Chap 28 Morphology Flashcards
What is acute neuronal injury?
- Involve “red neurons”
- Changes that occur from acute CNS hypoxia/ischemia
What are red neurons?
- Seen in acute neuronal injury by 12 to 24 hours after irreversible hypoxic/ischemic insult
What are the morphologic features of irreversible hypoxic/ischemic insult?
shrinkage of cell body, pyknosis of the nucleus, disappearance of the nucleolus, and loss of Nissl structures with eosinophilia of the cytoplasm
What is subacute and chronic neuronal injury?
- “degeneration”
- Neuronal death occurring as a result of progressive disease
- Ex. in neurodegenerative diseases (ALS and Alzheimers)
What are the histologic features of subacute and chronic neuronal injury?
- Cell loss- involving functionally related groups of neurons
- Reactive gliosis
What is the best indicator of subacute and chronic neuronal injury?
Associated reactive glial changes
What is an axonal reaction?
A change in the cell body during regeneration of the axon
*best seen in anterior horn of the spinal cord where motor axons are cut or damaged
What is the morphologic appearance of an axonal reaction?
- Increased protein synthesis
- Enlargement and rounding up of the cell body
- Peripheral displacement of nucleus
- Enlargement of the nucleolus
- Central chromatolysis
What is central chromatolysis?
Dispersion of Nissl substance from the center to the periphery of the cell
What are neuronal inclusions and where are they seen?
- Occur with aging
- Intracytoplasmic accumulation of complex lipids, proteins, or carbs
What viral infections can lead to abnormal intranuclear inclusions?
- Herpetic infection: Cowdry body is seen
- Cytoplasmic inclusions: Rabies with Negri body
What degenerative diseases of the CNS are associated with neuronal intracytoplasmic inclusions?
- Neurofibrillary tangles of Alzheimer Disease
- Lewy bodies of Parkinson Disease
- Abnormal vacuolization of perikaryon and neuronal cell processes in neuropil in Creutzfeldt-Jakob Disease
Appearance of a acute subdural hematoma
- Collection of freshly clotted blood along brain surface without extension into the sulci
- Subarachnoid space is clear
What is the sequence of a acute subdural hematoma?
- 1 week: lysis of the clot
- 2 weeks: growth of fibroblasts from dural surface into a hematoma
- 1-3 months: early development of hyalinized connective tissue
What are chronic subdural hematomas?
Multiple recurrent episodes of bleeding from thin-walled granuloma tissue
When is the risk of repeat bleeding of a subdural hematoma most likely?
In the first few months after the initial hemorrhage
What are the histologic features of traumatic injury of the spinal cord at the level of the injury in the acute phase?
Hemorrhage, necrosis, and axonal swelling in surrounding white matter
What occurs at the time central areas of neuronal destruction in a spinal cord injury?
The areas become cystic and gliotic
What is the morphology of the brain during global ischemia?
Brain is edematous and swollen, widening of gyri, narrowing of sulci, poor demarcation of gray and white matter
Early microscopic features of infarction (ischemic injury)
- Occur 12 -24 hours after insult
- Microvacuolization, eosinophilia in cytoplasm, nuclear pyknosis and karyorrhexis
Subacute microscopic changes of infarction
- Occur 24 hours - 2 weeks
- Tissue necrosis, influx of macrophages vascular proliferation, and reactive gliosis
Microscopic repair changes of infarction
- Occur at 2 weeks
- Removal of necrotic tissue, loss of normal CNS architecture, and gliosis
What is pseudolaminar necrosis and when is it seen?
