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NMSP Exam 1 > Intro to Neuropathology > Flashcards

Intro to Neuropathology Flashcards

1
Q

Why is gliosis important?

A
  • Histopathologic indicator of CNS injury
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2
Q

What is gliosis characterized by?

A
  • Hypertrophy and hyperplasia of astrocytes (astrocytes act as a metabolic buffer and detoxifer)
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3
Q

How do gemistocytes differ from dead red neurons?

A
  • Gemistocytes have a nucleus whereas dead red neurons do not
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4
Q

What are rosenthal fibers?

A
  • Thick, elongated, brightly eosinophilic, irregular structures occurring within astrocytic processes
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5
Q

What do rosenthal fibers contain?

A
  • Heat shock proteins( alpha-beta crystalline and HSP27)

- Ubiquitin

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6
Q

Where are rosenthal fibers typically seen?

A
  • In areas of long standing gliosis
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7
Q

What is corpora amylacea?

A
  • Polygucosan bodies
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8
Q

What stain is used for corpora amylacea?

A
  • PAS
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9
Q

What does corpora amylacea look like?

A
  • Round, faintly basophilic

- Concentrically laminated strictures located adjacent to astrocytic end processes (resembles onion skinning)

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10
Q

What does corpora amylacea contain?

A
  • Glycosaminoglycan polymers
  • Heat shock proteins
  • Ubiquitin
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11
Q

What is a correlation with corpora amylacea?

A
  • Increased with age (represents degenerative change)
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12
Q

What do rosenthal fibers look like?

A
  • Beaded sausage to cork-screw shaped hyaline bodies of variable size
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13
Q

What is the job of microglia?

A
  • Macrophages of the CNS
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14
Q

What surface markers are seen with microglia?

A
  • CR3

- CD68

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15
Q

What are microglial nodules?

A
  • When microglia aggregate around small foci of necrosi
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16
Q

What is neuronophagia?

A
  • Microglia concregate around cell bodies of dying neurons
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17
Q

What are ependymal granulations?

A
  • Small irregularities on ventricular surfaces

- Disruption of ependymal lining and proliferation of subependymal astrocytes

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18
Q

What is vasogenic edema?

A
  • Increased extracellular fluid due to BBB disruption and increased vascular permeability
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19
Q

What are some causes of vasogenic edema?

A
  • Fluid shift from intravascular compartment to intercellular spaces
  • Paucity of lymphatics impairs resorption of excess extracellular fluid
  • Localized or generalized injury
  • Often follows ischemic injury
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20
Q

What is cytotoxic edema?

A
  • Increased intracellular fluid secondary to neuronal, glial, or endothelial cell membrane injury
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21
Q

What are some causes of hydrocephalus?

A
  • Increased production –> choroid plexus papilloma
  • Obstruction –> interventricular foramina, congenital, or secondary
  • Decreased absorption –> outflow obstruction
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22
Q

What is an external sign of hydrocephalus?

A
  • Papilledema
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23
Q

What does a choroid plexus papilloma look like?

A
  • Broccoli stalk
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24
Q

What is pyogenic meningitis?

A
  • Suppurative exudate covering brainstem and cerebellum
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25
Q

How can pyogenic meningitis cause hydrocephalus?

A
  • Thickened leptomeninges
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26
Q

What should you think when you see pyogenic meningitis covering the base of the brain?

A
  • TB or neurosyphilis
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27
Q

What are some congenital causes of hydrocephalus?

A
  • Intrauterine infections (TORCH)
  • Agenesis/atresia/stenosis
  • AV malformation
  • Arnold chiari malformation
  • Dandy-Walker syndrome
  • Cranial Defects
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28
Q

What are some acquired causes of hydrocephalus?

A
  • Infections
  • Mass lesions
  • Inflammation
  • Post hemorrhage
  • Choroid plexus papilloma
  • Sagittal sinus thrombosis
  • Hypervitaminosis A
  • Idiopathic
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29
Q

What is communicating hydrocephalus?

A
  • CSF is not absorbed properly at the dural sinus level

- Ventricles tend to be symmetrically dilated

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30
Q

How does aqueductal stenosis cause hydrocephalus?

A
  • Aqueduct is 1/3 the size of normal so it reduces the flow significantly
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31
Q

What is seen in hydrocephalus ex-vacuo?

