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Neuromusculoskeletal & Psychiatry II Exam #2 > Introduction to Neuropathology > Flashcards

Introduction to Neuropathology Flashcards

1
Q

What shape is suggested by “astro” and “oligo”?

A

Astro: oval
Oligo: round

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2
Q

What is the stain for glia (astrocytes and oligodendrocytes)?

A

GFAP IHC

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3
Q

What is meant by the term “selective vulnerability”?

A

A set of neurons, not necessarily located together, that share one or more properties demonstrating response to one insult.

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4
Q

What is the earliest morphologic indicator of acute neurological insult?

What causes this morphology?

A

Red neurons

Shrinkage of cell body, pyknosis, loss of nucleolus, loss of Nissl substance with intense eosinophilia of cytoplasm.

  • hypoxia
  • hypoglycemia
  • trauma
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5
Q

What neurological change is indicative of subacute and chronic insult and the best indicator of neuronal injury?

A

Neuronal degeneration: cell loss, reactive gliosis, apoptosis.
-abnormal protein accumulation

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6
Q

What occurs in the Axonal Reaction?

What are 3 morphological changes of neurons (and the 1 major change)?

A

Increased protein synthesis associated with axonal sprouting.

  • enlarged/rounded cell body
  • peripheral displacement of nucleus
  • enlarged nucleus
  • Central chromatolysis: Nissl removed from center of cell to periphery
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7
Q

What accumulates intracellularly in neurons?

What are 4 pathologic examples?

A

Lipofuscin, proteins or carbs accumulate.

Negri bodies: Rabies
Neurofibrillary tangles: Alzheimer Dz
Lewy bodies: Parkinson’s Dz
Vacuolization and perikaryon and neuronal processes: C-J Dz

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8
Q

What are 2 examples of intranuclear neural accumulations?

A

Herpes: Cowdry body
CMV: both intranuclear and cytoplasmic inclusions

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9
Q

Both chromatolysis and lipofuscin accumulation are…

A

Normal processes

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10
Q

What is the most important histopathologic indicator of CNS, regardless of etiology?

What features characterize it?

A

Gliosis (astrogliosis)

-> Hypertrophy and hyperplasia of astrocytes

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11
Q

What happens to gemistocytes during CNS injury?

A

Nuclei enlarge, become vesicular and develop prominent nucleoli; cytoplasm expands and becomes bright pink and dislocates nucleus eccentrically.

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12
Q

What is an Alzheimer type 2 astrocyte?

What diseases is it seen in? (3)

A

Gray matter cell with a large nucleus (2-3x bigger) and pale staining chromatin, intranuclear glycogen droplet with a prominent membrane and nucleolus.

Hyperammononemia (chronic liver disease)
Wilson disease
Hereditary metabolic disorder of the urea cycle

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13
Q

What are Rosenthal fibers?

What 2 proteins exist within these fibers?

A

Thick, elongated, brightly eosinophilic irregular structures occurring within astrocytic processes.

2 heat shock proteins: alpha B-crystalline + HSP27 and Ubiquitin

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14
Q

What makes up Corpora Amylacea? What stain is positive?

What changes are seen on histology as a result?
Where is it found?

What does it represent generally?

A

Polyglucosan bodies; PAS+.

Round, faintly basophilic, concentrically laminated strictures located adjacent to astrocytic end processes.
Subpial and perivascular location.

Degenerative change: increases in number with age.

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15
Q

What is the origin of Microglia (CNS macrophages)?

What are the surface markers?

How do they respond to injury? (4)

A

Mesoderm phagocytic cells

CD68 + CR3 (same as peripheral Mo)

Respond to injury by:

  • proliferating
  • developing elongated nuclei (rod cell), as in neurosyphilis
  • microglial nodules (microglia aggregate around small foci of necrosis)
  • neuronophagia: microglia congregate around cell bodies of dying neurons
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16
Q

In which kind of disorders do Oligodendrocytes respond to injury?

What changes occur in the following:

  • Progressive multifocal leukoencephalopathy (PML)
  • Multiple system atrophy (MSA)
A

Demyelinating disorders and Leukodystrophies

PML - intranuclear inclusions
MSA - glial cytoplasmic inclusions = alpha-synuclein

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17
Q

What kind of cells are Ependymal cells?

What are ependymal granulations?
What infection affects these cells?

A

Ciliated columnar cells that line the ventricles.

Small irregularities on ventricular surfaces due to ependymal and subependymal change.
CMV damages ependymal cells; viral inclusions.

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18
Q

What leads to vasogenic edema?

What type of injury is usually the cause?

A

Increased extracellular fluid due to BBB disruption and increased vascular permeability.

  • fluid shift from intravascular compartment to intercellular spaces.
  • paucity of lymphatics impairs resorption of excess extracellular fluid.
  • localized

Ischemic injury

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19
Q

What leads to cytotoxic edema?

