Intro to Neuropathology Flashcards
Major cells of the CNS
- neurons
- glia
- astrocytes = scar formation
- oligodendrocytes = myelin
- ependyma =myoventricular system
- microglia = macrophages
Ependymal cells
- in contact w/the CSF
Neuron characteristics
- largest/longest cells in body
- most metabolically active cells
- non-replicative (@ adult)
- neurons that are lost are not replaced
- soma size parallels axon length
Neuronal responses to injury
- total necrosis = loss of neuron/removal
- chromatolysis = injury to axon ==> death OR regrowth of axon
- acquisition of viral particles w/in nucleas/cytoplasm
- acquisition of abnormal material w/in cytoplasm
Characteristics of ischemic/anoxic neurons
- “red dead”
- shrunken nucleus; loss of basophilic Nissl substance
- some populations more susceptible to ischemia
Characteristics of chromatolysis neurons
- cell attempts ot regroup and regrow a damaged axon
- ==> swollen cell body
Characteristics of neurodegenerative neurons
- show accumulations of abnormal proteins/mlx in cytoplasm
- e.g. Lewy body in Parkinson’s
Storage disorder characteristics
- unable to breakdown certain metabolic products
- accumulation of materials overwhelms neurons
- can lead to severe intellectual disability
Transection of axon reaction/process
- necrosis distal to transection = “Wallerian degeneration”
- may see swollen axonal processes @ injury site
- axons may disconnect from synapse and around foreign material (e.g. amyloid plaque)
Astrocyte reaction to injury
- scar-former of CNS
- expansion of cytoplasmic volume and synthesis of intracytoplasmic intermediate glial filaments (GFAP+)’
- chronic gliosis ==> network of cell processes but no extracell collagen
Other important job of astrocytes
- metabolic regulators
Cellular characteristics of oligodendocytes
- little cytoplasm
- perinuclear halo
- located in both grey and white matter
- myelinates axons of CNS
problems w/oligodendrocytes
Ependymal cells characterisctics
- line ventricular spaces
- ciliated
Microglial cell characteristics
- responds to tissue damage in CNS
- “sentinels” w/in brain
- w/large injury ==> microglia cells proliferate and respond to injury and be replaced by blood monocytes
Process of CNS tissue response to traumatic injury
- injury to tissues/blood vessels
- influx of blood borne cells/proteins
- hemostasis
- inflamation
- reestablish BBB
- cell recruitment
- axonal breakdown
- repair/remodelling = gliosis
Muscle structure
- m
Muscle fiber types
- Type I (red)
- more oxidative enzymes
- more mitochondria
- more myoglobin
- fire more tonically
- slower rates of contraction and relax
- Type II (white)
- more glycolytic enzymes
- mroe fatiguable
Myopathy vs. Denervation
- myopathy
- proximal weakness/atrophy
- elevated CK
- EMG changes
- Denervation
- distal weakness/atrophy
- normal CK
- unique EMG changes
EMG changes in myopathy vs. denervation
- normal muscle = normal MUP (motor unit potential)
- myopathic changes
- dying muscle cells ==> less contraction
- ==> small MUP
- denervation
- ==> muscle type grouping
- ==> large MUP
Myopathic changes in muscle
x
Neuropathic (denervation) changes in muscle
x
Basic patterns of injury @ peripheral nerves
- Axonal problems
- Wallerian degeneration
- Distal axonopathy
- Demyelination
- Segmental demyelination
Wallerian degeneration
- sharp transection of axon
- usually ==> axonal retraction
- can have death of cell body
- response: central chromatolysis
- protein synthesis increased
- soma = swollen
- growth cone develops
- macrophages/schwann cells ==> degrade myelin
- bands of bugner = basal laminal lined endoneuronal sheath for schwann cells
Rate of axonal regeneration
- primates = 1-2 mm/day
- humans rate decreases w/increasing distance from cell body
End-organ response to denervation
- atrophy of muscle
- over time (~2 years for muscle), end-organ can lose ability to receive a nerve fiber input; if this time passes the muscle cannot be functionally restored
Distal axonopathy
- e.g. drugs, toxins impact cell body ==> distal axon is first impacted if production is slowed
- “stocking-glove pattern”
Segmental demyelination + repair process
- autoimmune against myelin
- repair ==> onion bulb formation = hypertrophy of nerves
Nerve conduction studies
- axonal loss = decreased amplitude
- demyelination = decreased conduction velocity