A
  • Dilation of the ventricles
  • Shrinkage of brain substance
  • CSF pressure is normal (makes it different)`
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32
Q

What are some causes of the shrinkage of brain substance in hydrocephalus ex-vacuo?

A
  • Atrophy with increasing age
  • Stroke or other injury
  • Chronic neurodegenerative (huntington dz or Alz)
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33
Q

What is normal pressure hydrocephalus?

A
  • Symmetric type of hydrocephalus that usually occurs in patients older than 60
  • Develops slowly
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34
Q

What is normal pressure hydrocephalus typically confused with?

A
  • Alzheimers or Parkinson
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35
Q

What are the classic symptoms of normal pressure hydrocephalus?

A
  • Wet –> Urinary incontinence
  • Wacky –> Dementia
  • Wobbly –> Gait disturbances
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36
Q

What generally causes increased cranial pressure?

A
  • Generalized brain edema
  • Expanding mass lesion
  • Increased CSF volume
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37
Q

What is herniation?

A
  • Increased pressure beyond the compensatory ability of venous system to compress and displacement of CSF
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38
Q

What are some types of herniation?

A
  • Subfalcine
  • Transtentorial
  • Tonsillar
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39
Q

What is a subfalcine herniation?

A
  • Cingulate gyrus displaced under the falx
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40
Q

What is a transtentorial herniation?

A
  • Medial aspect of the temporal lobe compressed against the tentorium
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41
Q

What signs may be seen in a transtentorial herniation?

A
  • CN3 –> dilated pupil and impaired eye movement
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42
Q

What is a tonsillar herniation?

A
  • Cerebellar tonsils displaced through the foramen magnum
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43
Q

Why is a tonsillar herniation life threatening?

A
  • Respiratory and cardiac centers are compressed
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44
Q

What are some signs of increased intracranial pressure?

A
  • Headache, change in behavior, N/V
  • Change in pupil reaction
  • False localizing signs
  • Seizures
  • Decreased coordination, ataxia
  • Papilledema
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45
Q

What causes Kernohan’s notch phenomenon?

A
  • Compression of the cerebral peduncle against the tentorium cerebelli due to transtentorial herniation
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46
Q

What is seen in Kernohan’s notch phenomenon?

A
  • Ipsilateral hemiparesis or hemiplegia (on side of herniation)
  • Caused by compression of the contralateral peduncle
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47
Q

What is special about Kernohan’s notch phenomenon?

A
  • As it progresses, it may compress the other side against kernohan’s notch (cerebral peduncle and CNIII) causing ipsilateral weakness, contralateral dilated pupil (relative to original herniation)
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48
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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49
Q

What causes a duret hemorrhage?

A
  • Mass effect displaces the brain downward causing a disruption of the vessels that enter the pons along the midline, leading to hemorrhage
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50
Q

What kind of necrosis does the brain go through?

A
  • Liquefactive (no architecture remains)
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51
Q

What is the progression seen in cerebral infarcts?

A
  • First red dead neurons will show up
  • Around day 10, foamy macrophages are seen
  • Then there is tissue loss and gliosis
52
Q

What is a hygroma?

A
  • Separation of arachnoid from dura due to contraction of underlying brain parenchyma
53
Q

What accounts for most CNS malformations?

A
  • Neural tube defects
54
Q

What may be a big cause to neural tube defects?

A
  • Folate deficiency
55
Q

What is spina bifida occulta?

A
  • Asymptomatic, bony defect

- Flattened disorganized segment of cord associated with meningeal pouch

56
Q

What is a myelomeningocele?

A
  • Extension of CNS tissue through a defect in vertebral column (lumbosacral most common)
57
Q

What is a meningocele?

A
  • Only meninges protrude
58
Q

What symptoms are seen in a myelomeningocele?

A
  • Motor and sensory deficits of LE
  • Bowel and bladder control
  • Superimposed infections (through thin coverings of cord)
59
Q

What is an encephalocele?

A
  • Diverticulum of disorganized brain tissue extending through defect in cranium (usually posterior fossa)
60
Q

What is a nasal glioma?

A
  • Misnomer for extension of brain tissue through cribiform plate
61
Q

What is anencephaly?

A
  • Absence of most of the brain and calvarium

- Forebrain development disrupted at around 28 days GA

62
Q

What are some defects in neural tube formation in the first trimester?

