograde transneuronal degeneration
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Wallerian Degeneration
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Anterogade transneuronal Degeneration
loss of eye lateral geniculate body
lesion of optic nerve
lesions of fornix mamillary bodies
loss of sensory gracilis and cuneate
fibers in posterior nuclei
spinal columns
loss of cortico- pontine nuclei
pontine fibers
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(Central) Chromatolysis –
„axonal“ Reaction
rounding of perikaryon
loss of central Nissl bodies
peripheral displacement of nucleus
retraction of presynaptic terminals
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Retrograde Transneuronal
Degeneration
Lesions of the optic degeneration of retinal
radiation and cells ganglion
calcarine region
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Factors which impair Regeneration of
CNS Axons
Lack of matrix-proteins,
e.g. laminin and fibronectin
Lack of growth factors,
e. g. GAP 43
Formation of inhibitory proteins,
e.g. oligodendroglial glycoproteins
Formation of glial scars
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reactive
degenerative
axonal changes
regenerative
dystrophic
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Neuroaxonal Dystrophies
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Pathology of the Neuronal Perikaryon retrograde reaction
vacuolisation
cell death
atrophy
aggregation of
proteins
lysosomal substrates
viruses
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Cell Death
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Types of Cell Death
necrosis
apoptosis
autophagy
„loss“
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Necrophanerosis
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Elective Parenchymal
Necrosis
=
selective neuronal necrosis
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Causes of elective
Parenchymal Necrosis
Anoxia / Hypoxia
Cardiac arrest
Anaemia
CO intoxication
Pulmonary disease
Hypoglycaemia
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Regions of elective Parenchymal
Necrosis
Purkinje cells (cerebellar cortex)
Pyramidal cells of cortex, incl.
hippocampus (cerebral cortex)
Striatal neurons
Thalamic neurons
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Tissue Death
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Types of Tissue Necrosis
Coagulation necrosis
hemorrhagic necrosis
liquefaction necrosis
caseating necrosis (TB)
gummous necrosis (Syphilis)
fibrinoid necrosis (arteries)
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Infarct
focal tissue necrosis owing to
insufficient local blood supply
= Ischemia
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Coagulation necrosis
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Antemortem brain death
Dissociated (brain)death
Complete infarct of the brain
Antemortem autolysis of the brain
Respirator brain
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Morphological Criteria for:
Necrosis
Passive process
Apoptosis
Active process
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Morphology Necrosis Apoptosis
cell
nuclear chromatin
other organelles
cell membrane
surrounding tissue
swells
disintergrates
swell
ruptures, blebs
inflammation
shrinks
condenses, strand breakage
normal
remains intact, later: budding
phagocytosis
Morphological differences between necrotic
and apoptotic cell death
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Phases of Apoptosis:
Initiation phase: different stimuli
Effector phase: common to all cells
Degradation phase: metabolic enzymes
activated
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PROTEINS of the Bcl-2 family involved in Apoptosis:
Inducing: Suppressing: Bax Bcl-2
Bak Bcl-xL
Bcl-w
Mcl-1
A1
Virus proteins: BHRF1 (Epstein-Barr virus)
LMW5 HL (African swine fever virus)
E-1B 19K (Adenovirus)
Location: Endoplasmic reticulum
Nuclear membrane
Outer mitochondrial membrane
Dimeric partners
Bcl2 Bax
Bcl-xL Bak
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Apoptosis in Neuropathology
Axotomy – retrogade
Motor Neuron diseases
Alzheimer disease
Parkinson disease
Huntington disease
Ischemia
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loss of neurons
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Ageing
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Cell Biology of Aging
programmed aging
defective DNA-repair
degeneration of extracellular matrix
damage by free radicals
insufficiency of protein degradation
cumulating cell damage
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Aging and CNS
Loss of brain weight:
parenchyma, water content
shrinkage of large neurons (loss?)
