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NMSP 1 > Intro to Neuropathology > Flashcards

Intro to Neuropathology Flashcards

1
Q

True or False: neurons have a centrally-located nucleus

A

True; if it’s not in the center, look for inclusions that could indicate some kind of pathologic process

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2
Q

What type of cell looks like a “fried egg” on H and E stains?

A

-oligodendrocytes that produce the myelin; they are usually located right near neurons

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3
Q

What type of stain shows astrocytes well?

A

Glial Fibrillary Acidic Protein

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4
Q

What is the neuronal response to acute injury (12-24 hrs) such as hypoxia, hypoglycemia, and trauma?

A

“Red Neurons”

  • cell body shrinks
  • pyknosis (chromatin condenses)
  • loss of nucleolus, blurring of cellular features
  • loss of Nissl substance w/ intense eosinophilia
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5
Q

What is the neuronal response to subacute and chronic injury such as degeneration and progressive disease (ex: ALS, Alzheimer)?

A
  • -loss of functionally-related groups of neurons
  • -neuron death by apoptosis
  • -reactive gliosis (best indicator)
  • –hypertrophy and hyperplasia of astrocytes
  • –areas of gliosis are more firm to the touch
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6
Q

Describe axonal reaction, a change in the cell body during regeneration of the axon.

A
  • increased protein synthesis
  • enlarged and rounded cell body, enlarged nucleolus

-peripheral displacement of nucleus and Nissl substance (central chromatolysis)

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7
Q

What are some examples of intracytoplasmic neuronal inclusions?

A
  • -lipofuscin (wear and tear pigment, gold-ish)
  • -negri bodies in rabies (eosinophilic)
  • -neurofibrillary tangles in Alzheimer (teardrop shape)
  • -Lewy bodies in Parkinson
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8
Q

What are some examples of intranuclear neuronal inclusions?

A

–Cowdry bodies in HSV (acidophilic)

–CMV has basophilic owl’s eye nuclear inclusions as well as cytoplasmic inclusions

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9
Q

What is the most important histopathologic indicator of CNS injury?

A

Gliosis (hypertrophy and hyperplasia of astrocytes)

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10
Q

What is the role of astrocytes?

A
  • metabolic buffers and detoxifiers in the brain

- foot processes contribute to the blood brain barrier

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11
Q

Describe what happens to astrocytes in the process of gliosis.

A
  • nuclei enlarge and develop prominent nucleoli
  • nuclei become vesicular
  • cytoplasm expands and becomes bright pink
  • nuclei is displaced from the center of the cell
  • these types of cells are called gemistocytes
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12
Q

What are Alzheimer Type II Astrocytes that form during gliosis?

A
  • nucleus 2-3x larger
  • pale central chromatin
  • intranuclear glycogen droplet
  • prominent nuclear membrane and nucleolus
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13
Q

What types of diseases are commonly associated with Alzheimer Type II Astrocytes?

A
  • hyperammonemia (chronic liver dz)
  • Wilson Disease
  • hereditary metabolic disorders of the urea cycle
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14
Q

What is a craniopharyngioma?

A
  • -slow-growing tumor located above the sella turcica
  • -remnant of Rathke’s pouch
  • -contains keratin b/c it’s derived from epithelium
  • -children (5 to 15yrs), and adults > 65yrs
  • -hemorrhage, calcification, “machine oil” fluid cysts
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15
Q

What are Rosenthal Fibers?

A

–thick, elongated, eosinophilic, irregular structures that occur within astrocytic processes in areas of long-standing gliosis

–contain alphaB-crystalline and HSP27

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16
Q

What tumor is characteristically associated with Rosenthal Fibers?

A
  • pilocytic astrocytoma
  • -seen in younger people
  • also Alexander Disease
  • -leukodystrophy w/ mutation of gene encoding GFAP
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17
Q

What is Corpora Amylacea?

A
  • result of injury, increase w/ age and degeneration
  • PAS+ polyglucosan bodies
  • concentrically lamellated structures
  • subpial and perivascular locations
  • consist of glycosaminoglycan polymers and HSP’s
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18
Q

What are microglia?

A
  • -macrophages of the CNS, mesoderm-derived

- -surface markers CR3 and CD68 (

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19
Q

How do microglia respond to CNS injury?

A
  • proliferate
  • elongate their nuclei (rod cells in neurosyphilis)
  • microglial nodules (aggregate around foci of necrosis)
  • neuronophagia (congregate around dying neurons)
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20
Q

What are characteristics of oligodendrocytes in response to CNS injury and examples of diseases where oligodendrocytes are injured?

A

-apoptosis in acquired demyelinating disorders and leukodystrophies

  • PML (progressive multifocal leukoencephalopathy)
  • -viral intranuclear inclusions
  • MSA (multiple system atrophy)
  • -glial cytoplasmic inclusions of alpha-synuclein
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21
Q

How are ependymal cells (ciliated columnar cells that line the ventricles) affected by CNS injury?