- Pattern of injury
- When the cerebral neocortex has uneven neuronal loss and gliosis and preservation or destruction of different layers
Gross Appearance of a Nonhemorrhagic Infarct
- varies with time
- 6 hours- little change
- 48 hours- tissue becomes pale, soft, swollen, and corticomedullary junction becomes indistinct
- 2-10 days- brain becomes gelatinous and friable
- 10 days- 3 weeks- tissue liquefies, leaving a fluid filled cavity that expands until tissue is dead
Microscopic tissue reaction of nonhemorrhagic infarct after first 12 hours
- Ischemic neuronal change (red neurons)
- Cytotoxic and vasogenic edema
- Endothelial and glial cells swell
- Myelinated fibers disintegrate
Microscopic tissue reaction of nonhemorrhagic infarct up to 48 hours
- Neutrophilic emigration increases and then falls
- Phagocytic cells are prominent until 2-3 weeks
- Macrophages filled with myelin breakdown products or blood
When are reactive astrocytes seen in nonhemorrhagic infarcts?
- As early as 1 week after the insult
- As liquification and phagocytosis proceeds, astrocytes enlarge, divide, and develop extensions
Microscopic tissue reaction of nonhemorrhagic infarct after several months
Astrocytic response recedes, leaving behind a dense meshwork of glial fibers mixed with capillaries and connective tissue
What occurs during hemorrhagic infarctions?
Same as ischmeic infarctions with the addition of blood extravasation and resorption
When are spinal cord infarctions seen?
- In the setting of hypoperfusion or after traumatic interruption of branches leading to the aorta
Where can hypertensive intraparenchymal hemorrhages originate?
Putamen, thalamus, pons, cerebellar hemispheres
What are the characteristics of an acute hemorrhage?
Extravasation of blood with compression of the adjacent parenchyma
What is the appearance of an old hemorrhage?
Area of cavitary destruction of brain with a rim of brownish discoloration
What do early lesions of hypertensive intraparenchymal hemorrhages look like?
Central core of clotted blood surrounded by a rim of brain tissue showing anoxic neuronal and glial changes and edema
What occurs in the later stages of a hypertensive intraparenchymal hemorrhage?
Edema is resolved, hemosiderin and lipid-laden macrophages appear and proliferation of reactive astrocytes is seen at periphery of the lesion
What vascular abnormalities are usually associated with cerebral amyloid angiopathy (CAA)?
- Leptomeningeal and cerebral cortical arterioles and capillaries
- Dense and uniform deposits of amyloid
What is a distinguishing factor between cerebral amyloid angiopathy and arteriolar sclerosis?
In CAA there is no fibrosis but arteriolar sclerosis has fibrosis
What is an unruptured saccular aneurysm?
Thin-walled outpouching
*Usually in Circle of Willis
What is the usual size of a saccular aneurysm?
2-3 cm
Appearance of a saccular aneurysm
Red, shiny surface and a thin, translucent wall
What part of a saccular aneurysm does a rupture usually occur?
Arterial wall adjacent to the neck of the aneurysm
What is the aneurysm sac of a saccular aneurysm made up of?
Thickened hyalinized intima and covering of adventitia
What vessels are involved in arteriovenous malformation?
Vessels in the subarachnoid space or in the brain or both
What are some characteristics of arteriovenous malformations?
- Composed of greatly enlarged blood vessels separated by gliotic tissue
- Some arteries are duplicated and have fragmented internal elastic lamina
- Some arteries show thickening or partial replacement of the media by hyalinized connective tissue
- High flow channels
What are the components of a cavernous malformation?
Distended, loosely organized vascular channels arranged back to back with collagenized walls
- No parenchyma between vessels
- Low-flow channels
Where are cavernous malformations most common?
Cerebellum, pons, and subcortical regions
What are capillary telangiectasias?
Microscopic foci of dilated, thin-walled vascular channels separated by relatively normal brain parenchyma
Where are capillary telangiectasias usually found?
In the pons
Components of venous angiomas (varices)
Aggregates of dilated venous channels
What is Foix-Alajoyanine disease (angiodysgenetic necrotizing myelopathy)?
- Venous angiomatous malformation of the spinal cord and overlying the meninges
- Commonly associated with ischemic injury to the spinal cord and slowly progressive neurologic symptoms
Where is Foix-Alajoyanine disease mostly located?
lumbosacral region