dendritic proliferation
cellular gliosis
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Granulovacuolar
Degeneration
Simchowicz
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Simekowicz
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Intraneuronal (intraglial)
Aggegation
Proteins
Viruses
Lysosomal substrates
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Lipofuscin (Lipopigment)
Age pigment
Wear and tear pigment
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Lipopigments physiological
neuronal: lateral geniculate body
inferior olive
dentate nucleus
aging: large neurons
(pyramidal neurons)
pathological: neuronal ceroid-lipofuscinoses
Vitamin E deficiency
experimental: Feeding unsaturated fatty acids
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Hirano body
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Marinesco body
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Alzheimer Disease
NFT neurofibrillary tangles
PHF paired helical filaments
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AT8
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Lewy body
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Lewy body
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Lewy body NF
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James B. Leverenz et al. Journal Compilation Brain Pathology Volume 17, Number 2 , 2007; 139-145
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Disease Proteins Location
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bA4
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Amyloid (osis)
Organ specific - generalised
Hereditary - acquired
Primary/Systemic - secondary
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Viral inclusions in nerve cells Nucleus (Cowdry type A)
Herpes simplex / zoster virus
Papova/JC (progressive multifocal leuko-
encephalopathy)
Paramyxovirus (measles)
Cytomegalovirus
Cytoplasm
Negri / Lyssa bodies (Rabies)
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Negri body
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Tay-Sachs
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Oligodendroglial Reactions
Viral replication inclusions
Protein aggregation inclusions
lysosomal activation lysosomal storage
demyelination
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Primary and secondary
Demyelination
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Types of Demyelination
Diffuse - metabolic, toxic
Focal - unifocal: traumatic,
neoplastic
multifocal: inflammatory
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CLASSIFICATION OF PRIMARY
MYELIN DISEASES
Allergic and infectious diseases
Hereditary (metabolic) diseases
Toxic diseases
Nutritional diseases
Traumatic diseases
Vascular diseases
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Multiple Sclerosis
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Glia reactions
Microglia
Astrocytes
(Glial scar)
Mesenchymal reactions Vessels
Fibroblasts
Scar
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Microglia-rapid reaction
phagocytes
MHC I + II positive
express APP, complement receptor
produce cytokines, NO
present antigens
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Synaptic stripping by
microglia
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Kufs Disease
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Infarct CD 68
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Myelin Basic Protein
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old infarct
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Oil-red 0
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Orthochromatic
(sudanophilic) Degradation
metachromatic Degradation
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AIDS
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General Paresis
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Hepatic Glia
Hypertrophy of astrocytic nuclei
Alzheimer type I = Wilson disease
(hepato-lenticular
degeneration)
Alzheimer Type II = hepatic and uremic
encephalopathies
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Alzheimer type I glia:
M. Wilson = hepatolenticular
degeneration
Alzheimer type II glia:
hepatic encephalopathy
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Alzheimer II
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Gemistocytes
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normal caudate nucleus
Huntington Chorea
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Bergmann glia
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Isomorphic gliosis
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Multiple Sclerosis
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Corpora amylacea
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Rosenthal fibers: occurrence reactive
around craniopharyngeoma
around MS plaques
neoplastic (?)
pilocytic astrocytoma
genetic
Alexander disease
giant axonal neuropathy
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Types of reaction
Cell types Regressive/
degenerative
Progressive/hyper-
trophic-
hyperplastic
neuron many specific and
nonspecific
alterations
none
oligodendroglia limited none (limited)
astrocyte limited astrocytosis
microglia limited inflammation
phagocytosis
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Space occupying
Lesions
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Contents of the Cranial Cavity
- 70 % brain tissue
- 12 % cerebrospinal fluid
- 15 % blood
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normal adult
5-year old child
newborn
elevated
mild
moderate
marked
death
0-10 mm (upper limit 15 mm)
0-5 mm
0-3 mm
-25 mm
-30 mm
-37,5 mm (electrical activity ceases,
ischemia)
-60 mm
Intracranial Pressure
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Causes of space-occupying lesions
tubors
haemorrhages
inflammatory processes
blockage of CSF (hydrocephalus)
brain edema
trauma
ischemia / anoxia
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Herniations
Subfalcial herniation
right and left supratentorial cavities
Uncus herniation
supratentorial cavities infratentorial cavity
tonsillar herniation
infratentorial cavity spinal canal
Retrograde: cerebellum
infratentorial cavity supratentorial cavity
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MAINZ
Walther Wagner