A
  • subependymal astrocytes proliferate and cause ependymal granulations (small irregularities on the ventricular surface)
  • CMV causes viral inclusions in ependymal cells
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22
Q

In regards to cerebral edema, what is vasogenic edema?

A

–increased EXTRAcellular fluid (shift from intravascular compartment to intercellular spaces)

–due to blood-brain-barrier disruption and increased vascular permeability (ex: caused by ischemia - damaged vessel walls are leakier)

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23
Q

In regards to cerebral edema, what is cytotoxic edema?

A

-increased INTRAcellular fluid (secondary to cell membrane injury)

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24
Q

Why is excess extracellular fluid, as seen in vasogenic edema, difficult to resorb?

A

-there aren’t many lymphatics in the brain

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25
Q

What is the gross appearance of cerebral edema?

A
  • flattened gyri
  • narrow sulci
  • compressed ventricles
  • can lead to herniation
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26
Q

What is Hydrocephalus Ex Vacuo?

A
  • compensatory increase in ventricular volume due to a loss of brain parenchyma, but CSF pressure is normal
  • ventricles “inflate” to push the brain back out to decrease tension on subarachnoid bridging vessels
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27
Q

What are the physical changes in response to increased cerebral spinal fluid in the setting of hydrocephalus?

A
  • Papilledema (d/t increased intracranial pressure)
  • enlargement of the 3rd ventricle downward
  • stretching and perforation of the septum pellucidum
  • thinning of the cerebral mantle
  • elevation of the corpus callosum
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28
Q

What are possible obstructive causes of hydrocephalus?

A
  • blockage of the interventricular foramina d/t exudates, tumors, infection, hemorrhage or clots
  • congenital aqueduct stenosis or atresia of foramina
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29
Q

What is a possible cause of hydrocephalus due to overproduction of CSF?

A
  • choroid plexus papilloma (rare)
  • -has a thick fibrous core/stalk
  • -picture in the lecture looked like broccoli
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30
Q

Describe how pyogenic meningitis is an obstructive cause of hydrocephalus.

A
  • suppurative exudate covers the brainstem and cerebellum (most often seen in TB)
  • leptomeninges is thickened
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31
Q

What are congenital causes of hydrocephalus?

A
  • TORCH infections
  • AV malformations
  • Arnold Chiari malformations
  • Dandy Walker Syndrome
  • Cranial defects (achondroplasia, craniostenosis)
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32
Q

What are acquired causes of hydrocephalus?

A
  • meningitis, cysticercosis (T. solium), or brain abscesses
  • neoplasms (medulloblastoma, astrocytoma)
  • choroid plexus papilloma/carcinoma
  • sagittal sinus thrombus
  • hypervitaminosis A (softens skull, fontanelles bulge)
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33
Q

True or False: ventricles are enlarged symmetrically in communicating hydrocephalus.

A

True, the ventricular system is in communication with the subarachnoid space where absorption happens and the entire ventricular system is enlarged

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34
Q

What is Normal Pressure Hydrocephalus?

A
  • symmetric hydrocephalus in patients usually over the age of 60 that has developed slowly due to gradual blocking of the drainage of CSF; normally idiopathic
  • ventricles slowly enlarge so fluid pressure is normal
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35
Q

What are the symptoms of Normal Pressure Hydrocephalus?

A
  • dementia
  • gait disturbance (“magnetic gait”)
  • urinary incontinence

-“wet, wacky, wobbly” mnemonic

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36
Q

Is Normal Pressure Hydrocephalus reversible or irreversible?

A

Reversible

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37
Q

What is a subfalcine herniation?

A
  • when the cingulate gyrus is displaced below the falx

- aka “cingulate herniation”

38
Q

What is a transtentorial (aka uncinated or uncal) herniation?

A
  • when the medial aspect of the temporal lobe (the uncus on the parahippocampal gyrus) is compressed against the tentorium
  • CN3 defects (dilated pupil or impaired eye mvmt)
39
Q

What is a tonsillar herniation?

A

-when the cerebellar tonsils are displaced through the foramen magnum

–can be life-threatening d/t compression of the respiratory and cardiac centers

40
Q

What is Kernohan’s Notch Phenomenon?

A
  • when a transtentorial herniation is severe enough to push the cerebral peduncle to the opposite side and compress it, causing ipsilateral hemiparesis since the peduncle contains motor fibers that cross the body
  • a false localizing sign
41
Q

What are Duret Hemorrhages?

A

-when a transtentorial herniation progresses and causes hemorrhagic lesions in the midbrain and pons

–linear or flame-shaped lesions in the midline or paramedian, d/t distortion/tearing of vessels supplying upper brainstem

42
Q

What neurons are most sensitive to hypoxia?