A
  • Anencephaly
  • Encephalocele
  • Holoprosencephaly
63
Q

What are some defects of neuronal proliferation in the second trimester?

A
  • Microcephaly
  • Megalencephaly
  • Lissencephaly
  • Agenesis of corpus callosum
64
Q

What are some major causes of microcephaly?

A
  • Chromosome abnormalities
  • Fetal alcohol syndrome
  • HIV-1 acquired in utero
  • maybe Zike virus
65
Q

What is lissenencephaly?

A
  • Decreased number of gyri

- Brain looks smooth or has a cobblestone surface

66
Q

What is polymicrogyria?

A
  • Small, usually numerous, irregularly formed convolutions
67
Q

What is neuronal heterotopias associated with?

A
  • Epilepsy
68
Q

What are neuronal heterotopias?

A
  • Collections of neurons in inappropriate places along the pathway of migration
69
Q

What genes are implicated in neuronal heterotopias?

A
  • X chromosome (filamin A and DCX)

- Lissencephaly in males and subcortical band heterotopias in females

70
Q

What is holoprosencephaly?

A
  • Incomplete separation of cerebral hemispheres across midline
71
Q

What does someone look like with holoprosencephaly?

A
  • Cyclopia

- Arhinencephaly –> absence of olfactory cranial nerves

72
Q

What pathway causes holoprosencephaly?

A
  • SHH
73
Q

What genetic abnormality is most likely seen with holoprosencephaly?

A
  • Trisomy 13
74
Q

What does agenesis of the corpus callosum look like?

A
  • Bat wing on CT
75
Q

What is seen in Chiari type 2?

A
  • More severe, misshapen midline cerebellum with downward extension of vermis through foramen magnum
76
Q

What is associated with Chiari type 2?

A
  • Hydrocephalus

- Lumbar myelomeningeocele

77
Q

What is seen in Chiari type 1?

A
  • Low-lying cerebellar tonsils extend down vertebral canal
78
Q

How does Chiari type 1 present?

A
  • May be silent and show up incidentally

- May have headache or migraine due to CSF flow impairment

79
Q

What is seen in Dandy-Walker malformation?

A
  • Enlarged posterior fossa
  • Expanded roofless fourth ventricle
  • Cerebellar vermis absent or rudimentary
80
Q

What replaces the vermis in Dandy-Walker malformation?

A
  • Cyst with ependymal lining that is contiguous with leptomeninges on its outer surface
81
Q

What is Joubert syndrome?

A
  • Hypoplasia of vermis
  • Elongation of cerebellar peduncles
  • Altered brainstem shape
82
Q

How does Joubert syndrome look on scans?

A
  • “Molar tooth sign”
83
Q

What is syringomyelia (or syrinx)?

A
  • Fluid filled cleft like cavity in the inner portion of the cord
84
Q

What are the classic symptoms of syrinx?

A
  • Isolated loss of pain and temperature sensation in UE (cape like distribution)
85
Q

How is a syrinx treated?

A
  • Inserting a shunt to help drain the fluid OR

- Removing some of the bone (either from vertebrae or base of skull depending on the location of the syrinx)

86
Q

What is cerebral palsy?

A
  • Non-progressive neurologic motor deficit attributable to insults occurring during the prenatal and perinatal period
87
Q

What does cerebral palsy look like?

A
  • Spasticity
  • Dystonia
  • Ataxia/athetosis
  • Pareis
88
Q

Where does an intraparenchymal hemorrhage occur?

A
  • Seen in germinal matrix of premature infants

- Junction between thalamus and caudate nucleus

89
Q

When does an intraparenchymal hemorrhage occur?

A
  • Usually a few hours after birth but can occur at any time
90
Q

What is periventricular leukomalacia?

A
  • Infarcts in supratentorial white matter
91
Q

What does periventricular leukomalacia look like?

A
  • Chalky yellow plaques due to necrosis and calcification
92
Q

What is multicystic encephalopathy?

A
  • Extensive ischemic damage of both white and gray matter –> large destructive cystic lesions
93
Q

What is ulegyria?

A
  • Perinatal ischemic lesions in the depths of sulci

- Causes thinned out gliotic gyri

94
Q

How do people fall when awake vs loss of consciousness?

A
  • Awake: Fall backward onto occipital

- LOC: Fall forward onto frontal

95
Q

What is a diastatic fracture?

