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NMSP Exam 1 > Intro to Neuropathology > Flashcards

Intro to Neuropathology Flashcards

1
Q

Any tumor that would “spill” into/adjacent to brain parenchyma would produce what?

A

a localized injury and astrogliosis

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2
Q

What are some histologic characteristics of Rosenthal fibers?

A

beaded sausage to cork screw shaped hyaline bodies of variable size, bright red on Masson trichrome, blue with Luxol fast blue stain

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3
Q

Rosenthal fibers are evident after long standing gliosis due to what?

A

pineal cysts, hemangioblastoma, spinal lesions, etc

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4
Q

What are eosinophilic granular bodies?

A

protein droplets seen in gangliomas and PXA, mark of slow growing low grade prognostically favorable tumors, PAS+

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5
Q

What are the surface markers for microglia?

A

CR3 and CD68 (same as peripheral macrophages)

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6
Q

What are the two types of cerebral edema?

A

Vasogenic and cytotoxic

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7
Q

What is vasogenic edema?

A

increased extracellular fluid due to BBB disruption and increased vascular permeability; fluid shifts from intravascular compartment to intercellular spaces; paucity of lymphatics impairs resporption of excess ECF; localized (adjacent to inflammation or neoplasm) or generalized; often follows ischemic injury

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8
Q

What are the characteristics of generalized cerebral edema?

A

flattened gyri, narrowed sulci, compressed ventricles; can lead to herniation

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9
Q

What happens to ventricular volume with hydrocephalus?

A

ventricular volume increases out of proportion to volume of sulci

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10
Q

The largest width of the frontal horns (FH) should be _____ than half of the internal skull diametric in ___ hydrocephalus

A

greater; true

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11
Q

What is the response to increased CSF?

A

Absorption of tranventricular and nerve root sleeves, dilation of frontal and temporal horns, elevation of corpus callosum, thinning of the cerebral mantle, stretching/perforation of septum pellucidum, enlargement of 3rd ventricle downwards, papilledema (increased ICP)

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12
Q

What is the pathogenesis of hydrocephalus/increased CSF?

A
  • increased production of CSF due to choroid plexus papilloma (rare);
  • obstruction due to intraventicular foramina (exudates/tumors/blood clots), congenital (stenosis/atresia), or secondary (tumors/hemorrhages/infections);
  • decreased absorption due to outflow obstruction
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13
Q

What are causes of congenital hydrocephalus?

A

intrauterine infections (TORCH), genesis/atresia/stenosis, AVM, Arnold chiari malformation, Dandy Walker syndrome, cranial defects such as achondroplasia or craniostenosis

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14
Q

What are acquired causes for hydrocephalus?

A

infections (meningitis, meningoencephalitis, cysticercosis), mass lesions (neoplasms such as medulloblastoma or astrocytoma), inflammation from a brain abscess, post hemorrhage (IVH, SAH, injury), choroid plexus papilloma/carcinoma, sagittal sinus thrombosis, hypervitaminosis A, idiopathic

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15
Q

What are the features and sx of hypervitaminosis A?

A

softening of skull bones in infants and kids; blurred vision, bulging fontanelles, dizziness, alterations in alertness

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16
Q

What is communication hydrocephalus?

A

occurs when CSF is not absorbed properly at the dural sinus level thus ventricles tend to be symmetrically dilated; involves the leptomeninges but there is not a single point of obstruction

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17
Q

What can cause overproduction of CSF seen in communication hydrocephalus?

A

choroid plexus tumor, neurosyphilis or arachnoid fibrosis following meningitis

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18
Q

What is non-communicating hydrocephalus?

A

occurs if ventricular system is focally obstructed due to a mass in the 3rd ventricle or aqueductal stenosis

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19
Q

What is hydrocephalus ex-vacuo?

A

a compensatory increase in ventricular volume secondary to a loss of brain parenchyma; dilation of the ventricles occurs as well as shrinkage of brain substance due to frontal atrophy with increasing age, stroke or other injury, or chronic neurodegenerative dz such as Huntington or Alz; CSF pressure is normal;

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20
Q

Increased ICP is generally due to what?

A

generalized brain edema, expanding mass lesion (tumor, abscess, hemorrhage), or increased CSF volume

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21
Q

What is herniation?

A

increased pressure bestowing the compensatory ability of the venous system to compress and displacement of CSF –> tissue herniation past the rigid dural folds (falx and tentorium) or through the openings of the skull

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22
Q

What is a subfalcine (cingulate) herniation?