A

-neurons in the pyramidal cell layer of the hippocampus, especially area C1 (aka Sommer Sector)

  • cerebellar Purkinje cells
  • pyramidal neurons in the cerebral cortex
43
Q

What type of necrosis occurs in the CNS?

A

Liquefactive Necrosis

  • denaturation of intracellular proteins
  • enzymes from the lysosomes of the dying cell digest it
  • tissue becomes a viscous mass
  • no architectural remains
44
Q

True or False: in regards to malformations and developmental disorders, the earlier the malformation occurs, the more severe the phenotype

A

True

45
Q

What is the most common type of malformation?

A
  • neural tube defects d/t folate deficiency

- neural tube normally closes by Day 28 of gestation

46
Q

What is spina bifida occulta?

A
  • neural tube defect that’s only a bony defect
  • asymptomatic
  • a dimple or a tuft of hair over the region may exist
47
Q

Describe the more severe presentation of spina bifida.

A
  • flattened, disorganized segment of spinal cord

- associated w/ an overlying meningeal pouch

48
Q

What is an encephalocele?

A

–diverticulum of disorganized BRAIN tissue extending through a cranial defect (usually posterior fossa)

–called a “nasal glioma” (kind-of a misnomer) when the tissue extends through the cribriform plate

49
Q

What is anencephaly?

A
  • malformation of the anterior end of the neural tube

- absence of most of the brain and calvarium d/t disruption of forebrain development around 28 days gestation

50
Q

What is the Area Cerebrovasculosa?

A
  • only thing present in anencephaly
  • flattened remnant of disorganized brain tissue admixed w/ ependymal, choroid plexus, and meningothelial cells (posterior fossa may be spared)
51
Q

What is Lissencephaly?

A
  • a forebrain anomaly
  • reduction in the number of gyri
  • agyria = NO gyri
52
Q

What is Microgyria?

A
  • small, unusually numerous, irregularly formed cerebral convolutions
  • grey matter has four or fewer layers w/ meningeal tissue trapped at points of fusion that would normally be cortical surface
53
Q

What is hydranencephaly?

A
  • brain defect where cerebral hemispheres are mostly absent, and the cranial cavity is filled with a cystic sac
  • only remnants of the basal ganglia and posterior lobe are present
54
Q

What is a dermal sinus?

A

-indentation or opening between the cutaneous ectoderm and the neuroectoderm, usually over lumbosacral region

55
Q

What is a meningocele?

A

-extrusion of the meninges through a defect in the vertebral column

56
Q

What is a myelomeningocele?

A
  • expansion of CNS tissue through a defect in the vertebral column; accompanied by motor and sensory deficits in the lower extremities, as well as disturbances in bowel and bladder control
  • often complicated by infections that extend into the spinal cord from the thin, overlying skin
57
Q

What is an Arnold-Chiari malformation?

A
  • small posterior fossa
  • misshapen midline cerebellum
  • extension of vermis through foramen magnum

-almost always includes hydrocephalus and lumbar myelomeningocele

58
Q

What causes forebrain anomalies?

A

-abnormalities in the generation and migration of neurons

59
Q

What are characteristics of microcephaly?

A

-decrease in the number of neurons in the neocortex, resulting in simplification of gyral folding

  • usually associated w/ small head circumference
  • more common than megalocephaly

-d/t chromosome abnormality, fetal alcohol syndrome, HIV-1 acquired in utero, Zika virus

60
Q

What are neuronal heterotopias?

A
  • group of disorders caused by the presence of collections of neurons in inappropriate locations along the path of migration
  • associated w/ epilepsy
61
Q

What are two examples of neuronal heterotopias?

A

–mutations in the gene for filamin A, an actin-binding protein (on X chromosome); lethal in males

-DCX gene mutation (on X chromosome); lissencephaly in males, subcortical band heterotopias in females

62
Q

What is holoprosencephaly?

A
  • incomplete separation of cerebral hemispheres
  • midline facial abnormality, causing cyclopia
  • can have arrhinencephaly, absent olfactory CN’s
  • associated w/ Trisomy 13
  • can be d/t mutations in SHH pathway
63
Q

What are the characteristics of agenesis of the corpus callosum?

A

-absence of the white matter bundles that carry cortical projections between hemispheres

  • “batwing deformity” of lateral ventricles
  • mental retardation common, but not always present
64
Q

What is Dandy Walker Malformation?

A
  • enlarged posterior fossa
  • expanded roofless 4th ventricle
  • absent or rudimentary cerebellar vermis
  • -instead, replaced by cyst w/ ependymal lining that is contiguous w/ the leptomeninges on its outer surface
65
Q

What is Joubert Syndrome?

A
  • hyperplasia of the cerebellar vermis
  • elongation of the cerebral peduncle
  • altered brainstem shape
  • “molar tooth sign” on imaging
66
Q

What is Syringomyelia?

