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Flashcards in Neuro Deck (229)
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1

Acute Neuronal Injury

  • changes secondary to hypoxia/ischemia cell necrosis or apoptosis.
  • intense cytoplasmic eosinophilia and nuclear pyknosis = red neurons

2

Subacute and Chronic Neuronal Injury

  • degeneration = neuronal death and reactive gliosis
  • trans-synpatic degeneration when afferent inputs to neuron are lost.

3

Axonal Reaction

  • response of neuronal cell body to challenge of regenerating damaged axons.  
  • cell body rounds up and nucleoli enlarge.
  • Nissl substance dispersal and perinuclear cytoplasmic pallor (central chromatolysis) = ↑ protein synthesis and axonal sprouting

4

Neuronal Inclusions

  • manifestation of aging (lipofuscin), disorders of metabolism (storage material), viral diseases (inclusion bodies), or neurodegenerative diseases with aggregated proteins.

5

Astrocytes

  • principal cells for repair and scar formation in brain.
  • important for blood brain barrier.
  • with CNS damage, get enlarged vesicular nuclei and conspicuous eosinophilic cytoplasm (gemistocytic astrocytes)
  • astrocyte hypertrophy and hyperplasia ⇒ gliosis
  • directly injured ⇒ rosenthal fibers, corpora amylacea, alzheimer type II astrocytes.
    • rosenthal fibers = elongated, eosinophilic structure in astrocyte processes containing alphaB-crystallin and hsp27.  see in long-standing gliosis or pilocytic astrocytomas.
    • corpora amylacea = lamellated polyglucosan bodies and hsp.  ↑ with age, are degenerative change.
    • Alzheimer type II astrocytes = enlarged nucleus with intranuclear glycogen and pale chromatin.  occurs with hyperammonemia.

6

Glial Cell Injury

  • oligodendroglial cell apoptosis feature of demyelinating disorders and leukodystrophies.
  • viral inclusions in progressive multifocal leukoencephalopathy
  • alpha-synuclein inclusions in multiple system atrophy (MSA)
  • ependymal cells don't regenerate.  damage ⇒ proliferation of subependymal astrocytes = ependymal granulations

7

Cerebral Edema

  • vasogenic = ↑ vascular permeability ⇒ accumulate intercellular fluid.
    • focal or generalized.
    • absence of lymphocytes impairs resorption.
  • cytotoxic = ↑ intracellular fluid 2° to endothelial, neuronal, or glial injury.
  • interstitial = fluid from ventricular system transudates across ependyal lining from ↑ intraventricular pressure.

8

Hydrocephalus

  • obstruction of CSF flow ⇒ ventricular enlargement and ↑ CSF volume
  • from impaired flow or resorption, overproduction uncommon.
  • occurs prior to cranial suture closure ⇒ enlarged head.
  • occurs after cranial suture closure ⇒ ventricular expansion and ↑ ICP
  • non-communicating = enlargement of a portion of the ventricle system.
  • communicating = entire system expanded
  • hydrocephalus ex vacuo = extensive tissue loss ⇒ compensatory expansion of entire CSF compartment

9

Subfalcine Herniation

  • aka cingulate herniation.
  • from ↑  ICP.
  • can compromise branches of anterior cerebral artery.

10

Transtentorial Herniation

  • aka uncinate, mesial temporal herniation.
  • distorts adjacent midbrain and pons.  
  • 3rd CN compromise ⇒ pupillary dilation
  • compression of posterior cerebral artery ⇒ ipsilateral hemiparesis
  • Duret hemorrhages = tearing of feeding vesels.

11

Tonsillar Herniation

  • through foramen magnun ⇒ compress medulla and compromise cardiac and respiratory centers.

12

Neural Tube Defects

  • primary failure to close or secondary reopening.
  • abnormalities in some combo of neural tissue, meninges, and ovelrying bone and soft tissues.
  • risk factors: folate deficiency.
  • antenatal diagnosis through alpha-fetoprotein screening.
  • encephalocele, anencephaly, spina bifida, myelomeningocele.

13

Encephalocele

  • malformed CNS diverticulum extending through defect in cranium (occiput or posterior fossa)

14

Anencephaly

  • malformation of anterior neural tube ⇒ failure of cerebrum development

15

Spina Bifida

  • occulta = asymptomatic bony defect
  • or a severe malformation with flattened, disorganized cord segment with overlying meningeal outpouching.

16

Myelomeningocele

  • CNS outpouching through vertebral column defect.
  • mostly lumbrosacral region with lower extremity motor and sensory deficits and disturbed bowel and bladder control.

17

Forebrain Anomalies

  • issues with brain size: microencephaly, lissencephaly, agyria, megalencephaly.
  • issues with gyral formation and organization: polymicrogyria, neuronal heterotopias, holoprosencephaly, agenesis of corpus callosum.

18

Microencephaly

  • small brain.
  • too many periventricular cells proliferate too soon.
  • from chromosomal abnormalities, fetal alcohol syndrome, in uter HIV.

19

Lissencephaly

  • aka agyria.
  • smooth brain, few to no gyri.
  • too many periventricular cells proliferate too soon.
  • from chromosomal abnormalities, fetal alcohol syndrome, in utero HIV.

20

Megalencephaly

  • large brain.
  • too few periventricular cells proliferate at early stages ⇒ overproduction of neurons.

21

Polymicrogyria

  • small, overabundant cerebral convolutions from focal injury near end of neuronal migration.

22

Neuronal Heterotopias

  • abnormal clusters of neurons in inappropriate locations along normal migratory routes.  
  • associated with epilepsy.
  • mutations in filamin A or microtubule associated proteins.

23

Holoprosencephaly

  • incomplete separation of cerebral hemispheres.  
  • midline facial abnormalities (cyclopia).
  • mutation of sonic hedgehog or other genes in neural development.

24

Agenesis of Corpus Callosum

  • normal white matter interhemispheric bundles not formed.
  • may have mental retardation but clinically most are normal.

25

Posterior Fossa Anomalies

  • Dandy-Walker Malformation
  • Arnold-Chiari Malformation 
  • Chiari I malformation

26

Dandy-Walker Malformation

  • enlarged posterior fossa, absent cerebellar vermis, large midline cyst with brainstem nuclei dysplasias.

27

Arnold-Chiari Malformation

  • aka Chiari II malformation
  • small posterior fossa, malformed midline cerebellum, extension of vermis through foramen magnum, hydrocephalus, lumbar myelomeningocele.

28

Chiari I Malformation

  • low-lying cerebellar tonsils extend into vertebral canal.
  • clinically silent but can present with CSF flow obstruction.

29

Syringomyelia

  • formation of cleftlike cavity in spinal cord.
  • morphology: gray and white matter destruction surrounded by reactive gliosis.
  • presentation: loss of pain and temperature sensation in upper extremities.

30

Hydromyelia

  • expansion of central canal.
  • morphology: gray and white matter destruction surroudned by reactive gliosis.
  • presentation: loss of pain and temperature sensation in upper extremities.