A

cingulate gyrus displaced under the falx (can compress the ACA and lead to infarcts)

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23
Q

What is a transtentorial (uncinated, uncal, mesial temporal) herniation?

A

medial aspect of the temporal lobe compressed against the tentorium; CN3 –> dilated pupil and impaired eye movement on the side of the lesion

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24
Q

What is a tonsillar herniation?

A

cerebellar tonsils displaced through the foramen magnum; life threatening due to respiratory and cardiac center compression

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25
Q

What are the signs and sx of increased ICP?

A

HA, change in behavior, N/V, lethargy, change in pupil reaction, upward gaze, false localizing signs (e.g. 6th nerve palsy), seizures, decreased coordination, ataxia, papilledema

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26
Q

What is a duret hemorrhage?

A

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

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27
Q

What is an infarct?

A

area of necrosis resulting from sudden insufficiency of arterial or venous blood supply

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28
Q

What is the characteristics of neurons during hypoxia?

A

neuronal loss, with the remaining neurons being shrunken, eosinophilic and/or pyknotic; can be seen in purkinje cells of the cerebellum and pyramidal cells of sommer’s sector

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29
Q

What is necrosis?

A

denaturation of intracellular proteins and enzymatic digestion of lethally injured cells; enzymes that digest the cells derived from the lysosomes of the dying ell themselves

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30
Q

What is liquefactive necrosis?

A

digestion of tissue into liquid mass, no architectural remnants; occurs in the CNS; possibly due to bacterial infections (purulent material)

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31
Q

CNS infarct results in what type of necrosis?

A

liquefactive; all other organs undergo ischemic coagulative necrosis (architecture remains)

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32
Q

What are the events that occur during/after a cerebral infarct?

A

acute ischemic injury causes diffuse eosinophilia of neurons which are beginning to shrink; after 10 days the lesion is characterized by the presence of foamy macrophages and reactive gliosis with neovascularization

33
Q

Small infarcts are seen as what?

A

areas of tissue loss with residual gliosis

34
Q

What is hygroma?

A

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

35
Q

What can an old cystic infarct lead to?

A

destruction of cortex with cavitation

36
Q

What accounts for most CNS malformations?

A

neural tube defects

37
Q

What events occur during the first trimester?

A

formation of the neural tube

38
Q

What events occur during the 2nd trimester?

A

neural proliferation and migration

39
Q

What events occur during the 3rd trimester?

A

neural organization and myelination

40
Q

What defects in neural tube formation occur in the first trimester?

A

anencephaly, encephalocele, holoprosencephaly (arrhinencephalia)

41
Q

What defects in neural tube formation occur in the 2nd trimester?

A

a decrease in number of neurons leads to microcephaly, whereas an increase results in megalencephaly; defective neural migration results in lissencephalia or agenesis of the corpus callosum

42
Q

What is spinal dysraphism?

A

includes several conditions characterized by congenital failure of fusion of the midline structures of the spinal column; includes spina occulta, dermal sinus, meningocele, meningomyelocele, arnold-chiari, malformation

43
Q

What is cyclopia?

A

a rare form of holoprosencephaly and is a congenital disorder characterized by the failure of the embryonic prosencephalon to properly divide the orbits of the eye into two cavities; nose is either missing or replaced by a nonfunctioning nose (known as rhinencephaly or rhinocephaly)

44
Q

What are the effects of a syrinx?

A

Sx usually begin in 2nd or 3rd decade of life and include dissociated anesthesia (loss of pain and temperature sense in the UE), denervation atrophy of muscle, and kyphoscoliosis

45
Q

What are the effects of a Dandy Walker malformation?

A

The 4th ventricle dilated and the membrane that forms its roof balloons, creating a large posterior fossa cyst which pushes the tentorium upwards —> obstructs CSF flow —> hydrocephalus

46
Q

What are examples of perinatal brain injury?

A

Cerebral palsy, intraparenchymal hemorrhage, periventricular leukomalacia, multicystic encephalopathy and ulegyria

47
Q

What is cerebral palsy?

A

Non-progressive neurologic motor deficit attributable to insults occurring during the prenatal and perinatal period; will demonstrate spasticity, dystonia, ataxia/athetosis and paresis

48
Q

What is intraparenchymal hemorrhage?