A
  • Fracture that crosses a suture
96
Q

Why is the timing of fractures important?

A
  • New fractures lines do not extend across previous fracture lines
97
Q

What are some signs of a basal skull fracture?

A
  • Orbital or mastoid hematoma

- Otorrhea/rhinorrhea –> CSF drainage

98
Q

What could battle sign or raccoon eyes help point to?

A
  • Basilar skull fracture
99
Q

What is a concussion?

A
  • Clinical syndrome

- Altered consciousness secondary to head injury

100
Q

What are some direct parenchymal injuries?

A
  • Contusions (blunt trauma)

- Lacerations (penetrations or tearing of the tissue)

101
Q

What are the most common locations for direct parenchymal injuries?

A
  • Frontal lobes/orbital ridges and temporal lobes
  • Regions of the brain that overlie rough and irregular inner skill surface
  • Crests of gyri are most susceptible where direct force is greatest
102
Q

What does a contusion look like grossly?

A
  • Wedge shaped –> Broad at point of impacts
103
Q

What is a coup?

A
  • Contusion at point of impact
104
Q

What is a contrecoup?

A
  • Diametrically opposed to coup

- Contusion opposite point of impact due to rebound

105
Q

What are plaque jaune?

A
  • Depressed, retracted, yellowish brown patches involving crests of gyri
106
Q

What causes plaque jaune?

A
  • Old trauma lesions –> often countercoup inferior frontal cortex, temporal and occipital lobes
107
Q

What is diffuse axonal injury?

A
  • Axonal swelling +/- focal hemorrhagic lesions
108
Q

When does diffuse axonal injury present?

A
  • Typically within hours and will persist much longer
109
Q

What stain is used to help identify diffuse axonal injury?

A
  • Silver stain
  • Amyloid precursor protein (APP)
  • Alpha synuclein immunostains
110
Q

What can cause diffuse axonal injury?

A
  • Direct action of mechanical forces

- Angular acceleration alone can produce even in the absence of impact

111
Q

Why is shaking a baby bad?

A
  • Brains are very soft and not fully developed

- Shaking them causes brain damage but does not kill them

112
Q

How does several occasions of shaking a baby kill them?

A
  • Is like second concussion syndrome

- Don’t die instantly but after hours of brain swelling and DAI

113
Q

How is shaken impact syndrome recognized?

A
  • DAI/Cerebral edema
  • Subdural hematomas
  • Retinal hemorrhages
  • Sometimes, subgaleal hemorrhages
  • Sometimes, microscopic iron
114
Q

What is post-traumatic hydrocephalus?

A
  • Obstruction of CSF resorption due to hemorrhage in subarachnoid space
115
Q

What is chronic traumatic encephalopathy?

A
  • Dementing illness developed from repeated head trauma?
116
Q

What is seen in CTE?

A
  • Atrophy
  • Enlarged ventricles
  • Tau neurofibrillary tangles involving gyral depths
  • Perivascular regions in frontal and temporal lobes (characteristic pattern)
117
Q

What is a traumatic brain injury (TBI)? What is it associated with?

A
  • Some level of damage to the brain due to external mechanical force
  • Generally associated with diminished or altered state of consciousness
118
Q

What are some major features of CTE?

A
  • Neurofibrillary tangles/amyloid and tau depositions (similar to Alzheimer’s)
  • Depigmentation of substantia nigra (similar to parkinsons)
119
Q

What kind of paresis is seen in a spinal cord injury in the thoracic region?

A
  • Paraplegia (just legs)
120
Q

What kind of paresis is seen in a spinal cord injury in the cervical region?

A
  • Quadriplegia (all limbs)
121
Q

What kind of paresis is seen in a spinal cord injury in C4 or above?

A
  • Respiratory compromise and paralysis of diaphragm
122
Q

What do acute lesions of the spinal cord look like?

A
  • Hemorrhage
  • Necrosis
  • Axonal swelling
123
Q

What do chronic lesions of the spinal cord look like?

A
  • Central areas become cystic and gliotic
124
Q

What is the most likely cause of an epidural hematoma?

A
  • Rupture of the meningeal artery –> usually due to skull fracture
125
Q

What is the most likely cause of a subdural hematoma?

A
  • Rupture of bridging veins between the brain and superior sagittal sinus

NMSP Exam 1 (12 decks)

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