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Neuro > 72. Pathological Responses to Brain Injury > Flashcards

72. Pathological Responses to Brain Injury Flashcards

1
Q

What do the following cells normally look like on histology?

  • neurons
  • oligodendrocytes
  • astrocytes
  • microglia
  • ependyma
A

Neurons: (pyramidal neurons in layers 3/5), large triangular cell bodies, abundant cytoplasm, large nucleus, prominent nucleolus (Nissl substance: rouch ER, bluish granules)
Oligos: round dark nuclei with perinuclear halo (more common in white matter)
Astros: oblong nuclei with fine chromatin, cytoplasm blends in with background (white and grey matter)
Microglia: activated = rod cells (thin, elongated, dark nuclei)
Ependyma: single layer of cuboidal/columnar ciliated cells - line ventricles for blood-csf barrier

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2
Q

How do neurons change in response to injury over time?

How do cells change due to axonal injuries?

What do different types of neuronal inclusions suggest?

A
  1. Acute (12hrs-2days later): RED DEAD Neurons - earliest sign of irreversible neuronal injury (cell shrinkage, RED cytoplasm, pyknotic (small,dark) nucleus)
  2. Subacute/Chronic (2d-10d): “DEGENERATION” - reactive gliosis (astrocyte hyperplasia/hypertrophy)

Axonal Damage: cell body rounding/ballooning, CENTRAL CHROMATOLYSIS (Nissl Body dispersion to periphery)

Rabies: cytoplasmic Negri bodies
Herpes: intranuclear Cowdry bodies
Proteinopathies: aggregates of misfolded proteins in cytoplasm and nucleus
PD: Lewy Body; AD = neurofibrillary tangles

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3
Q

How do astrocytes change in response to injury?

What are Alzheimer Type 2 Astrocytes?

What are Rosenthal Fibers?

What is Corporal Amylacea?

A
  1. Gliosis - MOST COMMON response of CNS to Injury (1 week later) - hypertrophy (abundant eosinophilic cytoplasm)/hyperplasia (eccentric nuclei) of astrocytes, filling space of neurodegenerative disease; visualized with GFAP stains

Alz T2: NOT with AD; in pts with long-standing METABOLIC DISORDERS - Enlarged nuclei (3x) with light chromatin/nucleolus, (no eosinophilic cytoplasm)

Rosenthal Fibers: cytoplasmic inclusions in astrocytic processes - in areas of long-standing gliosis (cyst walls) and slow growing tumors)

Corpora Amylacea: in aging/long-standing injury - degenerative changes (round, blue/basophilic, concentrically layered structures of astrocyte end processes, calcified)

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4
Q

What 3 days do microglia change in response to injury?

A
  1. Activate = Rod Cells
  2. Microglial Nodules = aggregates around areas of necrosis (Giant Cells = HIV Encephalitis)
  3. Neuronophagia = surround dying neurons (seen in polio/ALS)
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5
Q

What do injured oligos represent?
What inclusions are in oligos?

What does injured ependyma look like?

A

Injury - demyelinating disorders/leukodystrophies
Inclusions - PML - nuclear; Cytoplasmic - MSA

Ependymal Granulations: nonspecific to injury, form ependymal canals
Inclusions: CMV/Viral

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6
Q

What are the types of Cerebral Edema?

What does cerebral edema look like macroscopically?

A
  1. Vasogenic Edema = High Extracellular fluid: disrupted BBB has more permeability
  2. Cytotoxic Edema = High Intracellular fluid: 2/2 injury of cells disrupting ion gradiant
    both types COEXIST

Gross: Gyri-flattening, Sulci-narrowing, Ventricular System Compression

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7
Q

Hydrocephalus: what it is, causes, 2 main types

A

High CSF volume 2/2 disequilibrium b/w CSF formation and resorption
Cause: impaired flow/absorption
1. Noncommunicating: obstructive, CSF blocked from reaching SubArachnoid - enlargement proximal to blockage
2. Communicating: enlargement of ENTIRE CSF system (due to choroid plexus papilloma - overproduction; scarring of arachnoid granulations from hemorrhage)

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8
Q

Herniation: what is it - 3 types

A

Displacement of tissue past dural partitions in skull or through skull openings

  1. Subfalcine (Cingulate) Herniation: cingulate gyrus goes under falx cerebri - can compress ipsi ACA
  2. Transtentorial (Uncal) Herniation: uncus/medial temp lobe through tentorium - compress ipsi CN3, PCA, cerebral peduncle (severe - push contralateral cerebral peduncle)
  3. Cerebellar tonsillar herniation: LIFE THREATENING - cerebellar tonsils through foramen magnum - compression of medulla’s cardio/resp centers

Duret Hemorrhages: rupture of BA perforators to pons due to transtentorial herniation

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9
Q

Causes of Focal Cerebral Ischemia (and where they most likely impact cerebrum)