A

Seen in germinal matrix of premature infants; junction b/w thalamus and caudate nucleus —> progression to ventricles and then SAH —> hydrocephalus and death

49
Q

What is periventricular leukomalacia?

A

Infarcts in supratentorial white matter; in premature infants consists of chalky yellow plaques with necrosis and calcification

50
Q

What is multicystic encephalopathy?

A

When damage from PML is xxtensive ischemic damage of both white and gray matter —> large destructive cystic lesions

51
Q

What is ulegyria?

A

Perinatal ischemic lesions in the depths of sulci —> thinned out gliotic gyri

52
Q

Lesions to what area result in ahtetosis?

A

Corpus striatum (occur along with sx of cerebral palsy)

53
Q

What is the long term sequalae of severe prenatal or perinatal ischemic injury associated with PML?

A

Large cystic spaces in the white matter

54
Q

If a person is awake which way would they fall?

A

Backward so occiput would be fractured

55
Q

If a person losses consciousness which way do they fall?

A

Forward so they would have frontal impact

56
Q

What is a diastatic fracture?

A

Fracture that crosses a suture line

57
Q

Later fracture lines do not extend across what?

A

Previous fracture lines

58
Q

What is a displaced/depressed skull fracture?

A

Bone displaced into cranial cavity by a distance > thickness of the bone

59
Q

what is a basal skull fracture?

A

Orbital and/or mastoid hematomas; can cause raccoon eyes, battle’s sign (bruise behind ear), hemotympanium, otorrhea/rhinorrhea (CSF drainage from ear or nose)

60
Q

What test is done to detect CSF in blood?

A

Dipstick with Beta transferrin

61
Q

What are plaque Jaune?

A

Remote contusions with a yellow color that reflects hemosiderin accumulation

62
Q

What is shaken baby syndrome?

A

Shaking a child violently to make it stop crying which induces brain damage; 75-80% dont die but develop brain damage; shaking a child on several occasions may be like 2nd concussion syndrome (some of them die after hours of brain swelling and DAI)

63
Q

How is shaken impact syndrome recognized?

A

Through a constellation of injuries including diffuse axonal injury/cerebral edema, subdural hematomas, retinal hemorrhages, sometimes subgaleal hemorrhages or microscopic iron (old bleeding, Prussian blue stain);

64
Q

What does injury to the thoracic or lower vertebra cause?

A

Paraplegia

65
Q

What does injury to the cervical spine cause?

A

Quadriplegia

66
Q

What does injury to C4 and above cause?

A

Respiratory compromise, paralysis of diaphragm

67
Q

What is a micro spinal injury?

A

Lesion tapers above and below level of injury

68
Q

What can acute micro injuries cause?

A

Hemorrhage, necrosis and axonal swelling

69
Q

What can chronic micro injuries cause?

A

Central areas become cystic and gliotic; secondary ascending and descending wallerian degeneration above and blow the lesion

70
Q

What is the etiology for epidural and subdural hemorrhages?

A

Trauma

71
Q

What are the features of an epidural hemorrhage?

A

Usually associated with skull fracture (in adults); rapidly evolving neuro sx requiring intervention; arterial

72
Q

What are the features for a subdural hemorrhage?

A

Level of trauma may be mild; slowly evolving neurologic sx often with a delay from the time of injury; venous

73
Q

What are the etiologies for a subarachnoid hemorrhage?

A

Vascular abnormalities (AVM or aneurysm) or trauma

74
Q

What are the features for a subarachnoid hemorrhage caused by vascular abnormalities?

A

Sudden onset of severe HA often with rapid neuro deterioration; secondary injury may emerge associated with vasospasm

75
Q

What are the features for a subarachnoid hemorrhage due to trauma?

A

Typically associated with underlying contusions

76
Q

What are the etiologies for intraparenchymal hemorrhage?

A

Trauma or hemorrhage conversion of an ischemic infarct

77
Q

What are the features for intraparenchymal hemorrhage caused by trauma (contusions)?

A

Selective involvement of the crests of gyri, where the brain may contact the inner surface of the skull (Frontal and temporal tips, orbitofrontal surface)

78
Q

What are the features for intraparenchymal hemorrhage caused by hemorrhagic conversion of an ischemic infarction?

A

Usually petechial hemorrhages in an area of previously ischemic brain, usually following the cortical ribbon

NMSP Exam 1 (8 decks)

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