A

Increased intracellular fluid secondary to neuronal, glial or endothelial cell membrane injury.

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20
Q

What changes occur to the brain when there is both vasogenic and cytotoxic edema present? What can it lead to?

A

Flattened gyri, narrowed sulci and compressed ventricles; can lead to herniation!

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21
Q

What are 3 potential pathogeneses of hydrocephalus?

A

Increased CSF production: choroid plexus papilloma (rare)

Obstruction

  • intraventricular foramina (exudates/tumors/clots)
  • congenital (stenosis/atresia)
  • secondary (infection/tumors/hemorrhage)

Decreased absorption: outflow obstruction

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22
Q

“Thick fibrous core/stalk”

A

Choroid plexus papilloma (increased fluid production hydrocephalus)

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23
Q

How does pyogenic meningitis lead to obstructive hydrocephalus?

A

Suppurative exudate covering brainstem and cerebullum leads to thickened leptomeninges (arachnoid + pia) and subsequent obstructive hydrocephalus.

24
Q

What are causes of congenital hydrocephalus? (6)

A 
Intrauterine infections (TORCH)
Agenesis/atresia/stenosis
AVM
Arnold Chiari malformations
Dandy-Walker syndrome
Cranial defects: achondroplasia, craniostenosis
25
Q

What is cysticercosis?

A

A calcified cyst that can lead to hydrocephalus, often due to ingestion of T. solium eggs by fecal contamination.

26
Q

What occurs in hydrocephalus ex-vacuo?

What can cause it?

What is the major distinction of this kind of hydrocephalus?

A

Dilation of the ventricles leads to shrinkage of brain substance.

  • atrophy with increased age
  • stroke
  • chronic neurodegeneration: HDz, ADz…

Normal CSF pressure

27
Q

What symptoms are seen in normal pressure hydrocephalus (NPH)?

A

Urinary incontinence, gait disturbance and dementia (“wet, wacky and wobbly”)

28
Q

What is the definition of herniation in the CNS?

What are the following types of hernation?

Subfalcine (cingulate)

Transtentorial (uncinated, uncal, mesial temporal)

Tonsillar

A

Increased pressure beyond the compensatory ability of the venous system to compress and displacement of the CSF. This causes tissue to herniate past the rigid dural folds (falx and tentorium) or through openings of the skull.

Subfalcine (cingulate): cingulate gyrus is displaced under the falx.

Transtentorial (uncinated, uncal, mesial temporal): medial aspect of the temporal lobe compressed against the tentorium; CN 3 affected and causes a dilated pupil and impaired eye movements.

Tonsillar: cerebellar tonsils displaced through foramen magnum; life-threatening due to compression of respiratory and cardiac centers of the brainstem.

29
Q

What is Kernohan’s notch phenomenon?

What is meant by a “false localizing sign”?

Which CN is implicated?

A

Compression of the cerebellar peduncle against the tentorium cerebelli due to transtentorial herniation. This produces ipsilateral hemiparesis or hemiplegia.
-> this produces a visible “notch” in the cerebellar peduncle.

It is caused by an injury to the opposite side of the brain. For example, if you have a right hemisphere transtentorial herniation it causes a KN in the left cerebellar peduncle, which results in right-sided motor impairment.

CN 6

30
Q

What is the average age of patients with normal pressure hydrocephalus (NPH)?

What is the onset?

The cause is usually…

A

60 y/o

Slowly over time

Idiopathic, but can be secondary due to hemorrhage, trauma, tumor, infection, etc.

31
Q

What is a Duret hemorrhage?

A

The progression of transtentorial herniation, often accompanied by secondary hemorrhagic lesions in the midbrain and pons.

32
Q

What kind of necrosis tends to occur in the CNS?

A

Liquefactive - digestion of tissue into a liquid viscous mass, without any architectural remnants.

33
Q

What is a hygroma?

A

Separation of arachnoid from dura due to contraction of the underlyig brain parenchyma after an infarct.

34
Q

What is a Myelomeningocele?

What is a Meningocele?

What symptoms might these patients have?

A

Myelomeningocele: extension of CNS tissue through a defect in the vertebral column (lumbosacral is most common).

Meningocele: only the meninges protrude.

Motor and sensory deficits of the LE, bowel, and bladder control, superimposed infections.

35
Q

What is an encephalocele? Where is it most common?

What is a “nasal glioma”?

A

Diverticulum of disorganized brain tissue extending through a defect in the cranium. Most common in the posterior fossa.

Misnomer for extension through the cribiform plate.

36
Q

What is anencephaly?

What is area cerebrovasculosa?

A

Absence of most of the brain and calvarium. The forebrain is disrupted at approx. 28 days.

A flattened remnant of disorganized brain tissue admixed with ependymal, choroid plexus and meningothelial cells. Posterior fossa structures may be spared.

