Intro into NeuroPathology Flashcards by Amy Kunduru

Describe the Acute Response to Neuronal Injury. When would you see it? What would you see?

12-24 hrs
Red Neurons
Shrinkage of cell body
Pyknosis
Intense eosinophilia of cytoplasm

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In what conditions will acute injury occur?

Hypoxia
Hypoglycemia
Trauma

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What would you see with a Subacute and Chronic Response to neuronal injury?

In what conditions, would you see this occur?

Degeneration; progressive
Cell loss and reactive gliosis; Apoptosis

Neurodegenerative dz or demyelinating dz

Abnormal protein accumulation
ALS
Alzheimer’s

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How do axons react to neuronal injury?

Increase protein synthesis with axonal sprouting

Enlarged cell body
Central chromatolysis = nissl substance to periphery (also nucleus)

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What are some intracytoplasmic inclusions?

Lipofuscin (increases with age)
Negri bodies - Rabies
Neurofibrillary tangles - ALZ
Lewy bodies - Parkinson

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What are some intranuclear inclusions?

Cowdry bodies - Herpes

CMV = intranuc and intracyt

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What is histologically characteristic of CMV infection?

Owl’s eye nuclear inclusions

damages ependymal cells

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What is the most important histopathologic indicator of CNS injury?

Astrogliosis!

Regardless of etiology

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Describe Alz Type 2 astrocytes. When would you see them?

Gray matter cell
Large nucleus
Pale staining central chromatin
Intranuclear glycogen droplet

Hyperammononemia (chronic lever dz)
Wilson Dz
Hereditary metabolic DO of urea cycle

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What cancer would you associate astrogliosis with? What other characteristics can be seen?

Craniopharyngioma

Rosenthal fibers
Keratin
Cystic tumor
Drainage like machine oil

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When would you see rosenthal fibers? What do they contain?

During a slow and benign process
At areas of long standing gliosis = Pilocytic astrocytoma

Contains 2 heat shock proteins = a-B-crystalline,HSP27
Ubiquitin

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What characteristics would you see with Corpora Amylacea?

Polyglucosan bodies
PAS+
Increase with age
Degenerative change

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What are the macrophages of the CNS? What are the surface markers? How do they respond to injury?

Microglia
CR3 and CD68

Respond by:
Proliferating
Microglial nodules - aggregate around necrosis
Neuronophagia - congregate around cell bodies of dying neurons

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What injuries do oligodendrocytes respond to? Name specific dz and what you see.

Demyelinating DOs, Leukodystrophies

PML = intranuclear inclusions
MSA (multiple system atrophy) = glial cytoplasmic inclusions (a-synuclein)

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Where do you see a-synuclein?

Parkinson’s
Lewy Body dementia
MSA
Diffuse axonal injury (DAI)

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Describe ependymal cells. What are ependymal granulations?

Line ventricles, ciliated columnar cells

Granulations = disruption of ependymal lining and proliferation of subependymal astrocytes

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Describe vasogenic edema. What does it often follow?

Increase in extracellular fluid due to BBB disruption and increased vascular permeability

Follows ischemic injury
No lymphatics to clear fluid away

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Describe cytotoxic edema.

Increase in intracellular fluid secondary to neuronal, glial, or endothelial cell membrane injury

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Which type of edema would you see more? What can it lead to?

Often see elements of BOTH vasogenic and cytotoxic edema = gyri flatten, sulci narrow, ventricles compressed –> HERNIATION

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What is the one bacterial dz that will affect the bottom of the brain? What pathology will it lead to?

Pyogenic meningitis = suppurative exudate covering brainstem and cerebellum

Thickened leptomeninges –> obstructive hydrocephalus

Wet, Wobbly, Wacky?

Gait disturbance, Dementia, Urinary incontinence

Seen with NPH

What are the different types of herniation? What conditions will they cause?

Subfalcine = cingulate gyrus under the Falx

Transtentorial = medial aspect of the temporal lobe compressed against tentorium
CN3 –> dilated pupil and impaired eye movement

Tonsillar = cerebellar tonsils through foramen magnum –> respiratory and cardiac compression

What is the Kernohan’s notch phenomenon? What does it cause?

Compression of CEREBRAL peduncle against tentorium cerebelli

Due to Transtentorial herniation

Ipsilateral hemiparesis or hemiplegia (on side of herniation) –> a RIGHT hemisphere herniation causes LEFT notch leading to RIGHT-sided motor impairment

What is Duret hemorrhage?

