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1111 NEUROBIOLOGY > Neuropathology > Flashcards

Neuropathology Flashcards

1
Q

Neural tube defects - time

A

22-26 days

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2
Q

The most severe form of neural tube defect - complete failure of primary neurulation

A

Cranioraschisis totalis

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3
Q

failure of rostral neuropore to close

A

anencephaly

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4
Q

defect in skull with protrusion of the leptomeninges +/- brain…maintain epidermal covering over the cranial neural tube closure defect

A

encephalocele

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5
Q

failure of closure of the posterior neuropore - seen in chiari II

A

Myelomeningocele

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6
Q

How is the primitive streak formed?

A

cells of the caudal half of the epiblast thicken, converge in the midline to form the primitive streak

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7
Q

What happens at the cranial end of the primitive streak?

A

cranial end thickens to form the primitive (Hensen’s Node)

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8
Q

What forms in the middle of the primitive streak?

A

Primitive groove

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9
Q

When does the primitive streak form?

A

14-16 days

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10
Q

Gastrulation

A

formation of three germ layers

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11
Q

With regard to neurogenesis what happens during gastrulation?

A

cells from Hensen’s node begin migrating cranially toward the buccopharyngeal membrane (prochondral plate) FORMING THE NOTOCHORDAL process

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12
Q

Once the notochord is formed what happens around day 18?

A

Neural plate morphogenesis - neuroectoderm - wide end lies rostrally
bilateral symmetry
regionalization

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13
Q

what occurs during primary neurluation

A 
neural tube folds
- first folds occur caudally at 22 days 
- closure proceeds bidirectionally 
- not simple zipper
takes 4-6 days, keeps paces with somites
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14
Q

secondary neurulation

A

caudal cells mass coalesces and fuses with area where posterior neuropore has closed to form sacral spinal cord (s3)

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15
Q

Which neural tube defects are also associated wtih tethering of spinal cord?

A

myelomeningocele
lipomyelomeningocele
dermal sinus tract
spina bifita oculta

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16
Q

time-line anencephaly

A

23-25 days

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17
Q

site of final closure of anterior neuropore

A

commissural plate - which is immediately anterior to the lamina terinalis at the site of the future anteiror commissure

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18
Q

encepholocele distinguished from anencephaly?

A

have an epidermal covering over the cranial neural tube closure defect

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19
Q

myelomeningocele

A

failure of the posterior neuropore closure

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20
Q

time - myelomeningocele

A

25-27

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21
Q

a skin covered CSF filled mass that is continuous with the CSF in the spinal canal

A

meningocele

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22
Q

lipomyelomeningocele

A

lipoma extends from subcutaneous tissue to the dorsal aspect fo the corde and tethering the cord inferiorly

this process reflects a premature separation of the cutaneous ectoderm druing the process of neurulation that allows mesenchyme to enter the unclosed neural tube and differentiate into fat

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23
Q

dorsal dermal sinus tract

A

ectoderm lined tracts that can transgress the dura and allow communication between the skin and CSF - can also cause tethering

24
Q

spina bifita oculta

A

at L5-S1 common incidental fidning - failure of verterbral arch to encricle appropriately

25
Q

where is conus medullaris in typical newborn and where should it not be below in adult

A

L3
not below L2
Usually between L1-2

26
Q

Consequence of neural tube tethering

A

Common incontinence due to UMN issues

27
Q

caudal cerebellar tonsillar ectopia, below the foramen magnum, associated with chronic tonsillar herniation with syringomyelia

A

chiari I

28
Q

complex malformation - myelominigocele, hydrocephalus, hindbrain and spina abrnomalities

A

chiari II

29
Q

Which of the chiari malformations is associated with neural tueb closure defects

A

II

30
Q

Universal symptoms of chiari type II

A 
hydrocephalus
meningomyelocele
small posterior fossa with kinking of brainstem 
herniation of cerebellum - vermis
synonymous with Arnold-Chiari
31
Q

chiari type I can be associated with

A

syringomyelia

32
Q

What is syringomyelia?

A

low lying cerebellar tonsils in chiari I can obstruct the aperture that allows CSF to exit the canal of the spinal cord into the subarachnoid space - leading to accumulation of CSF within the central canal - the CSF filled cyst can break out of the central canal and dissect into substance of the cord

33
Q

When is the prosencephalon developing

A

peak period 2-3 months gestation

34
Q

How does prosencephalic development occur

A

by inductive interations between the notochord/prechordal mesoderm and forebrain. This occurs ventrally at the rostral end of the embryo - ventral induction

35
Q

what does prosencephalic induction effect?

A

face and brain

36
Q

3 cleavages in prosencephalic development occur at 5-6 weeks gestation

A

horizontally
transversely
sagitally

37
Q

when a single centricle that exists in teh early embryonic forebrain fails to form properly into two lateral ventricles and one third ventricle

A

holoprosencephaly

38
Q

no evidence of division of cerebral cortex

A

alobar holoprosencephaly - most severe

39
Q

only partial cleavage with the cerebral hemisphere fused at the frontal region only

A

semilobar -

40
Q

cerebral hemispheres are separated anteriorly and posterioly with modest fustion of structures

A

lobar holoprosencephaly -

41
Q

common cause of holoposencephaly

A

SHH gene mutations

42
Q

when does the external granular layer develo

A

12 weeks :)

43
Q

Embryology of cerebellum - what happens with the cerebellum and 4th ventricle?

A

in early gestation the small cerebellum is found on top of the very large 4th ventricle - in time the cerebellum grows caudally and completely enfolds the cavity of the 4th ventricle

44
Q

Key features of Dandy Walker Malformation

A 
enlarged posterior fossa
high tentorium 
hypoplasia or agenesis of vermis
cystic dilatation of 4th ventricle that fills the posterior fossa
hydrocephalus
45
Q

What type of migration do we see in the cortex?

A

radial migration

- successive waves of neurogenesis migration past previously born neurons - inside out pattern

46
Q

3 causes of malformations of cortical development

A

abnormal neural/glia proliferation

abnormal cortical migration

abnromal organization

47
Q

micro and macro cephaly are disorders of

A

abrnomal proliferation

48
Q

agyria (lissencephaly)
polymicrogyra
hetertopia
are disorders of

A

neuronal migration adn gyral formaiton

49
Q

proencephaly
hydraencephaly
schizencephaly
are disorders of

A

late destructive gestational lesions

50
Q

what is schizencephaly

A

dysplastic gray matter lined clefts extending from the ependymal lining of the lateral ventricles to the pial covering of the cortex

both genetic and acquired causes

51
Q

what are three causes of fine structural abnromalities of myelin or dentrictic branching

A

downs
malnutrition
metabolic disorders

52
Q

principle cause of stroke in children

A

genetic malformation of heart or blood vessels

53
Q

childhood stroke hemorrhagic vs ischemic

A

55% ischemic

54
Q

strok in perinatal period in term infants

A

Ulegyria (mushroom gyri) is a result of perinatal watershed infarcts with subsequent growth of non-damaged parts of gyri

55
Q

Stroke in perinatal period in preterm infants

A

germinal matrix hemorrhages (subependymal hemorrhages) are major cause of morbidity and mortality

GMH occurs in preterm infats less than 32-34 weeks

56
Q

risk factors for GMH

A

immaturity of lungs
hypercapnia
low birth weight
acidosis

1111 NEUROBIOLOGY (6 decks)

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