37
Q

What are some common causes of microcephaly? (4)

A

Fetal alcohol syndrome, HIV-1, Zika virus, possible chromosomal abnormality.

38
Q

What forebrain anomaly is commonly associated with epilepsy?

What is the genetic basis for the anomaly?

A

Neuronal heterotopias - collections of neurons in inappropriate places along the pathway of migration.

X chromosome: Filamin A + DCV (causes Lissencephaly in males and subcortical band heterotopias in females).

39
Q

What is the developmental cause for Holoprosencephaly?

What features do these patients have?

What is the genetic/molecular association?

A

Incomplete separation of cerebral hemispheres across midline.

Cyclopia
Arrhinenceophaly: absence of olfactory CNs

Trisomy 13, sonic hedge hog signaling pathway

40
Q

What appearance is seen in brains of patients with agenesis of the corpus callosum?

What is the outcome?

A

“Bat-wing” lateral ventricles

Can be MR or have normal mentation; relatively common.

41
Q

Where do Arnold-Chiari malformations occur?

What is Chiari type 2 vs. Chiari type 1?

A

Small posterior fossa

Type 2: more severe, misshapen midline cerebellum with downward extnsion of the vermis through the foramen magnum.
-> hydrocephalus and lumbar meningocele.

Type 1: low-lying cerebellar tonsils extend down the vertebral canal. They are silent, but may be impaired if there is impaired CSF flow.

42
Q

What is a Dandy-Walker malformation?

A

An enlarged posterior fossa causing an expanded fourth ventricle. The cerebellar vermis is absent and replaced by a cyst with ependymal lining that is contiguous with the leptomeninges on its outer surface.

43
Q

What is Joubert syndrome?

What is the classic imaging finding?

A

Hypoplasia of the vermis, elongation of the cerebellar peduncles and altered brainstem shape.

“Molar tooth sign”

44
Q

What is Syringomyelia (Syrinx)?

What are the classic symptoms?

A

Fluid-filled cleft-like cavity in the inner portion of the cord. This interrupts fibers that cross through the white commissure.

Isolated loss of pain and temperature sensation of the upper extremities BL.

45
Q

What is a hydromyelia?

A

Expansion of ependymal-lined central canal of the cord.

46
Q

What is cerebral palsy?

What are some symptoms?

A

Non-progressive neurologic motor deficit attributable to insults occurring during the prenatal and perinatal period.

Spasticity, dystonia, ataxia/athetosis and paresis.

47
Q

Where in the brain is an intraparenchymal hemorrhage seen?

How can is progress?

A

The germinal matrix of premature infants.

At the junction of the thalamus and caudate nucleus it can enter the ventricles, then SAH.

48
Q

What is periventricular leukoplakia?

In which patients might you see periventricular leukoplakia?

What is seen on histology?

A

Infarcts in the supratentorial white matter.

Premature infants.

Chalky yellow plaques - necrosis and calcification.

49
Q

What is multicystic encephalopathy?

A

Extensive ischemic damage of both white and gray matter, causing large destructive cystic lesions.

50
Q

What is ulegyria?

A

Perinatal ischemic lesions in the depths of the sulci, causing thinned-out gliotic gyri.

51
Q

What is a diastatic fracture?

A

Fracture that crosses a suture

52
Q

What might occur as a result of a basal skull hematoma?

What is a common symptom?

A

Orbital and/or mastoid hematomas.

Otorrhea/rhinorrhea - CSF drainage from ear or nose.

53
Q

What occurs in a contusion to the brain parenchyma?

Define the following:

Coup
Countercoup
Plaque jaune

A

Wedge-shaped, broad-based at the point of impact.

Coup - contusion at point of impact.
Countercoup - diametrically opposed to coup (sudden deceleration).
Plaque jaune - depressed, retracted, yellowish-brown patches involving crests of gyri.

54
Q

What occurs in diffuse axonal injury (DAI)?

How long does it take to appear?

How is it found on histology?

What causes it?

A

Axonal swelling +/- focal hemorrhagic lesions.

Within hours and persist much longer.

+ silver stain or APP and alpha-synclein immunostains.

Physical trauma to the brain.

55
Q

What injuries might occur in a baby from shaken impact syndrome?

A 
DAI/cerebral edema
Subdural hematomas
Retinal hemorrhages
Sometimes, subgaleal hemorrhages
Sometimes, microscopic iron (old bleeding)
56
Q

What are features of trauma to the epidural space?

What are features of trauma to the subdural space?

A

Arterial - epidural space: skull fracture and rapidly evolving neurological symptoms, requiring intervention.

Venous - subdural space: more mild trauma with slowly evolving neurological symptoms, often with a delay from the time of injury.

57
Q

In which hematomas is the dura “peeled off” the skull?

A

Epidural hematoma

Neuromusculoskeletal & Psychiatry II Exam #2 (15 decks)

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