A
  • -fluid-filled cavity in inner portion of spinal cord
  • -generally manifests in teens and 20’s

–classic symptom: cape-like distribution of pain and temperature sensation loss of upper extremities

67
Q

What is Hydromyelia?

A

–expansion of ependymal-lined central canal of the spinal cord; same symptoms as Syringomyelia

68
Q

What are the symptoms of Dandy Walker?

A
  • slow motor development; lack of muscle coordination
  • irritability
  • vomiting
  • convulsions; unsteadiness
  • bulging at the back of the skull; heart malformations
69
Q

What is Cerebral Palsy?

A
  • -non-progressive neurologic motor deficit
  • -attributed to prenatal and postnatal insults

–symptoms: spasticity, dystonia, ataxia, athetosis (abnormal muscle ctx causing writhing mvmts), paresis

70
Q

What are intraparenchymal hemorrhages?

A
  • seen in the germinal matrix of premies, near the junction b/w the thalamus and the caudate nucleus
  • can lead to hydrocephalus d/t subarachnoid hemorrhage if the hemorrhage spreads into ventricles
71
Q

What is periventricular leukomalacia?

A
  • infarct of supratentorial periventricular white matter
  • chalky yellow plaques, necrosis, calcification
  • occurs in premies
72
Q

What is multicystic encephalopathy?

A
  • when both grey and white matter are damaged due to severe ischemia
  • large destructive cystic lesions develop throughout the hemispheres
73
Q

What is ulegyria?

A
  • perinatal ischemic damage to the cerebral cortex
  • the depths of the sulci suffer the most
  • result in thinned, gliotic gyri
74
Q

Where are head impacts common during falls while conscious versus falls during a loss of consciousness?

A

Awake: occipital impact
LOC: frontal impact

75
Q

What is a diastatic fracture?

A

-fracture that crosses a suture

76
Q

True or False: subsequent skull fractures can cross previous fracture lines

A

False; later fractures do NOT extend across previous fracture lines

77
Q

What is a displaced/depressed skull fracture?

A

-fracture where the bone is displaced into the cranial cavity by a distance greater than the thickness of the bone

78
Q

What are the characteristics of a basilar skull fracture?

A
  • orbital and/or mastoid hematomas
  • CSF drainage from the nose or ear
  • “raccoon” eyes
79
Q

What is a TBI?

A

-damage to brain resulting from external mechanical force

  • diminished/altered state of consciousness
  • temporary or permanent impairment of brain function
80
Q

True or False: head injury and TBI are synonymous

A

False

81
Q

What is Chronic Traumatic Encephalopathy?

A
  • brain disease linked with repeated blows to the head
  • can only be Dx by examining postmortem brain
  • progressive loss of normal brain matter
  • abnormal buildup of tau protein
  • combat veterans and contact sports athletes at risk
82
Q

What are symptoms of Chronic Traumatic Encephalopathy?

A
  • behavioral and mood changes
  • memory loss
  • cognitive impairment
  • dementia
83
Q

What is a coup contusion?

A

-contusion at the point of impact

84
Q

What is a contrecoup contusion?

A
  • diametrically opposed contusion from point of injury
  • occurs when the head is mobile at the time of injury
  • occurs during sudden deceleration
85
Q

What is Plaque Jaune?

A
  • old traumatic lesions
  • depressed, yellow patches on gyral crests
  • can become epileptic foci
  • most common at sites of contrecoup injuries
  • -inferior frontal cortex, temporal and occipital poles
86
Q

What are the characteristics of Diffuse Axonal Injury?

A
  • axonal swelling and focal hemorrhagic lesions
  • can occur d/t angular acceleration alone, w/o impact

-best seen with silver stain, or amyloid precursor protein and alpha synuclein immunostains

87
Q

True or False: about half of post-trauma coma patients have diffuse axonal injury, even w/o cerebral contusions

A

True

88
Q

What types of injuries might appear in a shaken baby?

A
  • diffuse axonal injury
  • cerebral edema
  • subdural hematomas (venous)
  • retinal hemorrhages
  • sometimes microscopic iron from old bleeding
89
Q

What are characteristics of trauma to the epidural space?

A
  • usually associated w/ a skull fracture in adults
  • rapid neurologic symptoms
  • arterial blood
90
Q

What are the characteristics of trauma to the subdural space?

A
  • level of trauma may be only mild
  • slow neurologic symptoms, often delayed from injury
  • venous blood
91
Q

What are characteristics of trauma to the subarachnoid space?

A
  • sudden onset of severe headache
  • rapid neurologic deterioration
  • secondary injury may arise d/t vasospasm
92
Q

What is the artery most commonly insulted in the brain?

A

-middle meningeal artery

NMSP 1 (9 decks)

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