A
  1. Embolism from distant source (affects MCA most - continuation of ICA)
  2. In situ thrombosis - atherosclerosis/plaque rupture - at carotid bifurcation, origin of MCA, either end of BA
  3. inflammatory process in vessels
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10
Q

Global Cerebral Ischemia

  • causes
  • most sensitive/vulnerable areas
A

Generalized reduction in CBF causes diffuse hypoxic-ischemic encephalopathy
Neurons are MOST SENSITIVE to any form of injury
1. Pyramidal neurons in CA1 region of HIPPOCAMPUS
2. Cerebellar Purkinje Neurons
3. Watershed Regions in cortical layers 3/5

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11
Q

Macroscopic Findings of Non-Hemorrhagic Infarcts (what happens grossly over time)

A
  1. Acute (AFTER 8 hours - 2 days)
    - blurring of grey-white junction, duskiness/softening of tissue
  2. Subacute (2-10d)
    - prominent softening, grey-white blurring, dusky discoloration, edema
    - tissue becomes progressively more gelatinous/friable
    - boundary becomes more distinct
  3. Resolving Infarct (10days - months)
    - liquefactive necrosis (gelatinous/friable) with progressive cavitation
  4. Remote Infarct (months - life)
    - CSF filled cystic cavity
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12
Q

Microscopic Findings of Non-hemorrhagic Infarcts (what happens histologically over time)

A
  1. Acute Infarct (AFTER 12 hrs - 2 days)
    - RED DEAD NEURONS (irreversible damage)
    - Edema, influx of neutrophils
  2. Subacute Infarct (2-10days)
    - Lipid Laden Macrophages predominate
    - Gliosis and capillary proliferations appear at 1 week and move inward
  3. Resolving Infarct (10d - months)
    - liquefactive necrosis: removal of necrotic tissue by macrophages
    - progressive cavitation, surrounding gliosis, vascular proliferation
  4. Remote Infarct (months - life)
    - some macs remain, cystic cavity with dense rim of reactive astrocytes
    - subpial tissue may remain intact
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13
Q

Lacunar Infarcts

  • where are they
  • what is the biggest risk factor
  • what structure is most commonly involved?
A

small, perivascular, ischemic, cavitary infarcts
RF: HTN (causes arteriosclerosis with vessel occlusion of deep penetrating vessels)
Location: PUTAMEN

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14
Q

What are the 3 types of Intraparenchymal Hemorrhage? (list)

A
  1. Ganglionic Hemorrhage
  2. Lobar Hemorrhage
  3. Secondary Hemorrhagic Infarcts
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15
Q

Ganglionic Hemorrhages

  • what are they, most common etiology
  • Gross features
  • Histo features
A

Deep, grey/white matter (usually PUTAMEN)
Etiology: HTN

Gross

  1. Acute: hematoma (core of clotted blood) compressing surrounding parenchyma
  2. Subacute: hematoma resorption, surrounding ischemic tissue becomes gelatinous/friable
  3. Resolving: liquefactive necrosis, cavitation
  4. Remote: cavitary lesion with BROWN RIM (hemosiderin-laden macrophages)

Histo:

  1. Acute: central hemorrhage and RED DEAD neurons
  2. Subacute: influx of hemosiderin/lipid - laden macrophages, hematoma resorption, gliosis/vascular proliferation
  3. Resolving: liquefactive necrosis, cavitation/gliosis
  4. cavitary lesion lined by gliosis + hemosiderin-laden macrophages
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16
Q

Lobar Hemorrhages

  • most common etiology
  • histo
A

Involves cerebral hemispheres
E: Cerebral Amyloid Angiopathy (CAA)
H: leptomeningeal/intracortical vessels appear rigid (filled with dense, glassy, pink amyloid), stains for beta-amyloid (same protein in AD)

17
Q

Secondary Hemorrhage Infarcts

  • what it is
  • cause
  • Gross
A

hemorrhagic transformation of non-hemorrhagic ischemic infarct
due to ischemia-reperfusion injury (thrombolysis/collateral circulation)

Gross: more petechial (small punctate) hemorrhages - multiple or confluent/large

18
Q

Subarachnoid Hemorrhage (SAH)

  • causes
  • risk factors
  • Gross
  • Histo
A

Trauma or Saccular “Berry” Aneurysm (90% at branch points of arterial circulation)
RF: +FHx, HTN, smoking, ADPKD, Ehlers-Danlos, NF
Gross: wide/narrow-necked thin walled outpouching, often translucent wall (usually at circle of willis branch point), complicated by atherosclerosis/calcifications/thrombus)
Histo: saccular wall lacks internal elastic lamina/smooth muscle media - made of thickened intima/adventitia

19
Q

Vascular Malformations

  • Gross
  • Histo
A

Gross: mass of irregular, tortuous “worm-like” vessels
Histo: large vessels subarachnoid or in brain parenchyma; show evidence of acute/chronic hemorrhage (hemosiderin-laden macrophages)

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