Progression of transtentorial herniation –> secondary hemorrhagic lesions in midbrain and pons

Describe liquifactive necrosis. What can cause this?

Digestion of tissue into liquid viscous mass, no architectural remnants Bacterial infections CNS Infarct

All other organs (except the brain) undergo this type of necrosis.

Coagulative Necrosis (architecture remains)

What is a hygroma?

Separation of arachnoid from dura due to contraction of underlying brain parenchyma s/p infarct

What accounts for the most CNS malformations? Describe it. What might be one reason that it is so common?

Neural Tube Defects failure of portion of neural tube to close or reopening after closure Folate deficiency = neural tube closure by 28 days before pregnancy is recognized

What is an encephalocele?

Diverticulum of disorganized brain tissue extending through defect in cranium (usually posterior fossa)

Which defects will you see in the 1st trimester? 2nd trimester? 3rd trimester?

1st = encephalocele, anencephaly 2nd = Lissencephalia, Microgyria 3rd = myelinating issues

B/w megalocephaly and microcephaly, which is more common? What can cause this?

Microcephaly - decreased number on neurons in neocortex ``` Usually assoc with small head circumference Chromosomal abnormalities Fetal Alcohol Syndrome HIV-1 in utero Zika virus ```

What is neuronal heterotopia? What is it commonly associated with? What genes are responsible?

Collections of neurons in inappropriate places Associated with epilepsy X-chromosome --> Filamin A protein and DCX = Lissencephaly in males and heterotopia in females

What is holoprosencephaly? Associations? Genes?

Incomplete separation of cerebral hemispheres across midline Assoc with cyclopia, arrhinenceophaly (absence of CN 1) Trisomy 13, SHH

What is polymicrogyria?

Small, unusually numerous, irregularly formed convolutions Entrapment of meningeal tissue

What do you see with agenesis of the corpus callosum?

Bat-wing lateral ventricles Mental retardation or normal mentation

Which is more serious Chiari Type 1 or 2? Describe them. What are their associations?

Small posterior fossa with Type 2 being more serious Type 2 = misshapen midline cerebellum with vermis through F magnum -Assoc = hydrocephalus, myelomeningocele Type 1 = Tonsils through FM, Silent, Sx if impaired CSF flow -Assoc = syringomyelia

What is a Dandy-Walker malformation? Characteristics?

Enlarged posterior fossa Expanded roofless 4th ventricle Vermis absent/rudimentary Cyst with ependymal lining contiguous with leptomeninges on outer surface

What is Joubert syndrome?

Hypoplasia of vermis Elongation of cerebellar peduncles and altered brainstem Molar tooth sign

What is syringomyelia?

Fluid filled cavity in the inner portion of spinal cord B/L loss of Pain and Temp of UE -Interrupts fibers that cross through anterior white commissure

What is Hydromyelia?

Expansion of ependymal-lined central canal of cord

Decribe characteristics of cerebral palsy.

Spasticity Dystonia Ataxia/Athetosis Paresis

Name the perinatal brain injuries. What might you see with them?

Cerebral palsy Intraparenchymal hemorrhage Periventricular leukomalacia (chalky yellow plaques) Multicystic encephalopathy (large destructive cystic lesions) Ulegyria (thinned gyri from ischemic lesions)

What is a diastatic fracture?

Crosses a suture

What are the sign of a basilar skull fracture?

Hemotympanum Battle's sign - bruising behind ear Racoon eyes Otorrhea/Rhinorrhea = CSF drainage form ear/nose

Describe a Traumatic Brain Injury (TBI).

Brain damage form external mechanical forces (rapid acceleration, impact, etc) Associated diminished or altered state of consciousness, brain function temp/perm impaired

How would you diagnose CTE? How do you get it? What happens?

DX only after examining brain after death ``` Get it from repeated head blows Progressive loss of normal brain matter and abnormal build up of Tau Microhemorrhages/DAD NF tangles/amyloid - 43% Depigmentation of substantia nigra ```

What is Plaque Jaune?

Depresses, retracted, yellowish brown patches involving crest of gyri Contusion - countercoup Old trauma lesions Temporal and occipital lesions

What is Diffuse Axonal Injury? What stains? Histologically significant?

Axonal swelling +/- focal hemorrhagic lesions (within hours) from mechanical forces Silver stain or APP/a-synuclein immunostains Axonal spheroids

Etiology of: epidural, subdural, SAH.

Epidural = trauma to Middle meningeal (dura peeled off) Subdural = trauma affecting venous system SAH = vascular/trauma, sudden onset of severe HA